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Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects (1986)

Chapter: HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS

« Previous: ASSESSING EXPOSURES TO ENVIRONMENTAL TOBACCO SMOKE
Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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9
Introduction

Epidemiologic and experimental studies seek to determine if a relationship exists between a particular exposure and particular health effects. When the exposure is via the air, as is the case with environmental tobacco smoke (ETS) exposure to nonsmokers, the organs that are directly exposed include the eyes, nose, throat, and lungs. Clinical, epidemiologic, and animal studies have shown, generally speaking, that air pollutants can have major health effects on the respiratory system (National Research Council, 1985). Experimental research using animals (Chapter 3) and research with biological markers in humans (Chapter 8) indicate that various constituents of the smoke are absorbed into the blood and, therefore, are transported to organs and tissues of the body. Consequently, the range of possible health effects of exposure to ETS may be very broad and vary enormously in their effect on the individual. Effects may be reversible or irreversible, discomforting, or life-threatening.

In the following chapters, several possible health effects that have received substantial attention are reviewed. Many of the health effects associated with active smoking have been evaluated in studies of nonsmokers exposed to ETS. These include: acute, noxious sensory irritation; nonmalignant respiratory symptoms and disease; decrease in pulmonary function; lung and other cancers; cardiovascular disease; relative growth, ear infections in children; and low birthweight of children of nonsmoking women.

Nonsmokers commonly complain of the perception of tobacco smoke and its irritating, noxious, or annoying qualities. However, in most such spontaneous instances, these complaints are voiced

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

because the subjects can see another person actively smoking in their vicinity. Chapter 10 reviews experimental studies that evaluate these acute comfort aspects under controlled conditions.

Chapters 11 and 12 assess and evaluate possible nonneoplastic and neoplastic pulmonary effects of exposure to ETS by nonsmokers. Over the past 15 years, a number of studies in children and in adults have assessed various possible acute and chronic pulmonary effects subsequent to long-term exposure to ETS. Individuals who have chronic lung diseases, such as patients with asthma, alpha-l-antitrypsin deficiency, or cystic fibrosis, are potentially hypersensitive to the effects of ETS exposures.

Chapter 13 reviews and evaluates reports of cancers other than lung that may be associated with exposure to ETS in nonsmokers.

Chapter 14 discusses the possible association of exposure to ETS with chronic and acute cardiovascular responses and cardiovascular diseases in nonsmokers. Individuals with chronic disease that compromise the cardiovascular system, such as patients with a history of angina pectoris, are at a high risk for developing abnormal cardiovascular responses following exposure.

Chapter 15 considers evidence that a number of other health effects are linked to ETS exposure in children of smokers, including lower relative growth, frequency of ear infections, and low birthweight (with nonsmoking pregnant mothers).

The studies reviewed here are epidemiologic and experimental. Epidemiologic studies include case-control studies, in which subjects are selected according to whether or not they have the health outcome being studied, and cohort (or prospective) studies, in which subjects are classified according to whether or not they have been exposed to ETS. Cross-sectional studies are those in which an assessment is made of a population at one point in time. Longitudinal studies follow a group of persons over time. In experimental studies, subjects are exposed to ETS under controlled conditions often using chamber studies. Most studies of ETS have been cross-sectional rather than longitudinal. To be informative, a study must evaluate a sufficient number of people to provide a precise estimate of the effect; obtain valid information regarding the history of exposure and health status of the individuals; and, of course, the statistical analyses must be appropriate to the study design. The appropriate design and use of these epidemiologic methods for the study of air pollution and possible health effects

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

are discussed in general terms in the monograph “Epidemiology and Air Pollution” (National Research Council, 1985).

REFERENCE

National Research Council, Committee on the Epidemiology of Air Pollutants. Epidemiology and Air Pollution. Washington, D.C.: National Academy Press, 1985. 224 pp.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

10
Sensory Reactions to and Irritation Effects of Environmental Tobacco Smoke

In this chapter, the acute sensory reactions from exposure to ETS are discussed. These reactions include perception of odor and irritation of eyes and upper airways. Methods for evaluating these psychosensory phenomena include controlled chamber studies, where ventilation and smoking rates are manipulated and evaluated in terms of reported perception by a small number of subjects.

ODOR

The perception of odor is often the earliest indicator of exposure to many airborne contaminants, but not for all. For some individuals, odor may merely be a nuisance. For others, odor is an early indicator of a complex reaction to exposure to ETS involving allergic and other physiologic responses.

Considerations of sensory reactions have a central role in the development of guidelines for ventilation requirements for occupied spaces. The amount of ventilation, or number of air exchanges, needed to eliminate unacceptable odors and irritation commonly exceeds that required to meet any other needs, such as control of carbon dioxide. For a number of years, quite apart from concerns about possible adverse health from exposure to ETS, ventilation engineers have viewed ETS as the most problematic common indoor contaminant (Leonardos and Kendall, 1971).

Efforts to derive functional relationships between the amount of a contaminant generated in a space and the amount of outdoor air, i.e., ventilation, necessary to control its odor began in the

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 10–1 Relationships between ventilation rate and air space per person in an environmental chamber according to three criteria: (A) maintenance of oxygen concentration; (B) control of carbon dioxide to a level of 0.6% (2.5 cubic feet per minute); and (C) control of body odor at a moderate level under sedentary conditions of occupancy, no smoking.

1930s (Yaglou et al., 1936). Function C in Figure 10–1 is derived from experiments of Yaglou et al. (1936), where judges assessed the odor generated by occupants sitting quietly in an environmental chamber. The function depicts the combination of air space per person and ventilation rate of the air space (outdoor air) per person necessary to maintain odor at a moderate, acceptable level under steady-state conditions. Theoretical functions A and B, which fall below C, implying less need for ventilation, represent the outdoor air needed to maintain oxygen at a minimum of 20% and the air necessary to hold carbon dioxide at a maximum 0.6%, respectively.

The decrease in curve C at low occupancy density (large air space per person) resulted most likely from the instability of occupancy body odor in Yaglou’s chamber. That is, occupancy odor decays relatively rapidly on its own (Yaglou and Witheridge, 1937; Clausen et al., 1984). Tobacco smoke odor, on the other hand, exhibits relative stability. When smoking has ceased in an unventilated room, the odor will remain at the about same level over many hours (Yaglou and Witheridge, 1937; Clausen et al., 1985). In a diagram such as Figure 10–1, a function for tobacco

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

smoke odor, like functions A and B, would be independent of the size of the space or of air space per occupant. In this respect, tobacco smoke odor behaves as a simple contaminant and ventilation requirements for reducing tobacco smoke odor should depend strictly on rate of smoking.

Twenty years after his study on occupancy odor, Yaglou (1955) reported a small experiment on tobacco smoke odor. Studying the very high smoking rate of 24 cigarettes per hour generated by six of nine occupants in his 1,410-cubic-foot chamber, he reported the need for 40 cfm (cubic feet per minute) per smoker, or 600 cubic feet per cigarette, in order to achieve moderate, acceptable odor. At about the same time, Kerka and Humphreys (1956), using similar psychophysical techniques, estimated the requirement at 2,250 cubic feet per cigarette, or 300 cfm per smoker smoking 8 cigarettes per hour. At a smoking rate of 2 cigarettes per hour, this would be 75 cfm per smoker.

Recent results have estimated ventilation needs closer to those of Kerka and Humphreys (1956) than those of Yaglou (1955), but have also uncovered limitations on ventilation as a solution to the odor problems produced by ETS. Figure 10–2 shows how tobacco smoke odor varied over time for three smoking rates and various ventilation rates (Cain et al., 1983). The line connecting the open squares in the left panel depicts the level of odor generated by nonsmoking occupancy with low ventilation. It shows that even in the presence of higher ventilation rates, smoking generated more odor than simple occupancy.

The psychophysical judges in the experiment, a mixed group of smokers and nonsmokers, assessed acceptability in addition to perceived intensity. Figure 10–3 shows the percent of dissatisfaction as a function of ventilation rate per cigarette. The ventilation rate that would lead to 20% of judges dissatisfied is 4,240 cubic feet per cigarette (shown by the vertical dashed line). Twenty percent dissatisfied is the maximum level allowed by recommendation of the American Society of Heating, Refrigeration and Air-Conditioning Engineers (ASHRAE, 1981). On the realistic assumption that the percentage of people actually smoking in a space at any given time will equal about 10%, ventilation rate per person (smokers and nonsmokers) would need to be 53 cfm (see Figure 10–3) to reduce odors to a level that would satisfy 80% of the judges.

Despite ASHRAE’s goal of satisfying at least 80% of visitors to a space, none of its recommendations for ventilation are as high

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 10–2 Intensity of odor during and after smoking in an environmental chamber for three different rates of cigarettes smoked per hour. Measurement of odor intensity was parts per million butanol matched to the test odor according to ASTM standard E544–75. Each point represents judgments taken over a 15-minute period. From Cain et al. (1983).

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 10–3 Percent of judgments of unacceptable odor quality of air versus ventilation per cigarette and ventilation per occupant, assuming that 10% of occupants in a space will be smoking at any time. Data from Cain et al. (1983).

as 53 cfm per occupant. For offices where smoking is allowed, the ASHRAE recommendation is 20 cfm per occupant. For many other smoking areas, however, the ASHRAE recommendation is 35 cfm per occupant. Such recommendations did not result from experiment, but rather from a consensus procedure of expert heating and refrigerating engineers that weighed available information. The bulk of the data on the acceptability of odor and irritation from ETS was not available at the time ASHRAE prepared its standard in 1981. The standard was, however, the first to specify the need for 4 to 5 times greater ventilation rates during smoking occupancy as compared with nonsmoking occupancy. The most common rate specified for smoking occupancy is 35 cfm per occupant, whereas 7 cfm per occupant is the most common rate specified for nonsmoking occupancy. This means that in a space where smoking is allowed, the pollution generated by smoking creates the greatest need for ventilation.

According to the data of Cain et al. (1983) (Figure 10–3), ASHRAE’s proposed ventilation rate of 35 cfm per occupant during smoking will lead to 25% of visitors being dissatisfied (75%

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

satisfied) with the odor. Data suggest that the difference in satisfaction between smoking and nonsmoking occupancy, and hence the difference in recommended ventilation rates, arises largely because of the intensity of the odors (Figure 10–4), rather than the quality of the odors. At equal odor intensity, the occupancy odor and tobacco smoke odor are disliked about equally.

An additional factor affecting annoyance with odor is that nonsmokers are much more likely than smokers to object to tobacco smoke odor. Figure 10–5 depicts relative dissatisfaction with tobacco smoke odor at various intensities, expressed in terms of equivalent levels of butanol. At 32 ppm (butanol level 2), 1% of smokers found the odor unacceptable, while 20% of nonsmokers found it so. The odor had to rise to 256 ppm (level 5) before as

FIGURE 10–4 Percent of judgments of unacceptable odor quality of air versus odor intensity assessed by means of a graphic rating procedure during various conditions of smoking and nonsmoking occupancy. Each point represents the outcome from a particular combination of contaminant generation (number of occupants or rate of smoking) and ventilation rate. Data from Cain et al. (1983).

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 10–5 Percent of judgments of unacceptable odor quality of air derived from tobacco smoke odor related to equivalent level of butanol (parts per million at top; log2 at bottom). Judgments accumulated across all conditions of smoking (2,357 judgments). Left: Data from all visitors. Right: Data from smokers and nonsmokers plotted separately. Data from Cain et al. (1983).

many as 20% of smokers found the odor unacceptable. In terms of practical solutions to the odor problem caused by tobacco smoke, the difference between smokers and nonsmokers may prove insurmountable. Under usual levels of smoking, no realistic level of ventilation will drive tobacco smoke odor as low as the equivalent of 32 ppm butanol (butanol level 2).

IRRITATION

Ventilating and air-conditioning engineers have typically concerned themselves with the reactions of visitors to enclosed spaces on the assumption that visitors will exhibit more sensitivity than occupants. As society has become more concerned with the health risks of smoking in the recent past, research on consequences of ETS exposure has focused on the occupant. Included within this concern have been the sensory reactions of occupants.

Figure 10–6 illustrates changes in tobacco smoke odor and irritation over time for occupants. Whereas perceived odor magnitude may fade due to olfactory adaptation, irritation may increase. Also apparent in this figure is a relationship between relative humidity and odor or irritation perception. In the low relative humidity conditions, both odor and irritation were exacerbated.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Receptors for irritation exist throughout the nasal, pharyngeal, and laryngeal areas and on the surface of the eyes. The receptors comprise free nerve endings of the fifth, ninth, and tenth cranial nerves and form the mediating elements of what is known as the common chemical sense. Although particularly sensitive to corrosive stimuli, the common chemical sense responds to almost any airborne organic material at high concentration (Cain, 1981).

The common chemical sense (or irritation perception) is characterized by a tendency to respond more vigorously over time (Cometto-Muniz and Cain, 1984). A person in an environment with a low-level irritant may even fail to notice any irritation at first. Once irritation has begun, however, it may persist even after removal of the stimulus.

FIGURE 10–6 Changes in odor and irritation during continuous, short-term exposure to cigarette smoke generated in a chamber. Ventilation equalled 14 cfm per cigarette and ambient temperature equalled 25°C. Relative humidity (RH) was 30% in one condition and 65% in the other. Adapted from Kerka and Humphreys (1956).

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 10–7 Eye irritation related to duration of exposure and concentration (parts per million carbon monoxide) of ETS. Left: Eye irritation index. Right: Eye blink rate. From Weber (1984).

Chamber Studies

A number of chamber studies have examined irritation and odor from tobacco smoke (Weber et al., 1976a,b; Weber et al., 1979a,b; Weber and Fischer, 1980; Muramatsu et al., 1983; Weber, 1984). The major findings include:

  • Irritation from ETS varies with both concentration (measured as an increment in carbon monoxide as a surrogate for ETS) and time over long durations, as shown in Figure 10–7.

  • The eyes are the most readily affected site for irritation, with the nose second.

  • Rate of eye blinking correlates well with estimates of eye and nose irritation when the level of ETS is high (i.e., level of ETS such that the carbon monoxide concentration is at least 5 ppm), though eye blinking seems a less sensitive index than psychophysical judgments (Figure 10–7).

  • Degree of annoyance (a composite index of impressions as defined by Weber) reaches a steady state much more rapidly than irritation, presumably because odor contributes to annoyance.

  • Degree of annoyance depend almost entirely on the gas phase of ETS. Filtration of the particles is followed by only a small, though relatively constant, reduction in annoyance.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
  • Eye irritation and increased eye blink rate depend almost entirely on the particulate phase of ETS. Particle filtration diminishes the sense of irritation greatly.

  • Weber (1984) suggested that ETS corresponding to CO concentrations of 1.5 to 2.0 ppm should form the maximum permissible level of exposure in environmentally realistic circumstances. At about 2 ppm of CO, almost 20% of occupants report “strong” or “very strong” eye irritation. Cain et al. (1983) and Clausen et al. (1985) found that incremental CO concentrations of 1 to 2 ppm led to 20% of visitors becoming dissatisfied with the air.

One of the more important issues with respect to control of ETS is whether filtration of the particles will reduce discomfort. As indicated above, Weber and colleagues found only a small reduction of annoyance when they filtered the particles with Cambridge pads. Since their criteria for annoyance largely assessed odor, their data largely agree with those of Clausen et al. (1985), who found that electrostatic precipitation of the particles caused no significant reduction in odor perceived by visitors to a chamber. Nevertheless, Weber and associates did find that filtration reduced reported eye irritation considerably. This led them to draw the conclusion that eye irritation derived largely from the particulate phase of ETS. Cain et al. (in press), on the other hand, found only a slight reduction of irritation following electrostatic precipitation of the particles. This disparity suggests the need for a more direct comparison of the sensory effects of the two filtration methods and for chemical analysis in order to determine whether Cambridge pads remove a vapor-phase constitutent of ETS that is left airborne by electrostatic precipitation.

Field Studies

Winnecke et al. (1984) argued that when people engage in social activities (e.g., playing cards or games) they become somewhat less critical of the environment and will tolerate a level corresponding to more than a 5-ppm increment in CO. It is suggested that when undistracted, occupants of chambers in experimental studies might complain about circumstances that would go unnoticed in life situations. On the other hand, irritation may prove relatively resistant to distraction. Restaurants would seem to offer a realistic proving ground for the interpretation of the chamber studies.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Weber et al. (1979a) found that more than 20% of occupants in restaurants included in a Zurich study reported eye irritation when CO, used as a surrogate for tobacco smoke levels, increased by 2 ppm above background. There was a direct relationship between reported irritation and CO concentration in four restaurants surveyed. In a study of more than 40 workrooms, Weber and Fischer (1980) also found a similar association between the concentration of CO and reported eye irritation.

Judgments of dissatisfaction, whether taken inside a chamber or in the field, may well vary as the social acceptance of certain odors, including ETS, changes with time. For this reason, judgments of some attribute, such as eye irritation, or judgments of odor intensity, particularly those that entail a reference such as butanol, should form the information of interest for long-term considerations. Dissatisfaction measures may be more variable.

HYPERSENSITIVE INDIVIDUALS

Individuals with chronic lung diseases, such as asthma and vasomotor rhinitis, may be more sensitive to the acute irritating effects of exposure to ETS (see Chapter 11). In addition, many people without active diseases report allergic or allergic-like symptoms as a result of exposure to ETS (e.g., Speer, 1968; Zussman, 1974). Reported symptoms include eye irritation, nasal symptoms, headache, cough, wheezing, sore throat, and nausea. The percent of people who report these responses varies with the nature of the exposure. These reports have led to the belief that a tobacco smoke allergy may exist.

Several investigators have studied immediate cutaneous hyper sensitivity to extracts of tobacco leaves. Zussman (1974) found that 16% of 200 atopic patients reported that they were clinically sensitive to ETS exposure. All of them did develop erythema during the intradermal tests. Becker et al. (1976) found that one-third (11 out of 31) of human volunteers, including smokers, exhibit hypersensitivity to a glycoprotein purified from cured tobacco leaves (TGP-L) and from cigarette smoke condensate (TGP-CSC). Reports of immediate skin reactivity suggest an immunological basis for clinical sensitivity to tobacco smoke.

Tobacco smoke has been shown to contain immunogens that can stimulate immune responses to tobacco leaf extract in experimental animals (Lehrer et al., 1978; Becker et al., 1979; Gleich and

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Welsh, 1979). However, the extracts differ and there is controversy concerning the purity of tobacco glycoprotein isolates (Becker et al., 1981; Bick et al., 1981).

In a recent study of Lehrer et al. (1984), skin prick tests of 93 subjects were done, including 60 of whom claimed clinical sensitivity to tobacco smoke. The group included atopic and nonatopic individuals. Approximately 50% of the atopic subjects had positive skin tests to leaf extracts or cigarette smoke condensate (CSC). Fewer than 5% of nonatopic individuals had a positive reaction, independent of whether they claimed to be sensitive to ETS exposure. Radioallergosorbent tests (RAST) were also conducted. Forty-five percent of atopic individuals and 6% of nonatopic individuals were positive for leaf extracts. There were no significant differences in specific serum IgE antibodies among smokers, exsmokers, or nonsmokers. Fewer than 6% of either group responded to CSC. Because there was no relationship between subjective tobacco smoke sensitivity and reaction to the various tests, the authors concluded that the reported subjective sensitivity is probably not related to hypersensitivity to tobacco leaf or smoke antigens.

In summary, experimental and clinical studies have indicated that there are immunogens in ETS and that a portion of the population is sensitive as shown by dermatological tests. However, the specific agent responsible for this reactivity has not been conclusively identified. Furthermore, there is some question as to whether reactions to skin tests are correlated with subjective complaints. It is clear, however, that a substantial number of atopic individuals will have positive skin tests to tobacco smoke or tobacco leaf extracts. More research needs to be done to characterize the immunogens and explain the relationship between subjective symptoms and skin tests.

SUMMARY AND RECOMMENDATIONS

There are a number of acute, noxious effects of exposure to ETS by nonsmokers that may occur. These include annoyance with odor, eye irritation, throat irritation, and immunological responses. The specific constituents that elicit these responses are not known.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
What Is Known
Odor
  1. ETS arouses odor responses. The objectionable odor generated by ETS greatly exceeds that generated by simple occupancy under comparable conditions of occupancy, density, temperature, and relative humidity, and is more persistent.

  2. Tobacco smoke odor is stable over time. Ventilation requirements for tobacco smoke odor will therefore vary in strict proportion to the number of cigarettes smoked.

  3. Rooms (and other spaces) where there is smoking require much more ventilation than spaces with nonsmoking occupancy. During smoking, ventilation requirements that satisfy at least 80% of visitors to a room exceed 50 cfm per occupant.

  4. Nonsmokers and visitors to rooms appear to set a more stringent criterion than smokers for acceptability of tobacco smoke odor. Current ventilation guidelines for smoking occupancy will apparently fail to satisfy a criterion level of 80% of visitors (mixed group). It is not clear that any practical ventilation rate could satisfy 80% or more nonsmokers under typical conditions of smoking occupancy.

Irritation
  1. Low humidity may exacerbate odor and irritation responses to ETS.

  2. Whereas odor will govern the reactions of visitors to a smoking space, irritation will largely govern the reactions of occupants. Over time, eye irritation grows to become the most important negative response of the occupant. Dissatisfaction observed in chamber studies is commensurate with that found in field studies.

  3. Eye blink offers a reasonable correlate of sensory irritation at high levels of smoke (i.e., levels of ETS such that the concentration of CO is at least 5 ppm), but not at low levels.

  4. Filtration of particles from ETS via an electrostatic precipitator causes no decline in odor to visitors and no meaningful decline in odor or irritation to occupants. This suggests that irritation and odor derive primarily from gas- or vapor-phase constituents.

  5. Filtration of particles via a Cambridge pad reduced irritation, but not odor, to occupants. Perhaps the Cambridge pad

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

removes some critical vapors from the smoke along with the particles.

  1. A substantial portion of atopic individuals are sensitive to tobacco leaf or tobacco smoke extracts as shown by skin tests. However, cutaneous sensitivity appears not to correlate with subjective symptoms.

What Scientific Information Is Missing
  1. The outcomes obtained in chambers regarding dissatisfaction created by the odor and irritation of ETS should be further verified in field situations. The chamber studies imply that there must be considerably more than 20% dissatisfaction in places where smoking occurs even when current ventilation standards are met.

  2. Prospects for abatement of discomfort through filtration of the vapor or particulate phases of ETS should receive attention.

  3. Objective physiological or biochemical indices should be sought to validate reports of chronic irritation of the eyes, nose, and throat.

  4. Research is needed to determine specific constituents that are the irritants in ETS.

  5. Information is needed on the prevalence and severity of allergic and hypersensitive responses to tobacco smoke in the general population and in atopic individuals.

  6. Further research needs to be done to determine the specific elements that are immunogenic in extracts of tobacco smoke and to relate immune response on skin tests to subjective complaints of sensitivity to tobacco smoke.

  7. Research is needed to evaluate the medical importance of positive reactions to RAST tests of tobacco leaf products for atopics.

REFERENCES

ASHRAE Standard 62–81. Ventilation for Acceptable Indoor Air Quality. Atlanta: ASHRAE, 1981. 19 pp.


Becker, C.G., T.Dubin, and H.P.Wiedemann. Hypersensitivity to tobacco antigen. Proc. Natl. Acad. Sci. USA 73:1712–1716, 1976.

Becker, C.G., R.Levi, and J.Zavecz. Induction of IgE antibodies to antigen isolated from tobacco leaves and from cigarette smoke condensate. Am. J. Pathol 96:249–254, 1979.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Becker, C.G., N.Van Hamont, and M.Wagner. Tobacco, cocoa, coffee, and ragweed: Cross-reacting allergens that activate factor-XXI-dependent pathways. Blood 58:861–867, 1981.

Bick, R.L., R.L.Stedman, P.L.Kronick, E.Hillman, and J.Fareed. Studies related to tobacco glycoprotein: A claimed activator of coagulation fibrolysis, complement, kinin and a claimed allergen. Thromb. Haemostasis 46:231, 1981.


Cain, W.S. Olfaction and the common chemical sense: Similarities, differences, and interactions, pp. 109–121. In H.R.Moskowitz and B. Warren, Eds. Order Quality and Intensity as a Function of Chemical Structure. American Chemical Society Symposium 148. Washington, D.C.: American Chemical Society, 1981.

Cain, W.S., B.P.Leaderer, R.Isseroff, L.G.Berglund, R.J.Huey, E.D. Lipsitt, and D.Perlman. Ventilation requirements in buildings. I. Control of occupancy odor and tobacco smoke odor. Atmos. Environ. 17:1183–1197, 1983.

Cain, W.S., T.Tosun, L.C.See, and B.P.Leaderer. Environmental tobacco smoke: Sensory reactions of occupants. Atmos. Environ., in press.

Clausen, G. P.O.Fanger, W.S.Cain, and B.P.Leaderer. Stability of tobacco smoke odor in enclosed spaces, pp. 437–441. In B.Berglund, T.Lindvall, and J.Sundell, Eds. Indoor Air, Vol. 3. Sensory and Hyperreactivity Reactions to Sick Buildings. Stockholm, Sweden: Swedish Council for Building Research, 1984.

Clausen, G., P.O.Fanger, W.S.Cain, and B.P.Leaderer. The influence of aging, particle filtration and humidity on tobacco smoke odor, pp. 345–350. In P.O.Fanger, Ed. Clima 2000, Vol. 4. Indoor Climate. Copenhagen, Denmark: VVS Kongress-VVS Messe, 1985.

Cometto-Muniz, J.E., and W.S.Cain. Temporal integration of pungency. Chem. Senses 8:315–327, 1984.


Gleich, G.J., and P.W.Welsh. Immunochemical and physicochemical properties of tobacco extract. Am. Rev. Respir. Dis. 120:995–1001, 1979.


Kerka, W.F., and C.M.Humphreys. Temperature and humidity effect on odor perception. ASHRAE Trans. 61:531–552, 1956.


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Lehrer, S.B., F.Barbandi, J.P.Taylor, and J.E.Salvaggio. Tobacco smoke “sensitivity”—Is there an immunological basis? J. Allergy Clin. Immunol. 73:240–245, 1984.


Muramatsu, T., A.Weber, S.Muramatsu, and F.Akermann. An experimental study on irritation and annoyance due to passive smoking. Int. Arch. Occup. Environ. Health 51:305–317, 1983.


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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

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Winnecke, G., K.Plischke, A.Roscovanu, and H.W.Schlipkoeter. Patterns and determinants of reaction to tobacco smoke in an experimental exposure setting, pp. 351–356. In B.Berglund, T.Lindvall, and J. Sundell, Eds. Indoor Air, Vol. 2. Radon, Passive Smoking, Particulates, and Housing Epidemiology. Stockholm, Sweden: Swedish Council for Building Research, 1984.


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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

11
Effects of Exposure to Environmental Tobacco Smoke on Lung Function and Respiratory Symptoms

This chapter discusses epidemiologic studies of nonsmokers exposed to tobacco product smoke that have evaluated lung function or respiratory symptoms, most of which have evaluated children. The effects of active cigarette smoking are briefly reviewed to recount the reasons why certain aspects of lung function have been studied in nonsmokers. The plausibility of finding similar effects in nonsmokers exposed to ETS is discussed and the studies found in the literature are assessed.

LUNG FUNCTION AND SYMPTOMS IN ACTIVE SMOKERS

Cross-sectional studies of smokers have demonstrated that smokers, compared with nonsmokers, have (1) an increased prevalence of chronic cough, chronic sputum production, and wheezing and (2) decreased lung function (see U.S. Public Health Service, 1984, for an extensive review). The effects of smoking on both respiratory symptoms and lung function may be seen within a few years of the onset of regular smoking (U.S. Public Health Service, 1979, 1984; Woolcock et al., 1984). Longitudinal studies have demonstrated that the mean rate of decline with age of the 1-second forced expiratory volume (FEV1) is greater in smokers than in nonsmokers. In some smokers, the rate of decline of FEV1 is rapid, leading to clinically important chronic airflow obstruction.

The structural changes associated with active cigarette smoking are seen in both the conducting airways and the pulmonary parenchyma (for a more detailed description, see U.S. Public

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 11–1 Known and suspected mechanisms for effects of tobacco smoke on airways. Solid lines=known mechanisms; dashed lines=suspected mechanisms.

Health Service, 1984). In the large airways there is hypertrophy and hyperplasia of the mucous glands. These changes are followed by an increase in mucus production that leads to increased cough and sputum production. Structural changes in smaller airways range from relatively mild inflammation to narrowing and closure of airways due to inflammation, goblet cell hyperplasia, and intraluminal mucus. Changes in the parenchyma include increased numbers of inflammatory cells and ultimately destruction of the alveolar walls, most commonly in the central part of the lobule, i.e., the development of centrilobular emphysema (see Figure 11–1).

The link between airway disease and parenchymal disease is poorly understood. Smokers with severe functional impairment usually have an appreciable amount of emphysema (U.S. Public Health Service, 1984).

Cessation of smoking leads to a rapid decrease in respiratory symptoms, an improvement in lung function, and a shift towards the nonsmoker’s rate of decline of FEV1 (U.S. Public Health Service, 1979, 1984). These improvements are usually seen regardless of the functional level at which cessation occurs.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Population-based studies of adults have generally shown a strong dose-response relationship between FEV1 with dose measured either in terms of years smoked, the number of cigarettes per day, or the integrated dose, i.e., pack-years (U.S. Public Health Service, 1984). It is worthwhile noting, however, that in two major studies (Burrows et al., 1977a; Beck et al., 1981) the active smoking dose accounted for only about 15% of the variation of FEV1 even after age and height adjustment. Most of the variance could be attributed to the naturally occurring large variability in pulmonary function. Another reason the active smoking dose did not explain much of the variance is that the number of cigarettes an individual smokes cannot readily be translated into the dose of smoke that is delivered into the airways and parenchyma. Many factors, such as puff volume and lung volume at which inhalation starts, clearance rates, and airway geometry of the lungs of exposed individuals, will influence the dose and the distribution of the smoke within the lungs. Variability in individual susceptibility to the effects of chemicals deposited in the lung has been demonstrated in studies of animals (Evans et al. 1971, 1975, 1978).

PLAUSIBILITY FOR AN EFFECT DUE TO PASSIVE SMOKING

The dose of cigarette smoke delivered to the lungs of nonsmokers exposed to ETS is both qualitatively and quantitatively different from mainstream smoke, being a small fraction of that delivered to the lungs of an active smoker (see discussions in Chapter 7). Exposure to constituents of tobacco smoke may begin in utero and continue throughout childhood through ETS exposure. During these periods, the lung is undergoing both growth and remodeling. Therefore, the lung of the fetus and young child may be particularly susceptible to environmental insults.

Despite qualitative differences between mainstream smoke, sidestream smoke, and ETS, it has been customary to assume that exposure to ETS approximates a low-dose exposure to tobacco smoke. The ability to measure responses to low doses depends on the shape of the dose-response curves, the sensitivity and specificity of the measurement tools available, and whether there is a threshold of exposure below which there is no response in any individual.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

The assumed shape of the dose-response curve determines what kinds of effects would be expected and the estimates of the probability of detecting them. If the dose-response curve were linear with a shallow slope, or a slope concave to the dose axis, the response at low doses might be so small that it would be difficult to detect. In such a situation, only the very susceptible portion of the population might have detectable effects. It is likely that there is a distribution of susceptibility to the effects of ETS within the population, such that there will be some persons who will respond at low doses and some persons for whom many years of heavy exposure may be needed to cause the same symptoms or change in lung function (Cockcroft et al., 1983).

If individuals who are most susceptible to the irritating effects of cigarette smoke on the lower respiratory tract do not start to smoke or, having started, soon quit as smokers, then a population of nonsmokers would be more likely to include the most susceptible individuals than a population of smokers. The existence of different subpopulations introduces an additional complication to the extrapolation from high-dose exposure in active smokers to the low-dose exposures of nonsmokers.

In addition, it is likely that the development of respiratory disease or symptoms, lung function level, and rate of decline reflect the cumulative burden of many environmental exposures and other insults, such as respiratory infections (Purvis and Ehrlich, 1963) to the lung. Furthermore, it might be hypothesized that the cumulative burden may interact with the individual’s genetically determined susceptibility.

METHODOLOGIC CONSIDERATIONS FOR EPIDEMIOLOGIC STUDIES

A recent report of the National Research Council (1985) is devoted to methodologic issues of epidemiology and air pollution. In this section, many of the problems are reviewed briefly.

Study Design and Analysis

Chronic pulmonary effects of ETS have been the subject of several recent reviews (Lee, 1982; Weiss et al., 1983; Surgeon General, 1984; Guyatt and Newhouse, 1985; Taylor et al., 1985) and symposium or workshop reports (U.S. Public Health Service,

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

1983; Gammage and Kaye, 1984; Rylander, 1984). Many of the studies reported in these reviews had not been originally designed to study chronic pulmonary effects of ETS exposure. Instead, these data sets were reanalyzed to address the question of the pulmonary effects of ETS. This use of these studies suggests the need for caution when interpreting their results.

Several analytic approaches were used in the reported studies. Independent risk factors, such as age and sex, usually need to be taken into account, but this was not always done. Several statistical approaches, such as stratification or regression analysis, are used to take into account the effects of potentially confounding variables. For most of the potentially confounding variables, researchers do not agree on the nature of the roles of the variables as confounders and, hence, on the appropriate ways to introduce these variables into the data analyses.

Assessing Exposure

Interpretation of epidemiological studies is hampered by the existence of factors that interact with and modify the response to exposure and by confounding factors that are associated with the same symptom complex as exposure to ETS, such as coughing, production of sputum, and wheezing (see Table 11–1). These variables must be assessed and accounted for in the statistical analyses where possible.

Unreported active smoking could lead to a large bias. Underreporting of smoking is likely in studies of older children, particularly when parents answer questionnaires for their children. Children who have parents who smoke are themselves more likely to smoke. Therefore, because active smoking is likely to have a considerably greater impact on respiratory symptoms and lung function than exposure to ETS, misclassification of the children who smoke will tend to overestimate the effect of exposure to ETS.

For blue collar males, occupational exposure can also be important and may interact with both direct cigarette smoke and ETS. Many pulmonary toxicants can exist in the workplace. Furthermore, ETS exposure can occur in the workplace. Similarly, comparison of inner-city-dwelling persons with less urban, or sub-urban, controls can lead to biases.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–1 Potentially Confounding and Effect Modifying Factors in Epidemiologic Studies of Exposure to Environmental Tobacco Smoke

Unreported active smoking

Tobacco products

Marijuana

Clove cigarettes

Developmental factors

Maternal smoking during pregnancy

Factors related to outdoor environment

Outdoor temperature, humidity

Respirable and nonrespirable particulates, e.g., fugitive dust

Pollens and other allergens

Factors related to indoor environment

Crowding

Number and age of siblings

Total number of people/animals in dwelling unit

Total number of smokers in dwelling unit

Household conditions

Frequency of air exchanges

Temperature and humidity

Use and condition of air conditioning units

Conditions of child care facilities

Unvented combustion products from heating/cooking stoves

Respirable and nonrespirable particulates, e.g., wood smokes

Pollens, molds, mites

Allergens and infectious organisms

Formaldehyde

Factors related to work/hobbies

Work/hobby-related exposure to gases, fumes, particulates

Miscellaneous factors

Annoyance response to tobacco smoking

Reporting biases

Assessing Respiratory Variables

Methods commonly used to assess the effect of passive smoking on the respiratory system, such as respiratory symptom questionnaires and measurement of lung function, may lead to some error.

The problems associated with the respiratory symptom questionnaires include:

  • Different questionnaires are used in studies. Differences in how the questions are asked can sometimes lead to large differences in answers. For instance, asking “Are you a smoker?” may elicit a “No” response from an exsmoker whereas the question “Have you ever smoked?” would be answered “Yes”.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
  • Some studies use a self-administered questionnaire, whereas other studies use a trained interviewer. Trained interviewers can determine whether the subject understands the questionnaire and can follow a prescribed set of probing questions that may help to resolve the specific nature of not-well-described symptoms.

  • Some studies have parents complete the questionnaires for the children, whereas other studies have the child answer the questionnaire. For older children, parents may not be aware of active smoking by the child and exposures to ETS in environments outside the home.

  • Questionnaires necessarily involve some subjective elements that are prone to recall bias. For example, a smoker who is symptomatic may be more likely to report the same symptom in his/her child (Schenker et al., 1983; Ferris et al., 1985).

Many tests are prone to measurement error, which tends to obscure differences between groups of subjects. For example, it may be necessary to repeat lung function measurements for a given individual and to average results to get a reliable estimate. Lung function tests are often not sensitive to the structural and functional changes associated with lung disease (Drill and Thomas, 1980).

CROSS-SECTIONAL STUDIES

In the following sections, selected cross-sectional studies of respiratory symptoms, lung function, and respiratory infections and longitudinal studies of lung functions are reviewed. The studies reviewed here are larger studies in which attempts have been made to standardize assessments and many of the data-gathering techniques, including interviews.

Studies of Respiratory Symptoms in Children

Almost all of the cross-sectional studies that have compared children of parents who smoke with the children of parents who do not smoke have reported increased prevalences of respiratory symptoms, usually cough, sputum, or wheezing, in the children of smoking parents. Some studies, including some that have not found a statistically significant increase in the prevalence of respiratory symptoms in ETS exposed children, have demonstrated

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

an increase in respiratory symptom prevalence with an increasing number of parents or other adults who smoke in the home (see below).

Three problems are especially important for studies of respiratory symptoms in children, i.e., underreported active smoking on the part of children, recall bias leading to overreporting of symptoms by parents, and the confounding variables of infections in parents. All three may lead to overestimation of symptom prevalences among children of smokers. Recall bias would occur if parents who have respiratory symptoms are more likely to report those symptoms in the children. (The possiblity also exists that parents with these symptoms would look upon them as so commonplace as not to be worthy of mention). Parents who are smokers are also more likely to have more respiratory symptoms and respiratory infections. Respiratory infections (and, as a consequence, symptoms) among children of smokers may be the result of direct transmission of infectious agents from the parent or may be caused by inflammation and irritation of lung tissues due to ETS exposure and consequent increase in susceptibility to infection. It has been observed that parents, especially mothers, who have a history of severe respiratory illness report higher rates of respiratory symptoms in their children (Schenker et al., 1983; Ferris et al., 1985).

Various ways of dealing with these potential sources of bias have been proposed. Restricting the study or analysis to children below age 8 is likely to eliminate bias due to underreporting of children who currently smoke. It is more difficult to handle the overreporting of symptoms in children when the parents have respiratory symptoms.

An additional problem for interpretation of parental reports of respiratory symptoms was noted by Schenker et al. (1983). In their study, children whose questionnaires were completed by fathers had significantly fewer symptoms reported than children with mother-completed questionnaires. There was no comparison of questionnaires completed separately by both mother and father for the same child. Because the rates for symptoms as reported by the mother were similar to what was found in other studies and because the fathers reported significantly fewer symptoms, the investigators suggested that fathers underreported symptoms in their children.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Table 11–2 reviews several selected cross-sectional studies of respiratory symptoms in children and adults. Lebowitz and Burrows (1976), reporting on children in the Tucson Epidemiologic Study of Obstructive Lung Disease, emphasized the need for controlling for parental symptoms. They reported that children had a higher prevalence of respiratory symptoms if they lived in households with adults with the same symptom, regardless of the family smoking habits. When the presence of symptoms in the adults was taken into account by partitioning households based on presence or absence of adult symptoms(s), the odds ratio that remained was greater than unity but was no longer statistically significant [Mantel-Haenszel odds ratio for all respiratory symptoms calculated from data presented is 1.35 (95% confidence limits of 0.91 to 1.98)]. Most symptoms were reported more frequently for children in currently smoking families.

Ferris et al. (1985) have argued that correcting for parental symptoms represents an overcorrection for respiratory symptoms in children since it also corrects for the parents’ smoking habits. In the Harvard Air Pollution Respiratory Health Studies (Six-Cities Study) of 10,106 white children aged 6–9 years, the variable indicating whether the parent had a history of bronchitis, emphysema, or asthma was found to be a highly significant independent risk factor for cough and wheeze and a history of respiratory illness among children (Figure 11–2). Children whose parents had a positive history had 72–155% higher symptom and illness rates than children whose parents had no history of these illnesses. Adjustment for parental respiratory history reduced the size of the estimated effects of maternal smoking on respiratory symptoms and illnesses by 20 to 30%, but the associations remained statistically significant for most of the outcome symptom and respiratory illness variables (odds ratios of 1.23 and 1.28, respectively).

In both the Lebowitz and Ferris studies, adjustment for parental symptoms or respiratory illness decreased the strength of the apparent association between exposure to ETS and respiratory symptoms, but did not eliminate it. This finding leads to the reasonable conclusion that the exposures typical of ETS are sufficient to cause respiratory symptoms in some children. The increases in frequency of cough were 20 to 50%, and as high as 90%, when there were smoking parents. The increases in frequency of wheezing were more variable, which may indicate the difficulty in

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–2 Effects of Passive Smoking on Respiratory Symptoms: Selected Cross-sectional Studies Involving Children/Adolescents

Study

Source of Subjects

Subjects

Exposure Assessment

Findings

Comments

Colley, 1974

Aylesbury, UK; seven public schools; 1971

1,328 boys, 270 girls; ages 6–14

Self-administered questionnaire from parents

  1. Close association of child cough and parent winter morning phlegm

  2. Prevalence of cough, 15.6% no smokers, 22.2% both parents smoke (ns)

Suggested cross-infection may be important cause; used different question from U.S. studies

Lebowitz and Burrows, 1976

Tucson, Ariz.; stratified cluster random sample of households; 1972–1973

1,655 households;

Anglo-white;

1,252 children <16,

2,516 children >15

Self-administered NHLBI questionnaire from children >15; otherwise from parents

  1. Prevalence of cough in young children, 7.8% no smokers, 10.4% smokers (p<0.05)

  2. Significance gone when parental symptoms considered

Less than 15 years old assumed to be nonsmokers; concluded familial aggregation important, potential confounder

Schilling et al., 1977

Survey of towns in Connecticut and South Carolina

816 children in 376 families;

607 children <16,

109 children >15

Respiratory Symptom Questionnaire, administered by interviewer

  1. No effect of parental smoking on children’s cough or wheeze

  2. Prevalence of wheeze in young children related to parental wheeze (p<0.01)

Tried to account for active smoking in children

Bland et al., 1958

Derbyshire, UK; 48 secondary schools; 1974

2,847 boys, 2,988 girls;

12 years old

Self-administered questionnaire by child

Prevalence of cough, 16% no smokers, 19% one smoker, 23.5% two smokers (p<0.01)

Effects of child’s and parent’s smoking independently analyzed.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Study

Source of Subjects

Subjects

Exposure Assessment

Findings

Comments

Tager et al., 1979

East Boston, Mass.; random sample in schools; 1975–1977

444 children; ages 5–9 years

NHLBI questionnaire administered by interviewer; if age <10, parent answered

No increase in respiratory illness with parental smoking

Controlled for family size

Weiss et al., 1980

See Tager et al., 1979

650 children; ages 5–9 years

See Tager et al., 1979

Persistent wheeze, 1% no smokers, 6.8% one smoker, 11.8% two smokers (p<0.02)

See Tager et al., 1979

Dodge, 1982

Three towns in Arizona; survey of schools; 1978–1979

558 children; ages 8–10 years

Self-administered by parents

Child’s wheeze (p<0.05), sputum (p<0.05), and cough (p<0.01) related to parental smoking

 

Schenker et al., 1983

Pennsylvania; survey of schools

4,071 children; ages 5–14

Self-administered by parents

Trend with number of smoking parents not significant for any symptoms

Not adjusted for parental symptoms although found to influence no. symptoms reported

Ware et al., 1984

Six U.S. cities; different regions survey of schools; 1974–1979

10,106 children; ages 6–13

Self-administered by parents

20–35% increased risk of all respiratory illness and symptoms with maternal smoking

Multiple logistic regression with gas cooking as other predictor

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 11–2 Relative odds of respiratory illness or symptoms versus average daily cigarette smoking by the child’s mother. Reference value is zero cigarettes per day. From Ferris et al. (1985).

assessing this symptom. Furthermore, there appears to be a dose-response relationship between exposure and the likelihood of the child’s developing respiratory symptoms or a respiratory illness. In the Harvard Study, a significant dose-response relationship was reported; the more mothers who smoked, the greater the risk of respiratory symptoms and illnesses among their children.

Studies of Lung Function in Children

A more quantitative measure of the impact of ETS on the lung is obtained by measures of lung function. Many of the studies that have examined the relationship between passive smoking and lung function have been cross-sectional.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Most studies have examined the effect of exposure to parental smoking rather than ETS exposure outside the immediate family. It is assumed that children are less likely than adults to be exposed to occupational irritants. The cumulative burden of respiratory It is often difficult (but not impossible) to measure lung function insults is, therefore, likely to be smaller in children than in adults. in young children and also hard to dissect out the relative contribution of ETS and that of natural variation and the effect of respiratory infections to pulmonary damage.

A majority of the studies (reviewed in Table 11–3) has shown a small decrease (up to 0.5% FEV1 per year) in rate of increase in lung function associated with normal growth in children living with one or more parents who smoke compared with those living with nonsmoking parents (Table 11–3 and Figure 11–3). These differences have usually been statistically significant. Although the mean effect is small, there are individuals in each study who have large decrements in growth of lung function. Some studies have found a dose-response relationship with the number of smokers in the home or the amount smoked (Hasselblad et al., 1981). Ware (1984) shows (see Figure 11–4) a highly significant negative association between maternal smoking level and FEV1 at both the baseline and follow-up examinations. For a child of a mother who smoked one pack of cigarettes per day compared with a child of a nonsmoking mother, the FEV1 was 0.7±0.2% lower at the baseline examination and 0.8±0.2% lower at the follow-up examination 1 year later. This amounts to a 10- to 20-ml difference for a child with an FEV1 between 1.5 and 2.5 L. In most studies, only the maternal effect was statistically significant. This may be because mothers usually spend more time with their young children than fathers.

A study carried out in Shanghai in the People’s Republic of China reported a clear paternal effect. Chen and Li (1986), in a cross-sectional study of 303 boys and 268 girls aged 8–16, found that the number of cigarettes smoked by fathers was linearly related to a decrease in FEV1 and FEF25–75%, the average forced expiratory flow during the middle half of the period of expiration. None of the mothers in this study were smokers; therefore, there was no maternal effect in that population. Differences in father’s smoking status accounted for 0.5% of the variation among individuals in FEV1 and 1.2% of the variation in FEF25–75%.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–3 Effects of Passive Smoking on Pulmonary Function: Selected Cross-sectional Studies Involving Children/Adolescents

Study

Source of Subjects

Subjects

Exposure Assessment

Findings

Comments

Lebowitz et al., 1982

Tucson, Ariz.; stratified cluster random sample of households; 1972–1973

1,655 households;

Anglo-white;

1,252 children <16,

2,516 children >15

Self-administered NHLBI questionnaire from children >15; otherwise from parents

No relationship of FEV1 with parental smoking when household aggregation of body mass taken into account

Less than 15-year-olds assumed to be nonsmokers; concluded familial aggregation important, potential confounder

Schilling et al., 1977

Survey of towns in Connecticut and South Carolina

816 children in 376 families;

607 children <16,

209 children >15

Respiratory Symptom Questionnaire, administered by interviewer

MEF 50% lower in younger children with maternal smoking (p<0.05); FEV1, PEF not significant

Tried to account for active smoking in children

Tager et al., 1979

East Boston, Mass.; random sample in schools; 1975–1977

444 children; ages 5–9 years

NHLBI questionnaire administered by interviewer; if age <10, parent answered

Lower z-scores for FEF25–75% in children with smoking parents

Controlled for family size

Weiss et al., 1980

See Tager et al., 1979

650 children; ages 5–9 years

See Tager et al., 1979

Lower z-scores for FEF25–75% with maternal smoking (p<0.005); FVC, FEV1 not significant

See Tager et al., 1979; also controlled for wheeze in child

Hasselblad et al., 1981

CHESS study, seven cities; survey of schools; 1970–1973

16,689 children; ages 5–13 years

Self-administered by parent (usually mother)

FEV0.75 dose-response relationship with mother’s smoking

No information on child’s smoking; small effect of maternal smoking (0.1% of variance)

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Study

Source of Subjects

Subjects

Exposure Assessment

Findings

Comments

Dodge, 1982

Three towns in Arizona; survey of schools; 1978–1979

558 children; ages 8–10 years

Self-administered by parents

No effect of parental smoking on any parameters, cough (p<0.01) related to parental smoking

Lung function tests not standardized

Ware et al., 1984

Six U.S. cities; different regions; survey of schools; 1974–1979

10,106 children; ages 6–13

Self-administered by parents

FEV1 significantly negative; FVC positive relation to maternal smoking

Multiple logistic regression with gas cooking as other predictor

Chen and Li, 1986

Shanghai, PRC, survey of two schools; 1984

571 children; ages 8–16 years

Self-administered questionnaire by parents

Paternal lifetime smoking related to z-scores of FEV1, MMEF, and FEF62.6–87.5%

No effect of maternal smoking, probably due to low prevalence of female smokers in PRC

Tashkin et al., 1984

Los Angeles County survey of four areas in city; 1973

971 nonsmoking, nonasthmatic children, ages 7–17

Modified NHLBI questionnaire administered by interviewer

Inconsistent effect of maternal smoking in younger boys and older girls

Effect in older girls probably due to unreported smoking by child

Ferris et al., 1985

See Ware et al., 1984

See Ware et al., 1984

See Ware et al., 1984

Significant effect of parental smoking on FEV1

See Ware et al., 1984

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 11–3 Mean percent lung function, by parental smoking, of nonsmoking males and females, ages 10–19, 1962–1965, from Tecumseh, Michigan. Burchfiel et al. (1986).

The most important contributors to variation in lung function among children are size-related factors such as sex, age, and height. These account for about 50–60% of the variation (Comroe et al., 1962).

It is not possible to determine whether ETS is directly causing the decreased lung function observed in children of smoking parents or if an increased infection rate in these children (see below) is responsible for the decrease. The annual small decrease in FEV1, which is related to exposure to ETS, is unlikely to be clinically significant. However, the effect may be important in two respects. First, the existence of statistically significant differences related to parental smoking leads to the conclusion that there are pathophysiologic effects of exposure to ETS in the lungs of the growing child. It may be an in utero effect, an effect on the growing and remodeling lung, or both. Second, it raises the question of whether the child who is adversely affected by parental smoking

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 11–4 Mean of pulmonary function residual (±1 SD) by mothers’ reported daily cigarette smoking, compared with children whose mothers have never smoked. Squares represent the first examination (n=7,112) and triangles represent the second examination (n=6,278). From Ware et al. (1984).

may be at an increased risk for the development of chronic airflow obstruction in adult life. An accelerated decline in lung function could increase the risk of chronic pulmonary disease (Samet et al., 1983).

Studies of Lung Function in Adults

White and Froeb (1980) studied 800 nonsmoking, middle-aged subjects, out of a total population size of 2,100, and found a small statistically significant decrease (8%) in FEF25–75% in both men and women who were nonsmokers exposed to ETS. The reported reduction in FEF25–75% for ETS exposed nonsmokers was almost identical to that of the smokers of 1–10 cigarettes per day. This raises questions about their findings. This study may suffer from problems of selection bias in the allocation of subjects to categories and the absence of any exsmokers (Adlkofer, et al., 1980; Aviado, 1980; Huber, 1980; Lee, 1982).

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

A cross-sectional study from France (Kauffmann et al., 1985) supports the conclusions that exposure to ETS may have an effect on lung function in nonsmoking adults. The French Cooperative Study surveyed more than 7,800 adult residents of seven cities in France in 1975 and found 1,675 were true nonsmokers. In men and women over 40, nonsmokers of either sex who had a spouse who smoked had a significantly lower FEF25–75% than those living with a nonsmoker. These differences were not explained by social class, educational level, air pollution, or family size. Among the women, there was also a significant difference in FEV1 and a dose effect was seen with the amount smoked by their husbands. These differences, only apparent in persons over 40, were small and were uncovered only following detailed examination of the data after the population had been stratified by age.

Two other cross-sectional studies involving adult women have found an effect of exposure to ETS on lung function. In a study of 220 married women aged 25 to 69 years from five U.S. cities, Kauffmann and coworkers (1986) reported that standardized residuals for FEV1 and FEV1/FVC* for the group identified as passive smokers were intermediate between the results of nonsmokers and current smokers. In a study of 163 nonsmoking women living in a rural area of the Netherlands, Brunekreef and coworkers (1985) found that those exposed to ETS tended to have slightly lower mean values for all of the lung function variables measured. These differences reached statistical significance for peak flow and FEF25–75% in the 40- to 60-year-olds. The numbers in each of their groups were small. No information was given on possible childhood exposures to cigarette smoke of the women studied.

Kentner and coworkers (1984), in a study of 1,351 white collar workers (941 men and 410 women) in northern Bavaria, and Comstock et al. (1981), a study that included 1,724 adults residents of Washington County, Maryland, examined the potential effects of ETS. In these studies, information was collected from subjects using questionnaires and the subjects were then classified as never smoked, exsmokers, and current smokers. The Kentner et al. study evaluated home and workplace exposures, whereas the Comstock et al. study evaluated only home exposures. In the Kentner et al. (1984) study, an additional classification was made for other smokers, representing those who were cigar and pipe smokers. These

*  

FVC is the forced vital capacity.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

investigators found no significant reductions in lung function with ETS exposure.

In view of the large number of factors that affect lung function, it is not surprising that it is difficult to document the extent to which a single type of exposure affects lung function. The lungs of adults have been subjected to many environmental exposures and potential insults over a lifetime, making it unlikely that a specific effect could be isolated. The variability in lung function due to differences of the other factors tends to obscure effects of a single variable. In addition, results in adults should be evaluated for possible misclassification of exsmokers or occasional smokers as nonsmokers, as well as possible confounding by occupational exposures to other pollutants or to ETS.

LONGITUDINAL STUDIES OF LUNG FUNCTION IN CHILDREN AND ADULTS

An important unanswered question is whether exposure to ETS affects the way the lungs grow and develop during childhood. Respiratory symptoms, by themselves, may have little clinical significance but would be important if associated with a change in the rate of lung growth and development or the development of pulmonary pathology at older ages.

There is evidence from two cohort studies (Table 11–4) that parental smoking may affect the rate of lung growth during childhood. Tager and coworkers (1983), who have followed 1,156 elementary school children in East Boston, Massachusetts, over a 7-year period, reported that maternal smoking was associated with a reduced rate of annual increase in FEV1 and FEF25–75%. There was a reported 3–5% decrease in expected lung growth over the 7-year period.

Burchfiel and coworkers (1986) examined pulmonary function in 3,482 children in Tecumseh, Michigan. Children 0 to 19 years old were followed for 15 years, during which time questionnaire information was collected from both parents. FEV1 and FVC values were significantly lower by 5% in male nonsmokers 10 to 19 years of age whose parents were current smokers.

The Harvard Air Pollution Respiratory Health Studies (Ferris et al., 1985; Berkey et al., 1986) (Figure 11–5) show a relatively smaller effect than that reported by Tager and coworkers (1983). The Harvard study included 7,834 children between the ages of

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–4 Effects of Passive Smoking on Pulmonary Function: Selected Longitudinal Studies Involving Children/Adolescents

Study

Source of Subjects

Subjects

Exposure Assessment

Findings

Comments

Tager et al., 1983

East Boston, Mass.; random sample in schools; 1975–1981

1,156 children from 404 families; ages 5–9 years

NHLBI questionnaire completed by parents

1-year change in FEV1 reduced in smoking families (p<0.02); 9% decrease over 2 years, 7% decrease over 5 years

Tried to account for child’s smoking; change scores corrected for age, sex, height, first FEV1

Ferris et al., 1985

Six U.S. cities; different regions; survey of schools; 1974–1981

8,380 white children; ages 5–19 years; 6 annual visits

Self-administered by parents

Growth rate in FEV1 reduced with maternal smoking (p<0.02), dose related

Assumed children did not smoke; controlled for city and SES

Berkey et al., 1986

Same as Ferris et al., 1985

7,867 white children ages 6–10 years

Same as Ferris et al., 1985

Maternal and paternal smoking not significantly related to FEV1 growth rate; however, number of cigarettes smoked by mother significant effect (p<0.05)

Corrected for parental education

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

6 and 10 years who were followed over a 5-year period. Children whose mothers smoked one pack of cigarettes per day had FEV1 levels, at age 8, that were 0.81% lower than children with nonsmoking mothers. Growth rates for FEV1 were approximately 0.17% per year lower. For a child aged 8 years with an FEV1 of 1.62 L, this corresponds to a deficit in rate of growth of FEV1 of approximately 3 ml per annum and a deficit of 13 ml by age 8. In contrast to the lower FEV1 seen in children whose mothers smoked, higher levels for FVC were observed in children with smoking mothers compared with children whose mothers did not smoke. For example, average FVC at age 8 for a child whose mother smoked one pack per day, was 0.33% higher than a child with a nonsmoking mother. On the other hand, the growth rate for FVC was 0.17% lower for a child with a smoking mother. This would be equivalent to a 2.8 percent decrease in pulmonary development throughout childhood and implies a decrease in the development of pulmonary function in children of smoking parents.

In view of the effects that climatic conditions can have on housing characteristics, and subsequent ventilation rates, it would be advantageous to conduct longitudinal studies in regions of the United States other than the Northeast. In any future studies, great care should be taken, as it was in the two cohort studies, to account for potential confounding variables in the analyses, such as socioeconomic status and gas cooking. Another aspect that deserves more attention in future studies is the effect on children’s pulmonary function when parents stop smoking.

THE EFFECT OF PASSIVE SMOKING ON RESPIRATORY INFECTIONS

There is now strong evidence that bronchitis, pneumonia, and other lower-respiratory-tract illnesses occur more frequently (at least during the first year of life) in children who have one or more parents who smoke (see Table 11–5). Evidence that this increased frequency of acute respiratory infections continues into later childhood is less convincing, although the evidence from both cross-sectional studies and cohort studies shows such a trend.

Harlap and Davies (1974) followed a cohort of 10,672 infants born in Israel between 1965 and 1968. Admissions to the hospital during the first year of life were recorded. Information about maternal smoking was obtained during the pregnancy only. Infants

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 11–5 Calculation of growth rate and level of ln(FEV1) for an individual child. The residuals in the upper panel, i.e., the difference between observed and predicted ln(FEV1), were regressed on age in the lower panel. From Berkey et al. (1986).

with major congenital malformations and those dying before their first birthday were excluded from the study. For the total population studied, there were 25.4 admissions per 100 babies under 1 year of age. The infants of mothers who smoked had a 27.5% greater hospital admission rate for pneumonia and bronchitis than children of nonsmoking mothers. A dose-response relationship was also found between the amount of maternal smoking and admissions to hospital for pneumonia and bronchitis.

Colley (1974; Leeder et al., 1976) carried out a similar study in London. The study involved a birth cohort of 2,205 infants born between 1963 and 1965. In this group of children, the incidence of pneumonia and bronchitis in the first year of life was associated with the parents’ smoking habits. This was true whether or not the parent has respiratory symptoms. The incidence was lowest for children of nonsmoking parents, highest in families where both

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–5 Childhood Respiratory Tract Illness and Passive Smoking

Study

Source of Subjects

Subjects

Exposure Assessment and Health Information

Findings

Comments

Harlap and Davies, 1974

Birth cohort; West Jerusalem; 1965–1969

All infants in cohort of 10,672 admitted to hospital in Jerusalem

Antenatal interview of mothers

  1. Significantly more admissions for bronchitis or pneumonia, especially in winter, in infants whose mothers smoke

  2. Dose-response for number of cigarettes by mother and excess of bronchitis and pneumonia

Information about mother’s smoking obtained prenatally, not concurrent with child’s admission; no information about father’s smoking obtained

Colley, 1974; Leeder et al., 1976

Birth cohort; Harrow, UK; 1963–1965

2,205 infants

Annual follow-up by health visitors for 5 yr; questionnaire administered by trained health visitor

  1. Incidence of pneumonia and bronchitis in first year associated with parental smoking: incidence lowest with both nonsmokers, highest with both smokers, intermediate with one smoker

  2. Associations inconsistent after 1 yr

  3. In first year of life, ETS exposure doubled risk for pneumonia/bronchitis

Most important determinant of respiratory illness was bronchitis or pneumonia in sibling; analysis not controlled for number of siblings

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Rantakallio, 1978

Birth cohort; Northern Finland; 1966

1,821 exposed, 1,821 unexposed; ages 0–5

Smoking determined in interview during pregnancy

Significant increase in hospitalization for respiratory illness

Only maternal smoking evaluated; categories based on smoking during pregnancy

Said et al., 1978

Cohort; France; 1975–1976

3,920 children; ages 10–20

Self-administered by children

Increase in tonsillectomy and/or adenoidectomy

Smoking by parents may not have coincided or preceded operations

Fergusson et al., 1981

Birth cohort; Christchurch, New Zealand; 1977

1,265 infants

Follow-up by structured interviews with mother at birth, 4 mo, 1, 2, and 3 yr; diaries kept by mothers on child’s history of medical care; check with hospital records

  1. Lower respiratory illness significantly related to mother’s smoking in first year of life, equivocal in second and absent in third

  2. No effect of paternal smoking

  3. Linear dose-response between maternal smoking and incidence of lower respiratory infections

Analysis controlled for maternal age, education, family size, family living conditions

Pedreira, 1985

Birth cohort from practice of four pediatricians in suburb of Washington, D.C.; 1976–1981

1,144 infants followed for 1 yr after birth

Interview with mother at first well baby exam carried out by doctor; all subsequent office visits in first year of life for lower respiratory tract infection

  1. Tracheitis and bronchitis significantly related to maternal smoking

  2. No dose-response relationship

  3. Bronchiolitis not related to parental smoking

No adjustment made for potentially confounding variables; relatively affluent area and low maternal smoking rate (19%)

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Study

Source of Subjects

Subjects

Exposure Assessment and Health Information

Findings

Comments

Speizer et al., 1980

Six U.S. cities; 1974–1979

8,120 children; ages 6–10

Questionnaire completed by parents

Parental smoking and sex of child related to respiratory disease before age 2

Recall bias a potential problem because children aged 6–10 at time of survey

Dutau et al., 1981

Survey in south of France; 1979–1980

892 children; ages 0–6 seen by pediatrician or admitted to hospital

Questionnaire administered to parents

Significant relationship between annual incidence of lower respiratory infections and total number of cigarettes smoked inside home

Pointed out importance of day care centers and nursery schools in increasing rates of lower respiratory infections and difficulty of adjustment for this

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

parents smoked, and intermediate where one parent smoked. This effect was not seen consistently over age 1.

A third birth-cohort study, involving 1,265 children in New Zealand, was reported by Fergusson et al. (1981). They studied the children from birth to age 3 years and found an increase in both bronchitis/pneumonia and lower respiratory illness during the first year in children whose mothers smoked. During the second year, the relationship between maternal smoking and lower respiratory illness was equivocal. The relationship disappeared by the third year. There was no effect observed of paternal smoking on the incidence of lower respiratory illness. Using logistic regression, they found that the rates of lower respiratory illness were related to maternal smoking. For each five cigarettes smoked per day by the mother, there was an increase of 2.5–3.5 lower respiratory “events” per 100 children at risk. Adjustment for maternal age, education, family size, and family living conditions did not change the relationship.

Rantakallio (1978) studied the effect of maternal smoking during pregnancy on morbidity and mortality of children to age 5 based on 12,068 births. Smoking status on the mother was only available from antenatal interview. Perinatal mortality was not higher among children of smokers, however, postneonatal mortality (between 28 days and 5 years) was significantly increased. Children of smokers were hospitalized for respiratory illness significantly more often than children of nonsmokers and the average duration of hospitalization was longer among children of smokers.

Two case-control studies evaluated smaller groups of children hospitalized for respiratory infection and nonhospitalized controls. Pullan and Hay (1982) studied 130 children who were hospitalized with a documented respiratory syncytial virus (RSV) infection in infancy and 111 controls. They found that children hospitalized with documented RSV infections were more likely to have mothers who smoked and that the children had an excess of wheeze and asthma and lower levels of pulmonary function, which persisted to age 10. Sims et al. (1978) also suggested that cigarette smoking by parents during a baby’s first year of life is associated with an increased risk of RSV infections.

Speizer et al. (1980) studied approximately 8,000 children, aged 6–10 years, from six communities in the United States as part of a prospective study of the health effects of air pollution (Harvard Air Pollution Respiratory Health Studies). Parental smoking and

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

sex of the child was associated with respiratory disease before age 2, after other variables had been taken into account. Children from households with gas cooking also gave a history of more frequent respiratory illness before age 2 than children from households with electric cooking.

Dutau et al. (1981) studied 892 children under age 6 in the south of France who were seen by a pediatrician or hospitalized for various reasons. They found a significant correlation between the annual incidence of pulmonary infections and the total number of cigarettes smoked inside the house.

Pedreira et al. (1985) followed all newborns (1,144 infants) seen by a group of pediatricians for a first well-baby examination between 1976 and 1981. They found that tracheitis and bronchitis occurred significantly more frequently (89% and 44%, respectively) in infants whose parents smoked and that maternal smoking imposed greater risks upon the infants than paternal smoking.

One study looked at the frequency of tonsillectomies and/or adenoidectomies in children (Said et al., 1978). They found the frequency was significantly increased among children with smoking parents. However, the smoking status reported for the parent may have been current smoking status, even though the operations had occurred 5 to 15 years previously.

All the studies that have examined the incidence of respiratory illnesses in children under the age of 1 year have shown a positive association between such illnesses and exposure to ETS. The association is very unlikely to have arisen by chance. It may represent a direct association between ETS exposure and disease (a causal explanation) and/or an indirect one (noncausal) arising because children living in homes of smokers are at risk of such diseases for other reasons. Some of the studies have examined the possibility that the association is indirect by allowing for confounding factors—such as social class, parental respiratory illnesses and birthweight—and have concluded that such factors do not explain the results. This argues, therefore, in favor of the causal explanation. Such an explanation is supported by the evidence of a dose-response relationship specific for respiratory disease (Tables 11–6 and 11–7). Also, the mother’s smoking is more likely to affect the infant than the father’s smoking, since the proximity of mother and child is closer during the child’s first year when the effect is more marked and consistent than later in childhood (see Fergusson et al., 1981). This also supports a causal, rather than

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

an indirect, explanation. Therefore, the evidence indicates that smoking in the home does increase the incidence of respiratory illness in infants.

The mechanism for this increase is less certain. It could represent a direct effect of ETS on the respiratory tract of the infant or it could be due to such infants’ being exposed to more parental respiratory infections as a result of their parents’ smoking. Either way, smoking in the home appears to increase the rate of respiratory illness in young children.

WHEN DO PULMONARY EFFECTS OF PASSIVE SMOKING OCCUR?

The weight of evidence is that there are clearly observable effects of ETS on the respiratory system. These effects include an increase in the incidence of acute respiratory infections in early infancy; increased prevalance of cough, sputum production, and wheezing; and a decrease both in lung function measured at an instant in time and in the growth of lung function. The finding of differences in symptom prevalence, respiratory infection rates, and lung function among children exposed and not exposed to ETS is often interpreted as evidence of a chronic effect of ETS on the airways. This is probably true, and it is unlikely that ETS is not an upper- and lower-respiratory-tract irritant in children.

The possibility that there is an effect of maternal smoking in utero as well must be considered. Evidence of an in utero effect in pregnant rats exposed to whole tobacco smoke has been reported by Collins et al. (1985). These investigators reported that pregnant rats exposed to smoke daily from day 5 to day 20 of gestation, when compared with control rats, showed reduced lung volume at term and saccules that were reduced in number and increased in size. The internal surface area of the lung was decreased. The relevance of this study to maternal smoking during pregnancy in humans is not yet clear and deserves further investigation.

Other factors that may alter the time when ETS effects during childhood include the relative immaturity of the immunologic system and the growth and remodeling that are occurring in the immature lung. The infant lung differs in a number of important ways from the adult lung: (1) T-lymphocyte and macrophage function are not fully developed at birth, (2) there is increased susceptibility to infection as a result of comparatively immature

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–6 Experimental Studies of Acute ETS Exposures for Asthmatic Patients

Study

Population

Exposure

Findings

Comments

Shephard et al., 1979a

Fourteen patients from the Gage Research Institute (nine male, five female); mean age 37 years

Room: 14.6 m3

Time: 2 h

Cig.: 7

CO: 24 ppm

Changes in pulmonary function slight; slight decrease in total lung capacity (helium mixing, p<0.02)

Patients on medication; associated chronic bronchitis or pulmonary emphysema in some patients; four patients claimed smoke sensitivity

Dahms et al., 1981

Ten patients from St. Louis Univ. Hospital Allergy Clinic; ages 16–39; 10 controls, ages 24–53

Room: 30 m3

Time: 1 h

Cig.: n.g.

CO: 15–20 ppm

Linear decrease in pulmonary function over time in patients; FEV1 decreased 21.4%; FEF25–75%, 19.2%; FVC, 20%; no change in controls

Patients on medication with restricted use of bronchodilators 4 h prior to test; five patients and five controls complained of irritation to ETS

Knight and Breslin, 1985

Six patients (4M, 2F); mean age 25.5 yr

Details not given

Significant decrease in 3/6 subjects; PC20FEV1 significantly decreased with histamine

No correlation of decreased function with chest symptoms

Wiedemann et al., 1986

Nine patients with near normal lung function; ages 19–30

Room: 4.25 m3

Time: 1 h

Cig.: n.g.

CO: 40–50 ppm

No change in expiratory flow rates; small decrease in bronchial reactivity; PD20FEV1 increased from 0.25 to 0.79 with methylcholine

Patients off medication; six patients with history of reaction to ETS

Abbreviations: n.g.=not given.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–7 Admission Rates in the First Year of Life for Bronchitis and Pneumonia per 100 Infants by Maternal Smoking and Number of Cigarettes Smoked Daily (Number of Infants in Parentheses)

Nonsmokers

 

Never Smoked

Former Smokers

Smokers

(Cigarettes per day)

Total

(8,900)

(786)

1–10

(747)

11–20

(179)

21+

(60)

(10,672)

9.6

7.8

10.8

16.2

31.7

9.8

NOTE: Differences among three categories of smoker p<0.001.

SOURCE: Harlap and Davies (1974).

lung defenses, (3) the internal diameter of the small airways is extremely small and vulnerable to obstruction, and (4) the newborn child has its full complement of airways at birth but only a small proportion of the alveoli. During childhood the airways grow in internal diameter, and the alveoli both multiply and increase in size.

The question of the timing of the effect of ETS on the growing and developing lung remains to be elucidated. If the effect is in utero, the question of how this carries over into infancy and childhood must be addressed. Likewise, the carryover effects of increased incidence of respiratory infections in infancy must be determined. In this regard, there is already some information relating early childhood respiratory illness to subsequent respiratory symptoms and impaired lung function later in childhood (Woolcock et al., 1984; McConnochie, 1985). Evidence is also accumulating that respiratory infections in early childhood are related to an accelerated decline of FEV1 in adult life (Burrows et al., 1977b; Lebowitz and Burrow, 1976). If this is so, and if exposure to ETS increases susceptibility to acute respiratory infections in infancy, ETS may have a carryover effect into adult life.

From the evidence to date, it appears that the effects of exposure to ETS may start in utero by altering the growth pattern of the fetal lung. In infancy, exposure to ETS may increase susceptilibity to viral respiratory infections that in turn may have a

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

carryover effect into later childhood and adult life. Direct effects of ETS as an airway irritant are also likely, although the dose by itself may be insufficient except for the most susceptible individuals to cause symptoms and/or functional impairment. It is unlikely that exposure to ETS can cause much emphysema. As one of the many pulmonary insults, however, ETS may add to the total burden of environmental factors that become sufficient to cause chronic airway or parenchymal disease.

STUDIES OF ACUTE PULMONARY EFFECTS

Several studies have examined acute responses to ETS. Because asthmatics may be hypersensitive to exposures to noxious agents, a number of studies have also searched for acute effects of exposure to ETS among asthmatic populations. Other studies have been conducted on normal healthy adults.

Normal Subjects

Pimm et al. (1978) compared various physiologic responses of nonsmokers to either room air or room air plus machine-generated cigarette smoke. Each smoke exposure consisted of combustion of four cigarettes to produce an extremely polluted room with high levels of carbon monoxide (24 ppm) and particles (greater than 4 mg/m3). Pulmonary function tests, nitrogen washout curves, blood carboxyhemoglobin levels, and heart rates were measured before, during, and after a 2-hour exposure. A few statistically significant differences between smoke and ambient air exposure days were found. The differences were small and were considered by the investigators to be of questionable importance. Subjective complaints were common in this and other acute cigarette smoke exposure studies, particularly eye irritation and cough. CO and suspended particles are thought to be less important than the phenols, aldehydes, and organic acids in producing this symptomatology (Hinds and First, 1975).

Shephard et al., (1979b) utilized a protocol similar to Pimm et al. (1978) but under conditions of intermittent moderate exercise (increasing the respiratory volume per minute 2.5 times). Moderate and heavy ETS exposures were considered, associated with CO concentrations of 20 and 31 ppm, respectively. Neither exercise

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 11–8 Pneumonia and Bronchitis by Parents Smoking in First Year of Follow-up, Annual Incidence per 100 Children (Number of Infants in Parentheses)

Both Nonsmokers

Both or One Exsmokers or Smoking Habits Changed

One Smoker

Both Smokers

All

7.8

(372)

9.2

(675)

11.4

(552)

17.6

(478)

11.5

(2,077)

 

SOURCE: Colley et al. (1974).

nor exposure level significantly influenced symptomatology. Small decrements (3–4%) in FVC, FEV1, Vmax50%, and Vmax25% (the volumes of air expired during the first half of the period of forced expiration or first quarter of the period, respectively) were noted in response to smoke exposures; however, static lung volumes were unaffected. Eye irritation and odor complaints were very common. One subject complained of wheezing and chest tightness, although his pulmonary function was not significantly impaired. Subjective symptom scores were higher overall for the higher smoke exposure (13.8 versus 10.3 points/subject at the lower exposure). A few subjects reported cough, nasal discharge, or stuffiness and throat irritation.

Asthmatic Subjects

A number of studies have examined acute pulmonary responses of asthmatic patients to exposure to ETS (Table 11–8). However, the mechanisms for bronchoconstriction among asthmatics differ. Therefore, the comparison between study populations and between individuals within studies is difficult.

Shephard et al. (1979a) examined asthmatic persons to determine whether their response to ETS exceeded that of normal subjects in a previous study. The subjects (9 men and 5 women; average age, 37 years) were exposed for 2 hours to machine-generated smoke (CO, 24 ppm). None of the patients had current respiratory infections, but some may have had associated chronic bronchitis or pulmonary emphysema. No significant alterations in dynamic lung volumes (FEV1, Vmax50%, and Vmax25%) were detected when the asthmatics’ responses to ambient air and cigarette smoke were

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

compared. A small, but significant, decrease in total lung capacity (TLC) was noted, although preexposure TLC was slightly higher than that on the same exposure day (96.5% and 103.5% relative to ambient air TLC, respectively). The lack of measurable change was interesting in light of a reported history of exacerbation with exposure to ETS by four subjects. Acute symptomatic responses during the experimental study were similar to those seen in the investigators’ previous study of normal individuals; however, more complaints of tightness in the chest (43% of subjects) and wheezing (36%) were made by asthmatic subjects. It was concluded that asthmatics did not have unusual measurable responsiveness to ETS exposure in this study.

The findings of Dahms et al. (1981) contrast with those of Shephard et al. (1979a). The exposure in this study was less intense, i.e., 1 hour at CO levels of 15–20 ppm. The patients were 16 to 39 years old, had mild impairment, and were on medication, except for the restriction that no bronchodilators might be used within 4 hours previous to the test. Five of the patients reported specific complaints when exposed to ETS. When compared with control subjects, asthmatics showed significant pulmonary function changes following 1 hour of smoke exposure. FVC decreased 20% and FEV1 declined 21.4% in the asthmatic subjects. These decreases are very large compared with the other studies. Based on a 0.40% increase in blood carboxyhemoglobin, the environmental CO concentration was calculated to be between 15 and 20 ppm—compared with approximately 24 ppm in the Shephard et al. (1979a) studies. Reasons for the discrepancy between the Dahms and Shephard studies results are not clear, nor do Dahms et al. (1981) cite or discuss the earlier Shephard et al. (1979a) findings.

Knight and Breslin (1985) evaluated six nonsmoking patients. The details of the subject population and exposure conditions were not specified. They measured a mean fall in FEV1 of 11% following exposure to ETS. Using a histamine inhalation test, they found that the provocative concentration (or dose) that produced a 20% fall in FEV1 (PC20FEV1 or PD20FEV1) decreased following exposure to ETS. This indicates an increased bronchial reactivity to histamine. The authors hypothesized that the airways may be primed to react more vigorously to other triggers.

Wiedemann et al. (1986) evaluated nine asthmatic individuals (aged 19 to 30 years) with normal or nearly normal lung function

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

for both lung function and airway reactivity following exposure to ETS. Six patients reported a history of reaction to ETS. These subjects, all of whom were off medication, were exposed for 1 hour (CO between 40 and 50 ppm). Their carboxyhemoglobin levels increased an average of 0.86% (p<0.001), FVC decreased 2% (p<0.01), and FEV1 declined 1% (not statistically significant). Airway reactivity was assessed using a methylcholine challenge test. The PD20FEV1 increased from 0.25±0.22 on the day before exposure to 0.79±1.13 postexposure (p<0.05), indicating a decrease in airway reactivity following exposure. The magnitude of this decrease was small, and the clinical meaning of the change is uncertain.

There are a number of possible reasons for the apparent inconsistency among these studies, not the least of which is small sample sizes. The subjects have not been characterized fully. As noted by the authors, the stability of patients and mechanisms of bronchoconstriction differ among subjects. For instance, patients were included in several of these studies, regardless of whether they were hypersensitive on the methylcholine challenge test. Further, some studies were performed on medicated patients. None of the studies could be performed blind to the presence of ETS. Therefore, the authors could not exclude the possibility that pulmonary function changes could be emotionally related to cigarette smoke exposure, especially in those patients who reported previous histories of adverse response to ETS exposure.

There are several issues that are unresolved by these studies. For instance, what proportion of a clearly defined population of asthmatics do react to ETS? If the patients are selected according to methylcholine or histamine responsiveness, criteria should be given for the extent of responsiveness, since it is a continuum. To address the issue of degrees of sensitivity, the appropriate case-control or cross-over studies, with carefully selected populations, need to be done.

Mechanisms of Response

The mechanisms responsible for eye irritation and rhinitis, as well as possible changes in airway size, are almost entirely unknown. They could represent irritant effects from gases such as oxides of nitrogen, acrolein, ammonia, and other reactive constituents. Lundberg et al. (1983) reported that throat irritation

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

and local edema may be due to vapor-phase components that stimulate substance P release from local capsaicin-sensitive afferent neurons in the airway mucosa. It is also possible that an allergic mechanism could be involved. Several authors have described allergic reactions to cigarette smoke (see, for example, Zussmann, 1970). Cutaneous hypersensitivity to tobacco antigens has been described in clinical settings (Becker et al., 1976). Constituents of tobacco smoke have also been shown to be immunogenic in laboratory animals (Becker et al., 1979; Gleich and Welsh, 1979).

During the last 10 years, Becker and colleagues (1979, 1981; Becker and Dubin, 1977) have isolated a tobacco glycoprotein both from cured tobacco leaves as well as from cigarette smoke condensate. Animals that were previously sensitized to this antigen had both pulmonary and cardiovascular changes when challenged (Levi et al., 1982). However, the role, if any, of this antigen, as well as other antigens that may be present in tobacco smoke, in the pathogenesis of cardiopulmonary disease in active smokers, let alone nonsmokers exposed to ETS, remains controversial.

SUMMARY AND RECOMMENDATIONS

There have been many studies of respiratory effects of exposure to ETS to children. In view of the weight of the scientific evidence that ETS exposure in children increases the frequency of pulmonary symptoms and respiratory infection, it is prudent to eliminate smoking and resultant ETS from the environments of small children.

What Is Known
  1. Children of parents who smoke compared with the children of parents who do not smoke show increased prevalences of respiratory symptoms, usually cough, sputum, and wheezing. The odds ratios from the larger studies, adjusted for the presence of parental symptoms, were 1.2 to 1.8, depending on the symptoms. These findings imply that ETS exposures cause respiratory symptoms in some children.

  2. Estimates of the magnitude of the effect of parental smoking on FEV1 function of children range from zero to approximately 0.5% decrease per year. This small effect is unlikely by itself to be clinically significant. However, it may reflect pathophysiologic

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

effects of exposure to ETS in the lungs of the growing child and, as such, may be a factor in the development of chronic airflow obstruction in later life.

  1. Bronchitis, pneumonia, and other lower-respiratory-tract illnesses occur up to twice as often during the first year of life in children who have one or more parents who smoke than in children of nonsmokers.

What Scientific Information Is Missing
  1. ETS exposure during childhood may influence the development of airway hyperresponsiveness in adult life. Research is needed to address this issue. To evaluate the timing of physiologic changes during development may require animal studies.

  2. Future cross-sectional studies of ETS exposure and lung function in adults need to be designed to control for other factors that may affect lung function.

  3. Little information is available from long-term longitudinal studies of the effect of exposure to ETS by nonsmokers on lung function in either children or adults. Studies need to be carried out in areas with different climates and characteristics of housing over long enough periods of time to assess the effects of changing smoking patterns. Animal studies may also be required to address these longitudinal questions. Intervention studies, in which parents stop smoking in the presence of children, should be done to assess the reversibility of these effects.

  4. The pathophysiologic mechanism of increased susceptibility to viral infections in very young children exposed to ETS has not been clarified.

  5. The extent to which normal and asthmatic adults are affected by short-term exposures to ETS needs to be studied further.

  6. The few studies of the effect of short-term ETS exposure of asthmatic patients and of nonasthmatics are not consistent. This may be because they have not been conducted under adequate control and have examined persons with considerable variability in the severity of asthmatic disease and airway responsiveness. Future studies should carefully define the populations when addressing issues of frequency of reaction to ETS and should be done separately on hyperresponsive and nonhyperresponsive patients when addressing issues of severity of reaction to ETS.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
  1. Studies of other patients with obstructive lung disorders, such as cystic fibrotic and alpha-1-antitrypsin patients, need to be done. Future studies need to identify susceptible subpopulations, if they exist, who are unusually vulnerable to the acute effects of ETS exposure.

  2. There is no consensus on how to deal with data on parental respiratory symptoms. Investigations should report on rates of childhood illness/symptoms using analyses that are both adjusted and unadjusted for parental symptoms.

  3. There is need for information on changes in pulmonary function between the end of the peak growth period and adult life to assess the possible reversibility of effects.

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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

12
Exposure to Environmental Tobacco Smoke and Lung Cancer

The risk of lung cancer in cigarette smokers is directly related to the number of cigarettes smoked. At low-to-average levels of smoking, this relationship is approximately linear and with no apparent threshold, although there are good theoretical reasons to believe that the true dose-response curve should be curvilinear and probably quadratic (Doll and Peto, 1978; Gart and Schneiderman, 1979). Among smokers, an increase in exposure leads to an increase in risk, as long as the additional tobacco smoke, whether through active or passive smoking, reaches the bronchial epithelium. Passive smoking would, therefore, be expected to cause some increase in risk of lung cancer in active smokers, as well as in any other persons in whom the appropriate tissues are exposed.

The studies reviewed in this chapter have attempted to address the questions of whether an increase in risk of lung cancer does occur in nonsmokers exposed to ETS and whether the dose-response relationship is similar to that in smokers. In part, this depends on whether there is a threshold dose of cigarette smoke exposure below which there is no increase in risk. Biological theory and current evidence on low-dose exposure to carcinogens do not provide evidence for such a threshold, and it is generally thought that one is unlikely (Office of Science and Technology Policy, 1985). If there is no threshold, it follows that exposure to tobacco smoke at low concentrations, such as that experienced by nonsmokers exposed to ETS, will cause an increased risk of lung cancer. The risk, of course, will be expected to be very much smaller than that associated with active smoking because of the much lower exposure of the bronchial epithelium to tobacco smoke.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 12–1 Urinary Cotinine (ng/ml) in Nonsmokers According to Number of Reported Hours of Exposure to Other People’s Tobacco Smoke Within the Past 7 Days (Including Day Urine Sample Was Collected)

Duration of Exposure

 

Urinary Cotinine, mean±SDa

Quintile

Limits (h)

No.

1st

0.0–1.5

43

2.8±3.0

2nd

1.5–4.5

47

3.4±2.7

3rd

4.5–8.6

43

5.3±4.3

4th

8.6–20.0

43

14.7±19.5

5th

20.0–80.0

45

29.6±73.7

All

0.0–80.0

221

11.2±35.6

aTrend with increasing exposure was significant (p<0.001).

SOURCE: Wald et al. (1984).

USING BIOLOGICAL MARKERS TO ESTIMATE RISK

Cotinine, a metabolite of nicotine, while of itself not considered a carcinogen, is a useful marker of exposure to tobacco smoke, whether through active or passive smoking. Table 12–1 shows that the mean urinary cotinine concentration increases with the estimated exposure to other people’s tobacco smoke over the past 7 days. Much of these data, collected in the United Kingdom (Wald et al., 1984), showed that nonsmokers had, on average, about 0.4% of the concentration of urinary cotinine found in active smokers. Similar work done in Japan suggested that nonsmokers had relatively high cotinine levels, about one-seventh the levels in average Japanese smokers (Matsukara et al., 1984). The reason for this difference is not known and it needs to be investigated. However, in both countries studies showed increasing urinary cotinine levels in proportion to the estimated increasing ETS exposure.

In most of the epidemiologic studies that assessed the relationship of lung cancer to ETS-exposed nonsmokers, the measure of exposure used was “living with a smoking spouse.” The observed risks of lung cancer for nonsmokers were compared for those living with a smoking spouse and those living with nonsmokers. While it is reasonable to believe that people living with smokers would be more heavily exposed to ETS than people living with nonsmokers,

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

this would seem to be a relatively insensitive measure of exposure. Many people who are exposed to other peoples’ smoke may not always be married to smokers. Even if they are married to smokers, they are likely to be exposed to their spouses’ smoke for only a relatively small proportion of the day. The possibility exists that they may be exposed to other people’s smoke, for instance, at work, or while in other public places.

A study using urinary cotinine levels as a measure of exposure, however, showed that “marriage to a smoker” may identify individuals who are more exposed to tobacco smoke in general, not simply from their spouses (Wald and Ritchie, 1984). Table 12–2 shows that the exposure to other people’s smoke was greater for men married to smokers than for men married to nonsmokers (median hours of reported exposure of 21.1 and 6.5 hours per week, respectively). Of particular relevance for epidemiologic studies is the fact that exposure is greater outside the home as well as within the home. A reasonable interpretation of this fact is that men married to smokers might be more tolerant of other people’s smoke than men married to nonsmokers and are less likely to seek out smoke-free environments outside the home. Similar results, based on questionnaire information, have been reported by others (Friedman et al., 1983).

These results corroborate the use of a spouse’s smoking history as a method of classifying nonsmokers into groups that have different exposure levels to tobacco smoke. Using data from the

TABLE 12–2 Urinary Cotinine Concentration and Number of Reported Hours of Exposure to Other People’s Tobacco Smoke Within the Past 7 Days in Nonsmoking Married Men According to Smoking Habits of Their Wives

Smoking Category of Wife

No. of Men

Urinary Cotinine Concentration, ng/ml

Exposure to Other People’s Smoke in Preceding Week, h

Total

Outside Home

Mean (SE)

Median

Mean (SE)

Median

Mean (SE)

Median

Nonsmoker

101

8.5(1.3)a

5.0

11.0(1.2)b

6.5

10.0(1.2)c

6.0

Smoker

20

25.2(14.8)

9.0

23.2(4.1)

21.1

16.4(3.3)

10.7

NOTE: Differences (nonsmoking wife versus smoking wife):

ap<0.05;

bp<0.001;

cp<0.06 (Wilcoxin rank sum test).

SOURCE: Wald and Ritchie (1984).

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

British study (Table 12–2), the relative urinary cotinine levels in three groups—nonsmoking men married to nonsmoking women, nonsmoking men married to smoking women, and men who were themselves active smokers—were in the ratio of 1:3:215 (actual mean values were 8.5, 25.2, and 1,826 ng/ml, respectively; Wald and Ritchie, 1984, and personal communication). Assuming a similar half-life of cotinine in smokers and nonsmokers, this suggests that exposure to ETS among nonsmokers who are exposed is about 1% (i.e., 25.2/1826) of that of active smokers. Similar results were reported by another United Kingdom study (Jarvis et al., 1984) and one from the United States (Haley et al., 1986). However, the half-life of cotinine in nonsmokers may be roughly 50% longer than in active smokers (Kyerematen et al., 1982; Sepkovic et al., 1986), thereby changing the estimate of relative exposure by up to 50%. Assuming a usage of 20 cigarettes (one pack) per day by active (male) smokers and assuming a linear relationship between number of cigarettes smoked per day and urinary cotinine level, this represents exposure to smoke equivalents of roughly 0.1 to 0.2 cigarettes per day. Others have estimated cigarette equivalent exposures of 0.2 to 1 cigarettes per day (Klosterkötter and Gono, 1976; Hugod et al., 1978; Vutuc, 1984).

Urinary cotinine is at present the best marker of tobacco smoke intake for passive smoking dosimetry because it is highly sensitive and specific for tobacco smoke. Because it can be measured directly in nonsmokers as well as active smokers, it makes it possible to estimate the relative exposures of the two groups (see Chapter 8). With other markers or with other substances in tobacco smoke, this is not currently possible. Estimates must be made of the extent to which these substances are inhaled in mainstream smoke, on the one hand, and released into room air, diluted, and then inhaled by nonsmokers, on the other (Chapter 7). Both of these estimates involve more assumptions in estimating the actual intake.

Whether a urinary cotinine measurement can provide a reasonable basis for computing a first estimate of the risk of lung cancer arising from ETS exposure depends in part on whether the intake of the relevant carcinogens in active and passive smokers is directly proportional to the relevant intake of nicotine, from which cotinine is derived. Our lack of knowledge of which specific smoke components are responsible for causing lung cancer and our

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

present inability to measure their intake directly creates uncertainty. But, as a first approximation, it is reasonable to assume proportionality.

Based on the above dosimetric considerations, the risk of lung cancer from ETS exposure among nonsmokers in the United Kingdom and United States would be small. Assuming linearity in the dose-response relationships, the risk would be about 1% of the excess risk in active smokers. This is equivalent to a relative risk of 1.14 in males, given that the relative risk in average male active smokers is 10 to 15 times greater than in nonsmokers (Hammond, 1966; Doll and Peto, 1978). For ETS-exposed women, the average relative risk may be less. If the cotinine data suggesting greater ETS exposures in Japan are correct, the excess risk in Japan would be greater.

ASSESSING THE RISK FROM EPIDEMIOLOGIC STUDIES OF LUNG CANCER AND EXPOSURE TO ETS

Some of the epidemiologic studies on the possible relationship between ETS exposure of nonsmokers and lung cancer have been discussed elsewhere (Rylander, 1984; Samet, 1985; IARC, 1986). The majority of studies of lung cancer in nonsmokers and ETS exposure classify subjects on the basis of whether the nonsmoker lives with a smoker. Eighteen such studies were identified, and the analysis presented below is based on 13 studies listed in Tables 12–3 and 12–4. The other 5 studies were excluded for the following reasons:

  • Knoth et al. (1983), no reference population was given;

  • Miller (1984), study reported all cancers but did not report on lung cancers separately;

  • Sandler et al. (1985), included very few lung cancer cases;

  • Koo et al. (1984), a more recent analysis of the population was presented in Koo et al. (1986); and

  • Wu et al. (1985), raw data were not presented.

Otherwise our analysis used data from all the studies, thereby reducing the possibility of bias arising out of selecting only some of the studies that met minimal standards.

Table 12–3 gives the characteristics of the 13 studies included in the analysis. The relative risk estimate, together with its 95%

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 12–3 Epidemiologic Studies of Lung Cancer and Exposure to Environmental Tobacco Smoke: Methodological Description of Studies Included in Analysis

Study

Subjects

Exposure Assessmenta

Comments

Type of Interview

Proxy Informants?

Not Married

Exsmokersb

Environments Assessed

Chan and Fung, 1982

Hong Kong, <39:84 cases (out of 189); 139 orthopedic controls

Interview, not blind

No criteria given

No criteria given

No criteria given

Home and workplace

Little information on methods or selection of controls; no adjustments of odds ratio; high cancer rate for South China

Trichopoulos, et al., 1983

Greece: 62 cases (out of 102); 190 orthopedic controls (out of 251)

Interview, not blind

No

“Unexposed”

Exclude if smoked within prior 20 yr; “nonsmoker” if no smoking in 20 yr; “exsmoker” if stopped 5–20 yr before

Spouse (current and former)

Excluded adenocarcinomas and terminal bronchial; original sample similar age and SES, no match on final sample

Correa et al., 1983

Louisiana: 30 (22F, 8M) cases (out of 35) 313 (133F, 180M) hospital controls (diseases not related to smoking)

Interview, blinded

Yes (24% of cases, 11% of controls)

Excluded, include “ever married”

Exclude; used pack yr of husband

Spouse, parents

No adjustment for age, race, or hospital admission; reported odds ratio for older than 40; excluded bronchioalveolar cancer

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Kabat and Wynder, 1984

Multicenter USA: 78 (25M, 53F) cases; 78 (25M, 53F) controls (nontobacco cancers)

Interview, not blind

No

24 cases and 25 controls had no spouse

Only data for 1 yr

Workplace, home

Cases, controls matched for age, sex, race, hospital, and date interviewed

Buffler et al., 1984

Texas: 41 cases (out of 460); 192 population-based controls (out of 482)

Interview

Yes

No criteria given

No criteria given

Spouse

Original population matched age, race, vital status, county; no match on final sample

Garfinkel et al., 1985

NJ, Ohio: 134 cases age 40+; 402 colon cancer

Interview, blinded

Yes

Used data on relative, otherwise “unexposed”

Exclude, exposed

Home, outside home

No dose-response effect; corrected for age, SES, date diagnosed

Pershagen et al., in press

Sweden: 67 registry cases; 347 controls

Mailed

Yes

“Unexposed”

Exclude

Spouse, parents, workplace

Previous interview 1961, 1963 with follow-up 1984; possible interaction with radon; adjusted for occupation, radon, urban; matched for age, vital status

Akiba et al., 1986

Japan: 113 (94F, 19M) cases (out of 164); 380 (270F, 110M) controls (match age, city, vital status)

Interview, not blind

Yes, (90% of cases, 88% of controls)

Excluded

Exclude; spouse “nonsmoker” if no smoking in prior 10 yr

Spouse, parents

Selected from atomic bomb survivors; average age more than 70; no adjustment for radiation dose

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Study

Subjects

Exposure Assessmenta

Comments

Type of Interview

Proxy Informants?

Not Married

Exsmokersb

Environments Assessed

Koo et al., in press

Hong Kong: 86 cases (out of 200); 136 controls (out of 200)

Interview, not blind

No

Used workplace

Exclude; exposed

Workplace, home, parents

Original sample matched for age, SES; no data on match in final sample; data on former spouses

Lee et al., 1986

England: 47 (32F, 15M) cases (out of 1,863); 96 (66F, 30M) controls

Interview

No

Excluded

Exclude

Home, workplace, leisure, daily travel

Follow-up; original sample matched for age, sex; not matched in final sample

Garfinkel et al., 1981

USA survey: 375,000 women (176,739 married) (total 153 cases)

Mailed

Yes

Used relative

Exclude

Spouse

Interviewed 1959, 1960 followed up 1972; adjusted for age, race, education, occupation, disease

Gillis et al., 1984

Scotland: 4,061 married pairs (total 6 cases)

Interview self-report

No

Excluded

Exclude

Spouse

Survey 1972, 1976 with mortality through 1982; age adjusted

Hirayama, 1981, 1984

Japan: 142,857 women age 40+ (91,450 married) (total 200 cases by death certificates)

Interview, blinded

No

Excluded

Exclude; calculated risk separately

Spouse (current)

Interviewed, follow-up 16 yr later; differences in age, occupation

aThese columns include the criteria for certain aspects of exposure assessment treated in the data analyses of the study.

bDisposition if subject is exsmoker; disposition if husband is exsmoker.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

confidence interval, is shown in Figure 12–1 for each of the studies. Also shown in Figure 12–1 is the summary estimate based on the studies combined. The relative risk estimates of lung cancer in nonsmokers in association with ETS exposure, together with the data used for calculating them, are given in Table 12–4. The data given in this table permit readers to combine any subset of the 13 studies which they may wish to consider. A summary estimate of the relative risk for the selected studies can then be calculated using the general method described in Appendix B. The method weights each study by its statistical precision and avoids making inappropriate comparisons across different studies. In the course of examining the data, several such subset analyses were conducted and the results are presented below.

The overall summary relative risk of lung cancer among nonsmokers in association with ETS exposure was 1.34 (95% confidence limits 1.18–1.53). For all women the relative risk was 1.32 (1.16–1.51); for men it was 1.62 (0.99–2.64). The wide confidence limits for men reflect the fact that most of the data were based on nonsmoking women rather than nonsmoking men. For studies conducted in the United States, the relative risk was 1.14 (0.92–1.40). Considering only the largest studies (those with expected number of lung cancer deaths of 20 or more), the relative risk estimate was 1.32 (1.15–1.52). The confidence limits on each of these estimates all include the overall summary estimate of 1.34.

CORRECTIONS TO ESTIMATES FOR SYSTEMATIC ERRORS

Two alternative explanations can be given for the finding of an increased risk in the epidemiologic studies. The finding may represent a direct and causal effect of ETS exposure on lung cancer in nonsmokers; or it could be due in whole or in part to bias, either in the form of systematic errors in the reporting of information or a confounding factor that is associated both with lung cancer and the fact of living with a spouse who smokes. An important question to answer is “What true risk, modified by a reasonable set of bias-producing factors, could lead to the average risk indicated by the epidemiologic studies?” In the following sections two computations are given that estimate how much the true relative risks might be modified as a result of these possible kinds of misclassification.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 12–4 Summary of Epidemiologic Studies of Risk Based on Exposure Assessed by Spouse Smoking Habits, When Available, or Smoking by the Household Cohabitants

Study No.

Study Authors

Location

Sex

Lung Cancers in “Exposed” Group

O–E

Var. of (O–E)

Riska

95% Confidence Limits

 

Obs.

Exp.

Case-Control Studies

1

Chan and Fung, 1982

Hong Kong

F

34

37.7

−3.7

13.01

0.75

0.44

1.30

2

Trichopoulos et al., 1983

Greece

F

38

29.3

8.7

11.70

2.13

1.18

3.78

3

Correa et al., 1983

U.S.A.

F

M

14

2

10.6

1.2

3.4

0.8

4.75

0.98

2.03

2.29

0.83

0.31

5.03

16.50

4

Kabat and Wynder, 1984

U.S.A.

F

M

13

5

13.7

5.0

−0.7

0.0

3.06

1.52

0.79

1.00

0.26

0.20

2.43

4.90

5

Buffler et al., 1984

U.S.A.

F

M

33

5

34.1

6.6

−1.1

−1.6

4.78

2.37

0.80

0.50

0.32

0.14

1.99

1.79

6

Garfinkel et al., 1985

U.S.A.

F

92

89.5

2.5

22.33

1.12

0.74

1.69

7

Pershagen et al., in press

Sweden

F

33

29.6

3.4

13.88

1.28

0.75

2.16

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

8

Akiba et al., 1986

Japan

F

M

73

3

67.4

1.8

5.6

1.2

14.19

1.38

1.48

2.45

0.88

0.46

2.50

13.06

9

Koo et al., in press

Hong Kong

F

51

45.3

5.7

13.19

1.54

0.90

2.64

10

Lee et al., 1986

England

F

M

22

8

21.9

7.3

0.1

0.7

4.71

2.56

1.03

1.30

0.41

0.38

2.47

4.42

Overall for Case-Control Studies

426

401.0

25.0

114.40

1.24

1.04

1.50

Cohort, Prospective Studies

11

Garfinkel, 1981

U.S.A.

F

88

81.8

6.2

30.82

1.18b

0.90

1.54

12

Gillis et al., 1984

Scotland

F

M

6

4

6.0

2.3

0.0

1.7

1.58

1.40

1.00b

3.25b

0.20

0.60

4.91

17.65

13

Hirayama, 1984

Japan

F

M

146

7

129.5

3.3

16.5

3.7

34.83

3.02

1.63

2.25

1.25

1.04

2.11

4.85

Overall for Prospective Studies

251

222.9

28.1

71.65

1.44

1.20

1.72

Overall for All Studies

692

637.7

53.1

186.0

1.34

1.18

1.53

aRisk is given as calculated odds ratios for case-control studies (see Appendix B for calculations) and published relative risk for cohort, prospective studies.

bRatio of age standardized mortality rates.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

FIGURE 12–1 Passive smoking and lung cancer. The relative risk (point estimate and 95% confidence interval) of lung cancer in nonsmokers whose spouses smoke compared with nonsmokers whose spouses do not smoke for each of the studies given in Table 12–4 and the summary estimate based on all the studies combined. The figures for females are shown first for studies based on male and female subjects. STUDIES: 1. Chan and Fung, 1982; 2. Trichopoulos et al., 1983; 3. Correa et al., 1983; 4. Kabat and Wynder, 1984; 5. Buffler et al., 1984; 6. Garfinkel et al., 1985; 7. Pershagen et al., in press; 8. Akiba et al., 1986; 9. Koo et al., in press; 10. Lee et al., 1986; 11. Garfinkel, 1981; 12. Gillis et al., 1984; 13. Hirayama, 1984.

Misclassified Exsmokers and the Tendency for Spouses to Have Similar Smoking Habits

One source of potential bias that would influence the estimates of relative risk is that some people who occasionally smoke or who have smoked in the past may report that they have never smoked. Having smoked, these people are somewhat more likely to develop lung cancer than would true lifelong nonsmokers. Because smokers tend to marry smokers, they are also more likely to have a spouse who smokes or did smoke in the past. Table 12–5 shows

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

that the bias produced by this misreporting could be serious. The arguments presented in this table are an extension of ideas discussed by Lee (Lehnert et al., 1984). From the table it is apparent that for this misclassification to fully account for the observed excess risk, it would be necessary that 8% or more of smokers and exsmokers report themselves as nonsmokers and that their smoking habits and history be identical with those of the self-reported smokers.

The proportion of people who say that they are nonsmokers, but who in fact do smoke, can be estimated using biochemical markers of tobacco smoke absorption. They appear to constitute about 0.5–3%, depending on the population studied and the questionnaire used (Wald et al., 1981; Saloojee et al., 1982). The proportion of people who smoke or have done so in the past but who say they have never smoked has also been estimated in two cohort studies (see Chapter 6). In one of these studies (N.Britten, England, personal communication University of Bristol, England; see Table 6–4), information on smoking was obtained in detail in a longitudinal study. A proportion (4.9%) of the subjects said they had never smoked as much as one cigarette a day in 1982, when in fact they had previously smoked and reported so in previous interviews. These subjects, however, had smoked at a rate of about half that of the current smokers and nearly all of them (93%) had stopped smoking 10 or more years earlier. Similar, or slightly higher, misreporting has been noted for older persons (see Chapter 6). However, older persons are likely to have smoked less and to have quit longer ago.

Table 12–5 is based on the assumption that people who fail to report that they have been smokers have the same risk of lung cancer as the average current smoker. As indicated in Table 6–4, “misclassified smokers” are more likely to have been exsmokers who failed to record the fact that they had smoked at some time in the past or, if they were current (or recent) smokers, they smoked fewer cigarettes per day than the average smoker (Table 6–4). In either event, their spouses’ risk of lung cancer would be lower than for the spouse of a current smoker.

The American Cancer Society’s study of smoking (Hammond, 1966) reported that women who smoked 20–30 cigarettes a day had a 4.9-fold increased risk of lung cancer compared with reported nonsmokers. The British Physicians’ Study (Doll et al., 1980) yielded an estimate of 6.4. Both studies were conducted a number

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 12–5 Illustration of a Bias Likely to Affect Passive Smoking Studies

 

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

of years ago. With the increased duration of smoking in women in recent years, these relative risks also should have increased. The relative risk estimate may be as high as 8.0. To the extent that this may be an overestimate, it will tend to exaggerate the effects of misclassification. The lung cancer relative risk for persons misclassified as nonsmokers is, for the reasons given, probably less than half of that for correctly classified active smokers (relative risk of 4) and probably closer to one-quarter (relative risk of 2).

Applying the same argument illustrated in Table 12–5, the misclassification effect on the relative risk is given in Table 12–6 (N.Wald and K.Nanchahal, personal communication), assuming that the risk of lung cancer of misclassified nonsmokers is half that of current smokers (relative risk=4.0) or one-quarter (relative risk=2.0).

Table 12–6 shows the possible effect of a nonrandom marriage (aggregation) pattern. In this table the extent of nonrandom association is described by an “aggregation” factor. The degree of aggregation is estimated by the ratio of the cross-products in a 2 ×2 table of smoking status of study subjects by spouse smoking status. For the computations in Table 12–6, three aggregation factors are assumed, 2.5, 3.5 and 4.5. The smoker aggregation factor (from epidemiologic studies) appears to be about 3 to 4 (see Table 12–7; Wald et al., personal communication).

The overall effect on an assumed true association between passive smoking and lung cancer, i.e., the “true” relative risk, is shown in Table 12–6 for relative risks ranging from 1.0 (i.e., no association) to 1.25 (i.e., 25% increase in lung cancer risk associated with passive smoking). It is assumed that 35% of women smoke and 50% of men smoke. Also, the effects of the misclassification of between 2% and 10% of smokers as nonsmokers is shown. The most plausible assumptions are a relative risk of 2.0 to 4.0, an aggregation factor of 3 to 4, and a misclassification rate of 2 to 7%. To use Table 12–6, locate the rows and columns that correspond the the above most plausible assumptions. The entries in the body of the table that are approximately 1.34, i.e., the observed overall relative risk, correspond to the set of parametric values that, with plausible assumptions of the bias, would inflate a true relative risk to the observed values. Inspection of the data within the body of Table 12–6 shows that an observed relative risk of 1.34, given the range of assumptions specified in the table, could come about if there were a true relative risk of no less than 1.15. That is,

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 12–6 Estimates of the Observed Relative Risk of Lung Cancer from Studies of Married Nonsmokers; Assuming 35% of Women and 50% of Men in the General Population Are Current Smokers

True Relative Risk

Marriage Aggregation Factorb

Proportion of Misclassified Smokers

Passive Smokers

Misclassified Smokersa

2%

4%

6%

8%

10%

1.00

2.0

2.5

1.01

1.02

1.03

1.04

1.04

 

 

3.5

1.01

1.03

1.04

1.05

1.06

 

4.5

1.02

1.03

1.04

1.06

1.07

4.0

2.5

1.03

1.05

1.08

1.10

1.12

 

3.5

1.04

1.08

1.11

1.14

1.17

 

4.5

1.05

1.09

1.13

1.17

1.20

8.0

2.5

1.06

1.12

1.17

1.21

1.25

 

3.5

1.09

1.17

1.24

1.30

1.36

 

4.5

1.11

1.20

1.29

1.37

1.43

1.05

2.0

2.5

1.06

1.07

1.08

1.08

1.09

 

 

3.5

1.06

1.08

1.09

1.10

1.11

 

4.5

1.07

1.08

1.09

1.11

1.12

4.0

2.5

1.08

1.10

1.13

1.15

1.17

 

3.5

1.09

1.12

1.16

1.19

1.21

 

4.5

1.10

1.14

1.18

1.22

1.25

8.0

2.5

1.11

1.17

1.21

1.26

1.29

 

3.5

1.14

1.21

1.28

1.34

1.40

 

4.5

1.16

1.25

1.33

1.41

1.48

1.10

2.0

2.5

1.11

1.12

1.13

1.13

1.14

 

 

3.5

1.11

1.12

1.14

1.15

1.16

 

4.5

1.12

1.13

1.14

1.16

1.17

4.0

2.5

1.13

1.15

1.17

1.19

1.21

 

3.5

1.14

1.17

1.20

1.23

1.26

 

4.5

1.15

1.19

1.23

1.26

1.30

8.0

2.5

1.16

1.21

1.26

1.30

1.33

 

3.5

1.19

1.26

1.33

1.39

1.44

 

4.5

1.20

1.30

1.38

1.45

1.52

1.15

2.0

2.5

1.16

1.17

1.17

1.18

1.19

 

 

3.5

1.16

1.17

1.18

1.20

1.20

 

4.5

1.17

1.18

1.19

1.21

1.22

4.0

2.5

1.18

1.20

1.22

1.24

1.26

 

3.5

1.19

1.22

1.25

1.28

1.31

 

4.5

1.19

1.24

1.27

1.31

1.34

8.0

2.5

1.21

1.26

1.30

1.34

1.38

 

3.5

1.23

1.31

1.37

1.43

1.48

 

4.5

1.25

1.34

1.43

1.50

1.56

1.20

2.0

2.5

1.21

1.22

1.22

1.23

1.24

 

 

3.5

1.21

1.22

1.23

1.24

1.25

 

4.5

1.21

1.23

1.24

1.25

1.27

4.0

2.5

1.22

1.25

1.27

1.29

1.30

 

3.5

1.24

1.27

1.30

1.33

1.35

 

4.5

1.24

1.28

1.32

1.36

1.39

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

True Relative Risk

Marriage Aggregation Factorb

Proportion of Misclassified Smokers

Passive Smokers

Misclassified Smokersa

2%

4%

6%

8%

10%

 

8.0

2.5

1.26

1.30

1.35

1.38

1.42

 

 

3.5

1.28

1.35

1.42

1.47

1.52

 

 

4.5

1.30

1.39

1.47

1.54

1.61

1.25

2.0

2.5

1.26

1.27

1.27

1.28

1.29

 

 

3.5

1.26

1.27

1.28

1.29

1.30

 

4.5

1.26

1.28

1.29

1.30

1.31

4.0

2.5

1.27

1.30

1.31

1.33

1.35

 

3.5

1.29

1.32

1.35

1.37

1.40

 

4.5

1.29

1.33

1.37

1.40

1.44

8.0

2.5

1.30

1.35

1.39

1.43

1.46

 

3.5

1.33

1.40

1.46

1.52

1.57

 

4.5

1.35

1.44

1.52

1.59

1.65

aSubjects who have smoked either in the past or currently, but claim to be lifelong nonsmokers.

bMarriage aggregation factor defined as ratio of cross-products of 2×2 table of smoking status of study subject by smoking status of spouse.

NOTE: The values inside the boxes indicate those situations that are most plausible, based on other sources of data for parameters, and yield observed relative risks of about 1.34.

TABLE 12–7 Number of Smokers and Nonsmokers According to the Smoking Habits of Their Spouses and the Odds Ratio Indicating the Extent of Such Marriage Aggregationa

Spouse

Females

Males

Smoker

Nonsmoker

Total

Smoker

Nonsmoker

Total

Smoker

53

17

70

20

11

31

Nonsmoker

47

83

130

53

80

133

All

100

100

200

73

91

164

Odds ratio

3.1

 

2.3

 

aBased on interviewing 200 women and 164 men attending a health screening center in London or working in the Civil Service in Newcastle in 1985.

SOURCE: Wald et al., personal communication.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

a true relative risk of 1.15 or more could, by a reasonable set of misclassification biases, be elevated to 1.30 in an epidemiologic study. Stated differently, this implies that reasonable misclassification does not account for the total increased risks reported by the epidemiologic studies, leaving the conclusion that the risk of lung cancer following exposure to other people’s smoke, as judged by whether a nonsmoker has a smoking spouse, would be increased by a minimum of 15%, and most probably increased by 25% (i.e., 1.25). (If the percentage of women smokers were as high as 50%, it would be 1.20.)

The study by Garfinkel et al. (1985) provides data relevant to the misclassification of exsmokers and the tendency for spouses to have similar smoking habits. In this study, subjects were interviewed if the hospital record indicated nonsmoker or made no mention of smoking status. From interviews by the investigators, it was determined that 40% of the women had actually smoked. Among these women who smoked, 81% had husbands who smoked, but only 68% of the women who were in fact nonsmokers had husbands who smoked, yielding an aggregation factor of 2.0.

Effects of Incorrectly Classifying Persons as Unexposed to ETS

In the studies that classify nonsmoker exposure based on whether or not the spouse smokes, some of the “unexposed” nonsmokers, i.e., married to nonsmokers, are likely to be exposed in other settings. For instance, some nonsmokers married to nonsmokers may be exposed to ETS in the workplace. Therefore, some individuals in the baseline, “unexposed,” group for these studies must have been exposed, and hence have risks greater than unity if there is an ETS effect. In the studies, which do ask about exposure to ETS in all environments, there still tends to be misclassification of some nonsmokers as “unexposed,” because there may be a tendency to overlook episodes of exposure.

The data from urinary cotinine studies and the observed relative risks can be used to estimate this effect. The only known source of cotinine in the body is from nicotine, which is virtually exclusively derived from tobacco, with the exception of nicotine chewing gum and nicotine aerosol rods. Therefore, if people who actively use tobacco or nicotine-containing aids to help stop smoking are excluded, cotinine can be used as an objective measure of

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

(recent) exposure to tobacco smoke in nonsmokers. For the following argument, the cotinine in body fluids is compared for the two groups of nonsmokers, those who reported exposure to ETS and those who reported no exposure. Since both groups are nonsmokers, the concern of whether or not the clearance rates for nicotine or nicotine metabolites differ between smokers and nonsmokers is not germane to these estimates.

In the study by Wald and Ritchie (1984), the urinary cotinine levels among nonsmokers exposed to smoking spouses were 3 times those of nonsmokers married to nonsmokers. Using a linear model of risk and assuming that the 3:1 ratio represents a lifetime difference, the implied relative risk of these two groups would be equal to:

(12–1)

where dN is the dose received by nonsmokers who are self-declared “unexposed” and β is the increase in risk per unit dose received (for details, see Appendix C). This equation assumes that the lifetime carcinogenic dose received by nonsmokers who say that they are “exposed” is 3 times that of truly unexposed nonsmokers, assuming cotinine levels to be a proxy for carcinogenic constituents of ETS.

When Equation 12–1 is set equal to the relative risk, one can solve for βdN. In the previous section, it was noted that the true relative risk is likely to be 1.25 and, as argued above, probably lies between 1.15 and 1.35. Consequently, relative risk values of 1.25, 1.15, and 1.35 will be considered. Using these values, βdN will be 0.14 (“ranging” 0.08 to 0.21). Therefore, the relative risk of self-identified “unexposed” nonsmokers compared with truly unexposed nonsmokers is:

(12–2)

which would be 1.14 (“ranging” 1.08 to 1.21). The relative risk of “exposed” nonsmokers compared with a truly unexposed nonsmoker is:

(12–3)

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

which would be 1.42 (“ranging” 1.24 to 1.61). That is, the increased risk of lung cancer as a result of chronic exposure to ETS, corrected for the effect of not identifying a truly unexposed reference group of nonsmokers, is likely to be at least as large as the observed risk.

We can say, therefore, that while the epidemiologic studies show a consistent and, in total, a highly significant association between lung cancer and ETS exposure of nonsmokers, the excess might, in principle, possibly be explained by bias. However, detailed consideration of the nature and extent of the bias shows that given some reasonable assumptions the bias would be insufficient to explain the whole effect. In fact, there are some types of bias that lead to underestimates of the effect. It must be concluded, therefore, that some, if not all, of the effect reported in spouse studies is causal.

OTHER CONSIDERATIONS

Some of the spouse-smoking studies show a dose-response effect with rates increasing with increasing exposure as measured by increasing levels of cigarette consumption by the smoking spouse (see Tables 12–8 and 12–9). A dose-response relationship also suggests a causal explanation, although biases could also operate to affect this estimation. It is possible that a person misclassified as a nonsmoker married to a smoker will have a cigarette consumption that is correlated with that of his or her spouse. A misclassified nonsmoker married to a heavy smoker would, therefore, have a higher risk of lung cancer independent of spouse is smoking than a misclassified nonsmoker married to a light smoker, thus giving the appearance of a dose-response relationship between ETS exposure and lung cancer.

This possible pseudo-dose-response effect arises only as a result of misclassifying smokers as nonsmokers. It is of interest, therefore, that one study has reported an effect of passive smoking in smokers as well as nonsmokers (Akiba et al., 1986). However, it does not appear that adjustment has been made for amount smoked. To the extent that smokers married to smokers may smoke more than the smokers married to nonsmokers, this would bias the results.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 12–8 Risk of Lung Cancer in Nonsmokers According to Cigarette Consumption of Spouse

Authors

Findings

 

Case-Control Studies

Trichopoulos et al., 1983

Exsmoker

1.0

 

1–20 cig. per day

2.4

 

21+ cig. per day

3.4

Garfinkel et al., 1985

1–19 total cig. per day

0.84

 

20–39 total cig. per day

1.08

 

40+ total cig. per day

1.99

 

Cigar/pipe

1.13

Akiba et al., in press

1–19 cig. per day

1.3

 

20–29 cig. per day

1.5

 

30+ cig. per day

2.1

Cohort Studies

Hirayama, 1984

1–19 cig. per day

1.45

 

20+ cig. per day

1.91

Garfinkel, 1981

1–19 cig. per day

1.27a

 

20+ cig. per day

1.10a

aMortality ratios, not relative risks.

NOTE: Relative risk for self-reported unexposed is assumed to be 1.0.

Most of the studies considered the histological type of lung cancer. In general they showed a higher proportion of adenocarcinoma in ETS-exposed nonsmokers than would be expected among active smokers. This is to be expected in view of the fact that the proportion of adenocarcinomas is, in general, higher among nonsmokers. Adding some nonadenocarcinoma-type disease, possibly as a result of ETS exposure, would reduce this proportion. It would nonetheless leave the proportion of adenocarcinomas higher than would be found among lung cancer cases among active smokers. If there were a high relative risk of adenocarcinoma associated with ETS exposure of nonsmokers, it would suggest a real effect, but the published data are insufficient or not presented in a way to allow assessing this issue at this time.

Two studies have examined the risk of lung cancer associated with passive smoking using parental smoking as a measure of exposure instead of spouse smoking (Correa et al., 1983; Sandler et al., 1985b). The first found an association with maternal smoking (RR=1.66, p<0.05) but not with paternal smoking (RR=

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

0.83). The second found no significant association with smoking of either parent.

The bias discussed in connection with spouse-smoking studies is likely to apply also to parental-smoking studies. In addition, these two studies included active smokers as well as recorded nonsmokers, and it is likely that the children of smokers start smoking at a younger age and possibly smoke more than do smoking children of nonsmoking parents (U.S. Public Health Service, 1984). This would also be a source of bias.

TABLE 12–9 Risk of Lung Cancer in Nonsmokers According to Duration of Smoking of Spouse or Other Measures of Exposure Not Shown in Table 12–7

Authors

Findings

 

Case-Control Studies

Trichopoulos et al., 1983

Total no. of cig. (in thousands):

 

1–99

1.3

 

 

 

100–299

2.5

 

 

 

300+

3.0

 

 

Correa et al., 1983

Total pack-years:

Males

Females

 

1–40

 

1.18

 

41+

 

3.52

 

All

 

2.0

2.07

Koo et al., 1984

Total hours:

 

 

 

1–3,499

1.28

 

 

3,500+

1.02

 

Any

1.24

Garfinkel et al., 1985

No. of h/day:

Last 5 yr

Last 25 yr

 

1–2

 

1.59

0.77

3–6

1.39

1.34

>6

0.94

1.14

Pershagen et al., in press

 

 

Kreyburg I

Kreyburg II

 

Less than 15 cig./day or 50 g tobacco/wk for less than 30 yr

1.8

0.8

More than 15 cig./day or 50 g tobacco/wk for more than 30 yr

6.0

2.4

Akiba et al., in press

Pack-days within last 10 yr:

 

 

 

<5,000

1.0

 

5,000–9,999

2.8

 

10,000+

1.8

 

NOTE: Relative risk for self-reported unexposed is assumed to be 1.0.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Pershagen et al. (in press) reported that the relative risk for lung cancer in women married to smokers and living in a home that had measurable radon levels was increased relative to the effects of living with a smoker or living in a home with radon. They suggested that this might represent an interaction between exposure to ETS and radon. Research needs to be done that explores this association further in light of recent reports of high radon concentrations in homes (Code of Federal Regulations, 1985).

SUMMARY AND RECOMMENDATIONS

The weight of evidence derived from epidemiologic studies shows an association between ETS exposure of nonsmokers and lung cancer that, taken as a whole, is unlikely to be due to chance or systematic bias. The observed estimate of increased risk is 34%, largely for spouses of smokers compared with spouses of nonsmokers. One must consider the alternative explanations that this excess either reflects bias inherent in most of the studies or that it represents a causal effect. Misclassification can have contributed to the result to some extent. Computations of the effect of two sources of misclassification were presented. Computations taking into account the possible effects of misclassified exsmokers and the tendency for spouses to have similar smoking habits placed the best estimate of increased risk of lung cancer at about 25% in persons exposed to ETS at a level typical of that experienced by nonsmokers married to smokers compared with those married to nonsmokers. Another computation using information from cotinine levels observed in nonsmokers and taking into account the effect of making comparisons with a reference population that is truly unexposed leads to an estimated increased risk of about one-third when exposed spouses were compared with a truly unexposed population. The finding of such an increased risk is biologically plausible, because nonsmokers inhale other people’s smoke and, as a result, absorb smoke components containing carcinogens.

What Is Known
  1. A summary estimate from epidemiologic studies places the increased risk of lung cancer in nonsmokers married to smokers compared with nonsmokers married to nonsmokers at about 34%.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Assuming linearity at low-to-average doses and a constant proportionality of nicotine and carcinogens in mainstream smoke and ETS, extrapolation from studies of active smokers using relative urinary cotinine places the risk at about 10%.

  1. To some extent, misclassification (bias) may have contributed to the results reported in the epidemiologic literature. However, bias is not likely to account for all of the increased risk. The best estimate, allowing for reasonable misclassification, is that the adjusted risk of lung cancer is increased about 25% (i.e., RR =1.25) in nonsmokers married to smokers compared with nonsmokers married to nonsmokers. When one allows for exposure to nonsmokers who report themselves as unexposed, the adjusted increased risk is at least 24%. The adjusted increased risk to a group of nonsmokers married to nonsmokers is at least 8% (i.e., RR=1.08) compared with truly unexposed subjects. This excess risk may come about from exposures in the workplace or other public places.

What Scientific Information Is Missing
  1. It would be useful to quantify the dose-response relationship between ETS exposure and lung cancer more precisely using biological markers of exposure. Studies should be done that incorporate these biological markers.

  2. Laboratory studies would be important in determining the carcinogenic constituents of ETS and their concentrations in typical daily environments and in facilitating understanding of possible dose-response relationships.

  3. The interaction between ETS and radon exposure, which can increase risk of lung cancer, is worth examining further.

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Akiba, S., H.Kato, and W.J.Blot. Passive smoking and lung cancer among Japanese women. Cancer Res. 46:4804–4807, 1986.


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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

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Jarvis, M.J., H.Tunstall-Pedoe, C.Feyeraband, C.Vesey, and Y.Saloojee. Biochemical markers of smoke absorption and self reported exposure to passive smoking. J. Epidemiol. Comm. Health 38:355–339, 1984.


Kabat, G.C., and E.L.Wynder. Lung cancer in nonsmokers. Cancer 53:1214–1221, 1984.

Klosterkötter, W., and E.Gono. Zum Problem das Passivrauchens. Zentrabl. Bakteriol. Hyg., I. Abt. 1: Orig. B 162:51–69, 1976.

Knoth, A., H.Bohn, and F.Schmidt. Passive smoking as a causal factor of bronchial carcinoma in female nonsmokers. Medizinisch Klin. 78:66–69, 1983.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Koo, L.C., J.H-C.Ho, and N.Lee. An analysis of some risk factors for lung cancer in Hong Kong. Int. J. Cancer 35:149–155, 1985.

Koo, L.C., J.H-C.Ho, J.F.Fraumeni, W.J.Blot, J.Lubin, and B.J.Stone. Measurements of passive smoking and estimates of risk for lung cancer among non-smoking Chinese females. Fourth World Conference on Lung Cancer, Toronto, Canada, Aug. 25–30, in press.

Kyerematen, G.A., M.D.Damiano, B.H.Dvorchik, and E.S.Vesell. Smoking-induced changes in nicotine disposition: Application of a new HPLC assay for nicotine and its metabolites. Clin. Pharmacol. Ther. 32:769–780, 1982.


Lee, P.N., J.Chamberlain, and M.R.Alderson. Relationship of passive smoking to risk of lung cancer and other smoking-associated diseases. Br. J. Cancer 54:97–105, 1986.

Lehnert, G., L.Garfinkel, T.Kirayama, D.Schmälh, K.Überla, E.L.Wynder, and P.Lee. Rountable discussion. Prev. Med. 13:730–746, 1984.


Matsukura, S., T.Taminato, N.Kitano, Y.Seino, H.Hamada, M.Uchihashi, H.Nakajima, and Y.Hirata. Effects of environmental tobacco smoke on urinary cotinine excretion in nonsmokers. N. Engl. J. Med. 311:828–832, 1984.

Miller, G.H. Cancer, passive smoking and nonemployed and employed wives. West. J. Med. 140:632–635, 1984.


Office of Science and Technology Policy. Chemical carcinogens: A review of the science and its associated principles, Feb. 1985, pp. 10371–10442. Fed. Regist. 50:50 (14 Mar. 1985).


Pershagen, G., Z.Hrubec, and C.Svensson. Passive smoking and lung cancer in Swedish women. Am. J. Epidemiol., in press, 1986.


Rylander, R. Environmental tobacco smoke and lung cancer. Eur. J. Respir. Dis. 133(Suppl.):127–133.


Samet, J.M. Relationship between passive exposure to cigarette smoke and cancer, pp. 227–240. In R.B.Gammage, S.V.Kaye, and V.A.Jacobs. Indoor Air and Human Health. Chelsea, Michigan: Lewis Pub., Inc.

Sandler, D.P., R.B.Everson, and A.J.Wilcox. Passive smoking in adulthood and cancer risk. Am. J. Epidemiol. 121:37–48, 1985a.

Sandler, D.P., A.J.Wilcox, and R.B.Everson. Cumulative effects of lifetime passive smoking and cancer risk. Lancet 1:312–315, 1985b.

Saloojee, Y., C.J.Vesey, P.V.Cole, and M.A.H.Russell. Carboxyhemoglobin and plasma thiocyanate: Complementary indicators of smoking behavior? Thorax 37:521–525, 1982.

Sepkovic, D.W., W.J.Haley, and D.Hoffmann. Elimination from the body of tobacco products by smokers and passive smokers. JAMA 256:863, 1986 (letter).


Trichopoulos, D., A.Kalandidi, and L.Sparros. Lung cancer and passive smoking: Conclusion of Greek study. Lancet 2:677–678, 1983.


U.S. Public Health Service. The Health Consequences of Smoking: Chronic Obstructive Lung Disease. A Report of the Surgeon General. DHHS (PHS) Publ. No. 84–50205. Rockville, Maryland: U.S. Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1984. 545 pp.


Vutuc, C. Quantitative aspects of passive smoking and lung cancer. Prev. Med. 13:698–704, 1984.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Wald, N.J. Validation of studies on lung cancer in nonsmokers married to smokes. Lancet 1:1067, 1984 (letter).

Wald, N.J., and C.Ritchie. Validation of studies on lung cancer in nonsmokers married to smokers. Lancet 1:1067, 1984.

Wald, N.J., M.Idle, J.Boreham, and A.Bailey. Carbon monoxide in breath in relation to smoking and carboxyhemoglobin levels. Thorax 36:366–369, 1981.

Wald, N.J., J.Boreham, A.Bailey, C.Ritchie, J.E.Haddow, and G.Knight. Urinary cotinine as marker of breathing other people’s tobacco smoke. Lancet 1:230–231, 1984.

Wu, A.H., B.E.Henderson, M.C.Pike, and M.C.Yu. Smoking and other risk factors for lung cancer in women. J. Natl. Cancer Inst. 74:747–751, 1985.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

13
Cancers Other Than Lung Cancer

The association of lung cancer with exposure to ETS has yielded relative risks of 2 or less for nonsmokers. As cancer of the lung is the cancer most strongly associated with active smoking, weaker effects would be expected for cancers that are less closely related to smoking. The first emphasis in this chapter is on smoking-related cancers, because these might be more plausibly associated with exposure to ETS. However, exposure to ETS occurs at earlier ages than active smoking; thus, there may be effects of ETS exposure on risk for other cancers.

SMOKING-RELATED CANCERS

Active tobacco smoking is an important cause not only of lung cancer, but also of bladder cancer, cancers of the pancreas and renal pelvis, and probably of the nasal sinus and kidneys. Oral, oropharyngeal, hypopharyngeal, laryngeal, and oesophageal cancers are also strongly associated with active smoking, especially in conjunction with the use of alcohol. Primary cigar and pipe smokers face a somewhat lower risk for cancer of the lung than cigarette smokers, but their risk for cancer of the larynx, pharynx, oral cavity, and esophagus is similar if not greater than that of cigarette smokers (U.S. Department of Health and Human Services, 1982). Also, lip cancer is associated with tobacco smoking, as well as pancreatic cancer and, perhaps, renal adenocarcinoma. An increased risk of cervical cancer has been observed in tobacco smokers, but

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 13–1 Studies of Passive Smoking and Cancers Other Than Lung Cancer with Significantly Increased Risks

Author

Study Design

Size (Cases and Population or Controls)

Tumor Outcome Studied

Odds Ratiosa

Hirayama, 1984

Cohort

34/91,540

28/91,540

Brain

Nasal sinus

3.0;6.3;4.3

1.7;2.0;2.6

Miller, 1984

Case-Control

123/537

All sites

1.40

Gillis, 1984

Cohort

Male: 8/827

Female: 43/1917

Sites other than lung

0.5 (M)

1.26 (F)

Sandler et al., 1985a (adulthood exposure)

Case-Control (total) includes smokers

518/518

All sites

Breast

Cervix

Endocrine glands

1.6

1.8

1.8

3.2

Sandler et al., 1985b (lifetime exposure)

Case-control (subset) includes smokers

869/409

All sites

Breast

Cervix

Leukemia and lymphoma

1.4;2.3;2.6

2.0;2.4;3.3

1.6;3.6;3.4

2.5;5.1;6.8

Sandler et al., 1985c (early life exposure)

Case-control (subset) includes smokers

438/470

All sites

Cervix

Hematopoetic tissue

1.5

1.7

2.4

aGiven with increasing dose, if available.

the causal relationship is unclear (International Agency for Research on Cancer, 1986). The risk for these cancers to nonsmokers exposed to ETS has been the subject of a few studies.

Hirayama (1984; see Chapter 12 and Table 13–1) examined cancers of the mouth, pharynx, oesophagus, bladder, pancreas, and cervix. The relative risks were not given, but they were reported to be insignificant. However, a relationship between ETS exposure in nonsmokers and nasal sinus cancer was noted, with rate ratios for the aforementioned exposure categories of 1.7, 2.0, and 2.6, respectively (see Table 13–1).

Sandler et al. (1985a; described in more detail below and in Table 13–1) also did not find a significant odds ratio for any of the smoking-related cancers (including lung cancer), except for cervical cancer (p<0.05). The odds ratios given for these cancers included smokers as well as nonsmokers. Therefore, since the odds ratios were not significant for the combined group, they would

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

not be expected to be significant for the nonsmokers analyzed separately.

CANCERS NOT RELATED TO SMOKING

Hirayama’s (1984) study, based on a cohort of 91,450 nonsmoking Japanese women, suggested an increased mortality from brain tumors among women whose husbands smoked. The rate ratios were 3.0, 6.3, and 4.3 for exposure to husbands smoking 1–14, 15–19, or 20 or more cigarettes per day, as compared with nonsmoking wives of nonsmoking husbands as the reference group. A trend was noted for all cancer sites, but the risk elevation became insignificant when lung, nasal sinus, brain, and breast cancers were excluded. No significant associations were found for cancers of the stomach, colon, rectum, liver, peritoneum, ovary, skin, or bone, or for malignant lymphoma or leukemia.

Sandler et al. (1985a,b,c), reporting on a case-control study from North Carolina, suggested an association of exposure to ETS at different periods during a lifetime with various types of cancer. People with cancer at any site, except basal cell cancer of the skin, were included in this study. The cases were drawn from a hospital-based tumor registry, irrespective of personal histories of smoking. Mailed questionnaires were used for collecting data on exposure, preceded by a telephone call for the control subjects, but not for the cases.

Many of the odds ratios reported in these articles are for the combined group, as briefly reported in Table 13–1. However, some results were reported separately for nonsmoking cases (No.=231) and controls (No.=235). The results discussed below are based on the latter group and thus reflect only 31% of the total eligible patient group.

The overall crude cancer risk among individuals who were ever married to smokers was 2.1 times that of those never married to smokers. Significantly elevated risks (p<0.05) were seen also for cancer of the cervix (odds ratio 2.1) and endocrine glands (odds ratio 4.4) (Sandler et al., 1985a). A nonsignificant odds ratio of 2.0 was obtained for cancer of the breast.

A subset of this study involved subjects who had lived with both natural parents for most of the first 10 years of life and had information on the smoking habits of both parents and spouses.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Overall cancer risks were found to increase steadily and significantly with each additional household member who smoked (Sandler et al., 1985b). The overall risk was significant only for adulthood exposure, either alone or in addition to childhood exposure (Sandler et al., 1985d). This trend appeared both for cancers traditionally associated with smoking and for other sites, with the strongest trend for the smoking-related cancers.

The transplacental and childhood exposures to ETS were specifically studied in another subset of the same study; however, the data were not adjusted for prenatal exposure (Sandler et al., 1985c). There were no significantly increased risks indicated for all sites or for specific cancers. Hematopoietic-tissue-cancer risk had an odds ratio of 2.3 when maternal smoking was considered and 2.4 when paternal smoking was considered (significance not given).

Cancers of hematopoietic tissues have been reported as increased in children whose mothers smoked during and after pregnancy. Neutel and Buck (1971) studied 65 cancer deaths among 89,302 children and found that the rate of leukemia among children of smokers was about twofold that of nonsmokers, but without a dose-response trend. The total number of leukemia cases in this study was 22. Manning and Carroll (1957) studied 187 cases of leukemia, 42 cases of lymphoma, and 93 other cancers among children, but found no effect of mothers’ smoking habits. Neither of these studies separated the effects of in utero exposure from the exposure to ETS after birth.

Two studies have evaluated all sites of cancer as a group. Miller (1984) questioned relatives of women who died between 1972 and 1976 in Erie County, Pennsylvania. He found a nonsignificant increased risk (1.40) of any cancer among women whose husbands smoked. In another study (Gillis et al., 1984), a population in Scotland was followed up 10 years after an initial screening survey for cardiovascular disease. The West of Scotland Cancer Registry was screened for subsequent incidence of cancer. Among the nonsmoking males, there were 8 cases of cancer other than lung cancer. The standardized mortality rates were actually decreased among men whose wives smoked (ratio=0.50). Among the nonsmoking women, there were 43 cases of cancer other than lung cancer, and the ratio of standardized mortality rates was nonsignificantly increased (1.26).

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

In the study by Preston-Martin et al. (1982) of childhood brain tumors, case and control mothers were similar in use of cigarettes during pregnancy. This is in contrast to the finding that significantly more case mothers than control mothers lived in a household with a smoker. The lack of an association of risk with maternal smoking, the association of smoking behavior with other lifestyle-related exposures, and the lack of apparent adjustment for smoking status of the mother make these uncorroborated results difficult to interpret.

INTERPRETATION

Interpretation of these observations regarding a possible association of ETS exposure and cancers with or without previously found associations with smoking is difficult. Only a few studies have been reported, on cancer and ETS exposure other than lung cancer.

The Sandler et al. (1985a,b,c) reports have been criticized for not maintaining matching (Higgins, 1985), for recruiting controls through two separate mechanisms, for conducting interviews in two different ways (telephone interviews or mailed questionnaires), and for insufficient information on other variables known to be risk factors for the various cancers that have been studied in these reports (Burch, 1985; Friedman, 1986; Mantel, 1986). The criticism of the lack of information on other known risk factors is of special concern and is also pertinent to the Hirayama study. For instance, alcohol use, reproductive and sexual histories, and occupational exposures are important risk factors for several of the cancers studied.

Considering increased risks for hematological malignancies, leukemia has not been thought to be smoking-related even though there have been reports of higher leukemia risks among smokers. However, there is a possibility that inhaled lead-210, originating from the tobacco or from radon daughters attaching to ETS, could end up in the skeleton, especially in young individuals who are building up their skeletons, and would result in irradiation of the bone marrow. Such an explanation is presently highly speculative, but increased concentrations of lead-210 have been found in the skeletons of adult smokers (Holtzman and Ilcewicz, 1966; Blanchard, 1967). Adults would be less sensitive to radiation than children. Austin and Cole (1986) suggest that, in addition to the

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

possible influence of radioactive elements, benzene, urethane, and nitrosamines may be contributing factors. All of these chemicals are found in cigarettes and ETS, and they have been shown to be leukemogenic in experimental animals, or in humans.

The findings of increased brain cancer associated with ETS exposure in the Hirayama (1984) study, and possibly in the Preston-Martin et al. (1982) study, are of note. N-nitroso compounds are potent nervous system carcinogens in animals (Magee et al., 1976; Preussman, 1984, 1986).

SUMMARY AND RECOMMENDATIONS

These recent observations on a possible connection between ETS and various forms of cancer have created much discussion and some confusion. The lack of consistency with other data on tumors among children of smoking mothers and the appearance of tumors that are not clearly smoking-related call for further epidemiologic research. Any new studies in this area will, hopefully, have a very careful, rigorous design, so that more definitive evaluation of this possible health hazard from ETS exposure is possible.

What Is Known
  1. There is no consistent evidence at this time of any increased risk of ETS exposure for cancers other than lung cancer.

What Scientific Information Is Missing
  1. Smoking-related cancers other than lung cancer need to be studied with adequate numbers and good exposure data and with consideration of the potential confounding effects from other known risk factors for these cancers.

  2. Some cancers not related to active smoking, especially lymphohematopoietic neoplasms, should be studied in relation to ETS exposure, particularly in childhood. Then the possibility of a etiologic role of inhaled decay products of radon (like bone-seeking lead-210) should be considered.

REFERENCES

Austin, H., and P.Cole. Cigarette smoking and leukemia. J. Chronic Dis. 39:417–421, 1986.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Blanchard, R.L. Concentration of 210Pb and 210Po in human soft tissues. Health Phys. 13:625–632, 1967.

Burch, P.R.J. Lifetime passive smoking and cancer risk. Lancet 1:866, 1985 (letter).


Friedman, G.D. Passive smoking in adulthood and cancer risk. Am. J. Epidemiol. 123:367, 1986 (letter).


Gillis, C.R., D.J.Hole, V.M.Hawthorne, and P.Boyle. The effect of environmental tobacco smoke in two urban communities in the west of Scotland. Eur. J. Respir. Dis. 33:S121–S126, 1984.


Higgins, I. Lifetime passive smoking and cancer risk. Lancet 2:867, 1985.

Hirayama, T. Cancer mortality in nonsmoking women with smoking husbands based on a large scale cohort study in Japan. Prev. Med. 13:680–690, 1984.

Holtzman, R.B., and F.H.Ilcewicz. Lead-210 and polonium-210 in tissues of cigarette smokers. Science 153:1259–1260, 1966.


International Agency for Research on Cancer (IARC) Monograph. Evaluation of Carcinogenic Risk of Chemicals to Humans, Vol. 38, pp. 163–314. Tobacco Smoking. Lyon: IARC, 1986. 421 pp.


Magee, P.N., R.Montesano, and R.Preussman. N-Nitroso compounds and related carcinogens. In: C.E.Searle, Ed. Chemical Carcinogens. Washington, D.C.: ACS Monogr. 173:491–625, 1976.

Manning, M.D., and B.E.Carroll. Some epidemiological aspects of leukemia in children. J. Natl. Cancer Inst. 19:1087–1094, 1957.

Mantel, N. Passive smoking in adulthood and cancer risk. Am. J. Epidemiol. 123:367–368, 1986 (letter).

Miller, G.H. Cancer, passive smoking and nonemployed and employed wives. West. J. Med. 140:632–635, 1984.


Neutel, C.I., and C.Buck. Effect on smoking during pregnancy on the risk of cancer in children. J. Natl. Cancer Inst. 47:59–63, 1971.


Preston-Martin, S., M.C.Yu, B.Benton, and B.E.Henderson. N-nitroso compounds and childhood brain tumors: A case-control study. Cancer Res. 42:5240–5245, 1982.

Preussman, R. Carcinogenic N-nitroso compounds and their environmental significance. Naturwissenchaften 71:25–30, 1984.

Preussman, R., and B.W.Stewart. Carcinogenic N-nitroso compounds and related carcinogens. In C.E.Searle, Ed. Chemical Carcinogens. 2nd Ed. Washington, D.C.: American Chemical Society 182:643–828, 1984.


Sandler, D.P., R.B.Everson, and A.J.Wilcox. Passive smoking in adulthood and cancer risk. Am. J Epidemiol 121:37–48, 1985a.

Sandler, D.P., A.J.Wilcox, and R.B.Everson. Cumulative effects of lifetime passive smoking on cancer risk. Lancet 1:312–315, 1985b.

Sandler, D.P., R.B.Everson, A.J.Wilcox, and J.P.Browder. Cancer risk in adulthood from early life exposure to parents’ smoking. Am. J. Public Health 75:487–492, 1985c.

Sandler, D.P., R.B.Everson, and A.J.Wilcox. The authors reply. Am. J. Epidemiol. 123:369–370, 1986 (letter).


U.S. Department of Health and Human Services. The Consequence of Smoking. Cancer. A Report of the Surgeon General. DHSS (PHS) Publ. No. 82–50179. Rockville, Maryland: U.S. Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1982. 302 pp.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

14
Cardiovascular System

The effects of active smoking on exercise tolerance, blood pressure, and the risk of developing cardiovascular disease have been reviewed elsehwere (U.S. Public Health Service, 1983). This chapter discusses studies of ETS exposure to nonsmokers and subsequent possible cardiovascular effects. The constituents that are thought to have the greatest effect on the cardiovascular system are carbon monoxide (CO) and nicotine. The possibility exists that the mechanisms, as well as the magnitude of the effects, for acute and chronic cardiovascular effects may be different for exposure to whole smoke and to ETS.

ACUTE CARDIOVASCULAR EFFECTS OF ENVIRONMENTAL TOBACCO SMOKE EXPOSURE

Administration of nicotine at level similar to those induced by active cigarette smoking is shortly followed by increases in heart rate and blood pressure (U.S. Public Health Service, 1983). Platelet aggregation has been shown to be increased in in vitro studies. CO rapidly combines with hemoglobin in the blood to form carboxyhemoglobin (COHb), thereby leading to some degree of tissue hypoxia. CO combines with muscle myoglobin, which is followed by some muscle hypoxia. The level of exposure of the nonsmoker to these cigarette smoke constituents, however, is less than that of the active smoker, and the effects are expected to be less.

Table 14–1 reviews some of the increases in COHb levels as seen in both experimental and observational studies. The levels of

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 14–1 Carbon Monoxide and Carboxyhemoglobin Levels in Nonsmoking Individuals

Experimental Studies (Controlled Chambers)

Study

No. of Cigarettes/h/10m3

No. of Subjects

CO, ppma

Carboxyhemoglobin

Control

Change

Anderson and Dalhamm, 1973

3.1

4.5

0.3

0

Dahms et al., 1981

10

15–20

0.6

+0.4

Harke, 1970

3.9

7

30

0.9

+1.2

Huch et al., 1980

2.3

12

1.3

+0.5

Hugod et al., 1978

2.5

10

20

0.7

+0.9

Pimm et al., 1978

2.4

10

24

0.5

+0.3

 

2.4

10

24

0.7

+0.2

Polak, 1977

6.7

15

23

2.0

+0.3

Russell et al., 1973

15.1

12

38

1.6

+1.0

Seppänen and Uusitalo, 1977

3.8

28

16

1.6

+0.4

Srch, 1967

50

90

2

+3

Observational Studies

Study

Subjects/Exposure

No. of Subjects

Nonexposed: Exposed

Carboxyhemoglobin, %

CO Expired, ppm

Foliart et al., 1982

Flight attendants/8 h

6

1.0:0.7

 

Jarvis et al., 1983

Normal/public house for 2 h

7

 

4.7:10.6

Lightfoot, 1972

Normal/submarine

 

—:1.0

 

Wald et al., 1981

Participants in health screening program

6,641

 

 

Jarvis et al., 1984

Normal/self report

10

0.9:0.8

5.7:5.5

Seppänen and Uusitalo, 1977

Restaurant for 5 h (CO:2.5–15 ppm)

47

2.1:2.1

 

 

Office for 8 h (CO:2.5 ppm)

15

2.3:2.3

 

aCarbon monoxide (CO) measured as a proxy to indicate the concentration of ETS in the chamber.

COHb commonly observed in active smokers are higher, ranging between 4 to 6 percent, rarely greater than 12 percent (Schievelbein and Richter, 1984). Because exposure of the nonsmoker is qualitatively different than exposure to smokers, a simple scaling down of effects observed in active smokers does not appear to be fully appropriate. Therefore, the effects of exposure to nicotine,

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 14–2 Resting Acute Cardiovascular Effects in Nondiseased Humans of Exposure to Environmental Tobacco Smoke

Authors

Study Population

Conditions

Results

Measured Variable

Before

After

Luguette et al., 1970

40 children

Room: 9 m3

No. cig.: 6

Time: 15 min

Heart rate

Blood pressure

89

116/67

97

120/72

Harke and Bleichert, 1972

10

Room: n.g.

No. cig.: 150

Time: 20 min

Heart rate

Blood pressure

Skin temperature (−°C/min)

72±8

123/84

0

74±12

121/84

0.0273

Rummel et al., 1975

56

Room: 30 m3

No. cig.: 6–8

Time: 20 min

Heart rate

Blood pressure

72±10

117/71

71±11

117/71

Hurshman et al., 1978

8

Room: n.g.

No. cig.: 2–6

Time: 10 min

Heart rate

Blood pressure

73

107/67

79

114/68

Pimm et al., 1978

10 males

10 females

Age=22.3

Room: 14.6 m3

No. cig.: 7

Time: 2 h

Heart rate

84(F)

77(M)

80(F)

70(M)

CO, or ETS need to be separately studied. In addition, consideration needs to be given to persons of different sensitivity or vulnerability.

Healthy Subjects

Table 14–2 lists studies that report on the consequences of exposure of nondiseased individuals to ETS for periods up to 2 hours under experimental, resting conditions. There were no significant changes noted in heart rate or blood pressure in school-aged children or in adult men and women.

Two studies evaluated the physiologic responses to exercise with and without exposure to ETS. In the first, Pimm et al. (1978) (see also Table 14–2) had subjects perform a 7-minute progressive exercise test on an electronic bicycle ergometer. During exercise, the women had higher heart rates after exposure to ETS when compared with control conditions (differences of 6.3 beats per minute at 2 minutes and 4.5 beats per minute at 7 minutes, p<0.01). The recovery heart rates were not significantly different. The men, however, showed little difference between test and

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

control conditions (differences of −0.1 beats per minute at 2 minutes and 1.5 beats per minute at 7 minutes). In the second study, Sheppard and colleagues (1979b) tested 11 males and 12 females at two different levels of ETS (i.e., 7 cigarettes over 2 hours, CO= 20 ppm, or 9 cigarettes over 2 hours, CO=31 ppm). Under both exposure conditions, contrary to expectations, both the increment in heart rate and average heart rate were less with ETS exposure.

In summary, for normal young adult males and females, no significant acute effects of ETS exposure on heart rate or blood pressure have been reported, either under resting or aerobic conditions.

There have been several studies of exposure of normal subjects under resting and aerobic conditions to low levels of CO but higher than those found with ETS exposure (reviewed in Environmental Protection Agency, 1984). No significant effects were found in healthy, exercising subjects during short-term exposure (e.g., Drinkwater et al., 1974; Raven et al., 1974a,b; DeLucia et al., 1983).

Angina Patients

Angina pectoris is a symptom complex involving feelings of pressure and pain in the chest, which is produced by mild exercise or excitement, presumably because of insufficient oxygen supply to the heart muscle. Under conditions of ETS exposure, the CO levels are increased, thus possibly placing individuals with angina at an increased risk of recurrent episodes.

Anderson et al. (1973) and Aronow and his colleagues, in a series of experiments (1973, 1974, 1978, 1981) (Table 14–3), studied angina patients under aerobic conditions with exposures to low levels of CO and to ETS. Ten patients with diagnosed angina pectoris, of whom two were smokers and eight exsmokers, were tested (Aronow et al., 1978). Significant increases in systolic blood pressure and heart rate, and decreases in time to onset of angina, were noted when the subjects were exposed to smoke in either ventilated or unventilated rooms (the actual levels of CO under these conditions were not noted). There were some subjective elements in the evaluation of these patients, and the physician conducting these tests was aware of the test conditions, i.e., smoking or not and ventilated or not. Consequently, the findings of this study, in

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

TABLE 14–3 Acute Cardiovascular Effects of Exposure to CO or Environmental Tobacco Smoke by Nonsmoking Angina Patients

Study

Design

No.

Conditions

Results

Anderson et al., 1973

Double-blind, Cross-over

10a

CO: 50 ppm or 100 ppm

Time: 4 h for 5 days

Mean duration before onset of pain shortened (50 ppm and 100 ppm); duration of pain longer (100 ppm only)

Aronow and Isbell, 1973

Double blind, Cross-over

10b

CO: 50 ppm

Time: 2 h

Times until onset decreased; decrease in BP and heart rate at angina

Aronow, 1978

Not blinded

10c

No. cig.: 15

Time: 2 h

Room: 30.28 m3

Earlier onset of angina; increased systolic BP and heart rate at angina

Aronow et al., 1979

Double-blind, Cross-over

20

COHb: 4%

Impairment in visualization test

Aronow, 1981

Double-blind, Cross-over

15

CO: 50 ppm

Time: 1 h

COHb: 2%

Time until onset decreased; decreased systolic BP and heart rate at angina

aIncludes five smokers and five nonsmokers.

bNot current smokers.

cIncludes eight exsmokers and two current smokers.

the absence of a true double-blind approach, require verification by other research workers.

The effects of rapid angina onset would be expected to be due to increased COHb levels. Anderson et al. (1973) and Aronow et al. (1973, 1981) exposed angina patients to low levels of CO. In these studies, angina pain appeared when COHb levels of patients were measured at 2 and 4%. These studies have been reviewed extensively as part of the Environmental Protection Agency’s (1984) activity in establishing air quality criteria for carbon monoxide. The review group found that the results were suggestive for effects at COHb levels above 3%, based on animal and theoretical models. There is concern that elevated levels of CO exposure may affect the electrical stability of the heart in previously compromised heart muscle, thus possibly leading to sudden death. The levels reviewed in Table 14–1 are close to the 3% level. This suggests that there is reason to be concerned with possible effects of exposure. However, a firm quantitative estimate of the risk to nonsmoking persons, under conditions of ETS exposure, cannot be made from the literature at this time.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

CARDIOVASCULAR DISEASE MORBIDITY AND MORTALITY

Possible pathophysiologic mechanisms for the atherogenic influence of cigarette smoking were reviewed in the 1983 Report of the Surgeon General. Experimental studies of subcutaneous or intravenous administration of nicotine in rabbits (Schievelbein et al., 1970; Schievelbein and Richter, 1984) and monkeys (Liu et al., 1979) have demonstrated that long-term exposure leads to arteriosclerotic lesions. Exposure to carbon monoxide also leads to atherosclerosis in rabbits, pigeons, and other animals (Astrup and Kjeldsen, 1979). Studies of whole tobacco smoke indicate that total serum cholesterol concentrations are increased and the ratios of the various lipoprotein fractions are changed (McGill, 1979). The contribution of whole tobacco smoke to modifying the lipoprotein fractions is not conclusive. However, there have not been experimental studies of the effects of ETS exposure or administration of ETS extracts.

Smoking and Cardiovascular Disease

The effects of active smoking on human health are summarized in the Surgeon General’s report The Health Consequences of Smoking: Cardiovascular Disease (U.S. Public Health Service, 1983). The principal conclusions are that cigarette smokers experience a 70% greater coronary heart disease (CHD) death rate than do nonsmokers and that smokers of more than two packs per day have 2 to 3 times greater CHD death rates than nonsmokers. The incidence of CHD in smokers is twice that of nonsmokers. Heavy smokers (more than two packs per day) have an almost fourfold increase. The relative risk in smokers for sudden death is greater than that for all deaths from CHD. The relative risk in young smokers is greater than that in older smokers. The relative risk for young women smokers, especially those who use oral contraceptives, is greater than 5.

The excess relative risk associated with smoking declines rapidly upon cessation of smoking, in some studies as much as 50% in 1 year. For exsmokers who previously smoked more than one pack per day, the residual excess risk also declines, but never completely disappears. The decline in risk on cessation of smoking cannot be explained by differences in known cardiac risk factors

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

between individuals who continue smoking and individuals who have quit. Smokers who have used only pipes or cigars did not appear to experience a substantially greater CHD risk than nonsmokers.

The rapid decline in risk associated with smoking cessation and the greater relative risk for sudden death suggest that active smoking can precipitate cardiac events in individuals with preexisting coronary artery disease. Autopsy evidence of increased arteriosclerosis in smokers, coupled with the fact that risk of exsmokers never returns to the levels found in nonsmokers, suggests that cigarette smoking is also implicated in the development of arteriosclerotic cardiovascular disease (ASCVD). The mechanism by which cigarette smoke may lead to the development of chronic ASCVD, sudden death, or acute myocardial infarction is unknown. There appears, however, to be no threshold in the number of cigarettes smoked below which there is no increase in risk.

Data on uptake of cotinine by nonsmokers exposed to ETS indicate that the exposure in nonsmokers chronically exposed to ETS is approximately 1% that of an active smoker (who smokes one pack per day) (see Chapters 8 and 12). If the excess relative risk for CHD mortality or morbidity is a linear, nonthreshold function of dose and, further, if the excess risk of CHD in a one-pack-a-day smoker is twofold, then the relative risk from CHD in nonsmokers exposed to ETS (compared to true nonsmokers) would be approximately 1.02. Such relative risks would be difficult to detect or estimate reliably in nonexperimental studies. Such small increases in relative risk are of the same order of magnitude as what might arise from expected residual confounding due to unmeasured covariates. Nonetheless, because of the large number of cardiovascular deaths each year, these possibilities deserve close attention and further study that could lead to firmer estimates of excess risk.

Studies of Environmental Tobacco Smoke Exposure and Mortality from Cardiovascular Disease

Garland et al. (1985) have reported that, in a prospective study of the effect of passive smoking, the age-adjusted rates of cardiac disease deaths in nonsmoking women whose husbands were former or current smokers were significantly elevated. It is

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

not certain, however, that the report is correct, because of a possible miscalculation or misuse of the Mantel-Haenszel statistic and some other methodologic problems. Data for the wives of former smokers were grouped with wives of current smokers. If this grouping were made after examining the data, which indicated that the risk was greater among the women whose husbands were former smokers, then this combination would be suspect. The p values based on the Mantel-Haenszel test may be inappropriate in view of the small sample sizes. The authors employ the Cox Proportional Hazard analysis to control for other factors associated with cardiovascular risk, such as age, blood pressure, cholesterol, obesity, years of marriage, etc. They report a relative risk for women married to current or former smokers compared with women married to never-smokers of 2.7 (Garland, 1985, corrected from an earlier report). The p value (<0.10) associated with this estimate is based on the asymptotic assumptions that are implicit in likelihood-based inference from the Cox model. These assumptions may not hold for small sample sizes. In summary, because of the small sample sizes, the significance calculations arising from this study must be looked upon as approximations.

Gillis et al. (1984) reported the results of a follow-up study of residents of two urban communities in Scotland. Nonsmokers exposed to cigarette smoke in their homes had a slightly higher rate of myocardial infarction than those unexposed. The sample size was small, so that few of the results were statistically significant, and other risk factors for myocardial infarction were not controlled for.

Hirayama (1984) reported the results of a 15-year prospective study of nonsmoking Japanese women classified at start of followup by the smoking status of their husbands. A relative risk from ischemic heart disease of 1.3 was found for nonsmoking women whose husbands smoked more than 19 cigarettes per day compared with nonsmoking women whose husbands did not smoke. A Mantel-Haenszel test for a linear trend was significant at the p<0.01 level.

It is unlikely that Hirayama’s results can be explained by chance. The potential biases inherent in this study (see Chapter 12) limit the weight that can be placed on these results. The observed relative risk of 1.3 is at the upper limit of the expectations derived from extrapolations from active smokers, unless the uptake of the active component of cigarette smoke to which

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

passive smokers are exposed is of the order of 10% of that of active smokers. Matsukura et al. (1984) have suggested that such high levels of uptake in passive smokers may be seen in Japan. If there were independent evidence that nonsmokers exposed to other people’s cigarette smoke do not differ on known risk factors for CHD from unexposed nonsmokers, more reliance could be placed on Hirayama’s results.

Svendsen et al. (1985) reported on the effect of cigarette smoke exposure to smoking wives among men participating in the Multiple Risk Factor Intervention Trial (MRFIT). MRFIT, which began in the mid-1970s, was a randomized primary prevention trial designed to test the effect of a multifactor intervention program on mortality from coronary heart disease in men with previous cardiac episodes. The men were chosen for participation if they had at least two of three risk factors for heart disease, including smoking, high cholesterol levels, or high blood pressure. The results reported by Svendsen et al. (1985), based on the group of men who never smoked but whose wives may or may not have been smokers, indicate no difference between exposed (i.e., smoking wives) and nonexposed (i.e., nonsmoking wives) of nonsmoking men for blood pressure or serum cholesterol. The MRFIT study demonstrates a roughly twofold increase in the risk of CHD mortality and morbidity among nonsmokers exposed to ETS. The sample size was small, and the results were not statistically significant. Adjustment for other risk factors for CHD did not change the estimates of effect.

SUMMARY AND RECOMMENDATIONS

What Is Known
  1. No statistically significant effects of ETS exposure on heart rate or blood pressure were found in healthy men, women, and school-aged children during resting conditions. During exercise there is no difference in the cardiovascular changes for men and women between conditions of exposure to ETS and control conditions.

  2. With respect to chronic cardiovascular morbidity and mortality, although biologically plausible, there is no evidence of statistically significant effects due to ETS exposure, apart from the study by Hirayama in Japan.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×
What Scientific Information Is Missing
  1. Experimental studies with animal models need to be performed with ETS to determine whether the cardiovascular changes seen following exposure to whole smoke also occur following exposure to ETS.

  2. Existing studies have not provided evidence of serious harm in people with heart disease. With regard to angina onset, the findings are uncertain and need to be repeated.

REFERENCES

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Anderson, E.W., R.J.Andelman, J.M.Strauch, N.J.Fortuin, and J.H. Knelson. Effect of low-level carbon monoxide exposure on onset and duration of angina pectoris. Ann. Intern. Med. 79:46–50, 1973.

Aronow, W.S. Effect of passive smoking on angina pectoris. N. Engl. J. Med. 299:21–24, 1978.

Aronow, W.S. Aggravation of angina pectoris by two percent carboxyhemoglobin. Am. Heart. J. 101:154–157, 1981.

Aronow, W.S., and M.W.Isbell. Carbon monoxide effect on exercise-induced angina pectoris. Ann. Intern. Med. 79:392–395, 1973.

Aronow, W.S., J.Cassidy, J.S.Vangrow, H.March, J.C.Kern, J.R.Goldsmith, M.Khemka, J.Pagano and M.Vawter. Effect of cigarette smosking and breathing carbon monoxide on cardiovascular hemodynamics on anginal patients. Circulation 50:340–347, 1974.

Aronow, W.S., R.Charter, and G.Seacat. Effect of 4% carboxyhemoglobin on human performance in cardiac patients. Prev. Med. 8:562–566, 1979.

Astrup, P., and K.Kjeldsen. Model studies linking carbon monoxide and/or nicotine to arteriosclerosis and cardiovascular disease. Prev. Med. 8:295–302, 1979.


Bridge, D.P., and M.Corn. Contribution to the assessment of nonsmokers to air pollution from cigarette and cigar smoke in occupied spaces. Environ. Res. 5:192–209, 1972.


Dahms, T.E. J.F.Bolin, and R.G.Slavin. Passive smoking: Effects on bronchial asthma. Chest 80:530–534, 1981.

DeLucia, A.J., J.H.Whitaker, and L.R.Byrant. Effects of combined exposure to ozone and carbon monoxide (CO) in humans, pp. 145–159. In S.D.Lee, M.G.Mustafa, and M.A.Mehlman, Eds. Advances in Modern Environmental Toxicology, Vol. V. International Symposium on the Biomedical Effects of Ozone and Related Photochemical Oxidants. Princeton, New Jersey: Princeton Scientific Publishers, 1983.

Drinkwater, B.L., P.B.Raven, S.M.Horvath, J.A.Gliner, R.O.Ruhling, and N.W.Bolduan, and S.Taguchi. Air pollution, exercise and heat stress. Arch. Environ. Health 28:277–282, 1974.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Environmental Protection Agency. Revised Evaluation of Health Effects Associated with Carbon Monoxide Exposure: An Addendum to the 1979 EPA Air Quality Criteria Document for Carbon Monoxide. Publ. No. EPA-600/8–83–033F. Washington, D.C.: U.S. Government Printing Office, 1984.


Foliart, D., N.L.Benowitz, and C.E.Becker. Passive absorption of nicotine in airline flight attendants. N. Engl. J. Med. 308:1105, 1982.


Garland, C., E.Barrett-Connor, L.Suarez, M.Criqui, and D.Wingard. Effects of passive smoking on ischemic heart disease mortality of nonsmokers. Am. J. Epidemiol. 121:645–650, 1985.

Gillis, C.R., D.J.Hole, V.M.Hawthorne, and P.Boyle. The effect of environmental tobacco smoke in two urban communities in the west of Scotland. Eur. J. Respir. Dis. 65(S133):121–126, 1984.


Harke, H.-P. Zum Problem des “Passiv-Rauchens.” Münch Med Wochenschr. 51:2328–2334, 1970.

Harke, H.-P., and A.Bleichert. Zum Problem des Passivrauchens. Int. Arch. Arbeitsmed. 29:312–322, 1972.

Hirayama, T. Lung cancer in Japan: Effects of nutrition and passive smoking, pp. 175–195. In M.Mizell and P.Correa Eds. Lung Cancer: Causes and Prevention. New York: Verlag Chemie, International, Inc., 1984.

Huch, R., J.Danko, L.Spatling, and R.Huch. Risks the passive smoker runs. Lancet 2:1376, 1980.

Hugod, C., L.H.Hawkins, and P. Astrup. Exposure of passive smokers to tobacco smoke constituents. Int. Arch. Occup. Environ. Health 42:21–29, 1978.

Hurshman, L.G., B.S.Brown, and R.G.Guyton. The implications of sidestream cigarette smoke for cardiovascular health. J. Environ. Health 41:145–149, 1978.


Jarvis, M.J., M.A.H.Russell, and C.Feyerabend. Absorption of nicotine and carbon monoxide from passive smoking under natural conditions of exposure. Thorax 38:829–833, 1983.


Lawther, P.J., and B.T.Commins. Cigarette smoking and exposure to carbon monoxide. Ann. N.Y. Acad. Sci. 174:135–147, 1970.

Lightfoot, N.F. Chronic carbon monoxide exposure. Proc. R. Soc. Med. 65:798–799, 1972.

Liu, L.B., C.B.Taylor, S.K.Peng, and B.Mikkelson. Experimental arteriosclerosis in Rhesus monkeys induced by multiple risk factors: Cholesterol, vitamin D and nicotine. Arterial Wall 5:25–38, 1979.

Luquette, A.J., C.W.Landess, and D.J.Merki. Some immediate effects of a smoking environment on children of elementary school age. J. Sch. Health 40:533–535, 1970.


Matsukura, S., T.Taminato, N.Kitano, Y.Seino, H.Hamada, M.Uchihashi, H.Nakajima, and Y.Hirata. Effects of environmental tobacco smoke on urinary cotinine excretion in nonsmokers: Evidence for passive smoking. N. Engl. J. Med. 311:828–832, 1984.

McGill, H.C. Jr. Potential mechanisms for the augmentation of atherosclerosis and astherosclerotic disease by cigarette smoking. Prev. Med. 8:390–403, 1979.


Pimm, P.E., F.Silverman, and R.J.Shephard. Physiological effects of acute passive exposure to cigarette smoke. Arch. Environ. Health 33:201–213, 1978.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Polak, E. Le papier à cigarette. Son rôle dans la pollution des lieux habites. Tabagisme passif: Notion nouvellee precise. Brux. Med. 57:335–340, 1977.


Raven, P.B., B.L.Drinkwater, R.O.Ruhling, N.W.Bolduan, S.Taguchi, J. Gliner, and S.M.Horvath. Effect of carbon monoxide and peroxyacetyl nitrate on man’s maximal aerobic capacity. J. Appl. Physiol. 36:288–293, 1974a.

Raven, P.B., B.L.Drinkwater, S.M.Horvath, R.O.Ruhling, J.A.Gliner, J.C.Sutton, and N.W.Bolduan. Age, smoking habits, heat stress, and their interactive effects with carbon monoxide and peroxyacetylnitrate on man’s aerobic power. Int. J. Brometeor. 18:222–232, 1974b.

Rummel, R.M., M.Crawford, and P.Bruce. The physiological effects of inhaling exhaled cigarette smoke in relation to attitude of the nonsmoker. J. Sch. Health 45:524–529, 1975.

Russell, M.A.H., P.V.Cole, and E.Brown. Absorption by nonsmokers of carbon monoxide from room air polluted by tobacco smoke. Lancet 1:576–579, 1973.


Schievelbein, H., and F.Richter. The influence of passive smoking on the cardiovascular system. Prev. Med. 13:626–644, 1984.

Schievelbein, H., V.Londong, W.Londong, H.Grumbach, V.Remplik, A. Schauer, and H.Immich. Nicotine and arterioscherosis. An experimental contribution to the influence of nicotine on fat metabolism. Z. Klin. Chem. Klin. Biochem. 8:190–196, 1970.

Seppänen, A., and A.J.Uusitalo. Carboxyhemoglobin saturation in relation to smoking and various occupational conditions. Ann. Clin. Res. 9:261–268 , 1977.

Shephard, R.J., R.Collins, and F.Silverman. “Passive” exposure of asthmatic subjects to cigarette smoke. Environ. Res. 20:392–402, 1979a.

Shephard, R.J., R.Collins, and F.Silverman. Responses of exercising subjects to acute “passive” cigarette smoke exposure. Environ. Res. 19:279–291, 1979b.

Srch M. On the significance of carbon monoxide in cigarette smoking in an automobile. Dtsch. Z. Gesamte. Gerichtl. 60:80–89, 1967.

Svendsen, K.H., L.H.Kuller, and J.D.Neaton. Effects of passive smoking in the Multiple Risk Factor Intervention Trial (MRFIT). AHA Circ. Monogr. 114(Suppl.):III-53, 1985. (Abstract 210)


U.S. Public Health Service. The Health Consequences of Smoking: Cardiovascular Disease. A Report of the Surgeon General. DHHS (PHS) Publ. No. 84–50204. Washington, D.C.: U.S. Department of Health and Human Services, Public Health Service, Office on Smoking and Health, 1983. 384 pp.


Wald, N.J., M.Idle, J.Boreham, and A.Bailey. Carbon monoxide in breath in relation to smoking and carboxyhemoglobin levels. Thorax 36:366–369, 1981.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

15
Other Health Considerations in Children

Several other health outcomes have been studied that relate to the growth and health of children. This chapter discusses studies of the influence of ETS exposure on birthweight of the offspring of nonsmoking pregnant women and its influence on childhood growth and ear infections. For all postnatal outcomes, it is often not possible to differentiate effects of in utero exposure to tobacco smoke constituent from subsequent childhood exposures to ETS.

ENVIRONMENTAL TOBACCO SMOKE EXPOSURE BY NONSMOKING PREGNANT WOMEN

The fetus of a smoking mother is exposed in a unique way to the chemicals produced in cigarette smoke. Many studies have documented the adverse effect this relationship has on intrauterine fetal growth, especially during the third trimester of pregnancy (U.S. Department of Health and Human Services, 1976). Maternal cigarette smoking apparently affects fetal oxygenation, due to high levels of carboxyhemoglobin in the blood of both mother and child (Abel, 1980). However, the effects on the fetus of a nonsmoking mother chronically exposed to ETS are not well documented. Some studies have indirectly approached this problem by evaluating paternal cigarette smoking and birth outcomes in nonsmoking pregnant women.

Some early studies of paternal smoking and birthweight demonstrated a dose-response relationship that was discounted as

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

“not easily acceptable as meaningful in terms of cause and effect” (Yerushalmy, 1962). An interview survey of 982 pregnancies indicated a strong dose-response association between paternal cigarette smoking and the percent of infants weighing less than 5 pounds, 8 ounces (Yerushalmy, 1962). In a later prospective study of nearly 13,000 births, Yerushalmy (1971) reported that paternal smoking was more strongly associated with low birthweight than was maternal smoking. The healthiest low-birthweight infants were found for couples where the wife smoked and her husband did not; the highest mortality rate was found among infants produced by couples where the husband smoked and the wife did not. These latter couples also had increased risks of producing premature offspring. The possibility that these differences in smoking were associated with differences in social class was not explored. On the bases of these data, Yerushalmy (1971) inferred that paternal smoking may be incidental to birthweight. When the mother’s smoking was considered, the importance of paternal smoking disappeared.

In a study of 12,192 births, MacMahon et al. (1966) confirmed the negative association between maternal smoking and birthweight of offspring and also found that infants of fathers who smoked weighed about 3 ounces less than those of fathers who did not smoke. They attributed this finding to the correlation between husbands’ and wives’ smoking habits, or to chance. MacMahon et al. (1966) referred to Yerushalmy’s (1962) observation of an association of father’s smoking habits with infant weight as “biologically nonsensical.”

In a study of 175 normal neonates and 202 neonates with congenital malformations, Borlee et al. (1978) found that paternal smoking was independently and significantly associated with reduced birthweight and higher perinatal mortality. They speculated that the effect occurred through its association with another factor. Gibel and Blumberg (1973) reported on a study of 5,000 children in which children of nonsmoking mothers whose fathers smoked more than 10 cigarettes per day had higher perinatal mortality than children whose parents were both nonsmokers. The incidence of severe malformations in children of fathers who were heavy smokers was double that of children of nonsmoking fathers, independent of parental age and social class.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

Using code sheets prepared at birth of 48,505 women in worldwide naval installations. Underwood et al. (1967) found that fathers’ smoking habits influenced pregnancy outcome. However, this was attributed to the increased numbers of wives who smoked when husbands smoked. For paternal smoking in the absence of maternal smoking, no association was found. Holmberg and Nurminen (1980) and Hughes et al. (1982) also reported no association of paternal smoking with low birthweight in cross-sectional reviews of several thousand births.

Rubin et al. (1986) provide a recent contribution to this subject based on a survey of 500 consecutive births. About two-fifths of the women reported smoking during pregnancy; 70 percent reported drinking. Paternal smoking was evaluated in terms of frequency and quantity of substance smoked, as reported in standardized interviews. They found that birthweight was reduced an average of 120 g per pack of cigarettes smoked per day by the father. This relationship remained statistically significant after controlling for relevant variables, including mother’s age, parity, maternal smoking, and alcohol and tobacco consumption during pregnancy. The effect was greatest in the lower social classes.

In a prospective study, Martin and Bracken (1986) studied 3,891 antenatal patients, 2,613 of whom did not smoke during pregnancy. One-third of the nonsmoking mothers (i.e., 906) were exposed to ETS for at least 2 hours per day. ETS exposure was related to lower birthweight in full-term babies (23.5 g, not significant). A logistic regression to control for gestational age, parity, ethnicity, and maternal age produced a significantly increased risk of delivering a low-birthweight baby, i.e., less than 2,500 g at birth for ETS-exposed mothers (relative risk=2.17, p<0.05). The retardation in fetal growth rate is small but appears to be clinically meaningful at the low end of the birthweight distribution. That is, exposure to ETS increases the risk that the infant will weigh less than 2,500 g and, therefore, will have a higher perinatal mortality.

GROWTH IN CHILDREN

A few studies have examined possible relationships between chronic exposure to ETS by children and parameters of growth and development. Many studies have demonstrated that smoking during pregnancy results in newborns who are lighter and shorter than other infants, even when gestational age has been taken into

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
×

account (Meredith, 1975; U.S. Department of Health and Human Services, 1976). This deficit in height and weight appears to persist into infancy and childhood (Goldstein, 1971; Butler and Goldstein, 1973; Dunn et al., 1976; Miller et al., 1976; Rantakallio, 1983).

Current smoking status of the mother also has been associated with decreased attained height (Rona et al., 1981; Berkey et al., 1984), although growth rate was not slower among these children (Berkey et al., 1984). These studies, however, did not differentiate between smoking during pregnancy and subsequent exposures during infancy and preschool years.

Rona and colleagues (1985) reanalyzed data from the National Study of Health and Growth (England) for a sample of 5,903 children aged 5 to 11 years, separating the effects of smoking during pregnancy from those of later smoking. After adjusting the data for social class and other social factors, they found that reduced height was associated with increasing numbers of cigarettes smoked in the home, regardless of whether the mother smoked during pregnancy and regardless of which parent smoked. There remained a small but significant effect on height—a reduction of approximately 0.05 standard deviations of height (approximately 0.3 cm) for each 20 cigarettes consumed daily in the home.

To verify this small change in height, other studies of comparable magnitude are needed. Growth is an especially difficult phenomenon to study. Many factors, such as genetics, nutrition, social class, and ethnicity play important roles, and it is difficult to assign proportionate causality to each factor. Recall bias in the mothers of school-age children regarding their smoking habits during the pregnancy may produce unreliable results, especially in light of the increasing publicity regarding ill effects on the fetus of maternal smoking during pregnancy. Moreover, height and weight ratios and other growth measures are not reliably obtained in standard pediatric surveys.

CHRONIC EAR INFECTIONS

A number of studies have linked household exposure to ETS with increased rates of chronic ear infections and effusions in children. Chronic ear infections or effusions in young children can lead to hearing loss and consequent speech pathology. Kraemer and colleagues (1983) conducted a hospital-based case-control study of 76 children with persistent middle-ear effusions contrasted with 76

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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children admitted for other types of surgery who were matched for age, sex, season, and surgical ward. They found that the daily exposure to ETS was greater among cases. They also reported that middle-ear effusions clear less readily in children heavily exposed to ETS. They concluded that a combination of several factors increased the risk of persistent middle-ear effusions, including recurrent otitis media, nasal catarrh, cigarette smoke exposure, and nasal allergies that chronically inflame the nasal and middle-ear cavities, causing persistent eustachian tube dysfunction. For children with regular exposure to ETS, atopy, and congestion, the relative risk for PPME was 6.3 (95% confidence interval, 1.9–21.1).

In another case-control study of 150 children hospitalized for chronic middle-ear effusions and 150 children hospitalized for other reasons (Black, 1985), the odds ratio for parental smoking was found to be significantly elevated (1.6). This effect was consistent across age groups, and became more evident in older children where effusions are less common. Pukander et al. (1985) reported that ETS was a significant risk factor for acute otitis media in 2-and 3-year-old children. They evaluated a number of important indoor environmental conditions, including relative humidity, carbon dioxide, and temperature. In this study, children of smoking parents also had 60% more middle-ear effusions than children of nonsmoking parents.

SUMMARY AND RECOMMENDATIONS

For all postnatal outcomes among children, it is difficult to differentiate effects of in utero exposure to tobacco smoke constituents from subsequent childhood exposures to ETS. However, for the above outcomes, there are indications that exposures to ETS may have effects on the fetus or child.

What Is Known
  1. Evidence has accumulated indicating that nonsmoking pregnant women exposed to ETS on a daily basis for several hours are at increased risk for producing low-birthweight babies, through mechanisms which are, as yet, unknown. Recent studies show a dose-response relationship between the number of cigarettes smoked by the father and birthweight of the children of nonsmoking pregnant women.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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  1. A few studies have reported that children of smokers have reduced growth and development. These require further corroboration to differentiate in utero exposure from subsequent childhood exposures.

  2. Household exposure to ETS is linked with increased rates of chronic ear infections and middle-ear effusions in young children. For children with nasal allergies and recurrent otitis media, ETS exposure may synergistically increase their risk of persistent middle-ear effusions.

What Scientific Information Is Missing
  1. Experimental studies should be developed to articulate possible mechanisms through which paternal smoking adversely effects fetal growth in nonsmoking pregnant women. Special emphasis should be placed on identifying relevant effects of pregnancy on excretion and absorption of ETS, including transplacental metabolism.

  2. Additional study is needed to corroborate one finding of a dose-response relationship between reduced height of children and increasing numbers of cigarettes smoked in the home, regardless of whether the mother smoked during pregnancy and regardless of which parent smoked.

  3. Research should be conducted to explore the mechanisms by which exposure to ETS might adversely affect the functioning of the ear and to study possible long-term consequences of ETS exposure for the auditory apparatus.

REFERENCES

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Black, N. The aetiology of glue ear—A case-control study. Int. J. Pediatr. Otorhinolaryngol. 9:121–133, 1985.

Borlee, I., A.Bouckaert, M.F.Lechat, and C.B.Mission. Smoking patterns during and before pregnancy: Weight, length and head circumference of progeny. Eur. J. Obstet. Gynecol Reprod. Biol. 8:171–177, 1978.

Butler, N.R., and H.Goldstein. Smoking in pregnancy and subsequent child development. Br. Med. J. 4:573–575, 1973.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Dunn, H.G., A.K.McBurney, S.Ingram, and C.M.Hunter. Maternal cigarette smoking during pregnancy and child’s subsequent development. I. Physical growth to the age of 6 1/2 years. Can J. Public Health 67:499–505, 1976.


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Kraemer, M.J., M.A.Richardson, N.S.Weiss, C.T.Furukawa, G.G.Shapiro, W.E.Pierson, and W.Bierman. Risk factors for persistent middle-ear effusions. Otitis media, catarrh, cigarette smoke exposure and atopy. JAMA 249:1022–1025, 1983.


MacMahon, B., M.Alpert, and E.J.Salber. Infant weight and parental smoking habits. Am. J. Epidemiol. 82:247–261, 1966.

Martin, T.R., and M.B.Bracken. Association of low birth weight with passive smoke exposure in pregnancy. Am. J. Epidemiol. 124:633–642, 1986.

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Miller, H.C., K.Hassanein, and P.A.Hensleigh. Fetal growth retardation in relation to maternal smoking and weight gain in pregnancy. Am J. Obstet. Gynecol. 125:55–60, 1976.


Pukander, J., J.Lustonen, M.Timore, and P.Karma. Risk factors affecting the occurrence of acute otitis media among two and three year old urban children. Acta Otolaryngol. 100:260–265, 1985.


Rantakallio, P. A follow-up study up to the age of 14 of children whose mothers smoked during pregnancy. Acta Paediatr. Scand. 72:747–753, 1983.

Rona, R.J., C.Du Ve Florey, G.C.Clarke, and S.Chinn. Parental smoking at home and height of children. Br. Med. J. 283:1363, 1981.

Rona, R.J., S.Chinn, and C.Du Ve Florey. Exposure to cigarette smoking and children’s growth. Int. J. Epidemiol. 14:402–409, 1985.

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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Yerushalmy, J. Statistical considerations and evaluation of epidemiological evidence. In G.James, Ed. Tobacco and Health. Springfield, Illinois: Charles C Thomas, 1962.

Yerushalmy, J. The relationship of parents’ cigarette smoking to outcome of pregnancy—Implications as to the problem of inferring causation from observed associations. Am. J. Epidemiol. 93:443–456, 1971.

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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APPENDIXES

Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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Suggested Citation:"HEALTH EFFECTS POSSIBLY ASSOCIATED WITH EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE BY NONSMOKERS." National Research Council. 1986. Environmental Tobacco Smoke: Measuring Exposures and Assessing Health Effects. Washington, DC: The National Academies Press. doi: 10.17226/943.
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This comprehensive book examines the recent research investigating the characteristics and composition of different types of environmental tobacco smoke (ETS) and discusses possible health effects of ETS. The volume presents an overview of methods used to determine exposures to environmental smoke and reviews both chronic and acute health effects. Many recommendations are made for areas of further research, including the differences between smokers and nonsmokers in absorbing, metabolizing, and excreting the components of ETS, and the possible effects of ETS exposure during childhood and fetal life.

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