9otH

TABLE 2. Methods used in retrospective and cross sectional studies of peptic ulcer and smoking (cont.)

 

 

 

 

 

 

Author,
year, Controls
country, Sex Number Method of selection Comments
reference Number Method of selection

Kasanen and M 43 Gastric. Successive male admissions with pep- 100 Successive men treated at medical A special questionnaire
Forsstrém, 57 Duodenal. tic ulcer treated at medical clinic clinic who had no gastrointestinal was used for the
1966, or outpatient department of Uni- symptoms or signs of CHD. interview.

Finland versity Hospital. Only patients

(13). under 65 years of age or those
who had been working were in-
cluded.

Gillies and Mand F 100 Gastric. Patients with peptic uleer were se- 150 Matched by age and sex from the Diagnosis well established
Skyring, 60 Duodenal. lected from hospital admissions in same ward at the same time and with X-ray, gastros-
1968, 1967. with absence of signs or symp- copy, or surgery.

1968, toms or past history of upper
Australia gastrointestinal disease.
(9).

Gillies and MandF 10 Gastric. 1,405 workers from a broadcasting 100 Two contro] groups: All information obtained
Skyring, 48 Duodenal. company, a manufacturing com- 1. 100 peptic ulcer patients pre- by question card. All
1969, 18 Uncertain pany, and a bus company were viously reported by authors. ulcers were proved by
Australia location. interviewed for a history of pep- 1,829 2. 1,829 workers without ulcer. X-ray or surgery.
(10). tic ulcer.

Monson, MandF 52 Gastric. 643 physicians from Massachusetts 625 Controls were physicians without Diagnosis established by
1970, 452 Duodenal. who responded affirmatively to a ulcer disease who were matched X-ray or surgery except
ULS.A, (15). 139 Not questionnaire sent to them in 1967 to ulcer patients by year of birth. for 46 “clinica]” cases.

specified. asking how many had had a pep-

tic ucer.

 
Ltr

TABLE 3.—Summary of results of retrospective and cross sectional studies of peptic ulcer and smoking

 

 

 

 

 

 

 

Author,

year, Percent nonsmoker Amount of tobacco used
country,
reference Cases Controls Cases Controls

Barnett, Total .......... 18.0 25.0
1927, Gastric ........ 15.0
U.S.A. Duodenal ...... 20.0
(2).

Trowell, Duodenal ...... 8.0 17.0 Average number:

1934, Cigarettes .. 12.0 perday..........11.1 per day
England Pipe ....... 1.6 ounces per week.. 2.15 ounces per week
(21).

Allibone and 38.0 54.0

Flint,
1958,
England

(1).

Doll et al., Gastric: Gastric: Percent amoking >>25 cigarettes per day
1958, Males ..... 1.3 47 Males ...... 10.6 11.3
England Females ... 51.1 66.8 Females .... 1.1 11
(7). Duodenal: Duodenal:

Males ..... 2.1 5.8 Males ...... 10.2 12.7
Females ... 53.7 62.0 Females .... 1.9 1.9

Edwards Percent of peptic ulcer by
etal, smoking category
1959, Never smoked ...........-¢2005- 6.0
England Formerly smoked .......--+025. 6.9
(8). Cigarettes:

1-9 perday .............. 9.4
10-19 perday .............. 9.8
>>20 per day ............4.- 12.0
Pipe oo. c cee cece eee e reece 6.5
Pipe and cigarettes 8.5

 
St

TABLE 3.—Summary of results of retrospective and cross sectional studies of peptic ulcer and smoking (cont.)

 

 

 

 

 

 

Author,
year, Percent nonsmoker Amount of tobacco used
country, —
reference Cases Controls Cases Controls
Kasanen “Peptic” . 10.0 40.0 Cigarettes per day:
and <10 ......., 10.0 7.0
Forsstr5m, 10-20 ...... 19.0 17.0
1966, 20 we... eee 42.0 26.0
Finland 20 2... 19.0 10.0
{78).
Gillies and Gastric -». 18.0 44.0 Mean number cigarettes per day:
Skyring, Duodenal - 62.0 71.0 Gastric .... 23.3 17.1
1968, Duodenal .. 23.2 23.0
Australia Duration of smoking (years) :
(9). Gastric .... 30.2 28.0
Duodenal .. 24.2 28.2
Gillies and Gastric +. 179 55.6
Skyring, Duodenal - 36.6
1969,
Australia
(20).
Monson, Duodenal - 82.1 46.7 Percent smoking >20
1970, Gastric ........ 19.2 cigarettes per day
U.S.A. Not Specified . 43.2 Age: Gastric Duodenal
(15). P| 38.8 27.3 30.1
30 oo... eee 45.7 43.0 47.1
45 Lo... 60.2 49.5 46.9
60 ......... B41 40.4 44.0

 
REFERENCES

(1) ALLIBONE, A., FLINT, F. J. Bronchitis, aspirin, smoking, and other fac-
tors in the aetiology of peptic ulcer. Lancet 2: 179-182, July 26, 1958.

(2) BARNETT, C. W. Tobacco smoking as a factor in the production of peptic
ulcer and gastric neurosis. Boston Medical and Surgical Journal
197 (12) : 457-459, September 22, 1927.

(3) BATTERMAN, R. C, EHRENFELD, I. The influence of smoking upon the
management of the peptic ulcer patient. Gastroenterology 12 (4) : 575-
585, April 1949.

(4) Cooper, P., Knicut, J. B., JR. Effect of cigarette smoking on gastric
secretions of patients with duodenal ulcer. New England. Journal of
Medicine 255(1): 17-21, July 5, 1956.

(5) Dot, R., Hz, A. B. Mortality in relation to smoking: 10 years’ obser-
vations of British doctors. Part I. British Medical Journal 1(5395):
1399-1410, May 30, 1964.

(6) Dox, R., Hitt, A. B. Mortality in relation to smoking: 10 years’ obser-
vations of British doctors. (concluded). British Medical Journal
1(5396) : 1460-1467, June 6, 1964. , ;

(7) Dott, R., Jones, F, A., Pycott, F. Effect of smoking on the production
and maintenance of gastric and duodenal ulcers. Lancet 1: 657-662,
March 29, 1958.

(8) Epwarps, F., McKeown, T., WHITFIELD, A. G. W. Association between
smoking and disease in men over sixty. Lancet 1: 196-201, January
24, 1959. .

(9) GiLiies, M., SKyRING, A. Gastric ulcer, duodenal ulcer and gastric car-
cinoma: A case-control study of certain social and environmental fac-
tors. Medical Journal of Australia 2(25): 1182-1136, December 21,
1968.

(10) Gries, M. A., SkyRING, A. Gastric and duodenal ulcer. The association
between aspirin ingestion, smoking and family history of ulcer, Medi-
cal Journal of Australia 2(6) ; 280-285, August 9, 1969.

(11) Hammonp, E. C. Smoking in relation to the death rates of 1 million men
and women. IN: Haenszel, W. (Editor). Epidemiological Approaches
to the Study of Cancer and Other Chronic Diseases. Bethesda, U.S.
Public Health Service, National Cancer Institute Monograph No. 19,
January 1966. pp. 127-204.

(12) Kaun, H. A. The Dorn study of smoking and mortality among US.
veterans: Report on 8% years of observation. IN: Haenszel, W. (Edi-
tor). Epidemiological Approaches to the Study of Cancer and Other
Chronic Diseases. Bethesda, U.S. Public Health Service, National
Cancer Institute Monograph No. 19, January 1966. pp. 1-125.

(18) Kasanen, A., Forsstrom, J. Social stress and living habits in the etiology
of peptic ulcer. Annales Medicinae Internal Fenniae 55(1): 13-22,
1966.

(14) Murty, W. F., Jk., Rousse.ot, L. M., DELANy, G. J. Smoking and its
relation to nutritional status of patients following gastrectomy; 2
five-year follow-up survey of 171 patients. Annals of Surgery 150(1):
76-84, July 1959.

(15) Monson, R. R. Cigarette smoking and body form in peptic ulcer. Gastro-
enterology 58(3) : 387-344, March 1970.

429
(16) Packarp, R. S. Smoking and the alimentary tract: A review. Gut 1:
171-174, 1960.

(17) Parmer, W. L. Peptic ulcer. Chapter 32. IN: Paulson, M. (Editor).
Gastroenterologic Medicine. Philadelphia, Lea & Febiger, 1969, pp.
710-757,

(18) ScHNeEDorRF, J. G., Ivy, A. C. The effect of tobacco smoking on the
alimentary tract. An experimental study of man and animals. Journal
of the American Medical Association 112(10): 898-904, March 11,
1939,

(19) STEIGMANN, F., DoLEHIDE, R. H., KAMINSKI, L. Effects of tobacco smok-
ing on gastric acidity and motility of hospital controls and patients
with peptic ulcer. American Journal of Gastroenterology 22: 399-409,
1954,

(20) THompson, J. H. Effects of nicotine and tobacco smoke on gastric secre-
tion in rats with gastric fistulas. American Journal of Digestive
Diseases 15(3) : 209-217, March 1970.

(21) TROWELL, O. A. The relation of tobacco smoking to the incidence of
chronic duodenal ulcer. Lancet 1: 808-809, April 14, 1934.

(22) U.S. Pupitic HEALTH SERVICE. NATIONAL CENTER FOR HEALTH STATIS-
Tics. Vital Statistics of the United States—-1967. Vol. JI—Mortality,
Part A. Washington, U.S. Department of Health, Education and Wel-
fare, Public Health Service Publication, 1969.

(23) Wet, J. M., DunN, J. E., JR. Smoking and mortality: A prospective
study. Cancer 25(1) : 105-112, January 1970.

430
CHAPTER 7

 

Tobacco Amblyopia
Contents

Page
Summary and conclusions .............. 00 eee eee eee 436
References 2.0.0... ccc eee ee eee neces 436

433
ToBacco AMBLYOPIA

Tobacco amblyopia (tobacco-alcohol amblyopia) is that syn-
drome of visual failure occurring in association with the use of
tobacco, with or without the concurrent use of alcohol, and with or
without concurrent nutritional deficits. The disease has a subacute
onset, leading to a loss of visual acuity and color perception (72).
It is characterized by centrocecal scotomas which are bilateral but
not necessarily symmetrical and which have sloping diffuse edges
and by the presence of nuclei of denser visual loss within the large
scotomas (22, 23). Such visual impairment is not unique to tobacco
amblyopia, as it is also seen in neurodegenerative disorders, such
as Leber’s hereditary optic atrophy (7, 25).

Clinical information on tobacco amblyopia has appeared in nu-
merous articles throughout the past century. This information has
been reviewed by Silvette, et al. (17) and, more recently, by
Dunphy (5). Pure tobacco amblyopia (TA), that is amblyopia
unassociated with excessive alcohol intake or the exposure to other
toxins, is rarely seen in the United States today (12). Walsh, et al.
(23) have observed that when TA is found it is usually present in
association with nutritional or idiopathic vitamin deficiencies.
Victor (22) recently observed that the type of visual defect seen in
tobacco amblyopia may be found in clinical circumstances in which
tobacco is clearly not a causative factor. He questions whether TA
is distinguishable from other forms of amblyopia.

The prevalence of this disorder has been variously estimated in
the past at from 0.5 to 1.5 percent of all eye clinic patients (20, 23).
However, currently in the United States, it appears to be a rare
condition. Silvette, et al. (17) have observed that the incidence of
tobacco amblyopia appears to have decreased substantially during
the past decades. Other authors (3, 15) have also commented on
this trend. Although reference has been made to the increased fre-
quency of certain types of tobacco usage in patients with this dis-
order, adequate population studies with proper controls have yet to
be performed. The association of this disorder with the use of
tobacco is strengthened by the frequent clinical observations of
improvement following the cessation of smoking although improve-
ment has been noted by some to occur without cessation.

Research into the pathogenesis of tobacco amblyopia has cen-

435
tered upon the interrelationships of cyanide metabolism, vitamin
B,., and other vitamin deficiencies. Three reviews of this material
have recently appeared (1, 12, 22). Numerous studies reviewed in
these articles suggest that tobacco amblyopia may result from the
incomplete detoxification of the cyanide present in tobacco smoke.
This failure of detoxification may stem from or be intensified by
inadequate dietary intake of necessary nutritional factors. This
may be the reason for the association of this disorder with exces-
sive alcohol intake and with its related nutritional deficits (2, 4, 6,
8,9, 10,11, 18, 14,16, 18, 19, 21, 24, 26, 27,28).

SUMMARY AND CONCLUSIONS

Tobacco amblyopia is presently a rare disorder in the United
States. The evidence suggests that this disorder is related to nutri-
tional or idiopathic deficiencies in certain detoxification mechan-
isms, particularly in handling the cyanide component of tobacco
smoke.

REFERENCES

(1) CANADIAN MEDICAL ASSOCIATION JOURNAL. Tobacco amblyopia. (Edi-
torial) Canadian Medical Association Journal 102(4) : 420, February
28, 1970.

(2) CHISHOLM, I. A., BRONTE-STEWART, J., FouLps, W. S. Hydroxocobalamin
versus cyanocobalamin in the treatment of tobacco amblyopia. Lancet
2(7513): 450-451, August 26, 1967.

($) Darsy, P. W., Witson, J. Cyanide, smoking, and tobacco amblyopia.
Observations on the cyanide content of tobacco smoke. British Journal
of Ophthalmology 51(5) : 336-338, May 1967.

(4) DreyFrus, P. M. Blood transketolase levels in tobacco-alcohol amblyopia
Archives of Ophthalmology 74(5) : 617-620, November 1965.

(5) Dunpuy, E. B. Alcohol and tobacco amblyopia: A historical survey.
American Journal of Ophthalmology 68(4): 569-578, October 1969.

(6) FouLps, W. 8., BRONTE-STEWwarT, J. M., CHISHOLM, I. A. Serum thio-
cyanate concentrations in tobacco amblyopia. Nature 218 (5141) : 586,
May 11, 1968.

(7) Foutps, W. 8., Cant, J. S., CHisHotM, I. A., BRoNTE-STEWaRT, J.,
WILson, J. Hydroxocobalamin in the treatment of Leber’s hereditary
optic atrophy. Lancet 1(7548): 896-897, April 27, 1968.

(8) Foutps, W. S., CHISHOLM, I. A., BRONTE-STEWaRT, J., WILSON, T. M.
Vitamin B,, absorption in tobacco amblyopia. British Journal of
Ophthalmology 538 (6) : 393-397, June 1969.

(9) Fourps, W. S., CHISHOLM, I. A., BRONTE-STEWART, J., WILSON, T. M.
The optic neuropathy of pernicious anemia. Archives of Ophthalmol-
ogy 82(4): 427-432, October 1969.

(10) FREEMAN, A. G., HEATON, J. M. The aetiology of retrobulbar neuritis in
Addisonian pernicious anaemia. Lancet 1(7183): 908-911, April 29,
1961.

436
(11) Heaton, J. M., McCormick, A. J. A., FREEMAN, A. G. Tobacco amblyo-
pia: A clinical manifestation of vitamin-B,, deficiency. Lancet
2(7041): 286-290, August 9, 1958.

(12) Knox, D. L. Neuro-ophthalmology. Archives of Ophthalmology 83(1):
103-127, January 1970.

(18) Linpstranp, K., WILSON, J.. MATTHEWS, D. M. Chromatography and
microbiological assay of vitamin B,, in smokers. British Medical
Journal 2 (5520): 988-990, October 22, 1966.

(14) LINNELL, J. C., SMitH, A. D. M., Smitu, C. L., WILSON, J.. MATTHEWS,
D, M. Effects of smoking on metabolism and excretion of vitamin B,,.
British Medical Journal 2(5599) : 215-216, April 27, 1968.

(15) ScHEpPeENs, C. L. Is tobacco amblyopia a deficiency disease- Transactions
of the Ophthalmological Society of the United Kingdom 66: 309-331,
1946.

(16) SCHIEVELBEIN, H., WERLE, E., SCHULZ, E. K., BAUMEISTER, R. The influ-
ence of tobacco smoke and nicotine on thiocyanate metabolism.
Naunyn-Schmiedebergs Archiv fiir Pharmakologie und Experimentelle
Pathologie 262(38) : 358-365, February 5, 1969.

(17) Sirvette, H., Haac, H. B., Larson, P. S. Tobacco amblyopia. The evolu-
tion and natural history of a “tobaccogenic” disease. American Journal
of Ophthalmology 50(1): 71-100, January 1960.

(18) SmitrH, A. D. M. Retrobulbar neuritis in Addisonian pernicious anae-
mia. (Letter) Lancet 1(7184): 1001-1002, May 6, 1961.

(19) Smiru, A. D. M., Duckett, 8. Cyanide, vitamine B,,, experimental
demyelination and tobacco amblyopia. British Journal of Experimen-
tal Pathology 46(6) : 615-622, December 1965.

(20) Traquair, H. M. Toxic amblyopia, including retrobulbar neuritis. Trans-
actions of the Ophthalmological Society of the United Kingdom 50:
851-385, 1930.

(21) Victor, M. Tobacco-alcohol amblyopia. A critique of current concepts of
this disorder, with special reference to the role of nutritional deficiency
in its causation. Archives of Ophthalmology 70(3) : 318-318, Septem-
ber 1963.

(22) Victor, M. Tobacco amblyopia, cyanide poisoning and vitamin B,, de-
ficiency. A critique of current concepts. Chapter 3. IN: Smith, J. L.
(Editor) Neuro-Ophthlamology. Symposium of the University of
Miami and the Bascom Palmer Eye Institute. Hallandale, Florida,
Huffman Publishing Co., 1970. pp. 33-48.

(23) Wa.sH, F. B., Hoyt, W. F. (Editors) Neurotoxic substances affecting
the visual and ocular motor systems, Chapter 15: IN: Clinical Neuro-
Ophthalmology, Volume 3, 3rd Edition. Baltimore, The Williams &
Wilkins Company, 1969. pp. 26138-2616.

(24) WATSON-WILLIAMS, E. J., BortromMLey, A. C., AINLEY, R. G., PHILLIPS,
C. I. Absorption of vitamin B,, in tobacco amblyopia. British Journal
of Ophthalmology 53(8) : 549-552, August 1969.

(25) Wiison, J. Leber’s hereditary optic atrophy: A possible defect of cya-
nide metabolism. Clinical Science 29(3): 505-515, December 1965.

(26) Witson, J., MaTrHEews, D. M. Metabolic inter-relationships between

cyanide, thiocyanate and vitamin B,, in smokers and nonsmokers.
Clinical Science 31(1): 1-7, January 1966.

437
(27) Woxes, F., Picarp, C. W. The role of vitamin B,, in human nutrition.
Clinical Nutrition 3(5) : 383-390, September—October 1955.

(28) WyYNorr, E. L., HOFFMANN, D. Certain constituents of tobacco products.
Chapter 8. K. Vapor phase of tobacco smoke. IN: Wynder, E. L.,

Hoffmann, I). (Editors). Tobacco and Tobacco Smoke. Studies in Ex-
perimental Carcinogenesis. New York, Academic Press, 1967. pp.
451-453.

438