THE HEALTH

CONSEQUENCES

OF SMOKING
FOR WOMEN

a report of the Surgeon General

u
ne DEPARTMENT OF HEALTH AND HUMAN SERVICES
as Health Service
One of the Assistant Secretary for Health
‘ce On Smoking and Health

ree
THE SECRETARY OF HEALTH, EODUCATION, AND WELFARE

WASHINGTON. D.C.20201

 

The Honorable Thomas P. O'Neill,Jr.
Speaker of the House of Representatives
Washington, D.C. 20515

Dear Mr. Speaker:

I hereby submit the 12th annual report that the
Department of Health, Education, and Welfare (DHEW) has
prepared for Congress as required by the Public Health
Cigarette Smoking Act of 1969, Public Law 91-222, and its
predecessor, the Federal Cigarette Labeling and Advertising
Act. This report is one of the most alarming in the series.

It clearly establishes that women smokers face the same
risks as men smokers of lung cancer, heart disease, lung
disease and other consequences. Perhaps more disheartening
is the harm which mothers' smoking causes to their unborn
babies and infants.

The report is not all bad news. It presents recent
data showing that women are turning away from smoking in
response to the warnings of government, voluntary agencies
and physicians, The precipitate rise in women's deaths from
lung cancer and chronic lung disease demand that this trend
away from cigarettes be accelerated. Our scientists expect
that by 1983, the lung cancer death rate will exceed that of
any other type of cancer among women,

Citizens of our free society may decide for themselves
whether to smoke cigarettes. The health consequences of
this decision make it imperative for their government to
assure that the decision is an informed one. This series
Of reports is one way in which DHEW is striving to meet
this critical responsibility.

Neer

Patricia Roberts Harris
PREFACE

This report is more than a factual review of the health conse-
quences of smoking for women. It is a document which chal-
lenges our society and, in particular, our medical and public
health communities.

This report points out that the first signs of an epidemic of
smoking-related disease among women are now appearing. Be-
cause women’s cigarette use did not become widespread until
the onset of World War II, those women with the greatest inten-
sity of smoking are now only in their thirties, forties, and fifties.
As these women grow older, and continue to smoke, their bur-
den of smoking-related disease will grow larger. Cigarette smok-
ing now contributes to one-fifth of the newly diagnosed cases of
cancer and one-quarter of all cancer deaths among women—
more cancer and more cancer deaths among women than can be
attributed to any other known agent. Within three years, the
lung cancer death rate is expected to surpass that for breast
cancer. A similar epidemic of chronic obstructive lung disease
among women has also begun.

Four main themes emerge from this report to guide future
public health efforts.

First, women are not immune to the damaging effects of
smoking already documented for men. The apparently lower
susceptibility to smoking-related diseases among women smok-
ers is an illusion reflecting the fact that women lagged one-
quarter century behind men in their widespread use of cigar-
ettes.

Second, cigarette smoking is a major threat to the outcome of
pregnancy and well-being of the newborn baby.

Third, women may not start smoking, continue to smoke, quit
smoking, or fail to quit smoking for precisely the same reasons
as men. Unless future research clarifies these differences, we
will find it difficult to prevent initiation or to promote cessation
of cigarette smoking among women.

Fourth, the reduction of cigarette smoking is the keystone in
our nation’s long term strategy to promote a healthy lifestyle
for women and men of all races and ethnic groups.

The Fallacy of Women’s Immunity

All of the major prospective studies of smoking and mortality
have reached consistent conclusions. Death rates from coronary
heart disease, chronic lung disease, lung cancer, and overall
mortality rates are significantly increased among both women
and men smokers. These risks increase with the amount
smoked, duration of smoking, depth of inhalation, and the “tar”

Vv
and nicotine delivery of the cigarette smoked.

In these studies, conducted during the past three decades,
relative mortality risks among female smokers appeared to be
less than those of male smokers. It is now clear, however, that
these studies were comparing the death rates of a generation of
established, lifelong male smokers with a generation of women
who had not yet taken up smoking with full intensity. Even
those older women who reported smoking a large number of
cigarettes per day had not smoked cigarettes in the same way as
their male counterparts. Now that the cigarette smoking char-
acteristics of women and men are becoming increasingly simi-
lar, their relative risks of smoking-related illness will become
increasingly similar.

This fallacy of women’s apparent immunity is clearly illus-
trated by differences in the timing of the growth in lung cancer
among men and women in this century. Lung cancer deaths
among males began to increase during the 1930s, as those men
who had converted from other forms of tobacco to cigarette
smoking before the turn of the century gradually accumulated
decades of inhaled tobacco exposure. By the time of the first
retrospective studies of smoking and lung cancer in 1950, two
entire generations of men had already become lifelong cigarette
smokers. Relatively few women from these generations smoked
cigarettes, and even fewer had smoked cigarettes since their
adolescence. Those young women who had taken up smoking
intensively during World War II were only in their twenties and
thirties. In 1950, women accounted for less than one in twelve
deaths from lung cancer.

Thereafter, the age adjusted lung cancer death rate among
women accelerated, and the male predominance in lung cancer
declined. Lung cancer surpassed uterine cervical cancer as a
cause of death in women. By 1968, as the findings of many large
population prospective studies were being published, women
accounted for one-sixth of all lung cancer deaths. These studies
found that women cigarette smokers had 2.5 to 5 times greater
death rates from lung cancer than women nonsmokers. By 1979,
women accounted for fully one-fourth of all lung cancer deaths.
Over the next few years, women cigarette smokers’ risk of lung
cancer death will approach 8 to 12 times that of women
nonsmokers, the same relative risk as that of men.

Lung cancer has four main histological types: epidermoid,
small cell, adenocarcinoma, and large cell carcinoma, As several
studies have shown, the incidence of each of these types of lung
cancer displays a clear relationship to cigarette smoking among
both men and women. Epidermoid and small cell lung cancer
appear to be more prominent among men, while adenocar-

vl
cinoma of the lung now appears to be more prominent among
women.

The recent acceleration of lung cancer incidence among
women has in fact been more rapid than the corresponding
growth of lung cancer among men in the 1930s. Again, this dif-
ference in the initial rate of acceleration of lung cancer inci-
dence does not refute the demonstrated causal relation between
cigarette smoking and lung cancer among both sexes. Instead,
differences in the rate of increase of lung cancer incidence may
reflect changes in the carcinogenic properties of cigarette
smoke, the style of cigarette smoking, or the interaction of
cigarette smoking with other environmental hazards. It is
noteworthy that those men who died of lung cancer in the 1930s
came from a generation that had gradually converted to
cigarettes from other, non-inhaled forms of tobacco. By con-
trast, the first regular tobacco users among women were almost
exclusively cigarette smokers.

The 1979 Report on Smoking and Health documented numer-
ous instances where cigarette smoking adds to the hazards of
the workplace environment among men. Among women, this
report reveals two such occupational exposures— asbestos and
cotton dust— which have been clearly demonstrated to interact
with cigarette smoking. The fact that evidence is limited among
women does not imply that women are protected from the
dangerous interactions of smoking and occupational exposures.

Pregnancy, Infant Health, and Reproduction

Scientific studies encompassing various races and ethnic
groups, cultures and countries, involving hundreds of
thousands of pregnancies, have shown that cigarette smoking
during pregnancy significantly affects the unborn fetus and the
newborn baby. These damaging effects have been repeatedly
shown to operate independently of all other factors that influ-
ence the outcome of pregnancy. The effects are increased by
heavier smoking and are reduced if a woman stops smoking
during pregnancy.

Numerous toxic substances in cigarette smoke, such as
nicotine and hydrogen cyanide, cross the placenta to affect the
fetus directly. The carbon monoxide from cigarette smoke is
transported into the fetal blood and deprives the growing baby
of oxygen. Fetal growth is directly retarded. The resulting re-
duction in fetal weight and size has many unfortunate conse-
quences. Women who smoke cigarettes during pregnancy have
more spontaneous abortions, and a greater incidence of bleed-
ing during pregnancy, premature and prolonged rupture of am-

vil
niotic membranes, abruptio placentae and placenta previa.
Women who smoke cigarettes during pregnancy have more fetal
and neonatal deaths than nonsmoking pregnant women. A rela-
tion between maternal smoking and Sudden Infant Death Syn-
drome has now been established.

The direct harmful effects of smoking on the fetus have long
term consequences. Children of mothers who smoked during
pregnancy lag measurably in physical growth; there may also
be effects on behavior and cognitive development. The extent
of these deficiencies increases with the number of cigaret-
tes smoked.

The damaging effects of maternal smoking on infants are not
restricted to pregnancy. Nicotine, a known poison, is found in
the breast milk of smoking mothers. Children whose parents
smoke cigarettes have more respiratory infections and more
hospitalizations in the first year of life.

Women who smoke cigarettes have more than three times the
risk of dying of stroke due to subarachnoid hemorrhage, and as
much as two times the risk of dying of heart attack in compari-
son to nonsmoking women. The use of oral contraceptives in
addition to smoking, however, causes a markedly increased risk,
including a 22-fold increase in the risk of subarachnoid hemor-
rhagic stroke and a 20-fold increase in heart attack in heavy
smokers.

Why Do Women Smoke?

Cigarette consumption in this country is now declining. An-
nual per capita consumption has decreased from 4,258 in 1965 to
an estimated 3,900 in 1979. From 1965 to 1979, the proportion of
adult male cigarette smokers declined from 51 to 37 percent. Not
only have millions of men quit smoking, but the rate of initia-
tion of smoking among adolescent males has now slowed.

From 1965 to 1976, the proportion of adult women cigarette
smokers remained virtually unchanged at 32 to 33 percent.
Since 1976, however, the proportion of adult women cigarette
smokers appears to have declined to 28 percent. Although adult
women are now beginning to quit smoking at rates comparable
to adult men, the rate of initiation of smoking among younger
women has not declined.

This report documents numerous differences by sex in the
perceived role of cigarette smoking, in attitudes toward health
and lifestyle, and in methods of coping with stress, anger, and
boredom. Yet the significance of these differences, and their
relation to differences in smoking patterns, remains poorly un-
derstood.

vill
Although it is frequently observed that women in organized
smoking cessation programs have more severe withdrawal
symptoms and lower rates of successful quitting than men,
these observations have not been systematically confirmed for
the general population. In the past, women may have attempted
to quit or succeeded in quitting smoking less frequently than
men. The recent decline in the proportion of women smokers,
however, suggests that women’s attempted and successful quit-
ting rates have now increased.

Although weight gain is a frequently cited consequence of
quitting smoking, the association of weight gain with cessation
of smoking has not been the subject of sufficient scrutiny. Con-
trolled studies with careful measurement on representative
populations of women do not exist. The impact of the fear of
weight gain after quitting has not been adequately examined. If
weight gain does result from cessation of smoking, its exact
mechanism must be determined.

Even more problematic are marked differences by sex in the
distribution of smoking prevalence by occupation. Men with ad-
vanced education and professional occupations have taken the
lead in quitting smoking, but women in administrative and
managerial positions have relatively high smoking prevalence
rates. Although 20 percent or fewer male physicians smoke, the
proportions of cigarette smokers among women health profes-
sionals, especially nurses and psychologists, remain disturb-
ingly high.

Recent changes in smoking prevalence among black women
and men have paralleled those of the general population. From
1965 to 1979, the proportion of black women cigarette smokers
declined from 34 to 29 percent, while the proportion of black men
smokers declined from 61 to 42 percent. However, differences by
race in the onset, maintenance, and cessation of smoking have
not been adequately explored. Little is known about cigarette
smoking among other ethnic and minority groups.

Adolescent Smoking

The health consequences of smoking evolve over a lifetime.
Evidence continues to accumulate, for example, that cigarette
smoking produces measurable lung changes in adolescence and
young adulthood. Young cigarette smokers of both sexes show
more evidence of small airway dysfunction, and a higher preva-
lence of cough, wheezing, phlegm production, and other respira-
tory symptoms. The health damage due to cigarette smoking
increases when an individual begins regular smoking earlier in
life. Yet, as this report documents, the average age of onset of

ix
regular smoking among women has continuously declined dur-
ing the last 50 years, and continues to decline.

According to a recent survey by the National Institute of
Education, cigarette smoking among adolescent girls now ex-
ceeds that among adolescent boys. In the 17-19 year age group,
there are almost 5 female cigarette smokers for every 4 male
cigarette smokers. The causes of this inversion are far from
clear. We do not yet understand the signal events in the initia-
tion of smoking among young women. It is possible that parents
set examples concerning lifestyle, health attitude, and risk-
taking much earlier in childhood. The beginning of junior high
school or entrance into the work force may be equally critical
events. We do not know enough about an adolescent’s sense of
competence and self-mastery, and how these roles differ among
women and men. Although smoking patterns among girls corre-
late with parental, peer and sibling smoking habits, educational
level, type of school curriculum, academic performance,
socioeconomic status, and other forms of substance abuse, the
practical significance of these empirical correlations is unclear.

Women and the Changing Cigarette

As this report documents, the proportion of men and women
smokers using brands with lowered “tar” and nicotine con-
tinues to grow. Adolescents of both sexes have followed this
trend, to the point where nonfilter cigarettes are relatively rare
among young adults.

Although the preponderance of scientific evidence continues
to suggest that cigarettes with lower “tar” and nicotine are less
hazardous, four serious warnings are in order.

First, the reported “tar” and nicotine deliveries of cigarettes
are standardized machine measurements. They do not neces-
sarily represent the smoker’s actual intake of these substances.
Evidence is now mounting that individuals who switch to
cigarettes with lowered “tar” and nicotine inhale more deeply,
smoke a greater proportion of their cigarettes, and in some
cases smoke more cigarettes.

Second, “tar” and nicotine are not the only dangerous chemi-
cal components of cigarette smoke. Many conventional filter
cigarettes, in fact, may deliver more carbon monoxide than non-
filter cigarettes.

Third, it has not been established that lower ‘tar’ and
nicotine cigarettes have less harmful effects on the unborn
fetus and baby; on women and men at high risk for developing
coronary heart disease, such as those with elevated cholesterol
or high blood pressure; or on workers with adverse occupational

x
exposures. It has not been established that switching to a lower
“tar” and nicotine cigarette has any salutary effect on indi-
viduals who already have smoking-related illnesses, such as
coronary heart disease, chronic bronchitis, and emphysema.

Fourth, even the lowest yield cigarettes present health
hazards for both women and men that are very much higher
than smoking no cigarettes at all.

The single most effective way for both women and men smok-
ers to reduce the hazards associated with cigarettes is to quit
smoking.

As this report demonstrates, little is known about the effects
of these product changes on the initiation, maintenance and
cessation of smoking, particularly among women. It has not
been determined whether the availability of cigarettes with
lowered “tar” and nicotine has made it easier for young women
to experiment with and become addicted to cigarettes. It is not
known whether smokers of the lowest yield cigarettes are more
or less likely to attempt to quit, or to succeed in quitting, than
smokers of conventional filtertip or nonfilter cigarettes. The
extent to which the act of switching to a lower “tar” cigarette
serves as a substitute for quitting may differ among women
and men.

Public Health Responsibilities

This report, which includes data compiled by individuals from
both inside and outside the Government, has confirmed in every
way the judgement of the World Health Organization that there
ean no longer be any doubt among informed people that
cigarette smoking is a major and removable cause of ill health
and premature death.

Each individual woman must make her own decision about
this significant health issue. Secretary Harris has noted that
the role of the Government, and all responsible health profes-
sionals, is to assure that this decision is an informed one. In
issuing this report, we hope to help the public heaith community
accomplish this purpose.

Julius B. Richmond, M.D.
Assistant Secretary for Health and
Surgeon General

xi
ACKNOWLEDGEMENTS

This report was prepared by agencies of the U.S. Department
of Health, Education, and Welfare under the general editorship
of the Office on Smoking and Health, John M. Pinney, Director.
Consulting scientific editors were David M. Burns, M.D., As-
sistant Clinical Professor of Medicine, Pulmonary Division,
University of California at San Diego, San Diego, California, and
John H. Holbrook, M.D., Associate Professor of Internal
Medicine, University of Utah Medical School, Salt Lake City,
Utan. Contributing scientific editors were Joanne Luoto, M.D.,
M.P.H., Medical Officer, Office on Smoking and Health,
Rockville, Maryland, and Kelley L. Phillips, M.D., M.P.H., Ex-
pert Consultant, Office on Smoking and Health, Rockville,
Maryland.

Introduction and Summary
Office on Smoking and Health

Patterns of Cigarette Smoking

Office on Smoking and Health

Jeffrey E. Harris, M.D., Ph.D., Associate Professor, Depart-
ment of Economics, Massachusetts Institute of Technology,
Cambridge, Massachusetts; Clinical Associate, Medical Serv-
ices, Massachusetts General Hospital, Boston, Mas-
sachusetts.

Mortality

National Heart, Lung, and Blood Institute

Eugene Rogot, M.A., Division of Heart and Vascular Diseases,
National Heart, Lung, and Blood Institute, National Insti-
tutes of Health, Bethesda, Maryland.

Thomas J. Thom, Division of Heart and Vascular Diseases,
National Heart, Lung. and Blood Institute, National Insti-
tutes of Health, Bethesda, Maryland.

Morbidity

National Center for Health Statistics

Ronald W. Wilson, M.A., Chief, Health Status and Demo-
graphic Analysis Branch, Division of Analysis, National Cen-
ter for Health Statistics, Hyattsville, Maryland.

Cardiovascular Diseases

National Heart, Lung, and Blood Institute

G. C. McMillan, M.D., Ph.D., Associate Director for Etiology of
Arteriosclerosis and Hypertension, Division of Heart and
Vascular Diseases, National Heart, Lung, and Blood Insti-
tute, National Institutes of Health, Bethesda, Maryland.

xill
Cancer

National Cancer Institute

Jesse L. Steinfeld, M.D., Dean, School of Medicine, Medical
College of Virginia, Virginia Commonwealth University,
Richmond, Virginia.

Non-Neoplastic Bronchopulmonary Diseases

National] Heart, Lung, and Blood Institute

Richard A. Bordow, M.D., Associate Director of Respiratory
Medicine, Brookside Hospital, San Pablo, California.

Claude J. M. Lenfant, M.D., Director, Division of Lung Dis-
eases, National Heart, Lung, and Blood Institute, National
Institutes of Health, Bethesda, Maryland.

Barbara Marzetta Liu, S.M., Division of Lung Diseases, Na-
tional Heart, Lung, and Blood Institute, National Institutes
of Health, Bethesda, Maryland.

Eric R. Jurrus, Ph.D., Division of Lung Diseases, National
Heart, Lung, and Blood Institute, National Institutes of
Health, Bethesda, Maryland.

Interaction Between Smoking and Occupational Exposures
National Institute of Occupational Safety and Health
Jeanne M. Stellman, Ph.D., Associate Professor, Columbia
University, School of Public Health, New York, New York.
Steven D. Stellman, Ph.D., Assistant Vice-President for
Epidemiology, American Cancer Society, New York, New
York.

Pregnancy and Infant Health

National Institute of Child Health and Human Development
Eileen G. Hasselmeyer, Ph.D., R.N., Associate Director for
Scientific Review, National Institute of Child Health and
Human Development, National Institutes of Health,
Bethesda, Maryland.

Mary B. Meyer, Sc.M., Associate Professor of Epidemiology,
Johns Hopkins University, School of Hygiene and Public
Health, Baltimore, Maryland.

Lawrence D. Longo, M.D., Professor of Physiology and of
Obstetrics and Gynecology, Loma Linda University School of
Medicine, Loma Linda, California.

Donald R. Mattison, M.D., Medical Officer, Pregnancy Re-
search Branch, National Institute of Child Health and
Human Development, National Institutes of Health,
Bethesda, Maryland.

Peptic Ulcer Disease

National Institute of Arthritis, Metabolism and Digestive

Diseases
Travis E. Solomon, M.D., Ph.D., Center for Uleer Research

X1V
and Education, Veterans Administration Wadsworth Medical
Center, and University of California, Los Angeles School of
Medicine, Los Angeles, California.

Janet D. Elashoff, Ph.D., Center for Uleer Research and Edu-
cation, Veterans Administration Wadsworth Medical Center
and University of California, Los Angeles School of Medicine,
Los Angeles, California.

Interactions of Smoking with Drugs, Food Constituents, and
Responses to Diagnostic Tests

Food and Drug Administration

Cheryl Fossum Graham, M.D., Division of Drug Experience,
Office of Biometrics and Epidemiology, Bureau of Drugs,
Food and Drug Administration, Rockville, Maryland.

Psychosocial and Behavioral Aspects of Smoking in Women
National Institute on Drug Abuse and National Institute of
Child Health and Human Development

Initiation

Ellen R. Gritz, Ph.D., Research Psychologist, Veterans Ad-
ministration Medical Center, Brentwood, and Associate Re-
search Psychologist, Department of Psychiatry and
Biobehavioral Sciences, School of Medicine, University of
California, Los Angeles, California.

Ann F. Brunswick, Ph.D., Senior Research Associate (Public
Health, Sociomedical Sciences), Center for Sociocultural Re-
search on Drug Use, Columbia University, New York, New
York.

Maintenance and Cessation

Karen L. Bierman, M.A., Department of Psychology, Univer-
sity of California, Los Angeles, California.

Ellen R. Gritz, Ph.D., Research Psychologist, Veterans Ad-
ministration Medical Center, Brentwood, and Associate Re-
search Psychologist, Department of Psychiatry and
Biobehavioral Sciences, School of Medicine, University of
California, Los Angeles, California.

The editors acknowledge with gratitude the many distin-
guished scientists, physicians, and others who assisted in the
preparation of this report by coordinating manuscript prepara-
tion, contributing critical reviews of the manuscripts or helping
in other ways.

Elvin E. Adams, M.D., M.P.H., Chairman, Texas Interagency

Council on Smoking and Health, Practicing Internal

Medicine, Fort Worth, Texas.

Josephine D. Arasteh, Ph.D., Health Scientist Administrator,
Xv
Human Learning and Behavior Branch, Center for Research
for Mothers and Children, National Institute of Child Health
and Human Development, National Institutes of Health,
Bethesda, Maryland.

Lester Breslow, M.D., M.P.H., Dean, School of Public Health,
University of California at Los Angeles, Los Angeles, Califor-
nia.

A. Sonia Buist, M.D., Associate Professor of Medicine and
Physiology, University of Oregon Health Sciences Center,
Portland, Oregon.

David M. Burns, M.D., Assistant Clinical Professor of
Medicine, Pulmonary Division, University of California at
San Diego, San Diego, California.

Thomas C. Chalmers, M.D., President and Dean, Mount Sinai
Medical Center, New York, New York.

Florence L. Denmark, Ph.D., Professor of Psychology, Hunter
College of the City University of New York, and President of
the American Psychological Association, New York, New
York.

Robert M. Donaldson, Jr., M.D., Chief, Medical Services,
Westhaven Veterans Hospital, and Vice-Chairman, Depart-
ment of Internal Medicine, Yale University School of
Medicine, New Haven, Connecticut.

Joseph T. Doyle, M.D., Professor of Medicine and Head, Divi-
sion of Cardiology of the Department of Medicine, Albany
Medical College of Union University, Albany, New York.
Elizabeth M. Earley, Ph.D., Chief, Section of Cytogenetics,
Division of Pathology, Bureau of Biologics, Food and Drug
Administration, Rockville, Maryland.

Bernard H. Ellis, Jr., Program Director for Smoking and Oc-
cupational Activities, Office of Cancer Communications, Na-
tional Cancer Institute, National Institutes of Health,
Bethesda, Maryland.

Diane Fink, M.D., Associate Director, National Cancer Insti-
tute, and Coordinator, Smoking, Cancer, and Health Program,
National Institutes of Health, Bethesda, Maryland.

Harold E. Fox, M.D., Associate Professor of Clinical Obstetrics
and Gynecology, Department of Obstetrics and Gynecology,
College of Physicians and Surgeons, Columbia University,
and Medical Director, Western and Upper Manhattan
Perinatal Network, New York, New York.

Joseph H. Gainer, D.V.M., Veterinary Medical Officer, Divi-
sion of Veterinary Medical Research, Bureau of Veterinary
Medicine, Food and Drug Administration, Beltsville, Mary-
land.

Stanley N. Gershoff, Ph.D., Director, Nutrition Institute and

XVI
Chairman, Graduate Department of Nutrition, Tufts Univer-
sity, Medford, Massachusetts.

Mary E. Guinan, M.D., Clinical Research Investigator, Clini-
cal Studies Section, Venereal Disease Control Division, Cen-
ter for Disease Control, Atlanta, Georgia.

Sharon M. Hall, Ph.D., Assistant Professor in Residence, Uni-
versity of California at San Francisco, Langley Porter Psy-
chiatric Institute, San Francisco, California.

Jane Halpern, M.D., Assistant Secretary for Policy Evalua-
tion and Research, Office of Health and Disability, United
States Department of Labor, Washington, D.C.

Beatrix A. Hamburg, M.D., Senior Research Psychiatrist,
Laboratory of Developmental Psychology, National Institute
of Mental Health, National Institutes of Health, Bethesda,
Maryland.

Virginia G. Harris, M.D., Director, Maternal and Child Health,
Onondaga County Health Department, Syracuse, New York.
John H. Holbrook, M.D., Associate Professor of Internal
Medicine, University of Utah Medical School, Salt Lake City,
Utah.

L. Stanley James, M.D., Professor of Pediatrics, and of Obstet-
rics and Gynecology, and Director, Division of Perinatal
Medicine, College of Physicians and Surgeons, Columbia Uni-
versity, New York, New York.

Hershel Jick, M.D., Boston Collaborative Drug Surveillance
Program, Boston University Medical Center, Waltham, Mas-
sachusetts.

Reese T. Jones, M.D., Professor of Psychiatry, Department of
Psychiatry, University of California at San Francisco,
Langley Porter Psychiatric Institute, San Francisco,
California.

Philip Kimbel, M.D., Chairman, Department of Medicine,
Graduate Hospital, Philadelphia, Pennsylvania.

Jan W. Kuzma, Ph.D., Chairman and Professor of Biostatis-
tics, Department of Biostatistics and Epidemiology, Loma
Linda University, Loma Linda, California.

Abraham Lilienfeld, M.D., M.P.H., D.Se., University Distin-
guished Service Professor, Johns Hopkins School of Hygiene
and Public Health, Baltimore, Maryland.

Harold A. Menkes, M.D., Associate Professor of Medicine and
Environmental Health Sciences, Department of Medicine,
Johns Hopkins University, Baltimore, Maryland.

Kenneth Moser, M.D., Professor of Medicine and Director,
Pulmonary Division, University of California at San Diego,
San Diego, California.

Mariquita Mullan, B.S.N., M.P.H., Special Assistant to the Di-

XV11
rector, National Institute of Occupational Safety and Health,
Center for Disease Control, Rockville, Maryland.

Janyce E. Notopoulos, Program Analyst, Office of Planning
and Evaluation, National Institute of Child Health and
Human Development, National Institutes of Health,
Bethesda, Maryland.

Albert Oberman, M.D., Director, Division of Preventive
Medicine, University of Alabama in Birmingham Medical
Center, Birmingham, Alabama.

Ralph S. Paffenbarger, M.D., D.R.P.H., Professor of
Epidemiology, Stanford University, School of Medicine, Stan-
ford, California, and Adjunct Professor of Epidemiology at the
University of California, School of Public Health, Berkeley,
California.

Richard Peto, M.D., Radcliff Clinic, Oxford University, Ox-
ford, England.

Malcolm C. Pike, Ph.D., Professor, Community and Family
Medicine, School of Medicine, University of Southern Califor-
nia at Los Angeles, Los Angeles, California.

Ovide F. Pomerleau, Ph.D., Professor of Psychology and Psy-
chiatry, University of Connecticut, School of Medicine, Far-
mington, Connecticut.

Phill H. Price, M.D., Medical Officer, Metabolic Products
Branch, Division of Metabolism and Endocrine Drugs,
Bureau of Drugs, Food and Drug Administration, Rockville,
Maryland.

Dorothy P. Rice, Director, National Center for Health Statis-
tics, Office of the Assistant Secretary for Health, Hyattsville,
Maryland.

Anthony Robbins, M.D., Director, National Institute of Occu-
pational Safety and Health, Center for Disease Control,
Rockville, Maryland.

Judith B. Rooks, C.N.M., M.P.H., M.S., Office of the Assistant
Secretary for Health, Washington, D.C.

Harold P. Roth, M.D., Associate Director for Digestive Dis-
eases and Nutrition, National Institute of Arthritis,
Metabolism, and Digestive Diseases, National Institutes of
Health, Bethesda, Maryland.

Philip Sapir, Special Assistant to the Director for Behavioral
and Social Sciences and Chief, Human Learning and Behavior
Branch, Center for Research for Mothers and Children, Na-
tional Institute of Child Health and Human Development,
National Institutes of Health, Bethesda, Maryland.

Marvin A. Schniederman, Ph.D., Associate Director for Sci-
ence Policy, National Cancer Institute, National Institutes of
Health, Bethesda, Maryland.

xvii
Irving J. Selikoff, M.D., Professor of Community Medicine and
Professor of Medicine, and Director of Environmental Sci-
ences Laboratory, Mount Sinai Medical Center, New York,
New York.

S. I. Shibko, Ph.D., Chief, Contaminants and Natural Toxic-
ants Branch, Division of Toxicology, Bureau of Foods, Food
and Drug Administration, Washington, D.C.

Jeremiah Stamler, M.D., Chairman, Department of Commu-
nity Health and Preventive Medicine, Northwestern Univer-
sity Medical School, Chicago, Tllinois.

John E. Vanderveen, Ph.D., Director, Division of Nutrition,
Bureau of Foods, Food and Drug Administration,
Washington, D.C.

Eve Weinblatt, Assistant Director for Research, Department
of Research and Statistics, Health Insurance Plan of Greater
New York, New York, New York.

Samuel S. C. Yen, M.D., Professor and Chairman, Department
of Reproductive Medicine, University of California, San Di-
ego, LaJolla, California.

The editors also acknowledge the help of the following staff
who among others assisted in the preparation of the report.

John L. Bagrosky, Associate Director for Program Opera-
tions, Office on Smoking and Health, Rockville, Maryland.
Jacqueline O. Blandford, Clerk-Typist, Office on Smoking and
Health, Rockville, Maryland.

Betty Budd, Secretary, Office on Smoking and Health,
Rockville, Maryland.

John F. Hardesty, Jr., Public Information Officer, Office on
Smoking and Health, Rockville, Maryland.

Patricia E. Healy, Technical Information Clerk, Office on
Smoking and Health, Rockville, Maryland.

Robert S. Hutchings, Associate Director for Information and
Program Development, Office on Smoking and Health,
Rockville, Maryland.

Margaret E. Ketterman, Secretary, Office on Smoking and
Health, Rockville, Maryland.

Richard A. Lasco, Ph.D., Bureau of Health Education, Center
for Disease Control, Atlanta, Georgia.

Joanne Luoto, M.D., M.P.H., Medical Officer, Office on Smok-
ing and Health, Rockville, Maryland.

Judith L,. Mullaney, M.L.S., Technical Information Specialist,
Office on Smoking and Health, Rockville, Maryland.

Marjorie L. Olson, Secretary, Office on Smoking and Health,
Rockville, Maryland.

xix
Kelley L. Phillips, M.D., M.P.H., Expert Consultant, Office on
Smoking and Health, Rockville, Maryland.

David L. Pitts, Public Health Advisor, Operations Branch,
Nutrition Division, Bureau of Smallpox Eradication, Center
for Disease Control, Atlanta, Georgia.

Donald R. Shopland, Technical Information Officer, Office on
Smoking and Health, Rockville, Maryland.

Linda R. Spiegelman, Administrative Assistant, Office on
Smoking and Health, Rockville, Maryland.

Carol M. Sussman, Technical Publication Writer/Editor, Of-
fice on Smoking and Health, Rockville, Maryland.

Ronald G. Thomas, Public Health Analyst, Office on Smoking
and Health, Rockville, Maryland.

Selwyn M. Waingrow, Public Health Analyst, Office on Smok-
ing and Health, Rockville, Maryland.

Ann E. Wessel, Public Health Analyst, Office on Smoking and
Health, Rockville, Maryland.

Carole L. Winn, Assistant Chief, Clinical Chemistry Stand-
ardization Section, Clinical Chemistry Division, Metabolic
Biochemistry Branch, Bureau of Laboratories, Center for
Disease Control, Atlanta, Georgia.

xx
TABLE OF CONTENTS

 

 

 

INTRODUCTION AND SUMMARY ..........5 se eeeeeee 1
PARTI
PATTERNS OF CIGARETTE SMOKING ................ 15
Introduction .... 0. ccc ccc ec eee eee eee en tenes 17
The Rise of Cigarette Smoking: 1900-1950 ........... 17
The Emergence of Filtertip Cigarettes: 1951-1963 .. 21
Increasing Public Health Awareness: 1964-1979 ..... 21
Exposure to Cigarette Smoking Among
Successive Birth Cohorts ......... ccc eee eee ees 28
Cigarette Smoking Among Young Women ........... 33
SuUMMary ... cee cee ccc eee eee eee eee ee tee tenes 36
References oo. cc cece ccc cece eee ee eee en een eens 39
PART II
BIOMEDICAL ASPECTS OF SMOKING
MORTALITY ...... 0... ccc ccc ence een eee eee nneaes 44
Introduction and Background ............. 000. eecaee 45
Mortality TrendS .......... cece cece eee ee ence nee 45
Epidemiological Studies ........ cece eee ee ees 46
The American Cancer Society
25-State Study ......... cc cece ee eee cece e eens 47
The Swedish Study ......... ccc eee ee ee eee eens 51
The Canadian Veterans Study ................06. 51
Japanese Study of 29 Health Districts ........... 51
The British Doctors Study ............... eee eens 51
The Framingham Heart Study ..............0065 52
The British-Norwegian
Migrant Study ....... ccc ccc e ec eee eee eee ences 52
Overall Mortality for Females—Cigarette Smokers
Versus Nonsmokers.......--- ee eee eee ere eens 53
Mortality Ratios .......... ccc cece ee ccc eee eens 53
Amount Smoked and Age ........ cece eee eee eee ees 54
Duration of Smoking ........... ccc eee eee ees 57
Age Began Smoking ......... 0... ec eee eee ee re eees 58
Inhalation ......... 00. c ccc cee ee teeter tenes 59
“Tar” and Nicotine Content of
Cigarettes ooo ccc ccc ccc ccc cece ee eee ene eee eee 59

XXi
CommentS ..ccccceccecec eter reece reese een e eases eee ees 61

Summary ..ceee cece cece e cece eee e eee esse ce cere e es 61
References ...ceeeeee rere renee ene rene erase reser ees 62
MORBIDITY ....-e eee e sere reer eee rete ere eee ees 65
Days Lost from Work .....---s+ eee srer settee 67
Limitation of Activity ......e cere ere reer eretteeeeres 68
Cigarette Smoking and Occupation ....-.++.seeeeeeee 69
Summary ..cce eee eee e rere eee e ects seen see esses sees 70
ReferenceS .cccecec cece ener rene nese ener rere cere ees 715
CARDIOVASCULAR DISEASES  .....-- eee ee errr teers V7
Introduction .....ceee eee e reer ee eee teen tena n neers es 79
Mortality Rates  ......e eee ee cree erent eens reeset es 79
Atherosclerosis ......eeecce tree reer reeneee rer eereees 84
Risk FactorS ...ccee cece cece eee tenn renee een reeeers 86
The Effect of Smoking .....--.eeeee ener errr ee eer tenes 86
Atherosclerosis ...cceeeee reece tenner neers eneaes 86
Coronary Heart Disease ....-.--e seer eee e recente 88

Cessation of Smoking and “Tar”
and Nicotine Content of

Cigarettes ...... cece eee eee ene e reer eee n ees 92
Angina PectoriS ......ssseee errr reer eer erer snes? 93
Cerebrovascular Disease .......eeeeeerrereerccces 93
Arteriosclerotic Peripheral
Vascular Disease... ee cece cence eee ener eenees 95
Aortic AN@ULySM .. se eee eee enter teen terete 96
Hypertension .....-.eseeee cree reser erence ecetees 96
Venous Thrombosis ......ccereeee eect cenreeness 97
High-Density Lipoprotein .....-.+++sesereerereees 98
Oral Contraceptive Use, Smoking, and
Cardiovascular Disease ....-..eeee errr er eeeertres 98
Carbon Monoxide ........eeee ener e eee eter rene erences 101
Comment ..cceec cece eee etree tenner eens enee nes aes 101
Summary ..cccecece cece eee eet eee eres seen sees sees 102
References ...cccccese cece cece nese ener eres sees enes ees 103
CANCER vce ccc eee eee e teen e renee een eeeeeer ener nesses 107
Introduction ...... cece eee e eee eee renee ete eee ents 109
LUNG cece eee cee eee eee een enn eter n teen eres eee e es 111
Geographic Differences .......++-+erereereseteces 116
Smoking Patterns Among Women ...-.+--++--++++ 117
Cessation of Smoking .....----.eeeee ec eeee eer eee 120
Experimental Carcinogensi§S ...-..eeeeee ee ee renee 121
LarynX oo. eee eee e ener ee eees ence eee eeeenaeeeenee 121
(0 7) 122
Esophagus .......eeeceee sree cree ee er eee r eer eeese reese 123

XXli
Urinary Bladder ........... eee e eee e eee rece e ence enees 125

Kidney ccc cece eee ener eee eee ee nee ence eees 125
PAncreaS i.e ee ccc cece ete cee ce ee eee eee eee ee eens 126
SUMMALY 2... cece eee eee e een enna tees 126
References ... cece ccc c cece eee e eee eee eee eee eee enenes 127

Non-neoplastic Bronchopulmonary

DiSCaASCS co cece ccc cece ce eee ee ee eee ene teeta en ean 133
Introduction ..... cece cece eee eee eee nee eee eees 135
DefinitionS . oo. c ccc cece eee ee cee tenner en eens 1385
Smoking and Respiratory Mortality ............+.5+- 137
Smoking and the Epidemiology and

Pathology of Cold 21... . cc cece erence rene ee eee eees 141
Smoking and Respiratory Morbidity ..........-..-+.- 146
Smoking and Pulmonary Function ..........+...0ee 156

Smoking and “Early” Functional
Abnormalities ....... cece cece eee ene 157
Smoking and Ventilatory Function ............-- 160
Summary ........ cece cece e eee een eet e eee e anaes 163
ReferenceS 2... cc cc cec ccc s cece cence nent een eee renee eees 1638
Interaction Between Smoking and

Occupational Exposures .........e reece teen eee 169
Smoking Patterns in Women ...........:seeee ere eeeee 172
Patterns of Employment .........ce eee ee cece eens 175
The Reproductive Role .......--- esse eee rece ee eeeeee 177
Specific Interactions Between Occupational

Exposure and Smoking .......-- ee see eee e ener eens 179
ASDOEStOS 2. cece cece cece rece eee e er een eee ene eens 179
Cotton Dust ..... ccc eee cee ence teen eens 181

Summary ..... ccc eee eee cece renee eee ee nnnenenes 186
ReferenceS oo. cece ccc cece ete e ee tee eee eee nent e ee enes 187
PREGNANCY AND INFANT HEALTH ...........-000e- 189
Introduction ...... ccc cee cee eee eee eee e nee eee e eens 191
Smoking, Birth Weight, and Fetal Growth ........... 191
Placental Ratios .......:cee cee cece tener e erence 194
Gestation and Fetal Growth ............ ee eeeeee 195
Long-Term Growth and Development ............ 196
Role of Maternal Weight Gain ..........-.. 5 eee 202
Smoking, Fetal and Infant Mortality,

and Morbidity  ......... cece eee e eee cree ne eee enee 206
Spontaneous Abortion ........cee reece ee ete eens 206
Congential Malformations ..........-sesee eee ees 207
Perinatal Mortality ........ 0... cece cece e nee e nee 211
Cause of Death oo... ccc cece eee eens 214

Complications of Pregnancy and Labor .............. 214
Preeclampsia ..... cece eee cere eee nee teen e eee zie
Preterm Delivery, Pregnancy
Complications, and Perinatal

Mortality by Gestation .........ee eee e eee ener 217
Long-Term Morbidity and Mortality .....-..--.+++++: 221
Sudden Infant Death Syndrome ...........++.+-- 225
Mechanisms ......cce cece c eee e ee ete eee eee een e eens 226
Experimental Studies .........se eee eee reenter ees 229
Tobacco Smoke ........ once e ee cee cece ence neres 229
Nicotine ... cc cece cee cee eee cee eee ene e en enenaes 229
Carbon Monoxide ....... see c cee eee cece ee eneeees 231
Polycyclic Aromatic Hydrocarbons ...........+-+-- 233
Other Components ......-.. eee cece eee eeeee 234
Fertility 0.0... cee cece cee eee eee nen een eeees 235
Smoking and Reproduction in Women ........-.- 235
Smoking and Age of Menopause .....-...+++++-+- 236
Smoking and Reproduction in Men ..........-.+- 236
Fertilization and Conceptus
Transport .... cece cece ee eee ene een eee eenens 237
SUMMALY ... ee cece eee e erect eee eens een eee 238
ReferenceS 1... cece cee cee cee eee ee tenner eeeeneeees 239
PEPTIC ULCER DISEASE _ ..... cee cece cece ee eee eees 251
Summary 2... cee eee ce eee eee eee tenes 254
ReferenceS oe ccevccccecc crete ccc en een ee eee eeeeenenes 254

INTERACTIONS OF SMOKING WITH DRUGS,
FOOD CONSTITUENTS, AND RESPONSES

 

TO DIAGNOSTIC TESTS 2... ce eee cnet e eee 259
Women Smokers and Nonsmokers and
Drug Consumption Patterns .........+.e sees eee ees 259
Altered Clinical Response to Drug Therapy
by Smokers as Compared to Nonsmokers .........: 261
Oral Contraceptives and Smoking .....+--..-+++eeees 262
Alterations in Normal Clinical Laboratory
Values in Women Smokers ......... 0c cece eeeeeeeecs 263
The Influence of Smoking on the
Nutritional Needs of Women .........0.. cece ee eeeee 264
Summary ....--. sec ce cece eee erect ence eee eee eeneee 265
ReferenCeS .cecceccccccecccee cece cee eeeeeeeeeeeerens 265
PART III
PSYCHOSOCIAL AND BEHAVIORAL ASPECTS
OF SMOKING IN WOMEN ........--. cee cee eee eee ceees 269
Introduction oo... ccc cece cece eee eee rere eens 271

XXIV
Initiation of Smoking in Adolescent Girls ............ 271

Concepts of Adolescent Behavior ...............6. 272
Prevalence and Patterns of
Adolescent Cigarette Use ......... 0. eee eee eee 278
Prevalence ..... cc ec ccc eee eee e ees 273
Age at Initiation of Smoking ................ 275
Number of Cigarettes Smoked ............... 277
Type of Cigarette Smoked ..................-. 278
Smoking Cessation ........... ccc eee eee eee 278
Smoking Prevalence and Ethnicity .......... 280
Alcohol and Marihuana Use ................. 280

Demographic and Psychosocial
Correlates of Smoking in

Adolescence oo... ccc cece ccc c eee e eee enes 281
Socioeconomic Influences ..............-0005- 281
Family Patterns ........... cece eee eee eee eens 282
Smoking Among Parents and Siblings ....... 282
Peer Group Influence ............. 0.00 cee eee 284
Scholastic Achievement and Aspirations ..... 285
Dynamic/Personality Factors ................ 286
Prediction of Future Smoking Behavior ..... 288

Prevention of Smoking and
Considerations for Future

Research  .... eee ccc cece eee eee eee eens 290

Prevention of the Initiation of
Smoking ......... eee eee ee eee eee ees 290
Research Goals ........ cee cee cee ee eee ences 291
Maintenance of Smoking Behavior ..............505 293
Patterns of Cigarette Smoking ...............0005 293
Smoking Prevalence and Ethnicity .......... 296

Pharmacological Effects of

Smoking ...... cece cece ee eee eee ence seen 297
Nicotine 1... cece cee eee cee ee ee eee enone 297
Peripheral Effects ............ cece eee ences 297
Central Effects ...... 0... cc cece eee cee eens 298

A Possible Role for Nicotine in
Smoking Maintenance .............seeeeee 298
Differences in Nicotine Metabolism .......... 300
Smoking and Stimulation Effects ................ 300
Smoking Cessation ....... 2. ee cece cece eet ee cee e ees 302
Demographics ......... cece eee ence ee een e ees 303
AGO Lice c eee cece eee cence ene nee enes 303
Education ..... cece ccc c ccc eee eee teen eens 303
INCOME 2. eee ect cere tee tee e ee eee 304
Occupation ..... eee eee ee ee eens 304
Psychology of Changing Smoking Habits......... 305
Treatment StudieS ......cc cece cece eee cette ences 306

The Smoking Withdrawal Syndrome ...........-. 315
Smoking and Weight Control .........+-e+eeeeees 315
Treatment Recommendations .........s-e eee eees 319
Conclusions ...cccc cece cece eect eect e eee eeeeeeees 321
Dissemination of Information About Smoking ....... 321
Health Attitudes and Behaviors .........++++.++- 321
Sources of Information ........cce eee eee e eee eeee 322
Health Care ProviderS ........cceeeeeeeeeeees 322
EducatorS ccc c cece cece ee ere eee ee eee eeeees 324
Peer Group... sce ccc eee eee eet e ee eneens 324
Family ...c cece cece ee eee cece een e ener eneeee 325
Media: Television, Radio, Film,
Newspapers, MagazineS ..-...seeeeeeeeeeee 325
Advertising ........cc cece eee eter cern eennees 325
The Failure to Disseminate
Information ....c cece cece eee ee eee reece eeenes 327
Stress at Work ..... ccc cece cece erect entree eee eeeness 327
Smoking Habits of Health Professionals ............. 329
Physicians ...... cece cece een ee eee recent ennnees 329
Psychologists .......cseceee eee renee ee eeeene eens 332
NurseS c.ccccccccc ccc cc cece eee ee renee ene eeeneens 333
The Pregnant Smoker—A Special Target ...........- 336
Sources of Information .......c cece cece eee eres 336
Physician Advice «6... cece ee eee eee eee e ne eeee 337
Prevalence of Smoking and Quitting
During Pregnancy ........- ss eee eee ener eee e cies 340
Psychosocial Factors in Quitting ............+-+- 344
Recommendations ........ceccee cece eee ene ceees 845
SuUMMAry oo cece cece cee eee eee nee e nent eee n ees 346
References ..ccscccc cece ence ec ee terete eee ee eee ennees 347

 
INTRODUCTION AND SUMMARY.
INTRODUCTION AND SUMMARY
The 1980 Report on the Health Consequences of Smoking fo-

cuses upon the evidence relating cigarette smoking to health
effects in women. It is not presented as a detailed discussion of
the entire range of effects of smoking on health. Such a detailed
review of all existing evidence can be found in the 1979 Report
of the Surgeon General on Smoking and Health. Instead, this
volume on smoking and women’s health is offered as a review
and reappraisal of smoking and major health relationships spe-
cifically in women. It is intended to serve the medical commu-
nity as a unified source of existing scientific evidence about
health effects of smoking cigarettes for women. As an examina-
tion of current knowledge, it will logically lend itself to applica-
tion in both the personal and public health arenas.

Its content is the work of numerous scientists within the De-
partment of Health, Education, and Welfare, as well as scien-
tific experts outside that organization.

_ This volume examines the major issues relating tobacco use
to women’s health including trends in consumption, the biomed-
ical evidence of the health effects of cigarette usage by women,
and determinants of smoking initiation, maintenance, and ces-
sation.

This section summarizes the principal findings of this report.
It is hoped that the entire volume will serve to highlight the
established risks of smoking for women and their children, as
well as to define the areas in need of further investigation.

Patterns of Cigarette Smoking

1. Women have differed from men in their historical onset of
widespread cigarette use, in the rate of diffusion of smoking
among each new birth cohort, in their intensity of cigarette
smoking and their use of various types of cigarettes.

2. Men took up cigarette smoking rapidly at the beginning of
the twentieth century, especially during World War I. Cigar-
ettes rapidly replaced other forms of tobacco.
ie 1925, approximately 50 percent of adult males were
qe smokers. Smoking among men accelerated rapidly
neil World War II. By 1950, the prevalence of cigarette use

3 Then approached 70 percent in some urban areas.
lagged b, onset of widespread cigarette use among women
adult wenind that of men by 25 to 30 years. The proportion of
until Pipa smoking cigarettes did not exceed one-quarter

e onset of World War II.
etween 1951 and 1963, increasing proportions of women

3
and men smokers converted to filtertip cigarettes. By 1964, 79
percent of adult women smokers and 54 percent of adult men
smokers used filter cigarettes.

5. After reaching a peak value of 4,336 in 1963, annual per
capita consumption of cigarettes declined in 1964, 1968-70, and
in the period since 1975. The most recent estimate of 3,900 _
cigarettes per capita in 1979 is approximately equal to that ob-
served in 1952.

6. From 1965 to 1978, the proportion of adult men cigarette
smokers declined from 51 to 37 percent. The preliminary esti-
mate of adult men’s smoking prevalence for 1979 is 36.9 percent.
From 1965 to 1976, the proportion of adult women smokers re-
mained virtually unchanged at 32 to 33 percent. Since 1976, the
proportion of women smokers has declined to below 30 percent.
For 1979, the preliminary estimate of adult women’s smoking
prevalence is 28.2 percent. The overall smoking prevalence of
32.3 percent for both sexes in 1979 represents the lowest re-
corded value in at least 45 years.

7. The proportion of adult smokers attempting to quit smok-
ing declined from 1970 to 1975, but increased in 1978-1979. In
contrast to past years, the proportions of women and men now -
attempting to quit smoking, and their reported quitting rates,
are indistinguishable. Approximately one in three adult smok-
ers now makes a serious attempt to quit smoking during the
course of a year. Approximately one in five of those who attempt
to quit subsequently succeed.

8. The proportion of adult smokers using lower “tar” and ~
nicotine brands has increased substantially. In 1979, 39 percent
of adult women smokers and 28 percent of adult men smokers
reported primary brands with F.T.C. “tar” delivery less than
15.0 milligrams. It is not known whether smokers of the lowest
“tar” cigarettes are more or less likely to attempt to quit smok-
ing, or to succeed in quitting, than smokers of conventional fil-
tertip or non-filter cigarettes.

9. The average number of cigarettes smoked by women and
men current smokers has increased. The relationship of this
finding to recent declines in the average F.T.C. “tar” and
nicotine deliveries of cigarettes is not well understood.

10. With each successive generation, the smoking character-
istics of women and men have become increasingly similar.

11. Among women, the average age of onset of regular smok-
ing progressively declined with each successive birth cohort—
from 35 years of age for those born before 1900, to 16 years of
age among those born 1951 to 1960. The average age of onset of
regular smoking among young women is now virtually identical

to that of young men.
4
12. Maximum smoking prevalence rates have declined sub-
stantially in recent birth cohorts of men. Men born 1931 to 1940
reached a peak smoking proportion of 61 percent during 1960-
62, while men born 1941 to 1950 reached a peak smoking propor-
tion of 58 percent in 1968-69. Men born 1951 to 1960 reached a
peak smoking proportion of 40 percent in 1976. Among recent
cohorts of women, peak smoking prevalence rates have declined
to a much smaller extent. Women born 1931 to 1940 reached a
peak smoking proportion of 45 percent in 1966-68, while women
born 1941 to 1950 reached a peak smoking proportion of 41 per-
cent in 1970-73. Women born 1951 to 1960 reached a peak smok-
ing proportion of 38 percent in 1976. Among the generation born
1951 to 1960, the porportions of women and men smoking
cigarettes are now virtually identical.

13. The proportions of women and men smokers in each age
group have declined. Among those born before 1951, this decline
in smoking prevalence resulted mainly from smoking cessation.
By contrast, the observed decline in smoking prevalence among
younger men born 1951 to 1960 has resulted from both smoking
cessation and a lower rate of smoking initiation. This decline in
the rate of onset of smoking among young men has not been
observed for young women.

14. Recent survey data on adolescent smoking habits reveal
that by ages 17 to 19, smoking prevalence among women ex-
ceeds that of men. This finding supports the conclusion that the
rate of initiation of smoking among young men— but not that of
young women—is declining. The future cigarette use of the
youngest generations of women is uncertain.

15. With each successive birth cohort, the accumulated years
of cigarette smoking per woman has progressively approached
the accumulated years of cigarette smoking per man. Each suc-
cessive birth cohort has also experienced progressively smaller
sex differences in the fraction of lifetime years of smoking that
represents filtertip cigarette use.

16. Among men born during this century, each successive
birth cohort has thus far experienced fewer cumulative years of
cigarette smoking, higher proportionate exposure to filtertip
cigarettes, and lower smoking prevalence rates. This relation-
ship between birth date and cigarette smoke exposure does not
hold for women. Women born 1921 to 1940 have experienced
substantially higher smoking prevalence rates than earlier
generations. Unless they quit smoking in substantial numbers,
these women, currently aged 40 to 59, will surpass older women
in total years of cigarette smoking per capita, the total years of
nonfilter cigarette smoking per capita, and in the total number
of cigarettes smoked. The health consequences of this enhanced

5
exposure to cigarette smoke among women are likely to be more
prominent in the coming decades.

Mortality

1. The mortality ratio for women who smoke cigarettes is
about 1.2 or 1.3.

2. Mortality ratios for women increase with the amount
smoked. In the largest prospective study the mortality ratio
was 1.63 for the two-pack-a-day smoker as compared to
nonsmokers.

3. Mortality ratios are generally proportional to the duration
of cigarette smoking; the longer a woman smokes, the greater
the excess risk of dying.

4. Mortality ratios tend to be higher for those women who
begin smoking at a young age as compared to those who begin
smoking later.

5. Mortality ratios are higher for those women who report
they inhale smoke than for those who do not inhale.

6. Mortality ratios for women tend to increase with the tar
and nicotine content of the cigarette.

7, Mortality ratios for female smokers are somewhat less
than for male smokers. This may reflect differences in exposure
to cigarette smoke, such as starting smoking later, smoking
cigarettes with lower “tar”? and nicotine content, and smoking
fewer cigarettes per day than men.

8. Women demonstrate the same dose-response relationships
with cigarette smoking as men. An increase in mortality occurs
with an increase in number of cigarettes smoked per day, an
earlier age of beginning cigarette smoking, a longer duration of —
smoking, inhalation of cigarette smoke, and a higher tar and
nicotine content of the cigarette. Women who have smoking
characteristics similar to men may experience mortality rates
similar to men.

Morbidity

The 1979 Report of the Surgeon General summarized the in-
formation on smoking and morbidity as follows:

1. In general, female current cigarette smokers report more
acute and chronic conditions including chronic bronchitis
and/or emphysema, chronic sinusitis, peptic ulcer disease, and
arteriosclerotic heart disease, than women who never smoked.

2. There is a dose-response relationship between the number
of cigarettes smoked per day and the frequency of reporting for
most of the chronic conditions.

6
3. The age-adjusted incidence of acute conditions (e.g., in-
fluenza) for women smokers is 20 percent higher for women who
had ever smoked than for nonsmokers.

Additional data from the Health Interview Survey (HIS) is
presented:

1. Currently employed women who smoke cigarettes report
more days lost from work due to illness and injury than working
women who do not smoke.

2. Limitation of activity is reported more commonly among
women under the age of 65 who have ever smoked than among
those who never smoked.

Cardiovascular Diseases

Coronary heart disease is the major cause of death among
both males and females in the U.S. population. The 1979 Sur-
geon General’s Report clearly demonstrated the close associa-
tion of cigarette smoking and increased coronary heart disease
among males. This report reviews the evidence associating
cigarette smoking and cardiovascular disease in women:

1. Coronary heart disease, including acute myocardial infarc-
tion and chronic ischemic heart disease, occurs more frequently
in women who smoke. In general, cigarette smoking increases
the risk by a factor of about two, and in younger women
cigarette smoking may increase the risk several fold.

2. Cigarette smoking is a major independent risk factor for
coronary heart disease in women; it also acts synergistically
with other coronary heart disease risk factors producing a risk
greater than the sum of the individual risks.

3. The use of oral contraceptives by women cigarette smokers
increases the risk of a myocardial infarction by a factor of ap-
proximately ten.

4, Women who smoke low “tar” and nic“tine cigarettes expe-
rience less risk for coronary heart disease than women who
smoke high “tar” and nicotine cigarettes, but their risk is still
considerably greater than that of nonsmokers.

5. Increased levels of high-density lipoprotein (HDL) are cor-
related with a reduced risk for an acute myocardial infarction;
women cigarette smokers have decreased levels of HDL.

6. Cigarette smoking is a major, independent risk factor for
the development of arteriosclerotic peripheral vascular disease
in women. Smoking cessation improves the prognosis of the dis-
order and has a favorable impact on vascular patency following
reconstructive surgery.

7. Women cigarette smokers experience an increased risk for
subarachnoid hemorrhage; the use of both cigarettes and oral

7
contraceptives appears to synergistically increase the risk for
subarachnoid hemorrhage.

8. Women who smoke cigarettes may be more likely to de-
velop severe or malignant hypertension than nonsmoking
women.

Cancer

1. Cigarette smoking is causally associated with cancer of the
lung, larynx, oral cavity, and esophagus in women as well as in
men; it is also associated with kidney cancer in women.

2. Cigarette smoking accounts for 18 percent of all cancers
newly diagnosed and 25 percent of all cancer deaths in women.
In 1980, 26,500 of the estimated 101,000 deaths, or over one
quarter of the deaths expected from lung cancer, will occur in
women.

3. Women cigarette smokers have been reported to have be-
tween 2.5 and 5 times greater likelihood of developing lung
cancer than nonsmoking women.

4. Among women the risk of developing lung cancer increases
with increasing number of cigarettes smoked per day, duration
of the smoking habit, depth of inhalation, and tar and nicotine
content of the cigarette smoked. The risk is inversely related to
the age at which smoking began.

5. A dose-response relationship has been demonstrated be-
tween cigarette smoking and cancer of the lung, larynx, oral
cavity, and urinary bladder in women.

6. The rise in lung cancer death rates is currently much
steeper in women than in men. It is projected that the age ad-
justed lung cancer death rate will surpass that of breast cancer
in the early 1980s.

7. The rapid increase in lung cancer rates in women is similar
to but steeper than the rise seen in men approximately 25 years
earlier. This probably reflects the fact that women first began
to smoke in large numbers 25-30 years after the increase in
cigarette smoking among men. Thus, neither men nor women
are protected from developing lung cancer caused by cigarette
smoking. ,

8. Cigarette smoking has been causally related to all four of
the major histologic types of lung cancer in both women and
men, including epidermoid, small cell, large cell and adenocar-
cinoma.

9. The use of filter cigarettes and cigarettes with lower levels
_ of “tar” and nicotine by women is correlated with a lower risk of
cancer of the lung and larynx compared to the use of high-“tar”
and-nicotine or unfiltered cigarettes. The risk posed by smoking

8
low-“tar” cigarettes, however, is clearly greater than that
among females who never smoked.

10. After cessation of cigarette smoking, a woman’s risk of
developing lung and laryngeal cancer has been shown to drop
slowly, equalling that of nonsmokers after 10-15 years.

11. Excessive ingestion of alcohol acts synergistically with
cigarette smoking to increase the incidence of oral and
laryngeal cancer in women.

Non-Neoplastic Bronchopulmonary Diseases

1. Recent statistics indicate a rising death rate due to chronic
obstructive lung disease (COLD) among women. The data avail-
able demonstrate an excess risk of death from COLD among
smoking women over that of nonsmoking women. This excess
risk is much greater for heavy smokers than for light smokers.

2. Women’s total risk of COLD appears to be somewhat lower
than men’s, a difference which may be due to differences in
prior smoking habits.

3. The prevalence of chronic bronchitis varies directly with
cigarette smoking, increasing with the number of cigarettes
smoked per day.

4, There is conflicting evidence regarding differences in the
prevalence of chronic bronchitis in women and men. Several
recent studies suggest that there is no significant difference in
the prevalence of chronic bronchitis between male and female
smokers. This may be the result, however, of increasingly simi-
lar smoking behavior of women and men.

5. The presence of emphysema at autopsy exhibits a dose-
response relationship with cigarette smoking during life.

6. There is a close relationship between cigarette smoking
and chronic cough or chronic sputum production in women,
which increases with total pack-years smoked.

7. Women current smokers have poorer pulmonary function
by spirometric testing than do female ex-smokers or nonsmok-
ers, a relationship which is dose-related to the number of
cigarettes smoked.

Interaction Between Smoking and Occupational Exposures

1. The 1979 Surgeon General’s Report identified the ways in
which smoking cigarettes may interact with the occupational
environment. They include:

a) Facilitation of absorption of physical contamination of
cigarettes,

b) Transformation of workplace chemicals into more toxic
substances,

9
c) Addition of the exposure to a toxic constituent of to-
bacco smoke to a concurrent exposure to the same con-
stituent present in the workplace,

d) Addition of a health effect due to environmental expo-
sure to a similar health effect due to smoking,

e) Synergy of exposures, and

f) Causation of accidents.

2. Women are entering occupational environments with
greater frequency, and thus may be experiencing greater expo-
sures to physical and chemical agents.

3. Cohorts of women with a greater prevalence of smoking are
currently reaching the ages of maximal disease occurrence, re-
placing earlier cohorts with lower cigarette exposures.

4. Physiologic differences in hormonal status between males
and females constitute a potential source of differing responses.

5. In the workplace women who are pregnant present a
nine-month exposure opportunity, including potential
teratogenic and perinatal mortality effects.

6. Concurrent exposure of women to smoking and asbestos
resulted in a clear excess of cancer of the lung.

7. Women smokers exposed to cotton dust run a higher risk of
developing byssinosis, bronchitic syndromes, and abnormal
pulmonary function tests than nonsmoking women.

Pregnancy and Infant Health

1. Babies born to women who smoke during pregnancy are, on
the average, 200 grams lighter than babies born to comparable
nonsmoking women.

2. The relationship between maternal smoking and reduced
birth weight is independent of all other factors that influence
birth weight including race, parity, maternal size,
socioeconomic status, and sex of child; it is also independent of
gestational age.

3. There-is a dose-response relationship between maternal
smoking and reduced birth weight; the more the woman smokes
during pregnancy, the greater the reduction in birth weight.

4. If a woman gives up smoking early during pregnancy, her
risk of delivering a low-birth-weight baby approaches that of a
nonsmoker.

5. The ratio of placental weight to birth weight increases with
increasing levels of maternal smoking, reflecting a considerable
decrease in mean birth weight and a slight increase in mean
placental mass; this may represent an adaptation to relative
fetal hypoxia.

10
6. The pattern of fetal growth retardation that occurs with
maternal smoking is a decrease in all dimensions including body
length, chest circumference, and head circumference.

7. Maternal smoking during pregnancy may adversely affect
the child’s long-term growth, intellectual development, and be-
havioral characteristics.

8. Maternal smoking during pregnancy exerts a direct
growth-retarding effect on the fetus; this effect does not appear
to be mediated by reduced maternal appetite, eating or weight
gain.

9. The risk of spontaneous abortion, fetal death, and neonatal
death increases directly with increasing levels of maternal
smoking during pregnancy; interaction of maternal smoking
with other factors which increase perinatal mortality may re-
sult in an even greater risk.

10. Excess deaths of smokers’ infants are found mainly in the
coded cause categories of “unknown” and “anoxia” for fetal
deaths, and the categories of “prematurity alone” and “respira-
tory difficulty” for neonatal deaths; this suggests that the ex-
cess deaths are due to problems of the pregnancy, rather than
to abnormalities of the fetus or neonate.

11. Increasing levels of maternal smoking result in a highly
significant increase in the risk of abruptio placentae, placenta
previa, bleeding early or late in pregnancy, premature and pro-
longed rupture of membranes, and preterm delivery—all of
which carry high risks of perinatal loss.

12. Although there is little effect of maternal smoking on
mean gestation, the proportion of fetal deaths and live births
that occur before term increases directly with maternal smok-
ing level. Up to 14 percent of all preterm deliveries in the United
States may be attributable to maternal smoking.

13. The incidence of preeclampsia is decreased among women
who smoke during pregnancy; however, if preeclampsia devel-
ops in a smoking woman, the risk of perinatal mortality is
markedly increased compared to preeclamptic nonsmokers.

14. An infant’s risk of developing the “sudden infant death
syndrome” is increased by maternal smoking during pregnancy.

15. There are insufficient data to support a judgement on
whether maternal and/or paternal cigarette smoking increases
she risk of congenital malformations.

16. Infants and children born to smoking mothers may expe-
‘ience more long-term morbidity than those born to non-
smoking mothers; however, studies usually cannot distinguish
»etween the effects of smoking during pregnancy and the ef-
ects of the infant’s or child’s passive exposure to cigarette
smoke after birth.

11
17. Studies in women and men suggest that cigarette smok-
ing may impair fertility.

18. Experimental studies on tobacco smoke, nicotine, carbon
monoxide, polynuclear aromatic hydrocarbons, and other con-
stituents of smoke help define pathways by which maternal
smoking during pregnancy may exert its aforementioned ef-
fects.

Peptic Ulcer Disease

The 1979 Surgeon General’s Report included evidence that
cigarette smoking in males was significantly associated with
the incidence of peptic ulcer disease and increased the risk of
dying from peptic ulcer disease by approximately two-fold. The
effect of smoking on pancreatic secretion and pyloric reflux
demonstrated among men may provide a mechanism by which
peptic ulcers develop.

1. Female smokers show a prevalence of peptic ulcer higher
than that of nonsmokers by approximately two-fold.

2. The effect of cessation on healing is not known.

Interactions of Smoking with Drugs, Food Constituents and
Responses to Diagnostic Tests

Most published studies investigating the effects of cigarette
smoking on drug use have been performed on mixed popula-
tions; factors specific for women have not been demonstrated to
date. It has, however, been clearly demonstrated that women
are prescribed and consume more prescription drugs than men.

1. Studies of selected drugs indicate that smoking may affect
clinical responses and alter the dose required for an effective
therapeutic result.

2. Smoking interacts with oral contraceptive use to increase
the risk of myocardial infarction and subarachnoid hemor-
rhage.

3. Common clinical laboratory parameters are altered in
smokers compared to nonsmokers; the health significance of
these changes is unknown.

4. Insufficient information exists for assessment of the im-
pact of smoking on the nutritional needs of women.

Psychosocial and Behavioral Aspects of Smoking in Women

1. The percentage of 17-18 year old women who smoke has
shown a steady rise between 1968 and 1979. It now appears,
however, that the increase in smoking prevalence among all
12-18 year old females has leveled off and begun to decline.
Young women born after 1962 show a substantially reduced

12
initiation of smoking and will probably have a much lower pre-
valence of smoking as adults.

2. Those young women who do begin to smoke are starting to
smoke regularly at a younger age, with more than half of the
male and female adolescents who begin to smoke starting before
the 10th grade.

3. The earlier tobacco is used and the greater the number of
cigarettes smoked per day, the less likely an attempt to quit will
be successful.

4. The percentage of women smokers who smoke more than
one pack per day is increasing.

5. Adolescent and adult women are more likely to use low-tar
and-nicotine cigarettes, smoke fewer cigarettes per day and in-
hale less deeply than do men, but the difference between the
sexes in these patterns of smoking is decreasing. Adolescent
and adult black women are more likely to be smokers than their
white peers, but they smoke fewer cigarettes per day.

6. Adolescents from low income families, single parent
families, and families with lower parental educational levels are
more likely to become smokers.

7. Female and male adolescents are more likely to begin
smoking if a parent or older sibling also smokes.

8. Adolescent smokers associate with peers who smoke and
nonsmokers associate with nonsmoking peers.

9. Adolescent girls overestimate the percentage of their peers
who smoke and they have a very positive image of the people in
cigarette advertisements, but they are less likely than adoles-
cent boys to see smoking as a social asset.

10. Adolescent girls who smoke tend to be more outgoing but
feel less able to influence their future.

11. Adolescents experience stress due to feelings of unattrac-
tiveness, incompetency in school achievement and personal re-
lations, limited opportunity for personal growth and concern
over future social and economic roles. This stress may be the
common mechanism producing the increased rates of smoking
in some groups.

12. The factors associated with successful quitting by adoles-
cents of either sex are lower number of cigarettes smoked per
day, higher educational aspirations and achievement, greater
acceptance of the health risk of smoking, and having more
nonsmokers among their friends.

_ 13. It is possible that women and men modify their smoking
i order to maintain a constant nicotine level.

14. Women are more likely than men to smoke in order to
reduce stress.

15. Women at higher education and income levels are more

13
likely to succeed in quitting. Additional factors associated with
successful quitting are a strong commitment to change, the use
of behavioral techniques and reliable social support for quit-
ting. Women have been reported to show lower rates than men
of successful cessation following organized cessation programs,
a difference which is less apparent in those programs that in-
clude social support.

14
PART I:

PATTERNS OF CIGARETTE SMOKING.
PATTERNS OF CIGARETTE SMOKING
Introduction

This chapter traces the evolution of cigarette smoking among
successive generations of American women and men during the
twentieth century. The available evidence demonstrates that
women have differed from men in their historical onset of wide-
spread cigarette use, in the rate of diffusion of smoking among
each new birth cohort, in their intensity of cigarette smoking,
and in their use of various types of cigarettes.

Four main conclusions emerge from this analysis. First, al-
though men rapidly took up smoking during the early decades of
this century, the proportion of adult female cigarette smokers
did not exceed one-quarter until the onset of World War II. The
peak intensity of smoking occurred among women born after
1920. Second, as a result of higher past rates of quitting and
lower past rates of initiation among men, as well as changes in
the type of cigarette consumed, the smoking characteristics of
women and men are now becoming increasingly similar. Third,
the prevalence of cigarette smoking among adult American
women and men is declining. This conclusion applies to all age
groups, but with less certainty to the youngest generation of
women. Fourth, increasing public awareness of the health con-
sequences of smoking has resulted in significant changes in the
nature of the cigarette product. Yet little is known about the
effects of these product changes on the initiation, maintenance
and cessation of smoking, particularly among women.

Since the last review of cigarette smoking in the 1979 Report
of the Surgeon General (24), two new national surveys have
been performed under the sponsorship of the National Center
for Health Statistics and the National Institute of Education.
This chapter relies in part on the recent, preliminary results of
these surveys.

The Rise of Cigarette Smoking: 1900-1950

Although the use of cigarettes in the United States was ob-
served as early as 1854 (42,48), consumption did not increase
dramatically until after 1900. As shown in Figure 1, per capita
consumption of all types of cigarettes increased by more than
tenfold from 1900 to 1920. Despite a transient decline during the
Great Depression, consumption increased from 665 cigarettes
per capita in 1920 to 3,522 cigarettes per capita in 1950 (50).

A continuous, nationally representative series of smoking
prevalence rates during the period 1900 to 1950 is not publicly
available. Nevertheless, numerous sources can be pieced to-

17
gether to characterize the differential growth of cigarette
smoking among women and men.

Figure 2 depicts estimates of the percentage of male and
female current cigarette smokers in the greater Milwaukee
area, as compiled by the Milwaukee Journal (38). In 1928, the
first reported year of this survey, 51.8 percent of males aged 18
years and over smoked cigarettes. Sixty percent of male
cigarette smokers also smoked pipes or cigars. In total, 87 per-
cent of adult males used some type of tobacco (38).

Although earlier survey estimates of male smoking rates are
unavailable, it appears that the rise of cigarette consumption
prior to 1923 reflected both the conversion of established male
non-cigarette tobacco users to cigarette smoking and the re-
cruitment of a new generation of younger male smokers during
World War I. Innovations in cigarette production and market-
ing have been cited as influential factors in this rapid growth
(39,48,67). Camel cigarettes, a blend of lighter Burley smoking
tobaccos with previously dominant Turkish cigarette tobaccos,
were introduced in 1913 and within months attained a national
market. Two similar brands, Lucky Strike and Chesterfield, fol-
lowed in 1916 and 1919, respectively (39,48,67). During World
War I, the War Industries Board estimated that soldiers of the
Allied Armies consumed 60 to 70 percent more tobacco than
they had used in civilian life (28,29).

Cigarettes continued to dominate other forms of tobacco
among male smokers throughout the 1920s and 1930s. By 1935,
62.5 percent of adult males in the greater Milwaukee area
smoked cigarettes (Figure 2), while the percentages of pipe and
cigar users had declined substantially. Average cigarette con-
sumption frequency among men smokers increased from 3.7
packs per week in 1923 to 4.8 packs per week in 1935 (38).

Consumption among men accelerated during World War II
(Figures 1 and 2). In 1944, more than 25 percent of cigarettes
produced in the U.S. were cistributed to overseas forces (29),
typically for free or at low cost (39), to the point where sub-
sequent shortages developed in the domestic market. By 1948,
67.1 percent of adult males in the Milwaukee area smoked
cigarettes (Figure 2). This estimate of the prevalence of
cigarette use among urban men is confirmed by other local con-
sumer surveys performed in that year. For example, in 1948,
adult male smoking rates were 69.1 percent in Omaha, 67.4 per-
cent in Birmingham, 69.4 percent in Philadelphia, 63.9 percent
in Seattle, and 63.4 percent in San Jose (37).

The growth of cigarette smoking among women occurred
much later in the face of strong social taboos. Gottsegen noted
that “the ultra smart set and women social leaders began to

18
smoke at the turn of the century” (13). By 1906, American “girl
stenographers” were reported smoking cigarettes clandestinely
(5). By 1919, some younger women in New York were reported
smoking at dinner parties “with a trace of defiance” (48). By
1922, New York women were smoking openly on the streets and
in bus tops (48).

The first advertisement showing a woman smoking was Loril-
lard’s 1919 publicity for Helmar cigarettes (43,48). In 1926, a
young women in a Liggett and Myers’ Chesterfield advertise-
ment did not smoke but pleaded, “Blow some my way” (6). In
April, 1927, a Philip Morris advertisement for Marlboro cigar-
ettes noted that “women, when they smoke at all, quickly de-
velop discriminating taste,” and that Marlboro cigarettes were
as “mild as May” (2). In 1928, a Lucky Strike advertisement
urged women to “reach for a Lucky instead of a sweet”
(31,39,48). In 1934, Eleanor Roosevelt smoked cigarettes pub-
licly (26). By 1940, handbags and cosmetic compacts were typi-
cally designed to hold cigarettes (13).

Although the Milwaukee Journal (38) reported that 16.7 per-
cent of adult women smoked cigarettes in 1934 (Figure 2), prior
estimates of women’s smoking prevalence are sporadic. Wessel
estimated that women consumed 5 percent of all cigarettes in
1924 (66). Moody’s Investors Service estimated that women
smoked 12 percent of all cigarettes smoked in 1929 (44). The
average daily consumption of women smokers, as compared to
men smokers, is not documented for that period. If men smokers
consumed approximately twice as many cigarettes per day as
women smokers (cf. the Milwaukee Journal’s 1934 survey report
that women’s consumption frequency was 135 packs per year as
compared to 244 packs per year for male smokers), and if the
estimates of male smoking prevalence rates in Figure 2 are
taken as nationally representative, and if there were approxi-
mately 5 percent more adult males than adult females during
the 1920 to 1930 decade (51), then Wessel’s estimate yields a 6
percent adult female smoking prevalence in 1924 and Moody’s
estimate yields a 16 percent prevalence in 1929.

The Milwaukee Journal series in Figure 2 must be interpreted
in light of changes in the type of survey respondent and the
wording of questions designed to elicit smoking practices (see
caption to Figure 2). Moreover, this urban population series
may not be representative of all American women. Neverthe-
less, the publicly available survey data sources are consistent
with the conclusion that smoking rates among women did not
exceed one-quarter until the onset of World War II.

Based on 10,000 applications for insurance policies during
1930 to 1940, Ley (32) estimated age-standardized smoking rates

19
of 63.9 percent of men and 20.8 percent of women aged 15 years
and over. In 1935, Fortune Magazine, in the first nation-wide
survey (12), reported that 52.5 pereent of adult men and 18.1
percent of adult women smoked cigarettes. (See Table 1). Among
those under 40 years of age, 65.5 percent of men and 26.2 percent
of women were smokers. Among those over 40 years, 39.7 per-
cent of men and 9.3 percent of women were smokers. Urban-
rural differences in smoking were significant. The proportion of
smokers ranged from 61.4 percent of men and 31.2 percent of
women in cities with population over one million, to 44.1 percent
of men and 8.6 percent of women in rural areas with population
under 2,500. A survey of 250 urban women by the Market Re-
search Corporation in 1937 reported 26 percent regular smokers
and an additional 23 percent occasional smokers (47).

After 1940, women’s smoking rates accelerated, as new gen-
erations of women, particularly younger women in urban areas,
entered the labor force (see also title “Occupation and Envi-
ronment” in this Report). In 1944, the Gallup Poll reported 48
percent adult male smokers and 36 percent adult female smok-
ers (4). In 1949, the Gallup findings were 54 percent male and 33
percent female (4). Local consumer surveys of urban areas in
1948 revealed 37.6 percent adult women cigarette smokers in
Milwaukee (see also Figure 2), 34.3 percent in Omaha, 35.6 per-
cent in Birmingham, 46.7 percent in Philadelphia, 38.3 percent
in Seattle, and 34.0 percent in San Jose (37). Conover, citing
“trade journal” surveys in the three or four years prior to 1950,
reported smoking prevalence rates of 65 to 70 percent among
men and 40 to 45 percent among women (9).

Although the differential growth of cigarette use among vari-
ous socioeconomic groups is not well documented, the available
data during this period suggest that male smoking rates de-
clined with increasing income, while the relation of women’s
smoking to income was less clear. The Milwaukee Journal in
1945 noted 58 percent of men with monthly rents over $50 were
smokers, and 75 percent of men with rents under $30 per month
were smokers (38). Among women, the corresponding propor-
tions were 32 and 37 percent respectively. In Mills and Porter’s
1947 survey of Columbus, Ohio (36), 28.3 percent of white
females and 64.9 percent white males smoked cigarettes,
whereas 36.4 percent black females and 68.9 percent black males
smoked cigarettes (estimates calculated from the age distribu-
tion data provided in Table 6 of (36)). Kirechoff and Rigdon, ina
survey of over 21,000 patients, visitors, and employees of hospi-
tals in Houston and Galveston, noted that 63.2 percent white
males, and 33.4 percent white females, 66.3 percent black males,
and 32.2 black females smoked cigarettes (30).

20
All of the above findings reinforce the conclusion that the
onset of widespread cigarette use among women lagged behind
that of men by 25 to 30 years. This historical delay in the growth
of cigarette smoking among women has also been documented
for the United Kingdom (8,46,49).

The Emergence of Filtertip Cigarettes: 1951-1963

As shown in Figure 1, total per capita consumption of cigar-
ettes declined during 1953 to 1954. This decline was coincident
with the appearance in the popular press of reports seriously
suggesting a link between cigarette smoking and lung cancer
(10,33,34,40). Thereafter, the consumption of filtertip cigarettes
increased rapidly (Figure 1). In 1953 filtertip cigarettes consti-
tuted 2.9 percent of cigarette production. By 1958, their share of
production had increased to 45.3 percent, and by 1963 it was 58.0
percent (50).

The transient decline during 1953 to 1954 in the number of
cigarettes consumed was not clearly matched by a decrease in
the proportion of cigarette smokers (27). At least in urban areas,
the proportion of women smokers continued to increase. From
1953 to 1958, the prevalence of adult female smoking increased
from 42.9 to 45:4 percent in Milwaukee (Figure 2), from 38.4 to
42.6 percent in Omaha, from 47.0 to 50.2 in Washington, D.C.,
and from 39.6 to 44.4 percent in San Jose (37).

At the same time, both women and men rapidly converted to
filtertip cigarettes. By 1958, filter cigarette use prevailed
among 61 percent of women smokers and 42 percent of men
smokers in Milwaukee, 54 percent of women smokers and 43
percent of men smokers in Omaha, 53 percent of women smokers
and 47 percent of men smokers in Washington, D.C., and 59 per-
cent of women smokers and 42 percent of men smokers in San
Jose (37). In a nation-wide 1964 survey reported by the National
Clearinghouse for Smoking and Health (64), 79 percent of adult
female smokers and 54 percent of adult male smokers used filter
cigarettes.

Increasing Public Health Awareness: 1964-1979

Per capita consumption reached a peak of 4,336 in 1963 (Fig-
ure 1). It declined transiently after the appearance in January
1964 of the first Report of the Advisory Committee to the Sur-
geon General (52). Per capita consumption continued to decline
during the subsequent period of increased publicity concerning
the health hazards of smoking (24,27). Since 1975, per capita
consumption has declined at an average rate of 1.4 percent an-

21
 

total

Nn

fA

/ filter

 

fg
‘,

 

 

L.

LS

 

5

cigarette consumption per capita

 

 

 

 

 

 

 

 

 

ST

feo
1900 ="10 20 30 ‘40 50 60 70 80
year

 

FIGURE 1.— Annual consumption of cigarettes and filtertip
cigarettes per person aged 18 years and over,
1900-1979*

*Total per capita consumption data for 1917-19 and 1940-79 include overseas
forces. Total per capita consumption for 1979 is preliminary estimate. Per
capita consumption of filtertip cigarettes derived from annual data on the
filtertip share of total cigarette production.

SOURCE: U.S. Department of Agriculture (50).

nually. The most recent 1979 estimate of 3,900 cigarettes per
capita closely approximates that observed in 1952.

Table 1 summarizes the results of selected, nationally repre-
sentative surveys of adult cigarette use during the period 1935
to 1979. Except for the Fortune survey of 1935 (12) and the sup-
plement to the Current Population Survey in 1955 (16), these
data were collected under the sponsorship of the National Cen-
ter for Health Statistics. The results of other recent national
surveys of adult cigarette use (34,57,58,61,62,64), revealing very
similar trends in the prevalence of smoking, were described in
the 1979 Surgeon General’s Report (24).

Among adult males, the prevalence of regular cigarette use
has declined continuously since 1965, with more marked de-
creases in the intervals 1965 to 1970 and 1976 to 1978. (The abso-
lute standard errors for the National Center for Health Statis-

22
tics estimates for 1970 to 1976 are less than 0.3 percent. The
absolute standard errors for 1978 and 1979 are 0.6 percent.)
Among adult women, the direction of change in smoking preva-
lence is less clear. The estimates for the interval 1976 to 1979,
however, suggest a recent downturn. The preliminary 1979 es-
timate of 32.3 percent for the overall prevalence of adult
cigarette smoking among both sexes represents the lowest re-
corded value in at least 45 years. (The overall prevalence of
cigarette smoking in the 1935 Fortune Magazine survey was
37.3 percent among adults of both sexes.)

TABLE 1.—Estimates of the prevalence of regular cigarette
smoking among adults, United States, selected
national surveys, 1935-1979

 

 

Year Females Males
1935 18.1 52.5
1955 24.5 52.6
1965 33.3 51.1
1970 31.1 43.5
1974 31.9 42.7
1976 32.0 41.9
1978 29.9 37.0
1979 28.2 36.9

 

Data for 1978 are revisions of preliminary estimates reported in Harris (26).
Data for 1979 are preliminary estimates based on a sample of over 13,000
interviews conducted during January-June 1979, provided by Health
Interview Survey, National Center for Health Statistics. 1955 data represent
persons 18 years and over. 1976 data represent persons 20 years and over.
Estimates for the years 1965, 1970, 1974, 1978 and 1979 represent persons 17
years and over.
SOURCE: Fortune Magazine (12), Haenszel, W. (16), U.S. Department of
Health, Education, and Welfare (54-56, 58-59).

These patterns of change in smoking prevalence applied to
both white and black adults. For white men, the prevalence of
regular smoking declined from 51.5 percent in 1965 to 36.3 per-
cent in 1979. For black men, the prevalence of regular smoking
declined from 60.8 percent in 1965 to 42.0 percent in 1979. For
white women, smoking prevalence declined from 34.2 percent in
1965 to 28.2 percent in 1979. For black women smoking preva-
lence declined from 34.4 percent in 1965 to 28.9 percent in 1979.
Racial differences in cigarette use are discussed in greater de-
tail in the chapter in this report entitled “Psychosocial and Be-
havioral Aspects of Smoking in Women.”

Although the Milwaukee area data for 1964 to 1979 do not
closely match these national estimates, Figure 2 does show a
marked decline in smoking rates for both sexes during 1964 to

23
 

MEN

 

 

 

 

 

 

PERCENT
8

} WOMEN

 

MIL

 

 

 

10

 

 

 

 

 

 

 

 

 

 

0
1800 1 1920 1930 1940 1950 1960 1970 1980

YEAR
FIGURE 2.— Percentage of adult current cigarette smokers in the
greater Milwaukee area, 1924-—1979*

*Prior to 1941, the wording of the question eliciting cigarette use and the type
of respondent are not recorded. From 1941 to 1954, men were asked, “Do you
smoke cigarets?’ From 1955 to 1959, all respondents were asked, “Do any
men (women) in your household smoke cigarets with (without) a filter tip?”
From 1960 to 1965 and in 1967, both men and women were asked “Have you
bought, for your own use, cigarets with (without) a filter tip in the past 30
days?” In 1966 and from 1968 to 1979, both men and women were asked,
“Have you bought, for your own use, cigarets with (without) a filtertip in the
past 7 days?” All percentages reflect adults aged 18 years and over. Data for
women from 1976 to 1979 (open circles) represent filtertip cigarette smokers
only.

SOURCE: Milwaukee Journal (38).

1970, a deceleration in the decline of smoking prevalence during
1971 to 1975, and a resumption of the decline in prevalence
among men in the last four years.

The cessation of cigarette smoking has been a significant fac-
tor in explaining this overall decline in smoking prevalence (24).
Column (i) of Table 2 presents estimates of the percentage of
recent smokers who made a “fairly serious attempt to quit”

24
TABLE 2.—Estimated rates of attempted and successful quitting
among adult, recent cigarette smokers, United
States, 1970-1979

 

(i) (ii) (iii)

 

Percent of Percent of Percent of
All Recent Smokers All Recent
Smokers Who Attempting to Smokers Who
Attempted to Quit in Past Reported
Quit in Past Year Who Successfully
Year Reported Quitting in
Successfully Past Year
Quitting
Women
1970 40.8 21.3 8.7
1975 30.2 19.5 5.9
1978 32.7 18.8 6.2
“1979 32.9 21.6 7.0
Men
1970 44.4 26.4 11.7
1975 28.3 20.1 5.7
1978 29.1 21.5 6.3
1979 31.4 21.3 6.7

 

1970 and 1975 data from surveys of persons aged 21 years and over, conducted
by National Clearinghouse for Smoking and Health. 1978 and 1979 data from
the Health Interview Survey of persons aged 17 years and over, conducted by
the U.S. National Center for Health Statistics. 1979 data are preliminary
estimates based on interviews during January-June of that year.

SOURCE: U.S. Department of Health, Education, and Welfare (54,61,62).

within one year of the interview date. (Recent smokers include
all current smokers plus those former smokers reported to have
stopped within one year of interview.) Column (ii) shows what
proportion of those attempting to quit regarded themselves as
former smokers. Column (iii) shows the proportion of all recent
smokers (whether or not they attempted or succeeded quitting)
who reported themselves as recent former smokers. These data
necessarily reflect respondents’ self-assessment of both the
seriousness of a quit attempt and their degree of success.
Nevertheless, they do provide an indication of the representa-
tive smoker’s annual probability of attempting to quit, the
probability of successful cessation given a quit attempt, and the
overall annual smoking cessation rate. (The absolute standard
errors in Table 4 are approximately 1.0 percent, 1.5 percent, and
0.3-0.5 percent for columns (i), (ii), and (iii), respectively.)

All three indicators of smoking cessation were highest for
men in 1970. Although a relatively large proportion of women
smokers attempted to quit smoking in 1970 (column (i)), their

25
probability of success in that year was significantly lower than
that of men (column (ii)). Quit attempt rates for both sexes (col-
umn (i)) declined by 1975, but have increased in 1978 to 1979.
With respect to the probability of attempting to quit and the
success rate, adult men and women cigarette smokers are now
indistinguishable.

Table 3 displays recent changes in the distribution of
cigarette brands according to F.T.C. “tar” contents. The propor-
tion of adults smoking cigarettes with F.T.C. “tar” delivery less
than 15 milligrams has increased from 9.5 percent of women and
2.9 percent of men in 1970 to 38.5 percent of women and 28.1
percent of me in the first half of 1979. A corresponding increase
in the proportion of smokers of cigarettes with F.T.C. nicotine
delivery less than 1.0 milligram was also observed.

TABLE 3.—Estimated percentage distribution of adult current
regular cigarette smokers according to F.T.C. “tar”
content of primary brand, United States 1970-1979

 

 

Less Than 5.0 to 10.0 to 15.0 to 20.0 mg

Year 5.0 mg 9.9 mg 14.9 mg 19.9 mg or More
Women

1970 0.7 2.0 6.8 67.1 23.4

1975 1.2 1.2 15.0 75.1 7.5

1978 5.3 8.8 21.1 59.2 5.7

1979 5.6 9.5 23.4 55.4 6.1
Men

1970 0.2 0.9 1.8 61.3 28.1

1975 0.6 1.1 11.0 68.1 19.2

1978 3.3 6.2 13.5 63.5 13.6

1979 2.6 8.5 17.0 60.1 11.8

 

1979 data are preliminary estimates provided by the National Center for
Health Statistics. 1970 and 1975 data represent adults aged 21 years and over.
1978 and 1979 data represent adults aged 17 years and over. Estimates
exclude those with unknown primary cigarette brand.

SOURCE: U.S. Department of Health, Education, and Welfare (54,61,62).

At the same time, the average daily cigarette consumption of
adult smokers has increased. Table 4 shows recent changes in
the distribution of reported daily cigarette consumption among
current smokers. These data must be interpreted in light of
possible underreporting biases (65) and, in particular, a strong
tendency for respondents to round off their reported daily con-
sumption to one pack. Nevertheless, the percent of women
smoking less than one pack per day has declined, while the pro-
portion smoking more than one pack per day has increased. Ex-
cept for 1979, a similar trend is observed for men. (The absolute

26
standard errors of the 1978 and 1979 estimates are approxi-
mately 1.0 percent.)

The data of Table 4 represent the more recent portion of an
apparently long run trend toward increasing daily cigarette
consumption among regular smokers. In 1924, Milwaukee men
smokers consumed an average of 10 cigarettes per day (38). In
1934, male smokers in Milwaukee consumed an average of 13.4
cigarettes per day, while women smokers consumed 7 per day
(38). If cigarette consumption in 1935 was 1,564 per adult (Fig-
ure 1 and (50)), and if the overall percentage of adult smokers
was 37.3 percent (12), then mean consumption per adult smoker
was 11.5 cigarettes per day. If consumption per adult was 3,597
in 1955 and if the prevalence of regular smoking was 37.6 per-
cent (16), then mean consumption per adult in that year was
26.2 cigarettes. The corresponding calculation based on 1979 per
capita consumption data and adult prevalence data (Figure 1
and Table 1) yields 33.3 cigarettes per day.

Numerous epidemiological studies and other surveys per-
formed during the period 1950 to 1965 have shown that for both

TABLE 4.—Estimated percentage distribution of adult current
cigarette smokers according to reported daily
consumption frequency, United States, 1965-1979

 

 

Percent Smoking Percent Smoking
Less Than 15 25 Cigarettes or
Year Cigarettes per Day More per Day
Women
1965 44.5 13.7
1970 39.1 18.0
1974 38.7 18.5
1976 36.5 19.6
1978 36.0 21.0
1979 34.6 22.4
Men
1965 29.6 24.5
1970 27.8 27.7
1974 26.3 30.6
1976 24,2 31.1
1978 23.4 34.2
1979 26.4 32.2

 

Data for 1976 represent persons aged 20 years and over. All other years

represent persons aged 17 years and over. Data for 1979 are preliminary

estimates based on interviews conducted during January-June of that year,

provided by the Health Interview Survey, National Center for Health

Statistics.

SOURCE: Harris, J. E. (26), U.S. Department of Health, Education, and
Welfare (54~56,58-59).

27
sexes, especially for women, the proportion of heavy smokers
was larger among the younger age groups (14,16,19,20,22,
30,36,61,64). These findings applied to current daily cigarette
consumption and lifetime maximum cigarette consumption.
They are consistent with the hypothesis that regular smokers
in past decades consumed fewer cigarettes per day than con-
temporary smokers.

The empirical relationships between rates of smoking cessa-
tion (Table 2), changes in F.T.C. “tar” and nicotine delivery of
cigarettes (Table 3), and increases in daily cigarette consump-
tion (Table 4) are poorly understood (25). It is not known
whether smokers of the lowest “tar” cigarettes are more or less
likely to attempt to quit, or to succeed in quitting, than smokers
of conventional filtertip or nonfilter cigarettes. The extent to
which the act of switching to a lower “tar” cigarette may serve
as a substitute for quitting may differ among women and men.
The observed increase in daily cigarette consumption among
current smokers could represent the effect of: higher cessation
rates among lighter smokers; an increase in the daily cigarette
consumption of continuing smokers; or an increased daily
cigarette consumption of new entrants into the smoking popu-
lation; or a combination of these effects (24). The relationship of
these possible mechanisms to the observed increase in the pro-
portion of filtertip cigarette and low “tar” cigarette smokers is
not well elucidated.

Exposure to Cigarette Smoke Among Successive Birth Cohorts

Figures 3 and 4 depict estimates of the prevalence of current
cigarette smoking from 1900 to 1978 among successive birth
cohorts of men and women. Each continuously graphed time
series corresponds to individuals born during a particular dec-
ade. For example, among women born from 1931 to 1940 (Figure
4), who are now 40 to 49 years old, the prevalence of smoking
rose rapidly during the post World War II period and reached a
peak of 45 percent by 1963. Thereafter, their overall prevalence
of smoking declined to 39 percent in 1978.

These prevalence data were constructed from the reported
lifetime smoking histories of over 13,000 respondents to the
Health Interview Survey during July to December, 1978. (For
related applications of this methodology, see 7,15,27). Although
the accuracy of survey recollection of age started smoking, age
of smoking cessation, and the duration of significant, temporary
periods of abstinence is not known, no particular source of recall
bias has been identified (15,16). However, the significantly
higher mortality rates of continuing smokers, as compared to

28
   

 

 

  

 

 

 

 

 

 

70 MEN "
ton zl. 1931-40
60 ; 1 RY ! 1941- 50
1901-1 ~ ay “
“00
oT] PT MLN
f
a 30
| h, :
20
i
‘ot —f | __}1951- 60

 

 

 

 

 

 

 

 

 

 

1900 1910 1920 1930 1940 1950 1960 1970. 1980
YEAR

FIGURE 3.—Changes in the prevalence of cigarette smoking
among successive birth cohorts of men, 1900-1978

Calculated from the results of over 13,000 interviews conducted during the last
two quarters of 1978, provided by Division of Health Interview Statistics, U.S.
National Center for Health Statistics.

SOURCE: U.S. Department of Health, Education, and Welfare (60).

nonsmokers or former smokers (1,11,17,18,41,45,46,52), intro-
duces a selection bias that may understate the prevalence of
past smoking for the oldest cohorts. For example, on the basis of
the insurance life tables recently reported by Cowell and Hirst
(11), a male cigarette smoker at age 32 has an estimated 25
percent probability of surviving to age 80, as compared to 49

29
I931- 40
WOMEN BI

50 |
1921-30 |

40 += eat

 

 

a rs
\

 

 

 

 

_ 30 KET igst- 60
2 1-20, |
2 “ ~
ra 1941-50
Do Y ‘
190140
0 \A }
=1900 “
_——

 

 

 

 

 

 

 

 

 

5 LL.

17900 «61910 1920 1930 1940 1950 1960 1970 1980

YEAR
FIGURE 4.— Changes in the prevalence of cigarette smoking
among successive birth cohorts of women,
1900-1978

 

Calculated from the results of over 13,000 interviews conducted during the last
two quarters of 1978, provided by Division of Health Interview Statistics, U.S.
National Center for Health Statistics.

SOURCE: U.S. Department of Health, Education, and Welfare (60).

percent for a nonsmoker. The estimated probabilities of surviv-
ing to age 60 are 80 percent for smokers and 93 percent for
nonsmokers, respectively. Therefore, the peak smoking preva-
lence rate of men born before 1900, calculated from 1978 survey
responses to be 46 percent in 1937, could actually have been as
high as 65 percent. Since individuals who quit smoking have a
higher survival than continuing smokers (18,45), the actual
point in time at which smoking rates peaked in this cohort may
have been later than 1937. This effect is less likely to be impor-
tant among men born after 1910, who are now approaching 70
years old. A similar calculation for men born, for example, be-
tween 1911 and 1920 reveals that their peak smoking rate may
have been understated by at most 2 or 3 percentage points.
This source of bias is likely to be less important for older
women. On the basis of age-specific mortality data reported by

30
Hammond in 1966 (18, Appendix Table 2b), women continuing to
smoke cigarettes from age 35 would have an estimated 48 per-
cent chance of surviving to age 80 years, as compared to 54
percent for nonsmokers. The estimated probabilities of survival
to age 60 would be 91 percent for smokers and 93 percent for
nonsmokers. If these survival data are currently applicable to
women smokers and nonsmokers, then the estimated peak pre-
valence rate of smoking among women born before 1910 could be
understated by only one to two percentage points.

Despite these possible biases, the predicted percentages of
current smokers in Figures 3 and 4 are consistent with past
survey and epidemiological data on the smoking habits of dif-
ferent age groups (12,14—16,19-23,30,35,36,55).

Comparison of Figures 3 and 4 reveals the following conclu-
sions. (a) The most marked differences in smoking prevalence
among men and women appeared in those individuals born be-
fore 1910, who are now over 70 years of age. (b) Women born
between 1921 and 1940, who are now approaching 40 to 59 years
of age, experienced the highest smoking prevalence rates.
These women have not yet reached the age where the absolute
excess deaths of smokers over nonsmokers are expected to be-
come substantial (1). (ec) Among successive cohorts of men and
women, the age of peak smoking prevalence has declined.
Among younger cohorts, the peak smoking prevalence rates are
declining, although the effect is less marked for women. Men
born between 1911 and 1920 reached a peak smoking prevalence
of 71 percent during 1946 to 1948, while those born 1941 to 1950
reached a peak smoking prevalence of 58 percent in 1968 to 1969.
Women born 1921 to 1930 reached a peak prevalence of 44 per-
cent in 1958 to 1960, while those born in 1941 to 1950 reached a
peak smoking prevalence of 41 percent in 1970 to 1973. (d)
Among men born 1951 to 1960, the rate of increase of smoking
prevalence was slower than in previous cohorts. This slowing of
the diffusion of smoking practices was coincident with the in-
creased publicity concerning the health risks of smoking and
the relatively high rate of quitting smoking among adult males
in the late 1960s. A similar effect is not clearly discernible for
young women in this cohort. In both sexes, among individuals
who are now approaching ages 20 to 29, the prevalence of smok-
ing has apparently peaked. Smoking rates among men and
women in this age group are now nearly indistinguishable.

Figure 5 depicts the mean age of starting regular smoking
among successive birth cohorts, calculated from the same data
as for Figures 3 and 4. The age of onset of smoking among
women declined continuously during this century, to the point
where it is nearly indistinguishable from that of men. As a re-

31
 

8

Oo
o

e

N
oO
T

t

Men

So. a
T T
L I

Mean Age Started Smoking (years)
on 8

 

 

1

941-50

1 1 1 1 4
09 901-10 220 199499193140 ,

 

951-60

Birth Cohort

FIGURE 5.— Mean age of onset of regular smoking among
successive birth cohorts of women and men
SOURCE: U.S. Department of Health, Education, and Welfare (60).

sult, each successive cohort of lifelong continuing women smok-
ers will have an increasing number of years of exposure to
cigarette smoke.

Figure 6 depicts the accumulated years of cigarette smoking
per capita, up to 1978, for each birth cohort. These magnitudes
correspond to the total areas under each cohort prevalence
curve in Figures 3 and 4. Among women, individuals born 1911
to 1920 have thus far experienced the largest total exposure per
capita. However, as seen from Figure 4, unless the smoking pre-
valence rates of women born during 1921 to 1940 decline more
rapidly in the future, the lifetime exposure of these latter
cohorts is likely to exceed that of the 1911 to 1920 cohort. It is
not clear, however, whether the lifetime exposure of men born

32
from 1921 to 1940, now 50 to 69 years of age, will exceed that of
previous generations. With each successive cohort, the ratio of
female to male exposure increasingly approaches one.

As a result of the rapid diffusion of filtertip cigarettes after
1950 (Figure 1), each successive birth cohort was exposed to a
different proportion of filtertip and nonfilter cigarettes. Details
of the respondent’s past history of cigarette brand use were not
obtained in the 1978 Health Interview Survey. Such data, how-
ever, are available from a series of over 2,000 interviews of cur-
rent and former smokers aged 21 years and over, conducted by
the National Clearinghouse for Smoking and Health in 1975
(62). Figure 7 depicts, for the same birth cohorts, the proportion
of lifetime years of smoking that represents filtertip cigarette
use. (The birth dates of the youngest cohorts in Figures 6 and 7
do not match due to differences in survey date and eligible age
group.) Among men, there is a distinct, monotonically increas-
ing relation between the proportion of filtertip cigarette expo-.
sure and birth date. The corresponding relationship among
women born before 1930 reflects their lower smoking cessation
rates and, therefore, their continued use of filter cigarettes (62).
A woman born in 1925, for example, who began smoking at age
21 (Figure 5), and who switched to filtertip cigarettes in 1957
(Figure 1), has now been smoking filtertip cigarettes for over
two thirds of her smoking career and 40 percent of her entire
life.

The prevalence of cigarette smoking, age of initiation, lifetime
duration of smoking, and the extent of use of various types of
cigarettes are not the only measures of cigarette smoke expo-
sure among a particular population. Trends in depth of inhala-
tion, fraction of cigarette actually smoked, and other dimen-
sions of the style of smoking also affect smoke exposure. How-
ever, as discussed in the 1979 Surgeon General’s Report (24),
these are difficult to determine from survey data. In view of the
concern over the accuracy of contemporaneous survey reports
of daily cigarette consumption (65); past accounts of the time
course of daily cigarette consumption would be difficult to as-
sess accurately. Nevertheless, the evidence presented in the
previous section is consistent with the conclusion that the aver-
age daily cigarette consumption among regular cigarette users
has increased among each successive birth cohort.

Cigarette Smoking Among Young Women

The more marked decline in peak smoking prevalence among
men born between 1951 and 1960, now approaching 20 to 29
years of age, reflected a slowing in the rate of initiation of smok-

33
 

 

 

 

MEN ——+

Gq
oO
ae Cee

 

 

+— WOMEN—>

 

 

 

 

8

 

—_
on
te
i
t
a
T

 

n

—_

oO
1 1
‘
!
t

'

'

i
T

 

 

Cumulative Years of Cigarette Smoking per Capita
Nh
On
ae Cy Be

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

oO

“1900 1901-10 1911-20 1921-30 193140 1941-50 1951-60
Birth Cohort

FIGURE 6.— Accumulated years of cigarette smoking per person
among successive birth cohorts of women and men,

1978
SOURCE: U.S. Department of Health, Education, and Welfare (60).

ing that was not observed in women of the Same age group. This
trend appears to be continuing in the next birth cohort.

Table 5 reports the results of nation-wide surveys of teenage
cigarette smoking during 1968 to 1979. The most recent survey,
conducted by the National Institute of Education during late
1978 and early 1979, presents the preliminary results of over
2,600 telephone interviews of individuals aged 12 to 18 years. In
this survey, but not in the others reported in Table 5, women
and men 19 years of age were also interviewed. Otherwise, the
survey sampling techniques and interview questions regarding
smoking practices were the same for all the surveys. (See notes
to Table 5).

The data in Table 5 support the conclusion that the rate of
initiation of smoking among even the youngest men is declining,

34
 

8

rece,

 

 

eaeeewemy
eseeweeee ad

 

+— WOMEN —

 

 

MEN ->

 

 

er |

gS 8a B B

weer erens

 

eens sean
aaeseneeee8

 

 

Bg

i

oO
Son ewe Se ewe ewe ewe eam mew,
scene ee eee Beeman enawané

 

=~
oO

 

 

 

 

Percent of Years Smoking Filter-tip Cigarettes

 

 

 

 

 

 

 

 

 

 

 

 

 

-1900 190140) = 1911-20 1921-30 1931-40 1941-50 1951-54

Birth Cohort
FIGURE 7.—Proportion of years smoking filtertip cigarettes
among successive birth cohorts of women and men,
1975

Caleulated from the results of over 2,000 smoking histories of men and women
who had ever smoked, collected by National Clearinghouse for Smoking and
Health.

SOURCE: U.S. Department of Health, Education, and Welfare (62).

an effect that is not present among young women. These results
must be interpreted in light of sampling variability. (The abso-
lute standard errors on the 1979 estimates for ages 15-16 and
17-18 are about 2 percent.) As in adult surveys, non-response
biases must also be considered. Nevertheless, the findings in
Table 5 are consistent with other nation-wide estimates of
smoking rates among young women and men. The prevalence of
Current regular smoking among respondents 17 to 19 years of
age in this survey was 28.1 percent for females and 22.8 percent
for males. The comparable rates for women and men aged 17 to
19 from the Health Interview Survey were 29.2 percent and 27.5
Percent, respectively. An analysis of the growth of smoking
Prevalence among this group, performed in the same manner as

35
TABLE 5.—Estimated percentage of current, regular cigarette
smokers, ages 12-18, United States, 1968-1979

 

 

Year Ages 12-14 Ages 15-16 Ages 17-18
Females
1968 0.6 9.6 18.6
1970 3.0 14.4 22.8
1972 2.8 16.3 25.3
1974 4.9 20.2 25.9
1979 4.4 11.8 26.2
Males
1968 2.9 17.0 30.2
1970 5.7 19.5 37.3
1972 4.6 17.8 30.2
1974 4.2 18.1 31.0
1979 3.2 13.5 19.3

 

Nation-wide surveys performed by National Clearinghouse for Smoking and
Health, 1968-1974, and National Institute of Education, 1979. Current regular
smokers in all surveys include all those who smoke cigarettes at least weekly. In
1979, approximately 90 percent of current regular smokers used cigarettes ona
daily basis. For 1979 only, 29.7 percent males and 31.9 percent females, aged 19,

were reported as regular smokers.
SOURCE: U.S. Department of Health, Education, and Welfare (63).

that of Figures 3 and 4, suggested that smoking rates among
this group of women grew rapidly and exceeded those of men by
1975. The future smoking habits of this generation of young
women cannot be accurately predicted.

Smoking among adolescent women is discussed in greater de-
tail in the chapter entitled “Psychosocial and Behavioral As-
pects of Smoking in Women” in this Report.

Summary

1. Women have differed from men in their historical onset of
widespread cigarette use, in the rate of diffusion of smoking
among each new birth cohort, in their intensity of cigarette
smoking and their use of various types of cigarettes.

2. Men took up cigarette smoking rapidly at the beginning
of the twentieth century, especially during World War I. Cigar-
ettes rapidly replaced other forms of tobacco. By 1925, approxi-
mately 50 percent of adult males were cigarette smokers. Smok-
ing among men accelerated rapidly during World War II. By
1950, the prevalence of cigarette use among men approached 70
percent in some urban areas.

3. The onset of widespread cigarette use among women lag-
ged behind that of men by 25 to 30 years. The proportion of adult

36
women smoking cigarettes did not exceed one-quarter until the
onset of World War II.

4, Between 1951 and 1963, increasing proportions of women
and men smokers converted to filtertip cigarettes. By 1964, 79
percent of adult women smokers and 54 percent of adult men
smokers used filter cigarettes.

5. After reaching a peak value of 4,336 in 1963, annual per
capita consumption of cigarettes declined in 1964, 1968-70, and
in the period since 1975. The most recent estimate of 3,900
cigarettes per capita in 1979 is approximately equal to that ob-
served in 1952.

6. From 1965 to 1978, the proportion of adult men cigarette
smokers declined from 51 to 37 percent. The preliminary esti-
mate of adult men’s smoking prevalence for 1979 is 36.9 percent.
From 1965 to 1976, the proportion of adult women smokers re-
mained virtually unchanged at 32 to 33 percent. Since 1976, the
proportion of women smokers has declined to below 30 percent.
For 1979, the preliminary estimate of adult women’s smoking
prevalence is 28.2 percent. The overall smoking prevalence of
32.3 percent for both sexes in 1979 represents the lowest re-
corded value in at least 45 years.

7. The proportion of adult smokers attempting to quit smok-
ing declined from 1970 to 1975, but increased in 1978-1979. In
contrast to past years, the proportions of women and men now
attempting to quit smoking, and their reported quitting rates,
are indistinguishable. Approximately one in three adult smok-
ers now makes a serious attempt to quit smoking during the
course of a year. Approximately one in five of those who attempt
to quit subsequently succeed.

8. The proportion of adult smokers using lower “tar” and
nicotine brands has increased substantially. In 1979, 39 percent
of adult women smokers and 28 percent of adult men smokers
reported primary brands with F.T.C, “tar” delivery less than
15.0 milligrams. It is not known whether smokers of the lowest
“tar” cigarettes are more or less likely to attempt to quit smok-
ing, or to succeed in quitting, than smokers of conventional fil-
tertip or non-filter cigarettes.

9. The average number of cigarettes smoked by women and
men current smokers has increased. The relationship of this
finding to recent declines in the average F.T.C. “tar” and
nicotine deliveries of cigarettes is not well understood.

10. With each successive generation, the smoking character-
istics of women and men have become increasingly similar.

11. Among women, the average age of onset of regular smok-
ing progressively declined with each successive birth cohort —
from 35 years of age for those born before 1900, to 16 years of

37
age among those born 1951 to 1960. The average age of onset of
regular smoking among young women is now virtually identical
to that of young men.

12. Maximum smoking prevalence rates have declined sub-
stantially in recent birth cohorts of men. Men born 1931 to 1940
reached a peak smoking proportion of 61 percent during 1960~-
62, while men born 1941 to 1950 reached a peak smoking propor-
tion of 58 percent in 1968-69. Men born 1951 to 1960 reached a
peak smoking proportion of 40 percent in 1976. Among recent
cohorts of women, peak smoking prevalence rates have declined
to a much smaller extent. Women born 1931 to 1940 reached a
peak smoking proportion of 45 percent in 1966-68, while women
born 1941 to 1950 reached a peak smoking proportion of 41 per-
cent in 1970-73. Women born 1951 to 1960 reached a peak smok-
ing proportion of 38 percent in 1976. Among the generation born
1951 to 1960, the proportions of women and men smoking
cigarettes are now virtually identical.

13. The proportions of women and men smokers in each age
group have declined. Among those born before 1951, this decline
in smoking prevalence resulted mainly from smoking cessation.
By contrast, the observed decline in smoking prevalence among
younger men born 1951 to 1960 has resulted from both smo<ing
cessation and a lower rate of smoking initiation. This decline in
the rate of onset of smoking among young men has not been
observed for young women,

14. Recent survey data on adolescent smoking habits reveal
that by ages 17 to 19, smoking prevalence among women ex-
ceeds that of men. This finding supports the conclusion that the
rate of initiation of smoking among young men— but not that of
young women—is declining. The future cigarette use of the
youngest generations of women is uncertain.

15. With each successive birth cohort, the accumulated years
of cigarette smoking per woman has progressively approached
the accumulated years of cigarette smoking per man. Each sue-
cessive birth cohort has also experienced progressively smaller
sex differences in the fraction of lifetime years of smoking that
represents filtertip cigarette use.

16. Among men born during this century, each successive
birth cohort has thus far experienced fewer cumulative years of
cigarette smoking, higher proportionate exposure to filtertip
cigarettes, and lower smoking prevalence rates. This relation-
ship between birth date and cigarette smoke exposure does not
hold for women. Women born 1921 to 1940 have experienced
substantially higher smoking prevalence rates than earlier
generations. Unless they quit smoking in substantial numbers,
these women, currently aged 40 to 59, will surpass older women

38
in total years of cigarette smoking per capita, the total years of
nonfilter cigarette smoking per capita, and in the total number
of cigarettes smoked. The health consequences of this enhanced
exposure to cigarette smoke among women are likely to be more
prominent in the coming decades.

References

(1)

(2)
(3)

(4)

(5)
(6)
(7)

(8)
(9)
(10)
(11)

(12)
(13)

(14)

(15)

(16)

(17)

(18)

ADAMS, E.E. Mortality. In: Smoking and Health. A Report of the Sur-
geon General. U.S. Department of Health, Education, and Welfare,
Public Health Service, Office of the Assistant Secretary for Health,
Office on Smoking and Health, January 1979, pp. 2-1 to 2-47.

ADVERTISING & SELLING. Marlboro makes a direct appeal. Advertis-
ing and Selling 8:25, March 28, 1927.

AMERICAN INSTITUTE OF PUBLIC OPINION (GALLUP). The Gal-
lup Opinion Index, September 1970, July 1971, July 1972, June 1978.
AMERICAN INSTITUTE OF PUBLIC OPINION (GALLUP). The Gal-
lup Poll Public Opinion, 1985-1971 Series, pp. 477-1501; 1972-1977

Series, pp. 274-1203.

BAIN, J., JR., WERNER, C. Cigarettes in Fact and Fancy. Boston, H.M.
Caldwell Co., 1906.

BONNER, L. Why cigarette makers don’t advertise to women. Advertis-
ing & Selling 7: 21, October 20, 1926.

BURBANK, F. U.S. lung cancer death rates begin to rise propor-
tionately more rapidly for females than for males: a dose-response
effect? Journal of Chronic Diseases 25: 473-479, 1972.

CAIRNS, J. The cancer problem. Scientific American 233(5): 64-78,
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42

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PART Il:

3IOMEDICAL ASPECTS OF SMOKING.
MORTALITY.
MORTALITY
Introduction and Background

Cigarette smoking has been cited as the single most impor-
tant environmental factor contributing to premature mortality
in the United States (17). A great many epidemiological studies
support this statement. The emphasis, in general, has been to
study males rather than females. Perhaps the main reason for
this discrepancy is that,.in the past, relatively few women
smoked whereas smoking was common among men. The upward
trend in lung cancer death rates in males observed in the 1950s
by Dorn and others stimulated epidemiologic studies of smoking
and health, especially among males (2,3).

According to the 1979 Surgeon General’s Report:

It is important that attention be called specifically to the
mortality that females experience as a result of cigarette
smoking. There has been an increase in smoking among teen-
age girls over the past 10 years. At present, the percentages of
teenage boys smoking and teenage girls smoking are nearly
identical. For some ages, there are more teenage girl smokers
than boy smokers. Over the past 10 years, there has been a
gradual reduction in the percentage of the adult population
that is smoking. Men have quit in greater numbers than
women. There has been only a modest drop in the percentage
of women who are smoking. In Canada and several European
countries, smoking is decreasing among men but increasing
among women.

The present report reviews some of the more important pro-
spective epidemiological studies on cigarette smoking and mor-
tality among women.

Mortality Trends

As background, this section reviews mortality levels by sex
and color in the United States, by examining recent trends in
overall mortality and in three causes of death which have been
strongly linked to cigarette smoking—ischemic heart disease,
lung cancer and the combined category of bronchitis, em-
physema and asthma.*. These trends are displayed in Figures 1
through 4.

For all causes of death (Figure 1), the trend for females was
downwards over the entire period from 1950 to 1977 with a
somewhat steeper decline in recent years. The trend in death
rates among males was essentially flat during most of the 1950s
and 1960s, but has been sharply downwards since the late 1960s.

*The category, chronic obstructive lung disease, may include asthma, a dis-
ease which is not causally related to smoking.

45
 

 

1500 1500
Nonwhite Males

"Pa geet ttene re gore nen)

sane
Rey oe eee teehee,
2

 

 

os
1000 F-="#+r- =z White Males~] 1000
eoPa, . Tee eae ™,
Nonwhite Females aman, os
700 Avs 700

 

4

P$~4O |

as
500 F— White Females a 500
omen

 

 

Rate Per 100,000 Population (Log Scale)

 

 

 

 

 

 

 

 

200 200
1950 1955 1960 1965 1970 1975

FIGURE 1.— Age-adjusted death rates* for all causes of death by
color and sex; United States, 1950-1977

* Adjusted by the direct method to the U.S. population, 1940.
SOURCE: National Center for Health Statistics (9).

For ischemic heart disease, the death rate trend for all sex
and color groups was upwards until it flattened in the 1960s. It
has been sharply downward since then (Figure 2).

For lung cancer the trend was sharply upwards during the
entire period, especially for females (Figure 8).

For bronchitis, emphysema and asthma, the death rate has
been sharply upwards for all sex and color groups except non-
white females. In recent years there appears to be a leveling off
for males but not for white females (Figure 4). Other inves-
tigators have studied these trends, especially ‘in relation to
changes in cigarette smoking habits in the United States and
their potential effect upon mortality from the smoking-related
diseases (8,12). There are inherent difficulties in interpreting
trend data and in particular in relating one trend to another.

Epidemiological Studies

During the past 30 years, there have been eight large pro-
46
 

 

 

 

 

 

    

 

 

 

 

 

 

 

 

 

400 400
White Males ~
— 300 peep =< 300
2 — Nonwhite Males IN
oO *” oepe® &,
S& 200 + a, 200
c Pree Nonwhite Females “te
3 ous aboootrnnn" ee, ~~ wen.
2 = ~
a wraen ee White Females ‘
2
6 100 100
i)
S
o
oO
2
«
50 50
1950 1955 1960 1965 1970 1975

<«—- 6th Rev. —» <«—— 7th Rev.—_—_»<——- 8th Rev. —__>

FIGURE 2.— Age-adjusted death rates* for ischemic heart
disease** by color and sex, United States,
1950-1977

*Adjusted by the direct method to the U.S. population, 1940.
**ICD 6th and 7th Rev. No. 420 and 8th Rev. Nos. 410, 413.
SOURCE: National Center for Health Statistics (9).

spective epidemiological studies specifically designed to de-
lineate the relationship between tobacco smoking and the de-
velopment of disease. In five of these studies data are available
on women as well as men. These studies are outlined below and
in Table 1 (1,2,4,5,7,10). To these published results are added
unpublished data from two other studies conducted by the Na-
tional Heart, Lung, and Blood Institute, and from the British
Doctors Study.

THE AMERICAN CANCER SOCIETY 25-STATE STUDY (6)

The largest study by far is the American Cancer Society study
of men and women in 25 states. In late 1959 and early 1960, the
American Cancer Society enrolled 1,078,894 men and women in
a prospective study. All segments of the population were

47
= TABLE 1.— Outline of prospective studies of smoking and mortality among women

 

 

 

Cederlof
Friberg Best Doll British-Norwegian
Hrubec Josie Gray Framingham Migrant Study
Hammond Lorich Walker Hirayama Peto Heart Study British Norwegian
Authors (5) (1) (4) (7) (2) (10) (10)
Probability Total pop. Sample plus Probability sample
Volunteers sample of Canadian of 29 health volunteers of British & Norwe-
Type of in 25 the Swedish _ pensioners districts British from Framingham, gian migrants to
subjects states population & dependents in Japan doctors Mass. (whites) U.S. in 12 states
Number of
female
subjects 562,671 27,7382 14,226 142,857 6,192 2,873 9,057 5,337
Age range
at baseline 35-84 18-69 <30 to 80+ 40 + 25 to 75 + 29-62 45-74 45-74
Year of
enrollment 1959 1963 1955 1966 1951 1948 1962 1962
Years of
follow-up
reported 4 10 6 5 22 26 5 5
Number of
female
deaths 16,773 1,955 1,794 1,508 1,090 662 588 354
Basic Person-yrs. Probability Probability Person-yrs. Person-yrs. Probability Probability of
statisti- death of death of death death death of death death in
cal measure rate in 10 yrs. in 6 yrs. rate rate in 26 yrs. in 5 years

 
 

 

 

 

     
 
 

 

 

 

 

 

 

 

 

 

50
White M
@
oO
° .
wn er
a <
Ss .” Nonwhite Males
c e
2 ." a
s " L°
3
2 A
a 10 ; * 10
o
o
oOo
°
= .
D Nonwhite Females 4
a
@O
a White Females
a 5 5
Lore
2 2

1950 1955 1960 "1965 1970 1975

<— 6th Rev. —»>~<——7th Rev. —»<——_ 8th Rev. ——_>

FIGURE 3.— Age-adjusted death rates* for malignant neoplasm
of trachea, bronchus, and lung,** by color and sex,
United States, 1950-1977

*Adjusted by the direct method to the U.S. population, 1940.
**ICD 6th and 7th Rev. Nos. 162, 163 and 8th Rev. No. 162.
SOURCE: National Center for Health Statistics (9).

included except groups that could not be traced easily. A lengthy
initial questionnaire contained information on age, sex, race,
49
 

 

30 30

hite Males —
W ite ——"

20 a 20

often, ;
*e

 

sane teone

of
Pad

4
/ ’ Nonwhite Males

o*. a” 10
7

*

 

Nonwhite Females

e ¢

 

 

 

Rate Per 100,000 Population (Log Scale)

 

 

 

 

 

 

 

a’? Par 2. 5
Je, ° *- eer! © i mer Lust
: * a
Sf White Females
2 2

 

1950 1955 1960 1965 1970 1975

<—-6th Rev. —>~+——7th Rev.—»<+——- 8th Rev.

FIGURE 4.— Age-adjusted death rates* for bronchitis,
emphysema, and asthma** by color and sex, United
States, 1950-1977

*Adjusted by the direct method to the U.S. population, 1940.
**ICD 6th and 7th Rev. Nos. 241,501,502,527.1 and 8th Rev. Nos. 490,493,549.3.
SOURCE: National Center for Health Statistics (9).

education, place of residence, family history, past diseases,
present physical complaints, occupational exposures, and vari-
ous habits. Information on smoking included: type of tobacco
used, number of cigarettes smoked per day, degree of inhala-
tion, age at which smoking began, and the brand of cigarettes
used from which the “tar” and nicotine content of the cigarette
could be calculated. Nearly 93 percent of the survivors were
successfully followed for a 12-year period. Only limited data

50
have been published for the 12-year period for women; the main
body of published data for women is based on the first 4-year
period of the follow-up.

THE SWEDISH STUDY (1)

A national probability sample of 55,000 Swedish men and
women was surveyed in 1963, by a mailed questionnaire to
which 89 percent of the sample responded. Information was col-
lected on smoking status at the time of the query and at
specified intervals during the previous 9 years according to type
and amount of smoking and degree of inhalation. The question-
naire identified age, sex, location (urban, nonurban), income,
and occuption of each subject. A 10-year follow-up on smoking-
related mortality was published in 1975.

THE CANADIAN VETERANS STUDY (4)

Beginning in 1955, the Department of National Health and
Welfare, Canada, enrolled 78,000 men (veterans on pension) and
14,000 women (mostly widows of veterans) in a study of
smoking-related mortality. Information was obtained on age,
detailed smoking history, residence, and occupation. During the
6 years of follow-up, 9,491 of the men and 1,794 of the women
died. No recent follow-up has been reported.

JAPANESE STUDY OF 29 HEALTH DISTRICTS (7)

In late 1965, a total of 265,118 men and women in 29 health
districts in Japan were enrolled in a prospective study. This
represented from 91 to 99 percent of the population aged 40 and
older in these districts. This study provides a unique opportu-
nity to examine the relationship of cigarette smoking to death
rates in a population with genetic, dietary, and other cultural
differences from previously examined Western populations. At
the time of the eighth year of follow-up 11,858 deaths had oc-
curred and there were 1,269,382 person-years of observation.
For women, however, the main body of published data is based
on 5 years of follow-up.

THE BRITISH DOCTORS STUDY (2)

In 1951, the British Medical Association forwarded to all
British doctors a questionnaire about their smoking habits. A
total of 34,400 men and 6,207 women responded. With few excep-
tions, all men who replied in 1951 have been followed for 20
years. Further inquiries about changes in tobacco use and some
additional demographic characteristics of the men were made in

51
1957, 1966, and 1972. More than 10,000 deaths have occurred in
this population during the past 20 years. For women, published
data are available for 11 years of follow-up, and unpublished
data are available for 22 years of follow-up.

THE FRAMINGHAM HEART STUDY (10)

The Framingham Study began in 1948 with a cohort of 2,336
white men and 2,873 white women who were age 29 to 62 at the
beginning of the study and were residents of Framingham,
Massachusetts. Persons were selected by a sample of house-
holds plus enlistment of volunteers. These individuals were re-
called and examined every 2 years thereafter.

The routine cardiovascular examination consisted of a medi-
cal history, physical examination, blood chemistries, body
measurements, vital capacity, chest x-ray and a 12-lead elec-
trocardiogram. Mortality and morbidity were documented in
detail from the routine biennial examination, hospital records,
death certificates, physician records and the next-of-kin.

Information on smoking was obtained at the first examina-
tion (and at several thereafter). A series of monographs and
over 200 articles on the Framingham Study have now become
part of the scientific literature.

Data on the relationship of cigarette smoking to cardiovascu-
lar morbidity and mortality, for both men and women, have
been reported in the Framingham literature, but the longest
reported follow-up period has been 18 years with relatively few
deaths having occurred by then, especially among the women
(11). Data given below are based on a longer follow-up period, 26
years, and have not been published. The study is presently in its
16th biennial cycle.

THE BRITISH-NORWEGIAN MIGRANT STUDY(10)

In October 1962, morbidity questionnaires requesting infor-
mation on personal and demographic characteristics, including
cigarette smoking, as well as symptoms of cardiorespiratory
disease were sent to approximately 32,000 British migrants and
18,000 Norwegian migrants to the United States residing in 12
states. These samples were drawn from the 25 percent random
sample of the entire population for which country of birth was
recorded in the 1960 United States Census. The 12 states in-
volved contained about three-fourths of the British and Norwe-
gian immigrants to the United States. The response rate to the
questionnaire was 86 percent. The respondents were then fol-
lowed for survivorship and cause of death data for 5 years, from
January 1, 1963 through December 31, 1967. The number of

52
morbidity questionnaire respondents and deaths occurring
among them from 1963 to 1967 for ages 45 to 74, by sex, were as
follows.

 

Males Females
Respondents Deaths Respondents Deaths
British 10,103 1,181 9,057 588
Norwegian 5,902 643 5,337 354

Several reports dealing with the prevalence survey and with
a related cross-sectional study of mortality, including data on
cigarette smoking for women as well as for men, have been pub-
lished (13,14,15,16). The main results of the prevalence study —
may be briefly summarized. Four syndromes were considered:
“persistent cough and phlegm,” “chronic bronchitis,” “angina,”
and “possible infarction.” The relation of smoking to the preva-
lence of these symptoms was clearly demonstrated for women
as well as for men. The main results of the cross-sectional mor-
tality study indicated substantial excess mortality for cigarette
smokers, as compared to nonsmokers, for both women and men.

Overall Mortality for Females— Cigarette Smokers Versus
Nonsmokers

MORTALITY RATIOS

In this report the mortality ratio is the basic means of com-
paring cigarette smokers with nonsmokers. It is usually ob-
tained by dividing a “death rate” (or other mortality measure)
for a classification of smokers by the “death rate” (or other
mortality measure) of a comparable group of nonsmokers. The
“death rate” may differ markedly from one study to another. In
Some studies it is calculated by means of person-years and is a
1-year measure; in others it is a probability measure; it may be
a 5-year, 10-year or, as in the Framingham Study, a 26-year
measure. Differences in mortality ratios may arise because of
these factors.

Because of the arithmetic nature of this ratio, there is a tend-
ency for lower ratios to result with higher underlying levels of
mortality. For example, with an underlying mortality level of 10
percent per year for nonsmokers, the mortality ratio for a group
of smokers can at most be 10 if all the smokers died within the
year. With a mortality level of 50 percent for nonsmokers, the
maximum possible ratio is 2. Since “death rates” increase with
age, there is a tendency for the mortality ratios to decline with
age, since its range is restricted.

53
TABLE 2.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age;
females in 24 states

 

 

 

 

Number of
cigarettes Age Total, 35-84
per day 35-44 45-54 55-64 65-74 75-84 Age-adjusted!
Nonsmokers 1.00 1.00 1.00 1.00 1.00 1.00

1-9 .90 .95 .99 1.09 1.07 .97
10-19 97 1.22 1.31 1.18 1.21 1.19
20-39 1.35 1.54 1.46 1.51 .85 1.45

40+ 1.56 1.96 1.23 1.42 * 1.63
All Smokers 1.12 1.31 1.27 1.31 1.14 1.26

 

‘Adjusted by the direct method using as standard the age distribution of all
women.

*Not shown—less than 5 expected deaths.

SOURCE: Hammond, E.C. (5).

TABLE 3.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age;
females in the Swedish study

 

 

 

 

Number of

cigarettes Age Total, 18-69
per day 18-39 40-49 50-59 60-69 Age-adjusted
Nonsmokers 1.0 1.0 1.0 1.0 1.0

1-7 1.0 1.6 1.1 9 1.0
8-15 2.3 2.2 1.7 1.4 1.5

16+ 4.5 2.2 1.5 2.2 2.0

All Smokers 1.8 1.9 1.3 1.1 1.2

 

SOURCE: Cederlof, R. (2).

For simplicity, however, mortality ratios are used throughout
this review; it is recognized that these ratios are not strictly
comparable from one study to another nor from one age group
to another.

AMOUNT SMOKED AND AGE

Overall mortality ratios by amount smoked and age are pres-
ented for several of the studies in Tables 2-7. Except for the
Swedish study (Table 3), age-adjusted ratios were calculated for
each level of smoking in each study. Adjustment was by the
direct method, using as standard the age distribution of all

54
TABLE 4.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age;
females in the Canadian study

 

 

 

 

Number of

cigarettes Age Total, 30+
per day 30-54 55-64 65-74 T5+ Age-adjusted!
Nonsmokers 1.00 1.00 1.00 1.00 1.00

1-9 1.59 1.09 1.05 92 1.20

10+ 2.25 .93 1.20 * 1.43

All Smokers 1.95 1.03 1.10 .95 1.31

 

1Adjusted by the direct method using as standard the age distribution of all
women.

*Not shown—less than 5 expected deaths.

SOURCE: Best, E.W.R. (1).

TABLE 5.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age;
females in the Framingham Heart Study

 

 

 

 

Number of
cigarettes Age Total, 29-62
per day 29-44 45-54 55-62 Age-Adjusted!
Nonsmokers 1.00 1.00 1.00 1.00
<20 1.42 1.21 1.07 1.30

20 1.84 1.48 1.13 1.62

21+ 2.25 1.14 * 1.72
All Smokers 1.62 1.28 1.07 1.43

 

1Adjusted by the direct method using as standard the age distribution of all
women.

*Not shown—less than 5 expected deaths.

SOURCE: National Heart, Lung, and Blood Institute (10).

women in the particular study. For the Swedish study the age-
adjusted values were taken directly from the report.

Mortality ratios shown in Table 2 are considered especially
important since they are derived from the study with the
largest survivorship experience. Mortality ratios generally rose
with the amount smoked for each age group except for the 75 to
84 age group. The age-ratios were .97 for the 1-to—9-cigarettes
per day group, 1.19 for the 10-to-19 per day group, 1.45 for the
20-39 group, and 1.63 for the 40-plus group. For all cigarette
Smokers the age-adjusted mortality ratio was 1.26. By age
group, mortality ratios were 1.12 for the 35-to—44 age group,

55
TABLE 6.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age;

 

 

 

 

British females

Number of
cigarettes Age Total, 45-74
per day 45-54 55-64 65-74 Age-adjusted!
Nonsmokers 1.00 1.00 1.00 1.00
<20 1.49 1.09 79 1.08

20+ 1.85 1,51 1.55 1.60
All Smokers 1.66 1.25 .98 1.25

 

1Adjusted by the direct method using as standard the age distribution of all

women.
SOURCE: National Heart, Lung, and Blood Institute (10).

TABLE 7.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day and age;
Norwegian females

 

 

 

Number of
cigarettes Age Total, 45-74
per day 45-64 65-74 Age-adjusted?
Nonsmokers 1.00 1.00 1.00
<20 1.54 1.07 1.33

20+ 1,41 89 1.18
All smokers 1.49 1.02 1.28

 

‘Adjusted by the direct method using as standard the age distribution of all
women.
SOURCE: National Heart, Lung, and Blood Institute (10).

1.31 for the 45-to-54 age group, 1.27 for the 55-to-65 group,
1.31 for the 65-to~74 group and 1.14 for the 75-to—84 age group.

Data from the Swedish study (Table 3) appear to be rea-
sonably consistent with the ACS data in Table 2. The 1-to-7-
cigarettes—per-—day group had an age-adjusted mortality ratio
of 1.0 (compared with .97 for the 1-to~9 group above) and 2.0 for
the 16-plus group (compared with 1.63 for the 40-plus group
above). For three of the four age groups, the mortality ratios
were directly associated with level of smoking. By age group,
the highest mortality ratios were observed for the two youngest
age groups and the lowest for the two oldest groups. The overall]
ratio for all cigarette smokers was 1.2.

For the other studies (Tables 4-7) mortality patterns were
generally similar in that mortality ratios tended to be highest

56
TABLE 8.—Mortality ratios for female cigarette smokers by
number of cigarettes smoked per day; females in the
British Doctors Study

 

 

 

Number of

cigarettes Total,

per day Age-adjusted?

Nonsmokers 1.00
1-14 0.94

15-24 1.54

25+ 1.66

All Smokers 1.23

 

1Based on annual death rates standardized for age.
SOURCE: Cederlof, R. (2).

with heaviest smoking and tended to be lowest at the oldest
ages.

For the Japanese study and the British Doctors Study, mor-
tality ratios by amount smoked and age were not reported.
However, an overall age-adjusted mortality ratio for female
cigarette smokers was reported in the Japanese study, while in
the British Doctors Study this ratio was obtained from unpub-
lished data based on 22 years of follow-up (Table 8). We list these
along with the overall ratios for the other studies:

Total mortality ratio

 

Study age-adjusted
American Cancer Society 1.26
Swedish 1.20
Canadian 1.31
Japanese 1.28
British Doctors 1.23
Framingham 1.43
British Migrants 1.25
Norwegian Migrants 1.28

All ratios here are greater than unity. The largest ratio is 1.43
for Framingham. The other seven ratios are close to one
another, ranging from 1.2 for the Swedish study to 1.31 for the
Canadian study.

DURATION OF SMOKING

Overall mortality ratios for women increased with duration of
the smoking habit based on data from the Canadian and

57
TABLE 9.— Age-adjusted mortality ratios of female cigarette
smokers, by number of cigarettes smoked per day
and age began smoking; subjects aged 45-54 at start
of study. 25-State Study

 

 

 

Number of Age began smoking
cigarettes
per day 25+ 15-24
Nonsmokers 1.00 1.00
1-9 0.95 0.88
10-19 : 1.17 1.23
20-39 1.33 1.61
40+ ** 1.85

 

**Ratio not shown—less than 10 expected deaths.
SOURCE: Hammond, E.C. (5).

TABLE 10.— Age-adjusted mortality ratios of female cigarette
smokers, by number of cigarettes smoked per day
and degree of inhalation. Subjects aged 45~—54 at
start of study. 25-State Study

 

 

 

Number of Degree of inhalation of smoke

cigarettes

per day None— Slight Moderate— Deep
1-9 0.85 1.04

10-19 1.27 1.17

20~39 1.41 1.58

40+ ** 2.19

 

**Ratio not shown—less than 10 expected deaths.
SOURCE: Hammond, E.C. (5).

Swedish studies (1,4). Among Canadian women who smoked for
10 or more years the mortality ratio, adjusted for age, was 1.37
compared to a ratio of 1.08 for women smoking less than 10
years. In the Swedish study an excess risk was found for women
smoking 30 or more years (1.4). For those smoking less than 30
years the ratio was 1.0.

AGE BEGAN SMOKING

Table 9 shows mortality ratios for women who were 45 to 54 by
number of cigarettes smoked per day and age began smoking
(5). Except for the light cigarette smokers (1-to-9-per-day),
those taking up the habit at ages 15 to 24 had higher mortality
ratios than those who started smoking at older ages.

58
TABLE 11.— Age-adjusted mortality ratios of female cigarette
smokers, by number of cigarettes smoked per day
and degree of inhalation and age. 25-State Study

 

 

 

Degree Age

of

Inhalation 35-44 45-54 55-64 65-74 75-84
Nonsmokers 1.00 1.00 1.00 1.00 1.00
None * 1.01 1.11 1.12 0.96
Slight 1.22 1.21 1.28 1.26 1.21
Moderate 1.05 1.30 1.32 1.41 *
Deep 1.40 1.78 1.64 “* +*

 

**Ratio not shown—less than 10 expected deaths.
SOURCE: Hammond, E.C. (5).

Mortality data for women smokers, according to age started,
are also available from the Swedish study (1); age-adjusted
ratios were reported as 1.7, 1.6, and 1.1 for age started less than
17, 17 to 18, and 19 plus, respectively.

INHALATION

Table 10 shows mortality ratios for female cigarette smokers
who were 45 to 54 years of age according to number of cigarettes
smoked per day and degree of inhalation of smoke (5). No clear
pattern emerges. The “moderate-deep” group had higher mor-
tality ratios than the “none-slight” group in two of three com-
parisons.

Table 11 shows mortality ratios for female cigarette smokers
by degree of inhalation and age (5). A fairly consistent general
pattern emerges; mortality ratios vary directly with degree of
inhalation. This is seen in each age group, except perhaps the
35-to-44 age group.

Mortality data for female cigarette smokers according to in-
halation are also available from the Swedish study (1); age-
adjusted ratios were reported as 1.1, 1.2, and 1.6 for the no inha-
lation, light inhalation, and deep inhalation groups, respec-
tively.

“TAR” AND NICOTINE CONTENT OF CIGARETTES

The relationship between overall mortality and the “tar” and
nicotine content of cigarette smoke was recently examined by
Hammond, et al. (6). In this study, “tar” and nicotine levels
(T/N) were defined as follows: “high” T/N, 25.8 to 35.7 mg “tar”
and 2.0 to 2.7 mg nicotine; “medium” T/N, 17.6 to 25.7 mg “tar”

59
TABLE 12.— Adjusted mortality ratios for males and females, by
“tar” and nicotine content of cigarettes usually

 

 

 

 

smoked
Mortality Ratios
“High” “Medium” “Low”
Sex TIN TIN TIN
Males 1.00 0.94 0.85
Females 1.00 0.88 0.83
Total 1.00 0.91 0.84

 

SOURCE: Hammond, E.C. (6).

TABLE 13.— Adjusted mortality ratios for males and females
smoking low “tar” and nicotine cigarettes and
subjects who never smoked regularly

Mortality ratios

 

 

Sex “Low” T/N Nonsmokers
Males 1.00 0.61
Females 1.00 0.74
Total 1.00 0.66

 

SOURCE: Hammond, E.C. (6).

TABLE 14.— Overall mortality ratios of cigarette smokers
compared to nonsmokers, by sex and by “tar” and
nicotine content of cigarettes usually smoked

 

 

 

Non- “Low” “Medium” “High”
Sex smokers TIN TIN TIN
Males 1.00 1.66 1.85 1.96
Females 1.00 1.37 1.45 1.65
Total 1.00 1.52 1.64 1.80

 

SOURCE: Hammond, E.C. (6).

and 1.2 to 1.9 mg nicotine; “low” T/N, less than 17.6 mg “tar” and
less than 1.2 mg nicotine.

Table 12 shows the overall mortality ratios of male and female
smokers by these “tar” and nicotine levels. In this instance, the
mortality ratio of the “high” T/N smokers was represented as
1.00 to illustrate the reduction in overall mortality that occurred
with lower T/N cigarettes. There was a small reduction in the
risk of dying with the use of lower T/N cigarettes. The mortality

60
ratio was reduced to 0.91 for the ‘‘medium” T/N smokers and
was further reduced to 0.84 for the “low” T/N smokers. The mor-
tality ratios were lower for women than for men.

In a separate analysis, a comparison was also made between
the mortality ratios of “low” T/N smokers and nonsmokers.
These data are presented in Table 13. The mortality ratio of the
“low” T/N group was designated as 1.00. Nonsmokers had over-
all mortality ratios that were considerably less than those of
“low” T/N smokers.

The combined data from Tables 12 and 13 are shown in Table
14 where mortality ratios were calculated using nonsmokers as
the reference. Combining these data from two separate
analyses that are not exactly comparable results in figures that
are only approximate.

Hammond also compared death rates of smokers of relatively
few (1 to 9) “high” T/N cigarettes with those of smokers who
smoked relatively large numbers (20 to 39) of “low” T/N cigar-
ettes (17). The death rates of these two groups were very simi-
lar.

Comments

Mortality ratios for women who smoke cigarettes ranged from
1.2 in the Swedish study to 1.43 in the Framingham study. As
with men, mortality ratios for women who smoke cigarettes var-
ied directly with amount smoked, depth of inhalation, “tar” and
nicotine content of the cigarette and duration of smoking, and
varied inversely with the age when smoking was started.

In attempting to study cigarette smoking and mortality
among women, a major difficulty is the lack of large-scale
epidemiological studies addressed specifically to female popula-
tions. The main findings of this review depend heavily on one
study, that of the American Cancer Society. For the other
studies reviewed here, the numbers of women—and of deaths
among them—are often too sparse to permit meaningful statis-
tical analyses. Thus, for example, little can be said about the
survivorship experience of women who give up cigarette smok-
ing. We strongly recommend, where possible, extending the
length of follow-up of women who are already enrolled in these
prospective studies. It is also highly recommended that new
studies be conducted that are specifically addressed to women
and smoking-related mortality.

Summary
1. The mortality ratio for women who smoke cigarettes is
about 1.2 or 1.3.
61
2. Mortality ratios for women increase with the amount
smoked. In the largest prospective study the mortality ratio
was 1.68 for the two-pack-a-day smoker as compared to
nonsmokers.

3. Mortality ratios are generally proportional to the duration
of cigarette smoking; the longer a woman smokes, the greater
the excess risk of dying.

4. Mortality ratios tend to be higher for those women who
begin smoking at a young age as compared to those who begin
smoking later.

5. Mortality ratios are higher for those women who report
they inhale smoke than for those who do not inhale.

6. Mortality ratios for women tend to increase with the tar
and nicotine content of the cigarette.

7. Mortality ratios for female smokers are somewhat less
than for male smokers. This may reflect differences in exposure
to cigarette smoke, such as starting smoking later, smoking
cigarettes with lower “tar” and nicotine content, and smoking
fewer cigarettes per day than men.

8. Women demonstrate the same dose-response relationships
with cigarette smoking as men. An increase in mortality occurs
with an increase in number of cigarettes smoked per day, an
earlier age of beginning cigarette smoking, a longer duration
of smoking, inhalation of cigarette smoke, and a higher “tar”
and nicotine content of the cigarette. Women who have smok-
ing characteristics similar to men may experience mortality
rates similar to men.

References

(1) BEST, E.W.R. A Canadian Study of Smoking and Health. Department of
National Health and Welfare, Epidemiology Division, Health Services
Branch, Biostatistics Division, Research and Statistics Directorate,
1966, 137 pp.

(2) CEDERLOF, R., FRIBERG, L., HRUBEC, Z., LORICH, U. The Rela-
tionship of Smoking and Some Social Covariables to Mortality and
Cancer Morbidity. A Ten Year Follow-up in a Probability Sample of
55,000 Swedish Subjects Age 18 to 69. Part I and II. Stockholm,
Karolinska Institute, Department of Environmental Hygiene, 1975,
201 pp.

(3) DOLL, R., GRAY, R., PETO, R. Mortality in Relation to Smoking: Ob-
servations on Female Doctors. (Unpublished manuscript)

(4) DORN, H.F. The relationship of cancer of the lung and the use of to-
bacco. The American Statistician 8(5): 7-13, December 1954.

(5) HAMMOND, E.C. Smoking in relation to the death rates of one million
men and women. In: Haenszel, W. (Editor). Epidemiological Ap-
proaches to the Study of Cancer and Other Chronic Diseases, National
Cancer Institute Monograph 19. Department of Health, Education,
and Welfare, Public Health Service, National Cancer Institute,
January 1966, pp. 127-204.

62
(6)

(7)

(8)

(9)

(10)

dy

(12)

(13)

(14)

(15)

(16)

(17)

HAMMOND, E.C., GARFINKEL, L., SEIDMAN, H., LEW, E.A. “Tar”
and nicotine content of cigarette smoke in relation to death rates. En-
vironmental Research 12(3): 263-274, December 1976.

HIRAYAMA, T. Smoking in relation to the death rates of 265,118 men
and women in Japan. A report of 5 years of follow-up. Presented at the
American Cancer Society's 14th Science Writers’ Seminar, Clearwater
Beach, Florida, March 24-29, 1972, 15 pp.

NATIONAL CENTER FOR HEALTH STATISTICS. Mortality from
Diseases Associated with Smoking: United States, 1950-1964. De-
partment of Health, Education, and Welfare, Public Health Service,
National Center for Health Statistics, Public Health Service Publica-
tion No. 1000-Series 20, 50. 4, October 1966, 45 pp.

NATIONAL CENTER FOR HEALTH STATISTICS, Office of Health
Research, Statistics, and Technology, Public Health Service, Depart-
ment of Health Service, Department of Health, Education, and Wel-
fare. (Unpublished data)

NATIONAL HEART, LUNG, AND BLOOD INSTITUTE. Proceedings
of the Conference on the Decline in Coronary Heart Disease Mortality.
Department of Health, Education, and Welfare, Public Health Service,
National Institutes of Health, NIH Publication No. 79-1610, May 1979,
399 pp.

NATIONAL HEART, LUNG, AND BLOOD INSTITUTE. Some charac-
teristics related to the incidence of cardiovascular disease and death:
Framingham Study, 18-year follow-up. In: The Framingham Study: An
Epidemiological Investigation of Cardiovascular Disease. Kannel,
W.B., Gordon, T. (Editors). DHEW Publication No. (NIH) 74-599, Feb-
ruary 1974.

NATIONAL HEART, LUNG, AND BLOOD INSTITUTE. Department
of Health, Education, and Welfare, Public Health Service, National
Institutes of Health, 1979. (Unpublished data)

PEARL, R.B., LEVINE, D.B., GERSON, E.J. Studies of Disease Among
Migrants and Native Populations in Great Britain, Norway, and the
United States. II. Conduct of Field Work in the United States. National
Cancer Institute Monograph 19. Department of Health, Education,
and Welfare, U.S. Public Health Service, National Cancer Institute,
1966, pp. 301-320.

REID, D.D. Studies of Diseases Among Migrants and Native Popula-
tions in Great Britain, Norway, and the United States. I. Background
and Design. National Cancer Institute Monograph 19. Department of
Health, Education, and Welfare, Public Health Service, National
Cancer Institute, 1966, pp. 287-199.

REID, D.D., CONFIELD, J.. MARKUSH, R.E., et al. Studies of Disease
among Migrants and Native Population in Great Britain, Norway, and
the United States. III. Prevalence of Cardiorespiratory Symptoms
Among Migrants and Native Born in United States. National Cancer
Institute Monograph 19. Department of Health, Education, and Wel-
fare, Public Health Service, National Cancer Institute, 1966, pp. 321-
346.

ROGOT, E. Cardiorespiratory disease mortality among British Norwe-
gian migrants to the United States. American Journal of Epidemiology
108(3): 181~191, 1978.

U.S. PUBLIC HEALTH SERVICE. Smoking and Health. A Report of
the Surgeon General. Department of Health, Education, and Welfare,
Public Health Service, Office of the Assistant Secretary for Health,
Office on Smoking and Health. DHEW Publication No. (PHS) 79- 50066,
1979, 1251 pp.

63
MORBIDITY.
MORBIDITY

The relationship between cigarette smoking and morbidity
has been summarized in the 1979 Surgeon General’s Report.
That report contained data from the National Center for Health
Statistics Health Interview Survey (HIS) showing the relation-
ship for both men and women between smoking and the preva-
lence of selected chronic diseases, the incidence of acute illness,
days lost from work, days of bed disability, and perceived health
status. This section will present additional data from the Health
Interview Survey on trends in days lost from work and limita-
tion of activity.

Days Lost from Work

Workers who smoke report losing more work days due to ill-
ness and injury than do nonsmokers. This relationship has been
observed for both men and women every year that the National
Health Interview Survey has included questions on cigarette
smoking. For example, in 1965 working women who smoked re-
ported 6.6 work-loss days; working women who had never
smoked reported only 4.8 work-loss days (see Table 1). Similarly,
in the 1977 HIS women who smoked reported 6.6 days lost from
work compared to 5.7 days lost from work by those who never
smoked.

The National Clearinghouse for Smoking and Health used the
earlier 1965 data to estimate the number of “excess” days lost
from work among cigarette smokers. This estimation was ob-
tained by calculating the expected number of work-loss days if
all workers had the same work-loss experience as those who had
never smoked cigarettes. It was estimated that approximately
20 percent of all work-loss days due to illness and injury could be
attributed to the higher rates of loss among current and former
smokers (2). The 1979 Surgeon General’s Report presented simi-
lar calculations, based on 1974 data, and again the estimate was
about 20 percent of all work-loss days. These calculations were
not sex specific. Certain modifications in the collection proce-
dures have lowered the male response rate for the smoking data
and may, thus, make comparisons of more recent data by sex
less than ideal. However, the data do show that in 1977 the
work-loss rate among women who never smoked was higher
than in 1965, while the rates among current smokers remained
about the same. This would tend to reduce the number of “‘ex-
cess” days among women attributable to smoking. There has
been a slight decrease in work loss among males who never
smoked. Former smokers reported fewer work-loss days in 1977
than in 1965. Although the difference in work-loss days between

67
TABLE 1.—Days lost from work per year due to illness and
injury, per currently employed persons 17 years
old and older, by smoking status, sex and age:
United States, 1965 and 1977

 

Present Former Never
Total! Smoker Smoker Smoked

 

Percent -of work-loss days

1965
Female
17+4 5.6 6.6 6.7 4.8
17-44 5.5 6.6 6.0 4.5
45-64 6.0 6.7 7.4 5.3
Male
17 +8 5.7 5.9 6.8 4.6
17-44 4.1 4.7 3.6 3.4
45-64 7.8 79 9.8 5.6
1977
Female
20 +3 6.0 6.6 5.4 5.7
20-44 6.1 6.8 5.4 5.4
45-64 6.4 6.5 5.9? 6.5
Male
20 +3 5.3 5.9 6.1 4.2
20-44 5.1 6.0 5.5 4.4
45-64 5.6 5.9 6.2 3.9

 

‘Includes unknown smoking status.

?Figure does not meet standards of reliability or precision.
5Includes ages 65 and over.

SOURCE: National Center for Health Statistics (1).

1965 and 1977 is small, it could be attributed to the assumption
that in recent years the former smoker groups have a greater
proportion of people who stopped smoking for preventive rea-
sons, that is, before they had experienced serious health conse-
quences.

Further study is needed to determine the association between
“excess” days lost from work by smokers and specific diseases.
Such an analysis would help explain the economic impact of
smoking in the work place.

Limitation of Activity

The Health Interview Survey also regularly collects data on
the long-term impact of chronic illness. Respondents were asked
if chronic illness limited their activities (3). Estimates of the
percent of the population with limitation of activity by cigarette

68
smoking status are shown in Table 2 for 1965 and 1977. Detailed
interpretation of trend data is difficult; however, there appears
to be a relationship between smoking and the impact of chronic
illness. In general, the 1977 data indicate that women under 65
who have ever smoked are more likely to have a limitation of
activity than those who never smoked. There are no marked
differences between current and former smokers. Among eld-
erly women in 1977, there were no differences in limitations of
activity by smoking status.

TABLE 2.— Percent of persons with limitation of activity due to
chronic conditions, by cigarette smoking status, sex
and age: United States, 1965 and 1977

 

Present Former Never
Total! Smoker Smoker Smoked

 

Percent with limitation

1965
Female
17+ 17.3 12.7 17.3 19.8
17—44 8.3 8.8 9.8 7.7
45-64 19.5 17.4 22.1 20.2
65+ 45.1 39.8 48.6 45.4
Male :
17+ 17.3 15.3 23.0 17.7
17-44 7.3 7 8.0 6.2
45-64 20.0 20.9 22.1 15.7
65 + 53.7 52.7 56.3 52.9
1977
Female
20 + 17.6 16.0 18.1 18.3
20-44 8.0 9.2 8.4 7.0
45-64 21.5 24.2 23.9 19.8
65 + 89.2 36.3 35.5 38.8
Male
20 + 20.0 20.5 24.1 17.6
20-44 9.6 12.4 8.3 75
45-64 25.7 27.5 25.7 25.7
65 + 47.5 52.7 47.6 42.5

 

‘Includes known smoking status.
SOURCE: National Center for Health Statistics (1).

Cigarette Smoking and Occupation*

The Health Interview Survey provides a considerable data
base on cigarette smoking behavior and occupational status.

*See: “Interaction Between Smoking and Occupational Exposures” in this
Report.

69
The data are available from a national probability sample of
about 40,000 households for the years 1965, 1966, 1970, 1974,
1976, 1977, 1978, and 1979. However, only minimal analysis has
been conducted on this potentially valuable data base (4). This
brief section presents data on smoking patterns for only two of
these periods—1970 and 1976. Researchers are encouraged to
investigate these data more fully through the purchase of pub-
lic use data tapes (1). The importance of this data base increases
as new evidence becomes available on the increased health risks
experienced by smokers in certain occupations. The problems of
relatively small sample sizes in high-risk occupations can be
partially overcome by combining several years of the HIS data
tapes.

Tables 3 and 4 show smoking characteristics of broad occupa-
tional groups—i.e., white collar, blue collar, service and farm
workers —for 1970 and 1976, respectively. Service and blue col-
lar workers, both women and men, are more likely to smoke
than are white collar and farm workers, but the differences are
much less among female workers. In 1970, there were virtually
no differences among female white collar, blue collar, and serv-
ice workers; more recently, however, there has been a slight
increase in smoking among the latter two groups. Caution
should be used in drawing conclusions from these data based on
differences of only a few percentage points since such dif-
ferences can be well within sampling error. White collar work-
ers who smoke tend to be heavier smokers than other types of
workers, and this pattern is more marked among female white
collar workers.

The proportions of cigarette smokers by more detailed occu-
pational classes are shown in Tables 5 and 6 for 1970 and 1976.
Within three of four subgroups of white collar workers —
professionals, managers, and sales people—the proportion of
smokers among women is the same as for men in the same occu-
pational group. This also appears to be true for laborers, who
show the highest levels of smoking among both women and men.

Summary

The 1979 Report of the Surgeon General summarized the in-
formation on smoking and morbidity as follows:

1. In general, female current cigarette smokers report more
acute and chronic conditions including chronic bronchitis
and/or emphysema, chronic sinusitis, peptic ulcer disease, and
arteriosclerotic heart disease, than women who never smoked.

2. There is a dose-response relationship between the number

70
TL

TABLE 3.—Percent distribution of the population 17 years and over by cigarette smoking status, according to
sex and occupation category, United States, 1970

 

 

 

 

 

 

Sex and
occupation category Percent distribution
Total Never Former Present Present smokers— no. of cigarettes per day?
population! smoked smokers smokers Total? <15 15-24 25+
Female
Total population 100.0 54.0 11.2 34.9 100.0 39.3 42.4 18.2
Total currently employed 100.0 54.3 111 34.6 100.0 38.7 43.3 18.0
White collar workers 100.0 53.2 12.6 34.2 100.0 37.6 42.8 19.6
Blue collar workers 100.0 55.1 8.5 36.5 100.0 40.7 44.4 14.9
Service workers 100.0 55.7 9.2 35.2 100.0 41.6 41.0 17.4
Farm workers 100.0 74.3 *7.5 18.6 100.0 *49.2 *33.3 *19.0
Male

Total population 100.0 28.8 24.9 46.2 100.0 25.8 45.1 29.1
Total currently employed 100.0 28.8 25.2 46.0 100.0 25.5 45.3 29.3
White collar workers 100.0 31.6 29.1 39.3 100.0 23.8 43.4 32.8
Blue collar workers 100.0 24.8 22.4 §2.8 100.0 25.5 46.4 28.0
Service workers 100.0 31.1 20.8 48.1 100.0 31.1 43.3 25.6
Farm workers 100.0 40.7 24.8 34.4 100.0 35.5 45.1 19.4

 

‘Excludes unknown if ever smoked.

?Excludes unknown amount of cigarettes smoked.

*Figure does not meet standards of reliability or precision.
SOURCE: National Center for Health Statistics (1).
oL

TABLE 4— Percent distribution of the population 20 years and over by cigarette smoking status, according to
sex and occupation category, United States, 1976

 

 

Sex and Total Never Former Present Present smokers—no. of cigarettes per day?
occupation category population! smoked smokers smokers Total? <15 15-24 25 +
Female

Total population 100.0 54.3 13.8 32.0 100.0 36.5 43.8 19.6

Total currently employed 100.0 50.8 13.3 35.9 100.0 36.5 44.0 19.5
White collar workers 100.0 61.1 14.6 34.3 100.0 35.3 42.4 22.3
Blue collar workers 100.0 50.7 10.2 39.0 100.0 38.0 44.3 17.6
Service workers 100.0 49.1 11.9 39.0 100.0 37.9 48.3 13.7
Farm workers 100.0 59.8 _ * 31.3 100.0 34.6 * *

Male

Total population 100.0 29.2 28.9 41.9 100.0 24.2 44.8 31.1

Total currently employed 100.0 29.5 27.1 43.4 100.0 21.9 45.4 32.8
White collar workers 100.0 34.0 29.4 36.6 100.0 20.8 43.6 35.6
Blue collar workers 100.0 24.3 25.3 50.4 100.0 21.2 47.4 31.5
Service workers 100.0 29.4 23.4 47.2 100.0 27.6 40.0 32.4
Farm workers 100.0 34.9 28.2 36.9 100.0 29.4 44.9 25.7

 

‘Excludes unknown if ever smoked.

*Excludes unknown amount of cigarettes smoked.

*Figure does not meet standards of reliability or precision.
SOURCE: National Center for Health Statistics (1).
TABLE 5.— Estimates of the percentage of current, regular cigarette smokers, adult ages 17 years and over,
according to labor force status, occupation, and sex, United States, 1970

 

 

Female Male
Total Total
17+ 17-44 45-64 17+ 17-44 45-64
Total 34.9 36.8 33.7 46.2 49.0 44,4
Currently employed 34.6 36.4 33.7 46.0 48.7 44,1
White collar total 34.2 34.9 34.3 39.3 41.1 38.4
Professional, technical
and kindred 28.1 29.4 26.3 31.7 32.8 30.6
Managers & administrators
except farm 40.8 48.4 38.3 42.8 47.4 40.0
Sales workers 34.6 35.3 35.7 44,9 46.8 46.1
Clerical & kindred workers 35.8 35.9 36.4 43.3 45.2 41.5
Blue collar total 36.5 39.9 33.5 52.8 56.1 49.2
Craftsmen & kindred
workers 40.4 44.4 37.0 51.7 56.1 47.2
Operatives and kindred
workers 36.5 40.0 33.5 54.7 57.5 50.7
Laborers, except farm *23.3 *25.6 *20.9 50.9 52.0 52.9
Service 35.2 39.3 33.5 48.1 48.3 51.7
Farm 18.6 *25.9 *15.5 34.4 38.7 37.7
Unemployed 38.4 40.8 32.9 52.3 54.4 53.0
Homemakers 29.7 37.3 32.3 NA NA NA

 

NOTE: Unknown if ever smoked excluded from calculation.
4 *Figure does not meet standards of reliability or precision.
oo SOURCE: National Center for Health Statistics (1).
= TABLE 6.— Estimates of the percentage of current, regular cigarette smokers, adults ages 20 years and over,

according to labor force status, occupation, and sex, United States, 1976

 

 

Female Male
Total Total
20+ 20-44 45-64 20+ 20-44 45-64
Total 32.0 36.9 34.8 41.9 47.6 41.3
Currently employed 35.9 37.0 36.1 43.4 46.8 39.7
White collar total 34.3 33.8 36.9 36.6 38.6 35.3
Professional, technical
and kindred 29.1 28.6 32.7 30.0 31.1 29.9
Managers & administrators
except farm 41.6 42.7 40.8 41.0 46.4 36.1
Sales workers 38.1 37.0 42.6 39.9 42.6 38.0
Clerical & kindred workers 34.8 34.7 36.0 40.4 40.1 44.2
Blue collar total 39.0 43.7 33.6 50.4 54.1 44.3
Craftsmen & kindred workers 40.5 46.9 35.6 48.0 52.1 41.6
Operatives and kindred
workers 37.6 42.5 31.2 52.3 55.3 46.2
Laborers, except farm 56.3 52.6 * 53.7 56.9 51.7
Service 39.0 42.8 37.2 47.2 51.1 44.8
Farm 31.3 51.0 * 36.9 45.4 35.0
Unemployed 40.0 41.0 39.2 56.8 59.9 53.8
Usual activity —homemakers 29.0 37.1 32.2 NA NA NA

 

NOTE: Unknown if ever smoked excluded from calculation.
“Figure does not meet standards of reliability or precision.
SOURCE: National Center for Health Statistics CD.
of cigarettes smoked per day and the frequency of reporting for
most of the chronic conditions.

3. The age-adjusted incidence of acute conditions (e.g., in-
fluenza) for women smokers is 20 percent higher for women who
had ever smoked than for nonsmokers.

Additional data from the Health Interview Survey (HIS) is
presented:

1. Currently employed women who smoke cigarettes report
more days lost from work due to illness and injury than working
women who do not smoke.

2. Limitation of activity is reported more commonly among
women under the age of 65 who have ever smoked than among
those who never smoked.

References

(1) NATIONAL CENTER FOR HEALTH STATISTICS. Standardized
Micro-Data Tape Transcript. Department of Health, Education, and
Welfare, Public Health Service, DHEW Publication No. 781-213, June
1978.

(2) NATIONAL CLEARINGHOUSE FOR SMOKING AND HEALTH. Smok-
ing and Illness. Department of Health, Education, and Welfare, Public
Health Service, Bureau of Disease Prevention and Environmental Con-
trol, National Center for Chronic Disease Control, National Clearing-
house for Smoking and Health, PHS Publication No. 1662, July 1967, 6

pp.

(3) WILDER, C.S. Limitation of activity due to chronic conditions, U.S. 1974.
Department of Health, Education, and Welfare, Public Health Service,
Health Resource Administration, National Center for Health Statistics,
Series 10, No. 111, Public Health Service Pub. No. (HRA) 77-1537, June
1977, 65 pp.

(4) WILSON, R.W. Cigarette smoking, disability days and respiratory condi-
tions. Journal of Occupational Medicine 15(3): 236-240, March 1973.

75
CARDIOVASCULAR DISEASES.
CARDIOVASCULAR DISEASES

Introduction

While the mortality and morbidity rates of coronary heart
disease (acute myocardial infarction and chronic ischemic heart
disease) (CHD) are lower for women than men, CHD still repre-
sents the major cause of death among women in the U.S. In 1976
the United States recorded 284,055 female deaths as attributa-
ble to this cause (Table 2). The difference in mortality rates
between the sexes is more marked for acute myocardial infarc-
tion, with males of all ages experiencing 189 deaths and females
111 deaths per 100,000 (Table 1). Observed differences by sex in
susceptibility to coronary heart disease are not fully understood
but appear to be affected by multiple specific risk factors within
any demographic group.

McGill and Stern have recently provided an extensive review
of sex differences in susceptibility to atherosclerosis in humans
and in experimental animals, including an analysis of factors
known to predispose to atherosclerosis and its dependent dis-
eases (25).

Mortality Rates

In the United States, the National Center for Health Statis-
tics has reported mortality rates from acute myocardial infarc-
tion and chronic ischemic heart disease classified by age, sex,
and race, for the years 1968 and 1976 (Tables 1-3) (33). These
tables show that mortality rates for acute myocardial infarction
among adults up to age 64 are highest for white men and are
succeeded by progressively lower rates for other men, other
women, and finally, white women. Mortality rates for chronic
ischemic heart diseases vary. The rates for white men are sec-
ond to those for other men and close to those for nonwhite
women; again, however, rates for white women are by far the
lowest. Both white and nonwhite women show consistently
lower rates until extreme old age. However, the differences nar-
row markedly in age in comparison with those in young adult-
hood and middle life (Table 1).

Male-to-female mortality ratios for acute myocardial infarc-
tion among adults in their 30’s and 40’s are approximately 5 to 6
for whites and 2 to 3 for nonwhites; among adults in their 70’s
and 80’s, they are roughly 1.6 and 1.4. The actual number of
deaths involved is very large; their distribution by age, sex, and
race is shown in Table 2. Between 1968 and 1976, a striking
decline occurred in the acute myocardial infarction mortality
rate for men and women of all ages and races. These are shown

79
08

TABLE 1.— Death rates* for acute myocardial infarction and chronic ischemic heart di

groups, by color and sex; United States, 1968-1976

sease for specified age

 

 

 

Total White All Other
Both Both Both
Year and age sexes Male Female sexes Male Female sexes Male Female
1976 Acute myocardial infarction

Allages ............,. 148.8 189.0 110.8 158.7 202.2 117.3 84.0 100.3 69.0
25-34 years ............. 2.8 4.6 1.1 2.6 4.3 0.9 4.2 6.4 2.3
35-44 years ............. 27.0 46.2 8.8 26.6 46.1 7.6 30.4 47.5 10.3
45-54 years ............. 111.7 186.9 41.3 111.8 190.1 37.7 111.2 159.8 68.9
55-64 years ............. 309.5 490.3 147.2 312.2 501.1 142.1 283.2 386.5 194.8
65-74 years ............. 660.1 989.8 406.8 674.5 1,024.7 406.5 524.6 667.9 409.9
75-84 years ............. 1,328.0 1,806.7 1,035.7 1,364.8 1,881.4 1,054.3 917.0 1,061.1 813.0
85 years and over ........ 2,038.0 2,564.7 1,790.3 2,135.0 2,709.6 1,869.9 1,126.5 1,369.1 990.1

1968

Allages ............. 185.4 243.0 130.6 195.9 258.0 136.7 109.5 133.2 87.7
25-34 years ............. 4.6 7.2 2.2 4.1 6.5 1.7 8.7 13.1 5.0
35-44 years ............. 42.3 70.9 15.2 40.3 69.6 12.1 57.9 81.6 37.9
45-54 years ............. 158.5 267.1 56.8 157.6 270.4 51.3 166.6 236.2 105.3
55-64 years ............, 420.8 668.3 197.1 423.9 684.3 188.4 390.5 512.5 281.0
65-74 years ............, 900.5 1,315.0 574.1 919.8 1,360.8 574.4 706.7 870.1 571.2
75-84 years ............. 1,687.1 2,228.4 1,316.5 1,732.1 2,306.5 1,342.8 1,103.1 1,291.4 961.1
85 years and over ........ 2,911.8 3,570.7 2,553.0 3,012.9 3,715.3 2,637.8 1,782.4 2,163.4 1,526.2
18

TABLE 1.— Death rates* for acute myocardial infarction and chronic ischemic heart disease for specified
age groups, by color and sex; United States, 1968—1976—(Continued)

 

 

 

Total White All Other
Both Both’ Both
Year and age sexes Male Female sexes Male Female sexes Male Female
1976 _ Chronic ischemic heart disease
Allages ............. 150.2 153.5 147.0 155.5 157.7 153.4 115.4 125.4 106.4
25-34 years ............. 1.6 2.4 0.8 1.2 1.9 0.5 4.2 6.1 2.5
35-44 years ............. 12.8 20.3 5.6 10.6 17.5 3.9 27.5 41.0 16.3
45-54 years ............, 57.7 90.9 26.7 50.4 82.6 20.1 116.1 160.7 77.4
55-64 years ............. 173.3 258.5 96.8 159.5 244.3 83.2 302.2 396.1 222.0
65-74 years ............. 487.4 674.8 343.4 467.8 660.5 320.4 672.1 805.8 565.2
75~—84 years ............. 1,621.5 1,947.4 1,422.6 1,626.0 1,968.0 1,420.4 1,572.0 1,742.7 1,448.8
85 years and over ........ 4,647.4 4,945.8 4,507.0 4,859.8 5,208.0 4,699.1 2,650.8 2,782.4 2,576.9
1968

Allages ............. 150.6 156.3 145.1 153.1 158.3 148.2 132.0 141.6 123.3
25-34 years ............. 1.6 2.3 11 1.0 1.6 0.4 6.2 7.2 5.3
'-44 years... oo .....,. 13.6 20.5 TA 10.4 17.0 4.0 38.8 49.8 29.5
45-54 years ............. 57.0 85.6 30.2 47.5 76.0 20.7 142.6 175.8 113.3
55-64 years ............, 190.6 273.4 115.7 169.2 253.4 93.0 393.1 468.6 334.8
65-74 years ............, 590.4 769.1 449.7 560.6 742.8 417.9 889.5 1,025.0 777.2
75-84 years ............. 1,826.0 2,075.5 1,655.3 1,833.9 2,093.7 1,657.8 1,724.6 1,858.1 1,628.0
85 years and over ........ 5,523.6 5,636.6 5,468.4 5,695.3 5,831.8 5,629.4 3,605.9 3,736.6 5 518.0

 

*Rates are deaths per 100,000 population. For acute myocardial infarction, rates are based on deaths assigned to category number 410
of the Eighth Revision of the International Classification of Diseases, adapted for use in the United States, adopted in 1965, and for
chronic ischemic heart disease, to category number 412 of this revision

SOURCE: Rosenberg, H.M. (33).
0o
bo

 

 

 

TABLE 2.— Number of deaths* for acute myocardial infarction and chronic ischemic heart disease for specified
age groups, by color and sex; United States, 1968 and 1976
Total White All other
Both Both Both
Year and age sexes Male Female sexes Male Female sexes Male Female
1976 Acute myocardial infarction
Allages ............. 319,477 197,429 122,048 295,613 183,820 111,793 23,864 18,609 10,255
25-34 years ............. 890 718 172 720 598 122 170 120 50
35-44 years ............. 6,223 5,182 1,041 5,838 4,558 780 885 624 261
45-54 years ............,. 26,405 21,361 5,044 23,479 19,407 4,072 2,926 1,954 972
55-64 years ............,. 62,091 46,516 15,575 56,623 43,072 13,551 5,468 3,444 2,024
65-74 years ............. 93,695 61,038 32,657 86,566 57,004 29,562 7,129 4,034 3,095
75-84 years ............. 89,969 46,395 43,574 84,852 43,912 40,940 5,117 2,483 2,634
85 years and over ........ 40,068 16,132 23,936 37,939 15,201 22,738 2,129 931 1,198
1968
Allages ............. 369,610 236,017 183,593 342,999 220,517 122,482 26,611 15,500 11,111
25-34 years ............. 1,099 838 261 846 664 182 253 174 19
35-44 years ............. 9,980 8,132 1,848 8,412 7,122 1,290 1,563 1,010 558
45-54 years ............. 36,032 29,368 6,664 32,261 26,860 5,401 3,771 2,508 1,263
55-64 years ............. 76,108 57,387 18,721 69,504 53,287 16,217 6,604 4,100 2,504
65-74 years ............. 109,672 70,564 39,108 101,863 66,205 35,658 7,809 4,359 3,450
75~84 years” ............. 100,312 53,838 46,474 95,613 51,436 44,177 4,699 2,402 2,297
85 years and over ........ 36,135 15,711 20,424 34,317 14,824 19,493 1,818 887 931
1976 Chronic ischemic heart disease
Allages ............. 322,382 160,375 162,007 289,572 148,372 146,200 32,810 17,003 15,807
25-34 years ............. 502 381 121 332 266 66 170 115 55
35-44 years ............. 2,937 2,273 664 2,137 1,734 403 800 539 261
&8

age groups, by color and sex; United States, 1968 and 1976—(Continued)

 

 

 

Total White All other
Both Both Both
Year and age sexes Male Female sexes Male Female sexes Male Female
45-54 years .........000. 13,649 10,391 3,258 10,593 8,426 2,167 3,056 1,965 1,091
55-64 years .....ss eee eee 34,765 24,525 10,240 28,929 20,996 7,933 5,836 3,529 2,307
65-74 years ...cec eee eee 69,176 41,612 27,564 60,042 36,745 23,297 9,134 4,867 4,267
75-84 years ......... eee 109,860 50,010 59,850 101,088 45,932 55,156 8,772 4,078 4,694
85 years and over ........ 91,368 31,109 60,259 86,358 29,217 57,141 5,010 1,892 3,118
1968

All ages .....eeceeeee 300,216 151,815 148,401 268,124 135,333 132,791 32,092 16,482 15,610
25-34 years 2.2... eee eee 390 262 128 211 166 45 179 96 83
35-44 years ............. 3,212 2,350 862 2,162 1,734 428 1,050 616 434
45-54 years .......-..4.. 12,953 9,412 3,541 9,727 7,545 2,182 3,226 1,867 1,859
55-64 years ...........4. 34,475 238,481 10,994 27,743 19,732 8,011 6,732 3,749 2,983
65-74 years ...........0. 71,905 41,270 30,635 62,076 36,135 24,941 9,829 5,135 4,694
75-84 years ........ 0 108,576 50,145 58,431 101,229 46,689 54,540 7,347 3,456 3,891
85 years and over ........ 68,548 24,801 43,747 64,870 23,269 41,601 3,678 1,532 2,146

 

*Number of deaths due to acute myocardial infarction are those assigned to category number 410 of the Eighth Revision of the
International Classification of Diseases, adapted for use in the United States, adopted in 1965; and for chronic ischemic heart disease
to category number 412 of this revision

SOURCE: Rosenberg, H.M. (33).
as percent changes in rate in Table 3. The percent change has
been larger at younger ages (Tables 2 and 3). The changes for
chronic ischemic heart disease are similar but less dramatic
(Table 3).

Atherosclerosis

Differences in heart attack mortality rates among men and
women parallel pathology data concerning atherosclerotic
plaques of the coronary arteries. The International
Atherosclerosis Project systematically collected autopsy obser-
vations on persons from 14 geographic locations and 19 ethnic
groups in different parts of the world, and found that women
from 11 of the 19 groups, when compared to their male counter-
parts, had as much or even more aortic atherosclerosis. Men
over age 39 had more raised plaques in their coronary arteries
than women (24).

These findings indicate that the occurrence of coronary
plaques was parallel to heart attack rates, but that the occur-
rence of aortic lesions was not. Coronary plaque severity had a
male-to-female ratio of 1.61 among whites and of 1.14 among
blacks. Studies of a white population in Sweden (40) and of west-
ern Europeans from five locations (18) demonstrate similar find-
ings: a clear excess of coronary atherosclerosis among men and
a similar severity of aortic atherosclerosis among men com-
pared to women.

Autopsy studies thus show a selective liability of the male
coronary arterial bed for atherosclerosis, as compared to the
female, especially among white men but also among men of
other races. The pathological findings are congruent with the
clinical data on heart attack mortality rates. Autopsy studies
also show that, among men or women with manifest coronary
heart disease, women patients have roughly the same preva-
lence of advanced atherosclerotic lesions of the coronaries as
men (41). These data suggest that the amount of atherosclerosis
necessary to precipitate a heart attack is the same, on the aver-
age, in both sexes. This generalization about the amount of
coronary atherosclerosis appears to hold for heart attacks at
younger and older ages, for recent and old infarcts, and coro-
nary occlusion without infarct, and for stenosis, as well as for
complicated and calcified lesions and raised plaques in the coro-
nary arteries (41).

It should be noted that the grading of atherosclerosis at au-
topsy is not a simple matter because there are several types of
lesions and several ways of evaluating or measuring them.
Moreover, the development of the different sorts of lesions is

84
TABLE 3.— Percent change* between 1968 and 1976 in death rates for acute myocardial infarction and chronic
ischemic heart diseases for specified age groups, by color and sex: United States

 

Total White All Other

Both Both Both
Age Sexes Male Female Sexes Male Female Sexes Male Female

 

Acute myocardial infarction

Allages ............, ~19.7 —22.2 ~15.2 -19.0 —21.6 -14.2 -23.3 ~24.7 —21.3
25-34 years ............. ~39.1 ~—36.1 -50.0 —36.6 —33.8 ~47.1 -51.7 -51.1 -54.0
35-44 years ............. —36.2 ~34.8 ~42.1 ~34.0 —33.8 ~37.2 -47.5 ~41.8 -57.0
45-54 years ............. —29.5 ~30.0 -27.3 ~—29.1 ~-29.7 ~26.5 —-33.3 —32.3 -34.6
55-64 years ............, —26.4 —26.6 ~25.3 —26.4 ~26.8 —-24.6 -27.5 —24.6 ~30.7
65-74 years ............. —26.7 —24.7 ~29.1 —26.7 —24.7 —29.2 ~25.8 ~-23.2 —28.2
75-84 years ............. -21.3 ~18.9 —21.3 —21.2 ~-18.4 -21.5 -16.9 -17.8 —-15.4
85 years and over ........ —80.0 ~28.2 —29.9 ~29.1 —27.1 ~29.1 —-36.8 ~36.7 ~35.1

Chronic ischemic heart diseases

Allages ............. -0.3 -1.8 1.3 1.6 -0.4 3.5 ~12.6 ~11.4 -13.7
25-34 years ............. 4.3 ~27.3 20.0 18.8 25.0 -82.3 ~15.3 -52.8
35-44 years ............, -5.9 -1.0 —21.1 1.9 2.9 —2.5 —29.1 -17.7 —44,7
45-54 years ............. 1.2 6.2 -11.6 6.1 8.7 -2.3 -19.6 ~8.6 -31.7
55-64 years ............. -9.1 —5.4 -16.3 ~5.7 -3.6 —10.5 —24.1 -15.5 ~33.7
65-74 years ............, -17.4 —-12.3 ~23.6 -16.6 —11.1 —23.3 —24.4 ~21.4 —27.3
75-84 years ............, ~11.2 -6.2 —14.1 ~-11.3 -6.0 -14.3 -8.8 ~6.2 -11.0
85 years and over ........ -15.9 ~12.3 -17.6 ~14.7 -10.7 -16.5 —26.5 -25.5 —26.8

 

*Percent changes are based on rates per 100,000 population. For 1968 and 1976, rates for acute myocardial infarction are based on

deaths assigned to category number 410 of the Eighth Revision of the International Classification of Diseases, adapted for use in the
2 United States, adopted in 1965, and for chronic ischemic heart disease, on category number 412 of this revision

SOURCE: Rosenberg, H.M. (33).
not necessarily parallel. Sternby provides a useful discussion of
issues in the grading of atherosclerosis (40). Nevertheless, the
major studies noted above provide strong evidence that women
have less coronary atherosclerosis on the average than men of
the same age in the same population

Risk Factors

Factors present in individuals which correlate with future
liability to disease are risk factors for that disease. In the case
of heart attack, for example, it has been shown that age, male
sex, cigarette smoking, hypertension, elevated blood cholesterol,
and several other conditions are positively and independently
associated with the probability of heart attack. The level of
high-density lipoprotein cholesterol in the serum has a negative
correlation with heart attack; that is, higher levels are protec-
tive. The various risk factors have been identified for both men
and women and have been shown on multivariate analysis to be
independent. A combination of risk factors is synergistic, pro-
ducing an associated risk greater than the simple sum of the
individual risks. Although the data for women are much less
extensive than for men, they indicate that cigarette smoking is
a major risk factor for heart attack in women.

The Effect of Smoking

ATHEROSCLEROSIS

There is little autopsy information about the amount of
atherosclerosis in women smokers. Sackett and his associates
reported on aortic atherosclerosis among both men and women:
of their 450 female subjects, 309 were nonsmokers, 52 smoked
less than a half pack per day, and 89 smoked more (34). Mean,
age-adjusted aortic atherosclerosis was found to increase in
conjunction with the amount and duration of smoking.

A study of the intramyocardial arteries and arterioles of the
heart in 13 women and 21 men who were nonsmokers, and 16
women and 27 men who were smokers, indicated that prolifera-
tive lesions in intramyocardial arteries were more advanced
relative to age in smokers than nonsmokers. It was also found
that subendocardial arterioles were thickened in smokers. A
separate analysis by sex was not performed, but the authors
remarked that the lesions developed as rapidly and as exten-
sively in women as in men in both smoking and nonsmoking
groups (28).

Studies of the severity of atherosclerotic plaques in the ar-
teries of women who smoked in comparison with those who did

86
48

TABLE 4.—Coronary heart disease mortality ratios related to smoking — prospective study

 

 

Author, Number and Follow- Number
year, type of Data up of
country populations collection (years) deaths Cigarettes/day Age Variation
Hammond 358,584 Questionnaire 6 14,819 M F Males
and males and follow-up NS ........ 1.00 1.00 40-49 50-59 60-69 70-79
Garfinkel, 445,875 of death certi- 1-9 ........ 1.27 0.81
1969, females age cate 10-19 ...... 1.00 1.22 NS ...... 1.00 1.00 1.00 1.00
U.S.A. 40-70 at 20-30 ...... 1.75 1.52 19 0... 1.00 1.50 1.48 1.14
entry. >40 ....... 1.77 0.61 10-19 ... 239 2.13 1.82 1.41
20-30 ... 3.76 2.40 1.91 1.49
>40 20... 3.51 2.79 171 1.47
Females
40-49 50-59 60-69 70-79
NS ...... 1.00 1.00 1.00 1.00
19) ....., 1.31 1.15 1.04 0.74
10-19 ... 2.04 2.37 1.79 0.98
20-30 ... 3.62 2.69 2.00 1.27
>40 20... +3.31 3.73 +2.02

 

Based on 5-9 deaths
NS = nonsmokers, M = males, F = females
SOURCE: U.S. Public Health Service (44,45).
not smoke involve too few subjects to be satisfactory. Inves.
tigating the relationship of these arterial lesions and cigarette
smoking in women is fundamental to understanding the occur-
rence of heart attack and other ischemic diseases.

CORONARY HEART DISEASE

Coronary heart disease (acute myocardial infarction and
chronic ischemic heart disease) occurs with greater frequency
in smoking than in nonsmoking women. The prospective study
of Hammond and Garfinkel, published in 1969, included data on
approximately 446,000 women between the ages of 40 and 79
(10). The inerease in mortality ratios in conjunction with in-
creasing numbers of cigarettes smoked per day for various ages
is shown below in Table 4 (43,44), Mortality ratios were higher
for younger ages and lower for older ages. The one-pack-a-day
smoker’s risk of death from heart attack was approximately
twice that of the nonsmoker. The prospective data of Shapiro
and colleagues are based on a population of 120,000 men and
women (36). Using a sampling factor of about one-thirtieth, they
examined 4,301 women at risk of a first myocardial infarction
between the years 1962 and 1964. The smokers compared with
nonsmokers had roughly twice as many rapidly fatal heart at-
tacks and heart attacks that were not fatal within 48 hours. The
ratio was approximately 2.9 among younger women aged 45 to
54 and 1.8 for the subjects aged 55 to 64. Heavy smokers had
higher ratios, but the data did not permit a detailed study of
dose relationships or of the experience of female ex-smokers.

A recent study examined the cause-specific mortality of 6,194
British women physicians over the period 1951 to 1973 (6). Table
5 presents the results of this study in conjunction with the pre-
viously published results among male physicians during the
same period (7). The clear association of cigarette smoking and
ischemic heart disease previously described in males was con-
firmed in female physicians. For women who reported smoking
15 or more cigarettes per day, mortality due to ischemic heart
disease was more than double that of nonsmokers.

Although the results demonstrated a similar effect of smok-
ing in the development of ischemic heart disease in both male
and female physicians, the association of smoking with heart
disease was less striking in women physicians. Ischemic heart
disease was less prominent as a proportional cause of death in
this population of women than in male colleagues (16 percent vs.
32 percent of all deaths). Ischemic heart disease mortality was
only 26 percent higher for all ever-smoked women than for
never-smoked women. However, for females who smoked heav-

88
68

TABLE 5.— Death from ischemic heart disease and smoking habits when last asked, British physicians 1951-1973

 

Annual Death Rate per 100,000

 

 

 

Persons Standardized for Age X?
Number Current Smokers - Dose Per Day Nonsmokers
Total of vs.
Popul. Deaths Nonsmokers Ex-smokers 1-14 15-24 > 25 others Trend
Women 6194 179 138 126 132 304 292 wee 21.14*
(number of cigarettes)
Men 34,440 3191 413 533 501 598 677 22.59% 53.56*
(any tobacco—grams)
(1 gram = 1 cigarette)
*P<0.001.

SOURCE: Doll, R. (6,7).
ily (= 25 cigarettes per day), the relative risk of death from
ischemic heart disease was 2.2, a finding consistent with that
demonstrated in males, who had a relative risk of 1.6.

In such studies, standardization for amount smoked daily by
each of the sexes does not, however, correct for differences in
age at initiation of smoking and degree of inhalation. This fact
greatly complicates comparison of the magnitude of biologic ef-
fect in the two sexes. This “cohort effect” (i.e., unmeasured but
documented dissimilarities in total smoking experience) may
lead to an erroneous interpretation that cigarette smoking is
less damaging to women than to men. This issue cannot be re-
solved until studies examine the effect of smoking in more re-
cent cohorts of women whose lifetime smoking behavior is more
similar to that of men.

Among 26,467 Swedish women observed during a 10-year
period, the risk of developing fatal coronary heart disease was
significantly higher among smokers than nonsmokers (50). The
relative risk was 1.9 at ages 40 to 49 and 1.3 at ages 50 to 59. An
extensive mortality study in Japan also reported a highly signif-
icant increase in deaths from ischemic heart disease among
female smokers, with a mortality ratio for smokers of 1.6 (29).

Coronary heart disease morbidity data are available on
women from prospective studies in Framingham, Mas-
sachusetts, Tecumseh, Michigan, and the greater New York
areas. The Tecumseh data of 1967 do not show a relationship of
such morbidity with smoking (Table 6) (8). The Framingham
Heart Study found an increased risk for women smokers, but
the associations were weak (19,20).

The study of Shapiro and colleagues considered both mortal-
ity and morbidity (36). It reported separately on deaths within
48 hours of onset and on all definite myocardial infarctions after
that time interval. Using this classification, the incidence of
coronary heart disease among women smokers was distinctly
higher than it was among nonsmokers.

While there is some variability in the strength of this associa-
tion, the data from the various prospective studies of mortality
and morbidity from coronary heart disease establish smoking as
a positive correlate, or risk factor, for women. However, the risk
ratios tend to be smaller than for men at a given level of
cigarette consumption in all age groups. This trend may result
from the different smoking patterns reported by men and
women who smoke the same number of cigarettes per day
(6,7,25). Men generally begin smoking at an earlier age and have
thus smoked for a longer time period than women. Men also
inhale more often than women and are more likely to smoke
more than half of a cigarette. These smoking styles would ex-

90
16

TABLE 6.—Coronary heart disease morbidity as related to smoking

 

 

Author, Number Follow- Number
year, and type of Data up of
country population collection years! incidents? Cigarettes/day® Pipes, cigars
Epstein, 6,568 male Initial medical 4 96 male, 92 Males Males
1967, and female examination female 40-59 60 and over 40-59
U.S.A. residents of and repeat CHD inelud- NS ...........005 1.00 (1) 1.00 (7) SM ........... 1.80 (2)
Tecumseh, follow-up ing deaths, | Op, 6.383 (10) 1.27 (11)
Mich. examinations. angina, and Cigarettes ....... 5.20 (36) 1.90 (23) 60 and over
myocardial SM ........--- 0.80 (6)
infarctions Females
40-59 60 and over
NS ...... eee eee 1.00 (21) 1.00 (47)
EX ..........005. 0.89 (3) 1.31 (5)
Cigarettes ....... 1.02 (14) 0.42 (2)

 

‘Reexamination of patients was spread over 142-6 year period, but data are reported in terms of 4-year incidence rates.
2Actual number of CHD incidents derived from data on incidence and total in smoking class.

3Risk ratios— actual number of CHD incidents shown in parentheses. SM = smokers, NS = nonsmokers, EX = ex-smokers.
SOURCE: U.S. Public Health Service (45).
pose men to a larger dose of smoke per cigarette and a larger
lifetime amount than that experienced by women.

Case control and retrospective studies of women who have
had heart attacks have suggested an increased incidence of
heart attack among smokers. For example, a case control study
of 55 women who had heart attacks before age 50 (an uncommon
event in women) found that 89 percent were smokers in contrast
to 55 percent in a control group without myocardial infarction.
Heavy smokers (35 or more cigarettes per day) had an estimated
myocardial infarction rate approximately 20 times that of the
nonsmokers. As far as possible, women using oral contracep-
tives and those with other identifiable risk factors were
excluded from the study (37).

Spain and his associates conducted a retrospective autopsy
study of women who had died suddenly of coronary heart dis-
ease and compared this verified diagnosis to the women’s smok-
ing habits as reported by the closest living relative (38). Only
witnessed sudden deaths were included in the data. Compari-
sons were made between women who had died of coronary heart
disease and women who died suddenly of causes other than
heart attack. It was found that 62 percent of the women suffer-
ing sudden cardiac death were heavy smokers in contrast with
only 28 percent of the control group. For those who smoked heav-
ily, the mean age at death was 19 years younger than that of
nonsmokers; lighter smokers died at an intermediate mean age.

In a retrospective study emphasizing psychosocial variables,
Talbott and associates reported on 64 white women who died
suddenly of arteriosclerotic heart disease (42). They found that
women who died suddenly smoked more cigarettes than the
comparison group. The relative risk for those smoking more
than a pack a day compared with those smoking less than a pack
a day was 3.9 (p<.004).

Smoking, as well as other risk factors, raises the already
somewhat higher risk of myocardial infarction among women
who use oral contraceptives. During the child-bearing years,
the use of oral contraceptives doubles the risk of myocardial
infarction; women who both smoke and use oral contraceptives
have approximately 10 times the risk of women who neither
smoke nor use oral contraceptives (14). These issues are consid-
ered below in a separate section.

Cessation of Smoking and “Tar” and Nicotine Content of
Cigarettes

Existing data are inadequate to determine the effect of smok-
ing cessation on the incidence of coronary heart disease in

92
women. Hammond and associates have reported that mortality
rates from coronary heart disease were lower in women who
smoked low-“tar” and low-nicotine cigarettes (as sold in the
1960s) than in those who smoked medium level products, and
still lower than for those who smoked high-“tar” and high-
nicotine products; even so, the mortality rate for those women
smoking low-“tar”, low-nicotine products was significantly
higher than that of nonsmokers (11).

Evidence considered below suggests that stopping smoking is
beneficial in the treatment of women suffering from peripheral
vascular disease.

ANGINA PECTORIS

The Framingham Heart Study reported that there was a posi-
tive association between smoking and angina pectoris among
men but not among women (20). In an extensive study con-
ducted in New York City, Shapiro and colleagues reported a
positive association between the development of angina pec-
toris and smoking among men and a nonsignificant positive
trend among women (37). Among patients with angina pectoris,
smoking lowers the exercise threshold for the onset of angina
(46). Only male patients have been studied thus far; equivalent
data apparently have not been published for women with an-
gina and angiographically proven coronary atherosclerosis.

CEREBROVASCULAR DISEASE

The incidence of stroke as a manifestation of cerebrovascular
disease appears to be somewhat greater in men than in women,
but the difference is small (21,30,43).

In an autopsy assessment of cerebrovascular atherosclerosis,
Sternby reported more atherosclerosis of the common carotid
artery and the carotid sinus in men than women. There was also
more intracranial atherosclerosis of certain vessels in men than
women. However, using the area-grading method, no sex dif-
ference was found in total intracranial atherosclerosis (40). The
International Atherosclerosis Project also reported a slight ex-
cess of cerebrovascular atherosclerosis among males (24). On
the whole, the available pathological evidence suggests a minor
increase in cerebrovascular atherosclerosis among men in com-
parison with women, although some studies fail to confirm this
conclusion (see 40).

It is not clear whether smoking is a risk factor among women
for the development of atherothrombotic stroke. Kannel has
discussed the issue and the current literature in some detail
(19). The Framingham Heart Study has reported a dose-related

93
¥6

TABLE 7.— Deaths from cerebrovascular disease related to smoking

 

 

Number of
Number deaths due
Author, and type underlying to
year, of popu- Data Follow-up CVD as Mortality
country lation collection years cause ratios
Hammond 358,584 Questionnaire 6 4,099 Age
and males and follow- Cigarettes/day 40-49 50-59 60-69 70-79
Garfinkel, 445,875 up of death Males
1969, females certificate Never smoked 1.00 1.00 1.00 1.00
U.S.A. 40-79 years 1-9 2... ee. eee 2.79 1.95 1.30 0.95
of age at 10-19 ......... 1.14 1.48 +1.44 0.92
entry. 20-380) ......... 2.21 2.08 1.62 1.22
>40 ....ceeeeee 1.64 2.40 1.72 +0.68
Females
Never smoked 1.00 1.00 1.00 1.00

L-9 Lecce cee eee eee 1.50 1.26 1.26 0.83
10-19... cece eee eee 2.60 2.70 2.15 +0.57
20-30 wo... eee eee 2.90 2.67 1.83 1.28
> 4D Lecce cece eee +5.70+3.52 — —

 

SOURCE: U.S. Public Health Service (44,45),
correlation between the incidence of atherothrombotic stroke
and cigarette smoking in men but not in women. The extensive
prospective study of Hammond and Garfinkel, which involved
almost 446,000 women and recorded 1,905 deaths from cere-
brovascular disease during a six-year period, found that smok-
ing was a positive correlate for such mortality (10); in both men
and women, the mortality ratio was increased by roughly 2 or
2.5 times (Table 7) (44,45).

That some of these deaths may have involved subarachnoid
hemorrhage rather than brain infarction, is suggested by a re-
cent report that found the incidence of subarachnoid hemor-
rhage to be positively associated with smoking for both men and
women (2). The relative risk for men was 3.9 and for women, 3.7.
The association appeared to relate to hemorrhage from rup-
tured cerebral aneurysms rather than to other conditions that
may give rise to subarachnoid hemorrhage. A synergism be-
tween smoking and the use of oral contraceptives and sub-
arachnoid hemorrhage is noted below (31). The Japanese study
cited in the discussion of ischemic heart disease has also re-
ported on 366 deaths from cerebrovascular disease among
women who smoked (29). The risk ratios for subarachnoid
hemorrhage and cerebral hemorrhage were both significantly
increased among women smokers (p<.001) as was the risk rate
for the category, “other forms of cerebrovascular disease”
(p<.05).

ARTERIOSCLEROTIC PERIPHERAL VASCULAR DISEASE

Clinicians have noted that arteriosclerotic peripheral vascu-
lar disease is more common in men than women. Sternby has
reported from autopsy studies that men generally have some-
what more atherosclerosis of the femoral and pelvic arteries
than women (40).

Kannel has reviewed the relationship of smoking to the inci-
dence of arteriosclerotic peripheral vascular disease (19). In the
Framingham Heart Study the incidence of peripheral vascular
disease was increased among smokers of both sexes; cigarette
smoking was as strong an independent risk factor in women as
in men. Heavy smokers had a threefold increased incidence.

Weiss studied 245 women with arteriosclerotic peripheral
vascular disease (49). Ex-smokers who had not smoked for 5
years or more had nearly a normal risk ratio of 1.06; those who
had not smoked for the last 1 to 5 years had a risk of 1.70;
continuing smokers of less than a pack a day, 5.15; pack a day
smokers, 11.53; and those smoking more than a pack a day, 15.56
(relative to nonsmokers, 1.00). The increased risk was particu-

95
larly associated with proximal (aortoiliac) disease, and there
was less association with distal (femoropopliteal) disease. Age-
standardized relative risk ratios for those smoking a pack a day
were 30.06 for proximal and combined proximal and distal dis-
ease and 6.32 for distal disease alone.

A retrospective study of 217 patients who underwent arterial
reconstructive procedures of various kinds for peripheral vascu-
lar disease has been reported by Myers and colleagues (27).
Diabetics were excluded from the report. There were 164 male
and 53 female patients. The late patency rate of the vascular
reconstruction was followed for 1 to 4 years. The authors re-
ported that the number of cigarettes smoked before surgery did
not influence the outcome, but cessation of smoking after
surgery had a favorable impact. There were no significant dif-
ferences in outcome between men and women. The patency rate
4 years after aortofemoral surgery was 90 percent in those who
smoked five or fewer cigarettes per day after surgery and 75
percent in those who smoked a greater amount. Following
femoropopliteal reconstruction, the 2-year patency rates were
95 percent for those who stopped smoking, 75 percent for those
smoking as many as 15 cigarettes per day, and 65 percent for
those who continued to smoke more than 15 cigarettes per day.

AORTIC ANEURYSM

Studies have not been reported for women with respect to
atherosclerotic aortic aneurysm and smoking. Deaths for
women are about one-fifth those for men (10).

HYPERTENSION

Smoking is not associated with an increased prevalence of
essential hypertension in men or women (39). However, smoking
does combine with hypertension (and other risk factors) as a
risk factor for heart attack, synergistically compounding the
risk.

Two recent case control studies of rapidly progressive, severe
or malignant hypertension have found that there is an overrep-
resentation of smokers among patients with this uncommon
phase of hypertension (3,13). In one study of 82 patients who
developed malignant hypertension, 67 were smokers. Thirty-
three of those were women. In the study, 77 percent of the
female patients with malignant hypertension smoked, and only
about 44 percent of those with essential hypertension and of the
general female population smoked. The difference is highly sig-
nificant. A similar and parallel study of 48 patients with malig-
nant hypertension contained 33 men and 15 women; 25 men (76

96
percent) and 8 women (53 percent) were smokers compared with
44 percent and 80 percent, respectively, of a group of 44 men and
44 women with nonmalignant hypertension. The difference is
significant for men but does not reach significance for women.

VENOUS THROMBOSIS

The section of the 1979 Surgeon General’s Report dealing with
venous thrombosis noted a case control study by Vessey and
Doll of 84 women who had venous thromboembolism (45). There
was no significant relationship to smoking, although there was
a trend (p=0.08) reasonably attributable to chance (46). Simi-
larly, Lawson, Davidson, and Jick reported no association with
smoking among 60 premenopausal women who used oral con-
traceptives and who had uncomplicated venous thromboem-
bolism (22).

The issue is reopened, however, by a recent paper derived
from the Walnut Creek Contraceptive Drug Study. The authors
analyzed 38 cases of venous thromboembolic events among the
approximately 16,700 women followed in the study. These
women were matched with 8,174 controls from the same cohort,
providing each case with 61 to 559 comparison subjects. The
relative risk of cigarette smoking was 2.6 with a one-sided p
value of less than 0.01. On multivariate analysis, the smoking
effect was independent and remained significant. Of the 17
idiopathic cases of thromboembolic disease, 65 percent occurred
in smokers, while 33 percent of the controls were smokers. The
relative risk for smokers was 4.2. Both smoking and oral con-
traceptive use were independent risk factors for venous throm-
boembolic disease in this cohort of women (32).

The same section of the 1979 Surgeon General’s Report noted
a controversy about whether smokers who suffered myocardial
infarction had a relative protective effect from leg vein throm-
bosis in the immediate post infarction period (45). The authors
did not provide an analysis for each sex.

A recent investigation of women undergoing gynecologic op-
erations has studied the incidence of deep vein thrombosis of
the leg in relation to smoking. In the prospective study of 231
women, their smoking habits during the month before the oper-
ation were determined. The occurrence of deep vein thrombosis
(DVT) was assessed by the radioactive fibrinogen technique,
with routine scans on the first, third, and sixth postoperative
days. Of the 231 patients, 99 smoked and 132 did not smoke.
Eight of the smokers (8.1 percent) and 29 of the nonsmokers (22
percent) developed DVT. Following an analysis of other factors,
the authors concluded that smoking provided an apparent “‘pro-

97
tective” effect against postoperative DVT, based on the fact
that smokers constituted only 21 percent of the patients with
DVT. They also noted that the women who developed DVT
weighed more than those who did not and that smokers who
developed CVT were more overweight than nonsmokers with
DVT (5).

In a continuing prospective study of the relationship of blood
clotting and blood thrombogenic properties to ischemic heart
disease, Meade and associates have reported on a number of
blood coagulation variables and their relationship to smoking
among 1,426 men and 638 women in England (26). Forty-three
percent of the men and 36 percent of the women were smokers.
Smoking was not found to have an effect in women on factors V
or VII, fibrinogen, fibrinolytic activity, antithrombin ITI,
platelet adhesiveness, or platelet count. Smoking decreased fib-
rinolytic activity in men and decreased factor VIII activity in
both men and women. Oral contraceptive users were found to
show an increase in fibrinolytic activity only if the women were
nonsmokers. :

HIGH-DENSITY LIPOPROTEIN

High-density lipoprotein (HDL) is a protein complex that
transports cholesterol in the blood. A higher level of HDL is
correlated with a reduced risk of heart attack. It has been ob-
served that women who smoke have lower levels of HDL than
expected (1,4,9).

Oral Contraceptive Use, Smoking, and Cardiovascular Disease

The association of oral contraceptive use and an increased
incidence of certain cardiovascular disorders has attracted
much interest. Smoking has emerged as a strong synergistic
risk factor, and an additional study has focused on smoking as
an independent risk factor.

The effects of smoking and of estrogen and progestin con-
traceptives on the level of high-density lipoprotein in women
have been studied by Bradley and associates. They measured
serum HDL among almost 5,000 women between the ages of 21
and 62 (4). They reported that the use of oral estrogens raised
the level of HDL significantly above the level in nonusers while
progestin use lowered it. Combination drugs tended to change
the HDL level according to their relative estrogen-progestin
formulation. The average HDL concentration was reduced by
smoking. Among nonsmoking women the HDL concentration
was 63.7 + 16.8 mg/dl. This was reduced by 2.2 mg/dl for those
smoking half a pack per day; and by 7.3 mg/d] for those smoking

98
one or more packs per day. A reduction in the HDL level among
women who smoked was also reported from Holland. This study
found an independent negative association with the HDL level
among oral contraceptive users (1).

It has been reported from long-term studies that women
using oral contraception have a two to threefold statistically
significant increase in risk of venous thromboembolic disease
when compared to those using other forms of contraception (47).
This study concluded that smoking did not significantly in-
crease the incidence of venous thromboembolism (46). By con-
trast, the Walnut Creek Study reported that smoking contrib-
uted to venous thromboembolism among both users and nonus-
ers of oral contraceptives (32). Conclusions about the effect of
smoking on venous thromboembolic phenomena, therefore,
must be regarded as uncertain at this time since there are few
relevant studies and they provide somewhat contrary conclu-
sions.

In 1973, the Collaborative Group for the Study of Stroke in
Young Women estimated that the relative risk of cerebral is-
chemia or thrombosis was approximately nine times greater for
women who use oral contraceptives than for those who do not. A
detailed analysis of smoking was not presented, but one of the
study’s striking findings was the high proportion of women with
stroke who currently or at some time smoked cigarettes regu-
larly (73.8 percent), compared with smoking rates of 43.4 percent
among neighborhood controls aged 17 to 44. The study also
found an increase in hemorrhagic strokes among white women.
Almost half of the hemorrhagic strokes were attributable to
bleeding from congenital aneurysms leading to subarachnoid
hemorrhage (5). Recently an association between smoking and
aneurysmal subarachnoid hemorrhage in both men and women
has been documented (2).

The Walnut Creek Contraceptive Drug Study reported that in
a cohort of approximately 16,700 women, the risk of sub-
arachnoid hemorrhage for smokers was 5.7 times that of
nonsmokers; the risk for oral contraceptive users was 6.5 times
that of nonusers; and the relative risk for women who used both
cigarettes and oral contraceptives was 22 times as great. Past
users of oral contraceptives also had an increase in relative risk,
but an analysis of risk was not possible because of the small
number of cases (31).

The risk of myocardial infarction in women is increased by
cigarette smoking and by the use of oral contraceptives, it is
compounded when both are used together. For example, Mann
and associates reported a retrospective study of 63 women
below the age of 45 with acute myocardial infarction. The pro-

99
portion of heart attack patients who had used oral contracep-
tives in the previous months was significantly higher than ex-
pected. The relative risk for myocardial infarction among
“women smoking 25 or more cigarettes per day was 11.3 times
greater than that among nonsmokers. Moreover, there was evi-
dence for synergism of the two risks (23).

Jick, et al. reported a case control study of 107 women under
age 46 who were discharged from the hospital after suffering
nonfatal, acute myocardial infarctions (15,16,17). The annual
risk of nonfatal myocardial infarction (MI) among healthy
women aged 39 to 45 who both smoked and used estrogens for
noncontraceptive purposes was approximately 1 in 750. They
noted that although an acute myocardial infarction is uncom-
mon in healthy young women, the risk appears to be substantial
in women over the age of 38 who both use estrogens and smoke
cigarettes (17).

In this same study, a relative risk of 14 was reported for oral
contraceptive users compared with nonusers (90 percent confi-
dence limits of relative risk from 5.5 to 37) (16). In women smok-
ing more than 25 cigarettes per day the relative risk rose to 34
times that of women who were both nonusers and nonsmokers.
While the number of subjects was small, the authors calculated
that for women exposed to either oral contraceptives or smok-
ing, but not both, the annual age-specific risks for nonfatal MI
were roughly 1 per 190,000 at ages 27 to 37; 1 per 47,000 at ages
38 to 40; 1 per 23,000 at ages 40 to 43; and 1 per 16,000 at ages 44
and 45. If, however, both cigarettes and oral contraceptives are
used, the annual age-specific risk is estimated to be much
higher and the respective risks become 1 in 8,400; 1 in 920, 1 in
540, and 1 in 250. The authors report that a dose-response rela-
tionship exists between smoking and risk among their popula-
tion of female myocardial infarction patients, such that smok-
ing 1 to 14 cigarettes per day carried a relative risk of nonfatal
myocardial infarction of 9.2; 15 to 25 cigarettes of 7.9; and 26 or
more cigarettes of 21, relative to those who never smoked (15).

In another recent study of 234 pre-menopausal women.who
had suffered a first myocardial infarction and 1,742 control pa- |
tients drawn from the hospital population, Shapiro and his co-
workers found an association between recent oral contraceptive.
use and smoking (35). They found no evidence that past use of
oral contraceptives was related to heart attack or that
heightened risk was associated with increased duration of use
of the oral contraceptives. For nonsmokers who used oral con-
traceptives, the rate of myocardial infarction increased fourfold
compared to nonusers and nonsmokers; in those women who
smoked 25 or more cigarettes a day but did not use oral con-

100
traceptives, the rate increased more than sevenfold; and in
those women who both smoked heavily and used oral contracep-
tives the rate increased at least twentyfold.

Carbon Monoxide

A study of male and female office workers found no sex dif-
ference in the relationship between carboxyhemoglobin (COHb)
levels and daily consumption of cigarettes. However, women
smoked fewer cigarettes on the average than men. The study
found that the COHb levels in smokers were higher among the
sedentary office workers than among physically active meat
porters and that both had higher levels of COHb than pregnant
women who smoked (12). The latter had COHb levels approxi-
mately three times higher than that of nonsmokers. Wald re-
ported from a cross-sectional study that carboxyhemoglobin
levels of smokers are a better indicator of the risk of
atherosclerotic cardiovascular disease than a reported smoking
history (48). The proportion of both men and women with
atherosclerotic disease increased with increasing levels of
COHb.

Comment

Women are less likely to experience a myocardial infarction
than men. Nevertheless, coronary heart disease is still a leading
cause of death and disability in women. The lower mortality
rates from acute myocardial infarction and chronic ischemic
heart disease of women as compared to men are paralleled by
less extensive and severe atherosclerosis in the coronary ar-
tieries of adult women. The severity of aortic atherosclerosis,
however, is about the same in both sexes.

The relationship of cigarette smoking to atherosclerosis,
heart attack,and other ischemic diseases secondary to
atherosclerosis has not been studied among women as exten-
sively as among men; moreover, most studies have been limited
to white women. It is not known whether atherosclerotic
plaques observed at autopsy are more extensive and severe in
women smokers than in nonsmokers. No data are available con-
cerning the incidence of death from atherosclerotic aneurysms
of the aorta among women who smoke relative to those who do
not, and inadequate data exist to indicate whether cessation of
smoking by women is associated with a beneficial reduction in
the risk of heart attack, as has been demonstrated in men. The
effect of smoking on the threshold for the onset of angina pec-
toris and on cardiac function in women with coronary heart
disease has not been studied.

101
Nevertheless, compelling data from prospective cohort
studies and from case control investigations indicate that
cigarette smoking is a major risk factor for fatal and nonfatal
heart attacks in women. In general, cigarette smoking in-
creases the risk by a factor of about two, and in younger women
cigarette smoking may increase the risk several fold. Women
who smoke low-“tar” and low-nicotine cigarettes have a greater
risk of suffering heart attacks than nonsmokers but appear to
have a smaller risk than women smoking moderate-to-high
“tar” and nicotine products.

Smoking is a major risk factor for arteriosclerotic peripheral
vascular disease in women, as it is in men. For both men and
women the successful outcome of surgical repair of this disorder
is enhanced by cessation of smoking. Smoking is a major risk
factor for subarachnoid hemorrhage and for the development of
malignant hypertension. Smoking is reported to depress the
natural relative elevation of high-density lipoprotein choles-
terol enjoyed by women. In women who use oral contraceptives,
smoking is a powerful synergistic risk factor for subarachnoid
hemorrhage and for myocardial infarction.

While data implicating smoking as a risk factor for various
cardiovascular diseases in women are neither as extensive nor
as complete as for men, the evidence nonetheless clearly estab-
lishes cigarette smoking as a major correlate for myocardial
infarction, arteriosclerotic peripheral vascular disease and
subarachnoid hemorrhage in women (45).

Summary

Coronary heart disease is the major cause of death among
both males and females in the U.S. population. The 1979 Sur-
geon General’s Report clearly demonstrated the close associa-
tion of cigarette smoking and increased coronary heart disease
among males. This report reviews the evidence associating
cigarette smoking and cardiovascular disease in women:

1. Coronary heart disease, including acute myocardial infarc-
tion and chronic ischemic heart disease, occurs more frequently
in women who smoke. In general, cigarette smoking increases
the risk by a factor of about two, and in younger women
cigarette smoking may increase the risk several fold.

2. Cigarette smoking is a major independent risk factor for
coronary heart disease in women; it also acts synergistically
with other coronary heart disease risk factors producing a risk
greater than the sum of the individual risks.

3. The use of oral contraceptives by women cigarette smokers

102
inereases the risk of a myocardial infarction by a factor of ap-
proximately ten.

4. Women who smoke low “tar” and nicotine cigarettes expe-
rience less risk for coronary heart disease than women who
smoke high “tar” and nicotine cigarettes, but their risk is still
considerably greater than that of nonsmokers.

5. Increased levels of high-density lipoprotein (HDL) are cor-
related with a reduced risk for an acute myocardial infarction;
women cigarette smokers have decreased levels of HDL.

6. Cigarette smoking is a major, independent risk factor for
the development of arteriosclerotic peripheral vascular disease
in women. Smoking cessation improves the prognosis of the dis-
order and has a favorable impact on vascular patency following
reconstructive surgery.

7. Women cigarette smokers experience an increased risk for
subarachnoid hemorrhage; the use of both cigarettes and oral
contraceptives appears to increase synergistically the risk for
subarachnoid hemorrhage.

8. Women who smoke cigarettes may be more likely to de-
velop severe or malignant hypertension than nonsmoking
women.

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CANCER.
CANCER
Introduction

For more than 40 years cancer has been second only to car-
diovascular disease as a cause of death in the United States.
With the exception of the very elderly, the death rate for adult
men exceeds that for adult women for both groups of diseases,
implying a difference in genetic susceptibility, environmental
exposures or lifestyles between the sexes, or a combination of
genetic and environmental factors.

Placing these generalizations about cause of death in per-
spective, current data from the National Center for Health
Statistics (28) reveal the following statistics:

There are 105 male births each year in the United States for
every 100 female births, but the higher death rate for males
results in a ratio of 100 men to 100 women at ages 20 to 24 and of
79:100 at ages 65 to 69, and of 47:100 at age 85. Life expectancy
in the United States in 1976 was 68.7 years for males compared
to 76.1 years for females.

Heart disease and cancer currently account for 60 percent of
deaths in the United States. In contrast to the decline in the
age-adjusted death rates for ischemic heart disease, the age-
adjusted death rate for cancer has increased. Hidden in this
small rise in the overall cancer statistics is a remarkable
increase—a veritable epidemic—of cancer of the lung in both
men and women. In the past quarter century, deaths from
cancer of the respiratory tract tripled in the white population
and quadrupled in the black population. The remarkable male-
to-female preponderence of lung cancer in the 1940s and 1950s
has been decreasing in the 1960s and 1970s; the rate of increase
in lung cancer in males is slowing while the rate of increase of
lung cancer in females is accelerating. As a cause of death, lung
cancer in women is now second only to mammary carcinoma and
will likely displace breast cancer as the Seading cause of cancer
mortality in women in the 1980s (1) (see Figure 1).

The 1964 Surgeon General’s Report reached the following
conclusion: “Cigarette smoking is causally related to lung
cancer in men; the magnitude of the effects of cigarette smoking
far outweighs all other factors. The data for women, though less
extensive, point in the same direction” (33). Since then, a
number of retrospective and prospective epidemiologic studies,
experimental animal carcinogenesis studies, and studies of
human tissues at surgery and autopsy have confirmed and ex-
tended those conclusions. Cigarette smoking is the major cause
of cancer of the lung in women. The risk increases with the
number of years the individual smoked, the number of ciga-

109
50

White Males
30 .
meee” 27

e
eo

¢

o onwhite Males

°
°

10

White Females

e

Rate Per 100,000 Population (Log Scale)

e##* *Nonwhite Females

 

2 2
1950 1955 1960 1965 1970 1975 1980 1985
6th Rev. ——»>*—7th Rev. —>*- 8th Rev. > 1

 

FIGURE 1.— Age-adjusted death rates* for malignant neoplasm
of trachea, bronchus and lung,** by color and sex
compared to rates for malignant breast neoplasm,
United States, 1950-1977; projection for white
females to 1985.***

* Adjusted by the direct method to the U.S. population, 1940.

**ICD 6th and 7th Rev. Nos. 162, 163 and 8th Rev. No. 162.

***Projection based on average annual rate of increase over last 10 years.

SOURCE: National Cancer Institute (25), National Center for Health Statis-
ties (27).

rettes smoked, the “tar” and nicotine level of the cigarette smoked
and the degree of inhalation, and is inversely related to the age
at which the individual began smoking, being higher for those
who begin smoking at younger ages. The risk of developing

110
cancer is diminished significantly by quitting smoking and is
lessened somewhat by switching to low-tar, low-nicotine filter-
tip cigarettes (43,45). Considerable evidence has also shown that
cigarette smoking is a significant cause—for women and
men—of cancer of the larynx, oral cavity, esophagus, urinary ,
bladder, kidney, and pancreas. Much of this information has
been summarized in previous issues of “The Health Conse-
quences of Smoking” or the Surgeon General’s Reports (33-48).

Table 1 lists the new cases and deaths estimated to occur in
1980 for those cancers which are causally associated with
cigarette smoking (1). Smoking will contribute to 43 percent of
the male and 18 percent of the female newly diagnosed cancer
cases in the United States in 1980 and to 51 percent of the male
and 26 percent of the female cancer deaths. This table does not
imply that cigarette smoking causes each of these individual
cancers. It does, however, identify the impact of cigarette smok-
ing on the major cancers now known to be associated with
cigarette smoking. Most of the cases of cancer of the lung and
larynx could have been prevented, as could a substantial pro-
portion of the cancer deaths at the other sites listed.

In this chapter, selected data on cancer and smoking among
women will be reviewed and summarized. Where necessary for
clarity, data previously reported will be summarized briefly.

Lung

The lung is a complex organ lined by at least five types of
epithelial cells, each of which theoretically might give rise to
one or more types of neoplasm. In addition to the epithelial cells,
blood vessels and connective tissue are prominent in the lungs.
Both visceral and parietal portions of the lung are covered by
synovial membranes, which also are subject to neoplastic trans-
formation. The World Health Organization’s classification of
malignant tumors (Table 2) includes multiple histologic types, of
which epidermoid, small cell, adenocarcinoma, and large cell
carcinoma are causally related to cigarette smoking and display
significant dose-response relationships in epidemiologic studies
(7,43). These four tumors are the most common histologic types
of lung cancer in both men and women. However, there are
differences in the distribution of the different types of lung
cancer in men and women and in smokers and nonsmokers.
Epidermoid carcinoma was the most common histologic type of
lung cancer in the male smoker, while adenocarcinoma was
most common in the female smoker and in nonsmokers of both
sexes in a series recently published from the Mayo Clinic (Table
3) (31).

111
ert

TABLE 1.—Estimated new cancer cases and deaths for sites associated with cigarette smoking, 1980

 

 

 

 

Estimated New Cases Estimated Deaths
Site Total Male Female Total Male Female
All Sites 785,000* 387,000* 398,000* 405,000 219,500 185,500
Lung 117,000 85,000 32,000 101,300 74,800 26,500
Pancreas 24,000 12,500 11,500 20,900 11,100 9,800
Urinary
Bladder 35,500 26,000 9,500 10,300 7,000 3,300
Oral 25,500 17,900 7,600 8,800 6,100 2,700
Kidney &
Other
Urinary 16,900 10,500 6,400 7,900 4,800 3,100
Esophagus 8,800 6,200 2,600 7,600 5,500 2,100
Larynx 10,700 9,000 1,700 3,500 2,900 600
All Tobacco
Related 238,400 167,100 71,300 160,300 112,200 48,100

 

*Carcinoma in situ is not included. There are 45,000 new cases of uterine cervical carcinoma in situ each year. Non-melanoma skin
cancer is not included. Approximately 400,000 new cases of non-melanoma skin cancer occur annually.
SOURCE: American Cancer Society (1).
TABLE 2.— World Health Organization classification of
malignant pleuro-pulmonary neoplasms

 

I. Epidermoid Carcinomas
Il. Small Cell Anaplastic Carcinomas
Ill. Adenocarcinomas
1. Bronchogenic

a. acinar

b. papillary with or without mucin formation
IV. Large Cell Carcinomas
V. Combined Epidermoid and Adenocarcinomas
VI. Carcinoid Tumors

VII. Bronchial Gland Tumors
1. Cylindromas
2. Mucoepidermoid tumors
VIII. Papillary Tumors of the Surface Epithelium
IX. Mixed Tumors and Carinosarcomas
X. Sarcomas
XI. Unclassified
XII. Melanoma
XIII. Mesotheliomas

SOURCE: Kreyberg, L. (22).

TABLE 3.—Histologic types of pulmonary cancers in smokers
and nonsmokers

 

 

 

 

Male Female
Non- Non-
Type Total Smokers Smokers Smokers Smokers
Epidermoid 992 892 7 80 13
Small Cell 640 533 4 100 3
Adenocarcinoma 760 492 39 128 101
Large Cell 466 389 16 46 15
Bronchioloalveolar 68 35 4 13 16
TOTAL 2,926 2,341 70 367 148

 

SOURCE: Resenow, E.C. (31).

Other centers have similar data, although the proportions by
histologic type may vary with the pathologic criteria used, pa-
tient population, geographic location, and other factors.

Earlier epidemiologic studies suggested that cigarette smok-
ers were more likely to develop squamous-cell and small-cell
lung carcinoma than other types. However, more recent inves-
tigations indicate that all four major histologic types of lung
ecancer—including adenocarcinoma, which appears to be in-
creasing rapidly in recent years—are related to cigarette smok-
ing in both men and women (48).

113
In 1980, of the estimated 117,000 newly diagnosed cancers of
the lung in the United States, 32,000 will be among women.
There will be an estimated 25,500 deaths from lung cancer in
women (1).

In 1950, women accounted for approximately 1 in 12 of all lung
cancer deaths. By 1968 the proportion was 1 in 6; in 1979 women
dying of lung cancer will represent over one-quarter of all lung
cancer victims. White women have death rates from lung cancer
which are similar to those of nonwhite women, while the rates of
white males remain below those of nonwhite males. These dif-
ferences may be due to differences in the smoking habits of
blacks and whites described elsewhere in this report.

Many prospective studies have found that the lung cancer
death rate for smokers was far in excess of the rates for
nonsmokers in both sexes; as previously mentioned, the rates
for male smokers dramatically exceeded the rates for female
smokers. However, even the nonsmoking male had a higher in-
cidence of, and death rate from, lung cancer than the nonsmok-
ing female (9). This evidence suggested that women might have
a decreased susceptibility to lung cancer. A more careful
examination of the data indicates that most of the differences
between male and female lung cancer rates can be explained by
differences in smoking habits and occupational exposures.

As discussed in other sections of this report, a smaller per-
centage of women than men smoke and, when they do smoke,
they are more likely to adopt smoking behaviors that have been
shown to have a lower risk of developing lung cancer. That is,
they smoke fewer cigarettes per day, inhale less, start smoking
later in life, and are more likely to smoke low-tar and low-
nicotine and filter cigarettes. In addition, it is important to con-
sider the cohort effects on the differences in rates between
males and females. Over 85 percent of those who smoke regu-
larly began between the ages of 12 and 25 (29). Men first began
to smoke in large numbers just before and during the First
World War. As each succeeding birth cohort passed through the
age of initiation (12 to 25), a larger percentage began smoking
until the groups born between 1915 and 1930 were reached (17).
In the birth cohorts born after 1930, fewer began to smoke regu-
larly. The risk of developing lung cancer increases exponen-
tially with age and duration of smoking, with the increase start-
ing 15 to 20 years after the beginning of regular smoking. This
accounts for the dramatic rise in the male lung cancer death
rates noted in the 1930s. As those birth cohorts with. higher
smoking rates replaced those with lower smoking rates, the
age-specific lung cancer rates rose steadily; and as each of the
heavy-smoking birth cohorts grew older, their lung cancer risk

114
continued to accelerate, resulting in a very steep rise in the
overall male lung cancer death rate. The overall cancer rates
among men will continue to rise (albeit more slowly) as those
birth cohorts with the heaviest smoking prevalence replace
those with lower prevalence in the older age groups where the
lung cancer death rates are the highest. As these birth cohorts
with high smoking prevalence pass through the age groups and
are replaced by birth cohorts with lower smoking prevalence,
declines in lung cancer rates should be noted.

They should be noted first in the age-specific death rates for
the younger age groups and later in the overall lung cancer
death rates. The first indications of this change have been noted
with a decline in the age-specific death rates in males born after
1930. It is therefore important to consider this cohort effect
when examining the differences between lung cancer rates of
men and women.

Women began to take up smoking in large numbers 20 to 30
years later than men (in the early 1940s). This rise in smoking
prevalence was produced by predominantly young women first
using tobacco as cigarettes. This is in contrast to the rise in men
which included a substantial percentage of men of all ages who
switched from other forms of tobacco use to cigarettes. The rise
in lung cancer rates in women occurred as those cohorts with
high smoking prevalence reached the ages where lung cancer
occurs with significant frequency (age 45 and over). Since most of
these women began smoking cigarettes prior to age 25 they
would have at least 20 years of exposure by age 45 in contrast to
the shorter durations of exposure at age 45 for those men who
switched to cigarettes from other forms of tobacco around the
time cigarettes first came into widespread use. This greater du-
ration of exposure at any given age for women in these first
heavy smoking birth cohorts compared to the first cohorts in
men, should result in a more abrupt rise in lung cancer rates in
women. This rapid rise in female lung cancer death rates began
to be observed in the late 1950s. As birth cohorts with higher
smoking prevalence continued to replace those with lower smok-
ing prevalence, the rates rose steeply, reproducing the
phenomenon noted in males 20 to 30 years earlier with some
indication that the rise is even steeper for women. If one sub-
tracts 25 years from the female cancer death rates in Figure 1,
the rates for women are only slightly below the rates for men.
This small difference is explained by lower prevalence of smok-
ing and less hazardous smoking patterns of women and their less
frequent exposure to occupational carcinogens. Thus, close
scrutiny of the trends reveals no substantial protective effect for
women on the risk of developing lung cancer but rather leads toa

115
TABLE 4.— Age-adjusted lung cancer mortality ratios—age
began smoking and degree of inhalation

 

 

 

 

Age Began Smoking Male Female
15 . 16.8 2.5
15-19 14.7 5.0
20-24 10.1 3.4
25+ 4,1 2.3
Depth of Inhalation Male Female
None 8.0 2.0
Slight 8.9 2.3
Moderate 13.1 3.5
Heavy 17.0 TA

 

SOURCE: Hammond, E.C. (11).

TABLE 5.— Age-adjusted relative risks of lung cancer by number
of cigarettes smoked

 

Number of Cigarettes
Smoked Daily

1-9 10-19 20-39 40+

 

 

 

 

ACS Study Male 4.6 8.6 14.7 18.8
Female 1.3 2.4 4.9 9.5
1-14 15-24 25+
British Male 7.8 12.7 25.1
Physicians Female 1.3 6.4 29.7

 

SOURCE: Doll, R. (6,8), Hammond, E.C. (11).

sobering projection of a reproduction of the male lung cancer
epidemic in women (Figure 1).

GEOGRAPHIC DIFFERENCES

Lung cancer death rates, including all histologic types, are
highest in industrialized countries where there has been a
higher smoking prevalence for a longer time. Women in Scotland
have one of the highest death rates from lung cancer of women of
any country. Their tobacco consumption per smoker approaches
that of English and Welsh men (19). Current tobacco consump-
tion by Scottish women is only a little lower than the consump-
tion of Scottish men 20 years ago. In England and Scotland,
where the upper socioeconomic classes have reduced their

116
TABLE 6.—Lung cancer mortality ratios for females by duration
of smoking: Swedish study

 

 

Duration of Smoking Mortality
in Years Ratios
Nonsmokers 1.0
1-29 years 1.6
30+ years 9.6

 

SOURCE: Cederlof, R. (4).

cigarette consumption in recent decades, there is a significantly
greater lung cancer mortality rate in the lower socioeconomic
classes among women (19).

Age-adjusted death rates for lung cancer in women in select
countries indicate that women in Hong Kong have the highest
rates, while those in Scotland are second and those in England
and Wales are third. The United States ranked sixth world
wide (1).

Among nonsmokers, lung cancer is found slightly more often in
urban than in rural areas; however, the marked increase in lung
cancer among smokers in urban areas suggests that urban living
exerts a potentiating rather than an additive effect on the inci-
dence of lung cancer. Urban living has little independent effect
on lung cancer induction in comparison with even modest smok-
ing of filtered low-tar and low-nicotine cigarettes (5,10).

SMOKING PATTERNS AMONG WOMEN

Although women tend to have different patterns of smoking
than men, the relative relationships between smoking and lung
cancer are the same. Lung cancer rates for women who smoke
increase with increased dosage as measured by several dosage
measures, including number of cigarettes smoked per day, dura-
tion of smoking habit, degree of inhalation, age of initiation of
smoking, and the “tar” and nicotine level of the cigarettes
smoked. These data, obtained from several prospective investi-
gations, are examined in Tables 4, 5, 6, 7, 9, and 10. The more
cigarettes an individual smokes, the more likely that individual
will die of lung cancer (Table 5). Overall, female cigarette smok-
ers have 2.5 to 5.0 times greater likelihood of dying from lung
cancer than nonsmokers (Table 7). As discussed earlier, when the
full impact of the cohort effect is felt, this ratio will probably
approach that for men (8 to 12).

Doll, et al. studied the cause-specific mortality experience
among approximately 6,200 female physicians in England during

117
TABLE 7.— Lung cancer mortality prospective studies

 

Age Adjusted Lung Cancer Death—Relative Risks

 

 

Cigarette

Nonsmokers Smokers
ACS Male 1.0 10.1
Female 1.0 2.6
British Male 1.0 14.0
Physicians Female 1.0 5.0
Swedish Study Male 1.0 8.2
Female 1.0 4.5

 

SOURCE: Cederlof, R. (4), Doll, R. (6,8), Hammond, E.C. (11).

the period 1951 to 1973 (6). The results of this study are presented
in detail in Table 8, which also includes data from a previous
report on male physicians (8).

It is apparent that smoking and lung cancer are similarly
related in men and women. In both sexes, lung cancer mortality
was at least three times as high in ever-smokers as in never-
smokers, at least twice as high in current heavy smokers (more
than 25 cigarettes) as in light smokers (less than 15 cigarettes),
and exhibited a significant dose-response relationship. The
magnitude of the smoking effect on lung cancer for females and
males was approximately the same. The relative risks for mortal-
ity from lung cancer for moderate (15 to 24 cigarettes per day)
and heavy (more than 25 cigarettes) smokers were 6.3 and 29.7
among females, and 10.6 and 22.4 for males.

The authors emphasize, however, that no conclusions can be
drawn from this data about the magnitude of the biologic effects
of smoking in men compared to women. Since the authors doc-
umented differences in lifetime smoke exposure (later age at
initiation and lower prevalence of inhalation among females),
lifetime smoking exposures between the sexes were not directly
comparable. This issue will be resolved only when studies
examine the effect of smoking in cohorts of women whose
lifetime smoking behavior more closely matches that of the men
to whom they are compared.

A number of retrospective studies have examined the rela-
tionship of smoking and lung cancer in women. The 1971 Health
Consequences of Smoking reviewed many of these investiga-
tions and showed a smoker-to-nonsmoker risk ratio ranging
from 0.2 to 6.8 for females. The reader is referred to this volume
for a more detailed discussion of these studies. Results of these
investigations reveal sex differentials similar to those found in

118
TABLE 8.—Death rates from lung cancer and smoking habit when last as

ked, British physicians 1951-1973

Annual Death Rate per 100,000
x2

Persons Standardized for Age
oT

Current Smokers— Dose Per Day Nonsmokers Trend

Total ee ee vs. (Dose/
Popul. # Deaths Nonsmokers Ex-Smokers 1-14 15-25 25+ Others Response)

 

 

 

 

 

 

Women 6,194 27 7 23 9 45 208 13.47* 61.59*
(cigarettes only)
Men 34,440 441 10 43 52 106 224 41.9* 197.04"
(any tobacco/grams)
(1 gram = 1 cigarette)
*(P<.001)

SOURCE: Doll, R. (6,8).

61T
TABLE 9.— Age-adjusted lung cancer mortality ratios* for males
and females, by tar and nicotine (T/N) in cigarettes

 

 

smoked
Males Females
High T/N 1.00 1.00
Medium T/N 0.95 0.79
Low T/N 0.81 0.60

 

*The mortality ratio for the category with highest risk was made 1.00 so that
the relative reductions in risk with the use of lower T/N cigarettes could be
visualized.

SOURCE: Hammond, E.C. (11).

the larger prospective studies, with males having higher overall
lung cancer rates compared to females. However, the lung
cancer rates of smokers are significantly higher than those of
nonsmokers for both sexes.

The women who smoke low-“tar”, low-nicotine cigarettes have
a lower age-adjusted lung cancer mortality rate than women
who smoke high-“tar”, high-nicotine cigarettes. Women who
smoke medium-“tar”, medium-nicotine cigarettes have mortal-
ity rates in between (12) (Table 9). However, even the low-“tar”
and low-nicotine cigarette smoker has a rate substantially
higher than the nonsmoker.

These data suggest some benefit from smoking low-“tar”,
low-nicotine cigarettes. However, a further comparison of
women who smoked less than one pack of high-‘‘tar”, high-
nicotine cigarettes daily with women who smoked more than
one pack of low-‘tar”’, low-nicotine cigarettes daily revealed
that the smoker of more than a pack a day of low-“tar’’, low-
nicotine cigarettes had over twice the age-adjusted lung cancer
mortality rate of the woman who smoked fewer cigarettes, but
with high “tar” and nicotine (Table 10).

In a retrospective study standardized for duration of smok-
ing, number of cigarettes smoked, inhalation and butt length,
long-term female smokers of filter cigarettes had a lower rela-
tive risk of developing cancer than smokers of non-filter
cigarettes (46).

CESSATION OF SMOKING

Although the risk of developing lung cancer increases with
age, both for smokers and nonsmokers alike, women in good
health who quit smoking will, over a period of years, experience
a reduction in their relative risk of developing lung cancer.
About 15 years after they have quit smoking, the risk of devel-
oping lung cancer approximates that of the nonsmoker.

120

 
TABLE 10.—Age-adjusted lung cancer mortality ratios* for
males and females, comparing those who smoked a
few high tar and nicotine (T/N) cigarettes with those
who smoked many low T/N cigarettes

 

 

1-19 high T/N . 20-39 low T/N

cigarettes/day cigarettes/day
Males 1.00 | 1.6
Females 1.00 ; 2.1

 

*The mortality ratio for the category with lowest risk was made 1.00 so the
increase in risk with smoking more cigarettes/day could be illustrated.
SOURCE: Hammond, E.C. (11).

EXPERIMENTAL CARCINOGENESIS

Tobacco tars, tobacco smoke, and single or mixtures of chemi-
cals found in tobacco smoke have been used with various species
of animals in carcinogenesis experiments involving skin paint-
ing, subcutaneous injections, tracheobronchial implantation,
-and/or instillation and inhalation. Some experiments have re-
ported sex differences in the occurrence of lung tumors follow- .
ing exposure to chromium oxide (26).

However, in a recent monograph on lung cancer, separate re-
views on tobacco carcinogenesis, radiation carcinogenesis in the
respiratory tract, and experimental models for studies of respi-
ratory tract carcinogenesis did not yield information suggesting
that the male lung of any of the species studied was more sus-
ceptible than the female lung to carcinogenic action by either
tobacco products or radiation (16). The reader is referred to pre-
vious Smoking and Health Reports for summaries of experi-
mental tobacco carcinogenesis studies. ,

Larynx

The larynx is a small, complex structure, which produces
speech, controls the flow of air in and out of the lungs, and
prevents aspiration during swallowing. In 1980 there will be an
estimated 1,700 new cases of laryngeal cancer and 600 deaths
from that tumor in U.S. women (Table 1). Laryngeal cancer has
occurred predominantly in men, but more and more women are
developing laryngeal cancer as their smoking and drinking
habits come to approximate those of men. The male-to-female
ratio for laryngeal cancer exceeds that of lung cancer.
Laryngeal cancer occurs in the fifth, sixth, and seventh decades
both in men and women. While the disease is uncommon, its
incidence has continued to rise over the past quarter century,

121
especially in women, substantially because of changes in their
smoking habits.

Cancer can occur either in the glottis (true cord, 70 percent of
cases), or in the subglottic or supraglottic region (false cord, 25
percent of cases). Usually the neoplasm is epidermoid car-
cinoma when examined histologically. Since a tumor that inter.
feres with speech gives rise to early symptoms, glottic cancers
are usually diagnosed at an early stage and are curable in over
60 percent of the cases. When the tumor arises in the subglottic
or supraglottic region, interference with phonation or speech
may not occur as early as when neoplasm begins on the glottis,
The tumor may, therefore, reach a greater size and be accom-
panied by significant local tissue invasion and destruction as
well as metastasis. Patients with tumors discovered when they
are still localized in the larynx have approximately an 80 per-
cent cure rate, while advanced lesions have a 33 percent 5-year
survival rate.

Laryngeal cancer displays a strong dose-response relation-
ship with smoking, increasing with the number of cigarettes
smoked per day, the “tar” and nicotine content of the cigarettes
smoked, the depth of inhalation and number of years cigarettes
were smoked. The risk of developing laryngeal cancer is in-
versely related to the age at which smoking began (43). A lower
risk for laryngeal cancer has been demonstrated in women who
used filtered cigarettes for 10 years or more compared to those
who smoked non-filtered cigarettes. Nonetheless, the risk re-
mained well in excess of that experienced by nonsmokers (45).

Excessive use of aleohol by nonsmokers also results in an in-
creased incidence of laryngeal cancer. Heavy drinkers of
alcohol—that is, greater than seven ounces of whiskey or its
equivalent per day— who also smoke cigarettes have a greater
risk of developing laryngeal cancer than if they either smoked
or drank to excess alone. There is a synergistic effect of smoking
and drinking on laryngeal cancer development (43,44).

When women quit smoking, their relative risk of developing
laryngeal cancer decreases until 10 years after cessation when
their risk approaches that of the nonsmoker (45).

A number of investigators have found an association between
exposure to asbestos and the subsequent development of
laryngeal carcinoma (438).

Oral

Oral neoplasms include cancer of the lip, tongue, gums, buccal
mucosa, hard and soft palate, salivary glands, floor of the
mouth, and oropharynx. In the United States for 1980, there

122
will be 17,900 new cases in men and 7,600 in women, resulting in
6,100 deaths in men and 2,700 deaths in women (1). While dif-
ferent histological types of cancer can occur in this group,
squamous cell carcinoma is by far the most common, except for
the tumors of the salivary glands. Five-year survival rates
range from 25 percent in those patients whose tumor is ad-
vanced when first diagnosed to 67 percent for those whose
tumor is localized at diagnosis.

In women, oral cancers account for 1.9 percent of all neoplasms,
while they account for 4.7 percent of all cancer occurring in men.
Deaths from the various oral cancers account for 1.4 percent of
cancer deaths in women and 2.8 percent of all cancer deaths in
men. Cigarette, pipe and/or cigar smoking are all associated with
increased oral cancers. Heavy alcohol use (over 7 ounces per day)
has been shown to be an independent causative factor (32,42).
When both are used together by women or men, synergism results
in an even greater incidence of oral cancer (3). Poor oral hygiene or
inadequate dentition is also a risk factor (15).

Most of the prospective epidemiologic studies have concen-
trated on men. In Japan a large prospective study showed the
mortality ratio for oral cancer to be 2.88 for the male cigarette
smoker and 1.22 for the female cigarette smoker compared with
the nonsmoker.

Leukoplakia or an abnormal thickening and keratinization of
the oral mucous membrane is recognized as a precancerous
condition. While found in the western world, it is most common
in Asian countries where a mixture of tobacco and betel nut or
lime ash chewing is common, and in those countries where re-
verse chutta (cigar) smoking occurs. Women in certain regions
of India are more likely to engage in reverse chutta smoking
than men, although both women and men develop carcinoma of
the hard palate after years of reverse chutta smoking (30).

Women and men with mouth, pharynx, and larynx cancer who
continue smoking after surgical treatment of the first neoplasm
have a 40 percent probability of developing another neoplasm of
the head and neck. Only 6 percent of the patients who quit
smoking develop a second cancer in the region. Less than 10
percent of oral cancer patients are nonusers of tobacco; almost
all have a well-differentiated carcinoma and a relatively high
cure rate (23).

Esophagus

Carcinoma of the esophagus will be diagnosed in 6,200 men
and 2,600 women in the United States in 1980 (1). The American
Cancer Society estimates that there will be 5,500 deaths in men

123
and 2,100 deaths in women from this disease (1). Median survi-
val time once esophageal carcinoma is diagnosed is 6 months,
The 5-year survival rate is only 3 percent. Esophageal car-
cinoma rates have declined in the white population over the
past 25 years. However, they have increased in the black popu-
lation in both sexes. This may reflect genetic or environmental
factors. In the Caspian littoral, there is a remarkable difference
in esophageal carcinoma incidence in people of comparable
background and socioeconomic status living only 400 kilometers
apart. There is a 30-fold higher incidence in women living in the
desert northwest section of Mazandran, Iran, compared with
the fertile Caspian rainbelt 400 kilometers to the west (20).

Data from a number of retrospective studies show that smok-
ing increases the risk of developing esophageal carcinoma.
Neither the relative risk of developing esophageal carcinoma
nor the steepness of the dose-response relationship with
cigarette smoking is as great as it is for carcinoma of the lung or
larynx (45). Individuals who stop smoking or switch to low-tar,
low-nicotine cigarettes will, after a lag period, experience lower
relative risks of developing esophageal carcinoma, although the
fall-off is not as steep as with lung and laryngeal cancer. In the
male, both retrospective and prospective studies show that pipe
and cigar smokers have mortality rates from esophageal car-
cinoma similar to cigarette smokers. There are no prospective
epidemiologic studies of female smokers in this country large
enough to permit development of a mortality ratio comparison
to nonsmoking females.

Ingestion of alcohol is also a major etiological factor in
esophageal carcinoma. A dose-response relationship exists,
with increasing alcohol ingestion resulting in an increased inci-
dence of esophageal carcinoma. As in the larynx, synergism of
the carcinogenic effect on the esophagus occurs with the use of
both tobacco and alcohol (45). Whether or not nutritional de-
ficiencies, which occur frequently with severe, chronic al-
coholism, play a role in carcinogenesis remains unknown, as
does the possible contribution of chronic iron deficiency found in
Plummer Vinson’s syndrome (Paterson-Kelly syndrome, sid-
eropenic dysphagia).

Ninety-eight percent of esophageal cancers are histologically
squamous cell in type. In an autopsy study, Auerbach found
more abnormalities of the esophageal tissues—including atypi-
cal nuclei, disintegrated nuclei, hyperplasia and hyperactive
esophageal glands—of tobacco smokers as compared with
nonsmokers (2).

Esophageal carcinoma can be produced experimentally by
both benz(a)pyrene and the nitrosamines. Both benz(a)pyrene

124
and a group of nitrosamines have been identified in tobacco
smoke. The appearance of experimentally-produced squamous
cell carcinomas can be accelerated by dissolving the carcinogen
in alcohol, a laboratory experiment duplicated daily by
thousands if not millions of our citizens (43).

Urinary Bladder

Cancer of the urinary bladder will occur in 26,000 men and
9,500 women in the United States during 1980 and it will kill
7,000 men and 3,300 women (1). Cancer of the urinary bladder is
frequently multicentric in origin. If found while still localized in
the bladder wall, the 5-year survival rate is 72 percent, in con-
trast to 14 percent for those patients whose disease had already
spread when the diagnosis was first established (1).

Bladder cancer has been associated with occupational expo-
sure to aniline dyes, leading to the study of aromatic amines as
potential carcinogens. 2-Naphthylamine, xenylamine, ben-
zidine, and 4-nitrobipheny] have all been implicated (43).

Numerous retrospective studies have shown a relationship
between smoking and urinary bladder carcinoma in both men
and women (17). The likelihood of either women or men develop-
ing bladder cancer increases with the number of cigarettes
smoked, the duration of smoking, and tar and nicotine content
of the cigarette smoked. Changing to low-tar, low-nicotine
cigarettes or more clearly, cessation of smoking, decreases the
relative risk of developing bladder cancer. The risk of an ex-
smoker developing urinary bladder cancer approaches that of
the nonsmoker years after cessation (46).

In prospective studies in Japan and Sweden, women who
smoke are 1.6 to 2.7 times as likely to develop bladder cancer as
nonsmokers (3,14). In an international study of successive birth
cohorts in the United States, United Kingdom, and Denmark,
Hoover and Cole found increasing rates of bladder cancer as-
sociated with increased cigarette smoking in men and women in
both suburban and rural areas and in all nationalities studied
(17). It has been estimated that 30 percent of urinary bladder
cancer in women can be attributed to cigarette smoking (48).

Kidney

Cancer of the kidney will occur in 10,500 men and 6,400 women
in the United States during 1980 (1). Some 4,800 men and 3,100
women will die of renal carcinoma (1). The 5-year survival rate
is between 40 and 50 percent (1). While the overall classification
of kidney carcinoma includes tumors of the renal pelvis and

125
ureter, the largest number of kidney carcinomas occur in the
renal parenchyma and are adenocarcinomas.

In retrospective studies, adenocarcinomas of the kidney are
found more frequently in smokers compared with non-smokers
in both men and women (43,44). In a large prospective study
among U.S. veterans, the kidney cancer mortality ratio in-
creased from 1.0 (the baseline for nonsmokers) to 1.34 for those
who smoked 10 to 19 cigarettes daily and to 2.75 for men who
smoked two packs or more each day (18). No large scale prospective
study of women and kidney cancer has been reported to date.

Pancreas

Carcinoma of the pancreas will occur in 12,500 men and 11,500
women in the United States during 1980, and 11,100 men and
9,800 women will die of pancreatic carcinoma (1). During the
past 25 years, there has been a steady increase in both the inci-
dence and mortality due to pancreatic cancer in both men and
women (1,21). Among the common human neoplasms, the rate of
increase of pancreatic cancer over the past quarter century has
been second only to that of the lung.

Most pancreatic carcinomas are adenocarcinomas, arising
from ductal cells (24). Most are relatively undifferentiated in
cell type. The median survival time from histologic proof of
diagnosis to death is 3.5 months in men and 4.5 months in
women. Survival time varies little with age at time of diagnosis,
duration of symptoms, location of primary lesion (head, body, or
tail of pancreas) or even degree of differentiation. The 5-year
survival rate is one percent, the most dismal survival rate for
any of the common neoplasms of either men or women (1).

Retrospective studies relating smoking to pancreatic car-
cinoma have been reviewed in previous reports. In a prospective
study of 143,000 women, the pancreatic cancer mortality ratio
was 1.94 for Japanese women smokers compared to nonsmokers
(14). In Sweden, a smaller prospective study showed that the.
mortality ratio for pancreatic cancer was 2.5 for women smokers
compared to women nonsmokers (4).

In the United States, the male to female ratio of pancreatic
cancer was 1.6 in the 1940s. It has. decreased to the current
estimate of 1.17 for 1979 and is consistent with the decreasing
male to female ratios of lung and laryngeal carcinomas.

Summary

1. Cigarette smoking is causally associated with cancer of the
lung, larynx, oral cavity, and esophagus in women as well as in
men; it is also associated with kidney cancer in women.

126
2. Cigarette smoking accounts for 18 percent of all newly diag-
nosed cancers and 25 percent of all cancer deaths in women. In
1980, 26,500 of the estimated 101,000 deaths, or over one-quarter of
the deaths expected from lung cancer, will occur in women.

3. Women cigarette smokers have been reported to have be-
tween 2.5 and 5 times greater likelihood of developing lung
cancer than nonsmoking women.

4, Among women the risk of developing lung cancer increases
with increasing number of cigarettes smoked per day, duration
of the smoking habit, depth of inhalation, and tar and nicotine
content of the cigarette smoked. The risk is inversely related to
the age at which smoking began.

5. A dose-response relationship has been demonstrated be-
tween cigarette smoking and cancer of the lung, larynx, oral
cavity, and urinary bladder in women.

6. The rise in lung cancer death rates is currently much
steeper in women than in men. It is projected that the age ad-
justed lung cancer death rate will surpass that of breast cancer
in the early 1980s.

7. The rapid increase in lung cancer rates in women is similar
to but steeper than the rise seen in men approximately 25 years
earlier. This probably reflects the fact that women first began
to smoke in large numbers 25-30 years after the increase in
cigarette smoking among men. Thus, neither men nor women
are protected from developing lung cancer caused by cigarette
smoking.

8. Cigarette smoking has been causally related to all four of
the major histologic types of lung cancer in both women and
men, including epidermoid, small cell, large cell and adenocar-
cinoma.

9. The use of filter cigarettes and cigarettes with lower levels
of “tar” and nicotine by women is correlated with a lower risk of
cancer of the lung and larynx compared to the use of high-“tar”
and nicotine or unfiltered cigarettes. The risk posed by smoking
low-“tar” cigarettes, however, is clearly greater than that
among females who never smoked.

10. After cessation of cigarette smoking, a woman’s risk of
developing lung and laryngeal cancer has been shown to drop
slowly, equalling that of nonsmokers after 10-15 years.

11. Excessive ingestion of alcohol acts synergistically with
cigarette smoking to increase the incidence of oral and
laryngeal cancer in women.

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131
VON-NEOPLASTIC
3RONCHOPULMONARY DISEASES.
NON-NEOPLASTIC BRONCHOPULMONARY DISEASES

Introduction

Chronic non-neoplastic bronchopulmonary disorders are a
major cause of death and disability in the United States.
Chronic obstructive lung diseases (COLD), including chronic
bronchitis and emphysema, comprise the majority of these
illnesses. In 1977, they were responsible for nearly 46,000 deaths
and millions of dollars in social security disability payments,
ranking second in economic cost only to heart disease (42).

Previous U.S. Public Health Service reports on the health
consequences of smoking have presented evidence that
cigarette smoking is the major cause of COLD (55-64). The
studies on which this is based have focused primarily on male
populations. This reflects the scientific interest generated by
the overwhelming male-to-female ratio in the prevalence of
COLD at the time these studies began. However, recent mortal-
ity statistics indicate a substantial increase in the death rate
from COLD among women (see Mortality section). Although
this increased death rate may partially reflect a greater aware-
ness and recognition of COLD, its magnitude suggests a true
increase in frequency of COLD among women. The following
text reviews a large number of studies analyzing the relation-
ship of smoking to COLD. These studies include appreciable
numbers of women, and many suggest that smoking may affect
men and women differently. Nevertheless, cigarette smoking
remains the most important cause of COLD regardless of sex or
other variables.

Definitions
The terms chronic bronchitis and emphysema have been used
diagnostically for many years. Physicians often use these terms
interchangeably to describe a patient with chronic airflow
obstruction. These conditions are, however, difficult to distin-
guish from each other in patients with chronic airflow obstruc-
tion because (a) both conditions may be present in the same
patient; (b) both disorders are characterized by expiratory flow
obstruction; and (c) patients with either disorder frequently
have the same symptom—dyspnea on exertion. Consequently,
the clinician often labels the patient with chronic airflow
obstruction as having chronic obstructive lung disease (COLD).
Many attempts have been made to establish criteria for the
diagnosis of chronic bronchitis and emphysema (1,27,28). The
most widely accepted definitions in the United States are those
135
TABLE 1.— Age-adjusted death rates from COLD (ICDA 490 - 492
and 519.3) 1960-1977 (per 100,000)

 

 

White Nonwhite
Male Female Male Female
1977 33.4 10.7 14.8 3.5
1976 33.5 10.1 14.9 3.2
1975 32.1 9.1 13.5 3.3
1974 31.1 8.4 13.7 2.8
1973 31.4 7.8 14.1 3.0
1972 29.9 7.0 14.0 2.9
1971 28.6 6.5 13.2 3.0
1970 28.2 6.0 13.3 2.6
1969 27.3 5.4 12.8 2.4
1968 22.3 3.8 13.7 2.5
1967 19.9 3.1 11.5 2.0
1966 19.7 3.0 11.0 1.9
1965 18.4 2.7 10.4 1.8
1964 16.1 2.4 9.2 1.6
1963 15.9 2.3 9.5 1.9
1962 13.1 2.0 7.9 1.8
1961 10.9 1.7 7.0 1.3
1960 10.4 1.7 6.7 1.4

 

SOURCE: National Center for Health Statistics (42).

of a joint committee of the American College of Chest Physi-
cians and the American Thoracic Society (1).

“Bronchitis: A non-neoplastic disorder of structure or func-
tion of the bronchi resulting from infectious or noninfectious
irritation. The term bronchitis should be modified by appropri-
ate words or phrases to indicate its etiology, its chronicity, the
presence of associated airways dysfunction or type of anatomic
change. The term chronic bronchitis, when unqualified, refers
to a condition associated with prolonged exposure to nonspecific
bronchial irritants and accompanied by mucous hypersecretion
and certain structural alterations in the bronchi. Anatomic
changes may include hypertrophy of the mucous-secreting ap-
paratus and epithelial-metaplasia, as well as more classic evi-
dence of inflammation. In epidemiologic studies, the presence of
cough or sputum production on most days for at least 3 months
of the year has sometimes been accepted as a criterion for diag-
nosis.”

“Pulmonary Emphysema: An abnormal enlargement of the
air spaces distal to the terminal nonrespiratory bronchiole, ac-
companied by destructive changes of the alveolar walls. The
term emphysema may be modified by words or phrases to indi-
cate its etiology, its anatomic subtype, or any associated airway
dysfunction.”

136
“Chronic Obstructive Lung Disease: This term refers to a dis-
ease of uncertain etiology characterized by persistent slowing
of airflow during forced expiration. It is recommended that a
more specific term, such as chronic obstructive bronchitis or
chronic obstructive emphysema, be used whenever possible.”

It should be noted that these definitions may have serious
inadequacies, particularly when applied to longitudinal studies
assessing the natural history of COLD (29,52). In the following

discussion, these limitations are recognized.

Smoking and Respiratory Mortality

Recent mortality statistics indicate a striking increase in
death rate from COLD among women (42). These data presented
in Table 1 indicate a nearly fivefold increase in reported mor-
talities due to COLD from 1962 to 1977 among white females and
a twofold increase among nonwhite females. Mortality rates
from these conditions for white and nonwhite males have also
increased since 1967 (by factors of 1.9 and 1.5, respectively), but
the rate of increase has not been as steep as that for women.

Seven large prospective studies have shown a greatly in-
creased mortality from COLD among smokers as compared to
nonsmokers (14,18,19,31,32,37). These studies, presented in
Table 2, represent over 13 million subject years of observation
and approximately 270,000 deaths from all causes. The number
of deaths related to COLD is probably underestimated since
some of the deaths attributed to pneumonia or myocardial dis-
ease may have been due to complications of COLD. In addition,
these mortality figures do not include an appreciable number of
individuals for whom COLD may have been a major contribut-
ory cause of death. For example, it is not uncommon for indi-
viduals to have COLD and lung cancer simultaneously.

Two of these prospective studies have included significant
numbers of women. Hammond prospectively followed 1,003,229
subjects aged 35 to 84 (31). Nearly 93 percent of the survivors
were observed for a 12-year period. Death rates from em-
physema among women were much higher in cigarette smokers
than nonsmokers. “Heavier” smokers (defined as either smok-
ers of 20 or more cigarettes a day regardless of age when smok-
ing was begun, or smokers of 10 or more cigarettes a day who
had begun smoking before age 25) had a sevenfold increased
mortality rate as compared to nonsmokers. Cederlof et al. fol-
lowed 55,000 Swedish subjects aged 10 to 69 for 10 years (14).
The overall mortality rate from all causes among female smok-
ers was 1.2 times higher than that of female nonsmokers. The
death rate from bronchitis, emphysema, and asthma among

137
BET

TABLE 2.—COLD mortality ratios + in seven prospective studies

 

 

Women in 25 Men in 25
Study British States States US. Canadian Men in California Swedish Subjects
(Reference) Doctors 45-65 45-64 65-79 Veterans Veterans 9 States Occupations Females Males
(18) (31) (31) (37) (8) (32) (19) (14)

Emphysema

and/or
bronchitis 24.7 _— _— —_ 10.08 _— 2.30 43 _— ~—
Emphysema

without
bronchitis _— 4.89 6.55 11.41 14.17 7.7 _ — — —
Bronchitis — — —_ — 4.49 11.3 _— — _ —
Bronchitis,
emphysema
and asthma — ~ — — _— _— _— _— 2.2 3.7*

 

* Death rate for smokers divided by death rate of a comparable group of nonsmokers.
*For all ages combined; increased mortality rate significant only for former smokers.
female smokers was 2.2 times that of female nonsmokers. How-
ever, the number of deaths due to COLD among women was
small in both of these studies; consequently, the relationship
with smoking is more difficult to evaluate. Nevertheless, a sig-
nificant excess risk for reported mortality from COLD was pres-
ent for female cigarette smokers as compared to female
nonsmokers.

Data collected by Doll et al. examine the association of smok-
ing and cause-specific mortality in 6,194 women physicians in
England, observed prospectively over the period 1951 to 1973
(17). Table 3 presents the results of this study, including previ-
ously published results of a similar study among male physi-
cians over the same period (18). The association of smoking and
chronic bronchitis clearly observed in males was confirmed in
women physicians. For both women and men who reported
smoking 15 or more cigarettes per day, the mortality rate due to
emphysema and chronic bronchitis was more than five times as
great as in nonsmokers. In both sexes, mortality due to em-
physema and chronic bronchitis was more than double that of
nonsmokers, was at least three times as high in ever-smokers as
in never-smokers, and was at least twice as high in current
heavy smokers (225 cigarettes) as in light smokers (<15
cigarettes).

The risk of death from emphysema and chronic bronchitis as-
sociated with smoking was approximately similar in men and
women. For moderate (1 to 14 cigarettes per day) and heavy
( =25 cigarettes per day) smokers, compared with nonsmokers,
the relative risk of death was 28.5 and 32 for women, respec-
tively, versus 16.7 and 29.3 for men. In this data, as well as that
for lung cancer, there is no support for the contention that
women are less susceptible to harmful effects of smoking than
are men. The authors emphasize that no conclusions can be
drawn from this data about the magnitude of the biologic effects
of smoking in men compared to women. Attempts to document
differences in lifetime smoke exposure (later age at initiation
and lower prevalence of inhalation among females)
demonstrate that lifetime smoking exposures between the
Sexes are not comparable. This issue will be resolved only when
studies examine the effect of smoking in cohorts of women
whose lifetime smoking behavior more closely matches that of
the men to whom they are compared.

In comparing the relative risks for mortality from COLD in
female and male smokers (Table 2), it is apparent that female
smokers have lower reported mortality rates than their male
counterparts. This difference in mortality rates may be due to
differences in female smoking patterns (31). Women tend to

139
OFT

TABLE 3.— Death rates from chronic bronchitis and emphysema by smoking habit when last asked, British
physicians 1951-1973

 

Annual Death Rate Per 100,000
Persons Standardized for Age

 

 

 

X2
Current Smokers— Dose Per Day Nonsmokers Trend
Total Non- Ex- vs. (Dose/
Popul. #Deaths Smokers Smokers 1-14 15-25 >25 All Others Response)
Women 6,194 13 2 10 21 57 64 12.34* 26.64*
(cigarettes only)
Men 34,440 254 3 44 38 50 88 25.58* 47.23*

(any tobaceo/grams)
(1 gram = 1 cigarette)
*(P >0.001)
SOURCE: Doll, R. (17,18).

 
smoke fewer cigarettes, inhale less deeply, and begin smoking
later in life than men. They more frequently smoke filtered and
low-tar and -nicotine cigarettes and have less occupational ex-
posure to lung irritants than men. Recent data suggest that
women are manifesting smoking patterns similar to those of
men. Moreover, more women are joining the labor force, includ-
ing occupations where exposure to lung irritants may occur.
(See section on Occupational Exposures.) Whether these women
will continue to have mortality rates different from those of
men remains to be determined.

In summary, recent statistics indicate a rise in the reported
death rate due to COLD among women. The two large prospec-
tive studies that included appreciable numbers of women found
significantly higher mortality rates due to COLD among women
smokers as compared to women nonsmokers. This relationship
was accentuated in heavier smokers. Mortality rates from
COLD among female smokers are considerably lower than
among male smokers. This may be due to different smoking pat-
terns and work exposure among men and women.

Smoking and the Epidemiology and Pathology of COLD

The prevalence of chronic bronchitis has been determined in
several populations in the United States and in other countries
(24,25,26,34,36,41,43,44,46,51). Table 4 lists several studies which
have included appreciable numbers of women. These studies
have documented a close relationship between cigarette smok-
ing and an increased prevalence of chronic bronchitis, and when
looked for, a dose-response relationship was also present (Table
3). The prevalence of chronic bronchitis in the United States
was determined in four cohort studies and ranged from 4 to 10
percent among women and 14 to 18 percent among men
(24,25,26,41,44,51). In both men and women a dose-response re-
lationship between the number of cigarettes smoked and the
prevalence of chronic bronchitis was apparent.

The observed differences between men and women noted in
these studies may be due in part to the smaller percentage of
women than men who were smokers in the population studied.
Moreover these women smoked fewer cigarettes than men.
When comparing current smokers, several studies of different
populations in the United States and in England did not find
significant differences in the prevalence of chronic bronchitis
between men and women (21,33,41).

The relationship between smoking and pathologic changes in
the lung have largely been obtained by necropsy studies. These
investigations are often skewed by physician and/or hospital

141
x TABLE 4.—Prevalence of chronic bronchitis by smoking classification (numbers in parentheses represent total
number of individuals in particular smoking group)

bo

 

S = Smokers.

NS = Nonsmokers

EX = Ex-Smokers

 

Author, Year

Number and Type

 

 

 

 

Country (Reference) of Population Men Women Comment
Higgins, 1958 94 men and 92 women NS woe eee eee ee 00 NS ................. 0.0
England (34) randomly chosen from Sve ceccccce cece cues 6.7 Soke cee aee .. 5.0
agricultural
communities
Oswald, 1955 . 8,602 males and 2,242 NS .......... 15.8 (474) NS .......... 12.1 (619) Chronic bronchitis
England (43) female clerical workers S ......... » 18.4 (1,940) S ............ 18.8 (579) defined by habitual
40-65 yrs. of age cough and sputum
production
Hubti, 1965 653 men and 823 women NS................ 5.7) NS ... cece cece ee 4.5 Ex-smokers represent
England (36) in a Finnish rural EX ....... cee eee 163 EX ............... 13.3 those who have stopped
community 40-60 yrs. S 1-14 ........... 88.0 S 1-14 ........... 10.4 for more than 1 month
of age 15-24 .... 41.4 15-24.......0..08.
2B Lecce cece eee 4.0 2B Lee e eee 57.0
Remington, 1969 41,729 men and 22,295 NS .......... 5.1 (9,055) NS......... 3.4 (12,351) Age-adjusted total
England (46) women participating in EX ......... 9.8 (6,510) EX ........... 3.9 (959) prevalence. Cigarette
mass miniature Cigarettes ..... (23,243) Cigarettes ...... (8,985) dosage gradient
radiography screening S 1-19............ 92 S 1-9............. 5.1 significant to P <0.001
10-19 ........... 15.0 10-19 ........... 10.6
ys | rn 20.6 >20 .... eee eee eee 18.5

 
§PT

 

 

 

Ferris, 1962 542 men and 625 women Overall Overall Age-specific rates
U.S.A. (23,25,26) residents of New NS .......... 13.8 (125) NS .......... 9.4 (378)
Hampshiretownchosen EX ........... 11.9(77) EX ........... 10.8 (37)
by random sampling of Cigarettes ... 40.3 (340) Cigarettes ... 19.8 (208)
census 1-10 ............. 29.8 1-10 ............. 13.1
11-20 ............. 34.2 11-20 ............. 22.2
21-30 ............. 42.3 21-80 ............... _—
31-40 ............. 61.1 31-40 ............. 27.3
Pal voce 0: a 9 _
Payne, 1964 5,140 adult residents of Overall ............. 8 Overall .............. 4 Prevalence rates
U.S.A. (44) Tecumseh, Mich. estimated from line
graph
Mueller, 1971 281 men and 328 women’ Overall ........ 17 (281) Overall ........ 10 (328)
U.S.A. (41) residents of Glenwood NS .......0.0008. 8(2) NS .............. 2 (3)
Springs, Colo. EX ......ccee eee 13(7) EX .............. 5 (1)
S 1-14.......... 11(3) S 1-14 .......... 14 (7)
15-24......... 20 (18) 15-24 ......... 25 (14)
>25 ..... eee 38 (21) >26 2... eee 33 (9)
Tager, 1976 227 men and 280 women Overall ...... 14.7 (227) Overall ...... 7.6 (285) Age-adjusted
U.S.A. (51) in East Boston, Mass. NS 2.0... eee ee eee 5.8 NS 2... eee eee 1.8 prevalence rate
age 15 or greater Sic cece eee e ee ees 24.2 S cle cee eee 17.6

 
interest and may not accurately represent a random popula-
tion. Moreover, observer variation occurs frequently, even
among “experts.” Data regarding smoking history are usually
derived from a hospital record or from close relatives and
friends; thus they may be unreliable.

Only a few of the studies examining the relationship of
cigarette smoking to the frequency and severity of pathological
changes have included significant numbers of female subjects.
Thurlbeck recently reviewed 30 reported surveys of the fre-
quency of emphysema at necropsy (53). Emphysema of some
degree was found in about 65 percent of men and 15 percent of
women. The emphysema found was also more severe in men
than in women.

The predominant pathological finding in chronic bronchitis is
the hypertrophied mucous gland in the submucosa of the large
cartilaginous bronchi. The ratio of bronchial gland thickness to
bronchial wall thickness (Reid index) is usually increased. In a
recent survey of 179 consecutive necropsies, Ryder et al. found
significantly greater bronchial mucous gland volume in smok-
ers compared to nonsmokers. There was no significant dif-
ference in mucous gland volume between male and female
smokers or male and female nonsmokers (48).

Mueller et al. examined the prevalence of chronic bronchitis
in one-fifth of the adult population of Glenwood Springs, Col-
orado (41). Among current smokers of varying smoking
categories (Table 4) there were no significant differences in the
prevalence of chronic bronchitis. Higgins and Cochran found no
significant difference in the prevalence of chronic bronchitis
between men and women smokers in 186 subjects randomly
chosen from an agricultural community (Table 4) (34). Similarly,
Oswald and Medvel found no significant difference in the preva-
lence of chronic bronchitis between men and women smokers in
5,844 clerical workers in England (Table 4) (43).

Auerbach et al. examined the relationship of smoking to em-
physema in whole-lung and microscopic sections at necropsy in
1,436 men and 388 women (4,5). Among the women, there were
97 current smokers, 16 of whom smoked two packs a day or
more. Data regarding smoking habits were obtained through
interviews with relatives. Female smokers had a significantly
higher rate of emphysema than female nonsmokers (Table 5).
Furthermore, the severity of the emphysema was dose-related
to the number of cigarettes smoked. The authors found similar
relationships in men.

Spain et al. examined consecutive whole-lung mounts from
necropsies of adult victims (49 women, 85 men) of sudden and
unexpected death (50). Smoking habits were ascertained by a
144
letter and questionnaire to the next of kin. The degree of em-
physema was graded from 0 to 100 by two observers independ-
ently and without prior knowledge of the source of the specimen
or any previous grading. There was aclose relationship between
cigarette smoking and the degree of emphysema in both men
and women. Furthermore, the data (Table 6) demonstrated a
dose-response effect between the number of cigarettes smoked
and the severity of pathological changes.

Thurlbeck et al. examined whole-lung sections in 1,742 ran-
dom necropsies in three different cities in different countries
with varying climates and environments (54). Using a standard
panel of grading pictures, pathologic changes in the lung were
graded from 0 to 100 by the three readers. In men and women
emphysema was more frequent and more severe in smokers
than nonsmokers; however, male smokers had higher average
emphysema scores and greater frequency of emphysema than
female smokers and nonsmokers. This difference between men
and women was also true when heavy smokers and ex-smokers
of both sexes were compared. The authors speculate that male-
female differences may exist because: (a) women are protected
by hormonal factors; (b) men may smoke more heavily than
women; (c) men may have different smoking patterns than
women, e.g., inhalation; and (d) men may be exposed to damag-
ing environmental factors at work.

TABLE 5.— Means of average degrees of findings* in nonsmokers
and current smokers standardized for age of total
study population, women

 

 

Subjects Who Current Cigarette
Never Smoked Smokers
Regularly <1 Pk. 1+Pk.

Number of subjects 252 33 64
Emphysema 0.05 1.37 1.70
Fibrosis 0.37 2.89 3.46
Thickening of arterioles 0.06 1.26 1.57
Thickening of arteries 0.01 0.40 0.64

 

*The pathologic findings recorded were: (1) degree of emphysema (four-point
scale ranging from zero for normal to four for advanced emphysema); (2)
degree of fibrosis (seven-point scale ranging from none to advanced diffuse
fibrosis); (3) degree of thickening of arterioles (four-point scale); (4) degree of
thickening of arteries (three-point scale); and (5) padlike attachments to
alveolar septa. Padlike attachment is a thickening of alveolar septa in focal
areas by fibroblasts, histocytes and collagen fibrils. This is recorded as
present or absent.

SOURCE: Auerbach, O. (4).

145
In summary, the prevalence of chronic bronchitis among
women in the United States has been reported to range from 4
to 10 percent. Women who smoke have a higher prevalence of
chronic bronchitis than those who do not smoke. Overall, how-
ever, chronic bronchitis is less common among women than men
in the United States. This may reflect the smaller proportion of
women who smoke, differences in their smoking behavior, and
less occupational exposure to lung irritants. When comparing
current smokers, several studies of different populations in the
United States and England did not find significant differences
in the prevalence of chronic bronchitis between men and
women. Pathological data suggest that female smokers have a
higher frequency of emphysema and bronchial mucous gland
hypertrophy than female nonsmokers. Furthermore, the sever-
ity of emphysema is dose-related to the number of cigarettes
smoked. Distinct female-male differences in the frequency and
extent of emphysema at autopsy have been reported, but it is
not clear whether these differences are due to intrinsic dif.
ferences in the way men and women respond to environmental
injury or to the differences in the degree of environmental in-
jury experienced by men and women.

Smoking and Respiratory Morbidity

A large number of recent studies have demonstrated a higher
frequency of respiratory symptoms, i.e., cough, sputum, wheez-
ing and dyspnea, in smokers as compared to nonsmokers. Many

TABLE 6.— Degree of emphysema* and cigarette smoking**

 

 

 

No. No. With Mean Age With

Cigarettes Over Mean Grade Grade 20 Grade 20
Per Day Age 30 of Emphysema Emphysema Emphysema
Men

0 30 8 (0-20) 3 (10%) 66
<21 14 11 (0-45) 5 (36%) 62
>20 41 14 (0-50) 16 (39%) 52
Women

0 21 2 (0-10) 0 —
<21 6 6 (0-20) 1 (17%) T0+
>20 22 8 (0-30) 5 (23%) 40

 

*x? test shows significance at the 1% level for the heavy smokers and
nonsmokers.

**Each whole lung paper mounted section was graded from 0 to 100 in
denominations of 5 up to grade 50 and then in denominations of 10 up to grade
100.

* One case.

SOURCE: Spain, D.M. (50).

146
of these studies have included appreciable numbers of women
(9,11,15,38,39,40,45,47,65). These investigations have examined
populations varying in age, geographic location, social class,
and exposure to air pollution.

Leibowitz and Burrows examined the quantitative relation-
ships between cigarette smoking and chronic productive cough
in a large randomized sample of the white non-Mexican Ameri-
can population of Tucson, Arizona (38). Their data (Table 7) con-
firm the close relationship between cigarette smoking and
chronic cough and/or chronic sputum production in men and
women. The effect of cigarette smoking was closely related to
the total pack-years smoked (Table 7). These data support the
male to female preponderance in prevalence of chronic bron-
chitis noted in several other epidemiologic surveys
(24,25,26,41,44,51). However, these data also indicate that males
and females with equivalent smoking histories have similar
rates of chronic cough and/or sputum production.

Woolf examined the frequency of respiratory symptoms in
women volunteers, aged 25 to 54, drawn from several large
commercial firms (Table 8) (65,66). The prevalence of cough and
sputum production was significantly greater in smokers than in
nonsmokers (p< 0.001). Heavier smokers complained of cough
and/or sputum production more frequently than nonsmokers or
ex-smokers. The prevalence of wheezing and exertional dysp-
nea increased progressively with the number of cigarettes
smoked. In addition, colds that “went to the chest” occurred
more frequently in moderate and heavy smokers than in
nonsmokers (p<0.005 and p<0.001, respectively). Woolf com-
pared his data with previously reported data among men (Table
9) and concluded that the relationship of cigarette smoking to
respiratory symptoms was similar among men and women.

Ferris resurveyed a 1967 sample of Berlin, New Hampshire,
residents in 1973 (22). As in 1967, the prevalence of cough and/or
sputum production in females and males was directly related to
the number of cigarettes smoked daily. When the group evalu-
ated in 1967 was examined by current inhaling and smoking
status (Figure 1), inhalers had a higher prevalence of symptoms
than noninhalers (22). Furthermore, the frequency of symptoms
was dose-related to the number of cigarettes smoked. Manfreda
et al. studied population samples in an urban and a rural com-
munity in Manitoba, Canada (39). Their data presented in Table
10 demonstrate a higher prevalence of cough, phlegm, and
wheezing among men and women who smoked than in
nonsmokers or ex-smokers. However, no significant differences
in the prevalence of symptoms were apparent in the two com-
munities.

147
PT

0 TABLE 7.— Comparison of prevalence of chronic cough* and/or chronic sputum production* in men and women,
by smoking habits*

 

(Number of Subjects) % With Symptoms

 

 

 

Never Smoked Ex-Smokers Presently 1-20/day Presently > 20/day

A. By age group Males Females Males Females Males Females Males Females

15-29 years (156) 7.2 (182) 8.2 (36) 8.8 (45) 17.7 (78) 25.7 (82) 20.8 (34) 41.2 (17) 41.1

30-44 years (43) 2.8 (82) 12.2 (45) 11.1 (41) 4.8 (48) 39.5 (40) 35.0 (40) 47.5 (30) 56.7

45-59 years (45) 11.1 (119) 10.9 (61) 21.3 (63) 20.6 (57) 43.8 (83) 36.2 (54) 61.1 (39) 51.3

60+ years (105) 18.1 (336) 14.6 (186) 36.0 (77) 20.8 (62) 51.6 (82) 34.1 (16) 81.3 (14) 57.1
B. By pack-years of smoking Present Smokers Ex-Smokers

Never smoked (350) 10.3 (719) 12,1 (350) 10.3 (719) 12.1

Smoked <6 pack-years (69) 29.0 (81) 21.0 (59) 5.3 (69) 15.9

6-20 pack-years (106) 35.8 (127) 33.1 (77) 14.8 (69) 15.9

21-40 pack-years (96) 47.9 (126) 40.5 (86) 34.9 (27) 18.5

40+ pack-years (113) 61.1 (53) 60.4 (106) 35.8 (30) 16.7

 

*Subjects with a history of childhood respiratory problems have been excluded from the analysis. Differences in rates by smoking
significant within each age-sex group (X? and z differences between proportions) and trend with smoking significant within age-sex
groups (X? trend). Trend of symptoms by pack-years significant for male present and ex-smokers and female present smokers (X?
trend). Never smokers always significantly different from present or ex-smokers (X2 and 2).

+Symptoms are those reported on a self-completion questionnaire and are derived from the National Heart and Lung Institute
modification of the British Medical Research Council respiratory questions. “Chronicity” of cough or sputum production refers to the
presence of the symptom “on most days for at least three months of the year.”

SOURCE: Leibowitz, M. (38).
6tTI

TABLE 8.—Prevalence of cough and sputum production in 500 women related to smoking habit

 

 

Nonsmokers Ex-smokers Light Smokers Moderate Smokers Heavy Smokers
No. % No. % No. % No. % No. %
a. Cough* 11 6.0 1 1.6 11 27.5 32 34.8 66 53.7
b. Sputum** 14 7.7 1 1.6 12 30.0 27 29.3 60 48.8
ec. Sputum volume
None 169 92.3 61 98.4 28 70.0 65 70.7 63 31.2
Morning blob 10 5.5 0 0.0 7 17.5 11 12.0 29 23.6
Tablespoonful 3 1.6 0 0.0 5 12.5 12 13.0 17 13.8
More than one
tablespoonful 1 0.5 0 0.0 0 0.0 4 4.4 12 9.8

 

*Includes women with cough with or without sputum.
**Includes women with sputum with or without cough.
SOURCE: Woolf, C.R. (65).
TABLE 9.—Prevalence of respiratory symptoms in men
compared with women*

 

 

 

 

Women
Men (Present
(Published Data) Investigation)
Cough Percent Percent
Nonsmokers 4 (46) 6
14-22 (47)
Light smokers 24 (48) 28
Moderate smokers 48-52 (48) 35
Heavy smokers 42 (46) 54
67-74 (47)
58-78 (48)
Sputum
Heavy smokers 42 (46) 49
Dyspnea
All smokers 21 (49) 27
Heavy smokers 33 (50) 33

 

*Numbers in parentheses are reference numbers.
SOURCE: Woolf, C.R. (65).

The relationship between smoking and several respiratory
symptoms was examined by Buist et al. in population samples of
three North American cities (11). Cough, sputum production,
and wheezing occurred more frequently among smokers than
nonsmokers regardless of sex.

Bewley and Bland examined the relationships between smok-
ing and the prevalence of respiratory symptoms in 14,033 chil-
dren aged 10 to 12% in two separate urban areas of the United .
Kingdom (9). In this questionnaire survey, 2.5 percent of the -
girls acknowledged smoking at least one cigarette per week
(“smoker”). Boys who smoked outnumbered girls who smoked
by 3:1 and were more frequent smokers of at least one cigarette
a day than were females by 11:1. Table 11 shows that, evenin -
this young age group, smokers have a higher frequency of morn-
ing cough, cough during the day and night, and cough for
3-months duration than their nonsmoking classmates.

In a questionnaire study of a large group of American high
school students in Rochester, New York, Rush found a strong
association between current smoking and respiratory
symptoms in both sexes (47). There were minor differences be-
tween sexes in the frequency of respiratory symptoms when

150
Males Females
70 +
(9 Non-iInhalers
60 + EES3 Inhalers
50 F
oO
oO
3
= 40 Fr
>
2
a
* 30F

 

 

 

 

 

 

 

      

1-14 35+

Cigarettes/Day

FIGURE 1.—Age-standardized rates (percent) of chronic
nonspecific respiratory disease* by inhaling and
current cigarette smoking

*Criteria for diagnosis were as follows:

(1) Chronic bronchitis: Affirmative response to the question— Do you bring
up phlegm from chest six or more times a day for four days a week for three
months a year for the past three years or more?

(2) Asthma: Affirmative response that bronchial asthma had been diagnosed
and was still present.

(3) Chronic obstructive lung disease: Affirmative response to one or more of
the following: wheezing or whistling in the chest occurred most days or nights;
the subject had to stop for breath when walking at his own pace on the level;
FEV: less than 60 per cent of the FVC.

These could occur in various combinations and were not mutually exclusive.

SOURCE: Ferris, B.G., Jr. (22).

smoking histories were comparable. Rawbone et al., in a ques-
tionnaire survey of 10,498 secondary school children aged 11 to
17 in London, found a significantly higher frequency of cough,

151
TABLE 10.— Respiratory symptoms and diseases in male (M) and
female (F) participants in Charleswood
(C)—urban— and in Portage La Prairie
(P)—rural—expressed as percent of respondents

 

Respiratory Nonsmokers Ex-Smokers Smokers
Symptom/Disease Cc P Cc P Cc P

 

Cough on most
days, at least 3

months/year
M 8.3 4.0 8.1 2.9 25.4 31.5
F — 4.0 _ 10.0 20.3 31.7

Phlegm on most
days, at least 3

months/year

M — 4.0 10.8 5.7 16.9 24.7
F — 4.0 _— 5.0 10.2 25.4
Wheezing apart

from colds

M 4.2 8.0 10.8 14.3 26.8 31.5
F 3.5 8.0 12.1 20.0 25.4 30.2

Attack of short-
ness of breath

and wheezing
M 4.2 8.0 13.5 11.4 11.3 17.8
F _— 12.0 6.1 15.0 13.5 20.6

Shortness of breath
compared to per-
sons of same sex

and age
M 8.3 4.0 5.4 5.8 5.6 12.3
F 7.0 12.0 6.1 5.0 22.1 17.5

 

SOURCE: Manfreda, J. (39).

colds, and exertional dyspnea in regular smokers as compared
to nonsmokers (45), There was no appreciable difference in the
frequency of cough between male and female smokers or be-
tween male and female nonsmokers. Colley et al. examined the
influence of smoking, lower respiratory tract illness under 2
years of age, social class of father, and air pollution on respira-
tory symptoms in a cohort of 20-year-olds followed since birth
(15). Their data (Table 12) suggest that respiratory symptoms
were closely related to current smoking. Symptoms were also
related to a history of lower respiratory tract infection in the
first 2 years of life but were not related to social class or air

pollution.
152
Sot

TABLE 11.—Smoking and the prevalence of respiratory symptoms in girls from two different cities in England

 

Prevalence of Symptom With Each Group

 

 

Experimental
Smoker* Smokert Nonsmoker

Symptom Residence N % N % N % Significance*
Cough in the morning Kent 10 31.3 51 9.8 73 6.9 P <0.001

Derbyshire 14 18.9 50 8.4 138 6.7 P <0.001
Cough day or night Kent 17 53.1 148 28.0 195 18.4 P <0.001

Derbyshire 35 47.3 176 29.5 458 22.1 P <0.001
Cough for 3 months of year Kent 5 15.6 43 8.2 55 5.2 P <0.01**

Derbyshire 10 13.5 32 5.4 82 4.0 P <0.001

 

+Smoker =a child who smoked at least one cigarette a week.

+Experimental smoker = a child who had smoked at sometime but less than one cigarette a week.

*Test for significant association of cough and smoking habit. Chi-square 2 x 3 table.
**Smokers and experimental smokers combined to give chi-square on a 2 x 2 table.

SOURCE: Bewley, B.R. (9).
cT

>

20-year-olds followed since birth

TABLE 12.—Prevalence (percent) of respiratory symptoms by sex and smoking habit in cohort of 3,898

 

 

 

Persistent
Winter Cough Day Cough 3 Winter Phlegm Day Phlegm 3 Cough and
Morning or Night Months in Morning or Night Months in Plegm
History of Cough in Winter Winter Phlegm in Winter Winter Q.1(e)
Cigarette Population Q.1(a)* Q.1(b)* Q.1(c)+ Q.2(a)* Q.2(b)* Q.2(c)* +2(c)t
Smoking M F M F M F M F M F M F M F M F
Never
smoked
cigarettes 802 1093 1.6 4.0 5.2 6.5 1.5 3.2 4.8 5.2 6.4 3.9 3.7 3.2 0.9 1.9
Ex-smokers
of cigarettes 101 57 3.0 18 TA 10.5 3.0 1.8 11.0 1.9 10.2 9.1 6.0 0.0 2.0 0.0
Present
smoker of
cigarettes 1009 678 13.0 13.2 13.9 16.0 8.1 ¥iR) 14.1 11.9 11.6 11.2 8.3 5.5 4.9 3.5
No data on
cigarette
smoking 92 48 8.7 11.8 9.1 18.8 4.5 0.0 0.0 6.7 48 0.0 4.8 0.0 4.8 0.0
All 2022 1876 7.7 74 9.8 10.2 5.0 4.7 9.9 1.6 9.3 6.7 6.2 3.9 3.0 2.4

 

+1, (a) Do you usually cough first thing in the morning in the winter?
(b) Do you usually cough during the day or at night in the winter?
If “Yes” to either question 1(a) or (b)
(c) Do you cough like this on most days for as much as three months each winter?
SCT

2. (a) Do you usually bring up any phlegm (spit from the chest) first thing in the morning in the winter?

(b) Do you usually bring up any phlegm (spit from the chest) during the day or at night in the winter?
If “Yes” to either question 2(a) or (b)

(c) Do you bring up phlegm (spit from the chest) on most days for as much as three months each winter?
SOURCE: Colley, J.R.T. (15).

TABLE 13.—Percentages of nonsmokers and smokers with abnormal test results in three North American
cities, using combined reference values“

 

 

Men Women
Nonsmokers Smokers Nonsmokers Smokers
AS i} Total AS NS} Total AS Ss Total AS Ss Total
(95)* (27) (122) (12) (115) (236) (145) (46) (191) (107) (98) (205)
Upper limit + 1.6 0.2 1.8 1.8 1.8 2.6 2.1 0.6 2.4 L7 1.7 2.4
Lower limit + 11.6 20.0 10.6 10.6 10.9 8.7 10.0 15.0 9.1 11.1 11.5 9.0
1. Abnormal test
FEV-FVC 6 11 q 5 7 6 4 20 8 7 25 16
CVIVC 2 q 3 13 17 15 6 11 7 23 26 25
CC/TLC 2 7 3 20 32 26 8 17 10 20 29 25
AN/L 1 qT 3 17 13 15 qT 24 11 27 37 32
RV/TLC 6 ll 7 9 9 9 8 9 8 11 13 12

 

*Reference values for nonsmokers derived from asymptomatic nonsmokers in the three cities.
**Numbers in parenthesis = number of subjects in each group.

*Upper and lower limits in the expected 5 percent abnormal results.

AS = asymptomatic; S = symptomatic

SOURCE: Buist, A.S. (11).
In a longitudinal study of elderly Edinburgh residents aged
61 to 90, Millne and Williamson found the prevalence of persist-
ent cough and sputum production was significantly greater in
smokers of both sexes than in their nonsmoking counterparts
(40). Male prevalence rates were three times higher than those
in females; however, no attempt was made to determine the
relationship of respiratory symptoms to life-time tobacco expo-
sure.

In summary, many recent studies demonstrate a higher fre-
quency of respiratory symptoms in women who smoke as com-
pared to women who do not smoke. This is true in surveys in-
cluding children, adolescents, young adults, working age, and
elderly women. The effect of cigarette smoking is related in
terms of both the number of cigarettes and years smoked. The
majority of studies indicate a greater prevalence of respiratory
symptoms among men who smoke than among women who
smoke; however, these differences often disappear when the
study is carefully controlled for smoking history.

Smoking and Pulmonary Function

The insensitivity of cough and sputum production in the adult
as a predictor of future development of COLD has been empha-
sized by Fletcher and Peto (29). Pulmonary function testing of-
fers an objective method for measuring the adverse effects of
smoking. However, current tests of pulmonary function display
a marked variability between individuals and may not detect
the development of COLD until irreversible damage of the lung
has occurred. Also, none of the presently used pulmonary func-
tion tests can predict which of those individuals with slightly
abnormal pulmonary function will progress to debilitating and
life-threatening emphysema and chronic bronchitis. Becklake
and Permutt have recently reviewed the objectives and prob-
lems of the tests of lung function commonly used for early de-
tection of COLD (7).

A large number of studies have established a higher fre-
quency of pulmonary functional abnormalities in smokers as
compared to nonsmokers. These studies have examined (a) the
relationship of smoking to abnormal tests of small airway func-
tion and (b) the relationship of smoking to measurements of
standard spirometry. The majority of epidemiologic surveys in-
vestigating the prevalence of functional abnormalities in smok-
ers have employed spirometric measurements, usually the
forced expiratory volume (FEV) and vital capacity (VC). Meas-
urements of airway resistance, diffusing capacity, lung volume,
and nitrogen mixing have been used much less frequently.

156
604 Males @ Portage ia Prairie
4 CJ Charleswood

iaodds

60 + Females

cm anile

RV%TLO = CV%VCE CC%TLC- Sipiil FEV,,%FVC

Percentage

 

Percentage
»
o
i

 

 

FIGURE 2.—Prevalence of lung function abnormalities among
smokers in an urban (Charleswood) and a rural
(Portage La Prairie) community
SOURCE: Manfreda, J. (39).

SMOKING AND “EARLY” FUNCTIONAL
ABNORMALITIES

The most widely used measurements for detecting early
change of chronic airflow obstruction are the single-breath ni-
trogen washout curve or a maximum forced expiratory volume
curve.

A limited number of recent studies using tests of small airway
function have included appreciable numbers of female subjects.
They have demonstrated a higher frequency of abnormalities in
tests of small airway function in smokers than in nonsmokers or
ex-smokers. A definite dose-response relationship has been
found in some of these studies but not in others (10,11,12). Table
13 shows the data from one of these studies (11). For all meas-
ures of small airway function, the frequency of abnormalities
was higher among smokers than nonsmokers in both men and
women. The frequency of abnormal measurements was consid-
erably higher in female smokers than in male smokers except
for closing capacity, in which equal proportions of male and

157
female smokers performed abnormally. However, the frequency
of abnormalities among female nonsmokers was also greater
than among male nonsmokers. The authors speculate that the
traditional view of chronic airflow obstruction as being predom-
inantly a disease of males may be accurate only when male
smokers outnumber female smokers and when males smoke
more cigarettes than females. They suggest that when women’s
smoking habits become comparable to those of men, the effect
on lung function may be similar.

Manfreda et al. used the single-breath nitrogen test in a large
group of subjects in two Canadian cities (Figure 2) (39). Almost
all smokers (85 percent) reported that they inhaled their
cigarettes. Smokers had a greater prevalence of abnormalities
than nonsmokers regardless of sex. The prevalence of abnormal
values in women who smoke was slightly less than in male
smokers.

In a volunteer population of 530 cigarette smokers attending
an emphysema screening center, Buist and Ross found an
equivalent frequency of abnormalities of the slope of phase III
among male and female smokers of less than 20 cigarettes per
day (Figure 3) with both sexes having significantly higher pre-
valence of abnormalities among smokers of more than 20
cigarettes per day (12). In the groups smoking more than 20
cigarettes a day, a greater proportion of females demonstrated
abnormalities than males. However, the age composition of
each group (male and female) was not identical.

A recent study of small airway function in 205 young volun-
teer smokers aged 18 to 25 has suggested that smoking may
exert its effects at different anatomic locations in the lungs of
men and women (21). All subjects smoked fairly heavily (more
than 20 cigarettes per day) for a short period of time (average:
2.4 pack-years). Male smokers showed frequent abnormalities in
tests of small airway function but female smokers did not ex-
hibit these abnormalities. Both male and female smokers
showed decreased forced expiratory flows at high lung volumes,
suggesting the presence of large-airway dysfunction in young
smokers. Male and female smokers differed significantly in
their response to He-O2z inhalation. Female smokers showed at
least as great an improvement in forced expiratory flows with
He-O, as did female nonsmokers. In contrast male smokers
showed a much smaller response to the He-O, at high lung vol-
umes. Thus, the predominant female response to habitual
cigarette smoking appears to have been involvement of the
large airways, but men who smoked appeared to have developed
abnormalities in small airway function. The reason(s) for the
differences in the data derived from this study and previously

158
Males | Females
n= 350 n=173

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

    

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

100%
100 -
80 + 74%"
60% t
60 be
% 45%
‘ 4 A2% qerega1%° peed
sok 38% mT
20+
0 scat =
137 74 173 77
<10 10-20 20-40

 

Cigarettes/Day

FIGURE 3.—Percentage of male and female cigarette smokers
with an abnormal change in nitrogen concentration
(ANz2) per liter according to their daily cigarette
consumption

*Indicates a significant difference between groups using 20 to 40 cigarettes
per day as the reference group (P <0.05).

*Indicates significant differences between males and females (P <0.05).
SOURCE: Buist, A.S. (12).

cited reports relating smoking to small airway dysfunction
(11,12,39) is unclear.

In summary, a limited number of recent studies have demon-
strated a higher frequency of abnormalities in tests of small
airway function in female smokers as compared to female
nonsmokers and ex-smokers. It is not clear whether these ab-
normalities are dose-related. Female smokers may have more
frequent abnormalities in the slope of phase III than male
Smokers. Male smokers may have more frequent abnormalities
In closing volume than female smokers. The meaning of these
differences is unclear. One study has suggested that the earliest

159
effects of smoking on lung function may occur in the large air.
ways in women and small airways in men.

SMOKING AND VENTILATORY FUNCTION

The majority of studies examining the relationship of smok.
ing to ventilatory capacity have used some measurement of
forced expiratory volume. Most of these studies have focused on
male populations and have found a close relationship between
cigarette smoking and the presence of abnormal pulmonary
function (2,6,16,20). Furthermore, the decrement in perform-
ance measured by simple spirometry is dose-related to the
numbers of cigarettes smoked (6,16,20). Relatively few studies
have included appreciable numbers of females.

Woolf examined pulmonary function in 500 women volunteers
(65). Smokers demonstrated significantly lower values for FVC,
FEV, FEF 25-75 percent, and specific conductance than
nonsmokers and ex-smokers who had not smoked for over a
year; this suggests that at least some abnormalities of pulmo-
nary function are reversible with smoking cessation.

Higgins and Keller examined the relationship of smoking to
seven derivatives of the forced vital capacity curve in 3,109
males and 3,256 females aged 10 and older (35). Nonsmokers
performed better than smokers in both sexes. Values consis-
tently decreased with increasing cigarette consumption. The
largest differences were in FEV and FEF 25-75 percent.

Seltzer et al. examined the relationship of smoking to FVC in
65,086 white, black, and Asian subjects aged 20 to 79 who had
attended a Kaiser-Permanente multiphasic health clinic (49).
The authors found a significant reduction in FVC among white
women who smoked as compared to nonsmoking white women.
No such differences were found for black and Asian subjects,
however. No explanation for this racial difference was apparent
from their data.

In a study by Buist et al., the prevalence of abnormalities of
FEVi/FVC was higher in female smokers than nonsmokers (11).
The frequency of abnormalities in FEV:/FVC among female
smokers was twice that of male smokers (Table 12). Gibson et al.
examined the relationship of smoking to measurements of the
forced vital capacity in 18,359 men and women in Australia (30).
Nonsmokers had better lung functions than smokers. Among
smokers of 10 or more cigarettes a day, men showed a greater
decrement in lung function than women.

Burrows et al. examined the relationship of smoking to
measurements of forced expiratory volume in 883 men and 1,166
women in Tucson, Arizona (13). Nonsmokers performed better

160
(34)

3.0
FvC

2.0 a a ae
(2)

w Nonsmoker
- a Heavy Smoker

 

 

1.0 4 i L 1 j
30 40 50 60 70 80

Age - Years

FIGURE 4.—Changes in forced vital capacity (FVC) by age in
various female cohorts

Results have been standardized to 155 cm and are body temperature and
pressure saturated (BTPS).

Numbers in parentheses are number in that cohort.

Heavy smokers are those who smoke 25 or more cigarettes per day.

SOURCE: Ferris, B.G., Jr. (23).

than ex-smokers or smokers, and ex-smokers performed better
than smokers in both sexes. Smokers of more than 20 cigarettes
per day performed worse than smokers of fewer than 20 cigar-
ettes per day. There were no significant differences in the re-
gression for FEV:/FVC on pack years in men and women,
suggesting that men and women with equivalent smoking
habits have similar decrements in FEV:/FVC.

The long-term effects of smoking on pulmonary function have
been scrutinized in two prospective studies. In the Framingham
study, 5,209 adults have been followed since 1948 with biennial
examinations including measurements of forced vital capacity
(3). Longitudinally, cigarette smokers showed a more rapid de-
cline in forced vital capacity than nonsmokers. Men and women
who continued to smoke had a more rapid decline in FVC than
those who had stopped. The rate of decline in pulmonary func-
tion was appreciably steeper in male smokers than female
smokers. The authors suggest that these differences could be
due to differences in smoking habits.

In a longitudinal study of residents of Berlin, New Hamp-
shire, Ferris examinéd the changes in pulmonary function by
smoking status in the various age cohorts (23). Among females,
heavy and moderate smokers had lower values for FVC and
FEV: as compared to nonsmokers, and the values fell more

161
3.0¢r

FEV,

2.0F (8)

 

a Nonsmoker

 

 

1.0F
LL a Heavy Smoker
I L i L l al
30 40 50 60 70 80

Age-Years

FIGURE 5.—Changes in forced expiratory volume in 1 second
(FEV, ,.) by age in various female cohorts

Results have been standardized to 155 cm and are body temperature and
pressure saturated (BTPS).

Numbers in parentheses are number in that cohort.

Heavy smokers are those who smoke 25 or more cigarettes per day.

SOURCE: Ferris, B.G., Jr. (23).

rapidly with age. These relationships for heavy smokers (25 or
more cigarettes a day) are presented in Figures 4 and 5.

In summary, women smokers perform worse on spirometric
testing than do female ex-smokers or nonsmokers. This rela-
tionship appears to be dose-related to the number of cigarettes
smoked. The differential effects of smoking on pulmonary func-
tion in males and females is unclear. One study demonstrated
that men and women with equivalent smoking habits have simi-
lar decrements in FEV:/FVC. The long-term effect of smoking
on pulmonary function has been evaluated in two studies which
included appreciable numbers of females. Longitudinally,
women who smoke show a more rapid decline in forced vital
capacity than women who do not smoke. Women who continue to
smoke have a more rapid decline in forced vital capacity than
those who stop; however, men who continue to smoke have an
even more rapid decline in pulmonary function than women
who continue to smoke. The long-term relationship between
respiratory symptoms and airflow obstruction in women is un-
known. One large prospective study could not find a relation-
ship between symptoms and the ultimate development of
chronic airflow obstruction in men (29).

162
Summary

1. Recent statistics indicate a rising death rate due to chronic
obstructive lung disease (COLD) among women. The data avail-
able demonstrate an excess risk of death from COLD among
smoking women over that of nonsmoking women. This excess
risk is much greater for heavy smokers than for light smokers.

2. Women’s total risk of COLD appears to be somewhat lower
than men’s, a difference which may be due to differences in
prior smoking habits.

3. The prevalence of chronic bronchitis varies directly with
cigarette smoking, increasing with the number of cigarettes
smoked per day.

4. There is conflicting evidence regarding differences in the
prevalence of chronic bronchitis in women and men. Several
recent studies suggest that there is no significant difference in
the prevalence of chronic bronchitis between male and female
smokers. This may be the result, however, of increasingly simi-
lar smoking behavior of women and men.

5. The presence of emphysema at autopsy exhibits a dose-
response relationship with cigarette smoking during life.

6. There is a close relationship between cigarette smoking
and chronic cough or chronic sputum production in women,
which increases with total pack-years smoked.

7. Women current smokers have poorer pulmonary function
by spirometric testing than do female ex-smokers or nonsmok-
ers, a relationship which is dose-related to the number of
cigarettes smoked.

References

(1) AMERICAN COLLEGE OF CHEST PHYSICIANS. AMERICAN
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167
INTERACTION BETWEEN SMOKING
AND OCCUPATIONAL EXPOSURES.
INTERACTION BETWEEN SMOKING AND OCCUPATIONAL
EXPOSURES

The 1979 Surgeon General’s Report on the health conse-
quences of smoking (18) examines the interaction of smoking
and occupational exposure. Ways in which smoking may inter-
act with the occupational environment are described and
examples of these interactions are discussed. Briefly, these
types of interaction are:

1. Tobacco products may serve as vectors by becoming con-
taminated with toxic agents found in the workplace, thus
facilitating entry of the agent by inhalation, ingestion, and/or
skin absorption of the agent.

2. Workplace chemicals may be transformed into more harm-
ful agents by smoking.

3. Certain toxic agents in tobacco products and/or smoke may
also inhabit the workplace, thus increasing exposure to the
agent.

4, Smoking may contribute to an effect comparable to that
which can result from exposure to toxic agents found in the
workplace, thus causing an additive biological effect.

5. Smoking may act synergistically with toxic agents found in
the workplace to cause a much more profound effect than that
anticipated simply from the separate influences of the agent
and smoking added together.

6. Smoking may contribute to accidents in the workplace.

Although few of the studies discussed in the 1979 Surgeon
General’s Report included enough women to adequately deter-
mine the health risks of smoking and the occupational environ-
ment, it is reasonable to hypothesize that women with the same
occupational exposure and smoking behavior as men would de-
velop health effects similar to those demonstrated in men. How-
ever, the interaction of smoking and the occupational environ-
ment and its effect on women differs in at least two ways:

First, smoking patterns among women are different from
those among men—women are less likely to smoke, and if they
do, they smoke fewer cigarettes per day, inhale less, and are
more likely to smoke lower “tar” and nicotine cigarettes
(7,14,18). Second, smoking and occupational exposure may ad-
versely affect the fetus or the health of the mother during preg-
nancy. Smoking and occupational exposure may also interact
with methods of contraception chosen by women.

This chapter reviews each of these reasons for a differential
health impact on men and women and examines two occupa-
tional exposures where interactions with smoking have been
clearly demonstrated for women workers.

171
TABLE 1.—Smoking habits of working women by title and

 

 

 

industry
Percent
of
Current Percent
Female
Labor Non- Ex-

Industry Foree* Smokers Smokers Present Smokers
<ilpack = 1 pack
perday per day

Professionals

Health 4.4 51.2 16.6 25.2 6.9
Teachers 6.8 63.5 14.0 19.8 2.7
Other 4.6 53.4 15.1 24.0 7.5

Managerial, incl.

office, rest.,

sales,

administrator 6.7 42.7 16.4 28.0 12.1
Sales 6.2 46.0 16.2 30.0 8.0
Clerical

Bookkeepers 4.6 53.1 12.2 26.5 8.2

Office machine

operators 1.3 52.8 15.7 23.1 8.4

Secretaries 13.3 52.0 14.7 26.3 7.0

All other 14.2 50.6 13.6 27.5 8.3

Crafts 2.4 46.4 13.1 31.8 8.6

Operatives 11.8 52.8 10.1 31.6 5.5

Service

Cleaning 2.5 51.9 12.8 81.2 4.1
Food 6.6 40.0 13.4 39.8 6.8
Health 6.9 52.1 10.5 32.2 5.2

Private Household

Workers 2.8 62.4 10.1 24.7 2.8

 

*Figures are subject to sampling errors and may therefore not agree with
those in other tables.
SOURCE: National Center for Health Statistics (6).

Smoking Patterns in Women

The male-female differences in smoking behavior and the
change in patterns of smoking behavior in women over time are
reviewed in other sections of this report. It is important, how-
ever, to consider the impact of these trends when evaluating the
interaction of smoking and the environment. Regular cigarette
smoking is a behavior that usually begins between the ages 12
and 25 (18). It is unusual to begin regular smoking after the age

172
TABLE 2.—Estimates of the percentage of current, regular
cigarette smokers, adults ages 20 years and over,
according to labor force status and occupation and
sex, U.S., 1976

 

Female Male
Total Total
20+ 20-44 45-64 20+ 20-44 45-64

 

Total 32.0 36.9 84.8 41.9 47.6 41.3
Currently employed 35.9 37.0 36.1 43.4 46.8 39.7
White collar total 34.3 33.8 36.9 36.6 38.6 35.3
Professional
technical
and kindred 29.1 28.6 32.7 30.0 31.1 29.9
Managers &
administrators
except farm 41.6 42.7 40.8 41.0 46.4 36.1
Sales workers 38.1 37.0 42.6 39.9 42.6 38.0
Clerical &
kindred workers 34.8 34.7 36.0 40.4 40.1 44.2
Blue collar total 39.0 43.7 33.6 50.4 54.1 44.3
Craftsmen &
kindred workers 40.5 46.9 35.6 48.0 52.1 41.6
Operatives and
kindred workers 37.6 42.5 31.2 52.3 55.3 46.2
Laborer, except
farm 56.3 52.6 * 53.7 56.9 51.7
Service 39.0 42.8 37.2 47.2 51.1 44.8
Farm 32.2 51.0 * 36.9 45.4 35.0
Unemployed 40.0 41.0 39.2 56.8 59.9 53.8
Usual activity —
homemaking 29.0 37.1 32.2 NA NA NA

 

NOTE: Unknown if ever smoked excluded from calculation.
*Figure does not meet standards of reliability or precision.
SOURCE: National Center for Health Statistics (6).

of 25 (7). In a cohort of individuals born in the same year, a
certain percentage of them will begin smoking by age 25. The
prevalence of smoking in any birth cohort after age 25 is pre-
dominantly determined by the rate at which people stop smok-
ing or die. The prevalence changes over time for each 10 year
birth cohort since 1910 for both men and women are presented

in the part of this report titled Patterns of Cigarette Smoking.
Women first began smoking cigarettes in large numbers im-
mediately before and during the Second World War (18). Thus,
the observed upswing in smoking among women occurred 25 to
30 years after that among men. The birth cohorts with the high-
173
TABLE 3.—Occupational distribution of men and women, 1978, by
percent of each sex employed in each category

 

 

 

 

Women Men
Professional, Technical 15.6 14.7
Sales 6.9 5.9
Clerical 34.6 6.2
Operatives & Transport 11.8 17.7
Service 20.7 8.7
All Other 2.5 11.7
Crafts 1.8 21.1
Managers 6.1 14.0
Total 100 100

 

SOURCE: Rones, F. (14).

est peak smoking prevalence were born from 1910 to 1980 (men)
and from 1920 to 1950 (women). As these cohorts with high pre-
valence of smoking grow older, they replace cohorts with lower
smoking prevalence. Since both occupational diseases and
smoking related illnesses increase separately with age, any in-
teraction between the two also could be expected to increase
with age. Men in the birth cohort from 1910 to 1930 are now in
the age range at which a high incidence of disease would be
expected, while those women born from 1920 to 1950 are just
beginning to enter the ages at which there is a high prevalence
of disease. As a result, the adverse effects of smoking and occu-
pational exposure would be expected to occur more frequently
in men, reflecting this difference in the age of the average male
and female smoker. This “cohort effect” might lead to the er-
roneous conclusion that women are protected from occupation-
smoking interactions, just as it has been used to suggest that
women are protected from the lung cancers induced by
cigarette smoking.

A second difference between male and female smoking habits
which must be considered is the prevalence of smoking by occu-
pation. Table 1 shows that the prevalence of smoking is rea-
sonably uniform among women employed in many different oc-
cupations (the exceptions are education and household area
workers with low prevalence and food area workers with high
prevalence). There is not the marked difference in smoking
habits between female blue collar and white collar workers that
has been observed in men (18) (Table 2). A slightly lower preva-
lence of smoking among professional women compared to other
white collar workers occurs similar to that seen in men (7).

The section on behavior in this report discusses the smoking
habits of several groups of health professionals. It shows that

174
women physicians and psychologists smoke more heavily than
their male counterparts. Thus, the relative levels of smoking
observed in the two sexes are reversed for these two occupa-
tional groups in comparison to the general population (14).
Nurses also have been shown to have a much higher prevalence
of smoking than women of the same age in the general popula-
tion (18). A final notable difference is that, among women, smok-
ing prevalence does not show the same marked inverse correla-
tion with socioeconomic status (7). The reasons for these dif-
ferences are beyond the scope of this section. However, an un-
derstanding of them forms part of the background for any dis-
cussion of the interaction of smoking and occupational expo-
sures among women.

Patterns of Employment

The percentage of women in the United States work force is
steadily growing. In 1973 women represented 38.4 percent of the
United States work force and in 1978 that percentage had risen
to 41.2 percent (15).

Approximately 39 million women are employed outside the
home. Table 3 clearly indicates that the distribution of women
in the labor force by category of work does not parallel that of
men. Women are more likely than men to be employed in the
clerical and service categories. Men are more likely to be em-
ployed in the management, crafts and operatives/transport
categories than women. Table 4 lists the number of women em-
ployed in a wide variety of occupations, including many of those
traditionally believed to be hazardous for men. In spite of this
diversity, the bulk of women are employed in a narrow range of
jobs. Over one-third of women in the paid labor force are em-
ployed in one of the 10 job categories listed in Table 5. All of
these categories have been traditional employment areas for
women. Thus, the recent gains by women in employment oppor-
tunity have not yet had a substantial impact on the actual dis-
tribution patterns of the female labor force. If a shift does occur
in employment patterns involving greater proportions of
women in occupations with significant exposures, we would ex-
pect a cohort effect to be apparent in the development of occu-
pational illness. That is, those women entering hazardous occu-
pations traditionally limited to male workers would be expected
to be women newly entering the work force and, thus, predomi-
nantly in the younger age groups. As these cohorts age, the
duration of both occupational and smoking exposures would in-
crease. It is only after these newer cohorts reach the ages where
disease is prevalent that we would be able to observe the full

175
TABLE 4.— Number of women in the current workforce,
classified by occupation (1978)

 

# of Women

# of Women

 

176

Occupation in Thousands Occupation in Thousands
White-collar workers 24,594 Blue-collar workers—cont’d
Professional & Technical 6,083
Biological scientists 22 Laundry and dry cleaning
Chemists 17 operatives, n.e.c. 118
Nurses, dieticians, & Meat cutters and butchers,
therapists 1,255 except manufacturing 13
Health technologists and Meat cutters and butchers,
technicians 353 manufacturing 33
Engineering and science Mine operatives, n.e.c. 4
technicians 132 Mixing operatives 3
Painters and sculptors 83 Packing and wrappers,
Photographers 13 excluding meat and
Managers and administra- produce 422
tors, except farm 2,365 Painters, manufactured
Sales workers 2,666 articles 30
Sales clerks, Photographic process workers 48
retail trade 1,672 Precision machine operatives 43
Clerical workers 18,456 Drill press operatives 15
Bookkeepers 1,660 Grinding machine operatives 10
Cashiers 1,222 Lathe and milling machine
Secretaries 3,561 operatives 11
Typists 1,009 Punch and stamping press
Blue-collar workers 5,770 operatives 47
Craft and kindred workers 694 Sawyer . 14
Printing craft workers 91 Sewers and stitchers M72
Upholsterers 14 Shoemaking machine
Operatives, except operatives 60
transport 4,317 Furnace tenders and stokers,
Assemblers 606 except metal 1
Bottling and canning Textile operatives 224
operatives 25 Spinners, twisters, and
Checkers, examiners, and ibe 100
inspectors; manufacturing 359 Welders and flare cutters 41
Clothing ironers and Winding operatives, n.e.c, 37
pressers 101 All other operatives, except
Cutting operative, n.e.c. 84 transport . 1,062
Dressmakers, except Transport equipment
factory 113 operatives 258
Drillers, earth 2 Nonfarm laborers 492
Dry wall installers and Service workers 8,037
lathers 1 Private households 1,135
Filers, polishers, sanders Child care workers 477
and buffers 38 Cleaners and servants 514
Furnace tenders, smelters, Housekeepers 117
and pourers, metal 3 Service workers, except
Garage workers, and gas households 6,901
station attendants 20 Cleaning workers 858
Table 4 (continued)

 

 

# of Women # of Women
Occupation in Thousands Occupation in Thousands
Service workers—cont’d. Health service workers—cont’d.
Lodging quarters cleaners 174 Practical nurses 390
Building interior cleaners, Personal service workers 1,302
n.e.c, 462 Attendants 175
Janitors and sextons 222 Barbers 11
Food service workers 2,951 Child care workers 103
Bartenders 111 Hairdresser and
Waiters’ assistants 45 cosmetologists 483
Cooks 678 Housekeepers, excluding
Dishwashers 82 private households —
Food counter and Welfare service aides 92
fountain workers 397 Protective service workers 115
Waiters 1,252 Firefighters 1
Foud service workers, Guards 53
n.e.c. 384 Police and detectives 28
Health service workers 1,660 Sheriffs and bailiffs 3
Dental assistants 128 Farm workers 509
Health aides, excluding
nursing 288 TOTAL— 38,910
Nursing aides, orderlies,
and attendants 902

 

NOTE: n.e.c. is an abbreviation for “not elsewhere classified” and designates
broad categories of occupations that cannot be more specifically identified.
SOURCE: U.S. Department of Labor (17).

impact of occupational exposures (or their interactions with
smoking) on the health of women.

Because of this cohort effect, any failure to demonstrate an
excess risk of a given occupational exposure in women must be
interpreted with considerable caution. It may mean only that
the women exposed were too young and the exposure too brief
for illness to have yet developed. This caution is doubly impor-
tant for those attempting to demonstrate an interaction be-
tween occupational exposure and smoking on the development
of disease in women. Thus, little comfort can be taken from the
current low prevalence of occupational disease in women. It is
reasonable to expect that any movement of large numbers of
women into hazardous occupations will be followed, after an
appropriate time lag, by a dramatic increase in the prevalence
of occupational illness in women.

The Reproductive Role

A third reason for examining the effects of occupational expo-
sures in women separately from those in men is the difference

177
TABLE 5.— Most common female job categories, by percentage of
the female work force employed

 

 

Percent of Percent of
Female Female
Job Work Force Job Work Force
Secretary 8.5 Private Household
Worker 2.9
Retail Sales Clerk 4.3 Registered Nurse 2.8
Bookkeeper 4.3 Elementary School
Teacher 2.8
Waitress 3.2 Typist 2.6
Cleaning Workers 2.2
Cashier 3.1 Sewer & Stitcher 2.0

 

SOURCE: Rones, P. (14).

in their reproductive roles. Toxic occupational exposures in
both men and women can reduce fertility and increase fre-
quency of teratogenic effects (see Table 6). In addition, however,
the 9-month duration of gestation provides many opportunities
for the fetus to share any adverse toxic exposure of its mother.
These risks may interact with the well-established risks of
cigarette smoking during pregnancy discussed elsewhere in this
report. Table 6 provides a list of hazardous substances in the
work environment, some of which are suspected of having ef-
fects on reproduction.

Another specific concern for women is that of contraception.
Substantial numbers of women in the United States use oral
contraceptives (18). These drugs have been shown to interact
with cigarette smoking to produce a greatly increased risk of
cardiovascular disease, as discussed in this report. In addition,
it is possible that oral contraceptives may interact in an adverse
manner with physical or chemical agents found in the work
place, or that the combination of smoking, occupational expo-
sure, and oral contraceptive use may bear special risks. The
answers to those questions can be found only through the study
of populations of working women.

One study approached this issue by examining the health
status of women involved in the manufacture of oral contracep-
tives. Poller, et al. have shown that women working in the man-
ufacture of oral contraceptives absorb enough of the drugs to
influence the clotting mechanism as well as alter menstrual
function (12). Unfortunately, the risk of cardiovascular
disease—and the effects of smoking in relation to it—could not
be estimated in this population. Because of the established ex-
cess risk of cardiovascular disease from concurrent smoking

178
and oral contraceptive use, examination of cardiovascular risk
in this group would be of interest.

The preceding discussion presents several areas where
female-male differences may significantly limit the direct
applicability of the results of male smoking studies to the
female population. These areas of potential difference present
research questions that justify significant, ongoing research
activities.

Specific Interactions Between Occupational Exposure and
Smoking

A review of all the potential risks of occupational exposure for
women is beyond the scope of this section. Table 6 lists a number
of agents found in the occupational environment and their ob-
served organ toxicity. Table 7 presents selected pulmonary ir-
ritants and sensitizers in specific occupational settings in rela-
tion to the number of women employed in those settings.

There is little specific data on the health effects of a given
occupational exposure in women. Two clear exceptions exist—
exposure to asbestos and to cotton dust. The data from studies
of women exposed to these two compounds provide examples of
established interactions between smoking and occupational ex-
posure in women.

ASBESTOS

Selikoff, et al. prospectively followed a group of 370 male as-
bestos insulation workers. They demonstrated a multiplicative
effect of asbestos exposure and cigarette smoking on the risk of
development of lung cancer (4,13). Workers who smoked cigar-
ettes developed lung cancer at arate 92 times that of non-exposed
nonsmokers. They observed no deaths from lung cancer among
87 nonsmokers, and 24 deaths from bronchogenic cancer among
283 regular smokers, a number well in excess of the 3 deaths
expected. Newhouse, et al. followed a cohort of 900 women first
employed between 1936 and 1942 in an asbestos factory making
both textiles and insulation materials (2,10,11). They analyzed
the group’s mortality experience between first employment and
1968, with a minimum of 26 years’ follow-up. There was an ex-
cess overall mortality partly accounted for by deaths from
cancer, observed even among those who worked in jobs with
low-to-moderate exposure to asbestos. An excess of cancer of
the lung and pleura was found among those who were severely
exposed and who had worked less than 2 years. In the group
with severe exposure for more than 2 years in the factory,
excess deaths from cancer of the lung, pleura, and non-

179
TABLE 6.—Chart of toxins and effects

DEFREITIVE SUSPECTED AiR STANDARDS”
TOUCKY CrFECTS:

 

 

 

 

 

 

 

 

 

 

 

 

ee SUBOESTED
H1E82 San = oe
AGENTS : PrCTS, , Teste (eusing) (proposed)
Codruum alejelele aje | Urine cogmam fume 0 | mg/e> ig
Quant low motecuir | dust 0.2 mg/Me
Leod «| [ele lel Jef G0Qd ead’ inorganic inorgorc
‘Biood ZN 0.2 myn Ol mg?
bronapoeDiNTE (Proposed ond
Unne ALA 01 mga? y Blood Lead
Une 80s.g/ 100gme
COpparpiyFR
‘Mercury | fe @| |e] Sood mercury snorganec 0.1 ma/M> wnorgonec:
Urine mercury organic 0.01 mg/h 0.05 mga
Orgentc setrenty |
Benzene (benzo) . *| . «] Unne phenots, 10 pom (emergency 1 pom
' coc proposal | ppm}
Hetogenoted mdrecervens |
2 chhorabuomene elelele; jo ofetele Liver funchon teat 25 pon ¥ ppm
<chworoprans)
‘Oibromochiorapropane ee eje ‘Sperm count 10 poe 10 poo
\ | Serum restos*erone Cemerency
: | proposed)
Epctiorohydnn: ‘ale . . Lever Runchon heat 20 mgit 2mgine
Emyiene oiorormice I+ . | . ole 20 ppm Tg?
Polychionngted a] jel 1 | Srverocne jelele Biood anoles. Compounds wath Lge

bipnanyes AgDONe tissue 427% crorina g/

(PCB's) ! ‘Sarum bronsomnose 54% chionne 0 5 mgs?
Tetrocniorcetnfene. ele . "| oe 100 pen SO pen
“Perctuorosttndane) oi
Vena change: ele) “| Acrosteoyss le. | | Liver tunichon rest 1 open 1 poet

idaa

Pf hyd
‘one eee mean
Corton moncmucle . a | «| Carboxy hemoglobin. 50 pom 35.0pm
Arashi, gees j fad {

\

Hotogenated: ete! | | | afelalels Ot specihed Hologenaled onesthencs.
8g halothane meray ' iq 2 pom based on wage

‘fyorone: i ‘ ot spectic gas somipled

i ‘ not >) hour
‘ ;
i
Pewicutes 1 :
Cortoryl a i | . 50 mg? 50 gi?
Chvonnored ! oe] | tet | Actpose neaue vones wth speci
Iydrocorbares 4 Onis COMPOMNES 0.)
(og chioraona) 1 : 1 | | 8k006 anak Chwcedone 0.5 mg/ M4?
Cmondecons wel |! | pweuneone de] ood anova emergency standard Tig
<nepone) to Jon! paws, : + gi
tegen compen | |i | -
Orethyis nies rot Pe “| ols \ 2| Blood ononvas: not specified not specrhedt
tli | I
Jenicing regenan 1
(vthete pety)
J-F@8 NO Doren rays ® Gaseo- nteatinal |e] eje} sje) Persone! fim badge: NCR? recomemendanon
Osorders. Gosmnetry 125 rad/quarver,
I Tremotumunsescent Soar
sommnenry ‘Pregnancy.
0.5 remvfuli pragnoncy
(@iaceRenseue subs tences
Corton cequition . 2] | Rennopatty a]e] |e] Unne dine azide met | 20 ppm Img.
Erenpene Omen eo} le eo} | car SO ppm 50 ppm

 

 

 

 

 

 

 

 

 

 

 

+ Animal and/or human data ©
Time weighted average 40-hr. week, 8-hr. day (OSHA), 10-hr. day (NIOSH).
In pregnancy, blood lead less than 4Q. 9/100 gms is suggested

° Evidence onty male ‘intertility; no data on females

SOURCE: National Institute for Occupational Safety and Health (9).
180
neoplastic respiratory disease were observed. The authors cal-
culated the excess annual mortality due to lung cancer. When
workers with low-to-moderate exposure experienced a mean ex-
cess lung cancer mortality of 63 deaths (per 100,000 years’ expo-
sure). Those severely exposed for less than 2 years experienced
an excess of 44 deaths, and those severely exposed for 2 years or
longer experienced an excess of 241 deaths. Interestingly, an
examination of deaths did not reveal any significant association
with age at first employment in the asbestos factory. In the
sub-sample of workers whose smoking histories were available,
those women who had both smoked and were heavily exposed
had a risk of developing lung cancer over 30 times that of non-
exposed nonsmoking women. The authors concluded that the
data suggested that asbestos and cigarette smoking exert mul-
tiplicative rather than merely additive effects.

In summary, the data on smoking and asbestos exposure in
women closely resemble the findings demonstrated for men.

COTTON DUST

Approximately 250,000 women were employed in the textile
industry in 1978; that population included approximately
100,000 women engaged in spinning, twisting, and winding op-
erations. Byssinosis is a syndrome characterized by tightness of
the chest and shortness of breath in workers exposed to dust of
cotton, flax, and hemp. In addition to these acute symptoms,
workers have been found to develop chronic bronchitis, and
some become severely disabled by their obstructive lung disease
(3). Berry, et al. studied the workers in 14 cotton and 2 man-
made fiber mills in England (1). They found that men had a
greater prevalence of byssinosis than women, and that smokers
of both sexes had 1.4 times greater prevalence of byssinosis
than nonsmokers. Byssinosis prevalence was also positively as-
sociated with length of exposure to cotton dust in both women
and men and was positively associated with dust level in the
working environment in women. Berry, et al. were unable to
determine if the observed difference in prevalence by sex repre-
sented a difference in physiologic response or differences in oc-
cupational exposure. They also found a higher prevalence of
bronchitis in exposed versus nonexposed workers of both sexes.
Smoking workers had higher bronchitis rates than nonsmoking
workers.

Bouhuys, et al. studied 645 active and retired cotton textile
workers (including 372 women), aged 45 and older, who had
worked an average of 35 years. Their respiratory symptoms and
flow-volume curves were compared to those of community resi-

181
28st

TABLE 7.— Example of pulmonary irritants and inorganic sensitizers in various occupations where women work

 

 

# of women
employed

Severe Inorganic in
pulmonary irritant sensitizers Occupation thousands
Beryllium & Compounds Platinum Salts Electronic Machinery,
Phosphorous Trichloride Equipment & Supplies 890
Tellurium (Hexaflouride) — Household Appliances 67
Zinc (Chloride fume) —Radio, T.V. &

Communication Equipment 216

—Electrical Machinery,

Equipment & Supplies 604
Ammonia Phthalic Anhydride Professional & Photo-
Chlorine graphic Equipment &
Ozone Watches 238
Sulfurie Acid —Scientifie & Controlling
Uranium Compounds Instruments 65
Vanadium Compounds —Optical & Health Services

(Pentoxide) Supplies 119
— Photographic Equipment

& Supplies 36
Acrolein Cobalt, metal Rubber & Misc. Plastic
Ammonia fumes & dust Products 257
Cadmium dust Phthalic Anhydride — Rubber Products 86
Chlorine —Misc. Plastie Products 171
Chromates

Dichloroethy] ether
Ethylene Oxide
Hydrogen Chloride
E8I

 

# of women

 

employed
Severe Inorganic in
pulmonary irritant sensitizers Occupation thousands
Hydrogen Fluoride
Hydrogen Suifide
Phosgene
Phosphorous Trichloride
Phthalic Anhydride
Sulfuric Acid
Tellurium (Hexafluoride)
Zinc Compounds
Ammonia Phthalic Anhydride Leather & Leather Products 177
Polyvinyl Chloride — Footwear, except rubber 13

Chromic Acid & Chromates —Leather Products, except
Chromium, metals & footwear 40

insoluble salts
Hydrogen Sulfide
Phthalic Anhydride
Sulphur Dioxide
Ammonia Fabricated Metal Products 299
Cadmium dust/fumes —Cutlery, hand tools, &
Chromic Acid & Chromates other hardware 52
Chromium, metal & —Fabricated structural

insoluble salts metal products 78
Fluorine —Serew machine products 26
Hydrogen Chloride —Metal stamping 43
Nitrogen Dioxide — Misc. fabricated metal
Sulfuric Acid products 101

Zinc Chloride fumes
S TABLE 7.—(Continued)

ra

 

# of women

 

employed
Severe Inorganic in
pulmonary irritant sensitizers Occupation thousands
Chlorine Detergents Personal Services
Hydrogen Fluoride (Enzymatic) — Laundering, Cleaning, &
. other Garment Services 231

Chlorine Detergents —Beauticians 492
Chlorine Dioxide (Enzymatic)
Chromium, metal & Cobalt

insoluble salts
Nitric Acid
Sulfur Dioxide
Sulfuric Acid
Ammonia Private Households 1,217
Chlorine Hotels & Motels 424
Beryllium & Beryllium Cobalt, metal Professional & Related

compounds fumes & dust Services 11,931
Chromic Acid & Chromates Detergentes —Hospital Workers 2,866
Chromium, metal & (Enzymatic) — Offices of Physicians 506

insoluble salts Platinum Salts --Offices of Dentists 242
Iodine — Health Services 473
Selenium Hexafluoride — Convalescent Institutions 869

Zinc Chloride fumes
 

# of women

 

employed

Severe Inorganic in
pulmonary irritant sensitizers Occupation thousands

Ammonia Cobalt dust Textile Mill Products 409

Antimony Phthalic Anhydride — Knitting Mills 126

Bromine — Yarn, thread & fabric mills 229

Cadmium dust/fumes — Misc. Textile mill products 23

Chlorine Apparel & other fabricated

Chromates textile products

Cotton dust, raw —Apparel & Accessories 995

Dichloroethyl ether — Misc. fabricated 898

Dimethylamine textile products 97

Ethylene Chlorohydrin

Ethylene Oxide

Hydrogen Sulfide

Methyl] Bromide

Nitric Acid

Nitrogen Dioxide

Sulfur Dioxide

Sulfuric Acid

Zinc Chloride fumes

Hydrogen Sulfide Meat Products 12,986

 

SOURCE: National Clearinghouse for Smoking and Health (8), Rones, P. (14), Stellman, J. (16).

G8T
dents who acted as controls (3). Textile workers of both sexes
had significantly increased prevalence of chronic cough, wheez-
ing, and dyspnea. Work in the textile mills was the major vari-
able associated with symptom prevalence, with smoking as an
additional significant variable. The lung function data con-
firmed the association of both smoking and working in the mills
with decreased lung function. Nonsmoking female workers were
slightly more likely to report chronic cough than nonsmoking
men, but smoking male workers were almost twice as likely to
report this symptom as smoking women. A similar pattern was
seen for wheezing and chest tightness, but not for dyspnea.

Kilburn, et al. studied the prevalence of byssinosis and bron-
chitis in 1,046 women textile workers and showed an interaction
of smoking and work exposure in producing a higher prevalence
rate of both byssinosis and bronchitis at a given dust level (5).

In summary, women have clearly been shown to have a
higher risk of developing byssinosis, chronic bronchitis, and
chronic obstructive lung disease because of exposure to cotton
dust in the workplace. Cigarette smoking has been shown to
interact with some work exposures to increase this risk, al-
though it is not established whether this interaction is additive
or multiplicative. Men employed in occupations where they are
exposed to cotton dust have a greater prevalence of bronchitis
and respiratory disability than women. Clarification is neces-
sary to determine whether this is a sex difference or a dif-
ference in exposure (either occupational or smoking).

Summary

1. The 1979 Surgeon General’s Report identified the ways in
which smoking cigarettes may interact with the occupational
environment. They include:

a) Facilitation of absorption of physical contamination of
cigarettes,

b) Transformation of workplace chemicals into more toxic
substances,

c) Addition of the exposure to a toxic constituent of to-
bacco smoke to a concurrent exposure to the same con-
stituent present in the workplace,

d) Addition of a health effect due to environmental expo-
sure to a similar health effect due to smoking,

e) Synergy of exposures, and

f) Causation of accidents.

2. Women are entering occupational environments with
greater frequency, and thus may be experiencing greater expo-
sures to physical and chemical agents.

186
3. Cohorts of women with a greater prevalence of smoking are
currently reaching the ages of maximal disease occurrence, re-
placing earlier cohorts with lower cigarette exposures.

4, Physiologic differences in hormonal status between males
and females constitute a potential source of differing responses.

5. In the workplace women who are pregnant present a
9-month exposure opportunity, including potential teratogenic
and perinatal mortality effects.

6. Concurrent exposure of women to smoking and asbestos
resulted in a clear excess of cancer of the lung.

7. Women smokers exposed to cotton dust run a higher risk of
developing byssinosis, bronchitic syndromes, and abnormal
pulmonary function tests than nonsmoking women.

References

(1) BERRY, G., MOLYNEUX, M.K.B., TOMBLESON, J.B.L. Relationships
between dust level and byssinosis and bronchitis in Lancashire cotton
mills. British Journal of Industrial Medicine 31: 18-27, 1974.

(2) BERRY, G., NEWHOUSE, M.L., TUROK, M.E. Combined effect of as-
bestos exposure and smoking on mortality from lung cancer in factory
workers. Lancet 2(7775): 476-479, September 2, 1972.

($) BOUHUYS, A., SCHOENBERG, J.B., BECK, G.J., SCHILLING, R.S.F.
Epidemiology of chronic lung disease in a cotton mill community. Lung
154: 167-186, 1977.

(4) HAMMOND, E.C., SELIKOFF, IJ. Relation of cigarette smoking to risk
of death or absestos-associated disease among insulation workers in
the United States. In: Boguvski, P., Gilson, J.C., Timbrell, V., Wagner,
J.C., Davis, W. (Editors). Biological Effects of Asbestos. International
Agency for Research on Cancer, Scientific Publication No. 8, Lyon,
France, International Agency for Research on Cancer, 1973, pp. 312-
317.

(5) KILBURN, K.H., KILBURN, G.G., MERCHANT, J.A. Byssinosis: Mat-
ter from lint to lungs. American Journal of Nursing 73(11): 1952-1956,
November 1973.

(6) NATIONAL CENTER FOR HEALTH STATISTICS. Health Interview
Survey, 1976. Department of Health, Education, and Welfare, Public
Health Service, National Center for Health Statistics. (Unpublished
data)

(7) NATIONAL CLEARINGHOUSE FOR SMOKING AND HEALTH.
Adult Use of Tobacco, 1975. Department of Health, Education, and
Welfare, Public Health Service, Center for Disease Control, Bureau of
Health Education, National Clearinghouse for Smoking and Health,
June 1976,

(8) NATIONAL CLEARINGHOUSE FOR SMOKING AND HEALTH. Sur-
vey of Health Professionals: Smoking and Health, 1975. Department of
Health, Education, and Welfare, Public Health Service, Center for Dis-
ease Control, Bureau of Health Education, National Clearinghouse for
Smoking and Health, June 1976, 42 pp.

(9) NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND
HEALTH. Occupational Diseases (Revised Edition). Department of
Health, Education, and Welfare, Public Health Service, Center for Dis-

187
(10)

(11)

(12)

(13)

(14)

(15)

(16)

(17)

(18)

188

ease Control, National Institute for Occupational Safety and Health,
June 1977, 608 pp.

NEWHOUSE, M.L. Cancer among workers in the asbestos textile indus-
try. In: Buguvski, P., Gilson, T.C., Timbrell, V., Wagner, J.C., Davis, W.
(Editors). Biological Effects of Asbestos. International Agency for Re-
search on Cancer, Scientific Publication No. 8, Lyon, France, Interna-
tional Agency for Research on Cancer, 1973, pp. 203-208.

NEWHOUSE, M.L., BERRY, G., WAGNER, J.C., TUROK, M.E. A study
of the mortality of female asbestos workers. British Journal of Indus-
trial Medicine 29: 134-141, 1972.

POLLER, L., THOMSON, J.M., OTRIDGE, B.W., YEE, K.F., LOGAN,
S.H.M. Effects of manufacturing oral contraceptives on blood clotting.
British Medical Journal 1: 1761-1762, June 30, 1979.

PROCTOR, N.H., HUGHES, J.P. Chemical Hazards of the Workplace.
Philadelphia, J.B. Lippincott Company, 1978, 533 pp.

RONES, P., LEON, C. Employment and unemployment during 1978: an
analysis. Special Labor Force Report 218. Department of Labor,
Bureau of Labor Statistics, 1979.

SELIKOFF, I.J., HAMMOND, E.C., CHURG, J. Asbestos exposure,
smoking, and neoplasia. Journal of the American Medical Association
204(2): 106-112, April 8, 1968.

STELLMAN, J., DAUM, S.M. Work is Dangerous to Health. New York,
Pantheon Books, 1973, 448 pp.

U.S. DEPARTMENT OF LABOR. Employment and unemployment dur-
ing 1978: An analysis. Department of Labor, Bureau of Labor Statis-
tics, Special Labor Force Report 218, 1979.

U.S. PUBLIC HEALTH SERVICE. Smoking and Health. A Report of
the Surgeon General. Department of Health, Education, and Welfare,
Public Health Service, Office of the Assistant Secretary for Health,
Office on Smoking and Health, DHEW Publication No. (PHS) 79-50066,
1979, 1251 pp.
PREGNANCY AND INFANT HEALTH.
PREGNANCY AND INFANT HEALTH

Introduction

A woman who smokes during pregnancy not only risks her
own health, but also changes the conditions under which her
baby develops. Studies have identified specific areas in which
the effects of maternal smoking during pregnancy may occur.
These include fetal growth, most often determined by compar-
ing birth weights of smokers’ babies with those of otherwise
similar nonsmokers’ babies; spontaneous abortions, fetal
deaths, and neonatal deaths; pregnancy complications, includ-
ing those that predispose to preterm delivery; possible effects
on lactation; and long term effects on surviving children. The
relationships between maternal smoking and these outcomes
have been established by clinical, pathological, and especially
epidemiological studies. Understanding of mechanisms by
which smoking may produce the observed effects has been
gained by physiological studies in humans and experimental
studies in animals.

The Chapter on Pregnancy and Infant Health in the 1979
Surgeon General’s Report is a detailed review of past studies of
the effects of smoking in pregnancy, with a comprehensive bib-
liography. This section summarizes current knowledge in major
areas of study, describes important new studies, and points out
areas requiring further research (146).

Smoking, Birth Weight, and Fetal Growth

Babies born to women who smoke during pregnancy are, on
the average, 200 grams lighter than babies born to comparable
women who do not smoke. Since 1957, when Simpson reported
this finding from her original study (138), it has been confirmed
in more than 45 studies of more than half a million births (146).
Results of these studies are expressed as mean birth weights of
smokers’ and nonsmokers’ babies or, alternatively, as the per-
centage of babies who weigh less than a specified amount, usu-
ally 2,500 grams.

To illustrate the association between maternal smoking and
an increased proportion of low-birth-weight infants, the results
of five studies with an aggregated total of almost 113,000 births
in Wales, the United States, and Canada are summarized in
Table 1. In these populations, 34 to 54 percent of the mothers
smoked during pregnancy and on the average the smokers had
twice as many low-birth-weight babies as the nonsmokers. Also
in these populations, from 21 to 39 percent of the incidence of

191
c61

TABLE 1.—Birth weight under 2,500 grams by maternal smoking habit, relative and attributable risks derived
from published studies

 

 

Nonsmokers Smokers Births < 2,500 grams Relative Attribut-
Non- risk able
Propor- smoker Smoker smoker: risk*
Study No. No. tion (%) (%) nonsmoker (%)
Cardiff 7,176 6,238 -465 4.1 8.1 1.98 31
US Collaborative
White 8,466 9,781 -536 4.3 9.5 2.21 39
Black 11,252 7,777 409 10.7 17.5 1.64 21
California, Kaiser
Permanente
White 3,189 2,145 .402 3.5 6.4 1.83 25
Black 934 479 338 6.4 13.4 2.09 27
Montreal 3,954 3,004 432 5.2 11.4 2.19 34
Ontario 27,316 21,062 435 4.5 9.1 2.02 31

 

*Percentage of total birth weights < 2,500 gm attributable to maternal smoking. Attributable risk in population = b(r—1) divided by
b(r—1) +1 where b = proportion of mothers who smoke and r = relative risk of low weight = smoker rate/nonsmoker rate.
SOURCE: Meyer, M.B. (86).
 

TUTTI TTT) Tt

 
 
  
   

10
—_——u=e= Nonsmokers

enesese Smokers

Percent
o

 

 

“ea guves
TTT tT TT?) lS

4 5 6
Birth Weight (Scale in Pounds: Intervals of 4 02.)

 

FIGURE 1.—Percentage distribution by birth weight of infants of
mothers who did not smoke during pregnancy and of
those who smoked one pack or more of cigarettes per
day

SOURCE: MacMahon, B. (77).

low birth weight could be attributed to maternal smoking
(3,15,38,86,102,106,107).

One study in which rates of low birth weight were simulta-
neously adjusted for multiple factors showed that maternal
smoking had a more significant relationship to birth weight
than did previous pregnancy history, hospital pay status,
mother’s prepregnant weight, height, age-parity, or sex of child.
Adjusted rates of birth weights under 2,500 grams were 49 per
thousand for nonsmokers, 76 per thousand for smokers of less
than a pack per day, and 114 per thousand for smokers of a pack
per day or more. The risk of having a low-birth-weight baby
therefore increased 53 percent and 130 percent for light and
heavy smokers, respectively, compared with nonsmokers (86).

Population studies that illustrate whole distributions of birth
weights by maternal smoking levels show a downward shift of
all birth weights in proportion to the amount smoked (74,
77,83,114,136,160) (see Figure 1).

193
These studies show that the relationship between smoking
and reduced birth weight is independent of all other factors that
influence birth weight, such as race, parity, maternal size,
socioeconomic status, sex of child, and other factors that have
been studied. It is also independent of gestational age. There is
a dose-response relationship: that is, the more the woman
smokes during pregnancy, the greater the reduction in birth
weight. If a woman gives up smoking by her fourth month of
gestation her risk of delivering a low-birth-weight baby is simi-
lar to that of a nonsmoker.

PLACENTAL RATIOS

Analyses of placental weights by maternal smoking habits
have noted that these weights were either not affected or were
less affected by maternal smoking than were birth weights
(57,61,91,104,155). The placental ratio, the ratio of placental
weight to birth weight, tended to be larger for smokers than for
nonsmokers, mainly because of the dose-related reduction in
birth weights with increasing number of cigarettes smoked.

Wingerd and colleagues have studied placental ratios based
on data from 7,000 pregnancies among members of the Kaiser
Foundation Health Plan in Oakland, California (156). Smoking
information was obtained early in pregnancy, and placentas
were handled according to Benirschke’s standardized protocol.
Figure 2 shows placental ratios by smoking level and gestation
for single live births. At each gestational age, from 37 through
43 weeks, the more the mother smoked during pregnancy, the
higher was the placental ratio. These ratios were higher for
black than for white women and tended to increase as maternal
hemoglobin level decreased (156).

Christianson’s recent report, based on standardized examina-
tions of these placentas, has shown that the increase in placen-
tal ratio with maternal smoking level was due to considerable
decreases in mean birth weight, accompanied by slight in-
creases in mean placental weight. In addition, smokers’ placen-
tas were significantly thinner than those of nonsmokers, and
their minimum diameters were larger (19).

Maternal smoking leads to significant increases in car-
boxyhemoglobin in maternal and fetal blood, with a consequent
reduction in the oxygen carrying capacity of both, and a reduc-
tion of the pressure at which oxygen is delivered to the fetal
tissues (70,72,146). Christianson discusses the similarity be-
tween studies of placental ratios by smoking level, altitude,
maternal anemia, and maternal cyanotic heart disease. She
suggests that the changes in placental ratio represent an adap-

194
15.5

 

 

15.0

Heavy smokers

aff’).

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

& 14.5 t

x

2 NK \ Light smokers

& 14.0 >

3s ~~

Cc

8 13.5 ~

a ™s Nonsmokers P

13.0

é e
af J

37 38 39 40 41 42 43
Week of gestation

FIGURE 2.—Reatio of placental weight to birth weight by length of
gestation and maternal smoking category

SOURCE: Wingerd, J. (156).

tation to relative fetal hypoxia (19). An adaptive advantage for
survival might occur because a larger placenta with an in-
creased area of attachment would deliver more oxygen, and a
smaller fetus would have a decreased oxygen demand. If so, it is
extremely important to know whether this reduction in size is
accompanied by any long-term costs in later growth and devel-
opment.

GESTATION AND FETAL GROWTH

In early studies the consistent finding that mean birth
weights were lower and the frequency of births under 2,500
grams higher for women who smoked during pregnancy than
for similar nonsmokers raised the obvious question of whether
this might be due to a smoking-related reduction in gestation.
This is not the case. Studies consistently show that mean gesta-
tion is minimally reduced by maternal smoking (less than 2
days) (3,13,146,159) and that birth weight is lower for infants of
smokers than for infants of nonsmokers at each gestational age
(3,15,83,146).

195
The finding that maternal smoking does not cause an overall
downward shift in the distribution of gestational ages, as was
shown for birth weights of smokers’ infants, leads to the conclu-
sion that the lower weight must be due to direct retardation of
fetal growth. In other words, these infants are small-for-dates
rather than preterm. The type of fetal growth retardation as-
sociated with maternal smoking is characterized by an abnor-
mally short crown-heel length for gestational age (89,90).
Smokers’ babies are smaller than corresponding nonsmokers’
babies in all dimensions measured, including length, head cir-
cumference, chest circumference, and shoulder circumference
(10,30,31,52,57,61,102,104,146,157).

Previous studies of these measurements at birth have in-
ferred that birth size reflects the rate of fetal growth; this has
been confirmed by a definitive study in which fetal biparietal
diameters were measured serially during gestation. Persson
and coworkers studied 5,715 pregnancies prospectively, making
ultrasonic measurements of biparietal diameters (BPD) from 18
to 20 weeks through term. Separate growth curves of BPD were
constructed for fetuses of smokers and nonsmokers who were
delivered between 266 and 294 days after the last menstrual
period. The BPD increased faster in the nonsmoking group; the
difference from the smoking group was significantly apparent
from the 28th week and was positively correlated with the aver-
age number of cigarettes smoked (Figure 3). Measurements
taken at birth showed that the distributions of birth weights
and lengths shifted downwards in proportion to the level of
smoking. Figure 4 illustrates this shift (114). These findings cor-
roborate Miller’s characterization of smokers’ babies as nor-
mally proportioned but short as well as light for dates, and
smaller in all dimensions than babies of nonsmokers (90). The
data are also consistent with the speculation that relative fetal
hypoxia results in a slower mitotic rate, a baby with fewer cells,
and a reduced oxygen demand.

LONG-TERM GROWTH AND DEVELOPMENT

Possible long-term consequences of maternal smoking during
pregnancy are also of concern. Several long-term studies pro-
vide evidence that children of smoking mothers have slight but
measurable deficiencies in physical growth, intellectual and
emotional development, and behavior (95).

Because these complex outcomes are affected by many known
and unknown factors, it is important to take these other factors
into account in any attempt to measure long-term effects of
maternal smoking. Several well-controlled studies have shown

196
mm

 

 

 

100 r
BPD =
30Pr SS SESS
===" ;
80 a —=—=——=s. ——
70r Tf
: @ nonsmokers
- : © heavy smokers

YW ——a
cl >=

i i f J

25 30 35 40

weeks

FIGURE 3.— Fetal Biparietal Diameters (BPD) values [means
and standard error of means (SEM)] of nonsmokers
and heavy smokers (10 cigarettes/day) plotted in
relation to postmenstrual age against the normal
range (shaded area depicts 95% confidence interval)

SOURCE: Persson, P.H. (114).
197
that the physical growth of smokers’ babies remains behind
that of nonsmokers’ babies as measured at 7 to 14 days (31); 1
year, 4 years, and 7 years (pairs of births matched for race, date
of delivery, maternal age and education, and sex of child) (52); 5
years (adjusted for other factors) (157); up to 642 years (prospec-
tive study) (35); and at ages 7 and 11 (follow-up studies of the
17,000 children from the British Perinatal Mortality Study, with
the adjustment for other social and biological factors) (16,30,33),

Associations have also been noted between maternal smoking
and deficiencies in neurological and intellectual development of
the child. Hardy and Mellits analyzed findings for 88 pairs of
children of smokers and nonsmokers, matched for race, date of
delivery, maternal age and education, and sex of the child. Al-
though they reported no significant differences in intellectual
function between children born to smoking and nonsmoking
mothers, the direction of difference on almost all tests was in
favor of the nonsmokers’ babies. Fewer smokers’ than
nonsmokers’ children had normal neurological status at age 1
year, both in the original 88 matched pairs and in the additional
set of 55 pairs of children of smokers and nonsmokers, matched
for birth weight as well as for the other cited factors. In both
sets, smokers’ children had lower scores on the majority of tests
of intelligence and intellectual function at ages 4 and 7 (52,146).

Similarly, Dunn evaluated neurological, intellectual, and be-
havioral status in a prospective study of low-birth-weight in-
fants, including 76 who were “small-for-dates” (term and pre-
term), 92 “truly premature” (preterm with birth weight be-
tween 11 and 89 percentile) and 151 full-birth-weight control
infants. Neurological abnormalities, including minimal cerebral
dysfunction and abnormal or borderline electroencephalo-
grams, were slightly more common among children born to
women who smoked (Table 2).

In a battery of psychological tests, the mean scores of children
of nonsmoking mothers were better than those of smokers’ chil-
dren in 45 out of 48 correlations, and the difference was signifi-
cant in 14 of these. Some significant differences in favor of
nonsmokers’ children were also demonstrated with respect to
behavior ratings and school placement (35). These results are
very similar to those of Hardy and Mellits in that the direction
of the differences was almost always in favor of the nonsmoker’s
child.

Small numbers and population selection factors were not a
problem in the longitudinal follow-up of the population origi-
nally included in the British Perinatal Mortality Study, com-
prising approximately 17,000 births, an estimated 98 percent of
all births in England, Scotland, and Wales during the week of

198
TABLE 2.—Incidence of neurological abnormalities at about 6%
years, by maternal smoking habits

Percent of Children with
Diagnosis
Maternal Smoking Habits

 

 

Diagnosis Smoker Nonsmoker P
Minimal cerebral dysfunction 20.0 11.0 <.05
Total neurological abnormalities 29.4 19.5 <.05
EEG borderline or abnormal
Low-birth-weight children 46.3 32.4 NS
Full-birth-weight children 28.2 21.6 NS

 

NS = not significant.
SOURCE: Dunn, H.G. (85).

March 8 to 9, 1958. These children have been traced and studied
again at ages 7 and 11, to describe their behavior, their health,
their physical development, their educational standards, and
their home environment. At ages 7 and 11 years, physical and
mental problems due to maternal smoking during pregnancy
were found, and these increased with the number of cigarettes
smoked.

Children whose mothers smoked 10 or more cigarettes a day
during pregnancy were on average 1.0 centimeter shorter and 3
to 5 months retarded in reading, mathematics, and general abil-
ity, as compared with the offspring of nonsmokers. After allow-
ing for associated social and biological factors, all of these dif-
ferences were highly significant, as illustrated in Figure 5
(p< 0.001) (16,30).

Denson’s case-control study of hyperkinesis reported a highly
significant association of hyperkinesis with heavy maternal
smoking, which at a mean level of 23.3 cigarettes per day was
more than three times the average for two control groups. The
authors concluded that their findings were “consistent with the
hypothesis that smoking during pregnancy is an important
cause of the hyperkinetic syndrome” (31).

A recent comparison by Saxton of behavioral patterns of in-
fants of mothers who smoked during pregnancy with infants of
mothers who did not smoke found that these patterns can be
influenced by smoking in pregnancy, and that the auditory
senses are particularly affected. Fifteen smokers of more than
15 cigarettes per day and 17 nonsmokers were selected for
study, matched for maternal age, social class, and parity. All
infants were spontaneous term deliveries of normal birth
weight. Sex distribution, length of labor, analgesia, and obstet-
rical factors were similar for the two groups. Examiners who did

199
aes NONSMOkers
_e me == Ali smokers

seenessee Heavy smokers /

 

 

1 * wen °F a mi,
44 46 48 50 52 54 56
Length, cm

FIGURE 4.—Distribution of birth lengths

SOURCE: Persson, P.H. (114).

not know the smoking status of the mother evaluated the in-
fants at 4 to 6 days of age, using the Brazelton Neonatal Behav-
ioral Assessment Scale. The scale includes a total of 20 tests and
maneuvers. While many of these showed no statistically signifi-
cant differences, auditory tests or tests with auditory compo-
nents were significantly different. Recorded “overall im-
pressions” of the infants at the end of the test showed that the
smokers’ infants tended towards “irritability, decreased ability
for self-control, and a general lack of interest, whereas the
nonsmokers, infants tended to be less irritable and better
oriented.” The author concluded that some effect on the normal

200
a) Reading Comprehension

 

@ 34
~ 24
e 4
3 04
c 1
cpm 7]
a= -24
ES -3!
gE -44
<6 654
2 -64
S  -7
a

a

 
 
  
  

Test for differences between
3 smoking categories after
adjusting for other factors
X? (2 D.F.) = 130.1; P < 0.001

n= 8,545) (n= 1,981) (n= 1,489)

 

qT

0 19 10+

Amount smoked per day after 4th month of pregnancy

b) Mathematics Ability

3
2
1
0

Deviation from
mean mathematics age
(months)

_7 Kin = 8,543 (n = 1,980)

 
 
  
  

Test for differences between
3 smoking categories after
adjusting for other factors
X? (2 D.F.) = 198.0; P <0.001

(n= 1,489)
0 1-9 10+

Amount smoked per day after 4th month of pregnancy

c) Height
144.55

—_
.—
>
°
i

Height (cm)

143.55

143.04

 

 
 
    

Test for differences between

3 smoking categories

after adjusting for other factors
X? (2 D.F.) = 60.4; P < 0.001

(nN = 7,649) (n= 1,729) (N= 1,316)
0 1-9 10+

Amount smoked per day after 4th month of pregnancy

FIGURE 5.—Tests of 11-year-old children by mothers’ smoking

habits after the fourth month of pregnancy

SOURCE: Butler, N.R. (16).

201
hearing mechanism had occurred in infants of smokers, possibly
due to a hypoxic effect of carbon monoxide on the cochlear
organ during development (132).

These studies suggest unfavorable effects of maternal smok-
ing during pregnancy on the child’s long-term growth, intellec-
tual development, and behavioral characteristics. Although
these changes are difficult to study because of the vast complex-
ity of possible antecedent and confounding variables, high
priority should be given to obtaining conclusive answers about
the long-term consequences of fetal exposure to cigarette
smoke.

ROLE OF MATERNAL WEIGHT GAIN

In the search for mechanisms through which maternal smok-
ing reduces birth weight, the question has been asked whether
it might be an indirect result of reduced appetite, less intake of
food, and lower maternal weight gain (84,127). Several early
studies reported no differences between smoking and nonsmok-
ing women in intake of food or in weight gain, and concluded
that the effect of maternal smoking on birth weight was not
mediated in this way (146).

Meyer analyzed the relationships between maternal smoking,
birth weight, maternal weight gain, and gestation, using data
based on 31,788 births from the Ontario Perinatal Mortality
Study (106,107). She found a significant downward shift in the
distribution of birth weights as maternal smoking level in-
creased, but no similar shift in the distribution of maternal
weight gain with smoking. Whereas the usual strong relation-
ship between the proportion of births under 2,500 grams and
maternal smoking level was found, there was no similar trend
for the proportion of mothers who gained less than 10 pounds
during pregnancy. Finally, the proportion of infants weighing
less than 2,500 grams increased directly with the amount
smoked within each maternal weight gain group from less than
5 pounds to 40 pounds or more, as shown in Figure 6 (83). From
Figure 6, one might conclude that smoking has a more pro-
nounced effect on low birth weight when maternal weight gain
during pregnancy is less than 20 pounds.

Other studies have indicated a lack of relationship between
smoking and maternal weight gain, while demonstrating a di-
rect relationship between smoking and fetal growth rate. The
German prospective study of 6,200 pregnant women, examined
every month from the first trimester through delivery, showed
no significant association between smoking habit and weight
gain. The usual relationships were found between smoking and

202
    
  

  
  
 
  

          

E 25 Private Hospital Status

oa 8

Se ° : [) Nonsmoker

N§ 15 By Wm <1 Pack/Day

ve 3 1 + Pack/Day

® 10 ed

oa oa

£~ 5 x

= = | ; ; , . bt

a 0 Ped a ; a, — -
0-4 5-9 10-14 15-19 20-24 25-29 30-34 35-39 40+

Maternal Weight Gain (pounds)

Ee 25 Public Hospital Status

g _ 2

N S 15

VS 10

oo a

= 5 £ o fs

oO 0 a x | > ” ~] & = 4 ry 3 cs
0-4 59 10-14 15-19 20-24 25-29 30-34 35-39 40+

Maternal Weight Gain (pounds)

FIGURE 6.—Percentage of birth weights under 2,500 grams by
maternal smoking level within maternal weight gain
group (five-pound intervals) by hospital pay status.
Births of 38+ weeks gestation (Ontario study)

SOURCE: Meyer, M.B. (83).

small-for-dates babies, with general retardation of weight,
length, and head circumference in proportion to the number of
cigarettes smoked during pregnancy (80). Miller and Hassanein
also found that the effects of smoking on fetal growth did not
appear to be related to maternal nutrition (93). Persson’s study
showing retardation of fetal growth of smokers’ babies by serial
measurement of biparietal diameters and by weight, length,
and other measurements at birth showed that the low birth
weights were independent of maternal weight gain. These au-
thors concluded that the fetal growth retardation resulted from
a direct pharmacological effect of smoking on the fetus “rather
than an influence resulting from nutritional deprivation” (114).
Hajeri and colleagues studied maternal weight gain in 105
smokers of 10 or more cigarettes a day with a control group of
nonsmokers who were similar with respect to gestation, age,
height, parity, and maternal weight at conception. Birth
weights, specific for sex, were significantly higher for infants of
203
TABLE 3.— Birth weight under 2,500 gm by maternal smoking
and prepregnant weight

 

Births <2,500 gm per 100
Total Births

 

 

Maternal Smoking Ratio
(Packs per day) Smoker:Nonsmoker

Prepregnant Total :
Weight Births 0 <1 1+ <1 1+
<120 lb

(<54 kg) 18,935 6.1 10.2 15.8 1.7 2.6
120-134 lb

(54-61 kg) 19,798 4.2 6.3 9.5 1.5 2.3
135+ lb

(>61 kg) 10,456 3.3 5.1 8.7 1.6 2.6

 

SOURCE: Meyer, M.B. (86).

nonsmokers, with a mean difference for boys of 330 grams and
for girls of 320 grams (p<.01). Mean extrauteral weight gain,
calculated as the difference between maternal weight gain and
the weights of fetus and placenta, was 7,044 grams for smokers
and 6,899 grams for nonsmokers (49),

Garn has compared mean birth weights, specific for gesta-
tional age, of babies of obese smokers, all nonsmokers, and all
smokers, using data from the Collaborative Perinatal Project of
the National Institute of Neurological and Communicative Dis-
orders and Stroke (NINCDS). Obesity was defined as the top 15
percent of the distribution of prepregnant weights, shown sepa-
rately for black and white women. Babies of the 1,383 obese
white smokers had mean birth weights similar to the total
group of white nonsmokers and higher than the total group of
white smokers. The 1,001 obese black smoking mothers had
babies whose mean birth weights were generally higher than
those of all black nonsmokers, leading Garn to conclude that
“maternal obesity (weight-defined) apparently counteracts the
smoking effect on the conceptus” (43). Because birth weight is
strongly correlated with maternal size, a more appropriate
comparison would have been between mean birth weights of the
babies of obese smokers and the babies of obese nonsmokers.
That such a comparison would show the usual relationship to
maternal smoking level is suggested by Meyer’s analysis of
birth weight by maternal smoking and prepregnancy weight
(Table 3). The correlation between maternal weight and the
proportion of low-birth-weight babies is clear at each smoking
level, and the independent relationship between smoking level
and low birth weight is clear at each level of maternal weight.

204
TABLE 4.— Mean birth weights in successive pregnancies to the
, same women, by smoking habit

 

Mean

Smoking Habits Smoking Habits Birth Weight (gm)

 

 

 

 

First Second Difference

pregnancy pregnancy N #1 #2 2nd-1st (gm)
Smoker ' Smoker 886 3204 =. 3228 +24
Nonsmoker Nonsmoker 988 3356 3388 +32
Difference: Nonsmoker - Smoker (gm) +152 +160
Smoker _ Nonsmoker 119 = 3271—S- 3881 +110
Nonsmoker _ Smoker 108 - 3323 3265 ~—58
Difference: Nonsmoker - Smoker (gm) +52 +116

 

SOURCE: Naeye, R. (93).

The relative increases in the proportion of low-weight births
with light and with heavy smoking are almost identical in the
three strata of prepregnant weight (86).

Studies of birth weight, maternal weight, and maternal
weight gain should also be carefully controlled for maternal age
and parity. In studies of successive births to the same mother
included in the Collaborative Perinatal Project of the NIN CDS,
Garn found that prepregnancy weights increased with succes-

_ Sive pregnancies by similar amounts for smokers and nonsmok-
ers (44). Naeye, using the same data base, reported that mater-
nal weight gain was less in the second pregnancy than in the
first pregnancy for smokers, for nonsmokers, and for women
who changed habits between pregnancies in either direction
(93). Second babies weighed on the average 24 grams more than
first babies if the mother smoked both times, and 32 grams more
if the mother smoked neither time (Table 4). If the mother
smoked during the first and not during the second pregnancy,
the second baby weighed an average of 110 grams more than the
first baby; in women who smoked during the second pregnancy
but not during the first pregnancy, second babies averaged 58
grams less than first babies (93).

The most careful analyses indicate that the effect of maternal
smoking is a direct one not mediated through an effect on mat-
ernal appetite, eating, or weight gain. In conclusion, as stated in
a Lancet editorial, “the appeal of the nutritional hypothesis is
that women might be more readily encouraged to eat more dur-
ing pregnancy than discouraged from smoking. ... However, if,

205
as now seems more likely, the growth-retarding effect of smok-
ing is due to fetal hypoxia, there is no short-cut to removing
this adverse influence” (63). This conclusion in no way obviates
the enormous importance of dietary factors during pregnancy.

Overt maternal malnutrition is associated with inadequate
growth. Recently, it has been suggested that more subtle alter-
ations in the maternal supply of essential nutrients combined
with compromised uteroplacental circulation may contribute to
reduced fetal growth. Crosby, et al. (26) observed that the con-
centrations of each of 14 amino acids and carotene were reduced
significantly in the blood of smoking mothers. These workers
postulated that, while these differences were on the order of 10
or 20 percent, they could be an important factor in producing
the small-for-gestational-age infants associated with maternal
smoking. In a study of over 1,100 pregnant women, Schorah, et
al. (135) noted an inverse correlation between the number of
cigarettes smoked and the leukocyte ascorbic acid concentra-
tion. For instance, the leukocyte ascorbic acid concentration
was about 22 percent less in the blood of women who smoked
more than 20 cigarettes a day as compared with controls. De-
spite a 15 percent increase in the number of circulating leuko-
cytes in the blood of smokers, the blood ascorbic acid concentra-
tion was still 10 percent less than in controls. These differences
were even more marked in women from lower socioeconomic
groups. The authors suggested that in addition to the role of
ascorbic acid in fetal nutrition, these lowered concentrations
might be related to the increased incidence of premature rup-
ture of the amniotic membranes in smoking women.

Smoking, Fetal and Infant Mortality, and Morbidity

SPONTANEOUS ABORTION

Past studies have demonstrated a statistically significant as-
sociation between maternal cigarette smoking and spontaneous
abortion (55,61,104), some showing a strong dose-response re-
lationship (110,144,162). Spontaneous abortions are difficult to
study because of problems of ascertainment. In prospective
studies, early abortions may be missed, and bias may occur if
one group tends to register earlier than the other. Retrospect-
ive studies allow more complete ascertainment but are subject
to errors of recall. Nevertheless, higher rates of spontaneous
abortion have been associated with maternal smoking in both
types of studies (61,104,162).

Kullander and Kallen found higher rates of “spontaneous
abortion” among smoking women, but noted that many of these

206
pregnancies were unwanted. Analysis of their data showed that
the relative risk of spontaneous abortion of smokers compared
with nonsmokers was 1.20 for wanted and 1.35 for unwanted
pregnancies (61). A case-control study of spontaneous abortion
with important variables held constant reported an 80 percent
increase in the odds of smoking among the cases compared with
controls (60).

Recent studies corroborated the finding of associations be-
tween smoking and spontaneous abortion risk. In a small retro-
spective study in New Zealand, Fergusson found that women
who smoked more than 20 cigarettes a day had almost twice the
nonsmoker risk of having had a previous spontaneous abortion,
and that the association could not be explained by differences in
maternal age, educational level, parity, race, socioeconomic
status or marital status (42). In a study of 12,013 consecutive
pregnancies in Dublin, Ireland, Murphy and Mulcahy found a
positive association between the number of cigarettes smoked
and the rates of spontaneous abortion, independent of the ef-
fects of maternal age and parity. The authors stated that in-
duced abortions are a negligible factor in Ireland and concluded
that maternal smoking leads to reduced reproductive efficiency
at all stages of pregnancy (92). Himmelberger and colleagues
surveyed a group of professional women in medicine concerning
the influence of maternal smoking on their 12,194 pregnancies
(54). After controlling for interfering variables, the risk of spon-
taneous abortion for certain subgroups of heavy smokers was
estimated to be as much as 1.7 times that for nonsmokers. Spon-
taneous abortion rates were lowest in the 25 to 29 year old cate-
gory, increasing with age to levels of 38 and 36 percent for
nonsmokers and smokers, respectively, at age 40 plus. The rela-
tive increase in risk associated with maternal smoking was
highest at the youngest ages and decreased with increasing age
(54).

An editorial in the British Medical Journal summarized these
findings and stated: “Cigarette smoking, one of the first man-
ifestations of women’s social emancipation, is emerging as a
possible threat to her procreative role.” The proportion of ab-
normal karyotypes in abortuses of women who smoke appears
to be reduced rather than increased (1). The mechanism under-
lying the smoking-related excess appears to be due to complica-
tions of pregnancy rather than to any fetal abnormality (13).

CONGENITAL MALFORMATIONS

Several studies have reported perinatal, fetal, or neonatal
Mortality rates by cause. In these comparisons, death rates due

207
TABLE 5.— Incidence of congenital abnormality (all single births)

 

Nonsmokers Smokers

 

Number Percent Number Percent

 

Total abnormal infants 2.37 2.73

Type of abnormality
Anencephaly 18 0.2 15 0.2
Spina bifida 20 0.22 23 0.3
Other C.N.S. abnormality 38 0.42 36 0.47
Cardiovascular abnormality 34 0.37 32 0.42
Gut abnormality 21 0.23 24 0.32
Genito-urinary abnormality 39 0.43 25 0.33
Bone abnormality 65 0.72 52 0.68
Cleft palate and/or hare lip 10 0.11 20 0.26
Other abnormality 19 0.21 18 0.24

 

x? (all abnormalities) = 2.22, p> 0.05.
x? (cleft palate and hare lip) = 5.36, 0.01< p<0.05.
SOURCE: Andrews, J. (3).

to congenital malformations have usually been lower for smok-
ers’ than for nonsmokers’ infants (3,22,46,87). This is compatible
with the finding that smoking-related spontaneous abortions
have a lower frequency of abnormal karyotypes and tend to
occur later than spontaneous abortions in nonsmokers. As pre-
viously described, increased losses of conceptus associated with
maternal smoking appear to be due to pregnancy problems and
complications rather than to abnormalities of the embryo or
fetus (41). Andrews and McGarry, in a community study of
18,631 pregnancies in Cardiff, Wales, reported that smokers’ in-
fants had lower mortality rates from malformations than those
of nonsmokers. Rates of stillbirths due to congenital malforma-
tions were 0.32 and 0.27 per 100 nonsmokers and smokers re-
spectively. Corresponding rates for neonatal deaths were 0.33
and 0.31 per 100 babies of nonsmoking and smoking mothers. On
the other hand, the incidence of congenital malformations
among all single births in Andrews’ population was higher
among smokers’ babies, overall, and specifically higher for cleft
palate and lip. Among other sites, some were higher for smokers
and some for nonsmokers, as is shown in Table 5 (3).

A significant positive association between cardiac malforma-
tions and maternal smoking was shown by Fedrick and col-
leagues, based on firm diagnoses among stillbirths, neonatal
deaths, and survivors to age 7 from the British Perinatal Mor-
tality Survey. However, this difference was largely due to the
inclusion of patent ductus arteriosus, which may or may not be
classified as a malformation (80).

208
.09 r
08 F *
07
06 F

05 F _—~
~— Moderate Smoker
~\ 2A
~

~~

    

04
03 F
0267
.O1F

Probability of Congenital Abnormality
/

 

18 22 26 30 34 38 42 46 50
Maternal Age

FIGURE 7.—Risk of congenital abnormality according to age and
smoking habit

SOURCE: Himmelberger, D.U. (54).

Some recent studies have shown a positive association be-
tween maternal smoking and congenital malformations, defined
in a variety of ways. Himmelberger and colleagues carried out a
mail survey of professional women in medicine (54). They were
interested in exposure to anesthetic gases in the operating
room, and evaluated possible effects on pregnancy outcome of a
number of factors including cigarette smoking. Information was
obtained and analyzed by a multiple logistic regression based
on 12,914 pregnancies, including 10,523 live births, which repre-
sented a response rate of 53.2 percent. After the effects of age,
exposure to anesthetic gases, and pregnancy history were con-
trolled, the risk of congenital abnormalities for babies of
mothers who smoke was estimated. A statistically significant
risk (p<.05) for maternal smoking was found. Figure 7 shows
the estimated risk of congenital abnormality as a function of
maternal age for nonsmokers, moderate smokers (1 to 19 per
day), and heavy smokers (20 plus per day). Relative risks for
heavy smokers compared with nonsmokers were as high as 2.3.
Rates of abnormalities in each general category were higher for
the children of smokers (see Table 6). The significant increase in
cardiovascular abnormalities among smokers’ children is in
agreement with Fedrick’s findings (40) and in general agree-

209
TABLE 6.—Comparison of congenital abnormality rates for
babies born of smokers and nonsmokers, by type of

 

 

abnormality

Smokers Nonsmokers p*
Abnormality % No. % No.
Cardiovascular 19.07+ (68) 13.65 (95) 0.02
Respiratory 15.15 (54) 12.07 (84) 0.10
Musculoskeletal 23.84 (85) 19.69 (137) ~—- 0.08
Gastrointestinal 13.46 (48) 9.48 (66) 0.04
Central nervous system 11.50 (41) 10.20 (71) (0.27
Urogenital 21.32 (76) 15.81 (110) ~—-0.02

 

*One-tail significance level for the test of the difference between two
proportions.

+Rate is number of congenital abnormalities per 1,000 live births. Rates
based upon 3,565 live births among the smokers and 6,958 live births among
the nonsmokers.

SOURCE: Himmelberger, D.U. (54).

ment with the study of Andrews and McGarry (3). Himmel-
berger, et al. point out that their findings are based on retro-
spective survey data, obtained by mail, and therefore subject to
bias from various sources, including that of a high nonresponse
rate. However, the study methods have been designed to elimi-
nate those effects (54).

A recent study by Borlee and Lechat controlled for confound-
ing variables by matching births with congenital malformations
to control births according to hospital and time of birth, mater-
nal age, sex of child, and socioeconomic level of parents. Two
hundred and two children with malformations diagnosed at
birth were compared with 175 controls, from a total of 17,970
consecutive births studied from June 1972 through May 1974.
No differences were found between cases and controls in the
distribution of smoking habits, including the number of cigar-
ettes smoked with or without filters. Sixty-six percent of
mothers of malformed infants and 68 percent of mothers of con-
trols were nonsmokers, Fathers’ smoking habits were also simi-
lar among cases and controls. Significantly more mothers of
malformed infants were heavy coffee drinkers (8 plus cups per
day). Because of the frequent association between heavy coffee
drinking and smoking, both habits should be included in studies
of environmental factors possibly related to the risk of congeni-
tal malformations (10). The same is true for consumption of al-
cohol in populations where drinking is prevalent.

Mau and Netter have reported births by gestation, birth
weight, perinatal mortality, and the incidence of congenital
malformations by smoking habits of fathers in 3,696 cases in

210
which the mother was a nonsmoker. Trends toward lower birth
weights and more preterm births with increasing levels of pat-
ernal smoking were not statistically significant. In the total
study of 5,200 births, regardless of maternal smoking habits,
there was a significant increase in the incidence of severe mal-
formations with increasing levels of paternal smoking; children
of heavily smoking fathers had about twice the expected inci-
dence. Although malformations in all systems were more fre-
quent if the father smoked over 10 cigarettes per day, only the
differences in facial malformations were significantly different
(p<.01) by smoking level. The authors state that the trends
with paternal smoking were independent of maternal smoking
level, maternal and paternal age, and social class (120).

More studies of these possible relationships are urgently
needed. As serious malformations are relatively rare, the case~
control approach is probably the method of choice, with careful
matching of cases with suitable controls.

PERINATAL MORTALITY

The 1973 report, The Health Consequences of Smoking and
the 1979 Report have summarized studies demonstrating a di-
rect relationship between level of maternal smoking and risk of
perinatal loss. The reports have also clarified reasons for the
variation in risk observed in these studies (146,147).

Two important reasons for variability between studies have
been demonstrated. First, other important variables such as
age, parity, race, and socioeconomic status influence the results
if they are unequally distributed between comparison groups of
smokers and nonsmokers (89). Second, cigarette smoking is
more harmful to the pregnancies of certain women than to
those of others. In general, women with other risk factors were
at greater risk from smoking than otherwise low-risk women
(3,15,22,128,144,159).

Table 7 illustrates these points. It shows that women charac-
terized by low social class, low level of education, being very
young or old during pregnancy, or being black, have higher
risks of perinatal mortality than their counterparts. Their in-
crease in risk due to smoking is relatively greater. Meyer, et al.
measured the perinatal mortality risks of light smokers (less
than a pack of cigarettes per day) and of heavy smokers (one
pack or more per day) relative to nonsmoker risks within sub-
groups of the population. The increased risk of perinatal mortal-
ity for light smokers who were young, low-parity, and non-
anemic was less than 10 percent. At the other extreme, mothers
characterized by high-parity, public hospital status, previous

211
TABLE 7.—Examples of perinatal mortality by maternal smoking status related to other subgroup
characteristics

bw

 

 

Perinatal or neonatal

 

 

 

 

 

 

 

No. of births deaths/1,000 births
Study Non- Non- Relative
Population Smokers Smokers Category smokers Smokers risk*
British Perinatal Mortality 11,145 4,660 Social class
Survey, England, all births 1,2 (high) 25.8 26.3 1.02
3-5 33.5 46.6 1.39
Washington Co. Maryland, 7,646 4,641 Father’s
white education
9+ years 14.4t 16.1¢ 1.12
<= 8 years 17.6t 38.0T 2.16
Northern Finland, white 8,898 2,346 23.2 23.4 1.01
California, middle to Race
upper middle class 6,067 3,726 White 11.0 11.3t 1.03
2,219 1,071 Black 17.1 21.5t 1.26
Boston City Hospital Race
Prenatal Clinic 513 892 White 29.2 31.4 1,08
1,225 636 Black 28.6 54.1 1.89
Quebec, 10% sample of 3,912 2,967 Maternal age
registered births <25 12.1 16.1 1.33
25-34 12.6 13.2 1.05
“35+ 23.0 41.7 1.81

 
Social Class

 

 

40r
1&2

Smoker

3

MBsas5
x
= 30 Non-
7 smoker
3
. di i
S
2
;
5
®O
x 10F
e Para Para Para Para Para Para

1, 2, 3 0 4+ 1, 2, 3 0 4 +
=—=-Under 35 years—=— —— 35 years +
0 be

FIGURE 8.—Theoretical cumulative mortality risk according to
smoking habit, in mothers of different age, parity,
and social class groups

SOURCE: Butler, N.R. (15).

low-weight births, or anemia had an increased perinatal] mortal-
ity risk of 70 to 100 percent when they were heavy smokers (88).

To help visualize the interacting effects of maternal smoking
and of other factors on perinatal mortality risk, Butler has cal-
culated theoretical mortality risks based on data from the
British Perinatal Mortality Study. In Figure 8, perinatal mor-
tality risks by social class, maternal age, and parity are ar-
ranged in order of increasing magnitude. The differences be-
tween smokers’ and nonsmokers’ risks are represented by the
height of the bars, which varies depending on other risk factors
(15).

These studies show that the risk of spontaneous abortion, of
fetal death, and of neonatal death increases directly with in-
creasing levels of maternal smoking during pregnancy. Studies
of smoking during pregnancy show a range of perinatal mortal-
ity risk ratios (smokers versus nonsmokers) from a low of 1.01 to
a high of 2.42, Variability between risk ratios in different study
populations may be due to lack of comparability between smok-
ers and nonsmokers in other respects, or to interaction between
smoking and other pregnancy risk factors. Studies failing to

213
take account of other important variables may show unusually
high or unusually low risk ratios.

CAUSE OF DEATH

The increased perinatal mortality associated with maternal
smoking is concentrated within a few cause-specific categories.
Excess stillbirths have been associated with antepartum
hemorrhage or abruptio placentae and with “unknown cause”
(3,46). Excess neonatal deaths were associated with immaturity,
asphyxia, atelectasis (23), and with the respiratory distress
syndrome (3).

Meyer and Tonascia (87) analyzed fetal and neonatal deaths
to identify causes of death which showed an excess if the mother
smoked. Fetal and neonatal deaths by coded cause and mater-
nal smoking habit are shown in Table 8. For each cause the
observed numbers for smokers were compared with the number
expected at nonsmoker rates. The differences between observed
and expected numbers indicate the number of deaths in each
category attributable to maternal smoking. ,

Fetal deaths showed a major smoking-related excess in the
category of “unknown” cause and some increase from “anoxia”
and “maternal cause.” By contrast, neonatal deaths related to
smoking were in the category of “prematurity alone,” or in the
related category of “respiratory difficulty.” The tentative con-
clusion to be drawn here is that fetuses and neonates whose
deaths were related to maternal smoking had no recognizable
pathology, but had died in utero from anoxia, maternal cause, or
unknown cause, or had suffered the consequences of preterm
delivery.

Complications of Pregnancy and Labor.

Studies have consistently found a direct relationship between
maternal smoking level and the incidence of placenta previa,
abruptio placentae, bleeding during pregnancy,and premature
rupture of membranes (3,24,46,61,86,87,94,95,130,144,145). The
association is independent of socioeconomic and racial back-
ground (144), parity (3) and many other factors (86) (Figure 8).

These complications carry with them a high risk of fetal and
neonata loss, and are frequently cited as the cause of death among
the offspring of women who smoke. Kullander and Kallen found a
significant increase in the frequency of abruptio placentae among
smokers’ children dying before the age of 1 week (61). In a prospec-
tive study of 9,169 pregnancies by Goujard and colleagues, a large
proportion of the increase in stillbirths among smokers was
caused by abrutio placentae (46).

214
TABLE 8.—Fetal and neonatal deaths by coded cause and
maternal smoking habit (Canadian English-speaking

 

 

 

 

mothers)
Observed Observed
——___—___—————- Expected Expected p+
Coded cause Nonsmoker Smoker smoker* difference value
Fetal] deaths
Unknown 75 125 81.4 43.6 0.003
Malformations 32 24 34.7 ~10.7 N.S.
Hemolytic disease 11 15 11.9 3.1 N.S.
Anoxia 16 29 17.4 11.6 N.S.
Maternal cause 31 45 33.u 11.3 N.S.
All others 8 13 8.7 4.3 N.S.
Total 173 251 187.9 63.1 0.003
Neonatal deaths
Unknown 52 51 56.5 -5.5 N.S.
Malformations 22 24 23.9 0.1 N.S.
Hemolytic disease 7 8 7.6 0.4 N.S.
Respiratory difficulty 46 63 50.0 13.0 N.S.
Prematurity alone 33 65 35.8 29.2 0.005
Maternal cause 2 6 2.2 3.8 N.S.
All others 16 16 17.4 -1.4 N.S.
Total 178 233 193.3 39.6 0.06
Total Births 15,240 16,549

 

N.S. = not significant.

*Based on nonsmoker rate.

p+ value derived from chi square based on a null hypothesis of no difference
between smokers and nonsmokers.

SOURCE: Meyer, M.B. (87).

Naeye reviewed the clinical and postmortem material from
the 3,897 fetal and infant deaths in the Collaborative Perinatal
Project of the NINCDS (102) and reported an association be-
tween perinatal mortality rates caused by abruptio placentae
and number of cigarettes smoked by the mother (95). Abruptio
placentae was the underlying cause identified in 11 percent of
all the deaths in this large study (94).

Analysis of data from the Ontario Perinatal Mortality Study
corroborated these findings. Increasing levels of smoking re-
sulted in a highly significant increase in the risks of placental
abruptions, placenta previa, bleeding in pregnancy, and prema-
ture and prolonged rupture of membranes. Fetal and neonatal
deaths were analyzed for associations between them and
smoking-related excesses of various coded complications of
pregnancy and labor. Although most diagnoses showed no asso-
ciation with excess mortality for smokers’ babies, a few stood

215
O Nonsmokers
@ Smokers

Plasma Volume (liters)

 

 

2.5
Ll | ! ! J | j

12 16 20 25 30 34 38
Gestation (weeks)

FIGURE 9.—Mean plasma volume in nonsmokers and smokers

SOURCE: Pirani, B.B.K. (117).

out as highly significant. Excess fetal deaths of smokers’ babies
were strongly associated with bleeding during pregnancy,
either before (P = 0.01) or after (p = 0.0005) 20 weeks gestation.
In other coded categories, a significant excess of fetal deaths
occurred among smoking mothers with abruptio placentae
(p= 90.0001) or other obstetrical problems. Similar comparisons
were made for neonatal deaths. A strong, significant relation-
ship between smoking-related excess neonatal deaths and a his-
tory of bleeding before 20 weeks of gestation was found
(p= 0.0001). Other categories that showed significant increases
of smoking-associated neonatal deaths were the admission
status of rupture of membranes only, other obstetrical compli-
cations, and duration of rupture of membranes over 48 hours
(87).

216

 
PREECLAMPSIA

Several published studies have reported that the incidence of
preeclampsia is declining as the number of cigarettes smoked
increases (109,145). Data from the British Prenatal Mortality
Study were cross-tabulated by parity, severity of preeclampsia,
and maternal smoking status. Smokers had lower rates of all
grades of preeclampsia than nonsmokers, whether they were
primiparae or multiparae (15). Andrews and McGarry showed
that the inverse relationship between cigarette smoking and
preeclamptic toxemia was independent of social class, maternal
weight before pregnancy, and maternal weight gain during
pregnancy (3). Despite this effect of smoking on the incidence of
preeclampsia, there is a greatly increased risk of perinatal mor-
tality if preeclampsia does develop in a smoker (3,34,129). Sev-
eral authors have suggested that this negative association may
be due to the hypotensive effect of thiocyanate, which is derived
from the cyanide present in cigarette smoke and is regularly
found in the blood of smokers (3,109). Because preeclampsia is
predominantly a complication of first pregnancies, it is possible
that the occasional finding of reduced rates of perinatal mortal-
ity in young, primiparous, light smokers who are otherwise
healthy is due to this relationship.

Pirani and MacGillivray performed seven serial mea-
surements from the end of the second trimester until term in 31
nonsmokers and 29 smokers. After 25 weeks gestation the
plasma volume of smokers failed to keep pace with that for
nonsmokers, the increases in volume being 25 percent less in
smokers (Figure 9). Plasma volume and total body water expan-
sion are related to birthweight, at least in primigravidas. After
30 weeks of gestation, total body water in smokers plateaued in
contrast to nonsmokers, so that by term their body water vol-
ume increase was about 25 percent less. Serum heat-stable al-
kaline phosphatase levels in smokers significantly exceeded the
concentration in nonsmokers from the 37th week of pregnancy
onward. This enzyme is of placental origin, and cigarette smok-
ing may contribute to this change by its effects on the placenta

(117).
Whether the reduction in the incidence of preeclampsia with

maternal smoking is due to the hypotensive effects of thiocyanate,
to the reduced size of the baby, to a smaller increase in maternal
blood volume, or to another process requires further study.

PRETERM DELIVERY, PREGNANCY COMPLICATION S,
AND PERINATAL MORTALITY BY GESTATION

Studies of large numbers of births to measure mean gestation
by smoking habit have demonstrated differences of only a day

217
or two. This finding led to the conclusion that maternal smoking
does not affect gestation (14,52,74,102,146,159). On the other
hand, abundant evidence has been presented that a smoking-
related increase in preterm delivery plays an important role in
the increased risk of neonatal death for infants of smokers.

When the proportion of preterm births is measured, rather
than the mean gestation, smokers have shown consistently
higher rates than nonsmokers, as illustrated in Table 9. In four
studies in which all births and perinatal deaths were included,
the risk of early delivery increased from 36 to 47 percent if the
mother smoked, and 11 to 14 percent of all preterm births could
be attributed to maternal smoking (3,15,38).

Figure 10, using data from the Ontario Perinatal Mortality
Study, shows percentage distributions by gestational age of
births to nonsmokers, light smokers, and heavy smokers, plot-
ted on a semilogarithmic scale to emphasize differences be-
tween smoking-level groups in very preterm births. There is
little difference between the means of these curves because the
great majority of births occur around term in all groups. There
is, however, a significant and dose-related increase in the pro-
portions of preterm babies born to women who smoke. These
preterm deliveries account for a small proportion of total births
but for a large proportion of the deaths (82,146).

As previously reviewed, Meyer and Tonascia have related the
excess fetal and neonatal mortality of smokers’ infants and the
excess incidence of pregnancy complications among women who
smoke to the gestational age of occurrence, using a life-table
approach. A starting population of all pregnancies in utero at 20
weeks was used to calculate the probabilities of fetal death, live
delivery followed by survival or death, or the occurrence of a
complication followed by fetal death or delivery. At 28 weeks
(the next point defined by the data), the population at risk in-
cluded those remaining in utero at that point. Figure 11 shows
the probability of perinatal death during each period of gesta-
tional age starting at 20 weeks. Risks for smokers’ infants were
significantly greater in the earlier weeks, but not different after
38 weeks gestation (87,146).

A similar approach was applied to determine the risk by ges-
tation of abruptio placentae, placenta previa, and premature
rupture of membranes for smokers and nonsmokers. The risk of
all these complications was higher for smokers throughout ges-
tation, but in all the differences were most significant in the
weeks of pregnancy from 20 to 32 or 36 weeks (87,146). The lower
limit of 20 weeks was built into the study design, which included
all single births of at least 20 weeks gestation (106,107).

These studies show that excess deaths of smokers’ infants are

218
612

TABLE 9.— Preterm births by maternal smoking habit: relative and attributable risks, derived from published

 

 

studies
Preterm Births* Relative
per 100 Risk Attributable
Smokers Total Births Smokers/Non- Risk
Study (proportion) Nonsmokers Smokers smokers %
Cardiff 465 6.7 9.2 1.36 14
Great Britain 274 4.7 6.9 1.47 ll
Montreal A382 V7 10.6 1.38 14
Ontario 435 7.4 10.1 1.36 14

 

*Cardiff and Ontario data are for <38 weeks. All others are for <37 weeks.

SOURCE: Andrews, J. (3), Campbell, J.M. (15), Fabia, J. (38), Meyer, M.B. (86), U.S. Department of Health, Education, and Welfare
(146).
80.0

      

 

 

4
60.0+ g
40.04 /

T ] = 95% Cl
20.04
10.0>F

-
6.07

Ss —

KS 407

oO -

c

S 2.0"

a

a

1+ Pack oo af
105 aa ceewaes
4 weet 1 Pack
0.6-- f° .
+ Fr
0.4 + Nonsmoker 4
0.27
o1t b+ +--+ ++ + +-+-+-+++
20 24 28 32 36 40 444+

Gestation: Weeks

FIGURE 10.—Percentage distribution by weeks of gestation of
births to nonsmokers, smokers of less than one
pack per day, and smokers of one pack per day or
more

SOURCE: Meyer, M.B. (82).

found mainly in the coded cause categories of “unknown” and
“anoxia” for fetal deaths, and in the categories of “prematurity
alone” and “respiratory difficulty” for neonatal deaths. This
finding indicates that the excess deaths result not from abnor-
malities of the fetus or neonate, but from problems related to

220
the pregnancy. Increasing levels of maternal smoking result in
a highly significant increase in the risks of placental abrup-
tions, placenta previa, bleeding early or late in pregnancy, pre-
mature and prolonged rupture of membranes, and preterm de-
livery, all of which carry high risks of perinatal loss. Although
there is little effect of maternal smoking on mean gestation, the
proportion of fetal deaths and live births that occur before term
increases directly with maternal smoking level. Up to 14 per-
cent of all preterm deliveries in the United States may be at-
tributable to maternal smoking. According to the results of one
large study, the most significant difference between smokers’
and nonsmokers’ risk of perinatal mortality and pregnancy
complication occurs at the gestational ages from 20 to 32 or 36
weeks.

These findings lead to the conclusion that maternal smoking
can be a direct cause of fetal or neonatal death in an otherwise
normal infant. The immediate cause of most smoking-related
fetal deaths is probably anoxia, which can be attributed to pla-
cental complications with antepartum bleeding in 30 percent or
more of the cases. In other cases, the oxygen supply may simply
fail from reduced carrying capacity and reduced unloading
pressures for oxygen caused by the presence of carbon
monoxide in maternal and fetal blood. Neonatal deaths occur as
a result of the increased risk of early delivery among smokers,
which may be secondarily related to bleeding early in preg-
nancy and premature rupture of membranes (146).

Long-Term Morbidity and Mortality

Studies of infant and child morbidity and mortality by the
mother’s smoking habits usually cannot distinguish between
the effects of smoking during pregnancy and the effect of the
infant’s or child’s passive exposure to cigarette smoke after
birth. Several studies have found that hospitalization rates for
pneumonia and bronchitis were higher during the first year of
life for infants of smoking mothers (20,21,53). Rates in children
were higher if the smoking parents also had cough and phlegm.
Harlap and Davies found that the risk of contracting
pneumonia or bronchitis in the first year of life more than dou-
bled if the parents smoked more than 24 cigarettes a day (53).

A unique and important study of morbidity and mortality in
smokers’ and nonsmokers’ children up to the age of five has now
been published by Rantakallio (119). The experience up to age 5
of over 12,000 children born in 1966 in Northern Finland, com-
prising 96 percent of all births in two provinces, was ascertained
through hospital and death records and questionnaires. Smok-

221
Nonsmokers Smokers

     
 

 

Total Births 27,420 21,465
Total Deaths 634 624
Probability of Death .023 .029
0.1
0.08
g 9.06 1= 95% CI
& 0.04
a
ro
x 0.02
£
©
a 0.01
2 0.008 cag DmOkers
= 0.006 i “eretteneonk,
2 -0.004
a
9
* 0.002
0.001
Totai Deaths —— (263) (198) (121) (110) (152) (149) (187) (78)
Smokers and p—+-—-}—+—+- +} +--+} —+- +--+ + 4
Nonsmokers 20 24 28 32 36 40 42+

Gestation: Weeks

FIGURE 11.—Probability of perinatal death for smoking and
nonsmoking mothers, by period of gestational age
(bars show 95% confidence intervals)

SOURCE: Meyer, M.B. (87).

ing was rare in this population, and the smokers tended to be
young and otherwise healthy. Fourteen percent of pregnant
women smoked fewer than 10 cigarettes per day (mean number
after the second month of pregnancy 3.9) and 3 percent smoked
more than 10 cigarettes per day (mean number 12.2); the re-
maining 83 percent of the population were nonsmokers. It was
therefore possible to remove the usual problems of confounding
variables by close individual matching of 1,750 smokers to
nonsmoking “controls”. Matching factors included marital
status, maternal age within 2 years, and place of residence, with
the latter category including many socioeconomic variables to
equalize the probable use of medical facilities and other dif-
ferences. Although the author states that perinatal mortality
did not show a statistically significant increase for smokers,

222
rates were 24 per thousand for controls, 26 per thousand for
light smokers, and 33 per thousand for “heavy” smokers (de-
fined as smoking 10 plus cigarettes per day). These rates are
similar to those found in other studies in which differences were
statistically significant. Postneonatal mortality, from 28 days to
5 years, was higher for smokers’ children with rates of 11.1 and
3.9 per thousand for smokers’ and nonsmokers’ children respec-
tively. Overall death rates of 24.7 per thousand births in smok-
ing women and 16.5 per thousand births in nonsmoking women
were reported for children under the age of 5, of which 12.6 and
8.8 were neonatal.

In addition, the children of the smokers were hospitalized
more frequently, had more visits to doctors, and had longer av-
erage durations of hospital stays than children of nonsmokers.
Respiratory diseases caused significantly more hospitalizations
among smokers’ children. It is of great interest that the chil-
dren born to a subgroup of women who stopped smoking during
the last 3 months of pregnancy showed no increase of post-
neonatal mortality or morbidity up to the age of 5, compared
with controls. However, these women had been very light smok-
ers before quitting. Table 10, derived from Rantakallio’s study,
shows that the various outcomes measured show increasing
rates of morbidity and mortality with increasing levels of smok-
ing. However, it may not be possible to distinguish between the
adverse effects of maternal smoking during pregnancy and the
adverse effects on infants and children exposed to cigarette
smoke in the home, because women who smoked during preg-
nancy probably also continued to smoke after pregnancy.

Because of the known carcinogenic potential of tobacco smoke
and the evidence that benzo(a)pyrene reaches the placenta,
Neutel and Buck investigated the relationship of maternal
smoking during pregnancy to the incidence of cancer in children
aged 7 to 10. A combined population of 89,302 births from the
Ontario Perinatal Mortality Study and the British Perinatal
Mortality Survey was used as a base population for a prospec-
tive study in which 65 cancer deaths and 32 cancer survivors
were identified. For cancer of all sites, the children of smokers
had a relative risk of 1.3, with 95 percent confidence limits of 0.8
to 2.2. A dose-response relationship was not observed. The num-
bers were not large enough to determine significant differences
by site. Excess cancer rates for children of mothers who smoke
and a possible dose-related progression were concentrated at
ages 0 to 24 months, but these rates were based on small num-
bers of cases. The authors conclude that “although a significant
excess is not demonstrable, a doubling of the cancer risk for
children of smokers cannot be ruled out.” Their equivocal re-

223
FSS

TABLE 10.—Long term effects of morbidity and mortality by level of maternal smoking

 

 

 

 

 

 

 

A. Mortality
Nonsmokers Light Smokers Heavy Smokers
Control 1 Control 2 (1-10 per day) (10+ per day)
Number of children 1300 258 1302 252
Doctor visits per child
(mean number) 71 61 76 83
Hospitalizations per child
(mean number) 19 15 22 .39
<Age 1 14 .08 17 30
Age 1-5 15 17 .22 .25
B. Perinatal and postneonatal mortality (28 days to 5 years) per 100 births, by maternal smoking
Nonsmokers Smokers
Control Light Total Heavy
Total births number 1844 1844
Perinatal mortality per 1,000 births 23.9 25.7 26.0 32.6
Postneonatal mortality 3.9 111
All mortality per 1,000 live births 16.5 24,7

 

SOURCE: Rantakallio, P. (119).
sults were reported to encourage other workers to add to the
data (99). This should certainly be done, with particular empha-
sis on the first 2 years of life.

Rantakallio, et al. also analyzed the use rates of ophthal-
mological services in their follow-up study of approximately
12,000 children, relating these rates of prenatal factors ascer-
tained during pregnancy. The incidence of squint among smok-
ers’ children was 22.5 per thousand, compared with 11.5 per
thousand among the children of matched, nonsmoking controls
(p < .05). On the other hand, rates of dacryostenosis and of other
congenital ocular malformations were higher among the chil-
dren of controls. The authors state that squint was inversely
correlated with birth weight and was more common among chil-
dren with other diseases, especially nervous or mental diseases
(121).

SUDDEN INFANT DEATH SYNDROME

Maternal smoking habits have been ascertained in several
studies of the sudden infant death syndrome (SIDS). In all of
these, an association has been found between maternal smoking
during pregnancy and the incidence of sudden infant death.
Steele and Langworth, in a study of 80 cases, each with two
matched controls, which were traced back to the Ontario
Perinatal Mortality Study population of 1960-61, found that
sudden infant deaths were strongly associated with the fre-
quency and level of maternal smoking during pregnancy
(p < .001). Thirty-nine percent of the cases were nonsmokers ver-
sus 60 percent of controls; 36 percent of the cases and 27 percent
of the controls smoked less than a pack per day; 24 percent of
the cases and 10 percent of the controls smoked a pack per day
or more. The habits of the remaining 1 to 2 percent of mothers
were unknown (139).

Bergman and Wiesner studied 56 families who lost babies to
the sudden infant death syndrome and 86 control families. They
reported that a higher proportion of SIDS mothers smoked dur-
ing pregnancy than controls (61 percent versus 42 percent),
more smoked after pregnancy (59 percent versus 42 percent),
and SIDS mothers smoked a significantly greater number of
cigarettes than controls. These authors indicate that exposure
to cigarette smoke (passive smoking) appears to enhance the
risk for SIDS for reasons not yet known (8). However, whether
prenatal or postnatal exposure is more important cannot be de-
termined.

Naeye, et al., in their analysis of 125 SIDS victims from the
population of the Collaborative Perinatal Project of the

225
NINCDS, stated: “The gestations that produced the SIDS vic-
tims were characterized by a greater frequency of mothers who
smoked cigarettes and had anemia” than was true for the whole
population of 53,721 infants or for a set of 375 controls matched
for important factors (96). Rhead, commenting on studies pub-
lished to date which demonstrate an increased incidence of
maternal cigarette smoking in SIDS, states: “It is now ... clear
that maternal cigarette smoking contributes to an infant’s risk
of dying from SIDS” (123).

Analysis of data from the prospective study of 19,047 births to
members of the Kaiser Foundation Health Plan (1960-1967)
also showed a strong association of SIDS with maternal smok-
ing. In the SIDS group, 70.6 percent of mothers smoked during
pregnancy, compared with only 35.3 percent of mothers of
babies who did not die of SIDS (p < .001). The relative risk of
SIDS for smokers versus nonsmokers was 4.4 (67).

Mechanisms

Clues to the mechanisms by which smoking may increase the
risk of pregnancy complications are available from pathological
and physiological studies of placentas, membranes, blood ves-
sels, circulatory patterns, and serum levels of substances im-
portant for cell and tissue integrity. For example, it is possible
that placental changes in smokers that serve as adaptations to
the hypoxic effects of carbon monoxide may also increase the
risk of placental complications.

Christianson has reported findings from carefully stand-
ardized gross examinations of 7,651 placentas from smokers and
nonsmokers. These examinations revealed that smokers’
placentas were thinner and larger in their minimum diameter
than those of nonsmokers. This significant change effectively
increased the surface area of the smokers’ placentas and must,
therefore, have increased their area of attachment to the
uterine wall. The distance from the edge of membrane rupture
to the placental margin was also less for smokers, and signifi-
cantly more smokers than nonsmokers had zero distance, which
is consistent with the diagnosis of placenta previa (19). These
findings suggest a possible mechanism to account for the signif-
icant dose-related increase in the frequency of the clinical diag-
nosis of placenta previa that accompanies maternal smoking
(86). A similar increase in this condition occurs with increasing
altitude (75).

Christianson’s study also revealed that smokers had signifi-
cantly more placental calcification, primarily of the maternal
surface, and patchy subchorionie fibrin, as shown in Table 11.

226
Loe

TABLE 11.—Selected results of gross examinations of placentas from smokers and nonsmokers

 

Percent of Placentas with Stated Condition

 

 

 

 

White Black
Nonsmoker Smoker Nonsmoker Smoker
N=3,461 N=2,239 P N=1,300 N=652 P
Calcification 49.5 60.8 <.0001 43.5 59.0 <.0001
Patchy Subchorionie Fibrin 26.2 35.3 <.0001 30.8 37.0 <.01
Infarcts 24.6 22.3 <.05 14.4 14.5 NS
Thickness (mean cm) 2.16 2.12 <,001 2.11 2.06 <.01
Ratio of smallest diameter to thickness 8.19 8.40 <.001 8.39 8.68 <.01
Shortest distance, edge of rupture of
membranes to placental margin (mean cm) 4,32 4.09 <.025 5.08 4.83 NS
Percent with zero distance 25.6 27.9 NS 18.6 20.3 <.05

 

SOURCE: Christianson, R.E. (19).
These changes are characteristic of maturation and aging of the
placenta and occur as normal gestation proceeds; however, they
occurred earlier in smokers than in nonsmokers (19). This find-
ing is compatible with other manifestations of accelerated aging
reported to be associated with cigarette smoking (28,108).

Asmussen compared placental vessels in smoking and
nonsmoking mothers by electron microscopy. In the smoking
group these vessels were characterized by subintimal edema
with destruction of the intimal elastic membranes, a marked
decrease in collagen content, and proliferation of myocytes.
Asmussen postulated that similar damage may occur in the
fetal and infant vascular system. To what extent such changes
may predispose to the subsequent development of vascular dis-
ease remains unknown. The author regarded most of the
changes observed in smokers’ vessels as degenerative, but men-
tioned the possibility that the thickening of the basement mem-
brane observed in smokers might be an attempt at repair (4,5).
Naeye (93) has described an increased frequency of placental
microscopic lesions associated with smoking. These include:
cytotrophoblastic hyperplasia, obliterative endarteritis,
stromal fibrosis, and small villous infarction. Smokers also
demonstrated an increased frequency of necrosis and inflam-
mation in the decidua capsularis and in the decidua basalis at
the placental margin. Placental features observed less fre-
quently in smokers’ placentas were excessive syncytial knots
and various thrombotic phenomena.

Naeye found increasing placental enlargement with smoking
level, accompanied by decreasing birth weight and a consequent
increase in the placental ratio. The author stated that “as smok-
ing increased, placentas developed microscopic lesions charac-
teristic of underperfusion of the uterus.” Naeye’s data showed
positive trends with maternal smoking level for some findings
and negative trends for others (93). Many of the changes cited
were of low frequency in all groups, and no clear pattern of
possible mechanisms of action emerged.

Other studies that may shed light on these complex interrela-
tionships include the report by Goujard and colleagues that
heavy alcohol consumption as well as smoking contributes to
the risk of stillbirth caused by abruptio placentae. In a prospec-
tive survey of 9,169 women, the risk of stillbirth was 21 per 1,000
in smokers who were light or nondrinkers, 20 per 1,000 in
nonsmoking drinkers of 45 ml equivalents or more of absolute
alcohol per day, and 8.5 per thousand for nonsmokers who drank
less than 45 ml per day. The small number of smokers who were
also heavy drinkers had stillbirth rates of 50.5 per 1,000 (95
women with 5 stillbirths). The proportions of these deaths that

228
were attributable to abruptio placentae increased with smoking
and with drinking, based on data unadjusted for the effects of
age, parity, and other factors (122).

More research is needed to define possible pathways of action
by which the active components of cigarette smoke affect preg-
nancy complications that may lead, in turn, to fetal death or to
preterm birth with or without survival.

Experimental Studies

TOBACCO SMOKE

Tobacco smoke contains more than 2,000 compounds includ-
ing: carbon monoxide, oxides of nitrogen, ammonia, polycyclic
aromatic hydrocarbons, hydrogen cyanide, vinyl chloride, and .
nicotine. For the pregnant woman and fetus the most important
- of these appear to be nicotine, carbon monoxide, and the
polycyclic aromatic hydrocarbons.

NICOTINE

The effect of nicotine on sympathetic and parasympathetic
ganglia, skeletal muscles, and the central nervous system is
similar to that of acetylcholine. At all three sites it first stimu-
lates, then depresses. Minute doses of nicotine stimulate the
chemoreceptors of the carotid and aortic bodies, causing reflex
hypertension. Nicotine also releases epinephrine from the ad-
renal medulla, thereby producing cardiovascular changes.
Thus, it can produce widely differing effects depending upon the
dosage and the particular site that is most sensitive to stimula-
tion.

Nicotine rapidly crosses the placenta to affect the fetus (142).
Relatively mature rhesus monkey fetuses respond to nicotine
infusion with a rise in blood pressure, bradycardia, acidosis,
hypercarbia, and hypoxia (141). Maternal nicotine administra-
tion in rats also has been shown to affect the fetal central ner-
vous system and its response to electrical stimulation during
the newborn period (56,78).

Quigley, et al. noted that in moderate to heavy smokers, after
84 weeks gestation, smoking two cigarettes in 10 minutes was
associated with a 60 percent increase in maternal plasma
norepinephrine and epinephrine and a 20 percent increase in
serum cortisol concentrations (118). These changes also were
associated with an increase in maternal pulse and blood
pressure. Lehtovirta and Forss measured changes in placental
intervillous blood flow using the 133 xenon method (66). Im-
mediately after smoking, intervillous flow decreased 22 percent.

229
These data correlate with the studies of Resnik, et al. (122),
showing nicotine-induced increases in catecholamines and de-
creased uterine blood flow in sheep, and of Haberman, demon-
strating decreased uteroplacental blood flow in women, using
thermography (48).

Sastry and his colleagues have carried out a series of studies
on the effect of nicotine on the human placenta. Nicotine added
to a calcium-containing medium caused a 33 percent increase in
the rate of acetylcholine release from isolated placental villi
(131). The authors postulated that this effect could account for
the decrease in placental amino acid transport (125,154) pro-
duced by nicotine-mediated cholinergic blockade (105). Rowell
and Sastry also demonstrated that nicotine caused a 41 percent
decrease in uptake of alpha amino isobutyric acid in an experi-
mental placental system (126). Their studies indicate that under
normal circumstances acetylcholine exhibits a muscarinic ef-
fect facilitating placental amino acid uptake. Nicotine blockade
of the facilitating effects of acetylcholine on amino acid uptake
may result in fetal growth retardation (126). These data agree
with the 1977 work of Crosby, et al. in humans (26).

Nicotine injection in rats results in prolonged gestation with
lower than normal newborn weights. A possible cause of this
prolonged gestation is nicotine-induced delay in ovum implan-
tation. Yoshinaga, et al. tested this hypothesis, administering
7.5 mg nicotine tartrate twice daily from the morning of proes-
trus until the day of sacrifice on days 1 to 5 of pregnancy (161).
The nicotine-injected animals demonstrated a delay of about 12
hours in ovum cleavage from the two- to the four-cell stage, and
each step of development after the four-cell stage was thereby
delayed. In addition, ovum entry into the uterus, blastocyst
formation, shedding of the zona pellucida, and implantation
were delayed. Nicotine injection also was associated with a
“crowding” of implantation sites toward the tubal ends of the
uterine horns.

During the preimplantation period the serum concentrations
of progesterone, luteinizing hormone, and prolactin were lower,
while the concentrations of estrogen and follicle stimulating
hormone were higher than in control animals. These workers
suggested that the delayed ovum implanation followed a de-
layed increase in progesterone secretion required to prepare
the uterus for the implanting blastocyst, and that the delayed
progesterone secretion results in part from nicotine-induced
disturbed hypothalamus pituitary balance.

Hamosh, et al. observed that, while administration of 100 mg
kg-'day~' nicotine to pregnant rats from day 14 gestation onward
failed to affect the mother or fetus, administration of 1 mg kg" ‘day”’

230
(a dose “comparable” to that of a 20 cigarette-per-day smoker) re-
sulted in a decrease in litter size and an increase in stillbirth rate.
Although administration of 100 mg kg~'day“' nicotine failed to affect
newborn birth weight by 12 days of age continued maternal nicotine
administration resulted in a 9 percent decrease in body weight and a
40 percent decrease in weight of the stomach contents. These de-
creases presumably resulted from lower milk production by the
nicotine-treated animals (51).

CARBON MONOXIDE (CO)

Carboxyhemoglobin concentrations of 4 to 5 percent are as-
sociated with numerous physiologic alterations in adults.
Cigarette smoking raises the carboxyhemoglobin concentration
4 to 5 percent per pack smoked per day. Although CO diffuses
across the placenta relatively slowly [ the half time equals 1.5 to
2 hr (72)], fetal carboxyhemoglobin concentrations reflect those
of the mother, and under steady state conditions are 10 to 15
percent higher than maternal levels (71). Elevated car-
boxyhemoglobin concentrations in the fetus are associated with
decreased fetal blood oxygen tensions. These decreased oxygen
tensions are associated with a redistribution of fetal blood flow
to the brain, heart, and adrenal glands (146).

Carboxyhemoglobin concentrations have been described
under several conditions of pregnancy. Davies, et al. (31) com-
pared carboxyhemoglobin concentrations and “available oxy-
gen” (a function of O, content in ml dl blood-') in women who
stopped smoking for 48 hours during the last trimester of preg-
nancy, with women who did not stop smoking, and with
nonsmoking women. In those women who stopped smoking, car-
boxyhemoglobin concentrations decreased. “Available oxygen”
increased about 8 percent due both to an increase in functioning
hemoglobin and a shift in the oxyhemoglobin saturation curve;
this increase in “available oxygen” should contribute to im-
proved fetal oxygenation.

Exposure of rabbits (6) and rats (39) to CO during gestation
resulted in decreased fetal weights and increased perinatal
mortality. Such CO-exposed newborn animals showed less activ-
ity as well as decreased lung weights and decreased concentra-
tions of brain protein, DNA, and the neurotransmitters
norepinephrine and serotonin (45). Cellular hypoxia is the final
common pathway mediating the adverse effect of CO on the
developing fetus.

Recent experimental studies have explored various aspects of
CO-induced biochemical changes in the fetus and the newborn.
Newby, et al. demonstrated a persistent effect of CO exposure in
8- and 18-day-old rats following a single 5-hour exposure to 1,500

231
120—
@—=8 CO 9 n=8
@-=-@ CO FT n=15
Om=Q CONT 2 n=9
100 F Oseep CONT oN =9

 

 

 

S 80b

°

>

2

@ 60F

Co

2

z

<< 40F

20F

L i i i
1 2 4 16

Intensity (Candlepower/9.4 x 10‘)

FIGURE 12.—Effect of prenatal CO upon peak-to-peak
amplitudes of the first positiive to the first
negative component of the flash evoked potential
recorded from the rat visual cortex. Vertical bars
represent + standard error of the means

SOURCE: Dyer, R.S. (36).

parts per million (0.15 percent CO) (100). In these animals alpha
methyl-p-tyrosine, a potent inhibitor of the enzyme tyrosine
hydroxylase, was injected 1 hour before the CO exposure, and
the extent of catecholamine depletion was taken as an index of
the rate of catecholamine turnover. CO-treated rats showed in-
creased steady state dopamine concentrations with decreased
rates of dopamine turnover. In addition, the CO effect on
dopamine turnover persisted for at least 3 to 6 weeks after a
single exposure of 8-day-old rats. There was no CO effect on
norepinephrine concentrations or turnover rates, and the effect
was not produced in rats exposed to 8 percent oxygen instead of
carbon monoxide. This is consistent with the data of Coyle and
Campochiaro, which indicates that a maturational event occurs
in the striatum of the 8-day-old rat (25). Whether this event
represents the age of functional maturity, initiation of

232
dopaminergic transmission, or maturation of cholinergic inter-
neurons is unclear.

Prenatal CO exposure may have long-term consequences on
central nervous system function. For instance, Dyer, et al. ex-
posed female Long-Evans hooded rats to 150 ppm CO through-
out pregnancy (36). At birth the litters and mothers were placed
in room air without CO. On day 65 electrodes were placed in the
young rats’ skulls, and 2 weeks later visually evoked potentials
were recorded. Figure 12 illustrates the effect of such prenatal
exposure on the peak-to-peak amplitudes of the P1-N1 (first pos-
itive to first negative) component of the visual evoked potential
from the cortex. Females showed a significant increase in P1-N1
amplitude at each of four flash intensities. Although the exact
nature of this amplitude increase could not be determined, it
suggests altered cell populations at the retinal, geniculate, and
cortical levels, and may represent impaired inhibitory mecha-
nisms, rendering other neurons more excitable.

The question of the posible teratogenicity of CO has never
been resolved. Schwetz, et al. exposed mice to 250 ppm CO for 7
or 24 hours per day, from days 6 through 15 of gestation, and
rabbits to the same concentration from days 6 through 18 (137).
Blood carboxyhemoglobin concentration ranged from 10 to 15
percent. The fetuses of mice exposed to CO for 7 and 24 hours
per day were slightly heavier and lighter, respectively, than
those of the control animals. The only increase in teratogenic
effects were minor skeletal variants such as extra lumbar ribs
and spurs.

POLYCYCLIC AROMATIC HYDROCARBONS

The polycyclic aromatic hydrocarbons (PAH), such as ben-
zo(a)pyrene, are widely distributed mutagens and carcinogens.
These substances, produced by incomplete combustion of or-
ganic material, are important constituents of tobacco smoke.
Exposure of cells to PAH induces the enzyme, aryl hydrocarbon
hydroxylase. The inducibility of this enzyme system has been
used by some workers to demonstrate, indirectly, that ben-
z0(a)pyrene and other polycyclic hydrocarbons reach the
placenta and fetus.

The placental concentration of benzo(a)pyrene is highly corre-
lated with the amount which a pregnant woman smokes (97,
111). In pregnant rats exposed to this substance higher doses
were required to induce enzyme activity in the fetus as com-
pared with the dose required to stimulate placental enzyme ac-
tivity (153), suggesting that the placenta may protect the fetus
from these substances. However, the placenta is not imperme-

233
able to benzo(a)pyrene (134). The placenta is involved in com-
plex hormonal interrelations between mother and fetus, and
oxidative enzyme pathways in the placenta are important in
maintaining hormonal and nutrient balance for normal fetal
development. The hydroxylation of polycyclic hydrocarbons and
the active transport of various compounds by trophoblast cells
may share common enzyme systems. Thus, the induction of var-
ious enzymes by polycyclic hydrocarbons may interfere with
normal transport systems.

Another unanswered question concerns the carcinogenic risk
for progeny exposed in utero to polycyclic aromatic hydrocar-
bons. The offspring of mice that were injected with ben-
zo(a)pyrene late in gestation showed an increased incidence of
neoplasms of the lungs, liver, and mammary glands (101). Pel-
konen, et al. determined that placental aryl hydrocarbon hyd-
roxylase activity correlated closely with both the amount the
mother smoked and newborn weight (112). These authors
suggested that the placental concentration of this enzyme may
be used as a measure of fetal exposure to maternal cigarette
smoking. Vaught, et al. also reported much higher aryl hyd-
rocarbon hydroxylase activity in the placental microsomes of
smokers compared with nonsmokers (148).

Although currently available data do not allow a quantitative
assessment of the genetic risk to man from cigarette smoking,
such risk may occur since so many components of cigarette
smoke are mutagens (as well as carcinogens) (11). Male
cigarette smokers may have an increased number of abnormal
spermatozoa (150). Paternal and maternal chromosomal aber-
rations (103) and sister chromatid exchanges may be increased
in smokers (62). Because the proportion of smokers in the popu-
lation is so high (between 30 and 50 percent), even a relatively
weak mutagenic effect could have a significant effect on the
gene pool (11).

OTHER COMPONENTS

Cyanide, another constituent of cigarette smoke, may con-
tribute to retarded infant growth and increased perinatal mor-
tality. Smokers have increased levels of cyanide and thiocyan-
ate in body fluids. Serum concentrations of vitamin Biz, used in
cyanide metabolism, are decreased as well. Several workers
have recorded increased thiocyanate concentrations in both
women who smoke and in their fetuses (2,140,154). Pettigrew, et
al. compared cyanide and thiocyanate concentrations in smok-
ers and nonsmokers, matched for age, height, parity, and
socioeconomic status (116). Cyanide and thiocyanate concentra-

234
tions were two to four times greater in the blood and urine of
smokers and in the urine of smokers’ infants as compared with
controls. Meberg, et al. reported that thiocyanate concentra-
tions were correlated with cigarette consumption and inversely
correlated with birth weight (81).

Cadmium, another constituent of tobacco smoke, is concen-
trated in the placenta of smokers (124). Webster exposed preg-
nant mice to 10 to 40 ppm cadmium and noted an inverse corre-
lation between cadmium concentration and fetal weight (152).

Lauwerys, et al. examined the effects of epidemiology factors
on heavy metal and CO concentrations in the blood, placenta,
and fetus of smoking women (65). Cadmium concentrations in
maternal blood were twofold greater than concentrations in
fetal blood, suggesting that the placenta acts as a barrier to this
metal. They reported a correlation between maternal cadmium
and carboxyhemoglobin concentrations (13,65). They also found
that the cadmium concentration of smokers’ placentas was
about 25 percent greater than in a control group and that the
placental cadmium concentration exceeded that of maternal
blood about tenfold (124).

Fertility

Fertility results from the successful completion of a complex
step-wise process beginning with gametogenesis (sperm and egg
production), continuing through gamete release (ejaculation
and ovaluation), gamete interaction (fertilization), conceptus
transport through the fallopian tube into the uterus, and end-
ing with implantation of the embyro into the endometrial wall.
An adverse effect of smoking on any of these steps may impair
fertility.

SMOKING AND REPRODUCTION IN WOMEN

Several epidemiologic studies have suggested that smoking
decreases fertility in women (50,115,143,149). The retrospective
study of Tokuhata demonstrated that 21 percent of women who
regularly smoked cigarettes were infertile while only 14 percent
of those who never used tobacco regularly were infertile (148).
After several characteristics (cause of death, age at and year of
death, education, occupation and frequency of marriage as well
as husbands’ smoking habits, education and occupation) were
controlled, a 46 percent excess of infertility was found in women
who smoked.

In a study on the return of fertility after discontinuing con-
traception, Vessey, et al. found a suggested reduction in fertility
among women smoking 15 or more cigarettes per day (149). Pet-

235
tersson, et al. found a tendency toward a greater prevalence of
secondary amenorrhea among smokers (4.8/100 women) than
among nonsmokers (3.7/100 women) (115). Hammond found that
49 percent of the nonsmoking women between 40 and 49 years
had regular menses while only 40 percent of those smoking
more than one pack a day had a regular menses (50). Conversely
only 18 percent of nonsmokers had irregular menses while 24
percent of those smoking one or more packs of cigarettes per
day said they had irregular menses. Smoking women were also
more likely to have an unusual vaginal discharge and vaginal
bleeding than nonsmokers. Experimental studies have demon-
strated alterations in luteinizing hormone release and a de-
creased ovulatory response in rats exposed to tobacco smoke (76).

The effect of smoking on ovulation may result from direct
effects of nicotine on the hypothalamus or pituitary. This would
alter the release of gonadotropin releasing hormones from the
hypothalamus or impair the pituitary response to releasing
hormones.

SMOKING AND AGE OF MENOPAUSE

Substantial data demonstrate that smoking lowers the age of
spontaneous menopause (7,9,27,58,68,69). The recent study by
Jick, et al. revealed a dose dependent decrease in the age of
menopause in smoking women who live in Sweden and the
United States (58). The median age of menopause in nonsmok-
ers was 50; among those smoking one-half pack/day it was 49; in
those smoking 1 or more pack/day, it was 48. Similar studies
have been published indicating an earlier onset of menopause in
smoking women in the United States (29), in England (7), in
Germany (9), and in Sweden (68,69). The mechanism of early
menopause in smokers may be related to ovotoxins in cigarette
smoke (37) or to toxic alterations in the hormonal regulatory
mechanisms controlling the hypothalamic- pituitary-—ovarian
axis (76). One group of ovotoxins may be polycyclic aromatic
hydrocarbons which have been demonstrated to be metabolized
by ovarian enzymes to toxic products which destroy oocytes in
rat and mouse ovaries (47,79).

Evidence collected by Daniell (29) and Lindquist (68) suggest
that the earlier menopause of smokers is not related to weight
differences between smokers and nonsmokers but is a direct
result of some component of cigarette smoke.

SMOKING AND REPRODUCTION IN MEN

Spermatogenesis, sperm morphology, sperm motility
(17,64,133,150) and androgen secretion (12,113) appear to be al-

236
tered in men who smoke. Viczian (150) has demonstrated de-
creased sperm density, a cigarette-dose-dependent decrease in
sperm motility, and a cigarette-dose-dependent increased ab-
normal sperm morphology among smokers.

In metabolic studies of alcoholic men admitted to a clinical
research center, an inverse relationship between number of
cigarettes smoked and reduction of testosterone levels was seen
(113). Briggs (12) has reported lower plasma testosterone among
smoking men compared to matched nonsmoking controls and
has shown that cessation of smoking resulted in increased tes-
tosterone levels in these men. Wintermitz and Quillen (158) in a
study on the acute effects of smoking in men demonstrated in-
creases in plasma cortisol and growth hormone during the
smoking period. Growth hormone returned to the presmoking
level shortly after the smoking period, and cortisol fell gradu-
ally to the presmoking level by 90 minutes after cessation of
smoking. Urinary catecholamines were higher on the smoking
day than the nonsmoking day. No acute changes were observed
in gonadotropins or testosterone in these men. These studies
demonstrate stimulatory effects of smoking on growth hormone
and cortisol.

Studies in experimental animals have also shown that to-
bacco smoke impairs spermatogenesis (37,151). Smoking also
lowers sexual activity in male rats (18).

These data suggest two possible mechanisms of action of
smoking on male reproduction. A component of cigarette smoke
may have a direct action on the testes, disrupting gamete pro-
duction. This would be consistent with the suggested effect of
cigarette smoke on the ovary. In addition, cigarette smoke is
known to contain compounds which are mutagenic (59). Alter-
natively, cigarette smoke may interfere with the regulatory
mechanisms controlling the hypothalamic-pituitary-testicular
axis.

FERTILIZATION AND CONCEPTUS TRANSPORT

The effect of smoking on sperm-egg interaction (fertilization)
has not been studied in mammalian species. Evidence from
sub-mammalian species demonstrates that nicotine promotes
polyspermy (the entrance of more than one sperm into the oo-
cyte) (73). Polyspermy would result in abnormal embryonic de-
velopment and early abortion, which is one known effect of
smoking (60).

The effect of smoking on conceptus transport in the fallopian
tube or entry into the uterus is unknown; however, some evi-
dence suggests that smoking can alter the amplitude and tone

237
of contractions measured during the Rubin uterotubal insu ffla-
tion test (a combined measure of uterotubal junction and tubal
patency) (98), suggestive that smoking may alter conceptus
transport in the fallopian tube or its entrance into the uterus.

In summary, cigarette smoking appears to exert an adverse
effect on fertility. Further studies are needed to quantify the
effects, identify etiologic agent(s), and define the mechanism(s)
of action.

Summary

1. Babies born to women who smoke during pregnancy are, on
the average, 200 grams lighter than babies born to comparable
nonsmoking women.

2. The relationship between maternal smoking and reduced
birth weight is independent of all other factors that influence
birth weight including race, parity, maternal size,
socioeconomic status, and sex of child; it is also independent of
gestational age.

3. There is a dose-response relationship between maternal
smoking and reduced birth weight; the more the woman smokes
during pregnancy, the greater the reduction in birth weight.

4, If a woman gives up smoking early during pregnancy, her
risk of delivering a low-birth-weight baby approaches that of a
nonsmoker.

5. The ratio of placental weight to birth weight increases with
increasing levels of maternal smoking, reflecting a considerable
decrease in mean birth weight and a slight increase in mean
placental mass; this may represent an adaptation to relative
fetal hypoxia.

6. The pattern of fetal growth retardation that occurs with
maternal smoking is a decrease in all dimensions including body
length, chest circumference, and head circumference.

7. Maternal smoking during pregnancy may adversely affect
the child’s long-term growth, intellectual development, and be-
havioral characteristics.

8. Maternal smoking during pregnancy exerts a direct
growth-retarding effect on the fetus; this effect does not appear
to be mediated by reduced maternal appetite, eating or weight
gain.

9. The risk of spontaneous abortion, fetal death, and neonatal
death increases directly with increasing levels of maternal
smoking during pregnancy; interaction of maternal smoking
with other factors which increase perinatal mortality may re-
sult in an even greater risk.

10. Excess deaths of smokers’ infants are found mainly in the
coded cause categories of “unknown” and “anoxia” for fetal

238
deaths, and the categories of “prematurity alone” and “respira-
tory difficulty” for neonatal deaths; this suggests that the ex-
cess deaths are due to problems of the pregnancy, rather than
to abnormalities of the fetus or neonate.

11. Increasing levels of maternal smoking result in a highly
significant increase in the risk of abruptio placentae, placenta
previa, bleeding early or late in pregnancy, premature and pro-
longed rupture of membranes, and preterm delivery—all of
which carry high risks of perinatal loss.

12. Although there is little effect of maternal smcking o.:.
mean gestation, the proportion of fetal deaths and live births
that occur before term increases directly with maternii smok-
ing level. Up to 14 percent of all preterm deliveries in the United
States may be attributable to maternal smoking.

13. The incidence of preeclampsia is decreased among women
who smoke during pregnancy; however, if preeclampsia devel-
ops in a smoking woman, the risk of perinatal mortality is
markedly increased compared to preeclamptic nonsmokers.

14. An infant’s risk of developing the “sudden infant death
syndrome” is increased by maternal smoking during pregnancy.

15. There are insufficient data to support a judgement on
whether maternal and/or paternal cigarette smoking increases
the risk of congenital malformations.

16. Infants and children born to smoking mothers may expe-
rience more long-term morbidity than those born to nonsmok-
ing mothers; however, studies usually cannot distinguish be-
tween the effects of smoking during pregfancy and the effects
of the infant’s or child’s passive exposure to cigarette smoke
after birth.

17. Studies in women and men suggest that cigarette smok-
ing may impair fertility.

18. Experimental studies on tobacco smoke, nicotine, carbon
monoxide, polynuclear aromatic hydrocarbons, and other con-
stituents of smoke help define pathways by which maternal
smoking during pregnancy may exert its aforementioned ef-
fects.

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247
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248

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the Assistant Secretary for Health, Office on Smoking and Health.
DHEW Publication No. (PHS) 79-50066, 1979, 1251 pp.

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1963.

249
PEPTIC ULCER DISEASE.
PEPTIC ULCER DISEASE

There is little information dealing specifically with the rela-
tionship between smoking and peptic ulcer disease in women.
The data which are available suggest the same trend toward
higher prevalence of peptic ulcer disease among women who
smoke as is observed among men who smoke. Table 1, extracted
from the 1979 Surgeon General’s Report, shows that the preva-
lence of “peptic ulcer” in female smokers was higher in two out
of three studies of women, which showed a twofold or 1.6 fold
higher prevalence (7). The one study which failed to demon-
strate an increased prevalence was conducted in rural Poland
where very few women smoke (only 7 percent) (6). The median
ratio of smoking ulcer patients to nonsmoking ulcer patients
has been reported to be 1.7 for men (7). Thus, women smokers
seem to show greater susceptibility to ulcer disease than do
nonsmokers.

The population of women with ulcers contains a greater pro-
portion of smokers than does the group of women without ul-
cers. Alp et al. performed a retrospective analysis of 638 pa-
tients with gastric ulcer, 230 of whom were women (2). There
were 1.9 times as many smokers in the group of women ulcer
patients as in an age-matched control group. However, even
among the ulcer patients, only 39 percent were smokers. In a
smaller series of 31 female patients admitted to hospitals with
hemorrhage from, or perforation of, gastric or duodenal ulcers,
the prevalence of smoking was 26 percent in both ulcer patients
(8/31) and controls (8/31) (1).

In a report examining the effect of smoking on healing rates
of gastric and duodenal ulcers, Doll et al. studied 92 women with
gastric ulcer and 54 women with duodenal ulcer (3). Smoking
was 1.6 times more common in women gastric ulcer patients as
in controls matched for age and place of residence (p < 0.01).
There was no significant excess in the proportion of smokers in
the group with duodenal ulcer. The effect of smoking on healing
rate was reported for men and women grouped together, so no
conclusion regarding specific effects on women is possible.

Although some studies of etiological factors in smoking-
induced ulcer disease (gastric acid secretion, pancreatic secre-
tion, etc.) have included women, the number of women has been
small, or the data from women have not been presented sepa-
rately.

In summary, the evidence currently available documents an
increased prevalence of peptic ulcer disease in women who
smoke. No data are available concerning specific effects of
smoking in women on gastric acid secretion, gastric emptying,

253
TABLE 1.— Prevalence of peptic ulcer in smoking and
nonsmoking women (number per 100)

 

 

No.

with
Reference ulcers Smokers Nonsmokers Ratio*
Higgins, M.W.
(1966) (5) 47 2.8 1.4 2.0
Friedman, G.D.
(1974) (4) 1092 6.3 3.9 1.6
Jedrychowski, W.
(1974) (6) 26 0.8 1.3 0.6

 

. Prevalence among smokers
*Ratio = &

Prevalence among nonsmokers

pancreatic secretion, or other processes which might be in-
volved in the pathogenesis of peptic ulcer disease.

Summary

The 1979 Surgeon General’s Report included evidence that
cigarette smoking in males was significantly associated with
the incidence of peptic ulcer diease and increased the risk of
dying from peptic ulcer disease by approximately two-fold. The
effect of smoking on pancreatic secretion and pyloric reflux
demonstrated among men may provide a mechanism by which
peptic ulcers develop.

1. Female smokers show a prevalence of peptic ulcer higher
than that of nonsmokers by approximately two-fold.

2. The effect of cessation on healing is not known.

References

(1) ALLIBONE, A., FLINT, F. J. Bronchitis, aspirin, smoking and other
factors in the aetiology of peptic ulcer. Lancet 2: 179-182, July 26, 1958.

(2) ALP, M. H., HISLOP, I. G., GRANT, A. K. Gastric ulcer in south Au-
stralia 1954-1963. 1. Epidemiological factors. Medical Journal of Au-
stralia 2: 1128-1132, December 12, 1970.

(3) DOLL, R., JONES, F. A., PYGOTT, F. Effect of smoking on the produc-
tion and maintenance of gastric and duodenal ulcers. Lancet 1: 657-
662, March 29, 1958.

G4) FRIEDMAN, G. D., SIEGELAUR, A. B., SELTZER, C. C. Cigarettes,
alcohol, coffee and peptic uleer. New England Journal of Medicine
290(9): 469-473, February 28, 1974.

(5) HIGGINS, M. W., KJELSBERG, M. Characteristics of smokers in
Tecumseh, Michigan. II. The distribution of selected physical meas-
urements and physiological variables and the prevalence of certain

254
diseases in smokers and nonsmokers. American Journal of Epidemiol-
ogy 86: 60-77, 1967.

(6) JEDRYCHOWSKI, W., POPIELA, T. Association between the occur-
rence of peptic ulcers and tobacco smoking. Public Health London
88(4): 195-200, 1974.

(7) U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE.
Smoking and Health: a Report of the Surgeon General. Department of
Health, Education, and Welfare, Public Health Services, Office of the As-
sistant Secretary for Health, Office on Smoking and Health. DHEW Pub-
lication No. PHS) 79-50066, 1979, 1251 pp.

255
INTERACTIONS OF SMOKING WITH
DRUGS, FOOD CONSTITUENTS,
AND RESPONSES TO DIAGNOSTIC

TESTS.
INTERACTIONS OF SMOKING WITH DRUGS, FOOD
CONSTITUENTS, AND RESPONSES TO DIAGNOSTIC TESTS

Since most published studies investigating the effect of
cigarette smoking on measures of health were performed in
mixed populations, it is difficult to demonstrate specific factors
applicable only to women. Neither the differences between men
and women regarding the metabolism and action of drugs nor
the pharmacological basis for differences between smokers and
nonsmokers is well understood. The same is also true of the
observed variations in laboratory values and nutritional needs.
Thus, the associations for women between smoking, drugs, var-
iations in clinical laboratory values, and nutritional needs re-
quire further study.

Women Smokers and Nonsmokers and Drug Consumption
Patterns

The drug consumption pattern of women as compared to men
has been studied by a number of investigators using different
methodologies. The results consistently show that women are
prescribed and take more prescription drugs than men (7,17). In
one study where 1-year drug histories were used, the percent-
age of women using prescription drugs was 29 percent as com-
pared to 13 percent for men (17). Another study which examined
only drugs consumed within 48 hours of the interview showed
that 60.2 percent of the women had taken medication compared
to 41.8 percent of the men (7). The two studies cited are unique
in the realm of drug usage studies because they measure actual
self-administration of drugs rather than counting physician
prescriptions or pharmacy dispensing patterns. Unfortunately,
neither of these studies quantified information according to
whether the subjects were smokers or nonsmokers.

Other reports show that smokers tend to use more drugs, es-
pecially of the psychotherapeutic type and drink more coffee
and alcoholic beverages than nonsmokers (18,26). In only one
study have women smokers and nonsmokers been compared for
use of all drug categories; these data were derived from a self-
administered questionnaire asking about drug use for the past
year (21). As Table 1 shows, women smokers take more of almost
every type of drug than nonsmokers. When the data were or-
ganized according to age groups, the 15-to-19-year-old group of
women showed a marked elevation in drug use among smokers
(Table 2).

Although the data are preliminary, a trend that female smok-
ers consume drugs with greater frequency than female
nonsmokers is suggested. It is beyond the scope of this chapter

259
TABLE 1.—Ratio of percent usage of drug classes, women
smoker/nonsmoker status

 

 

Drug class White Black Asian
Antihistamine or allergy medicine 0.8 0.9 0.6
Cough medicine 1.7 1.8 0.7
Asthma medicine 0.9 1.0 0.9
Aspirin-containing drugs 1.2 1.2 0.9
Pain medicine 1.2 1.2 1.0
Codeine, morphine, Darvon,

Percodan, Demerol 1.5 1.6 1.2
Phenobarbital or other barbiturates 1.3 1.8 1.6
Sleeping pills 1.2 1.3 1.3
Tranquilizers 1.5 1.6 1.8
Anticoagulants 1.3 0.8 0.0
Digitalis or other heart medication 1.0 0.8 0.1
Antihypertensives 0.8 1.1 0.9
Diuretics 11 1.0 1.3
Cortisone-type medication 1.0 1.2 1.0
Hormones 1.2 1.3 1.4
Insulin or diabetic pills 0.9 0.8 0.9
Iron or anemia medications 0.9 0.9 0.9
Thyroid medication 1.1 1.3 2.3
Pills to control periods 1.3 1.2 16
Contraceptives 1.2 1.1 1.3
Benzedrine or Dexedrine 1.6 1.1 11
Weight reduction medication 11 0.9 1.3
Penicillin or other antibiotics 1.2 1.2 1.0
Sulfa drugs 11 1.2 0.8
Stomach or digestion medicine 1.2 1.2 1.3

 

SOURCE: Seltzer, C.G. (21).

TABLE 2.—Percentage of positive responses among females in
age group 15-19

 

 

Question Smokers Nonsmokers
Taken phenobarbital or barbiturates? 2.3 1.0
Taken codeine, morphine, etc.? 16.0 6.5
Taken Benzedrine or Dexedrine? 4.9 0.3
Taken penicillin or other antibiotics? 33.0 25.8
Taken pills to prevent pregnancy? 27.0 9.7

 

SOURCE: Seltzer, C.G. (21).

to differentiate between the behavioral components of this
phenomenon or to address the argument that women who
smoke are less healthy than nonsmokers. It is beneficial, how-
ever, to examine the few reports that address the differences in

260
drug action between smokers and nonsmokers, regardless of the
reasons for drug use.

Altered Clinical Response to Drug Therapy by Smokers
Compared to Nonsmokers

The number of studies investigating the differences in the
clinical responses to a drug by smokers and nonsmokers are far
fewer in number than the studies examining the alterations in
metabolism and biochemistry of drugs in smokers. The 1979
Surgeon General’s Report included an extensive review of the
alterations in drug disposition that occur in smokers (25). That
information is useful for clarifying mechanisms by which smok-
ing alters drug metabolism, absorption, excretion, and other
functions. The clinical significance of these alterations has not
been clarified, however.

The most exhaustive examination of alterations in smokers’
clinical response to drugs was done by Jick and his associates in
the Boston Collaborative Drug Surveillance Program (BCDSP).
Over the past several years, this group has investigated the
clinical response of smokers and nonsmokers to six different
drugs: propoxyphene (Darvon) (4); diazepam (Valium) (3); chlor-
diazepoxide (Librium) (3); phenobarbital (3); chlorpromazine
(Thorazine) (24); and theophylline tea (19). The differences ob-
served between smokers and nonsmokers were consistent
among men and women, except for the theophylline study, in
which the toxic effects of therapy were slightly more frequent
among women (13.4 percent) than among men (9.19 percent).
Only in the chlorpromazine study (24) did the study group (those
taking chlorpromazine) contain more women than men, an ob-
servation that supports other reports that women use major
tranquilizing agents more frequently than men (18).

Since the published BCDSP data is not organized according to
groups of women smokers and nonsmokers, any difference in
drug use between these groups is not reflected in the data
analysis. However, it is important to note that these studies,
except as noted in the chlorpromazine study, predominantly in-
volved men. It has been shown that women report more fre-
quent use of the minor tranquilizers such as diazepam and
chlordiazepoxide (17). Thus these studies should not be inter-
preted as reflecting drug response among the general popula-
tion (17).

The studies on chlorpromazine, diazepam, and chlor-
diazepoxide showed a lessened frequency of the adverse effect
of drowsiness among smokers as compared to nonsmokers (4,24).
Conversely, no difference was reported for phenobarbital (3).

261
The analgesic effect of propoxyphene was reduced in smokers,
an effect which was not observed in smokers on aspirin, codeine,
acetaminophen, or combinations of these drugs (4).

The evidence for increased theophylline metabolism in smok-
ers is well established and predicts the observed clinical re-
sponse to theophylline (13). The BCDSP study of theophylline
showed that smokers not only required larger doses of theophyl-
line for efficacy, but alzu were less likely to report adverse ef-
fects than nonsmukers, even though they required larger doses.

Theoretically, then, because of a decreased clinical response
to a drug, the tendency would be for the smoker to require in-
creased doses to achieve the same therapeutic effect as a
nonsmoker.

Therapeutic efficacy and adverse side effects in relationship
to gender, smoking history, and drug consumption patterns
have not been adequately studied, although the preliminary
evidence would indicate an area of potential toxic drug effects
and/or therapeutic failures.

Oral Contraceptives and Smoking

Chronic estrogen therapy has a profound interaction with
chronic tobacco use. Again, the BCDSP has been most instru-
mental in assessing the influence of these two factors on the
health status of women.

In assessing the relative risk of stroke in women who smoke
and take oral contraceptives, the data from the Collaborative
Group for the Study of Stroke in Young Women show that smok-
ing alone increased the risk of hemorrhagic stroke (i.e., sub-
arachnoid) from 1.0 for a nonsmoker who did not use oral con-
traceptives, to 2.6 for a smoker who did not use oral contracep-
tives. A smoker taking oral contraceptives had a relative risk of
6.1 or 7.6 (depending on the control group) (6). Similar increases
in risks do not seem to occur for thrombotic stroke in the smoker
taking oral contraceptives, but the risk of a thrombotic stroke
for a woman using oral contraceptives alone is about nine times
greater than that for a noncontraceptive user (5).

Again using the BCDSP data, the risk of nonfatal myocardial
infarction among women under 38 is very low among nonsmok-
ers, whether or not they use oral contraceptives. However, the
risk to women who both smoke and use oral contraceptives is
substantially higher, ranging from an estimated one per 8,400
annually in women aged 27 to 37 years to one per 250 for women
aged 44 to 45 years (16). In a similar study of noncontraceptive
estrogens, similar risks were demonstrated for women who both
smoke and use estrogens (15). These findings are in agreement

262
with studies done in Great Britain where oral contraceptives
were associated with an overall increase in cardiovascular dis-
ease in young women (20).

Another group which has investigated the link between smok-
ing, oral contraception, and myocardial infarction reported that
there is a considerable interaction between smoking and con-
traceptive use. The group found that rate of acute myocardial
infarction among female smokers on oral contraceptives is
greater than could be accounted for by either smoking or con-
traceptives alone (22). In earlier studies this same group con-
cluded that there was a dose-response relationship between
smoking and myocardial infarction in women, and that among
women smoking 35 or more cigarettes per day, the rate of
myocardial infarction was estimated to be 20 times higher than
among those who never smoked (23).

These data lend themselves to the prediction of risk in only a
very general way and provide no particular measures by which
a woman—smoker or nonsmoker—can evaluate her own risk of
experiencing one of the adverse effects described.

The following section reviews some of the laboratory values
that are altered by smoking. Unfortunately, many of the largest
studies on the correlation between smoking and alterations in
clinical laboratory values have focused on men.

Alterations in Normal Clinical Laboratory Values in Women
Smokers

Only a few investigators have studied clinical laboratory
values in women smokers and nonsmokers (1,8-12,14,27). Many
of these studies show statistically significant differences in a
variety of common parameters. The clinical significance of
these differences may not be apparent, however, since the ac-
tual differences between women smokers and nonsmokers are
small. For example, a study of packed red cell volume (PCV) and
hemoglobin (Hb) in women smokers and nonsmokers showed the
PCV and Hb for nonsmokers to be 41.95 and 13.85 compared to
42.94 and 14.16 for smokers, a difference significant at p < 0.05,
but a discrimination which physician or patient may find dif-
ficult to assess (14).

Small differences in laboratory values between smokers and
nonsmokers can be seen in a number of serum chemistry and
hematologic tests. One measurement that shows a wide enough
variation between smokers and nonsmokers to be recognized
clinically is the leukocyte count of a smoker (11,12). It is impor-
tant to recognize that a WBC of 12,000 per mm? is within the
normal range for a heavy cigarette smoker, and that the dif-

263
ferential count remains normal (11). In one study, individuals
with chronic bronchitis were excluded from evaluation of leuko-
cyte counts, and the same relative increase in leukocyte count
was observed (12).

In several studies of triglyceride and cholesterol values in
smoking and nonsmoking women, an elevation of both values,
which was not statistically significant, was seen in smokers.
The addition of oral contraceptive use to smoking caused a sig-
nificant elevation over the nonsmoker, noncontraceptive user.
The nonsmoker values were 79 + 6.8 mg/100 ml for triglycerides
and 157 + 7.5 mg/100 ml for cholesterol. In the smoker they were
110 + 14.8 mg/100 ml and 174.3 + 8.8 mg/100 ml respectively,
whereas the smoker using oral contraceptives had a triglyceride
value of 150.0 + 14.1 mg/100 ml and a cholesterol value of 186.1 +
mg/100 ml. In this same study, there was no significant difference
between the levels of vitamins A, E or C in smoking and
nonsmoking women (27).

A number of investigators have measured vitamin C levels in
smoking and nonsmoking women, with extreme variation in re-
sults. Some showed decreased plasma and leukocyte vitamin C
levels in smokers, and others showed no differences between
smokers and nonsmokers. The discrepancies in these results
may in part be related to the amount of dietary vitamin C
habitually consumed by the subjects in the various studies (27).

Changes in serum proteins were the subject of another study
of women smokers and nonsmokers (26). Significant differences
in all serum protein fractions were found in cigarette smokers
compared to nonsmokers. In general, the effects increased with
the amount smoked. Past smokers showed globulin values that
were significantly below those of women who never smoked, but
there was no difference observed in the other serum protein
fractions between past smokers and those who had never
smoked.

The Influence of Smoking on the Nutritional Needs of Women

Outside of a possibly increased need for vitamin C in women
who smoke, there is very little information about other nutrient
requirements in smokers. In recent years a great deal of time
has been spent studying the influence of smoking on fetal de-
velopment, a subject covered elsewhere in this volume. The spe-
cial nutritional needs of the nonpregnant smoking woman have
not been dealt with in any systematic way.

A recent study involving obese women looked at the influence
of smoking cessation on body weight (2). Although the data are
innately biased because the study group consisted of women
264
enrolled in a weight loss program, the results showed that
women who smoked less than a half pack of cigarettes a day
gained 4 pounds after they quit. Heavy smokers consuming over
two packs a day gained an average of 30 pounds over several
decades. Moderate smokers gained an intermediate amount.
This study does not contradict a commonly held notion that
women gain weight when they stop smoking; however, it pro-
vides no behavioral or physiological hypothesis for this
phenomenon.

Summary

Most published studies investigating the effects of cigarette
smoking on drug use have been performed on mixed popula-
tions; factors specific for women have not been demonstrated to
date. It has, however, been clearly demonstrated that women
are prescribed and consume more prescription drugs than men.

1. Studies of selected drugs indicate that smoking may affect
clinical responses and alter the dose required for an effective
therapeutic result.

2. Smoking interacts with oral contraceptive use to increase
the risk of myocardial infarction and subarachnoid hemor-
rhage.

3. Common clinical laboratory parameters are altered in
smokers compared to nonsmokers; the health significance of
these changes is unknown.

4. Insufficient information exists for assessment of the impact of
smoking on the nutritional needs of women.

References

(1) BILLIMORIA, J. D., POZNER, H., METSELAAR, B., BEST, F. W.,
JAMES, D. C. D. Effect of cigarette smoking on lipids, lipoproteins,
blood coagulation, fibrinolysis and cellular components of human
blood. Atherosclerosis 21(1): 61-76, January-February 1975.

(2) BLITZER, P. H., RIMM, A. A., GIFFER, E. E. The effect of cessation of
smoking on body weight in 57,032 women: cross sectional and longitud-
inal analysis. Journal of Chronic Diseases 30(7): 415-429, July 1977.

(8) BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM.
Clinical depression of the central nervous system due to diazepam and
chlordiazepoxide in relation to cigarette smoking and age. New Eng-
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(4) BOSTON COLLABORATIVE DRUG SURVEILLANCE PROGRAM.
Decreased clinical efficacy of propoxyphene in cigarette smokers. Clin-
ical Pharmacology and Therapeutics 14(2): 259-263, March-April 1973.

(5) COLLABORATIVE GROUP FOR THE STUDY OF STROKE IN
YOUNG WOMEN. Oral contraceptives and increased risk of cerebral
ischemia or thrombosis. New England Journal of Medicine 288(17):
871-878, April 26, 1973.

(6) COLLABORATIVE GROUP FOR THE STUDY OF STROKE IN

265
(7%)

(8)

(9)

(10)

(11)

(12)

(13)

(14)

(15)

(16)

(17)

(18)

(19)

(20)

(21)

(22)

(28)

266

YOUNG WOMEN. Oral contraceptives and stroke in young women.
Journal of the American Medical Association 231(7): 718-722, February
17, 1975.

CRAIG, T. L., VANNATTA, P. A. Current medication use and symptoms
of depression in a general population. American Journal of Psychiatry
135(9): 1036-1039, September 1978.

DALES, L. G., FRIEDMAN, Q. D., SIEGELAUB, A. B., SELTZER, A.C.
Cigarette smoking and serum chemistry tests. Journal of Chronic Dis-
eases 27(6): 293-307, August 1974.

DALES, L. G., FRIEDMAN, Q. D., SEIGELAUB, A. B., SELTZER, A.C.,
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ron 20: 163-170, 1978.

DESMOND, P. V., ROBERTS, R. K., WILKINSON, Q. R., SCHENKER,
S. No effect of smoking on metabolism of chlordiazepoxide. New Eng-
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FRIEDMAN, Q. D., SIEGELAUB, A. B., SELTZER, C. C., FELDMAN,
R., COLLEN, M. F. Smoking habits and the leukocyte count. Archives
of Environmental Health 26(3): 187-143. March 1973.

HELMAN,N., RUBENSTEIN, L. S. The effects of age, sex, and smoking
on erythrocytes and leukocytes. American Journal of Clinical Pathol-
ogy 63: 35-44, 1975.

HUNT, S. N., JUSKO, W. J., YURCHAK, A. M. Effect of smoking on
theophylline disposition. Clinical Pharmacology and Therapeutics 1%5,
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ISAGER, H., HAGERUP, L. Relationship between cigarette smoking
and high packed cell volume and haemoglobin levels. Scandinavian
Journal of Haemotology 8(4): 241-244, 1971.

JICK, H., DINAN, B., ROTHMAN, K. J. Noncontraceptive estrogens and
nonfatal myocardial infarction. Journal of the American Medical Asso-
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JICK, H., DINAN, B., ROTHMAN, K. J. Oral contraceptives and non-
fatal myocardial infarction. Journal of the American Medical Associa-
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PARRY, H. F., BALTER, M. B., MELLINGER, Q. D., CISIN, I. H.,
MANHEIMER, D. I. National patterns of psychotherapeutic drug use.
Archives of General Psychiatry 28: 769-783, June 1973.

PARRY, H. F., CISIN, I. H., BALTER, M. B., MELLINGER, Q. D.,
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PFEIFER, H. J.. GREENBLATT, D. J. Clinical toxicity of theophylline
in relation to cigarette smoking. Chest 73(4): 455-459, April 1978.

ROYAL COLLEGE OF GENERAL PRACTITIONERS ORAL CON-
TRACEPTION STUDY. Mortality among oral contraceptive users.
Lancet (4): 727-733, October 8, 1977.

SELTZER, C. G., FRIEDMAN, Q. D., SIEGELAUB, A. B. Smoking and
drug consumption in white, black, and oriental men and women.
American Journal of Public Health 64(5): 466-473, March 1974.

SHAPIRO, S., SLONE, D., ROSENBERG, L., KAUFMAN, D., STOL-
LEY, P.D., MIETTINEN, O. S. Oral contraceptive use in relation to
myocardial infarction. Lancet (1): 743-747, April 7, 1979.

SLONE, D., SHAPIRO, S., ROSENBERG, L., KAUFMAN, D. W.,
HARTZ, S. C., ROSSI, A. C., STOLLEY, P. D., MIETTINEN O. §. Rela-
tion of cigarette smoking to myocardial infarction in young women.
New England Journal of Medicine 298(23): 1273-1276, 1978.

(24) SWETT, D. Drowsiness due to chlorpromazine in relation to cigarette
smoking. Archives of General Psychiatry 31: 211-213, August 1974.

(25) U.S. PUBLIC HEALTH SERVICE. Smoking and Health. A Report of
the Surgeon General. U.S. Department of Health, Education, and Wel-
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Health, Office on Smoking and Health, DHEW Publication No. (PHS)
79-50066, 1979, 1251 pp.

(26) WINGERD, J., SPONZILLI, E. E. Concentrations of serum protein frac-
tions in white women: effects of age, weight, smoking, tonsillectomy
and other factors. Clinical Chemistry 23(7): 1310-1317, 1977.

(27) YEUNG, D. L. Relationships between cigarette smoking, oral contracep-
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terol. American Journal of Clinical Nutrition 29: 1216-1221, 1976.

267
PART III:

PSYCHOSOCIAL AND BEHAVIORAL
ASPECTS OF SMOKING IN WOMEN.
PSYCHOSOCIAL AND BEHAVIORAL ASPECTS OF SMOKING
IN WOMEN

Introduction

Currently, women are rapidly approaching men in the rate of
initiation and prevalence of cigarette smoking, but seem to have
a lower rate for successful cessation of smoking. (See also Part I
of this report, Patterns of Cigarette Smoking.) While an increasing
percentage of the U.S. population is giving up smoking, nationwide
surveys and cessation studies suggest that a smaller proportion of
women than men are quitting successfully.

This part discusses tobacco use by women, with comparative
reference to men’s use wherever appropriate. Special attention
is directed to the patterns of initiation, the rise in smoking
among girls, and the factors important in the maintenance of
smoking behavior, including pharmacological effects, smoking
patterns, information dissemination, and stress management.
The differences in successful quitting between men and women
smokers are discussed with the hope of generating new ideas for
research and intervention.

A separate analysis of smoking patterns among women in the
health professions is presented. In addition, a section is devoted
to the pregnant smoker because the impact of smoking, both on
the fetus and on the pregnant woman, makes this a period of
particular importance in the life of the women smoker.

Initiation of Smoking in Adolescent Girls

Cigarette smoking, particularly cigarette smoking among
young girls, is a changing phenomenon. Shifts in smoking at-
titudes and behaviors reflect broader social forces, including
changes in sex roles and gender differences in responses to pub-
lic information programs and to social sanctions against smok-
ing.

The trend in adolescent smoking, as in other “adult-like” be-
haviors such as alcohol use or sexual activity, is toward earlier
onset. For example, before the mid-1970s, girls were less likely
to start smoking than boys, and when they did, they started
later. Neither of these differences holds true any longer.

A number of psychosocial variables correlate highly with ado-
lescent smoking trends. These include the attitudes, percep-
tions, and behaviors of adolescent girls, their social setting
(family, peer groups) and those broad demographic factors
(race, education, family income, urbanicity) that help to define
an individual’s position within the society.

271
CONCEPTS OF ADOLESCENT BEHAVIOR

Discussions of adolescence with its attendant problems have
seldom differentiated between boys and girls, and no theory or
model of adolescent behavior has been developed specifically for
girls. However, gender differences in development, cognitive
processes, sex-role acquisition and achievement have recently
been examined and a number of psychological differences have
been identified (24,26,51,68,98,211).

The essence of adolescence is growth, transition, and change.
The rate of physical growth in adolescence is more rapid than at
any other stage of development except the neonatal stage. Ado-
lescent development is a complicated process which involves in-
creasing self-awareness, intellectual and emotional growth, and
physiological changes.

What adults characterize as risk taking in adolescence may be
exploration of the limits of identity and capability. Adolescents
are attempting to resolve the competing and conflicting de-
mands stemming from childhood experience on the one hand
and expectations of adulthood on the other: dependency and
compliance versus autonomy and independent decision-making;
orientation toward family versus orientation toward peers.
They face increasing demands for social and cognitive achieve-
ment and for developing the self-control required to handle new
psychological, physical, and social situations. Inadequate expe-
rience with these challenges or failure to meet them may result
in low self-esteem and increased anxiety and stress.

Numerous formulations contributing to a general model of
adolescent development have emerged. These include life-span
theory and cohort change (52,131), adolescent sexuality (32), and
differences between early and late adolescence (85).

Douvan and Adelson have identified issues that distinguish
adolescence: for girls they are sexuality, interpersonal-
intimacy, and identity issues; for boys they are sexuality,
autonomy —assertion—independence and identity issues (51). In
this study, conducted in the 1950s, girls evidenced conflict be-
tween the social roles for which they were preparing (further
education and careers) and the future role they desired
(marriage—-motherhood). La Farge described a similar female
adolescent conflict between social rules and individual percep-
tions (109). Research published in the 1970s shows that young
women still have role conflicts different from those of young
men (68).

Research on gender-role differentiation in childhood has
provided some insight into developmental differences between
girls and boys. Maccoby suggests that these differences may

272
derive from different role models for boys and girls; from the
varying responses of significant adults to their behaviors; from
biological differences; and from a combination of these (116).
Block and Maccoby and Jacklin report that the differences in-
clude girls having less confidence in their ability to handle a
new task and less sense of control over what happens to them
(18,117). Girls also show greater susceptibility to expressed anx-
iety, greater need for help and reassurance, greater closeness to
friends, and more concern for what is socially desirable.

Adolescent behaviors—social or antisocial, adaptive or
maladaptive—are a function both of individual choice and of the
opportunities for growth and development which a society pro-
vides its youth (36). “Not only is the term ‘adolescence’ a social
definition, but what society perceives as an adolescent problem
is also socially defined” (52). Similarly, the development of
values, motivations, and controls that foster healthy growth
and deter the onset of smoking and other undesirable behaviors
depends on the opportunities and resources that society makes
available to the adolescent.

PREVALENCE AND PATTERNS OF ADOLESCENT
CIGARETTE USE

National surveys of adolescent smoking behavior have pro-
vided information on gender differences, secular trends, and
age subgroupings within the adolescent period. Surveys of
smoking patterns, ages 12 to 18, were conducted by the National
Clearinghouse for Smoking and Health (NCSH) in 1968, 1970,
1972, and 1974 and by the National Institute of Education (NIE)
in 1979 (130,197). Two other periodic surveys, both sponsored by
the National Institute on Drug Abuse (NIDA), ineluded
cigarette consumption (2,101). A number of studies in specific
geographic locales or among specific populations, such as high
school students, have also been carried out (198). Differing defi-
nitions of a current regular adolescent smoker make compari-
sons among these studies particularly difficult. In the NCSH
and NIE surveys, a regular smoker is defined as one who
smokes cigarettes at least weekly. In the NIDA surveys, regu-
lar smoking is defined as occurring within the past 30 days.

Prevalence

Table 1 summarizes adolescent cigarette smoking prevalence
between 1968 and 1979, by age and gender, as surveyed by
NCSH and by NIE. Between 1968 and 1974 there was a signifi-
cant increase in the percentage of girl smokers in each age cat-
egory at each point in time, in contrast to the relatively stable

273
prevalence of current regular smoking among boys. A decline in
the average age of smoking initiation for both sexes is
suggested by the small but significant increase in smoking pre-
valence among 12 to 14 year olds. (198). Trends in the data from
a national study of high school seniors also support the
hypothesis of an earlier age of initiation (101).

In the five years from 1974 to 1979, the proportion of 17 to 18
year old girls who smoked changed little, but the proportion of
boys who smoked dropped by a third. It was this difference
among 17 to 18 year olds that created the overall higher smok-
ing rate for girls as compared with boys in 1979. However, at
ages 15 to 16, the drop from 1974 to 1979 was greater for girls ©
than boys, suggesting that the initiation of smoking is also be-
ginning to decline in those girls born after 1962.

The differences in the within-age-group changes in the smok-
ing prevalence of girls may represent an isolated effect on the
cohort of girls born in 1963 and 1964. The change was essentially
confined to the 15 to 16 year old subgroups who were born dur-
ing these years. The precise nature of the interaction of social
influences on the development and maturation of this cohort is
unclear. However, other data suggest that a marked secular
change occurred in cigarette smoking attitudes and behavior
which was secondary to an increased awareness of the health
risks of smoking.

An alternate hypothesis is that the isolated decline in the 15
to 16 year old subgroup may be an artifact produced by the
combined trends of reduced initiation of smoking and the initia-
tion at a younger age. Thus, the decline in prevalence among 15
to 16 year old girls would reflect the decreasing percentage of
young women who are taking up smoking, but this trend will be
masked in the younger age group by the tendency of those girls
who are going to take up smoking to do so at a younger age. The
1979 NIE Survey reports that:

The increasing prevalence of teenage smoking that was ob-

served in the period between 1968 and 1974 has come toa halt,

and a decrease in the smoking rates of both boys and girls has
taken place. The decrease in boys’ smoking was greater than
that of girls, resulting in a higher smoking rate for girls than
for boys in 1979. Smoking among boys leveled off in the early
1970s, and then began to decrease. It appears that girls are
now following this pattern: the smoking rate has leveled off
among 17 and 18 year olds, and probably can be expected to

decrease over the next few years (130).

Other surveys (Table 2) support these trends in adolescent
girls’ smoking behavior. Differences between studies in abso-
lute prevalence rates reported are at least partly due to the

274
TABLE 1.— Estimates of the percentage of current, regular
cigarette smokers, adolescents, aged 12 to 18, United
States, 1968-1979

 

 

 

Ages 12-14 Ages 15-16 Ages 17-18 Ages 12-18
Year Male Female Male Female Male Female Male Female
1968 2.9 0.6 17.0 9.6 30.2 18.6 14.7 8.4
1970 5.7 3.0 19.5 14.4 87.3 22.8 18.5 11.9
1972 4.6 2.8 17.8 16.3 30.2 25.3 15.7 13.3
1974 4,2 4.9 18.1 20.2 31.0 25.9 15.8 15.3
1979 3.2 4.3 13.5 11.8 19.3 26.2 10.7 12.7

 

NOTE: Current regular smoker includes respondent who smokes cigarettes at

least weekly.
SOURCE: National Clearinghouse for Smoking and Health (197), National
Institute of Education (130).

difference in the definition of a smoker, and differences in
survey technique. The National Institute of Education Sur-
vey included as current regular smokers both those who smoke
one or more cigarettes per week and those who smoke one or
more cigarettes a day. The prevalence rates of Abelson, et al. (2)
and Johnston, et al. (101) refer to any cigarette smoking in the
past 30 days.

The Abelson, et al. data, which were collected 2 years before
that of NIE, show the predicted decline, but to a lesser degree
(2,130). The Johnston, et al. data suggest that there was an in-
crease in adolescent girls’ smoking as measured in samples of
high school seniors between 1975 and 1977 (101). Johnston’s fig-
ures were retrospectively reported and refer only to youngsters
born before and during 1960, and therefore, would not be ex-
pected to reflect changes occurring in those cohorts born after
1962 where the decline has occurred. This may explain why the
Johnston, et al. 1977 sample did not reflect a downturn, and re-
ports of later cohorts of high school seniors should show a
stabilization and then a decline in female smoking rates. Re-
sults from a study by the same group in 1978 show the predicted
downturn in the smoking habits of high school senior girls (from
39.6 percent in 1977 to 38.1 percent in 1978) as well as boys (from
36.6 percent in 1977 to 34.5 percent in 1978) (103).

Age of Initiation of Smoking

The data in Table 1 show that the prevalence of smoking in
girls aged 12-14 increased steadily between 1968 and 1974 to a
level equal to or slightly higher than boys of the same age. Be-
tween 1974 and 1979 the prevalence of smoking stabilized in

275
girls and may have begun to decline. The prevalence of smoking
by boys of this age peaked in 1970 and has shown a steady de-
cline since that time. These trends may represent fewer adoles-
cents taking up smoking, with those who do beginning at an
earlier age.

Well over one-half of high school seniors—male and
female—who smoke regularly, reported first smoking in the
ninth grade or earlier (101). It is hard to know whether this
earlier onset reflects something specific to cigarette smoking or
is attributable to the more general pattern of earlier onset of all
“adult-type” behaviors.

This trend toward early initiation of smoking behavior may
have a significant impact on the future health of these adoles-
cents, as many of the health risks associated with smoking in-
crease with both earlier onset of smoking and duration of the
smoking habit. In addition, the earlier the use of a substance is
begun, the longer it is likely to be continued and the more heav-
ily it is likely to be used (26,102,137).

These national surveys do not permit a detailed examination
of the initiation process. ‘“Experimenters,” those who have
smoked at least a few puffs of a cigarette, but not more than 100
cigarettes, are grouped with “never smokers’, those who have
never taken even a few puffs. “Occasional” smokers are defined
as those who smoke less than one cigarette a week but more
than 100 cigarettes in a lifetime. Occasional or intermittent
smoking is rare among adults. Examining the proportion of
“experimenters” at each age and following their subsequent
smoking behavior might help clarify the determinants of the
initiation process (126).

In one major British study, smoking only a few cigarettes
usually led to becoming a regular smoker; only 15 percent of
those who smoked more than a single cigarette escaped adop-
tion of smoking as a regular behavior (126). The estimate in this
study of 8 percent “occasional smoking” in adolescence is based
on a definition of smoking less than daily, but at least one
cigarette a week for as long as 1 month. The difference in defini-
tion of occasional smoking makes comparison with current U. S.
data on adolescents difficult. From 1968 to 1979, the percentage
of current occasional smokers (less than once per week) varied
between 0.4 percent and 1.6 percent for girls, and 0.4 percent
and 2.3 percent for boys (130). McKennell and Thomas estimated
that the mean length of time between smoking the first
cigarette and adopting regular (daily) smoking was slightly less
than 3 years for boys and slightly more than 2 years for girls
(126). The difference is probably due to earlier experimentation
among boys. The transition from experimental or occasional

276
TABLE 2.—Percent of adolescents currently using* cigarettes,
alcohol and marihuana, by sex: three national
surveys compared

 

Ages 12-17 Ages 17-19
Ages 12-18 Abelson, et al. High School Seniors
NIE (1979) (1977) Johnson, et al. (1977)

 

Ages 1974 1979 Ages 1974 1977 Ages 1975 1977

 

Current Cigarette Use
12-14 F 51 4.3 12-13 13 10 _ _

M 4.2 3.2

15-16 F 216 12.3 14-15 25 22 _ _
M 181 14.6

17-18 F 26.4 27.0 16-17 38 35 _— _
M 32.6 19.6

12-18 F 15.9 13.1 12-17 F 24 22 17-19 F 35.9 39.6
M 16.3 «11.1 M 27 23 M 37.2 36.6

 

Current Alcohol Use

16-17 F&M 51 52
12-17 F 29 25 17-19 F 62.2 665.0
M 39 37 M 75.0 177.8

 

Current Marihuana Use

16-17 F&M 20 29
12-17 Fil 13 17-19 F 22.5 30.0
M 12 19 M 32.3 40.7

 

*NOTE: Definition of current use varies by study. Cigarettes: NIE
(1979)—current regular smoker (one or more cigarettes during the past week
over and above a minimum five packs) and current occasional smoker (less
than one cigarette per week); Abelson, et al. (1977) and Johnston, et al.
(1977)—smoked within the past 30 days. Alcohol and marihuana: use within
the past month (smokers and nonsmokers).
SOURCE: Abelson, H.I. (2), Johnston, L.D. (10D, National Institute of
Education (130).

smoking to regular smoking is an extremely important one to
study because it may provide a crucial period for intervention
before psychosocial or pharmacological dependency is estab-
lished.

Number of Cigarettes Smoked

In the NCSH/NIE survey (130), a smaller percentage of
female smokers than male smokers smoked 10 or more cigar-
ettes per day (61.8 percent versus 73.8 percent in 1974, and 59.0

277
percent versus 65.6 percent in 1979). The high school senior sur-
vey showed male-female rates to be equivalent at the half-pack
per day rate, with boys exceeding girls at heavier levels (101). In
that study, the proportion of females currently smoking as
much as a half-pack per day increased between 1975 and 1977,
while the proportion of males smoking at that rate remained
constant. The American Cancer Society survey also suggested
an increase in the proportion of heavy smokers among adoles-
cent girls compared with stable rates in boys between 1969 and
1975 (216). It reported a fourfold increase in the percentage of
female smokers who smoked at least a pack a day, from 10 per-
cent to 39 percent, compared with an unchanged rate of 31 per-
cent among males. The equality in smoking behavior may be
extending to the number of cigarettes smoked.

Type of Cigarette Smoked

In adolescent smokers of both sexes, there has been a definite
trend toward smoking cigarettes with lower “tar” yields be-
tween 1974 and 1979. Figure 1 shows the decline in the “tar” and
nicotine levels of the cigarettes smoked by adolescents. Girls
appear to be slightly ahead of boys in the use of lower “tar”
cigarettes. The trend can be attributed to three factors: the
increased marketing of low “tar” cigarettes; the decreased “tar”
levels of existing cigarettes; and increased awareness of dif-
ferential health hazards associated with different kinds of
cigarettes (130). It should be noted, however, that the midpoint
on the cumulative percentage continuum has dropped only
about 1 mg “tar” between 1974 and 1979, from approximately
17.5 mg to approximately 16.5 mg, and the percentage of adoles-
cents smoking the lowest category of “tar” (less than or equal to
10 mg) is still very small.

Smoking Cessation

Are there differences between girls and boys in patterns of
smoking cessation comparable to those observed in adults? A
greater proportion of adult males than adult females have quit
smoking (see the section on adult smoking cessation in this
part). Two national surveys have shown more ex-smokers
among adolescent boys than among girls (101,130). Looking at
either the percentage of ex-smokers among all adolescents or at
the quit rates (number of former smokers divided by number of
ever smokers), boys exceed girls in every survey between 1968
and 1979 (130). However, if experimental smokers are elimi-
nated from the analysis, there are no differences between the

boys and girls. For the two most recent surveys, the quit rates
278
6L¢6

ew «@ 1974
x eees x 1979

 

 

 

 

 

 

 

 

 

 

% %
100- Girls L400
90- - 90
80- -- 80
70- r- 70
60- + 60
50+ -- 50
40-4 - 40
30-4 - 30
20- - 20
10- - 10
L. Jk
c CO FF v T qT q ! V4 ‘ w/a | 1 ' 1 '
<=10 11-168 16 617 18 19 >20 <10 11-15 16 #17 #18 19 >20
(0.6) (0.8) (1.1) (1.1) (1.2) (1.2) (1.45) (0.6) (0.8) (1.1) (1.4) (1.2)(1.3) (1.45)
Mg “tar” (and median mg nicotine) Mg “‘tar’’ (and median mg nicotine)

FIGURE 1.—Cumulative percentage of adolescent smokers by the tar level of cigarette smoked, 1974
and 1979

SOURCE: Federal Trade Commission (61), National Institute of Education (130).
were as follows: 33.2 percent of female and 36.0 percent of male
smokers had quit in 1974; 30.5 percent of female and 42.3 per-
cent of male smokers had quit in 1979. In contrast, Reeder found
no difference in quit rates between boys and girls aged 13 to 19
in national surveys conducted in 1965 (boys 28 percent, girls 29
percent) and in 1975 (boys 34 percent, girls 35 percent) (148).
Therefore, it is unclear whether adolescent girls show the same
patterns of quitting smoking found in adult women. It should
also be remembered that research on both smoking cessation
and illicit drug use has shown that quitting is often not a per-
manent state (100,147,173).

Smoking Prevalence and Ethnicity

There are no data based on a national sample examining ado-
lescent smoking in different racial groups. However, beginning
in 1969-1970 Brunswick has conducted a longitudinal personal
home interview survey of a representative sample of 668 urban,
non-Hispanic black youths in Harlem, New York City. She found
that more 16 to 17 year old girls than boys smoked (62 percent
versus 50 percent). This was well before national rates had
shown smoking among girls equaling and then exceeding that
among boys. This greater smoking prevalence in girls continued
into the young adult years. The same subjects were re-
interviewed 6 to 8 years later, when the youths were aged 18 to
23. Sixty-two percent of young black women (N =258) were cur-
rent smokers and 18 percent were currently smoking at least a
pack a day. This is compared with 57 percent of the black men 18
to 23 years old (N =277) who were current smokers, 16 percent of
whom regularly smoked at least a pack a day. These prevalence
rates are well above the rates for adult black women found in
national survey data, but are only slightly higher than the rates
found in adult black men (198). This study is of substantial in- -
terest, but may not be representative of national black adoles-
cent smoking patterns.

Aleohol and Marihuana Use

Cigarette use should be viewed in the context of other sub-
stance use behaviors. Abelson, et al., provided information on
the use of other substances in the age range of 12 to 17 by
current cigarette smokers and by those not currently smoking
(2). Smokers far exceeded nonsmokers in reporting use of al-
cohol, marihuana and/or hashish, or “stronger” drugs (hal-
lucinogens, cocaine, heroin, and other opiates): positive replies
for alcohol were 80.0 percent versus 44.8 percent; for marihuana
and/or hashish, 68.3 percent versus 16.7 percent; and for

280
stronger drugs, 26.3 percent versus 4.1 percent respectively (24,
103,130,216). Similar figures for alcohol use by 138 to 17 year old
girls were reported by Yankelovich, et al.: 81 percent of the
smokers drank compared with 42 percent of nonsmokers, but
somewhat lower estimates were reported for marihuana
use—25 percent of the smokers versus 3 percent of the
nonsmokers (203). Strong associations between alcohol use and
cigarette smoking and/or between marihuana use and cigarette
smoking in adolescents and college students have also been
identified in a number of other investigations (86,97,153,
177,181).

DEMOGRAPHIC AND PSYCHOSOCIAL CORRELATES OF
SMOKING IN ADOLESCENCE

Smoking is a complex behavior, and it is likely that adolescents
start to smoke for multiple reasons. Strong correlations be-
tween smoking and a number of demographic and psychosocial
variables have been reported, but causal connections have not
been established. Neither has the set of “predisposing factors”
been often subjected to multivariate analysis. It is rare that
more than one or two variables have been tested simulta-
neously. What appear to be separate determinants of smoking
behavior (for example, peer pressure and socioeconomic status)
may actually be reflecting a single underlying pattern. For
example, aspects of self-confidence, academic achievement,
types of parental and/or peer relations, and/or socioeconomic
factors cluster in certain ways to influence susceptibility to
smoking cigarettes. A few multivariate analyses have been
conducted (111,113,188).

Socioeconomic Influences

A number of studies have examined smoking in relation to
socioeconomic status. The findings consistently point to a rela-
tionship between lower parental status—income and
education—and higher smoking prevalence among these par-
ents and their children (20,130,148,161). Adolescents from low-
income families may also begin to smoke earlier than others
(33,126). The findings that girls who work have higher rates of
smoking may also reflect a relationship to lower economic
status (9,130). Srole and Fischer observed a relationship be-
tween downward mobility and smoking in adults (180). This may
be an important dynamic to explore in adolescent initiation of
smoking.

A relationship between parental education and adolescent
smoking also exists (130). When one or both parents attended

281
college, 9.9 percent of boys and 10.6 percent of girls smoked,
compared with 10.9 percent of boys and 14.8 percent of girls
from homes where neither parent attended college.

Family Patterns

In single-parent households (19.3 percent of those households
surveyed in 1979), adolescent smoking rates were approxi-
mately double those of households in which both parents were
present (130). This relationship holds for both boys and girls, in
every age group, and across all five NCSH/NIE surveys; it has
also been identified by others (111). In the 1979 survey, 19.3
percent of the boys and 21.2 percent of the girls in single-parent
households are smokers, compared to 8.6 percent and 10.7 per-
cent of those in homes with both parents present.

Parental modeling may underlie this association in two ways.
First, adult smoking rates are higher for divorced or separated
men and women. Second, female single parents who head
households are likely to work outside the home, and smoking is
more prevalent among working women than among homemak-
ers (182).

Smoking Among Parents and Siblings

Adolescents are more likely to smoke if either or both parents
smoke than if they do not (9,15,20,161,213). In the 1979 NIE Sur-
vey this pattern was found across age and gender (130) (See
Table 3.) Looking at the data slightly differently, when both
parents smoke, 13.5 percent of sons and 15.1 percent of
daughters smoke; when one parent smokes, 9.1 percent of boys
and 12.7 percent of girls smoke; and in homes where neither
parent smokes, 5.6 percent of boys and 6.5 percent of girls smoke
(130).

There are conflicting reports on the relationship between the
sex of the smoking parent and smoking habits of the offspring.
In two-parent homes in which only one parent smokes, 17 to 18
years olds appear to be more likely to smoke if the mother does
(130). Other studies have identified a relationship between the
child’s smoking and that of the parent of the same sex (9,15,213).
Allegrante, et al. found a relationship between the mother’s
smoking behavior and that of sons, but not of daughters, and no
relationship of the father’s smoking behavior to smoking by
children of either sex (3). In contrast to all of these findings,
Schneider, et al. were unable to relate parental smoking to that
of offspring (166).

Explanations for the association between parental and chil-
dren’s smoking behavior include the effect of role-modeling, pa-

282
82

TABLE 3.—Percentage of adolescents who smoke by the smoking behavior of parents and older

 

 

siblings
Have No Have No Older Older Older Older
Older Sibling Older Sibling Sibling Sibling Does Sibling Sibling Does
Smokes Not Smoke Smokes Not Smoke
One or Both Neither One or Both One or Both Neither Neither
Parents Parent Parents Parents Parent Parent
Smoke Smokes Smoke Smoke Smokes Smokes
Boys:
12-14 2.8 0.0 6.3 2.7 0.0 0.0
15-16 17.6 4.0 18.8 6.3 21.1 2.1
17-18 15.0 1.9 25.4 16.7 31.7 0.0
Total 8.2 2.9 17.0 1.5 19.5 0.6
Girls:
12-14 3.7 0.0 8.5 1.3 3.4 2.9
15-16 8.2 5.7 20.0 13.0 15.2 2.4
17-18 29.7 15.4 32.9 19.6 25.0 6.7
Total 9.7 4.1 20.3 9.7 15.3 4.1

 

Base: Both parents present in household

SOURCE: National Institute of Education (130).
rental permissiveness (real or imagined), and availability of
cigarettes in the home (125).

Older siblings seem equally important or more important
than parents as potential role models for smoking (9,130,148).
There is a greater likelihood that an adolescent will smoke if one
or more older siblings smoke than if no older siblings smoke;
this is true in those households where neither parent smokes as
well as in those where one or both parents smoke. In the 1979
survey, boys with older siblings who smoked were more than
three times as likely to smoke as boys with nonsmoking older
siblings. The increase is about twofold for girls. The highest
smoking rate for girls was found when at least one parent and
an older sibling smoked (20.3 percent). The corresponding rate
for boys (17.0 percent) was slightly lower than where an older sib-
ling but neither parent smoked (19.5 percent) (130). (See Table 3.)

Peer Group Influence

Adolescents’ smoking behavior is highly correlated with re-
ports of having friends who also smoke (15,132,133,155,162,216).
Most multivariate analyses have established this factor as
being of prime importance although one such analysis found no
relationship at all (3,113,138). It has been pointed out that pat-
terns of drug use in adolescents are very similar among best
friends (121). It has not been demonstrated, however, that it is -
the behavior of friends rather than inclinations of the adoles-
cent which influences him or her to smoke (3,130,166).

Inquiring about the smoking behavior of the “four best -
friends” of adolescent respondents, the NIE study reported that
87.6 percent of boys and 94.0 percent of girls who smoked stated
that at least one of those friends also smoked. In addition, only
10.2 percent of boys and 5.9 percent’of girls who smoked had no
regular smokers among their four best friends, and an even
smaller fraction (2.2 percent of boys and 0 percent of girls) re-
ported that none of their friends had even experimented. In a
parallel vein, it was found that nonsmokers also congregate to-
gether. Approximately one-third of the nonsmokers (33.8 per-
cent of boys, 32.9 percent of girls) reported having at least one
best friend who smoked, while over two-fifths (43.0 percent of
boys, 44.1 percent of girls) had no best friend who smoked regu-
larly. Over one-fifth (22.4 percent of boys, 23.0 percent of girls)
had no best friends who had even experimented.

Thus, “peer pressure” to smoke may be operative when the
adolescent belongs to or would like to belong to a group in which
smoking is part of the life-style (180). When the peer group be-

284
havior does not include smoking, there may be little pressure on
the adolescent to begin to smoke.

Conformity pressures and peer influence are very strong in
early adolescence. Therefore, if smoking were considered a be-
havior which was adopted by the majority of adolescents, exper-
imentation and initiation might occur because of the impor-
tance of conformity in this age period (63). Unfortunately, there
are suggestions that most adolescents tend to overestimate the
proportion of their peers who are smokers. Eighty-two percent
of all girls surveyed in the 1975 American Cancer Society Sur-
vey thought of adolescents as smokers rather than nonsmokers
(216). In that same survey, the professions of teachers, execu-
tives, housewives, and feminist leaders were all characterized
as smokers by approximately two-thirds of girls, with only doc-
tors and athletes considered nonsmokers.

Heterosexual peer considerations may also be important. Girl
smokers are very likely to have boyfriends who also smoke (72
percent), compared with nonsmoking girls (27 percent) (216).
Similar percentages apply to the fraction of all male friends who
smoke (69 percent for girl smokers and 32 percent for nonsmok-
ers). Yet girls are less likely than boys to see smoking as a social
asset (37 percent versus 55 percent) and they even consider it a
drawback (52 percent girls versus 31 percent boys).

The kinds of images projected by the people shown in
cigarette advertisements may lend support to peer influences to
smoke. Girl smokers characterized such people as attractive (69
percent), enjoying themselves (66 percent), well-dressed (66 per-
cent), sexy (54 percent), young (50 percent), and healthy (49 per-
cent).

Prevention efforts aimed at making actual statistics on smok-
ing prevalence available to teens in order to correct the above
beliefs may help counter the advertising. Popular personages in
various professions and lifestyles which girls mistakenly per-
ceive as smoker-dominated could be recruited in this effort.

Scholastic Achievement and Aspiration

Achievement in school has been one of the most frequently
investigated correlates of smoking, with a study as early as 1923
showing an association between poor school grades and smok-
ing (15,83,121,187,143,161,212). Two studies have reported this
association specifically for girls (35,216). Comparing the three
factors—parental smoking, socioeconomic status, and scholastic
performance—Borland and Rudolph identified scholastic per-
formance as the strongest correlate of smoking in a sample of
high school students (20). Studies of achievement, aspirations

285
and expectations in relation to smoking have found that re-
duced motivation and lower aspiration are associated with a
higher prevalence of smoking (3,33,101,180). High school stu-
dents in college preparatory courses were far less likely to
smoke than students in any other type of curriculum (130).
Smoking rates for boys and girls preparing for college (9.0 per-
cent and 12.0 percent, respectively) were 50 to 60 percent of
those in other curricula (18.3 percent of boys, 20.1 percent of
girls). The same trend was found in a previous study (216).
Smokers are less involved in extracurricular school activities
and have a higher rate of absenteeism (9,35,137).

These factors are undoubtedly interrelated with social class
and other factors. Sense of competency and sense of efficacy (or
personal control) are linked to school achievement. Smokers
have been reported to have less confidence that they can control
what they will become (130). McAlister, et al. comment that high
academic achievement is probably also associated with admis-
sion into a peer group in which smoking is not accepted (125).
Furthermore, they state, “Educationally deprived young people
may be somewhat less aware of the risks of smoking, but they
also experience more stress and greater pressure to adopt be-
haviors that signal independence and maturity” (125).

Dynamic/Personality Factors

Up to this point, adolescent smoking has been described and
analyzed in terms of discrete variables, many of which are truly
not independent of one another. From them, a composite picture
of the environment of the female smoker begins to emerge. Par-
alleling the behavioral descriptors is a set of individual/
personality factors which include attitudes, values, beliefs, and
perceptions which relate the adolescent to the world around
her. Vitally important are feelings of self-worth, aspirations and
expectations for the future, and feelings of efficacy, competence
and the girl’s view of her own smoking behavior.

Yankelovich, et al. have provided a thought-provoking de-
scription of the evolution in values which has occurred over the
past 20 years (216). Smoking is just one behavior which may
have been “suppressed” by social norms prescribing appropri-
ate behavior for women in the past, and which now may be
“disinhibited” in a very real sense.

Accompanying this shift in sanctions on female behavior is an
increase in expressed rebelliousness among girl smokers, which
was formerly more characteristic of boys. A higher percentage
of female smokers than nonsmokers are annoyed by “experts”

286
who define what is good for them (53 percent versus 34 percent),
agree that there is too much regulation of people’s lives (50
percent versus 39 percent), and do not want to follow their par-
ent’s wishes regarding their behavior (almost 50 percent versus
26 percent) (216). Factor scores of male and female smokers
similarly reflect a more negative “feeling toward authority” or
dislike of adult-imposed restrictions than those of nonsmokers,
and are approximately equal for both sexes (130). Clausen noted
that girls who smoked were less acquiescent to their parents,
more autonomous, and “strikingly higher in quest for power”
than nonsmoking girls (83).

The evolution in values and sex-role behaviors has resulted in
some interesting differences between male and female smokers
(216). The male smoker remains more socially uneasy, expresses
a greater need to be popular with the opposite sex, and consid-
ers smoking more of a social asset than the female smoker. The
female smoker, compared with her nonsmoking peer, is more
likely to consider parties a favorite leisure time activity, to have
a boyfriend, and to have had sexual relationships (see also 174).
In addition, she is less likely to feel nervous meeting new people.
Finally, while she is more willing to admit that smoking is a
drawback, she shows less acceptance than the male smoker of
the stereotype that adolescents begin to smoke cigarettes to
gain peer acceptance and approval (130,216). Nonsmokers show
the greatest acceptance of this stereotype and the one which
describes the smoker as a “show-off (216), who believes that
smoking makes one look “cool” or “grown-up.”

In other studies of smoking behavior, self-esteem has usually
been investigated in terms of the adolescent’s self-confidence in
interpersonal relationships. Smoking is ego enhancing and
facilitates social functioning (122,123). This has been observed
specifically among adolescent girls and female undergraduates
who smoke (174,216). Smoking is correlated with a wish to be
older (130). Both boys and girls who differed from the norms of
their high school peers on tests of self-concept were more likely
to smoke cigarettes as well as to use other drugs (95).

Adolescent smoking has been consistently correlated with low
educational and occupational aspirations. In a review which in-
cluded “locus of control” as a measured variable, Smith con-
cluded that smokers were more externally oriented and felt that
they had limited control over what happened to them (176).
Pflaum reviewed findings on the positive relationship between
smoking and feelings of helplessness and hopelessness (143).
Adolescent smokers express less desire and ability than
nonsmokers to control future events—for example, to determine
what kind of person they will become (130). Girls scored slightly

287
higher than boys on this factor, indicating a greater sense of
future control.

Finally, response to stress has been suggested as a basic
dynamic in cigarette smoking (122). Feelings of unattractive-
ness, a sense of incompetency and inefficacy in school achieve-
ment and personal relations, limited opportunities for personal
growth and for future social and economic roles all contribute to
stress in adolescence. Changes in social settings, such as transi-
tion from elementary to junior high shool, which occur simulta-
neously with physical and emotional changes must also be ac-
knowledged. Theoretical formulations of life-change events and
their effects on health might also be worth considering in study-
ing the onset of cigarette smoking among girls (47).

Prediction of Future Smoking Behavior

In 1979, a longitudinal study was undertaken by the National
Institute of Education involving the re-interview of 46.8 percent
(N= 1,194) of the 2,553 adolescents first surveyed in 1974 (130).
In 1974, 152 respondents were smokers and 1,042 were
nonsmokers. By 1979, 27 percent (N = 41) of the smokers had
quit, while 73 percent (N = 111) had continued to smoke. During
the same time period, 20.8 percent (N = 217) of the nonsmokers
had taken up smoking, while 79.2 percent (n = 825) had not.
Thus, the proportion of smokers who had quit was greater than
the proportion of nonsmokers who had taken up the habit. How-
ever, because the percentage of nonsmokers was much higher
than the percentage of smokers, the net effect was an increase
in the percentage of the population who were smokers (12.7 per-
cent to 27.5 percent).

With each increase in age group, the proportion of boys who
initiated smoking became smaller, so that boys who reached age
17 or 18 as nonsmokers were not likely to start in the next five
years. Only 15.4 percent did so, compared with 19.3 percent of 15
to 16 year olds, and 21.6 percent of 12 to 14 year olds. For girls,
the pattern is less clear. Fifteen to 16 year old nonsmokers in
1974 showed the greatest proportion of initiators (27.1 percent)
by 1979. In the 12 to 14 age group, 22.8 percent took up smoking,
and only 14.7 percent in the 17 to 18 age group did so.

Demographic and psychosocial relationships studied in 1974
were reexamined in this group now aged 17 to 23. The influence
of older siblings became less powerful than the influence of
peers, but educational attainment was still inversely correlated
with smoking status.

Those smokers who had quit had a shorter lifetime history of
smoking and were lighter smokers than those who were current

288
smokers in 1979. Of the former smokers, 24.7 percent said they
had been smoking less than daily just before quitting, and
another 34.5 percent smoked 1 to 14 cigarettes per day. Only 7.6
percent of current smokers report less than daily consumption.
This suggests that the former smokers may have been less de-
pendent (psychologically or physiologically) upon cigarettes and
may have found giving up the habit easier than heavier smok-
ers. In fact, 50 percent of the former smokers succeeded in quit-
ting on their first attempt, while 61.6 percent of current smok-
ers had made one or more unsuccessful attempts to quit.

These young smokers were concerned about health issues.
Sixty percent of current smokers had made at least one at-
tempt, and another 20 percent would have been willing to quit if
there were an easy way to do so. A greater percentage of young
women than men (91.0 percent and 85.2 percent, respectively)
expressed a concern about health effects of smoking. The risk
associated with oral contraceptive use and smoking and the
harmful effects on the fetus of smoking during pregnancy (130)
may be responsible for this increased concern. Young women
were more likely than young men to say that all cigarettes are
equally hazardous (33.7 percent and 25.9 percent, respectively).

Multiple regression analysis was used to identify those ado-
lescents most likely to take up smoking, and discriminant func-
tion analyses were used to predict future smoking for each
stage—nonsmoker, experimenter, regular smoker, and ex-
smoker. The best predictor of future smoking behavior was the
adolescent’s own perception of his or her future smoking behavior.

The best predictors of future smoking for never-smokers and
experimenters were smoking by an older sibling, scores on at-
titude scales, and age. The chance that a nonsmoker will start
smoking become smaller as the nonsmoker grows older. Once
regular smoking was initiated, the variables of higher dosage,
lower educational aspirations, friends who smoked, and lack of
acceptance of the health risks of smoking predicted continued
smoking behavior.

In summary, this study revealed that former smokers seemed
more similar to experimenters than to regular smokers. Their
smoking histories were shorter, and they had a lower dosage
and did not have much difficulty quitting. Regular smokers, on
the other hand, tried to quit or expressed an interest in doing so,
and were bothered by the health hazards associated with smok-
ing. Five years previously, they were able to accurately predict
their current smoking status. Smoking was also more likely to
be a behavior of their older siblings and peers. And lastly, both
educational aspirations and attainments were lower for this
group.

289
PREVENTION OF SMOKING AND CONSIDERATIONS FOR
FUTURE RESEARCH

Prevention of the Initiation of Smoking

There are a number of ongoing interventions which attempt
to prevent the initiation of smoking (34,58,59,125,198). These
studies are directed at elementary, junior high, and high school
students, and use an “inoculation” approach to prevention. Ex-
posure to a small amount of information about pressures to
smoke is accompanied by practice in coping and assertiveness
strategies. The main types of influences in which students are
instructed are peer pressures, parental modelling, and media
pressures. Peer instructors are often used to maximize influ-
ence. Compliance in self-reporting smoking behavior is in-
creased by the use of physiological measures of smoking, for
example, salivary nicotine or expired air carbon monoxide,
which may or may not be analyzed for the entire subject sam-
ple.

Dissemination of information about the health risks of smok-
ing seems to be successful, at least on a superficial level.
Ninety-six percent of all adolescents (and 91.6 percent of smok-
ers) “strongly or mildly agreed” that smoking is harmful to
health (130). Percentages were similar for boys and girls, and
nonsmokers scored higher on all health-related questions than
smokers. Almost 90 percent of adolescent smokers (87.9 percent
of boys and 89.9 percent of girls) “strongly or mildly agreed”
with the statement, “I believe the health information about
smoking is true.” Fishbein has pointed out, however, the poten-
tial importance of the difference between strong and mild
agreement with such statements, and the lack of direct personal
attribution involved (63). Only 60 to 65 percent of adolescent
smokers expressed strong agreement, compared with approxi-
mately 80 percent of nonsmokers. Either reduction of cognitive
dissonance by denial or actual lack of information may underlie
this response pattern. Finally, a surprisingly high percentage of
smokers feel (strongly or mildly agree) that it is all right to
smoke if “you don’t smoke too many.” On this item, fewer girls
(25.6 percent) were willing to endorse this statement than boys
(43.3 percent).

Somewhat lower estimates of the acceptance of health infor-
mation comes from the 1975 American Cancer Society (ACS)
Survey (216). Of all adolescent girls 74 percent agree that smok-
ing is as harmful for women as it is for men; 71 percent agree
that smoking is harmful for young people as well as for older
people; 56 percent agree that it is not safe to smoke low “tar”
cigarettes; and 56 percent agree that smoking is as addictive as

290
illegal drugs. Comparable figures are not provided for boys, nor
are the data broken down by smoking and nonsmoking
categories. This survey further reports that 68 percent of the
girls sampled were not warned about smoking by their doctors.

While 60 percent of female smokers began to smoke before the
age of 13, only 48 percent attended an antismoking education
program in school, and a mere 4 percent attended such a pro-
gram in the sixth grade when they were approximately 12 years
old.

These statistics suggest that smoking education and coping
strategies should begin earlier in schools and should begin ear-
liest for high risk groups.

Research Goals

The best evidence suggests that female cigarette smoking
rates are declining. This change has occurred in more recent
adolescent cohorts—those born after 1962. National surveys are
likely to underestimate true rates, whether school, household,
or telephone samples are used. Drop-out, absenteeism, lack of
telephone accessibility, and belonging to a minority group all
contribute to the sampling errors, which include under-
representation of population subgroups whose rates are sub-
stantially higher than the norm. Accurately measuring these
subgroups would enable scientists to better target interven-
tions. Young black females appear to be one such group whose
smoking rates well exceed the national average (33).

There is good reason to expect the heaviest cigarette use and
other “problem behaviors” among those segments of the adoles-
cent population who feel cut off from socioeconomic opportunity
and mobility. The review of correlates of adolescent smoking
shows that many of the variables that predict cigarette smoking
bear a remarkable similarity to ones identified as predictors of
marihuana and/or other illicit drug use. It is recommended that
greater attention be given to models of behavior and socializa-
tion processes.

More prospective longitudinal studies need to be undertaken,
based on varied samples of children. Data need to be collected
about physical and emotional status, psychosocial outlooks and
attitudes, family and peer relations, academic and recreational
activities, family and school settings, and family and residential
background. This information must be gathered early in child-
hood to record significant socialization influences which pre-
cede the onset of smoking behaviors and should be collected
frequently enough to record significant changes close to the
time they occur.

291
666

TABLE 4.—Smoking parameters observed in Hamburg, Germany,

in 1971 and 1974

 

Puff Duration

Puff Interval

Total Puff Duration

 

 

 

Puff Number
1971 1974 1971 1974 1971 1974 1971 1974
Men 10.2 10.9 1.47 1.47 52.9 42.1 15.0 16.0
Women 10.9 13.3 1.31 1.17 46.0 40.7 14.3 15.5
All 10.5 11.8 1.41 1.34 50.3 41.5 14.8 15.8

 

SOURCE: Schulz, W. (167).
Maintenance of Smoking Behavior

PATTERNS OF CIGARETTE SMOKING

Smoking patterns differ between the sexes. Schulz and
Seehofer studied the smoking behavior of male and female
smokers observed surreptitiously in public places. Puff number,
duration and interval were measured (167). Women were found
to leave a significantly longer butt length (approximately 2mm
longer) and had shorter puff durations than men (Table 4).
However, they took a greater number of puffs and, therefore,
had the same total puff duration (puff number x puff duration).
These authors do not report gender data on inhalation patterns,
which are crucial to determining dose. However, Creighton and
Lewis reported no sex differences in puff volume in a small study
of the inhalation patterns of eight men and eight women (39).

Data on smoking patterns were collected in surveys con-
ducted in 1964, 1966, 1970 and 1975 by the National Clearing-
house for Smoking and Health (NCHS) (see Table 5). In each
survey a greater proprotion of men than women reported inhal-
ing deeply into the chest and inhaling almost every puff. Men
therefore may extract a greater dose of nicotine and the other
constituents of cigarette smoke than do women. However, there
is an increasing proportion of women who report smoking their
cigarettes “as far as possible,” in contrast to a decline in the
proportion of men who reported this behavior (167,192,193,194).
A slightly higher proportion of males reported letting “very lit-
tle” of their cigarette burn without smoking it: 1970, 20.6 per-
cent male vs. 18.0 percent female; 1975, 20.9 percent male vs.
18.6 percent female (193,194). These changes are often a corre-
late of heavier smoking. In sum, the observational data suggest
that men and women have equal total duration of smoking per
cigarette, and the national survey data suggest a larger propor-
tion of males inhale deeply. In general, men smoke in a more
hazardous way than do women. However, the smoking patterns
of women are changing toward “more hazardous” smoking (see
Part I of this Report).

In contrast to the minor changes that have occurred in the
way an individual cigarette is smoked, there have been sub-
stantial changes in the percentage of both male and female
smokers who smoke more than a pack per day (Table 6). A
number of explanations may be offered for these data: (1) more
lighter than heavier smokers may be quitting, resulting in a
mean increase in daily consumption; (2) continuing smokers
may be increasing consumption; (3) smokers newly initiating
the behavior may be smoking more heavily than already estab-

293
v66

TABLE 5.—Respondent-reported styles of cigarette smoking, current, regular cigarette smokers, selected
categories, adults, United States, 1964-1975

 

 

 

1964 1966 1970 1975
Male Female Male Female Male Female Male Female

1. Inhaling deeply

into the chest 36.5% 22.5% 31.8% 15.5% 34.38% 17.5% 30.3% 16.4%
2. Inhaling almost

every puff 63.1 54.8 63.0 52.1 60.5 47.2 58.5 50.7
3. Smoking cigarette

as far as possible 15.9 V5 13.5 10.0 9.6 10.4 10.9 12.9

 

1. In 1964 and 1966, the questionnaire response was “as deeply into the chest as possible.” In 1970 and 1975, the questionnaire
response was phrased “deeply into the chest.”

2. In each survey year, the questionnaire response was “inhale almost every puff of each cigarette.”

3. In 1964 and 1966, the respondent was asked to draw a line on a diagram of a cigarette, indicating the average length of the
discarded cigarette butt length. In 1970 and 1975 the verbal questionnaire response was smoking cigarette “as far as possible.” The data
for 1964 and 1966 correspond to those respondents indicating a discarded cigarette butt length no greater than 20 mm.

SOURCE: National Clearinghouse for Smoking and Health (192,193,194).
6d

TABLE 6.—Estimates of the percentage of current, regular cigarette smokers who consume more than one pack

per day, adults, United States, 1955-1976

 

 

 

 

Supplement to Current Health Interview National Clearinghouse
Population Survey Survey for Smoking and Health
(17 yrs. and over) (17 yrs. and over) (21 yrs. and over)
21 cigarettes or 25 cigarettes or 25 cigarettes or
more daily more daily more daily
Year Total Male Female Total Male Female Total Male Female
1955 20.2} 25.5 9.8
1964 25.7 32.4 17.7
1965 19.9 24.5 13.7
1966 21.6 26.3 15.7 27.2 34.7 16.9
1967 21.9 26.2 16.3
1968 22.4 26.5 16.8
1970 23.3 27.6 18.1 25.2 31.1 17.1
1974 24.7? 30.3 18.4
1975 30.1 36.0 22.8
1976 25.3 30.8 19.4

 

118 years and over.

2Data provided by Health Interview Survey, National Center for Health Statistics.
320 years and over.

SOURCE: U.S. Department of Health, Education, and Welfare (198).
TABLE 7.—Estimates of the percentage of current, regular
cigarette smokers among white and black adults,
aged 20 years and over, United States, 1965-1978

 

White Black
a SS
Year Male Female Male Female
1965 51.5 34.2 60.8 34.4
1970 43.7 31.9 54.0 33.1
1974 41.9 31.8 55.3 36.8
1976 41.2 31.8 50.5 35.1
1978* 36.4 30.1 42.8 30.2

 

*NOTE: Results displayed as percentage of respondents with known smoking

status aged 17 years and over.
SOURCE: U.S. Department of Health, Education, and Welfare (198).

lished smokers; and (4) declining “tar” and nicotine contents of
cigarettes may be leading to compensatory increases in number of
cigarettes smoked in order to maintain nicotine dosage (198).

Regarding type of cigarette smoked, the 1975 NCSH survey
reported that more women than men smoked filter tip cigar- -
ettes (all types), 90.6 percent vs. 79.3 percent. Women seem to be
innovators in changing smoking practices. Sixty-one percent of
women and only 10 percent of men acknowledge changing
brands at least once, and women lead the trend in adopting
king-size, filter-tip and 100 mm cigarettes. On the other hand,
women smoke cigarettes almost exclusively. Cigars and pipes
are currently used by 18 percent and 25 percent of men, respec-
tively, but by less than 0.5 percent of women. Less than 2 per-
cent of women use snuff or chewing tobacco compared with 2.5
percent and 4.9 percent of men, respectively.

SMOKING PREVALENCE AND ETHNICITY

The prevalence of smoking in the population varies not only.
with age, sex, and socioeconomic status, but also with race and
cultural background.

Table 7 presents smoking prevalence among white and black
adults form 1965 to 1978 (198). Smoking has declined among men
of both races, but prevalence has decreased only slightly among
white and black females. Congruent estimates of prevalence
and lower cessation rates among blacks have been obtained in
other studies (66,183,201).

Despite their greater prevalence of smoking, black men and
women smoke fewer cigarettes per day than whites (66,183).

Black women may suffer the worst aspects of sexism and rac
ism with respect to occupational opportunity and financial com
pensation. Cigarette smoking may be related to assertion, inde

296
pendence, and rebellion or to identification with behavioral pat-
terns of black males. Adolescent dynamics have been studied
more than those of adults (see the section on adolescent smok-
ing cessation in this Part). Warnecke, et al. found that social and
psychological correlates among black women are similar to
those observed among white women (201).

Friedman, et al. examined smoking prevalence among Asian
men and women—Chinese, Japanese, Korean or unknown—
from the Kaiser Permanente Health Plan and found a smaller
percentage of cigarette smokers than among whites or blacks.
Asian women had the least frequency of current, established
cigarette smokers, 23.1 percent, compared to 39.2 percent of
white women and 42.1 percent of black women. Asians were also
the least likely to inhale among most age-sex groups of smokers.
There were fewer cigarette smokers among Chinese than
among Japanese; this was particularly true for women and
younger men (66).

PHARMACOLOGICAL EFFECTS OF SMOKING

One or more of the constitutents of cigarette smoke may play
a role in the maintenance of smoking behavior and help account
for the difficulties many individuals experience when they try
to quit smoking (198).

Nicotine

Nicotine is absorbed rapidly from the oral and intestinal mu-
cosa, lungs, and skin. It is distributed throughout the body and
is metabolized by several organs, including the liver. It is then
rapidly cleared, primarily through the kidney. Nicotine has ef-
fects on several organ systems, including the autonomic ner-
vous system, voluntary muscles, stomach, intestines, heart, and
brain. Most of the pharmacological actions of nicotine are
thought to result from its interaction with receptors of
cholinergic nervous systems. Analysis of the physiological ef-
fects of nicotine is complicated by the abundance of those ef-
fects. Many organs receive input from several neuronal systems
which are altered directly or indirectly by cholinergic activity.
Furthermore, the effects of nicotine itself depend both on the
dose and on the time course of drug administration: brief expo-
sure or low doses cause excitation of cholinergic systems, while
long exposure and high doses result in inhibition and paralysis.

Peripheral Effects

Nicotine produces a variety of changes in the autonomic ner-
vous system due to simultaneous effects on both sympathetic

297
and parasympathetic systems. The end result is an increased
heart rate and blood pressure; cold, clammy skin; increased acid
production in the stomach; increased intestinal activity; and
biphasic changes in salivation, with an initial increase followed
by a decrease. Nicotine also increases respiration.

Central Effects

Nicotine produces tremors and causes water retention by a
central effect on antidiuretic hormone release. Nicotine-
induced nausea and vomiting reflect a complex interaction be-
tween central and peripheral effects. To date, no specific effects
on complex emotions and behaviors have been demonstrated.
Animals will self-administer nicotine under certain circum-
stances, indicating that it may have pleasurable effects.

A Possible Role for Nicotine in Smoking Maintenance

A strong argument has been made for classifying smoking as
an addiction, with nicotine as the leading candidate for the ad-
dictive agent. Inhalation of cigarette smoke offers an effective
way to administer nicotine. Absorbed rapidly, it travels as a
highly concentrated bolus through the heart and directly to the
brain and is then rapidly cleared. A smoker who smokes one
pack per day can average around 70,000 such nicotine “‘injec-
tions” per year. In behavioral terms, smoking has many poten-
tial conditioned stimuli, ranging from the taste, sight, and feel
of the cigarette itself, to the many social settings in which smok-
ing takes place. If nicotine were a strong unconditioned
stimulus, particularly when inhaled, then it would be easily un-
derstandable that smoking can become a remarkably persistent
habit through connection of this unconditioned stimulus with
the many associated stimuli.

Although nicotine has effects on essentially all major organs
in the body, including the brain, the role of those actions in
maintaining the smoking habit remains an important but unre-
solved area of research.

The nicotine hypothesis of smoking states that the phar-
macological actions of nicotine are “reinforcing.” The most
likely site of this rewarding or reinforcing action is the brain,
with the precise locus of reinforcement not yet determined. In-
haling smoke insures rapid delivery of nicotine to the brain. It
takes approximately 13.5 seconds for an intravenous injection
of nicotine in the arm to reach the brain; but by inhalation, the
delivery time is 7.5 seconds (158). The plasma half-life of nicotine
is approximately 30 minutes, and the pack-a-day smoker lights

298
up approximately every 30 to 40 minutes of the day. This
suggests that the smoker is attempting to maintain a constant
level of nicotine.

The nature of the reinforcing effect is sometimes described as
an alteration of arousal. Stimulation may be subjectively expe-
rienced as increased alertness, a facilitation of concentration, or
an aid to continued efficient performance in fatiguing tasks.
Sedation, on the other hand, may be experienced as a tran-
quilizing or calming effect or as a reduction of some dysphoric
state, such as anger. Smoking has been described as distinctly
pleasurable following a meal or accompanying xanthines (coffee
and tea) or alcohol. Pharmacologic and psychologic components
to these subjective reports are beginning to be identified (70,78).

There is extensive literature describing acute and chronic
nicotine administration in animals including a limited number
of self-administration models. Tolerance to nicotine has also
been described (81,88,112).

A number of studies have examined the hypothesis that hu-
mans self-administer tobacco in order to obtain nicotine.
Studies have also examined compensatory adjustments in the
number of cigarettes and manner of smoking by subjects in re-
sponse to experimenter-induced increases or decreases in
cigarette nicotine content, cigarette size, availability, or sup-
plemental nicotine administration. Chewing gum containing
nicotine, nicotine tablets, intravenous nicotine and central or
peripheral nicotinic blocking agents have been used to supple-
ment or block the effects of the nicotine absorbed from the
smoke. A titration effect is said to occur if subjects change their
cigarette smoke intake in the appropriate direction in response
to these experimental manipulations.

A modest amount of compensation has usually been demon-
strated (79,158). Smokers seem to titrate along the nicotine,
rather than the “tar” continuum but an optimum ratio of nicotine
to “tar” probably exists for effective delivery to the lung. Experi-
ments involving the intravenous administration of nicotine
have been inconclusive, with both positive and negative effects
on the suppression of subsequent smoking having been ob-
served. When compensation occurs, it is seldom complete. This
may be due to a number of factors: (1) the inability to accurately
measure the smoker and/or nicotine dose delivered to the sub-
ject; (2) technical problems in experimental design (79,198); (3)
secondary reinforcing effects of smoking which mask titration;
and (4) the fact that people may smoke for reasons other than
regulation of nicotine level.

Some have even suggested that nicotine controls smoking beha-
vior only at the extremes, and then as an aversive agent (163).

299
Too much smoking might lead to such high serum concentra-
tions of nicotine that toxic effects encourage lower intake;
and toc little smoking or smoking of low-nicotine cigarettes
could lead to such low concentrations that withdrawal side ef-
fects encourage resumption of smoking. This hypothesis states
that, between those two extremes, other factors such as psycho-
logical and social pressures are far more influential in deter-
mining smoking patterns.

Differences in Nicotine Metabolism

The metabolism of nicotine may be different in men and
women. Measurement of nicotine and cotinine (the principal
metabolite of nicotine) excreted in the urine after intravenous
administration of nicotine hydrogen tartrate suggested dif-
ferences in metabolism based on sex and smoking status (73). In
nonsmokers, men excreted less nicotine but more eotinine than
women, suggesting greater initial metabolism among men.
However, there were no clear differences between male and
female smokers.

Schievelbein, et al. studied nicotine and cotinine excretion in
both regular smokers and nonsmokers after they smoked
cigarettes with differing tar and nicotine levels (165). Women
excreted significantly lower amounts of nicotine and cotinine
compared with men for three of the four brands tested. The
gender difference was found for the excretion of nicotine and
cotinine when tested separately and together. The number of
cigarettes smoked per day did not differ between the sexes, but
the carboxyhemoglobin (COHb) levels, which are often taken as
a correlate of depth of inhalation, were lower in the women. The
female subjects, therefore, may have received a lower dose of
nicotine because of a different smoking pattern.

SMOKING AND STIMULATION EFFECTS

The literature suggests that women are more likely to smoke in
situations of high arousal than low arousal and when experienc-
ing “negative affect” (69,96). The effects of smoking, which are
often perceived as tranquilizing, might then be sought as a
major coping mechanism. However, it can also be argued that
the stimulant effects of nicotine, which are usually considered
the predominant central nervous system action, might be
equally useful as a mobilizer. These related and commonly held
beliefs will be examined in some depth.

Frith (69) studied British male and female employees in a
psychiatric institute; they ranged in age from 28 to 50. Subjects -
rated the strength of the desire to smoke in 22 hypothetical

300
situations. The 12 high-arousal items involved either emotional
strain and anxiety or demanding mental activity; the ten low-
arousal items concerned boredom and relaxation or repetitive
tasks and physical fatigue. A factor analysis of the entire ques-
tionnaire and t-tests performed on male versus female scores
for the most extreme situations on the continuum led Frith to
state that men had a greater desire to smoke in situations in-
ducing boredom and tiredness and women had a greater desire
to smoke in stress-inducing situations. However, men rated the
desire to smoke significantly higher than did women on all three
of the questions representing low-arousal situations, whereas
women rated the desire to smoke significantly higher on only
one of the three questions representing the high-arousal ex-
treme of the continuum (69).

Using Frith’s questionnaire, Barnes and Fishlinsky were un-
able to replicate his findings in a sample of Canadian under-
graduates (12). Within the male sample, there was no significant
relationship between desire to smoke and the arousal value of
the situation in the question, and female subjects indicated a
greater desire to smoke in the low-arousal situations. The au-
thors point out the possible importance of sampling differences.

Elgerot studied light, medium, and heavy smokers in an at-
tempt to control potential differences in inhalation patterns be-
tween men and women (cited by Frith as a possible explanation
for his results) (57). Subjects were Swedish university students.
The 42-item questionnaire was similar, but not identical, to
Frith’s. There was no gender difference for low-arousal situa-
tions. There was no sex difference in the light and medium
smoker subgroups, but women in the heavy smoker subgroup
expressed a greater desire to smoke in stress-inducing circum-
stances.

Russell and his colleagues devised a 34-item questionnaire
covering a wide variety of smoking motives. It was adminis-
tered to 175 normal smokers and then subjected to factor
analysis (160). Six factors, representing six types of smoking,
were identified. Women scored significantly lower on what was
termed “sensorimotor” smoking, and significantly higher on
“sedative” smoking. Thus, the sex difference on “sedative”
smoking (reduction of arousal) was supported.

Ikard and Tomkins (96) found evidence that women smoke in
situations involving negative affect. Negative affect smoking is
defined as smoking which serves to reduce unpleasant feelings.
It includes smoking to reduce the dysphoric feelings accom-
panying rejection by a social group as well as smoking to satisfy
a craving for a cigarette (i.e., deprivation negative affect). Posi-
tive affect smoking involves the arousal of pleasant feelings.

301
For example, smoking from curiosity would be classified this
way because of the feelings of excitement and interest gener-
ated. Ikard and Tomkins showed two films, one intended to
evoke positive affect (a slapstick comedy), and another to evoke
negative affect (a documentary on Nazi atrocities) to college
students who smoke. To be characterized as either positive- or
negative-affect smokers, the subjects had to smoke during the
appropriate film and indicate a congruent mood on an affect
checklist. The major finding was that 73 percent of the female
sample of 15 subjects exhibited solely negative-affect smoking
compared to only 36 percent of the sample of 39 males. While 80
percent of the females indicated that they were likely to smoke,
in positive as well as negative-affect conditions, their behavior
did not match the self-report in this experiment. It is difficult to
determine if the environment of the experiment altered normal
behavior patterns, or if perhaps smokers are not accurate in
describing the types of situations in which they smoke.

Nationwide surveys conducted in 1964, 1966, and 1970 also
suggested that a higher percentage of women than men are
negative-affect smokers and that little or no difference exists
between men and women in the percentage who are positive-
affect smokers (192,193). A greater percentage of women cur-
rent smokers endorsed the statement, “It relaxes me.” (192).
This supports the hypothesis that reduction of negative affect is
a more important factor for women smokers. The statements
assessing positive-affect smoking did not show a clear gender
difference. In 1964, slightly more men than women endorsed the
statement “enjoys it” as a reason for smoking, but in 1966 there
was no difference between sexes and in 1970 slightly more
female than male current smokers agreed that “cigarettes are
pleasurable” (79.6 percent of women versus 77.0 percent of
men).

To summarize: smoking affects arousal; it is not known
whether women smoke to maintain a given arousal level, to
change that level, or to adjust a physical blood level of nicotine.
There are a number of studies which suggest that women use
cigarettes more in high-arousal situations than do men. Studies
which combine self-report with experimental situations provid-
ing a good approximation of natural smoking conditions are
needed to shed some light on the validity of evaluation by ques-
tionnaire alone.

Smoking Cessation

There is an assumption in the treatment literature that men
have greater success than women in quitting smoking. The

302
basis of this assertion lies partially in the demographic analyses
of cessation rates and partially in the literature on smoking
cessation clinics and experimental programs.

This section presents the results of both demographic and
experimental analyses of smoking cessation. A critical ap-
praisal is made of the relative success of men and women in
giving up smoking and in remaining ex-smokers. Psychosocial
and behavioral factors relating to abstinence and difficulties
encountered in quitting are discussed. Finally, recom-
mendations are presented for treatment and future research.

DEMOGRAPHICS

The quitting rates of smokers are calculated by dividing the
number of former smokers by the number of ever smokers
within each relevant demographic category. The following
statistics are taken from the 1975 U.S. Department of Health,
Education, and Welfare (USDHEW) survey on Adult Use of To-
bacco (194). Former smokers are defined as those who once
smoked but no longer do so. The term “former smokers” in-
cludes both those who have quit on their own and those who
have received outside help. Quitting rates of women lag behind
those of men, for each category reviewed.

Age

The USDHEW tables divide adult age groups into six
categories: ages 21 to 24, 25 to 34, 35 to 44, 45 to 54, 55 to 64, and
65 and over (194). There is a trend toward increasingly larger
percentages of former smokers in each successive age group for
both men and women. However, within each age group, the per-
centage of smokers who have quit is higher for men than it is for
women. For example, in the youngest age category, the per-
centage of female smokers who have quit is 22.6 percent while
that for males is 27.9 percent. For a middle-aged category (45 to
54), the female and male percentages are 32.0 percent and 46.7
percent respectively. In the oldest age group, 51 percent of
female ever smokers are former smokers, whereas the percent-
age is 60 percent for males. Bosse and Rose state that the
sex differences in quitting are vanishing at younger ages, but
Dicken argues persuasively that the absolute amount of con-
vergence is small, and that men remain substantially more
likely to stop smoking than women (21,45).

Education

Higher levels of education are associated with higher rates of
quitting for both men and women. Among those with a college

303
TABLE 8.—Most frequently endorsed reasons for resuming
smoking: Fall 1964 and Spring 1966 household
interview survey, responses of current smokers

 

Q: People give all sorts of reasons for either not being able to or not wanting to
stay off cigarettes. What were your reasons for going back to cigarettes?
(Asked if made a serious attempt to stop smoking.)

 

Current Smokers

 

 

 

1964 1966
N % N %
Selected total M 705 55.7 112 §4.9
F 542 50.6 588 57.1
No will power M 291 23.0 278 19.8
F 209 19.5 191 18.5
It relaxes me M 212 16.8 181 12.9
F 245 22.9 192 18.6
Enjoys it M 144 11.4 123 8.7
F 102 9.5 90 8.7
Helps keep weight down M 65 5.1 40 2.8
F 15 7.0 57 5.5
Smoke to be sociable M 98 U7 43 3.1
F 70 6.5 46 4.5

 

NOTE: More than one answer was allowable for each respondent.
SOURCE: U.S. Department of Health, Education, and Welfare (192).

education or higher, 52.1 percent of the men and 48.1 percent of
the women who have ever smoked have quit. For all other levels
of education, 40.5 percent of men smokers and 31.3 percent of
women smokers have given up smoking. Although the discrep-
ancy is less in the most advanced education category, the per-
centage of female quitters is smaller at both levels of schooling.

Income

Higher levels of income are associated in both sexes with
higher rates of cessation. For those ever smokers with incomes
under $10,000, the rates of quitting for men and women are 34.7
percent and 30.3 percent respectively. For those with incomes of
$10,000 or above, the rates are 45.7 percent for men and 36.2
percent for women. Quitting rates of men exceed those of
women for all but one ($5,000 to $7,499) of the seven income
levels.

Occupation

There is a difference of only 7.6 percentage points between the
proportion of male and female quitters in the category of pro-
3804
fessional, technical, and kindred workers, with the male quit-
ting rate at 49.4 percent and the female quitting rate at 41.8
percent. A dramatic increase in this difference occurs, however,
among managers, officials, and proprietors. In this category the
quitting rate for men is 47.1 percent and that for women is only
26.5 percent. Among sales and clerical workers, 40.1 percent of
the men and 25.8 percent of the women have quit. The quitting
rate of homemakers (33.9 percent) is in the mid range of the
rates for women in other occupations.

In general, then, women are quitting at lower rates than men
across the major demographic categories.

PSYCHOLOGY OF CHANGING SMOKING HABITS

A two-year follow-up of over 500 former smokers identified in
the 1964 nationwide survey provides support for the demo-
graphic data showing higher proportions of ex-smokers among
males than females (56). Men were significantly more likely
than women to remain successful abstainers. Men and women
made approximately the same number of attempts to quit, and
current smokers made more attempts than former smokers
(168). Furthermore, successful quitters have usually made at
least one abortive attempt to quit before succeeding. A survey
of young women, aged 18 to 35, revealed that light smokers had’
the greatest success in stopping smoking (216). This finding is
not entirely consistent with that of Eisinger (56), however, who
reported that long-term smoking was a predictor of successful
abstinence. The difference in study samples may account for the
lack of “fit” of the two results, as Eisinger’s survey included all
adults 21 years of age and older. The “reinterview” (follow-up)
aspect of Eisinger’s study gives further credence to his conclu-
sions since they are based on data actually obtained at two
points in time.

Those factors which consistently seem to differentiate be-
tween those who can quit or reduce intake and those who can-
not are: the presence of strong motivation and commitment to
change; the use of behavioral techniques; and the availability of
social support. Those who successfully quit or reduce smoking
use behavioral techniques such as substituting candy and gum
for cigarettes, and some form of self-reinforcement of desirable
behaviors to maintain abstinence (140,216). Successful reducers
use behavioral techniques more consistently and for a longer
period of time than those who fail to reduce smoking (140). Suc-
cessful quitters experience cravings when they stop, but the use
of substitutes seems partially to alleviate these feelings (139).
Furthermore, those smokers who do reduce intake are more

305
motivated and committed to personal change (140), and long-
term abstainers have more confidence in their ability to remain
ex-smokers (56). Successful reducers receive more positive rein-
forcement from others and the best known acquaintances of
successful abstainers are former smokers (56,140). Warnecke, et
al. reported female relatives to be the primary role models for
women who quit smoking (201).

TREATMENT STUDIES

Most smokers who attempt to quit do not seek outside help to
stop smoking. The population that seeks treatment may be one
that experiences severe difficulty in giving up smoking.
Thirty-nine treatment studies on smoking have reported suc-
cess rates for males and females, and have used the criterion of
total abstinence. Two exceptions were made for programs that
reported “success” in terms of 90 to 100 percent reduction.

The studies reviewed here fall into five categories of treat-
ment: education, physician advice, pharmacotherapy,
psychotherapy, and behavior modification (Tables 9-13). The
categorization is, by necessity, only a rough separation of
treatment modalities. Evaluation of the gender difference ques-
tion, however, does not rest directly on the categorization
schema.

Many of the studies listed in the tables did not report significant
evaluations for male/female quitting rates. Therefore, a chi
square statistic or Fisher exact probability test was calculated
wherever sufficient data were available. Because of the limited
number of studies identified for analysis and the often limited
sample size, results of borderline (0.05 <p <0.10) and acceptable
(p <0.05) levels of significance are reported for the reader’s infor-
mation.

The end-of-treatment cessation rates are high for all types of
treatment, but the maintenance of cessation tends to be much
lower. In 1971, Hunt, et al. demonstrated that recidivism curves
of heroin, alcohol, and smoking are almost identical, with long-
term cessation falling off steeply from the end of treatment (94).
Within three months approximately 35 percent of successful
quitters are still not smoking, and by one year, the figure is
closer to 20 percent. In 1978, another reviewer cited virtually
the same figures (147). There have been reports of improvement
in techniques for obtaining abstinence and in maintaining it,
using rapid smoking (an aversive conditioning technique), hyp-
nosis, and group therapy. The long-term cure rates of 60 percent
or higher at six months claimed in some studies have not been
reproducible in other settings. The smoking cessation literature
has been recently reviewed in detail (80,147,168, 198).

306
Across all treatments, women have more difficulty giving up
smoking than men, both at the end of treatment and at long-
term points of measurement. No studies have been reported in
which women do significantly better than men. Several of the
larger studies show higher abstinence rates by men, but many
show no difference. Results in the tables are based primarily on
those who complete treatment programs. Attrition rates are
very difficult to evaluate because most studies do not discuss
the issue of subjects who drop out of treatment.

Because of the emphasis placed on the role of physician advice
in increasing smoking education and promoting cessation, an
estimate of its effectiveness is relevant. From retrospective
data, it is estimated that 35 percent of people who have been
advised by a doctor either to quit or to cut down sharply, actu-
ally do quit (139). Twenty-five percent of those who have not
talked to a physician about smoking quit, and only 12 percent
who have been told by a physician that it was permissible to
continue smoking quit.

The prospective treatment literature yields varying esti-
mates of the impact of physician advice. Ten to 25 percent of
patients advised by a physician to quit or cut down actually do
so (198). Gender does not seem to exert a particular influence.
The primary variables associated with the ability to quit after
physician admonition were good psychosocial assets, psycholog-
ical stability, and the ability to verbalize depression (54).

Success in treatment in general seems to relate to personal
characteristics. A shorter smoking history and lower cigarette
consumption also predict a greater likelihood of cessation
(104,144,204). In addition, those subjects most likely to succeed
in treatment are highly motivated, believe they will succeed,
and are confident of their ability to stop smoking (82,136,187).

One group of women that seems to have great difficulty in
giving up smoking in treatment is homemakers. Homemakers in
the age range of 18 to 35 tend to be heavy smokers, and heavy
smoking is one predictor of failure in treatment (216). Kanzler, et
al. found that homemakers were less successful at quitting, par-
ticularly at long-term follow-up (104). However, as previously
discussed, homemakers have quit rates in the mid-range of
those of women in other occupations; therefore, the difference
may apply only to those homemakers who seek help through
treatment programs.

Wilhelmsen found significant male/female differences in
treatment success rates and stated that the poorer performance
of women related almost exclusively to the unsuccessful results
of homemakers (209). These women explained that cigarettes
served as companions and they reported the difficulties of being

307
& TABLE 9.—Education-Smoking cessation treatment results by sex

8

 

Percent Abstinence

 

 

 

 

 

End-of- Six
Treatment Months Long Term
Study Treatment N (%) (%) (%)
1. Guilford, 1967** (82) Five-Day Plan* unaided 75M 23M \ 2
100F 12F
Aided 82M 27M |
91F 29F
2. Peterson et al., Five-Day Plan 134M&F 7T9M&F 19M (18 mo. follow-up
1968** (141) 19F on 121 Ss)
3. Berglund, 1969** (4) Five-Day Plan 895M&F 87M 382M } 31M }
R4F o7F 2 23F 1 (4-18 mo.)
4. Delarue, 1973 (44) Education, small groups 472M&F 34M (12 mo.)
21F
5. Danaher et al., Education; skill training group 11F 50 (of 8 Ss 50 (9 mo.)
1978f (41) finishing
treatment)
6. Ochsner & Damrau, Pamphlets* 20M sort i
1970 (136) 33F 52F
7. Pyszka et al., American Cancer Society Clinics 131M 39M&F 28M (18 mo.)

19738** (146) 223F 20F

 
608

TABLE 9.—Education— Smoking cessation treatment results by sex—(Continued)

Percent Abstinence

 

 

 

End-of- Six
Treatment Months Long Term
Study Treatment N (%) (%)
8. Kanzler et al., 1976 (104) Smokenders 210M 70M om 1 (48 mo.)
343F 69F 30F ,
9. Dubren, 1977* (53) T.V. spots 92M eM 1
218F TF

 

ly <0.05

20.05 <p <0.10

*Success = 90-100% reduction in smoking.

**Results based only on those completing treatment or contacted for follow-up.

+Pregnancy intervention study.
OTs

TABLE 10.— Physician advice— Smoking cessation treatment results by sex

 

Percent Abstinence

 

 

 

 

 

 

End-of-
Treatment Six Months Long Term
Study Treatment N (%) (%) (%)
1. Burns, 1969 (27) M.D. advice to resp. dis. pts. 66M 53M 1(3mo.)
28F 32F
2. Handel, 1973 (87) Anti-smoking message in 45M 388M 1 (12 mo.)
med. exam 55F 11F ,
3. Burnum, 1974 (28) M.D. advice 84M 29M
40F 18F
4. Baric et al., 1976 (112) M.D. advice 134F
(spont. quitters) 24 83
(intervention) 63 14
(control) 47 14
5. Donovan, 19771(49) M.D. advice 552F 50%
reduction

 

1p <0.05
+Pregnancy intervention studies.
without adult company all day and of being deprived of outside
activities as obstacles to giving up smoking. Cigarettes have
also been described as a means of temporally partitioning the
day, of achieving physical autonomy from children, and of pro-
viding role differentiation (74).

Frieze, et al. reported women face more life stress than men
and have more symptoms of psychological distress (68). Waters
reports that women show more overt signs of neuroticism than
men (203). Furthermore, he finds an association in women be-
tween degree of neuroticism and amount smoked. Burns also
found that female smokers had higher neuroticism scores than did

female nonsmokers. No such differences were found in men (27).
Some studies have shown that women who smoke are both

more subject to psychological stress and more outgoing than
women who do not smoke. In a prospective study on women and
smoking, Cherry and Kiernan measured personality traits in
young women before the onset of smoking (31). They found that
smokers had high neuroticism and extroversion scores before
taking up the habit. They add that current women smokers are
more extroverted and also more neurotic than nonsmokers.
There is evidence that women smokers are more independent-
minded, assertive, self-opinionated and forthright (151,216). The
latter authors report that women smokers are also charac-
terized by apprehension and tension, and that these character-
istics are related to an inability to give up smoking.

The presence of psychological distress has also been shown to
affect the success of women in treatment. Peterson, et al. found
that, while 23 percent of the men who had participated in a
smoking program cited nervousness as the principal reason for
resuming smoking, 43 percent of the women cited this reason
(141). Russell reports that the presence of depression was re-
lated to dropping out of treatment, and that depression was
more frequent and severe among the women in his sample (156).
In a later study, Russell found that within the treatment group,
women had worse psychiatric adjustment scores than did men
(159). Furthermore, although the degree of psychiatric adjust-
ment did not differ between male treatment successes or fail-
ures, treatment successes among women were significantly
more likely to have good adjustment scores. Rode found that
success in a smoking withdrawal program was related to lack of
tension and apprehension for women (150). That smoking might
indeed act as a method of coping with psychological and social
stress is illustrated by the fear reported by many women that
they will engage in symptom substitution—specifically
overeating—if they stop smoking (14,23,27). It is also possible
that underlying stress in women impedes the strength of the

311
nw

wo
TABLE 11.—Pharmacotherapy—Smoking cessation treatment results by sex

 

Percent Abstinence

 

 

 

 

 

 

End-of- Six
Treatment Months Long Term
Study Treatment N (%) (%) (%)
1. Turle, 1958* (191) Hydroxyzine 23F 4F
2. Whitehead and Methylphenidate 10M 20M 0M a2
Davies, 1964 (208) Diazepam 6F OF OF mo.)
3. Wilhelmsen, 1968 (209) Methylscopolamine 291M 56M\, (12 mo.)
tranquilizer 200F 41F ,
4. Wetterqvist, 1971* (207) Methylscopolamine 192M 50M 19M 9M
1973* (206) 98F 33F {) jap (12m) oF (60 mo.)
5. Arvidsson, 1971* (5) Anticholinergics, 50M 85M 48M 1 (12 mo.)
Group aversion therapy 50F 85F 22F .
6. Merry and Preston, Lobeline 45M 29M
1963* (127) 31F 32F
7. Golledge, 1965* (72) Lobeline & placebo 19M 63M
8F 73F
8. Ross, 1967* (152) Lobeline 728M 40M 21M
Amphetamine 745F 29F 1 12F 1 (10-57 wks.)
STs

TABLE 11—Pharmacotherapy—Smoking cessation treatment results by sex— Continued

Percent Abstinence

 

 

End-of- Six
Treatment Months Long Term
Study Treatment N (%) (%) (%)
9. Schauble et al., Lobeline 33M 18M 1

1967* (164) Amphetamine 35F 26F
Lobeline, amphetamine 14M 57M
and education 17F 26F

10. West et al., Lobeline, amphetamine 255M 43M 22.0M

288F 33F |! 13.4F EY mo:)

1977* (204)

 

1p <0.05

*Results based only on those completing treatment or contacted for follow-up.
VIE

TABLE 12.— Psychotherapy —Smoking cessation treatment results by sex

Percent Abstinence

 

 

 

 

 

End-of- Six
Treatment Months Long Term
Study Treatment N (%) (%) (%)
1. Moses, 1964 (129) Hypnosis, discussion 35M 83M 2 11M 8M (12
15F 53F 12F 12F (12 mo.)
2. Mann and Janis, 1968 (119) Emotional role-playing 26F 23-50F (18 mo.)*
3. Streltzer and Koch, 1968 (185) Emotional role-playing 30F OF (4 wks.
post)
4. Lichtenstein et al., 1969 (115) Emotional role-playing 54F 9F (1-5 wks.
post)
5. Fee and Benson, 1971 (62) Group therapy 306M 56M 1 16M
204F 38F oF { } 6-12 mo.)
6. Bozzetti, 1972 (23) Group therapy 7™M 57M 85M (12 mo.)
TF 43F 57F ,
7. Tamerin, 1972 (187) Group therapy 16F 69F
1p <0.05
20.05 <p <0.1

*% reduction in smoking.
determination required to cease such behaviors as smoking and
overeating. Weight gain is a frequently reported consequence of
giving up smoking (173).

THE SMOKING WITHDRAWAL SYNDROME

Few of the studies reviewed here mentioned gender as a con-
nection with withdrawal symptoms, and none suggested that
men and women differ in the severity of smoking withdrawal
symptoms. However, Shiffman (173) analyzed Guilford’s raw
data (82), and stated that 15 of the 18 major symptoms reported
by subjects demonstrate sex differences (80,173). Thirteen of
those 15 symptoms were more frequently reported by women.
Other studies show similar, although not statistically signifi-
cant, trends. (141,190,215).

Factors contributing to relapse, such as craving and nervous-
ness, were reported to be similar for men and women (141).
Women who experienced the greatest craving during the initial
five days of abstinence were most likely to relapse (82). Since
women score higher than men on measures of anxiety as a gen-
eral rule, it is possible that they would be more susceptible to
relapse if smoking had been their customary means of reducing
such dysphoria. Women may also pay more attention to somatic
symptoms than men, as they make more frequent use of all
health care services, and specifically (because of the relative
symptomatology) for headache and and weight gain (114).

It is likely that the abstinence syndrome is a major factor in
recidivism during the first few weeks of cessation when relapse
is most common, and that the number of cigarettes smoked per
day is an important variable in determining the severity of the
withdrawal. The issue of a gender difference in withdrawal se-
verity is a major area where research is needed.

SMOKING AND WEIGHT CONTROL

Women who smoke are, on the average, thinner than women
who do not smoke. The reported mean weight difference ranges
from 1.2 to 4.5 pounds (7,17,93). Weight gain has been a fre-
quently documented consequence of quitting smoking, both in
males and females, (17,37,65,71,141,190,209,215).

Studies of males have reported weight gains among former
smokers which range from 1 to 12 pounds greater than those
who continue to smoke. In one such study, the authors observed
that, while 60 percent of continuing smokers gained weight,
among quitting smokers the observed proportion was 85 percent
(37). These figures gave rise to an observed-to-expected ratio of
1.4, suggesting that those who quit are 40 percent more likely to

315
= TABLE 13.— Behavior modification— Smoking cessation treatment results by sex

 

Percent Abstinence

 

 

 

 

 

 

End-of- Six
Treatment Months Long Term
Study Treatment N (%) (%)
1. Keutzer, 1968 (105) Breath holding, coverant 73M 18M
control, negative practice, 73F 29F
attention placebo
2. Suedfeld and Ikard, 1973 Sensory deprivation 3M 100M 67M 3
(186) 2F 50F 50F ( mo.)
8. Delahunt and Curran, Negative practice or self-control 50F 61 22
1976 (43) Negative practice and self- 89 56
control 1
Control 15 0
Nonspecific treatment 56 11
4. Tongas et al., 1976* Covert sensit., smoke aversion, 88M WM 2 sor} 2 (12 mo.)
(189) group therapy, combined 34F 39F 32F .
treatment 48M
18F } 2 (24 mo.)
5. Russell, 1970 (156) Electric shock aversion 10M 70M 40M (12 mo.)
4F 50F 50F °
LT&

TABLE 13.—Behavior modification— Smoking cessation treatment results by sex—(Continued)

Percent Abstinence

 

 

End-of-
Treatment Months Long Term
Study Treatment N (%)
6. Chapman et al., 1971 (30) Electric shock, self-
management, post-treatment
therapist monitoring: 2 weeks: 4M 75M 25M 25M
8F 100F 37F 29F
(12 mo.)
11 weeks: 4M 100M 50M 50M
TF 86F 57F 57F
7. Berecz, 1972 (13) Electric shock aversion, 56M sed
imagined vs. real smoking 32F
8. Russell et al., 1976 (159) Electric shock and controls 28M 64Mt
28F 57Ft

 

tp <0.05
20.05 <p <0.10
*Results based only on those completing treatment.

**Percent reduction, little for F; more for M in imagined-smoking condition.

tTwo weeks post-treatment.
gain weight than those who continue to smoke; but a significant
proportion of observed weight gain among men who quit smok-
ing would have occurred even if they had continued to smoke.

The single major report on lifetime smoking and weight pat-
terns in women examined data provided by approximately
57,000 female members of a national weight-reduction program
(17). Cross-sectional analysis indicated that current smokers
weighed less than nonsmokers by 1.2 pounds and 4.0 pounds less
than former smokers. Inhalers were significantly less obese by
5.7 pounds than current smokers who did not inhale. A 40-year
longitudinal analysis of weight in relation to reported lifetime
smoking history revealed that between ages 30 and 50 (the two
decades after the majority of those who quit had discontinued
smoking), the former smokers gained more weight than continu-
ing smokers, both for inhalers and non-inhalers. The calculated
weight gain after cessation varied substantially by amount
smoked; heavy smokers who inhaled ( > 41 cigarettes) gained 30
Ibs., while light smokers who inhaled (1 to 10 cigarettes) gained
only 4 pounds. The observed differences in weight persisted
through age 60. Conclusions of this study may not, in fact, be
directly applicable to the total female population. This study
raises the issues of reporting and recall bias among this obese
population (mean group weights ranging from approximately
171 to 180 pounds), as well as self-selection into continuing or
former smokers.

The implications of such studies are important. The image of
the slender, attractive female pervades our culture and is cer-
tainly present in tobacco advertising (84). Do women perceive
weight gain as a significant and unavoidable sequel to discon-
tinuing smoking? There is evidence suggesting that fear of
weight gain may keep women from quitting smoking. Women
are more concerned with weight than men are. In the 1975
NCSH survey, the percentages of female and male smokers who
responded “strongly agree” or “mildly agree” to the statement,
“Being afraid of gaining a lot of weight keeps people from quit-
ting cigarettes” are shown in Table 14.

Attempts have been made to examine the cause of such re-
ported weight gains. The mechanism of weight gain with cessa-
tion of smoking has not, however, been elucidated. Trahair and
others have reported that appetite increased with smoking ces-
sation, and the resulting increased caloric intake caused weight
gain (190). Other studies have suggested that smoking may, in
fact, directly affect metabolism. Glauser, et al. studied seven
males before and one month after cessation. Body weight and
surface area increased, while heart rate, serum calcium, sugar,
and oxygen consumption decreased (71). Conversely, however,

318
TABLE 14.—Percent affirmative responses to statement: “Being
afraid of gaining a lot of weight keeps people from
quitting cigarettes”

 

 

Smoking Status Women (%) Men (%)
Never Smoked 59.0 51.5
Formerly Smoked 63.1 53.6
Currently Smoked 59.9 47.3

 

SOURCE: National Clearinghouse for Smoking and Health (194).

Sims observed no change in resting metabolic rate, thermic re-
sponse to exercise or meals, and no change in serum T3 or T,4
(175).

Further research is necessary to define the degree of weight
gain after cessation of smoking, the mechanisms by which it
occurs and the ability to modify it by educational or behavioral
interventions during and after cessation attempts.

TREATMENT RECOMMENDATIONS

Perri, et al. recommend that smoking cessation programs with
a behavioral emphasis be comprehensive, multifaceted, long-
term, and that they include self-reinforcement and problem-
solving procedures (140). Given the difficulty for some women in
simultaneously dieting and attempting to quit smoking, smoking
withdrawal programs should adopt a total approach to health,
including advice on dieting, exercise and the immediate benefits
of abstinence (150).

Marlatt and Gordon write that relapse potential is greater for
individuals whose daily schedule fails to include some rewarding
or pleasurable activity (120). It would appear useful to attend to
this issue in smoking treatment programs.

A social support hypothesis is frequently cited in the treat-
ment literature to explain gender differences in quitting. It is
often suggested that women do better than men in programs
that provide amaximum amount of social support, and tend to do
worse in situations where program support is low or outside
factors militate against quitting. For example, Resnikoff, et al.
were able to differentiate between those women (but not men)
who did poorly in group-plus-medication treatment and those
who did well using the Social Introversion Scale of the Minnesota
Multiphasic Personality Inventory (149). This scale measures
the degree of discomfort in social situations and the presence of
outgoing tendencies. Women scoring high on this scale (shyer,
more socially introverted) were less likely to quit than low-

319
scoring women. This study provides just one example of th
observation that social support seems to be of lesser consequenc
to men in quitting smoking, although spousal support is impo
tant (170).

As the overall categories in Tables 9-13 show, women do mor
poorly in treatments characterized by less individual attentior
such as education and pharmacotherapy, compared with th
categories of psychotherapy and behavior modification, wher
contact is usually maximized in a small group or in a
individual-to-therapist setting.

Dubren reports that twice as many women as men participate
in a television stop smoking campaign, but that fewer wome
stopped smoking—presumably because of a lack of support (52
Guilford found that when men and women participated in grou
programs, success and failure rates were the same for both sexe
(78). When they did not attend group programs, men maintaine
the same success rates, but women achieved markedly lowe
rates. There is also support for the notion that groups are pa
ticularly effective for women if they are sexually homogeneot
(44,78). Tamerin writes that the group can provide support, en
pathy, and shared identification with others going through
similar process (187). The group also provides an avenue fi
affective expression, so that the relevance of cigarettes to psyc!
osocial events and the personal meaning of giving them up can }
discussed. Given the differential reaction of men and women *
quitting smoking, as well as the traditionally greater willingne:
of women to discuss affective issues, it is not surprising th:
all-female smoking-cessation groups have been particularly a
tractive.

Marlatt and Gordon studied the circumstances under whic
smoking relapse is most likely to occur (120). They claim th:
experiencing stress in the form of a negative emotional stat
social pressure, or interpersonal conflict is likely to lead to smo
ing among those who are attempting to abstain. The occurren:
of a full-blown relapse, however, can be attributed to the cogr
tive reaction to stress-induced smoking. Many individuals wl
are trying to abstain view a single slip as evidence that they ha:
failed, rather than as a natural and predictable reaction to
stressful situation. Marlatt and Gordon advocate teaching tho
who are trying to quit the importance of not viewing relapse in :
all-or-none manner. Rather, they suggest teaching smokers
“plan for a relapse,” to become psychologically prepared to a
cept a slip as a natural part of the difficult process of quitting

Another factor that appears to influence the success of wome
in treatment programs is smoking by significant others in the
environment. Kanzler, et al. found a significant trend for wom

320
to give up smoking if no one in their daily environment was a
regular smoker (104). This trend was only slight for men, al-
though spousal encouragement was related to success in one
large study of smoking cessation treatment in men (170). The
influence of the smoking behavior of significant others on female
_ attempts to quit has been repeatedly pointed out (14,201,204).
Sensitizing friends and relatives who are smokers to this prob-
lem, and advising discretion in smoking behavior on their part,
might increase treatment effectiveness for women.

CONCLUSIONS

‘Treatment programs should specifically deal with means of
handling anxiety and tension, ways to combat weight gain, and
should prepare smokers for mini-relapses. Social support should
be maximized. It may be increased through choice of treatment
modality, networks of “buddies,” friends and relatives, and the
involvement of spouses.

It should be possible to capitalize on the heavy commitment of
women to the health care system, both in terms of their own use
and their role as family providers. Health professionals need to
devise targeted interventions for women with this in mind.

Dissemination of Information About Smoking

HEALTH ATTITUDES AND BEHAVIORS

The extraordinarily serious health consequences of smoking
have not deterred almost 30 percent of the adult female and 37
percent of the adult male population from smoking regularly.
Seventy to 80 percent of these smokers agree that cigarette
smoking is harmful, is a health hazard that requires action, and
causes disease and death (194). Former smokers and nonsmokers
take a much stronger stand on these three points, ranging from
87 to 96 percent agreement. Gender differences are very slight.

The value placed on health compared to other positive life
goals was slightly lower for smokers than nonsmokers, and high-
est for ex-smokers (194). Out of a maximum factor score of six,
current smokers averaged 4.66 (M = 4.55, F= 4.81), and nonsmok-
ers averaged 4.82 (M = 4.68, F = 4.9) and ex-smokers averaged 4.89
(M = 4.78, F = 5.06). The higher scores of women support their
traditional concern with health in our culture but they are in-
congruent with recent smoking trends (114).

Fewer current smokers than nonsmokers and ex-smokers re-
port having personally known someone with coronary heart dis-
ease, lung cancer or emphysema/chronic bronchitis. This finding
may be attributable to a process of denial. Only about one-third

321
of current smokers admitted knowing someone personally whose
“health” was adversely affected by smoking while over 60 per-
cent of nonsmokers knew such a person. Clearly, mechanisms
must be operating in smokers to reduce cognitive dissonance
caused by their behavior and their knowledge of the health con-
sequences of their behavior. One of these mechanisms may be to
deny that the health problems of others are connected to smok-
ing.

A related issue is that of compliance. The term encompasses a
host of behaviors, all related to following medical recom-
mendations: seeking care when serious symptoms appear, tak-
ing medications, having follow-up examinations and procedures,
and doing breast self-examination, to name only a few. A large
number of studies have been performed in this area, and there is
no evidence that one sex shows greater propensity to be com-
pliant than the other (90,114).

Thus, we would have no reason to expect that women and men
would respond differentially to doctors’ advice to change their
smoking behaviors, at least from this literature.

Women in our society are more involved with health care serv-
ices (114). They arrange for those services and act as role-models
for children. This function would have great information deliv-
ery potential.

SOURCES OF INFORMATION

There are a variety of ways that people can learn about the
health consequences of tobacco use. The information gathered
from and effects of tobacco company advertising will be dis-
cussed separately below. The major sources of information fall
into a number of categories.

Health Care Providers

The influence of physicians and nurses as communicators of
information and as exemplars of healthy life styles has been the
subject of much research (198). The greater concern about health
among women, and their greater contact with health profession-
als, provides an obvious avenue of intervention (114). Health
professionals should be continuously reminded of their potential
impact and advised to use it to influence women to reduce smok-
ing. Physicians are considered the most authoritative source,
with the greatest potential for influencing patient behavior.

From the self-report of adults, physicians are not delivering
enough anti-smoking information and advice. In 1975, a full 64.6
percent of male and 60.8 percent of female current smokers

322
claimed that they had never received advice from any doctor
about quitting, cutting down, or continuing smoking (194). About
19 percent of male and 21 percent of current female smokers had
been advised to quit. Combining advice to quit and/or cut down,
the percentages rose to 34.8 percent of men and 37.7 percent of
women. In 1970, the percentages of men and women who re-
ported such advice were 30.2 percent and 34 percent, respectively
(193). A somewhat lower estimate of physician advice was ob-
tained from an ongoing nationwide study involving approxi-
mately 8,000 people (184). Advice to quit or cut down was reported
by 22.4 percent of the subjects, and lack of advice by 77.6 percent;
there were no significant gender differences.

A survey of physicians’ opinions about smoking and health in
the mid-1960s revealed that 38 percent claimed they advised
“all” or “almost all” (95 to 100 percent) of their patients who did
not have smoking-related disorders to quit or cut down (76).
Eighty-eight percent of physicians claimed they gave such ad-
vice to patients with lung and pulmonary conditions.

Nurses spend more time in direct patient contact than do
physicians and can exert a major role in delivering information
as well as serving as exemplars. Most nurses are aware of this
responsibility (60,75,135,195). Only 10 percent of nurses claimed
to discuss smoking and health with “almost all” or “most” (65 to
99 percent) of their patients or students (135), Another 21.5 per-
cent claimed to have discussed it with 35 to 64 percent of patients
or students. Only 50 percent of current smokers, compared to 65
percent each of former smokers and nonsmokers, suggested
stopping to 5 percent or more of their patients and students.

While the identical question was not asked of nurses in the 1975
survey, a number of valuable questions relating to exemplar
status were posed (196). In almost every case, current smokers
took the weakest position on exemplar role, former smokers were
in between, and nonsmokers were strongest. For all questions,
the proportion of nurses who agreed “strongly” or “somewhat”
with the statements of exemplar role is reported here. Regarding
their own behavior, 69.5, 91.7, and 94.5 percent of current, former
and nonsmoking nurses respectively felt that they should set a
good example by not smoking. This percentage varied according
to work location. Lowest percentages were given for hospital
duty (70.0, 83.8, and 89.2 percent for current, former and
nonsmokers respectively), intermediate for private physician’s
office (79.9, 86.7, and 90.5 percent, respectively, and highest for
private duty (91.1, 91.4, and 94.4 percent, respectively). A much
lower rate of agreement about not smoking in public while in
uniform was obtained; only 44.4 percent of current smokers, 67.1
percent of former smokers, and 72.8 percent of nonsmoking

323
nurses concurred. Nurses believe that it is their responsibility to
convince people to stop smoking (64 percent of smokers, 74 per-
cent of former smokers, and 64.8 percent of nonsmokers). Approx-
imately 54 percent of smokers, 81.3 percent of former smokers,
and 82 percent of nonsmokers said they had tried to persuade
someone other than patients to quit, and a much higher percent-
age reported convincing someone not to start (83.4, 78.6, and 75.8
percent, respectively). Finally, 52.1, 78.2, and 85.4 percent of the
respective groups agreed strongly or somewhat that nurses
should be more active in speaking to lay groups.

Given the possible role modeling effect of female nurses, a need
exists for adequate preparation of all health professionals in
smoking and health counseling. This preparation should include
education on the health hazards of smoking as well as effective
methods of counseling patients.

There is little information available about the role played by
other health care providers in dissemination of information or
discouragement of smoking behavior. Nationwide campaigns are
currently being aimed at physicians and dentists to increase
their commitment to and involvement with this task. Other
health care providers should be encouraged to take a more active
role and adopt exemplar status as well.

Educators

Adult educators include those in schools and colleges, job
training, community organizations (churches and other reli-
gious groups, Young Women’s Christian Associations, and Red
Cross, civic organizations, social service groups, cultural groups)
and in school-based programs for parents. There are large
number of sources of information about smoking available from
educators in adult settings and in programs for parents. These
have been studied in-depth and reviewed elsewhere (188, 198).
The frequent contact with and involvement of women in the
school system should provide excellent opportunities to provide
female-oriented information.

Peer Group

This group is an important, influential source of information
on behavior. Evidence is strongest for the effect on initiation
(addressed earlier in this Part). In two studies of British work-
ing class women, the peer group was an important source of
information about smoking and pregnancy (11,74). Other strong
relationships within the lay adult community have also been
reported (118,201).

324
Family

Significant others, especially within the family, have been
shown to be primary sources of information to pregnant women
(11,74). The female relative may serve as a particularly impor-
tant role model for black women (201). Smoking initiation is
strongly influenced by parental smoking habits in teenagers
(addressed earlier in this Part). In married couples, smoking
patterns tend to be congruent; this almost enforces a sharing of
information and makes it especially important in quitting ef-
forts that couples stop together or are very supportive of the
new ex-smoker (77,118,170,216).

Media: Television, Radio, Film, Newspapers, Magazines

The use of the mass media as a source of information as well
as a tool in effecting cessation has been extensively developed
in recent years (55,188,193,198,202,214).

Since women are almost exclusively the target audience of
women’s service magazines, effort should be devoted to using
this medium to provide information on smoking and health, ces-
sation techniques, and clinic availability. These magazines
have not adequately disseminated information on smoking and
health.

One of the principal reasons suggested for this failure is the
power that tobacco companies wield through the economic in-
centive of advertising (178). Only one women’s service magazine
does not accept cigarette advertising in the United States.
Frank admission of the economic dependency upon such adver-
tising has been made. Not a single leading national woman’s
magazine that accepts cigarette advertising in 7 years of publi-
cation printed an article “... that would have given readers any
clear notion of the nature and extent of the medical and social
havoc being wreaked by the cigarette-smoking habit’ (178).
Smith goes on to point out that those magazines that do not
accept cigarette advertising, or have no advertising at all, have
done considerably better at informing their readers of the
health risks of smoking.

Advertising

In recent years, advertising in the United States has been
directed specifically towards the women’s market, with themes
as diverse as the emancipation of women, the first woman (bi-
blical reference), romantic love, and the independent single
woman. Most girl smokers have a positive impression of the

325
individuals pictured in cigarette advertisements. The latter are
seen as attractive (by 69 percent), enjoying themselves (by 66
percent), well dressed (by 66 percent), sexy (by 54 percent),
young (by 50 percent), and healthy (by 49 percent). There is no
comparable data on how girl nonsmokers or young adult women
view advertising (216).

Thus, advertisers have been successful in creating a sense of
mystery, sophistication, and power around the behavior of
smoking. Although smoking was once frowned upon for women,
people now respond less negatively to a woman smoking (16).
There is evidence that, for some women, smoking is linked with
attitudes and behaviors that comprise a socially valued and
successful self-image, and that giving up smoking is a threat to
that image (123). ,

A majority of former smokers and nonsmokers of both sexes
in the 1975 Adult Use of Tobacco Survey (194) agreed with the
statement, “Cigarette advertising should be stopped com-
pletely.” The percentages for men were 56.9 percent for
nonsmokers and 56.4 percent for former smokers, and for
women, 68.2 percent for nonsmokers, and 62.5 percent for
former smokers. However, only 42.6 percent of male smokers
and 42.5 percent of females smokers agreed with the statement.
It appears that adult smokers value cigarette advertisements,
but why they do—whether for information about brand charac-
terization and availability, identification with the image por-
trayed, or some other reason—is not known. Fishbein concluded
that cigarette advertising influences the decision to smoke. as
well as the choice of brand. Furthermore, he points out that
cigarette advertising may serve as a discriminative stimulus for
smoking behavior. Advertising can influence the initiation of
smoking, the choice of brands smoked, and the level of consump-
tion. Commenting that the tobacco industry asserts that adver-
tising serves only to influence brand choice and not initiation or:
consumption, Fishbein maintains that it is somewhat unrealis-
tic to assume that an advertisement which can do one of these
things is not also capable of doing the other. While additional
research on the effects of cigarette advertising is clearly neces-
sary, this review suggests that cigarette advertising does affect
cigarette consumption (63).

Restrictions have now been placed on advertising in many
countries in the world, including the United States. There is no
uniform agreement that the ban on televised cigarette advertis-
ing in the United States and the United Kingdom significantly
reduced consumption. However, it is generally believed that
each action of this sort—including the U.S. Surgeon General’s
Reports and the Reports of the Royal College of Physicians, as

326
well as other smoking control measures such as taxation and

legislation—has a cumulative effect on per capita consumption
(8,142,202),

THE FAILURE TO DISSEMINATE INFORMATION

Many of the critical evaluations of public health campaigns
conveying anti-smoking information maintain that little at-
titudinal or behavioral change is ever effected (188). Fishbein
(63) argues that there is insufficient information describing the
complex relationships between cigarette smoking behavior and
beliefs, attitudes, and intentions to make this conclusion. He
further maintains that it is necessary to know to what extent
decisions regarding initiation, reduction, increase or cessation
are under attitudinal (individual, personal) or normative
(society-influenced) control. The importance of personalizing
the health message, and the failure of the public to personalize ~
the health messages that they have received is emphasized. For
example, over 80 percent of smokers agree with the statement
that smoking is hazardous to health. However, on the question,
“Are you in any way concerned about the possible effects of
cigarette smoking on your health?” only 25 percent of current
smokers in the 1975 NCSH survey stated that they were “very
concerned,” another 22.6 percent were “fairly concerned,” 18.9
percent were “only slightly concerned,” and a final 31.9 percent
were “not concerned” (194). Fishbein maintains that the public
is not effectively informed about the general danger to health
posed by smoking and is even less informed about the connec-
tion with specific diseases. He concludes that the content of an
effective message is fourfold: that continued smoking leads to
negative outcomes; that stopping smoking leads to positive out-
comes; that personal relevance must be established; and that
normative influences must be appealed to by maintaining that
significant others think an individual should quit.

Stress at Work

A general model of stress at work (38) is worthy of considera-
tion. Examination of the sources of stress at work (Figure 2)
reveals a number of items that are especially salient for women.
Discrimination against women in employment, role conflict, au-
thority problems, inequity in promotions, exclusion from
decision-making processes and the “old boys” network have
been frequently discussed (68). Individual characteristics may
be considered from a gender viewpoint as well; for example,
some types of psychological disorders, such as anxiety and de-

327
8a8

Sources of Stress
At Work

Individual
Characteristics

 

Intrinsic to job:

Poor physical working conditions
Work overload

Time pressures

Physical danger, etc.

   

The individual:

 

Role in organization:

Role ambiguity

Role conflict
Responsibility for people
Conflicts re organizational
boundaries (internal

and external), etc.

 
   

  

Level of
anxiety

  
  
 

  
 
 

Level of
neuroticism

 

Tolerance for

 

Career development:
Overpromotion
Underpromotion

Lack of job security
Thwarted ambition, etc.

    
 

 

ambiguity

Type A behavioural
pattern

    

 

Relationships at work:

Poor relations with boss,
subordinates, or colleagues
Difficulties in delegating
responsibility, etc.

 

     

  

Extra-organizational
sources of stress:

 

Organizational structure and
climate:

Little or no participation

in decision-making
Restrictions on behaviour
(budgets, etc.)

 

Office politics

J tees of effective consultation, etc.

    

  

Family problems
Life crises
Financial difficulties, etc.

    

 

FIGURE 2.—A model of stress at work

Symptoms of Occupational Disease
ill Health

 

Diastolic blood pressure

 
     
   
 
   

Coronary
heart
disease

Cholesterol level
Heart rate
Smoking

Depressive mood

  

Mental
il
health

 
   

Escapist drinking

Job dissatisfaction

 

Reduced aspiration, etc.

 
pression, are more prevalent among women than men (48,68).
The Type A behavior pattern, which is associated with male
cardiovascular disease, has been shown to be unrelated to sex
once socioeconomic status is taken into consideration (172).

An additional set of stressors originates in the extraorganiza-
tional environment. A prospective study of the relationship of
employment status and employment-related behaviors to coro-
nary heart disease (CHD) incidence was conducted by Haynes
and Feinleib (91). Working women scored higher on scales
measuring daily stress, marital dissatisfaction, and aging wor-
ries than men. They were also less likely to display overt anger
than either homemakers or men. While incidence rates of coro-
nary heart disease in working women were not significantly
higher than in homemakers, an excess risk of CHD was iden-
tified among women who were employed in clerical jobs and had
children. The risk factors for CHD in this group included family
responsibilities, suppressed hostility, a nonsupportive super-
visor, and low job mobility over the preceding 10-year period.

Smoking Habits of Health Professionals

There are relatively few studies available which present
gender-specific smoking rates in various professions. Health
professionals were selected for analysis because they were more
likely to be aware of the health consequences of smoking than

the general public; this group has also been studied more exten-
sively.

PHYSICIANS

The smoking habits of male and female physicians in five
nations are presented in Table 15. Smoking rates in the general
population are provided for comparison when supplied by the
authors. No breakdowns by gender are available for the United
States. Separate estimates of smoking rate in a small group of
women physicians age 36 to 46 at the time of survey (205) and in
a large sample of predominantly male (93 percent) physicians
(195) are listed in the table. In addition, the wives of 3,990
physicians were queried about their own smoking habits and
those of their husbands; no information is provided on the
occupations of these women (77).

Examination of the table shows that smoking rates of
physicians, both male and female, tend to be much lower than
general population rates. The only exception is the higher rate
of current smokers among female physicians in Finland (200).
The percentage of current smokers among the sample of U.S.
female physicians is higher than that reported in other

3829
& TABLE 15.—Smoking habits of male and female physicians in selected countries

0

 

 

 

 

 

 

 

 

 

Percent Smokers
Pop. Pop. Pop.
Author Country Number Never Est. Current Est. Former Est.
1. Bourke, et al., 1972 (22) Ireland M 1359 17.9 —  19.7* 48.5 — 67.6" 33.6 — 12.7%
F 221 51.5 53.9 26.7 — 38.6* 22.2 — 7.5*
2. Vuori et al., 1971 (200) Finland M 843 38 34 60 27
F 66 26 20 8
3. Wilhelmsen & Faith-Ell, 1974 (210) Sweden ? 33 38 29
54 27 19
4. Aaro et al., 1977 (1) Norway M_~ 740 35.3 —  53* 3nO 27'*
F 398 21.7 — 36* 38: — 20'*
5. Westling-Wikstrand et al., 1970 (205) USA F 81 42 35.8 13.6
6. Greenwald et al., 1971? (77) USA M 3990 325 24 433
F 3990 35° 36 273
7. USDHEW, 1976 (195) USA M 36574 21 39 64! 43}
34}

 

*Significant difference between percentages paired by (—).

former smoker

‘Stopping rate = ever smoker

2Sample consisted of physicians and their wives whose profession was undefined.

3Percentages estimated from graph, not specified in text.

4Approximate total of M and F, estimated to be 93% male.
countries and approaches the rates in the general population
(205). Prevalence of smoking has a strong relation to
demographic variables such as profession, income, and
education. We would expect physicians to be in the highest
category on each of these variables and, therefore, to have
lower prevalence rates. Therefore, it would be relevant to
examine the cross-tabulations for smoking prevalence by
socioeconomic status, according to sex.

According to the three studies providing comparative data,
both female and male physicians are quitting at rates higher
than the general population. The percentage of former smokers
among female physicians, and estimates of quit rate, are lower
than among male physicians in all but one of the studies listed.
This trend may represent a time lag in the smoking behavior of
women as compared to that of men, or there may be a lower quit
rate among women physicians.

In two studies, female physicians smoked more cigarettes per
day than women in the general population (1,22). In contrast,
wives of physicians smoked fewer cigarettes on the average
than their husbands (77). A greater percentage of the wives of
physicians than physicians themselves were smokers in every
age group except the oldest. The percentage of current smokers
appeared to be inversely related to age in the group of wives,
but virtually stable across age for the physician-husbands.
Husbands and wives tended to have similar smoking habits.

Based on a small sample of women graduates of a single U.S.
medical school, Westling-Wikstrand, et al. (205) reported that
58.8 percent of the current smokers belonged to the category
“professor” (academic appointment of assistant professor or
above, with or without board attainment) when ranked on pro-
fessional attainment. The other categories were “boards” (spe-
cialty board certification but not professional appointments),
“no boards” (in practice without board certification or profes-
sional appointment), and “not in practice.” The “professor”
group was characterized by greater likelihood of being single
and having fewer “habits of nervous tension.” Compared to
other groups, this group had the lowest depression scores, aver-
age anger scores, and the highest anxiety scores. The authors
comment that this group of women was the most similar to their
male colleagues. They may also have experienced fewer prob-
lems with ambivalence about sex roles, self-image, or conflict
over aggressive behavioral patterns. The presence of the high
anxiety scale, however, casts some doubt on this generalization.

Women in U.S. medical schools are subjected to significant
psychological pressures and often experience emotional prob-
lems and lack of confidence about achieving the goal of gradua-

331
tion (205). Female physicians also experience significant role
conflict (19).

The relevance of indices of stress to smoking patterns is again
one of inference. If smoking serves as a coping mechanism—a
means of reducing negative affect—then it is understandable
that female physicians, or any other professional with elevated
stress levels, would have higher current smoking rates than the
general populace. It is also understandable that they might ex-
perience more difficulty in quitting.

PSYCHOLOGISTS

A survey of psychologists in California state universities and
colleges found that female psychologists were much more likely
to smoke than their male colleagues (46). The rate of smoking
was slightly higher than in male health professionals, and ap-
proximately the same for female psychologists (38 percent) and
nurses (195) (see Table 16).

This smoking rate is significantly above the rate among pro-
fessional women in general (25.6 percent) and was due to lower
cessation rates among psychologists rather than higher initia-
tion rates. The most common reasons given for smoking are the
stress of work or school, and personal stress. Frieze, et al. state
that professional women have to exhibit “male-like” character-
istics in order to survive in their jobs, but that these character-
istics are often met with criticism and hostility (67). Thus, social
and occupational demands are at odds with each other. Fur-
thermore, there is evidence that female psychologists face very
real sex discrimination in the evaluation of their work (67).

Dicken and Bryson (46) report a high degree of power fan-
tasies among female psychologists who smoke. This supports
Fisher’s finding that female smokers in general seem preoc-
cupied with the issue of power (64). He speculates that cigar-
ettes are used defensively against feelings of powerlessness,
weakness, and inferiority.

Elevated suicide rates are another correlate to the evidence
of excessive stress and difficulty in coping experienced by some
female professionals. These higher rates, compared with the
general female population, have been observed among women
psychologists, chemists, and physicians (124,164). Factors such
as ambivalence about success, role conflict and marginality
were offered as dynamics. However, it is not possible to deter-
mine whether these higher suicide rates are due to the self-
selection of suicide-prone women into these and possibly other
professions, or to the difficulties encountered in professional
training and practice (or to an interaction of both).

332
NURSES

A number of studies have shown a higher rate of smoking
among nurses than in the general female population in the
United States. The most recent assessment of nurses’ smoking
behavior was conducted in 1975 (199). In Table 16, smoking
habits of nurses are compared with those of adult U.S. women
and other groups of health professionals.

Between 1969 and 1975, the proportion of nurses who were
current smokers rose from 37 to 39 percent. Every other cate-
gory of health professional (physician, dentist, and pharmacist)
had substantially reduced smoking rates. The membership of
these three professions is predominantly male and current
smoking rates vary from 21 to 28 percent. If one examines quit
rates in 1975 among the four categories of health professionals,
it is clear that the majority of physicians, dentists, and pharma-
cists who ever smoked cigarettes have quit: 64, 61, and 55 per-
cent respectively. Among nurses, only 36 percent have quit,
which does, however, compare favorably with adult women (34
percent) and working women (30 percent) (199).

Noll surveyed smoking behaviors of nurses by work setting
(see Table 17) (135). The overall percentage of current smokers
in this survey was 37 percent, compared to a national average
(for 1966) of 33.7 percent in women. There was a smaller per-
centage of never smokers (41.3 percent) among nurses in that
survey than among the female population (56.8 percent),
suggesting a higher quitting rate at that time as well. From
Table 17 it appears that there is no selective recruitment into
the various nursing specialties; the proportion of never smokers
is fairly equal across work settings. Differences do appear, how-
ever, in the proportion of current smokers according to work
setting. Highest rates of smoking are found in psychiatric and
pediatric settings, and lowest rates in the four categories con-
nected to education and community involvement: nursing edu-
cation, working in the community, elementary or high school
nursing, and working in a doctor’s office.

In Great Britain, only 26 percent of maternity nurses smoked
regularly, compared to 37 percent of those in general nursing
(106). In the United Kingdom, approximately the same propor-
tion of nurses smoke as women in the general population —44
percent (106,154).

Knopf Elkind reports differences in smoking among different
types of ward nursing staff. Trained nurses had 41 percent cur-
rent smokers, learners had 28 percent, nursery nurses had 14
percent, and auxiliaries had 61 percent current smokers (106).

Lampman reported a similar excess of smokers among nurses

333
ree

TABLE 16.— Percentages of cigarette smokers (S), former smokers (FS), and ever smokers (ES) and cessation
ratio (FS/ES) among psychologists, nurses, and other selected health professionals

 

 

Sample N Ss FS ES FS/ES
Male and predominantly male samples
CSUC male psychologists 258 28 35 62 55
Eminent experimental psychologists— 90% male
(Lawton and Goldman, 1961) q2 53 11 64 17
Psychiatrists —% male not reported
(Tamarin and Eisinger, 1972) 309 42 27 69 39
American Public Health Association male members
(Eyres, 1973) 3,569 21 40 61 66
Physicians—93% male (USPHS, 1977) 8,657 21 42 63 67
U.S. adult males (USDHEW, 1976) 5,702 39 29 69 42
Female and predominantly female samples
CSUC female psychologists 86 38 19 57 33
American Public Health Association female members
(Eyres, 1973) 1,973 31 31 62 50
Nurses— 98% female (USPHS, 1977) 2,429 39 22 61 36
U.S. adult females (USDHEW, 1976) 6,327 29 14 43 33

 

NOTE: CSUC = California State University and Colleges.
SOURCE: Dicken, C. (46).
TABLE 17.— Cigarette smoking status by work setting for nurses

 

 

 

(percent)
Cigarette Smoking Status Total*
Work Setting Current Former Never Percent N
Surgical Units 41.2 19.4 39.4 100.0 529
Medical Units 37.8 18.2 43.9 99.9 476
Operating, Labor, Delivery
Emergency Room 39.8 15.2 45.0 100.0 485
Maternity Unit 36.2 17.2 46.6 100.0 197
Pediatrics Unit or Setting 46.6 8.8 44.6 100.0 80
Psychiatric Unit or Setting 49.9 18.2 32.0 100.1 135
Nursing Education Setting 24.6 26.8 48.7 100.1 90
In the Community 26.1 33.4 40.6 100.1 264
Elementary or High School 27.5 36.4 36.1 100.0 217
Doctor’s Office 24.2 33.8 41.9 99.9 338
Out-Patient Clinic 42.5 15.1 42.5 100.1 113
Other and Mixed 41.3 18.4 40.3 100.0 1,078

 

*Total N = 6,012
SOURCE: Noll, C.E. (135).

aides (95.2 percent female) in a large metropolitan hospital in
the United States (110). Fifty-two percent of that group smoked,
compared with 36 percent of the medical nurses (99.3 percent
female) and 40 percent of the student nurses (95.6 percent
female). This survey was aimed at identifying smoking within
the hospital. Thus, true prevalence in this sample can only be
higher.

Compared to other female health professionals (see Table 16)
in the United States, nurses’ quit rates are above some (psy-
chologists, U.S. adult women) and below others (American Pub-
lic Health Association female members). Knopf Elkind points
out that in the British population other female-dominated pro-
fessions, such as primary school teachers, health visitors and
domiciliary midwives, have noticeably lower rates of smoking
than hospital nurses (106). Entry into the profession of nursing
is associated with taking up daily smoking but the degree of
occupational stress in a population of 300 British student
nurses was not different for smokers and nonsmokers (92). This
finding does not rule out the use of smoking as a stress-
reduction mechanism, however.

Other factors which might contribute to a high smoking rate
among nurses are work overload and frustration in professional
relationships with physicians.

Knowledge of health consequences of smoking is high among
nurses, but it has been shown that student nurses are less well-
informed than medical students (154). Nurses who quit smoking

335
do cite protection of future health as a major reason (75,92).
Nurses who smoke are less likely than nonsmokers to agree that
not smoking is a preventive measure against cancer (106). Simi-
lar refusal to acknowledge health risks of smoking is found
among smokers in the general population (194). Whether this
represents a real lack of knowledge or a method of reducing
cognitive dissonance through denial is unknown. The problem is
particularly critical for nurses (and other health professionals)
since they serve both as exemplars and as providers of informa-
tion (106).

The Pregnant Smoker—a Special Target

The pregnant woman is in a unique life situation. Every sub-
stance she ingests and every behavior that she manifests can
affect the present and future health status of the fetus she is
carrying. If she smokes, the nicotine, carbon monoxide, and hy-
drogen cyanide which she inhales all cross the placental barrier
and enter the bloodstream of the fetus. The risk factors for both
mother and fetus have been extensively reviewed elsewhere in
this volume as well as in previous reports from the Surgeon
General (198). (See also Pregnancy and Infant Health in Part II
of this Report).

It is estimated that between one-quarter and one-third of
pregnant smokers quit smoking for the duration of pregnancy
and that another third cut down.

This section reviews the current literature on sources of in-
formation available to the pregnant smoker, summarizes avail-
able data on prevalence of current smoking and smoking cessa-
tion during pregnancy, and discusses the problem of cessation
from a behavioral viewpoint.

SOURCES OF INFORMATION

The same classes of information discussed in the previous sec-
tion are available to the pregnant smoker. How the pregnant
smoker uses these sources and her degree of confidence in the
information provided seems to be a function of socioeconomic
status and parity. Information is distributed through health
professionals (primarily physicians and nurses), peers and fam-
ily, community resources, and the media.

Women in lower socioeconomic classes tend to rely more on
lay referral systems, such as peers and family, than upon mass |
media or medical sources (10,74). Personal transmission of in-
formation seems to be more highly valued and readily adhered
to (71). Middle and upper class women are more likely to utilize

386°
impersonal sources such as mass media and physician-supplied
information (74).

In one study of predominantly working class British women,
the mode of exposure to smoking information ranked as follows:
84 percent had seen it on television; 65 percent were told by
family or friends; 52 percent had seen posters and leaflets; 37
percent had been told by husbands; 34 percent used books and
magazines; and 25 percent had been told by a medical source (16
percent from a doctor, and 9 percent from a nurse) (11). The
authors comment that television, posters, and leaflets are in-
adequate for the delivery of statistical information; books,
which are better sources, were used much less than these other
sources. Baric and MacArthur present a discussion of health
norms in pregnancy (10). Seventy-nine percent of the sample
were aware of some norm relating to smoking in pregnancy: 39
percent thought they were expected not to smoke at all, and an
additional 40 percent thought they were expected to reduce
their smoking. All of the women could name at least one source
of information; 98 percent had been exposed to mass-media
messages to quit smoking. Smoking seemed to be undergoing a
change in norm status, from generality to specificity, i.e., from
being a general health menace to one with specific conse-
quences, such as a threat to the health of the baby.

The issue of normative behavior in smoking and personaliza-
tion of message should be crucial to informational campaigns,
according to Fishbein’s theory (63). Social support from a spouse
should also be critical, as would be involvement of significant
others.

Women about to have their first baby are more likely to be-
lieve educational materials than multiparous women (11,50).
This finding suggests that different modes of intervention or
different emphases should be developed for primiparous and
multiparous women.

Physician Advice

The physician represents one of the most knowledgeable fig-
ures the pregnant woman will encounter as a source of informa-
tion. Consequently, estimates of the frequency with which the
physician delivers advice on smoking are of importance.

Three such estimates are available from national samples in
the United States. In the first study, conducted in the mid-
1960s, 37 percent of physicians reported that they advised all or
almost all (95 to 100 percent) of their pregnant patients to quit
smoking or cut down sharply. Obstetricians were more likely to
deliver such advice to pregnant patients (49 percent) than were
physicians in general practice (38 percent) (76).

337
 

YJ Major n= 5401

 
  

PS] Contributing Cause
ua Association
No Association
100 F- 93.2 90.4 92.6 =

  
  

ox

Sd
bo
52

 
   

     

 

o,
2

 
     
   

   
  

 

 

5 80r oe s 7
5 60F y Y
a Y
Y
40 GZ
Y
20 Y
0 AES
Neonatal Coronary Chronic Pulmonary = Lung
Death Artery Bronchitis Emphysema Cancer
Disease

FIGURE 3.—Beliefs of OB-GYN specialists about the association
of maternal smoking with neonatal death and other

selected diseases
SOURCE: Danaher, B.G. (40).

The Physician Advice Survey conducted by the Center for
Disease Control examined the beliefs and behavior of physi-
cians specializing in Obstetrics and Gynecology (OB-GYN) in
the United States (40). The OB-GYN specialty practice includes
preventive medical care in the form of specific suggestions re-
garding hygiene and family planning and, during pregnancy,
active participation in directing perinatal care (40). The beliefs
of OB-GYN specialists about the relationship between maternal
smoking and neonatal death are presented in Figure 3, along
with their belief about some of the more common diseases as-
sociated with smoking. Because neonatal death can result from
a great many factors, the attribution of causality is somewhat
lower than for the other conditions represented. However, it is
notable that 23.6 percent of the physicians deny the existence of
any relationship. Congruent with the estimate from the 1960s,
45.3 percent of OB-GYN specialists in this survey claimed to
instruct all or almost all of their patients to quit or cut down on
smoking (see Figure 4). Another 13.1 percent delivered such ad-
vice to most or many (65 to 95 percent). A noticeably smaller
fraction of physicians who are current smokers deliver this
message than ex-smokers or nonsmokers.

The 1975 Survey of Adult Use of Tobacco, sponsored by the
National Clearinghouse on Smoking and Health, included a

338
70

NjAdvise All + Almost All Patients
60 Most + Many
EFew + None

50 45.3

40

Percent

30

20

10

   

0
Total Current Former Non-
(n = 3208) Smokers Smokers Smokers
(n =622) (n = 1187) (n = 1404)

FIGURE 4.— Percentage of patients advised to quit or cut down
their smoking by the smoking behavior of the advis-
ing obstetrician-gynecologist

SOURCE: Danaher, B.G. (40).

questionnaire directed at smoking habits in pregnant women. A
preliminary analysis of the results has been made (89). Out of
12,029 respondents interviewed in 1975, a total of 1,225 women
(814 current smokers and 411 former smokers) were adminis-
tered questions about their smoking habits during pregnancy.

Each of the 983 respondents (664 current smokers and 319
former smokers) who had ever been pregnant was asked
whether her doctor suggested that she quit smoking or cut
down during her last pregnancy. Table 18 displays the results
by year of last pregnancy. The percentage of women reporting
such advice from their doctors rose steadily. Only 14.6 percent of
women who had last been pregnant from 1965 to 1969 claimed to
have been advised by their doctor either to stop or cut down;
23.7 percent of women last pregnant from 1970 to 1975 remem-
bered such advice. These estimates are considerably smaller
than those supplied by physicians themselves (40,76). There are
several possible explanations for the discrepancy: the women
were reporting retrospectively, and memory may have been dis-
torted; a selective under-reporting of advice may have occurred;
or the populations of physicians and patients may be entirely
nonoverlapping. Retrospective data have been shown to be un-
reliable in one pregnancy study (49). Unfortunately, sample
sizes were too small to provide reliable estimates of the per-

339
TABLE 18.—Distribution of responses of current former
smokers who were ever pregnant to the question
“Did your doctor suggest that you cut down or stop
smoking cigarettes during your last pregnancy?”

 

Percent by Year of Last Pregnancy
(Prior to (1965- (1970- (1965-

 

 

 

Physician's Advice 1965) 69) 75) 75)
Quit smoking 5.6 6.2 10.8 9.3
Cut down smoking 5.7 8.4 12.9 11.4
No advice given 70.5 64.1 65.6 65.1
Not smoking at the time 16.4 20.6 9.1 12.9
Had no doctor 0.5 0 0.2 0.1
Don’t know or no answer 1.3 0.8 1.3 0.9
Number of respondents 466 215 291 506

 

SOURCE: National Clearinghouse for Smoking and Health (194).

centage of women who followed the advice of a physician to stop
smoking during pregnancy. Such data might have yielded an
estimate of the effectiveness of such advice.

In sum, over 50 percent of physicians claim to advise their
pregnant patients to eliminate or sharply curtail their smoking
during pregnancy, but a much smaller percentage of pregnant
women recall such advice.

PREVALENCE OF SMOKING AND QUITTING DURING
PREGNANCY

The prevalence of smoking in pregnant women (before special
cessation efforts) should be roughly equivalent to the preva-
lence of smoking in the female population in the same age
range, corrected for socioeconomic status. Ten studies con-
ducted in developed countries, reported between 1971 and 1973,
show a range from 23.4 percent to 47.6 percent in prevalence of
tobacco use (145). The median rate is 42.75 percent smokers for
the entire sample. A survey (conducted during the course of the
pregnancy) of 9,553 pregnant women who represent a cross sec-
tion of the general population in the Riverside-San Bernadino-
Ontario (California) area was recently completed (108). Prelimi-
nary results indicate that 44.5 percent of all women surveyed
either continued to smoke during pregnancy or had smoked be-
fore, but not during, this pregnancy. Since the precise time of
cessation is not clear, a more conservative estimate is that 33.3
percent of women continued to smoke for the duration of their
pregnancy. This estimate is well within the range of those de-
rived from the Population Report analysis (145).

340
There is a paucity of race-specific information on smoking
prevalence during pregnancy. Niswander and Gordon (134), ina
study encompassing 14 U.S. cities, reported greater prevalence
of smoking among white than black women (53.65 percent vs.
41.85 percent, respectively). This is a high estimate and reversal
of the prevalence rates presented in Table 7. The finding is simi-
lar to the previously presented data, in that white women
smoked more cigarettes per day than black women: only 3.3
percent of black women smokers consume a pack a day or more,
compared to 13.4 percent of white women in this study. Smoking
is slightly less prevalent in black than in white women in the
sample of Kuzma and Phillips (108): 57.3 percent of black women
and 53.3 percent of white women have never smoked. For His-
panic women, the percentage is somewhat higher, 61.9 percent
never-smokers. Table 19 summarizes the results of 11 studies
reporting rates of discontinuing smoking during pregnancy.
The overall rate of cessation among regular smokers ranges
from 0.9 percent to 35 percent, which is the figure most often
anecdotally cited. The median is closer to 20 percent.

Only one study provides ethnic data on smoking cessation
during pregnancy (108). In this study, it should be remembered,
stopped smokers are women who smoked prior to, but not dur-
ing the pregnancy, so that quitting may not have been
pregnancy-specific. Rates are very similar for white, black and
Hispanic women: 24.5 percent, 24.9 percent and 28.7 percent,
respectively, were stopped smokers in this study.

Even acute abstinence from cigarette smoking may be of
value, if it occurs immediately prior to giving birth. In the
United Kingdom, women are often admitted as early as 48 hours
before elective delivery; abstaining from smoking for that
period of time was found to result in a net percent increase in
available oxygen as COHb was excreted (42). Such a temporary
benefit may actually be critical under acutely stressful condi-
tions, and where there is chronic placental insufficiency.

Cutting down on smoking during pregnancy would appear to
be better than no change in behavior, especially for those ad-
verse effects upon the fetus which show a dose-response rela-
tionship. However, cutting down on number of cigarettes does
not always imply a reduction in delivered dose of nicotine or
other tobacco smoke constituents (79,80). When smoking behav-
ior was measured over the course of pregnancy in regular
smokers (5 to 30 cigarettes per day for at least 5 years), a de-
crease in number of puffs per cigarette occurred as pregnancy
progressed (6). Like puffing rate, the COHb concentration also
decreased over time in pregnancy. However, in these subjects
there was no significant change in nicotine dose extracted from

341
= TABLE 19.—Percentage of current smokers who altered smoking behavior during pregnancy

 

Change in Smoking Habit— Percent of Women

 

 

 

 

 

 

 

 

 

 

Cut
Quit Down No Miscellaneous,
Author and Date N Quit Temporarily Only Increased Change or Comment
1. Kullander & Kallen, 1971 (107) 2,806 0.9 1.3 97.3 +0.5 Initiated
2. Andrews & McGarry, 1972 (4) 6,733 14.7 Maternities only
3. Butler et al., 1972 (29) 841 18.4 Quit by end of 4th month
4. Schwartz et al., 1972 (171) 1,188 31.0 10.0
5. Baric et al., 1976! 134 14.9 3.0 82.1 Quit by 1st ante-natal visit
6. Graham, 1976 (74) 50 33.3* 33.3* 33.3 *1/3 quit or cut down;
1/3 cut down temporarily
7. Baric & MacArthur, 1977! (10) 133 22.5 6.0 33.1 5.3 26.3 +6.8 reduced temporarily
8. Donovan, 1977 (49) 959 12.5 5.6
9. Yankelovich et al., 1977 (216) ? 35.0 32.0
hE

TABLE 19.—Percentage of current smokers who altered smoking behavior during pregnancy—Continued

 

Change in Smoking Habit— Percent of Women

 

 

Cut
Quit Down No Miscellaneous,
Author and Date N Quit Temporarily Only Increased Change or Comment

10. Harris, 1979 (89) 4092 26.5 24.8 7.9 36.9 +3.9 changed brand or
switched to filter cigarettes
82.2 of quitters resumed
smoking after delivery

11. Kuzma & Phillips, 1979 (108) 4,249 25.1 13.4 of quit smokers were

again smoking at 1-5 mo.
post-delivery

 

NOTE: !These two studies may be composed of overlapping samples.
2Of the 506 women in the NCSH survey whose last pregnancy occurred during 1965-75, 409 reported smoking either before or
during pregnancy.
’Percent who smoked prior to, but not during this pregnancy, calculated as part of smoker sample.
the cigarette over the duration of the pregnancy. Some alter-
ation in puffing pattern, presumably in inhalation, produced
the compensation. Thus, caution must be exercised in the in-
terpretation of “cutting down.”

There is even less information available on the percentage of
quit-smokers who return to smoking after delivery. Table 19
provides two extremely divergent estimates: 82.2 percent (89)
and 13.4 percent (108). Because we are dealing with relatively
small sample sizes, the reliability of such data is not very high.
Much more information must be accumulated before any firm
statements about recidivism can be made. Women who quit dur-
ing pregnancy have an excellent opportunity to change a behav-
ior for life, with benefits both to themselves and to their chil-
dren (see Recommendations).

PSYCHOSOCIAL FACTORS IN QUITTING

Health reasons, primarily centering around preventing harm
to the fetus, are most often given as reasons for quitting. Yan-
kelovich, et al. (216) report that 62 percent of young women
smokers believe that smoking can harm the fetus and norms
against smoking have been discussed (10). The sickness experi-
enced as a part of pregnancy can also be a reason to give up
smoking (11). It has also been reported that women who smoke
before pregnancy show a significantly increased incidence of
appetite cravings and aversions, which may be associated with
quitting (41).

A closely related aspect of maternal health is weight gain.
Preventing excessive weight gain has even been given as a rea-
son to continue smoking during pregnancy (50). Baric and
MacArthur included control of weight gain as a norm during
pregnancy; 24 percent of this sample expressed awareness of
social expectations in this area (10). The issue of how much
weight it is appropriate to gain in pregnancy varies according to
time and culture, so the generality of this finding is unclear.

Little is known about problems in quitting during pregnancy.
The role of cigarettes as stimulants or tension reducers may be
altered during this period. Abstinence symptomatology has also
not been documented.

A composite picture of the successful quitter has been drawn
by Baric, et al. and also by Kuzma and Phillips (11,108). Baric, et
al. list educational qualifications as being positively related to
quitting, followed by sickness in early pregnancy. Other distin-
guishing characteristics are smoking fewer cigarettes before
pregnancy (also see 49,171), having started smoking at an older
age, having stopped previously for at least 6 months, having

344
heard about harmful effects of smoking from more sources,
firmly believing that smoking was harmful to the baby, and
finally, being encouraged to stop or being joined in the cessation
effort by their husbands (47,166).

Kuzma and Phillips identified a number of similar character-
istics: higher educational level; greater family income; being
married; being employed; more frequent church attendance;
having a spouse who does not smoke; and no illicit drug use
(106,108).

The characteristics described—advanced educational level,
higher socioeconomic status, wider information base, belief in
stopping for the sake of the fetus, and spousal support—all fit
with a model of behavior change involving information, per-
sonalization, and social norms (63).

Three studies evaluate smoking cessation interventions for
pregnant women (11,41,49). Tables 9 and 10 show reported abs-
tinence figures for two studies. One study (11) showed no dif-
ference between intervention and control groups, and the sec-
ond study (41) showed 50 percent abstinence at 9-month follow-
up for those completing treatment (11,41). This latter result is
very encouraging but is based on a very small sample in an
affluent community where the aforementioned factors of educa-
tional level, high socioeconomic status and orientation toward
professional advice are operative.

RECOMMENDATIONS

The preceding discussion has revealed a number of findings
which may be useful in improving methods of reaching the
pregnant woman and offering her cessation interventions.

1, Pregnant women seem to know that smoking is harmful to
health, and most acknowledge that it can be directly harmful to
the fetus. This information about the baby’s health should be
made as specific as possible, and the mother’s own health should
be intricately interwoven in the theme. Quitting is for the good
of both mother and baby, not the baby alone. The harmful as-
pects of smoking and the benefits of not smoking must be
equally emphasized.

2. Mass media, such as television and film, are particularly
good avenues for portraying women of varying ethnicity in a
number of geographical and socioeconomic settings. Because of
gender identification it is important to utilize women as the
transmitters of information and advice. Information should be
dispensed by as many different sources of contact in the pre-
natal clinic (or doctor’s office) as possible, not solely by the

345
physician. The awazeness of various health professionals
should be raised in this regard.

3. Social norms and lay referral systems should be used as
part of information dissemination and modeling influences.
This is particularly true for women of lower socioeconomic
status. It is important to involve the father of the child in the
normative belief system and in a direct supportive effort of
quitting. This should be particularly timely in an era when more
and more couples are experiencing pregnancy and birth as a
two-person process.

4. Much more emphasis must be placed on permanent smok-
ing cessation rather than just during the time of pregnancy.
Positive aspects of remaining an ex-smoker include better
health for the mother and child and the future impact of role
modeling as the child grows.

Summary

1. The percentage of 17-18 year old women who smoke has
shown a steady rise between 1968 and 1979. It now appears,
however, that the increase in smoking prevalence among all
12-18 year old females has leveled off and begun to decline.
Young women born after 1962 show a substantially reduced in-
itiation of smoking and will probably have a much lower preva-
lence of smoking as adults.

2. Those young women who do begin to smoke are starting to
smoke regularly at a younger age, with more than half of the
male and female adolescents who begin to smoke starting before
the 10th grade.

3. The earlier tobacco is used and the greater the number of
cigarettes smoked per day, the less likely an attempt to quit will
be successful. ,

4. The percentage of women smokers who smoke more than
one pack per day is increasing.

5. Adolescent and.adult women are more likely to use low “tar”
and nicotine cigarettes, smoke fewer cigarettes per day and in-
hale less deeply than do men, but the difference between the
sexes in these patterns of smoking is decreasing. Adolescent
and adult black women are more likely to be smokers than their
white peers, but they smoke fewer cigarettes per day.

6. Adolescents from low income families, single parent
families, and families with lower parental educational levels are
more likely to become smokers.

7. Female and male adolescents are more likely to begin
smoking if a parent or older sibling also smokes.

346
8. Adolescent smokers associate with peers who smoke, and
nonsmokers associate with nonsmoking peers.

9. Adolescent girls overestimate the percentage of their peers
who smoke and they have a very positive image of the people in
cigarette advertisements, but they are less likely than adoles-
cent boys to see smoking as a social asset.

10. Adolescent girls who smoke tend to be more outgoing, but
feel less able to influence their future.

11. Adolescents experience stress due to feelings of unattrac-
tiveness, incompetency in school achievement and personal re-
lations, limited opportunity for personal growth and concern
over future social and economic roles. This stress may be the
common mechanism producing the increased rates of smoking
in some groups.

12. The factors associated with successful quitting by adoles-
cents of either sex are lower number of cigarettes smoked per
day, higher educational aspirations and achievement, greater
acceptance of the health risk of smoking, and having more
nonsmokers among their friends.

13. It is possible that women and men modify their smoking
in order to maintain a constant nicotine level.

14. Women are more likely than men to smoke in order to
reduce stress.

15. Women at higher education and income levels are more
likely to succeed in quitting. Additional factors associated with
successful quitting are a strong commitment to change, the use
of behavioral techniques and reliable social support for quit-
ting. Women have been reported to show lower rates than men
of successful cessation following organized cessation programs,
a difference which is less apparent in those programs that in-
clude social support.

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