Summary

of the Health
Consequences
of Smoking

 

CHRONIC OBSTRUCTIVE
LUNG DISEASE

 

A Report of the

Surgeon General

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service

National Institutes of Health

National Heart, Lung, and Blood Institute
 

U.S. NATIONAL
LIBRARY
OF
MEDICINE

 
 
   

Copies of this summary can be obtained by writing the Public Inquiries and
Reports Branch, Building 31, Room 4A21, National Heart, Lung, and Blood
Institute, National Institutes of Health, Bethesda, MD 20205. Single copies of
the Report on the Health Consequences of Smoking: Chronic Obstructive Lung
Disease DHHS (PHS) 84-50205 can be obtained from the Office on Smoking
and Health, Parklawn Building, Room 1-58, 5600 Fishers Lane, Rockville, MD
20857.
Two decades have passed since Dr. Luther Terry issued the first Surgeon
General’s report on smoking and health. That report pointed out in great detail
many of the health hazards of cigarette smoking and was the beginning of a
concerted effort to. change the smoking habits of the American public.

The Report of the Surgeon General on the Health Consequences of Smoking
for 1984 concentrates on chronic obstructive lung disease (COLD), which
comprises emphysema and chronic bronchitis. The evidence brought forth in
this report indicates that COLD would almost disappear if Americans quit
smoking. Some 80 to 90 percent of COLD mortality is associated with smok-
ing; most of the rest is the result of a relatively rare genetic defect in which the
patient lacks a certain enzyme that protects against lung damage.

The importance of the report of the Surgeon General is very substantial. It
underscores the overwhelming evidence that has been amassed over the years
which clearly establishes the cigarette as public enemy number one for a
healthy lung. I hope it provokes the medical community to be even more
vigorous in counseling their smoking patients to quit. What follows is an
extraction of the overview and conclusions of the report, which we hope will
serve as a convenient summary.

Claude Lenfant, M.D.
Director

National Heart, Lung,
and Blood Institute
Overview

Scientists from a variety of disciplines have investigated the role of
cigarette smoking in the development of COLD; today we can trace
the progressive decline in lung function in smokers with increasing
smoke exposure. We can describe the concurrent pathologic changes,
demonstrate that both COLD prevalence and COLD death are
limited largely to smokers, and perhaps most important, we can
describe in detail a plausible mechanism by which cigarette smoking
can lead to the development of emphysema. Some gaps in the
understanding of the details of this process may still exist, but the
experimental and epidemiologic evidence leaves no room for reason-
able doubt on the fundamental issue: cigarette smoking is the major
cause of COLD in the United States.

The earliest recognized response to cigarette smoke is an increase
in airway resistance that occurs with the inhalation of smoke by the
smoker. This increase in resistance is a response to the irritants in
the smoke, as is coughing, which is known to be more frequent in
smokers than in nonsmokers, even in adolescents. By the time
smokers become young adults, a substantial proportion of them_will
have developed pathologic changes in their small airways. These
abnormalities are demonstrable using a variety of physiologic tests,
and result from pathologic changes of inflammation in the airways
less than 2 mm in diameter. Part of this small airways response, but
perhaps a later manifestation of it, is the development of smooth
muscle hypertrophy, goblet cell hyperplasia, and mild peribronchio-
lar fibrosis. The prevalence of abnormalities on tests of small
airways function increases as these young smokers grow older and is
greater in heavy smokers than in light smokers. While it is clear
that changes in the small airways represent an early response to
cigarette smoking and that they are a significant finding in the

1
pathophysiology of COLD, it is not clear that abnormal function of
the small airways, per se, is useful as a marker for identifying who
will progress to develop symptomatic COLD. It may identify a large
group of smokers who manifest an irritant response to smoke in the
small airways, of whom only a subset actually develop symptomatic
airflow obstruction.

Measurable differences in tests of expiratory airflow exist between
smokers and nonsmokers after age 25. Smokers as a group have a
more rapid decline in FEV, with age than that observed in
nonsmokers, and the decline is even greater among heavy smokers.
However, this increased rate of decline in lung function is not
distributed evenly, even among smokers with similar smoking
histories. Some smokers have a far more rapid decline than the
average smoker, and clearly those individuals who have developed
symptomatic chronic airflow obstruction have had a larger total
decline in lung function than the average smoker. This has led to the
suggestion that individuals with a particularly rapid decline in FEV,
early in life may represent a group especially susceptible to the later
development of symptomatic COLD. The nature of this susceptibility
remains unclear, but differences in depth or pattern of inhalation,
variations in the cellular and biochemical response of the lung to
smoke, differences in immune or repair mechanisms, and childhood
infections or exposure to environmental tobacco smoke as a child
have been suggested as potential factors.

The accumulation of lung damage, marked by the excess decline in
FEV, and other measures of expiratory airflow, can lead to shortness
of breath and other symptoms that characterize clinically significant
COLD. These symptoms result in disability due to ventilatory
limitation and may vary from patient to patient in severity and
duration; many patients with clinically disabling COLD die with
their disease rather than because of it. Death from COLD usually
results only after extensive lung damage and commonly occurs
because of failure of the severely damaged lungs to maintain
adequate gas exchange.

The cessation of cigarette smoking has a substantial impact on the
incidence and progression of COLD. Cigarette smokers who quit
prior to developing abnormal lung function are unlikely to go on to
develop ventilatory limitation; when the abnormalities are demon-
strable only on tests of small airways function, cessation often
results in a reversal of these changes and a return to normal
function. The presence of significant fixed reduction in measures of
expiratory airflow usually reflects the presence of substantial lung
damage. Cessation of smoking at this stage of COLD results in a
slowing in the rate of decline in lung function with age. After a
period of cessation, this rate of decline in function may approximate
the rate found in nonsmokers, but there is little evidence to suggest

2
that those who quit are able to regain their prior excess functional
decline. Therefore, those who quit continue to have reduced lung
function when compared with those who have never smoked, but
their lung function begins to decline less rapidly with age when
compared to the lung function of those who continue to smoke.

The importance of cigarette smoking as a causative factor in
COLD is emphasized by cross-sectional studies of the populations in
the United States where the only major predictor for developing or
dying of COLD is smoking behavior. In the absence of cigarette
smoking, clinically significant COLD is rare.

As the smoker enters the sixth decade of life, pathologically
definable pulmonary emphysema begins to become evident. In older
age groups, mild to moderate emphysema is present in most smokers
and is rare in nonsmokers. Once again, however, only a small
number of smokers develop severe emphysema, and this minority
includes a disproportionate number of heavy smokers.

A mechanism for smoking-induced emphysematous lung injury
has been proposed and continues to evolve as our understanding of
cellular and biochemical responses of the lung increases. Emphyse-
ma can be produced by the presence of excessive amounts of elastase
(an enzyme capable of degrading the structural elements of lung
tissue) or by the absence of a,-antiprotease (an enzyme that inhibits
the action of elastase). As part of the inflammatory response to
cigarette smoke, an increased number of inflammatory cells are
present in the lungs of smokers; these cells may result in an
increased amount of elastase being present in the lung. In addition,
cigarette smoke can oxidize the a,-antiprotease in the lung, further
contributing to the imbalance between levels of elastase and levels of
a,-antiprotease. The net result can be excess levels of elastase,
leading to degradation of elastin in the lung, destruction of alveolar
walls, and development of emphysema.

The text of this Report discusses in detail the relationship of
cigarette smoking to COLD morbidity and mortality, the pathology
of smoking-induced COLD, some of the mechanisms by which
smoking results in COLD, the impact on the lung of low tar and
nicotine cigarettes and of involuntary smoke exposure, the deposi-
tion and toxicology of tobacco smoke, and the role of the physician
and of community intervention programs in smoking cessation.

The overall conclusion of this Report is clear: Cigarette smoking
is the major cause of chronic obstructive lung disease in the
United States for both men and women. The contribution of
cigarette smoking to chronic obstructive lung disease morbidi-
ty and mortality far outweighs all other factors.
Conclusions of the 1984 Report

COLD Morbidity

1. Cigarette smoking is the major cause of COLD morbidity in the
United States, and 80-90 percent of the COLD in the United
States is attributable to cigarette smoking.

2.In population-based studies in the United States, cigarette
smoking behavior is often the only significant predictor for the
development of COLD. Other factors improve the predictive
equation only slightly, even in those populations where they
have been found to exert a statistically significant effect.

3.In spite of over 30 years of intensive investigation, only
cigarette smoking and a,-antiprotease deficiency (a rare genet-
ic defect) are established causes of clinically significant COLD
in the absence of other agents.

4. Within a few years after beginning to smoke, smokers experi-
ence a higher prevalence of abnormal function in the small
airways than nonsmokers. The prevalence of abnormal small
airways function increases with age and the duration of the
smoking habit, and is greater in heavy smokers than in light
smokers. These abnormalities in function reflect inflammatory
changes in the small airways and often reverse with the
cessation of smoking.

5. Both male and female smokers develop abnormalities in the
small airways, but the data are not sufficient to define possible
sex-related differences in this response. It seems likely, how-
ever, that the contribution of sex differences is small when age
and smoking exposure are taken into account.

6. There is, as yet, inadequate information to allow a firm
conclusion to be drawn about the predictive value of the tests of
small airways function in identifying the susceptible smoker
who will progress to clinical airflow obstruction.

7. Smokers of both sexes have a higher prevalence of cough and
phlegm production than nonsmokers. This prevalence in-
creases with an increasing number of cigarettes smoked per
day and decreases with the cessation of smoking.

8. Differences between smokers and nonsmokers in measures of
expiratory airflow are demonstrable by young adulthood and
increase with number of cigarettes smoked per day and with
age.

9.The rate of decline in measures of expiratory airflow with
increasing age is steeper for smokers than for nonsmokers; it is
also steeper for heavy smokers than for light smokers. After
the cessation of smoking, the rate of decline of lung function
with increasing age appears to slow to approximately that seen
in nonsmokers of the same age. Only a minority of smokers will
develop clinically significant COLD, and this group will have
demonstrated a more extensive decline in lung function than
the average smoker. The data are not yet available to
determine whether a rapid decline in lung function early in life
defines the subgroup of smokers who are susceptible to
developing COLD.

10. Clinically significant degrees of emphysema occur almost
exclusively in cigarette smokers or individuals with genetic
homozygous a,-antiprotease deficiency. The severity of em-
physema among smokers increases with the number of ciga-
rettes smoked per day and the duration of the smoking habit.

COLD Mortality

1. Data from both prospective and retrospective studies consis-
tently demonstrate a uniform increase in mortality from COLD
for cigarette smokers compared with nonsmokers. Cigarette
smoking is the major cause of COLD mortality for both men
and women in the United States.

2. The death rate from COLD is greater for men than for women,
most likely reflecting the differences in lifetime smoking
patterns, such as a smaller percentage of women smoking in
past decades, and their smoking fewer cigarettes, inhaling less
deeply, beginning to smoke later in life, and more frequently
smoking filtered and low tar and nicotine cigarettes.

3. Differences in lifetime smoking behavior are less marked for
younger age cohorts of smokers. The differences in male and
female mortality rates from COLD are decreasing because of a
more rapid rise in mortality from COLD among women.

4.The dose of tobacco exposure as measured by number of
cigarettes or duration of habit strongly affects the risk for
death from COLD in both men and women. Similarly, people
who inhale deeply experience an even higher risk for mortality
from COLD than those who do not inhale.

5. Cessation of smoking leads to a decreased risk of mortality
from COLD compared with that of continuing smokers. The
residual excess risk of death for the ex-smoker is directly
proportional to the overall lifetime exposure to cigarette smoke
and to the total number of years since one quit smoking.
However, the risk of COLD mortality among former smokers
does not decline to equal that of the never smoker even after 20
years of cessation.

6. Several prospective epidemiologic studies examined the rela-
tionship between pipe and cigar smoking and mortality from
COLD. Pipe smokers and cigar smokers also experience higher
mortality from COLD compared with nonsmokers; however,
the risk is less than that for cigarette smokers.
7. There are substantial worldwide differences in mortality from
COLD. Some of these differences are due to variations in
terminology and in death certification in various countries.
Emigrant studies suggest that ethnic background is not the
major determinant for mortality risk due to COLD.

Pathology of Cigarette-Induced Disease

1. Smoking induces changes in multiple areas of the lung, and the
effects in the different areas may be independent of each other.
In the bronchi (the large airways), smoking results in a modest
increase in size of the tracheobronchial glands, associated with
an increase in secretion of mucus, and in an increased number
of goblet cells.

2. In the small airways—conducting airways 2 or 3 mm or less in
diameter consisting of the smallest bronchi and bronchioles—a
number of lesions are apparent. The initial response to
smoking is probably inflammation, with associated ulceration
and squamous metaplasia. Fibrosis, increased muscle mass,
narrowing of the airways, and an increase in the number of
goblet cells follow.

3. Inflammation appears to be the major determinant of small
airways dysfunction and may be reversible after cessation of
smoking.

4. The most obvious difference between smokers and nonsmokers
is respiratory bronchiolitis. This lesion may be an important
cause of abnormalities in tests of small airways function, as
well as being involved in the pathogenesis of centrilobular
emphysema. The severity of emphysema is clearly associated
with smoking, and severe emphysema is confined largely to
smokers.

Mechanisms of COLD

1. Increased numbers of inflammatory cells are found in the
lungs of cigarette smokers. These cells include macrophages
and, probably, neutrophils, both of which can release elastase
in the lung.

2. Human neutrophil elastase produces emphysema when in-
stilled into animal lungs.

3. Alpha, -antiprotease inhibits the action of elastase, and a very
small number of people with a homozygous deficiency of a,-
antiprotease are at increased risk of developing emphysema.
The a,-antiprotease activity has been shown by lung lavage to
be reduced in the bronchoalveolar fluids obtained from ciga-
rette smokers and from rats exposed to cigarette smoke.

4. The protease-antiprotease hypothesis suggests that emphyse-
ma results when there is excess elastase lytic activity as the
result of increased concentrations of inflammatory cells in the
lung and of decreased levels of a,-antiprotease secondary to
oxidation by cigarette smoke.

5. Cigarette smokers have been shown to have a more rapid fall in
antibody levels following immunization for influenza than
nonsmokers. Whole cigarette smoke has been shown to depress
the number of antibody-forming cells in the spleens of experi-
mental animals.

6. Cigarette smoke produces structural and functional abnormali-
ties in the airway mucociliary system.

7. Short-term exposure to cigarette smoke causes ciliostasis in
vitro, but has inconsistent effects on mucociliary function in
man. Long-term exposure to cigarette smoke consistently
causes an impairment of mucociliary clearance. This impair-
ment is associated with epithelial lesions, mucous hypersecre-
tion, and ciliary dysfunction.

8. Chronic bronchitis in smokers and ex-smokers is characterized
by an impairment of mucociliary clearance.

9. Both the particulate phase and the gas phase of cigarette
smoke are ciliotoxic.

Low Tar and Nicotine Cigarettes

1. The recommendation for those who cannot quit to switch to
smoking cigarette brands with low tar and nicotine yields, as
determined by a smoking-machine, is based on the assumption
that this switch will result in a reduction in the exposure of the
lung to these toxic substances. The design of the cigarette has
markedly changed in recent years, and this may have resulted
in machine-measured tar and nicotine yields that do not reflect
the real dose to the smoker.

2.Smoking-machines that take into account compensatory
changes in smoking behavior are needed. The assays could
provide both an average and a range of tar and nicotine yields
produced by different individual patterns of smoking.

3. Although a reduction in cigarette tar content appears to reduce
the risk of cough and mucous hypersecretion, the risk of
shortness of breath and airflow obstruction may not be
reduced. Evidence is unavailable on the relative risks of
developing COLD consequent to smoking cigarettes with the
very low tar and nicotine yields of current and recently
marketed brands.

4.Smokers who switch from higher- to lower-yield cigarettes
show compensatory changes in smoking behavior: the number
of puffs per cigarette is variably increased and puff volume is
almost universally increased, although the number of ciga-
rettes smoked per day and inhalation volume are generally

7
unchanged. Full compensation of dose for cigarettes with lower
yields is generally not achieved.

5. Nicotine has long been regarded as the primary reinforcer of
cigarette smoking, but tar content may also be important in
determining smoking behavior.

6. Depth and duration of inhalation are among the most impor-
tant factors in determining the relative concentration of smoke
constituents that reach the lung. Considerable interindividual
variation exists between smokers with respect to the volume
and duration of inhalation. This variation is likely to be an
important factor in determining the varying susceptibility of
smokers to the development of lung disease.

7. Production of low tar and nicotine cigarettes has progressed
beyond simple reduction in tobacco content. Additives such as
artificial tobacco substitutes and flavoring extracts have been
used. The identity, chemical composition, and adverse biologi-
cal potential of these additives are unknown at present.

Passive Smoking

1. Cigarette smoke can make a significant, measurable contribu-
tion to the level of indoor air pollution at levels of smoking and
ventilation that are common in the indoor environment.

2. Nonsmokers who report exposure to environmental tobacco
smoke have higher levels of urinary cotinine, a metabolite of
nicotine, than those who do not report such exposure.

3. Cigarette smoke in the air can produce an increase in both
subjective and objective measures of eye irritation. Further,
some studies suggest that high levels of involuntary smoke
exposure might produce small changes in pulmonary function
in normal subjects.

4. The children of smoking parents have an increased prevalence
of reported respiratory symptoms, and have an increased
frequency of bronchitis and pneumonia early in life.

5. The children of smoking parents appear to have measurable
but small differences in tests of pulmonary function when
compared with children of nonsmoking parents. The signifi-
cance of this finding to the future development of lung disease

- is unknown.

6. Two studies have reported differences in measures of lung
function in older populations between subjects chronically
exposed to involuntary smoking and those who were not. This
difference was not found in a younger and possibly less exposed
population.

7. The limited existing data yield conflicting results concerning
the relationship between passive smoke exposure and pulmo-
nary function changes in patients with asthma.
Deposition and Toxicity of Tobacco Smoke in the Lung

1.The mass median aerodynamic diameter of the particles in
cigarette smoke has been measured to average approximately
0.46 m, and particulate concentrations have been shown to
range from 0.3 x 10° to 3.3 x 10° per milliliter.

2. The particulate concentration of the smoke increases as the
cigarette is more completely smoked.

3. Particles in the size range of cigarette smoke will deposit both
in the airways and in alveoli; models predict that 30 to 40
percent of the particles within the size range present in
cigarette smoke will deposit in alveolar regions and 5 to 10
percent in the tracheobronchial region.

4. Acute exposure to cigarette smoke results in an increase in
airway resistance in both animals and humans.

5. Exposure to cigarette smoke results in an increase in pulmo-
nary epithelial permeability in both humans and animals.

6. Cigarette smoke has been shown to impair elastin synthesis in
vitro and elastin repair in vivo in experimental animals
(elastin is a vital structural element of pulmonary tissue).

The Role of the Physician in Smoking Cessation

1. At least 70 percent of North Americans see a physician once a
year. Thus, an estimated 38 million of the 54 million adults in
the United States who smoke cigarettes could be reached
annually with a smoking cessation message by their physician.

2. Current smoking prevalence among physicians in the United
States estimated at 10 percent.

3. While the majority of persons who smoke feel that physician
advice to quit or cut down would be influential, there is a
disparity between physicians’ and patients’ estimates of cessa-
tion counseling, with physician advice being reported by only
approximately 25 percent of current smokers.

4. Studies of routine (minimal) advice to quit smoking delivered
by general practitioners have shown sustained quit rates of
approximately 5 percent. Followup discussions enhance the
effects of physician advice.

5. A median of 20 percent of pregnant women who smoke quit
spontaneously during pregnancy. That proportion can be
doubled by an intervention consisting of health education,
behavioral strategies, and multiple contacts.

6. Large controlled trials of cardiovascular risk reduction have
demonstrated that counseling on individual specific risk fac-
tors, including smoking cessation techniques, can be effective.

7.Studies of pulmonary and cardiac patients indicate that
severity of illness is positively related to increased compliance

9
in smoking cessation. Survivors of a myocardial infarction have
smoking cessation rates averaging 50 percent.

8. Nicotine chewing gum has been developed as a pharmacologi-
cal aid to smoking cessation, primarily to alleviate withdrawal
symptoms. Cessation studies conducted in offices of physicians
who prescribe the gum have produced mixed results, however,
with outcome depending on motivation and intensive adjunc-
tive support or followup. .

9. Physician-assisted intervention quit rates vary according to the
type of intervention, provider performance, and patient group.
In general, quit rates in recent research appear lower than in
older studies.

Community Studies of Smoking Cessation

10

1.Community studies of smoking cessation and prevention are
becoming an established paradigm for public health action
research. Such studies emphasize large-scale delivery systems,
such as the mass media, and include community organization
programs seeking to stimulate interpersonal communication in
ways that are feasible on a large-scale basis.

2. Although there are methodological limitations to nearly all
communitywide studies, the results yield fairly consistent
positive results, indicating that large-scale programs to reduce
smoking can be effective in whole populations. Person-to-
person communication appears to be a necessary part of a
successful community program to reduce smoking.

3. Further research is needed, with both improved methodology
and more emphasis on low socioeconomic status groups that
have not yet shown population trends toward reduced smoking.

4. Several promising directions for research are clear, but the
most important future trends will be toward the establishment
of smoking reduction programs within existing health services,
the combination of chronic disease prevention with mental
health promotion via mass media and community intervention,
and the development of social policy to establish integrated
strategies for smoking cessation and prevention.

® U.S. GOVERNMENT PRINTING OFFICE: 1984-461-320:4882