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The Effect of Tobacco on the Normal Angioscotoma*
T H E E F F E C T O F TOBACCO ON T H E NORMAL ANGIOSCOTOMA* S. P.
MATHUR, + M.S.,
AND K.
N.
MATHUR,
M.S.
New Delhi, India Angioscotomas were first described1 in 1926. They signify "defects of the visual field resulting from the blindspot of Mariotte and related in form and pattern to distribution of the retinal vessel tree." They were first thought to be shadows of retinal vessels but this view was modified because: The degree of widening of an angioscotoma is often so great and rapid that a retinal vessel would burst were it to dilate with cor responding speed; the widened shadow may be six to 10 times larger than normal; when pressure is made upon the globe the retinal vessels narrow, while the angioscotoma widens; and in conditions known to cause vasodilation, the degree of widening of the angioscotoma is greater than the widening of corresponding vessels seen ophthalmoscopically. The fact that an angioscotoma corresponds in form to the retinal vessel tree makes it seem likely that those structures and func tions most intimately related to the vessel should receive first consideration. After ex tensive research these shadows have been in terpreted as arising through modification of the retinal perivascular spaces2 and in the retinal synaptic junctions. Since the time of its introduction, angioscotometry has been used for clinical in vestigation in various diseases. It has also been used for studying the action of various therapeutic drugs and the effect of high altitudes on the visual field3 during World War II. It was only recently that Fink 4 showed an interest in the effect of smoking on the normal angioscotoma. As a result of his study he came to the following conclusions: 1. The smoking of a certain popular brand * From the Department of Ophthalmolog}', S.N. Medical College. t Research Fellow, Indian Council of Medical Research.
of cigarette (containing about two-percent nicotine) produces a widening of the an gioscotoma. 2. Cigarettes containing one tenth the nic otine produce an alteration in the angiosco toma of lesser degree than that observed by the popular brand. 3. Inhalation of an unlighted cigarette produced no alteration of the angioscotoma. Fink therefore attributed all these changes to the stimulation of the sympathetic ner vous system by the nicotine in the tobacco, the degree of widening of angioscotoma being in direct proportion to the amount of nicotine in tobacco. Since the use of tobacco in various ways is so widespread over all the world and the habit so common, it was thought that s the knowledge of its effect on the eye might be of clinical interest and might throw some light on the early diagnosis of tobacco amblyopia. According to the graphic representa tions of Fink,4 the degree of widening of the angioscotoma could also suggest the best form, the more harmless ways, and the safe limits of consuming tobacco. In the present studies, the nicotine con tent of the tobacco in various commonly used cigarettes, and also in the main stream of its smoke, was estimated. After determin ing the amount of nicotine passing over with the smoke of a cigarette, changes in the an gioscotoma were plotted. Later, varying quantities of tobacco containing different amounts of nicotine were given and varia tions on the angioscotoma with each were noted. MATERIAL
The campimeter used for plotting the angioscotoma was made according to the details given by Evans. 5 Monocular fixa tion was employed. The patient was per mitted to rest for about 10 minutes before the actual mapping was begun; during this
923
924
S. P. MATHUR AND K. N. MATHUR
time the patient was told various details of the procedure. The disappearance of the test object was indicated by tapping. The diame ter of the test object used varied from 0.4 to 0.6 mm., a 0.5 mm. test object being used in most cases. The chart was illuminated by about 15 foot-candles. The blindspot was first plotted, taking the object from the visible to the invisible area at right angles to the border of the defect. The main two superior and two inferior scotomas were plotted. The method was prac ticed many times before actually starting the work so that a satisfactory plotting could be made in a short time. PROCEDURE AND OBSERVATIONS
A total number of 72 eyes were examined. All of the subjects were males, whose ages varied between 20 to 40 years ; most of them were between 25 to 30 years. They were divided in various groups: Ten normal persons were examined, three of whom were smokers (10 to 20 cigarettes per day), the rest were nonsmokers. None of them smoked for at least four hours be fore they were studied. Their angioscotomas were plotted, after which they were given a market-brand cigarette containing about twopercent nicotine in tobacco, which was smoked until two cm. were left. The angioscotoma was again plotted just after smoking and then every 15 minutes (fig. 1). It was noted that the angioscotoma widened, together with the blindspot; the maximum widening took place just after smoking, vary ing from three to eight degrees, after which
//
%
\ / / \ %^ y s
'5/iqoi
\
it decreased to return to normal in 45 to 60 minutes. Seven subjects were given an equal weight of cigar tobacco, containing about two-per cent nicotine. After smoking, a similar change in the angioscotoma was noted which was neither quantitatively nor qualitatively different from that produced by the cigarette. It returned to normal in 45 to 60 minutes. Next, an equal amount of pipe tobacco containing three-percent nicotine was given to five persons. The changes in angiosco toma after smoking were the same and lasted for an equal time as those produced by one market-brand cigarette. Five subjects were given an equal weight of "bidi" tobacco containing four-percent nicotine. The angioscotometric changes were in no way different from those produced by one cigarette. Ten subjects were given a "du-Maurier" filter-tipped cigarette, the smoke of which contains only 33 percent of the nicotine pres ent in the smoke of a nonfilter-tipped ciga rette, although the tobacco of both contain about two-percent nicotine. The widening of angioscotoma was almost the same in extent and intensity as with a normal cigarette and took the same time to return to normal. Five subjects received half a cigarette, and changes in angioscotoma were plotted. The same subjects were given two cigarettes, one after the other. Changes in the angioscotoma in both instances were similar in intensity and duration as those produced by one cigarette. These observations show that the changes in the angioscotoma do not in any way de-
/ \
°"S/H» * " * "
V
\ / \
■K
A
t
mm
\ / \ mt
—
•%, *X
Jl ]f
t«*y
arS
li<>o »>.■■—
Fig. 1 (Mathur and Mathur). Effect of smoking one cigarette on a normal angioscotoma. The angioscotoma was plotted every IS minutes.
TOBACCO AND NORMAL ANGIOSCOTOMA pend on the amount of nicotine in tobacco or its smoke. To find if tobacco alkaloids are at all re sponsible for these angioscotometric changes, cigarettes were rolled with tobacco from which the alkaloids had been removed. To bacco was treated with a mixture of ether and petroleum ether for four days, with two to three changes every day. It was then washed with water several times and tested for the alkaloids by Mayer's reagent. When this did not give a precipitate, the tobacco was dried and mixed with a thick sugar solu tion, which helped in binding, and rolled into cigarettes, the weight of tobacco being equal to that of a market-brand cigarette. Ten subjects were given such an alkaloidfree cigarette. The changes in the angiosco toma were similar to those with the marketbrand cigarette containing nicotine. It was evident therefore, that alkaloids were not responsible for the changes in the angiosco toma. During these investigations, a few subjects could not inhale the smoke and simply puffed it out of the mouth. In these subjects, the angioscotoma remained unchanged even after 45 minutes, showing that it was necessary for the smoke to be inhaled before any change in the angioscotoma was produced. In the next group of 10 cases, the factor of smoke was eliminated by testing with chewing tobacco which was equivalent in terms of nicotine contained to the smoke of one cigarette. All these subjects were habituated to chewing tobacco but of a much lesser quantity at a time. No change in the angioscotoma could be detected, even after one hour. This further confirmed that the smoke as such was responsible for the changes in the angioscotoma and not the nicotine, which still went into the system during chewing. Further, in 10 subjects, after plotting the normal angioscotoma, the throat was irritated with a swab stick. Surprisingly, in all of them the angioscotoma widened, of course lesser in amount and for a shorter duration.
925
This suggests that the irritation of throat, probably by the smoke during smoking, is responsible for the angioscotometric changes and not the alkaloids contained in tobacco or its smoke. CONCLUSIONS
The dilation of the angioscotoma due to tobacco smoking does not depend on habitual smoking nor even on the brand of tobacco, its nicotine content, or the nicotine in its smoke. These points have been made evident by the fact that the intensity and duration of dilation of the angioscotoma was the same when an equal weight of market-brand of cigarette, cigar, pipe, and bidi tobacco was given, containing two percent, two percent, three percent, and four percent nicotine, re spectively. Further these changes were not different when a filter-tipped "du-Maurier" cigarette was given, the smoke of which con tains only 33 percent of the nicotine present in the smoke of an ordinary market cigarette. These findings were further confirmed by the subjects who first smoked half a cigarette and later two cigarettes in succession. The changes in the angioscotoma in both tests differed in no way. These observations are in complete dis agreement from those of Fink 4 who thinks that the changes in angioscotoma are directly proportional to the amount of nicotine in tobacco. In those subjects who were given alkaloidfree cigarettes, the angioscotometric changes were similar as after an ordinary cigarette. This seemed conclusive proof that the alka loids of tobacco are not responsible for these changes. The subjects who did not inhale the smoke did not show changes in angioscotoma, al though nicotine was detectible in the saliva, which gave a white precipitate with Mayer's reagent. If nicotine were responsible for the dilatation of the angioscotoma, that absorbed by the mucous membrane of mouth, which is said to possess the power of absorption, could have effected the change.
S. P. MATHUR AND K. N. MATHUR
926
The findings in subjects who were given tobacco to chew have been most interesting. No changes in the angioscotoma could be noted in spite of the fact that the tobacco contained an amount of nicotine equal to the smoke of one cigarette. This observation is in complete agreement with our view that tobacco alkaloids are not responsible for changes in the angioscotoma. The factor in the smoke that produced all these changes in the angioscotoma may be due to irritation of the throat. It is common to find habitual smokers with a badly inflamed throat, the so-called, "chronic throat." This is prob ably due to deposition of easily condensible volatile products of tobacco smoke which ir ritate the mucous membrane of the throat. It was with this idea that 10 subjects had their throat irritated with a bland swab. The an gioscotoma widened, although less in extent and duration than after smoking a ciga rette because irritation with the swab was for a shorter period.
brand of tobacco, its nicotine content, or the nicotine content of smoke. T h e alkaloids of tobacco are not responsible for the widening of the angioscotoma because similar changes could be produced by smoking an alkaloidfree cigarette. After chewing tobacco, no changes in angioscotoma could be detected. T h e changes in the angioscotoma are prob ably due to the irritation of the mucous mem branes of the throat by various volatile prod ucts of smoke. T h a t the throat is the site of the changes was shown by those subjects who did not inhale and who did not show changes in the angioscotoma. Further, similar changes in the angioscotoma were produced by me chanical irritation of the throat. It is fair to conclude that these changes in the angioscotoma are of little value in the early clinical diagnosis of cases of tobacco amblyopia, or in finding the best form, the harmless way, and the safe limit of consum ing tobacco. Irivin Hospital.
SUMMARY
We wish to express our gratitude to the Indian Council of Medical Research for the financial assistance without which the work would have been impossible.
T h e effect of tobacco smoking on the nor mal angioscotoma does not depend on the
REFERENCES
1. Evans, J. N.: A preliminary report of the retinal vessel scotoma. Am. J. Ophth., 9:118-119 (Feb.) 1926. 2. : Angioscotometry. Am. J. Ophth., 9 :489-S06 (July) 1926. 3. Evans, J. N., and McFarland, R. A.: Effects of oxygen deprivation on visual fields. Am. J. Ophth., 21:968-980 (Sept.) 1938. 4. Fink, A. I.: Clinical study of effect of tobacco on the normal angioscotoma. Read before the Brook lyn Ophthalmological Society, April 19, 194S. 5. Evans, J. N.: An Introduction to Clinical Scotometry. New Haven, Conn., Yale Univ. Press, 1938, p. 175.
MATHUR, + M.S.,
AND K.
N.
MATHUR,
M.S.
New Delhi, India Angioscotomas were first described1 in 1926. They signify "defects of the visual field resulting from the blindspot of Mariotte and related in form and pattern to distribution of the retinal vessel tree." They were first thought to be shadows of retinal vessels but this view was modified because: The degree of widening of an angioscotoma is often so great and rapid that a retinal vessel would burst were it to dilate with cor responding speed; the widened shadow may be six to 10 times larger than normal; when pressure is made upon the globe the retinal vessels narrow, while the angioscotoma widens; and in conditions known to cause vasodilation, the degree of widening of the angioscotoma is greater than the widening of corresponding vessels seen ophthalmoscopically. The fact that an angioscotoma corresponds in form to the retinal vessel tree makes it seem likely that those structures and func tions most intimately related to the vessel should receive first consideration. After ex tensive research these shadows have been in terpreted as arising through modification of the retinal perivascular spaces2 and in the retinal synaptic junctions. Since the time of its introduction, angioscotometry has been used for clinical in vestigation in various diseases. It has also been used for studying the action of various therapeutic drugs and the effect of high altitudes on the visual field3 during World War II. It was only recently that Fink 4 showed an interest in the effect of smoking on the normal angioscotoma. As a result of his study he came to the following conclusions: 1. The smoking of a certain popular brand * From the Department of Ophthalmolog}', S.N. Medical College. t Research Fellow, Indian Council of Medical Research.
of cigarette (containing about two-percent nicotine) produces a widening of the an gioscotoma. 2. Cigarettes containing one tenth the nic otine produce an alteration in the angiosco toma of lesser degree than that observed by the popular brand. 3. Inhalation of an unlighted cigarette produced no alteration of the angioscotoma. Fink therefore attributed all these changes to the stimulation of the sympathetic ner vous system by the nicotine in the tobacco, the degree of widening of angioscotoma being in direct proportion to the amount of nicotine in tobacco. Since the use of tobacco in various ways is so widespread over all the world and the habit so common, it was thought that s the knowledge of its effect on the eye might be of clinical interest and might throw some light on the early diagnosis of tobacco amblyopia. According to the graphic representa tions of Fink,4 the degree of widening of the angioscotoma could also suggest the best form, the more harmless ways, and the safe limits of consuming tobacco. In the present studies, the nicotine con tent of the tobacco in various commonly used cigarettes, and also in the main stream of its smoke, was estimated. After determin ing the amount of nicotine passing over with the smoke of a cigarette, changes in the an gioscotoma were plotted. Later, varying quantities of tobacco containing different amounts of nicotine were given and varia tions on the angioscotoma with each were noted. MATERIAL
The campimeter used for plotting the angioscotoma was made according to the details given by Evans. 5 Monocular fixa tion was employed. The patient was per mitted to rest for about 10 minutes before the actual mapping was begun; during this
923
924
S. P. MATHUR AND K. N. MATHUR
time the patient was told various details of the procedure. The disappearance of the test object was indicated by tapping. The diame ter of the test object used varied from 0.4 to 0.6 mm., a 0.5 mm. test object being used in most cases. The chart was illuminated by about 15 foot-candles. The blindspot was first plotted, taking the object from the visible to the invisible area at right angles to the border of the defect. The main two superior and two inferior scotomas were plotted. The method was prac ticed many times before actually starting the work so that a satisfactory plotting could be made in a short time. PROCEDURE AND OBSERVATIONS
A total number of 72 eyes were examined. All of the subjects were males, whose ages varied between 20 to 40 years ; most of them were between 25 to 30 years. They were divided in various groups: Ten normal persons were examined, three of whom were smokers (10 to 20 cigarettes per day), the rest were nonsmokers. None of them smoked for at least four hours be fore they were studied. Their angioscotomas were plotted, after which they were given a market-brand cigarette containing about twopercent nicotine in tobacco, which was smoked until two cm. were left. The angioscotoma was again plotted just after smoking and then every 15 minutes (fig. 1). It was noted that the angioscotoma widened, together with the blindspot; the maximum widening took place just after smoking, vary ing from three to eight degrees, after which
//
%
\ / / \ %^ y s
'5/iqoi
\
it decreased to return to normal in 45 to 60 minutes. Seven subjects were given an equal weight of cigar tobacco, containing about two-per cent nicotine. After smoking, a similar change in the angioscotoma was noted which was neither quantitatively nor qualitatively different from that produced by the cigarette. It returned to normal in 45 to 60 minutes. Next, an equal amount of pipe tobacco containing three-percent nicotine was given to five persons. The changes in angiosco toma after smoking were the same and lasted for an equal time as those produced by one market-brand cigarette. Five subjects were given an equal weight of "bidi" tobacco containing four-percent nicotine. The angioscotometric changes were in no way different from those produced by one cigarette. Ten subjects were given a "du-Maurier" filter-tipped cigarette, the smoke of which contains only 33 percent of the nicotine pres ent in the smoke of a nonfilter-tipped ciga rette, although the tobacco of both contain about two-percent nicotine. The widening of angioscotoma was almost the same in extent and intensity as with a normal cigarette and took the same time to return to normal. Five subjects received half a cigarette, and changes in angioscotoma were plotted. The same subjects were given two cigarettes, one after the other. Changes in the angioscotoma in both instances were similar in intensity and duration as those produced by one cigarette. These observations show that the changes in the angioscotoma do not in any way de-
/ \
°"S/H» * " * "
V
\ / \
■K
A
t
mm
\ / \ mt
—
•%, *X
Jl ]f
t«*y
arS
li<>o »>.■■—
Fig. 1 (Mathur and Mathur). Effect of smoking one cigarette on a normal angioscotoma. The angioscotoma was plotted every IS minutes.
TOBACCO AND NORMAL ANGIOSCOTOMA pend on the amount of nicotine in tobacco or its smoke. To find if tobacco alkaloids are at all re sponsible for these angioscotometric changes, cigarettes were rolled with tobacco from which the alkaloids had been removed. To bacco was treated with a mixture of ether and petroleum ether for four days, with two to three changes every day. It was then washed with water several times and tested for the alkaloids by Mayer's reagent. When this did not give a precipitate, the tobacco was dried and mixed with a thick sugar solu tion, which helped in binding, and rolled into cigarettes, the weight of tobacco being equal to that of a market-brand cigarette. Ten subjects were given such an alkaloidfree cigarette. The changes in the angiosco toma were similar to those with the marketbrand cigarette containing nicotine. It was evident therefore, that alkaloids were not responsible for the changes in the angiosco toma. During these investigations, a few subjects could not inhale the smoke and simply puffed it out of the mouth. In these subjects, the angioscotoma remained unchanged even after 45 minutes, showing that it was necessary for the smoke to be inhaled before any change in the angioscotoma was produced. In the next group of 10 cases, the factor of smoke was eliminated by testing with chewing tobacco which was equivalent in terms of nicotine contained to the smoke of one cigarette. All these subjects were habituated to chewing tobacco but of a much lesser quantity at a time. No change in the angioscotoma could be detected, even after one hour. This further confirmed that the smoke as such was responsible for the changes in the angioscotoma and not the nicotine, which still went into the system during chewing. Further, in 10 subjects, after plotting the normal angioscotoma, the throat was irritated with a swab stick. Surprisingly, in all of them the angioscotoma widened, of course lesser in amount and for a shorter duration.
925
This suggests that the irritation of throat, probably by the smoke during smoking, is responsible for the angioscotometric changes and not the alkaloids contained in tobacco or its smoke. CONCLUSIONS
The dilation of the angioscotoma due to tobacco smoking does not depend on habitual smoking nor even on the brand of tobacco, its nicotine content, or the nicotine in its smoke. These points have been made evident by the fact that the intensity and duration of dilation of the angioscotoma was the same when an equal weight of market-brand of cigarette, cigar, pipe, and bidi tobacco was given, containing two percent, two percent, three percent, and four percent nicotine, re spectively. Further these changes were not different when a filter-tipped "du-Maurier" cigarette was given, the smoke of which con tains only 33 percent of the nicotine present in the smoke of an ordinary market cigarette. These findings were further confirmed by the subjects who first smoked half a cigarette and later two cigarettes in succession. The changes in the angioscotoma in both tests differed in no way. These observations are in complete dis agreement from those of Fink 4 who thinks that the changes in angioscotoma are directly proportional to the amount of nicotine in tobacco. In those subjects who were given alkaloidfree cigarettes, the angioscotometric changes were similar as after an ordinary cigarette. This seemed conclusive proof that the alka loids of tobacco are not responsible for these changes. The subjects who did not inhale the smoke did not show changes in angioscotoma, al though nicotine was detectible in the saliva, which gave a white precipitate with Mayer's reagent. If nicotine were responsible for the dilatation of the angioscotoma, that absorbed by the mucous membrane of mouth, which is said to possess the power of absorption, could have effected the change.
S. P. MATHUR AND K. N. MATHUR
926
The findings in subjects who were given tobacco to chew have been most interesting. No changes in the angioscotoma could be noted in spite of the fact that the tobacco contained an amount of nicotine equal to the smoke of one cigarette. This observation is in complete agreement with our view that tobacco alkaloids are not responsible for changes in the angioscotoma. The factor in the smoke that produced all these changes in the angioscotoma may be due to irritation of the throat. It is common to find habitual smokers with a badly inflamed throat, the so-called, "chronic throat." This is prob ably due to deposition of easily condensible volatile products of tobacco smoke which ir ritate the mucous membrane of the throat. It was with this idea that 10 subjects had their throat irritated with a bland swab. The an gioscotoma widened, although less in extent and duration than after smoking a ciga rette because irritation with the swab was for a shorter period.
brand of tobacco, its nicotine content, or the nicotine content of smoke. T h e alkaloids of tobacco are not responsible for the widening of the angioscotoma because similar changes could be produced by smoking an alkaloidfree cigarette. After chewing tobacco, no changes in angioscotoma could be detected. T h e changes in the angioscotoma are prob ably due to the irritation of the mucous mem branes of the throat by various volatile prod ucts of smoke. T h a t the throat is the site of the changes was shown by those subjects who did not inhale and who did not show changes in the angioscotoma. Further, similar changes in the angioscotoma were produced by me chanical irritation of the throat. It is fair to conclude that these changes in the angioscotoma are of little value in the early clinical diagnosis of cases of tobacco amblyopia, or in finding the best form, the harmless way, and the safe limit of consum ing tobacco. Irivin Hospital.
SUMMARY
We wish to express our gratitude to the Indian Council of Medical Research for the financial assistance without which the work would have been impossible.
T h e effect of tobacco smoking on the nor mal angioscotoma does not depend on the
REFERENCES
1. Evans, J. N.: A preliminary report of the retinal vessel scotoma. Am. J. Ophth., 9:118-119 (Feb.) 1926. 2. : Angioscotometry. Am. J. Ophth., 9 :489-S06 (July) 1926. 3. Evans, J. N., and McFarland, R. A.: Effects of oxygen deprivation on visual fields. Am. J. Ophth., 21:968-980 (Sept.) 1938. 4. Fink, A. I.: Clinical study of effect of tobacco on the normal angioscotoma. Read before the Brook lyn Ophthalmological Society, April 19, 194S. 5. Evans, J. N.: An Introduction to Clinical Scotometry. New Haven, Conn., Yale Univ. Press, 1938, p. 175.