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Cigarette Smoking |
[Determination
of Extent of Exposure][Acute
Effects of Involuntary Smoking][Chronic
Effects of Involuntary Smoking]
The involuntary exposure to another person's cigarette smoke is termed "passive smoking," and represents a particularly insidious form of tobacco smoke exposure. Unfortunately, involuntary smoke exposure is extraordinarily common as many non-smoking people know, are forced to work with, or have chosen to live with a smoker (for better or for worse). These innocent non-smoking people are constantly exposed to smoke extruding from the tips of burning cigarettes. The monumental extent of this involuntary exposure becomes evident when compared to the incidence of voluntary smoking. While 30% of the adult population in the United States smokes (34), the number of people (adults and children) who have a significant exposure to this smoke is much larger. When sensitive biochemical markers for cigarette smoke are used (such as the degradation product of nicotine excreted in the urine- cotinine), the vast majority of non-smoking adults are shown to have at least some exposure (35). Additionally, approximately 70% of children in the United States live in homes in which at least one adult smokes. The potential for serious health risk to developing lungs can easily be appreciated. Unfortunately, however, it has been rather difficult to definitively ascertain the extent of the health hazard produced by this exposure, even though it has been a topic of many report. Since the original 1964 report by the Surgeon General of the United States, there have been over 20,000 articles written about the effect of cigarette smoke upon health. Unfortunately, fewer than 1% of these reports have dealt with the even more common risk of involuntary smoking. Since there are so many people exposed to cigarette smoke, even a very small excess health risk could produce large numbers of innocent victims. This chapter will attempt to review some of the literature dealing with involuntary cigarette smoke exposure, and determine the excess risk, if any, to health. Determination of the Extent of Exposure Implicit in any discussion on the health risks of cigarette smoking is that the degree of this involuntary exposure is significant. In other words, just casual, infrequent exposure to cigarette smoking would be unlikely to have important detrimental health consequences. However, constant exposure in a closed environment might prove a different story. Understanding the risks of involuntary cigarette smoking requires investigation of the chemical constituents of cigarette smoke. When discussing cigarette smoke, it is important to remember that there are really two types of smoke produced by the burning cigarette; mainstream and sidestream. Mainstream smoke is that smoke inhaled by the smoker, and generally filtered by the tobacco it is pulled through and by a filter on the mouth-end of the cigarette. This smoke would naturally be expected to be different from the sidestream stmoke, that smoke that is produced by the end of the cigarette and which is delivered to the environment without benefit of any filtering. The different temperatures of combustion, filtration, and amont of tobacco consumed all lead to the different concentration of mainstream and sidestream smoke (1,2,3). For instance, toxic gas phase chemicals are in higher concentrations in sidestream smoke than in mainstream (3), and nearly 85% of the smoke in a room is from the sidestream smoke. Sidestream smoke, however, is considerably diluted by the volume of air in the room into which it is inhaled. Therefore, the potentially toxic effects of sidestream smoke are dramatically affected by the type and number of cigarettes burned, the rate at which they are burned, the volume of air in the room in which they are burned, and the room's ventilation rates, among others. Thus, no simgle measurement is able to accurately characterize the risk of sidestream smoking or the degree of exposure of occupants such a room to any given chemical. Even with all these difficulties considered, there have been a few studies attempting to quantitate the risk of involuntary smoking. Only a few chemical constituents of cigarette smoke have been found to be significantly elevated in these studies. These include nitrogen oxide, carbon monoxide, nicotine, and particulate matter. Some studies have also found carbon dioxide to be significantly elevated. Nitrogen oxide is rapidly converted to nitrogen dioxide in room air, and probably is not too different from outside air, especially in regions where there is a significant amount of car exhaust. Exposure to nicotine is elevated, but only marginally so. It is estimated that nicotine exposure is only 0.04 cigarette equilivants/hour (2). The concentration of particulate matter indoors increases with the number of cigarette smokers, with the excess risk determined by the outdoor level, since particulates can also be greatly increased in urban environemnts. Carbon monoxide can pose an especially dangerous risk, however, especially when compared to these other compounds. This is because a small elevation in carbon monoxide level will have its effect greatly magnified by the strong binding of carbon monoxide to hemoglobin in preference to oxygen. Carbon monoxide has an affinity for hemoglobin that is 210 times as great as oxygen, so a small elevation in its concentration can produce marked reduction in hemoglobin oxygen concentration. The potential importance of this relationship can be appreciated when it is realized that sidestream smoke from a burning cigarette can have carbon monoxide concentrations well over 200 parts per million (ppm) which is well into the dangerous range (the national air quality standard for carbon monoxide is 9 ppm). While this high concentration of carbon monoxide is quickly diluted by the volume of room air, it is still significant enough to raise the blood carbon monoxide or carboxyhemoglobin considerably. The Acute Effects of Involuntary Smoking The effects of involuntary smoking can be grossly divided into whether the effects occur rapidly and then dissipate (the acute effects), or whether the effects take much time to develop but are more permanent (the chronic effects). Generally, there is much more data to establish the acute effects of cigarette smoking, partly because they are much easier to establish and do not require the time and expense of studies trying to establish chronic effects. The acute effects of smoking can be studied either in normal subjects, or in those with significant cardiopulmonary disease. Eye irritation is the single most common complaint offered by normal people involuntarily exposed to cigarette smoke. In one study, 69% of subjects had this complaint (4). Other complaints offered by about a third of normal study candidates were headache, nasal irritation, and cough (5,6). Several environmental factors seem to be important in the severity of the irritaiton symptoms including the amount of smoking, the size of the area in which the smoking is located, and the humidity and temperature of the ambient air. It is unknown whether people develop tolerance to these irritation effects, and the precise constituents of cigarette smoke responsible are likely unknown. Pulmonary function tests have been performed in normal patients exposed to cigarette smoke to determine whether any significant changes occur. When non-smoking adults are exposed to cigarette smoke, there was a significant elevation of blood carboxyhemoglobin from baseline values. Additionally, the pulmonary function tests showed a reduction of expired air flow at lower lung volumes at rest in men and with exercise in women. However, the magnitude of this change was quite small; only 7 percent reduction in males and 14 percent reduction in females. Thus, there does seem to be a small effect on the pulmonary function of normal people exposed to sidestream smoke, although the change is minimal and probably of no clinical importance (7). The situation may be quite different in people who already have underlying cardiopulmonary disease, however. Small changes in their carboxyhemoglobin level or reduction in their already deteriorated pulmonary function may have significant effects upon their general health. For example, Aronow (8) studied patients with stable angina (heart pain caused by a reduction of blood flow and which may develop into a heart attack). These patients were then exposed for two hours tocigarette smoke under conditions of either good or poor room ventilation. There was a significant elevation of the carboxyhemoglobin concentration in either instance, rising from 1.22% to 1.77% with good ventilation, and from 1.30% to 2.28% with poor room ventilation. The patients were then exercised to determine whether exercise time until the development of angina differed between the two groups. There was a 22% reduction in exercise time to angina under well ventilated conditions, but a highly significant 38% reduction in exercise time to angina under poorly ventilated conditions. Thus study indicates that it may be dangerous for patients with significant heart disease to even be in the same room as people who smoke since they may develop anginal episodes much more easily and under much less exertion than would otherwise be the case. Patients with bronchial asthma may also be more susceptible to the damaging effects from involuntary smoking. Dahms (9) studied ten patients with asthma and ten normal subjects who were exposed to involuntary smoking conditions. After exposure, the blood carboxyhemoglobin was again significantly elevated in the two groups comensurate with the degree of their cigarette smoke exposure, although the carboxyhemoglobin levels were not different between the asthmatic group and the normal control group. Patients with bronchial asthma suffered a significant reduction in some of their pulmonary function tests (FVC, FEV1, MMEFR) when compared to normal subjects who suffered no abnormalities. The asthmatic subjects began to suffer these abnormalities only 15 minutes after commencement of exposure, and worsened over the hour time period of the study to approximately 75% of their pre-exposure values. This study has been rightly criticized since it was not under "double blind" conditions; the asthmatic subjects knew that they were going to be exposed to possibly irritating cigarette smoke and might then have become very anxious. Since it is known that when asthmatic subjects become upset or anxious, they can have significant deterioriation in their lung function, their reduction in some pulmonary function tests after smoke exposure could be due only to anxiety. To study this possibility, Shepherd and coworkers (10) designed a similar study in which asthmatic patients had a two-hour exposure to cigarette smoke in a closed environemtn with a significant elevation of their carbon monoxide levels. However, there was another group of asthmatic patients who were placed into a ximilar box but who were not subjected to cigarette smoke inhalation. Data from this investigation revealed no significant difference in the pulmonary function after smoke exposure between the asthmatic patients exposed to cigarette smoke and those who were not. Thus, it is possible that the reductions in pulmonary function seen in the Dahms study were merely due to patient anxiety and not to a real effect from the cigarette smoke. Certainly, more studies are needed to resolve this issue, but the effect of cigarette smoke on pulmonary function even in asthmatic patients is not large if indeed it is present at all. Chronic Effects of Involuntary Smoking The chronic effects of involuntary cigarette smoking may be much more important to the health of society than the acute effects. While there is only minimal if any reduction of pulmonary function in asthmatics and normal persons acutely exposed to cigarette smoke, the accumulative effect of years of similar exposure may turn out to be significant. When the vast number of children and adults living with cigarette smokers is considered, the potential enormity of the problem can be understood. Childhood exposure-Children seem to be especially vulnerable
to the detrimental effects of cigarette smoking during their first year
of life. For instance, an Israeli study in 1965 and 1968 examined
10,672 birth and observed that infants born to mothers who said they smoked
had a 27.5% greater hospital admission rate for lung infections than did
children of non-smoking mothers (11). Additionally, there was a dose
response relationship established such that the more the mothers smoked,
the more their children required hospital admissions for lung diseases.
A similar study (12) was also conducted by British investigators between
1963 and 1965 on live births in London. As with the Israeli infants,
there was a greater hospital admission rate for bronchitis and pneumonia
during the first year of life when the mothers were smokers; this study
also established a dose-response relationship. Interestingly, however,
the increased incidence in hospital admission rate seems to be primarily
in infants younger than 1 year of age, and does not occur in older children.
A study published in 1981 from New Zealand (13) examined 1,265 children
from birth to three years of age and found similar results. There
was an increase in both bronchitis and pneumonia in children during their
first two years of life. This study was somewhat more thorough than
the previously cited studies in that this increased incidence was independent
of maternal age, family size, and socioeconmic status. The amount
of lung disease experienced by these children declined with increasing
child age, and with decreasing maternal smoking.
Older Children-Older children (5 to 20 years old) can also be adversely affected by parental smoking. Several studies have demonstrated a greater incidence of many illnesses in these children including acute respiratory diseases (14), chronic cough with phlegm and/or persistent wheeze (15-18). A consistent finding in all these studies in an increase in symptoms with increased smoke exposure from the family. There has also been some support for the notion that chronic childhood wheezing may be associated with parental smoking. While many studies have significant study design flaws, there are three studies that are worth examining. Lebowitz and Burrows (19) studied 463 children below 15 years old from both smoking and non-smoking households to determine the incidence of wheezing. The study found that there was a trend toward more wheezing days in households with smoking adults, but the rates were not significant when examined statistically. A preliminary report from one of another large study (20), the smoking habits of 8000 children aged 6 to 11 were examined from 6 communities. There was a persistent relationship demonstrated between the smoking behavior of the parents and the risk of childhood wheezing. This risk increased with greater maternal smoking also suggesting a direct relationship. Finally, Dodge (21) studied 3rd and 4th graders and demonstrated simnilar resulrs; wheezing symptoms were greater in children of parents who smoked. In summary, multiple studies suggest that there is a significant increase in the incidence of chronic respiratory complaints in older children (aged 5 to 20 years) that was linked to parental smoking behavior. However, the data is not very complete, and the literature is replete with poor tests using poor study designs. For example, there is little data concerning the level of involuntary smoking exposure that is necessary to produce symptoms in the non-smoking children, and whether youthful exposure to cigarette smoke will affect future lung growth and development. Nonetheless, I believe that there is a real cause for alarm in that while the risks may be small, there are a huge number of children involuntarily exposed to this small, preventable risk while might in the long run have serious detrimental health consequences. Pulmonary Function and Involuntary Smoking The reaction of the adult lung to involuntary smoking is also of concern to very many people. Is there any good evidence that lung function deteriorates when exposed to the sidestream smoke from cigarettes? While relatively few studies have been performed in attempts to answer this very important question, the answer does seem to be a qualified "yes". In children, about the same number of studies seem to show a positive association between passive cigarette smoke exposure and deterioration of pulmonary function tests as those which do not. In some investigations, there seems to even be a dose response relationship (22,23) in that the most cigarettes smoked, the greater the lung function deterioration. These studies show that younger children seem to be the most severely affected, and that maternal smoking habits (possibly since young children are with their mothers more than with their smoking fathers) are more important (22). However, other investigations in warm, dry areas of the United States show no association between deterioration in lung function and parental smoking habits (24,25). Unfortunately, however, all of these investigations suffer from not having a clearly defined estimate of the degree of exposure to cigarette smoke. This means that it is impossible to tell whether in one study, the children had a greater cigarette exposure than in another study. For example, it is possible that the studies which did not find an association between deterioration in lung function and involuntary smoking in warm, dry climates may simply be that children in these climates are more frequently outdoors, and that their exposure to paternal cigarette smoking is comparatively less. The correlation of adult pulmonary function deterioration with relation to involuntary smoking is similarly difficult to prove. The White and Froeb study (26) is a frequently quoted investigation which attempted to prove this association. They reported on 2,100 asymptomatic otherwise healthy adults that was about to enter into a fitness program. They found significant reduction in some pulmonary function tests (FEV1 and MMEFR) in adults exposed to tobacco smoke in the work environment compared to those who did not have this exposure. The change in pulmonary function tests was not severe, but was comparable to that which might be seen in smokers of 1 to 10 cigarettes a day. Additionally, the investigators attempted to determine the degree of exposure to cigarette smoke (the lack of this determination being the principle difficulty with similar studies performed in children - see above). They found that carbon monoxide levels in the workplace were in agreement with the working history of the study groups. The picture is obscured, however, by Comstock and associates (27) who performed a similar study on 1,724 subjects. They found no statistically significant reduction of pulmonary function (FEV1) in non-smoking men whose wives were smokers at home. A similar correlation between non-smoking women whose husbands smoked at home could not be done. Another similar study by Shilling and associates (24) also found no significant reduction in pulmonary function that could be associated with involuntary smoking. A criticism of many of these studies is that they did not control well for the years of exposure to involuntary tobacco smoke. It can be shown that many years of exposure are probably necessary before any significant reduction in pulmonary function should be anticipated. In one study in France, Kaufmann and associates (28) studied a large group of 1,985 nonsmoking women who were from 25 to 59 years old in which 58% were exposed to a smoking husband. In these women, there was a statistically significant reduction in pulmonary function (MMEFR) only in those women who were over 40 years old. These changes were small but were present and suggest that future studies should control for age of the non-smokers or years of involuntary exposure to tobacco smoke. Additionally, the results agree with our perception that lung disease may take many years to develop, even in those who are actively smoking, and does not occur with only incidental exposure. The function significance of these small reductions in only some of the pulmonary function studies is unclear. Most likely, however, most people are not too symptomatic from these minor changes, and it seems unlikely that most people without other risk factors for chronic lung disease would sustain significant damage to their lungs with involutary smoking exposure. However, it is not at all clear whether those subjects with underlying lung disease, such as asthma, might not be significantly more sensitive to involuntary smoking than the normal population. Also, the causes of asthma, especially in children, are largely unknown, and it is certainly not outside the realm of possibility that repeated involuntary exposure to cigarette smoke may have some role in its development. Also, there is the unfortunate statistic that children whose parents smoke are twice as likely to become active cigarette smokers than children of parents who do not have this unfortunate habit (29); this association is certainly much more important than the minor lung impair that involuntary smoking might impart. Involuntary Smoking and Lung Cancer While everybody would be concerned if there were a strong link between reduction in pulmonary function, wheezing, and childhood lung infections associated with involuntary smoking, there could be little doubt that as associationg between lung cancer would be far more serious. The possibility that passive smoking could be associated with a greater risk of lung cancer has also been investigated in several studies with rather alarming results. A large investigation by Hirayama (30) concerned 91,540 non-smoking married women with 13 years of follow-up. The lung cancer rate was approximately 1.6 times greater among those who were married to men who smoked less than 1 pack per day, but 2.1 times greater among women whose husbands smoked more than 1 pack a day. For comparison, women who smoke had a risk of lung cancer 2.1 times greater than the women with involuntary smoke exposure, who in turn had an average of 1.7 times greater risk for lung cancer than women whose husbands did not smoke. Another study that investigated the possible relationship between passive smoking and lung cancer was performed by Trichopoulos and associates (31). In this study, non-smoking women with husbands who smoked had a 2.4 times greater risk of developing lung cancer than did those women married to husbands who did not smoke. The risk increased to 3.4 times greater for women married to husbands who smoked greater than 1 pack per day. Finally, Garfinkle (32) examined lung cancer mortality rates in the United States through analysis of the American Cancer Society study and the Dorn study of American veterans. The Garfinkle study included 176,739 nonsmoking women who were married to men who smoked. Those women married to husbands smoking less than a pack a day had only 1.3 times the risk of lung cancer than did those women married to nonsmoking husbands, and those women married to husbands who smoked greater than 1 pack a day had only 1.1 times greater risk. Neither of these results were statistically significant. There were several differences in methodology between the American and the Japanese studies. First, the American study did not investigate 72.9% of the husbands of nonsmoking women in comparison with only 27.7% of the same missing data in the Japanese studies. Additionally, the larger homes and higher divorce rates in the United States could also potentially affect the data since there might be less smoke exposure (18). A more recent study by Repace and Lowery (36) has attempted to derive an approximate number of lung cancers which are caused by passive smoking. They examined the differences in lung cancer mortality between Seventh-Day Adventists who never smoked, and a group of comparable nonsmoking, non-Seventh Day Adventists. The investigators then made use of a nujber of simplifying assumptions (such as the entire difference in the lung cancer death rate between non-smoking Seventh Day Adventists and non-smoking non-Seventh Day Adventists is due entirely to passive smoking, that Seventh Day Adventists are not at all exposed to passive cigarette smoke while the non-Seventh Day Adventists are uniformly exposed, and that there are no differences in lung cancer death rates between women and men). Even though these assumptions are possibly questionable and over simplistic, the resulting figure of 7.4 lung cancer deaths per 100,000 person-years is remarkably similar to the figure of 6.8 lung cancer deaths per 100,000 person-years derived by Hirayama from the best available studies (30,36,37). Replace and Lowery then calculated that approximately 4,666 lung cancer deaths per year, or 5% of all lung cancer deaths and 30% of all nonsmoker annual lung cancer deaths, are due to passive smoking. Similar results were obtained in a recent study reported in the New England Journal of Medicine (38). This study tried to determine whether there was an increased risk of lung cancer associated with household exposure. To do this, the investigators compared two groups of patients; one group had lung cancer and never smoked cigarettes, and another group was the control or comparison group, of patients who did not smoke and did not have lung cancer. The lung cancer group was obtained by examining the medical records of patients in the seven Standard Metropolitan Statistical Areas (Buffalo, Rochester, Syracuse, Utica-Rome, Albany-Schenectady-Troy, Binghamton, and greater New York (excluding the five boroughs of New York)). To be enrolled in the study, the lung cancer patients had to be between 20 and 80 years old, and never have smoked more than 100 cigarettes during the ten years prior to diagnosis. The control group consisted of subjects drawn from records of the New York State Department of Motor Vehicles who were selected to be as closely matched to the cancer patients with respect to age, sex, and county of residence. 191 control subject-cancer patient pairs were entered into the study. After analysis of the data, the results indicated that household exposure to 25 or more smoker years during childhood and adolescence doubled the risk of lung cancer in later life; less than this degree of exposure did not increase the risk of lung cancer. Additionally, in this study, exposure to a spouse's smoking was not associated with an increased risk for developing lung cancer. The authors of this paper further point out that these findings are consistent with recent findings that passive smokers have elevated levels of some cancer causing agents in their blood (39). Consensus of Opinion on Dangers of Passive Smoking The American Lung Association has reported that a consensus of opinion concerning the dangers of passive smoking has been established between the 1986 Surgeon General's Report on Involuntary Smoking and the recent National Academy of Science Report on Enviromental Tobacco Smoke (40). More specifically, the following comparisons of opinions were made: Surgeon General National Academy of Science "Involuntary smoking is a cause of disease, including lung cancer, in healthy nonsmokers." Considering the evidence as a whole, exposure to ETS (environmental tobacco smoke) increases the incidence of lung cancer in nonsmokers."Summary In summary, estimates have been made several years ago that the
risk of developing lung cancer in nonsmokers who are regularly exposed
to passive smoking is 30% greater than for those not exposed (33).
These estimates have been proven to be correct by more recent investigations.
The problem of passive smoking is particularly tragic since those exposed
often have little influence over the degree of their exposure, especially
if children of smoking parents. Perhaps these recent investigations
demonstrating that these children have an increased chance for developing
respiratory problems in youth and adulthood, for reduction in rate of growth
of their children's lungs, and an increased chance for developing lung
cancer in latter life may influence parents to stop smoking.
References Involuntary Smoking 1. U.S. Public Health Service, Smoking and Health. A Public Health
Service Review, U.S. Department of Health, education and Welfare, Public
Health Service, Department of Health, education and Welfare, Publication
Number (PHS) 79-50066, 1979.
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