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7 EXPOSURE TO ENVIRONMENTAL TOBACCO Smoke Involuntary exposure to environmental tobacco smoke (ETS), or passive smoking, has been extensively investigated with re- spect to its potential health effects, particularly on respiratory health. There is a significant body of research on its potential ef- fects regarding the incidence, prevalence, and exacerbation of es- tablished asthma. While attention has focused upon possible as- sociations with childhood asthma, associations with asthma in adults also have been investigated. The following analysis relies heavily on several very detailed and comprehensive reviews, in- cluding those of the U.S. Environmental Protection Agency (EPA) (U.S. EPA, 1992), the California EPA s Office of Environmental Health Assessment (California EPA, 1997), the World Health Or- ganization (WHO) International Consultation on Environmental Tobacco Smoke (ETS) and Child Health (WHO, 1999), the report of the United Kingdom s Scientific Committee on Tobacco and Health (SCOTH, 1998), and the series of ten meta-analyses (to date) of the health effects of ETS by Cook, Strachan, and col- leagues (Anderson and Cook, 1997; Cook et al., 1998; Cook and Strachan, 1997, 1998, 1999; Strachan and Cook, 1997, 1998a-1998c). 263

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264 CLEARING THE AIR DEFINITION OF ENVIRONMENTAL TOBACCO SMOKE (ETS} Environmental tobacco smoke has been defined (Daisey et al., 1994) as: . . . the smoke to which non-smokers are exposed when they are in an indoor environment with smokers. It is composed largely of sidestream tobacco smoke (SS), the smoke emitted by the smolder- ing end of a cigarette between puffs, with minor contributions from exhaled mainstream smoke (the smoke which is directly inhaled by the smoker) and any smoke that escapes from the burning part of the tobacco during puff-drawing by the smoker. ETS differs from SS in that it is highly diluted and dispersed within a room and it undergoes aging. Tobacco smoke contains many chemical products with known or suspected adverse health effects. These products include eye and respiratory irritants, systemic toxicants, mutagens and car- cinogens, and reproductive toxicants (California EPA, 1997~. ETS consists of solid particulates, and semivolatile and volatile organic compounds (VOCs). The solid particulates have a mean diameter of 0.32,um (National Research Council, 1986~. "The aging process includes volatilization of nicotine, which is present in the particu- late phase in mainstream smoke but is almost exclusively a com- ponent of the vapor phase of ETS" (U.S. EPA, 1992~. The mean and standard deviation of the total emission factor for PM 2 5, de- termined for six commercial cigarettes and Kentucky reference cigarette 1R4F, is 8,100 + 2,000 ,ug per cigarette. Bacterial endot- oxin (lipopolysaccharide), previously associated with environ- mental lung diseases, has been reported to be a respirable con- stituent of both mainstream and sidestream smoke (Hasday et al., 1999~. Significant amounts of nearly 30 volatile organic compounds have been measured, including acetaldehyde, formaldehyde, nicotine, 3-viny~pyridine, toluene, pyridine, benzene, pyrrole, xy- lene, 2-butanone (methyl ethyl ketone iMEK]), phenol, and oth- ers. Many of the more volatile VOCs (such as aldehydes) remain in the air for prolonged periods of time following the smoking of a cigarette (at least four hours) and do not appear to undergo significant chemical reactions within this period. Some of the less volatile compounds and particulates appear to decrease over time

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE 265 due to deposition as well as ventilation effects. With the excep- tion of nicotine, the emission factors for VOCs are significantly greater in ETS than in SS (U.S. EPA, 1992~. Additional information on the physical and chemical proper- ties of ETS and the biological activities can be found in the U.S. and California EPA reports (California EPA, 1997; U.S. EPA, 1992~. FACTORS CONTROLLING EXPOSURE TO ETS Variations in Concentration of ETS in Indoor Environments Exposure Assessment Nicotine and particulate matter (PM), in addition to carbon monoxide, have been the constituents most extensively measured as a means of assessing ETS concentrations in indoor air. Nicotine is considered an adequate tracer for PM under certain conditions, and, possibly, for VOCs ranging from slightly to very volatile compounds (Dailey, 1999~. Among the documented conditions influencing the concentration of nicotine are emission rates, ven- tilation, and (for VOCs/SVOCs) resorption and Resorption from surfaces (Dailey, 1999~. The EPA (1992) and Guerin et al. (1992) summarized more than 25 studies of nicotine concentration in more than 100 different indoor environments and found that the average concentrations of nicotine ranged from 0.3 to 30,ug/m3, a hundredfold difference. In residences with one or more smokers, the typical range was from 2 to 10 ,ug/m3, typically being higher in winter than in summer. Bars and smoking sections of commer- cial airplanes recorded the highest levels up to 50-75 ,ug/m3, although nonsmoking regulations and ordinances have signifi- cantly altered this. In general, the concentrations of nicotine have been found to increase with the number of smokers and number of cigarettes consumed in a given indoor environment (U.S. EPA, 1992~. One study involving personal monitor measurement of approximately 100 individuals in 16 metropolitan areas in the United States reported mean 24-hour time weighted average nico- tine concentrations of 3.28 ,ug/m3 for those exposed to ETS both

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266 CLEARING THE AIR at work and away from work; 1.41,ug/m3 for those exposed away from work only; 0.69 ,ug/m3 for those exposed at work only; and 0.05 ,ug/m3 for those exposed at neither location Jenkins et al., 1996; Jenkins and Counts, 1999~. Particulate concentrations, un- like nicotine, are not specific to ETS as a source. However, al- though not unique to the combustion of tobacco, the quantity of respirable particulates produced by cigarette smoking, is large- significantly greater than the amounts produced by other com- mon combustion sources within the home, such as wood-burning fireplaces, gas stoves, and kerosene space heaters (California EPA, 1997~. Respirable suspended particles in homes with at least one smoker average about 20-100 ,ug/m3 higher than the levels in similar nonsmoking homes. The highest concentrations have been reported in restaurants and bars a maximum of 1,379,ug/m3 and a range of average concentrations of 35-986 ,ug/m3 (U.S. EPA, 1992~. Ott et al. (1996) documented a 77/O decrease in the average concentration of respirable suspended particles in a northern California tavern after a prohibition against smoking was insti- tuted. In addition to the influence of the number of smokers and the amount smoked on the concentration of ETS in a given indoor environment, concentration is affected by the ventilation rate. Long-term exposure to ETS has been of most concern from the standpoint of effects on lung development and cancers. How- ever, ETS concentration varies over an extreme spatial and tem- poral range in indoor and outdoor environments, making it in- feasible to comprehensively assess the ETS exposure history of an individual over their lifetime by direct exposure assessment or air sampling in all of the relevant environments. Critical aspects of this history can, however, be determined and more compre- hensive and accurate assessment is often feasible for infants and very young children. Because of the difficulties involved, epide- miologists have tended to use questionnaires and interviews to determine individual history with regard to ETS exposure, classi- fying people into categorical groups to provide a semiquantitative measure of exposure. Direct measurement of exposure at or near the breathing zone is often done via personal monitors and can provide an assessment of integrated exposure, but this is feasible for monitoring only over a relatively limited period of time.

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE Biomarkers of Exposure 267 The most direct assessment of exposure involves the measure- ment of ETS constituents or their breakdown products in body fluids. To date, the most reliable of these biomarkers is cotinine, a metabolite of nicotine (Benowitz, 1999~. Cotinine has an average half-life of approximately 16-19 hours (Benowitz and Jacob, 1994; larvis et al., 1988), making it highly useful for the assessment of integrated ETS exposure over the two to three days prior to the measurement. In infants and children, the half-life is appreciably longer, from approximately 40 hours in children more than 18 months old to approximately 65 hours in neonates (U.S. EPA, 1992~. Because urinary cotinine excretion varies markedly among individuals as a result of renal function, urinary flow rate, and urinary pH (Benowitz et al., 1983), results often are expressed as nanograms of cotinine per milligram of creatinine, rather than simply in nanograms per milliliter of fluid. However, the produc- tion of creatinine is a function of muscle mass; hence excretion varies with age, sex, and other individual factors. In particular, the low level of creatinine produced in children means that the cotinine-to-creatinine ratios in children may fall into the range reported for active smokers (Watts et al., 1990~. The levels of exposure of nonsmokers to ETS are sufficient that nicotine and cotinine are detectable in their urine, blood, and saliva (Benowitz, 1996~. Values are typically in the range of 0.5 to 10-15 ng/mL in the saliva and plasma, respectively, of nonsmok- ers, with urinary concentrations approximately three times higher as much as 50 ng/mL or more (Guerin et al., 1992; U.S. EPA, 1992~. A cutoff of 90 ng/mL has been used to distinguish active smokers from exposed and unexposed nonsmokers (Cummings et al., 1990), and studies consistently have been able to distinguish active smokers from exposed and unexposed non- smokers Jarvis et al., 1987~. It has been more difficult to distin- guish exposed from non-exposed non-smokers for a variety of reasons related to the validity of self-reported smoking status and ETS exposure, variability in nicotine metabolism, variability in sampling procedures, and the limits of sensitivity of the assay methods used (Idle, 1990~. Increasing levels of cotinine have been generally found to be associated with increasing levels of self

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268 CLEARING THE AIR reported ETS exposure (NRC, 1986; U.S. DHHS, 1986; U.S. EPA, 1992~. As would be expected from the results of measurement of ambient concentrations of nicotine, the maximum reported expo- sure levels have occurred in bars and restaurants and on commer- cial airline flights approximately 30 ng/mg creatinine (Mattson et al., 1989~. One study in which adults in an enclosed area were exposed to sidestream smoke from four cigarettes being smoked simultaneously and injected into the room continuously by ma- chine, with ventilation conditions equivalent to those in the aver- age office environment, found the air concentration of nicotine rapidly reached a stable level of 280,ug/m3. Average nicotine con- centration in saliva reached a maximum of 880 ng/mL after 60 minutes of exposure, and cotinine concentrations reached 3.4 ng/ mL in serum and 55 ng/mg creatinine in urine, a little more than six hours after exposure. A number of studies have compared biomarkers in active smokers with those in exposed and nonexposed nonsmokers. larvis and Russell (1984), for example, found mean urinary cotinine levels in these three groups of 1,390.0,7.7, and 1.6 ma/ mL, respectively (p < .001 between exposed and nonexposed non- smokers). Cotinine concentrations of self-reported smokers and nonsmokers have generally been found to overlap. In infants and children exposed to ETS, levels of cotinine have been found to be significantly higher in exposed than in nonexposed children. Direct exposure assessment has detected cotinine in the urine on the first day of life in neonates of both active smokers and ETS-exposed nonsmokers with significantly higher levels in the latter than in neonates of unexposed non- smokers Jordanov, 1990~. Henderson et al. (1989) found that air nicotine concentration in the home was significantly associated with the average log urinary cotinine level (r = 0.68, p = .006~. Greenberg et al. (1989) found a median concentration of 121 ng cotinine/mg creatinine (range 6-2,273 ng cotinine/mg creatinine) in children with any detectable cotinine. Chilmonczyk et al. (1990) found median levels of urinary cotinine of 1.6 mg/mL in non- smoking households, 8.9 mg/mL where someone other than the mother smoked, 28 mg/mL where only the mother smoked, and 43 mg/mL where both the mother and someone else smoked.

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE Exposure Prevalence 269 In reviewing studies of ETS exposure prevalence, the Califor- nia EPA (1997) concluded, "Taken as a whole, the various studies [at least 10 separate investigations including large representative sample surveys] . . . indicate that within California and the United States, exposure to ETS was widespread during the time period of the studies (1979 through 1992~. Analysis of ETS exposure within California indicated that the workplace, home, and other indoor locations contributed significantly to the exposure of adults. For children, the home was the most important single lo- cation contributing to ETS exposure. In all studies using both self- reporting and a biological marker (cotinine level) as measures of exposure, prevalence was higher when determined using the bio- logical marker." It further cited indirect evidence that "the preva- lence of ETS exposure in the rest of the U.S. population is higher than that in California." It is particularly noteworthy that despite aggressive antismok- ing education and regulation, and documented reductions in smoking rates (to 16.7% of the adult population in 1995 [CDHS, 1995~), in 1992 an estimated 9.4% of California women pregnant within the previous five years had smoked throughout pregnancy, and an estimated 19.6% of those 17 years of age may be exposed to ETS in their homes (Pierce et al., 1994~. By inference from stud- ies of adult smoking, it also would appear that the rates may be appreciably higher in specific subpopulations. Influence of Activity Patterns on Exposure The activity patterns of both children and adults have been studied in relation to exposure to ETS. For all ages, the home is the location in which the average person spends the most time 921 minutes per day for adults and 1,078 minutes per day for children in California. Time within the home is spent primarily in the bedroom an average of 524 minutes per day for adults and 674 minutes per day for children (Wiley et al., 1991~. The next greatest amounts of time are spent by children in school or child care (an average of 109 minutes for all children and 330 minutes for those attending school), in other people's homes (80 minutes

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270 CLEARING THE AIR average and 251 minutes for those doing this), and in-transit (69 minutes overall and 83 minutes for those traveling). Overall, chil- dren spend an average of 1,230 min. (20.5 hours) each day in- doors, 141 minutes outdoors, and 69 minutes in enclosed transit. Infants and other children ages 2 and under spend the most time indoors (an average of 21.6 hours), but somewhat less in enclosed transit (48 minutes). For adults, the times are 1,253 minutes in- doors, 73 minutes outdoors, and 111 minutes in enclosed trans- portation, with time in the workplace replacing time spent in school or child care by children. For children, the home is clearly the most likely source of ex- posure to ETS and the place that the child is most likely to sleep. While smoking is not permitted in schools or day care facilities and is prohibited in some states in licensed child care in private homes when children are present, the fact that many children are in nonlicensed child care arrangements or in states or communi- ties where smoking prohibitions are not well enforced means that significant regular exposure may occur in home settings. Expo- sure during travel in the private automobile is another potential source of exposure. For adults, research in California (Lum, 1994a, 1994b) has shown that exposure in the workplace is the most prevalent loca- tion for exposure of nonsmokers to ETS, with the home as the second most prevalent location. To the extent that workplaces adopt antismoking regulations, this exposure source may dimin- ish in importance. The private automobile represents another po- tentially significant location for adult exposure. It is possible for both adults and children to be exposed to ETS the majority of the time they are indoors, both during the day and at night. For the average preschool child, this could be virtu- ally all of the time, for the school-aged child as many as 15.5 hours a day, and for adults anywhere from 12 hours (for those working in a nonsmoking environment) to 24 hours for those working as well as living in environments in which smoking is permitted. The only reliable exception would be time spent in school, public buildings, or public transit where smoking is prohibited. There is no reason to believe that the activity patterns of persons with asthma differ significantly from those of nonasthmatics, except for the possibility of their having lower activity levels that could

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE 271 result in more time spent indoors and hence greater exposure to any ETS present in indoor environments. Further, there are ques- tions as to whether the sensitization of children to allergens (e.g., dust mites, cockroaches) in the home environment may be in- creased by the presence of ETS, as well as whether increased time spent in the indoor environment, if this occurs, results in greater exposure to ETS as well as to indoor allergens. One study of children between the ages of 2 and 12 in Scot- land, having at least one parent who smoked, found that salivary cotinine levels were nondetectable in only four children, all of whom had only a father who smoked (Irvine et al., 1997~. In the remaining 493 children, the levels ranged from 0.5 ng/mL (barely detectable) to 21.2 ng/mL, with a mean of 4.35 ng/mL. The au- thors cite two studies in which levels of 14.3 ng/mL or higher have been taken as indicative of active smoking by a child. How- ever, 13 of the 18 children who scored between 14.3 and 21.2 ng/ mL were younger than 6 years of age and are presumed not to be active smokers. This study found that the age of the child, cotinine level and self-reported amount smoked in the home by the index parent, self-reported frequency of smoking in the same room as the child, whether the index parent's partner smoked, whether the child had contact with other smokers, the number of persons per room in the home, and whether the home had a yard or gar- den were all significantly and independently related to the child's cotinine level. EVIDENCE OF A RELATIONSHIP BETWEEN ETS AND ASTHMA Action of ETS on the Lungs Tobacco smoke, whether mainstream, sidestream, or ETS, is a lung irritant. From a pathophysiologic point of view, active smok- ing is associated with significant structural changes in both the airways and the pulmonary parenchyma (U.S. DHHS, 1984), in- cluding hypertrophy and hyperplasia of the upper airway mu- cous glands, leading to an increase in mucous production with associated increased prevalence of cough and phlegm. Chronic inflammation of the smaller airways also occurs, leading to bron

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272 CLEARING THE AIR chial obstruction. In addition, airway narrowing may occur con- sequent to destruction of the alveolar walls, decreased Jung elas- ticity, and development of centrilobular emphysema (U.S. EPA, 1992~. Smoking also may increase mucosal permeability to aller- gens, increasing total and specific immunogiobulin E (IgE) levels (Zetterstrom et al., 1981) and blood eosinophi] counts (Halonen et al., 1982~. The adverse health effects and pathophysiologic changes as- sociated with active smoking have been observed at low-dose ex- posures, suggesting that ETS might have similar adverse effects, a suspicion that was heightened by the fact that ETS contains some volatile substances in greater quantities than are found in mainstream smoke (U.S. EPA, 1992~. In addition, since large pro- portions of the population are involuntarily exposed to ETS, in- cluding more susceptible infants and children, the index of suspi- cion for adverse effects of ETS is high. Exposures early in life, when the lung is undergoing significant growth and remodeling, could plausibly alter Jung development and increase the risk of various respiratory illnesses, including asthma. It is also plausible that, in addition to the marked susceptibility of young lungs, there is variable individual susceptibility in other respects, including genetic predisposition, lung injury such as bronchopulmonary dysplasia consequent to premature birth, and greater contact with a primary caregiver who smokes. Maternal Active Smoking During Pregnancy Exposure of the fetus to the products of maternal tobacco smoking is a form of "environmental" exposure to tobacco smoke, although not in the same proportions as in airborne ETS and not to all constituents of ETS (notably, not the particulates). It is plau- sible that virtually all products of active maternal smoking that enter the bloodstream of the mother, including products arising from mainstream and sidestream smoke, cross into the fetus through the placenta with a diffusion gradient. This has been con- firmed in the case of carbon monoxide (Longo, 1970) and cotinine. A biomarker for nicotine exposure, cotinine has been detected in the amniotic fluid of ETS-exposed women and the urine of their neonates in significantly higher concentrations than in

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE . . 273 nonexposed nonsmoking women Jordanov, 1990~. Transplacen- tal passage of the bloodborne products of passive maternal ETS exposure also would be expected, although at lower levels and with a different chemical com Position than if the mother were an active smoker. Active maternal smoking has been associated with reduced size of the placental arteries (Asmussen, 1979), a reduction in av- erage birthweight of 75~00 am. (Abell et al., 1991; Asmussen, 1979; Lodrup Carisen et al., 1997; Miiner et al., 1999; Sherwood et al., 1999; Wang et al., 1997), and altered lung function measured shortly after birth (Lodrup Carisen et al., 1997~. Small but statisti- cally significant deficits in forced expiratory volume in one sec- ond (FEVER and other spirometric indices (forced vital capacity [FVC], mid expiratory flow iMEF], and end expiratory flow [EEF]) have been fairly consistently demonstrated in school-aged chil- dren (data reviewed in Cook and Strachan, 1999) and as early as three days after birth (Lodrup Carisen et al., 1997), thereby strongly implicating maternal smoking during pregnancy as the cause of these deficits. However, in Turkey, where there is heavy smoking by men and virtually none by women, exposure of chil- dren also has been associated with significant deficits in lung function (e.g., Bek et al., 1999~. Experimental studies in animals have demonstrated that ETS exposure of pregnant rats is associ- ated with reduced Jung volume, number of saccules and septal crests, and elastin fibers in fetal lungs (Collins et al., 1985~. More recently, Sekhon et al. (1999) reported that nicotine alone, when administered to pregnant rhesus monkeys, altered the expression of nicotine receptors in the developing fetal lung, leading to lung hyperplasia with structural alterations and reduced complexity of the gas-exchange surface. ETS and Children's Respiratory Health Recent reviews of an extensive body of cross-sectional, case- control, and longitudinal epidemiologic research on the effects of parental smoking on children's respiratory health have come to very similar, although not identical, conclusions. These reviews include both systematic, quantitative meta-analyses (Cook and Strachan, 1999) and narrative reviews (California EPA, 1997; U.S.

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE 287 the outset of the study, and no intervention effect was observed. This differential self-reported exposure of infants of maternal smokers was not, however, accompanied by a significant differ- ential in the cotinine-to-creatinine ratios of the intervention and control children. In fact, the proportion with detectable urine cotinine levels tended to increase over the year of follow-up in both groups. The incidence of all acute lower respiratory illnesses (ALRIs) and of severe acute respiratory illnesses did not decrease in the intervention group, and in fact, there was a small but statis- tically significant difference in all ALRIs favoring the control group. There was a significant difference in the frequency of per- sistent lower-respiratory symptoms in the maternal smoking subsample, but only where the head of household had a high school education or less. The authors interpret the results as indi- cating that mothers took steps to protect the infant from exposure by removing them from the vicinity of the smoker and that the infants were nevertheless subsequently exposed to residual nico- tine but not to other ETS products, "which may be more likely than nicotine to have acute and chronic toxicity for passive smok- ers." The authors did not discuss whether parental report could have been biased in the direction of reduced reporting of expo- sure, and the unplanned subgroup analysis means that the posi- tive results with regard to persistent lower-respiratory symptoms are merely suggestive. Chilmonczyk et al. (1992) reported an unsuccessful phy- sician's office-based intervention strategy that used feedback from the physician to the parent on infant urine cotinine measurements in an attempt to reduce the infant's exposure to ETS. The 6% re- duction of urine cotinine levels for the intervention group at fol- low-up two months later was not statistically significant. This lack of success was in contrast to the investigator's previous success in getting women to stop smoking during pregnancy based on feedback on their own urine cotinine levels (Haddow et al., 1991), suggesting there may be greater motivation and ability of women to cease smoking and eliminate exposure of their fetus than to prevent exposure of infants and older children. An earlier unsuc- cessfu] attempt to reduce passive smoking in infancy was re- ported by Woodward et al. (1987~. Hovell et al. (1994) and Wahigren et al. (1997) have reported

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288 CLEARING THE AIR that among children with asthma, a preventive medicine counsel- ing intervention was associated with a greater reduction in self- reported and air monitor-verified ETS exposure than a monitored or usual care control condition. McIntosh et al. (1994) did not re- port a significant benefit of a cotinine-assisted, minimal-contact intervention. Where positive results and promising interventions have been reported, there is a need for replication and, if possible, extension to other populations. Extensions of interventions should be made to populations including those who tend to be more resistant to cessation efforts and may be more typical of those whose children are being exposed to significant levels of ETS and are at risk for poor asthma outcomes for a variety of reasons. Wilson et al. (1996) i] have found that both adults with asthma who smoke and smok- ing parents of children with asthma are less likely than nonsmok- ers to attend an asthma education program, making it less likely that they will modify the child's exposure or experience the other benefits of such asthma education programs. None of the studies to date that have investigated educational nterventions to reduce ETS exposure have extended this to in- clude asthma outcomes either doctor-diagnosed asthma or wheezing illness incidence, or the prevalence or exacerbations of established asthma. Until this is done, it leaves unanswered the question of whether any ETS exposure reduction that may be achieved is sufficient to alter these disease outcomes, as well as whether there is any safe ETS exposure level. This is particularly important when the intervention aims to reduce infant exposure by means other than cessation of smoking by all caregivers and others in the child's environment. For this reason it also is impos- sible to directly answer questions regarding the cost-effectiveness of mitigation and prevention strategies. CONCLUSIONS REGARDING ETS SOURCE CONTROL OR MITIGATION: FEASIBILITYAND BENEFITS Conclusions Regarding the Effects of Complete Avoidance of ETS Exposure Based on reasoning from the epidemiologic evidence pre

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE 289 sensed above, the following conclusions can be reached regard- ing the potential benefits of essentially complete avoidance of ETS exposure, if this could be achieved: There is sufficient evidence to conclude that complete avoidance of ETS exposure would be associated with a lower like- lihood of exacerbations of asthma in preschool children with es- tablished asthma. There is limited evidence suggesting that complete avoid- ance of ETS exposure would be associated with a lower likeli- hood of exacerbations of asthma in older children and adults. There is sufficient evidence to conclude that complete avoidance of ETS exposure, if this could be achieved, would re- duce the probability of the development of wheezing with respi- ratory illness in younger children. There is limited or suggestive evidence that complete avoidance of ETS exposure, if this could be achieved, would re- duce the likelihood of the persistence of asthma or of new-onset asthma in children and adults. Conclusions Regarding Mitigation Through Source Control There is sufficient evidence to conclude that increased ven- tilation and air-cleaning methods are technologically capable of reducing the concentration of ETS particulates in indoor air. There is no evidence as to how readily the necessary venti- lation and air-cleaning methods or technologies would be adopted and how effectively they actually would be used to re- duce ETS concentration. There is no evidence of whether interventions designed to encourage the use of the requisite ventilation and air-cleaning methods would be associated with a reduction in ETS concentra- tion, in the exposure of persons with asthma to ETS, or in asthma prevalence or exacerbations. There is inadequate evidence to conclude that interven- tions intended to establish smoke-free homes where a family member has asthma and to require smokers to smoke only out- doors are associated with a reduction in ETS exposure or asthma exacerbations.

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290 CLEARING THE AIR RES"RCH NEEDS A better understanding is needed of the mechanisms by which ETS and its individual constituents may impair the normal development of the airways in the fetus, promote allergic sensitization, promote respiratory infections, promote early wheezing illness, and (possibly) induce pathophysiologic changes that may pro- mote the establishment of asthma. Research is also needed to understand the nature of the inter- actions, both at the population or epidemiologic level and at the molecular and cellular levels, between the genetic predispositions to allergic sensitization and bronchial hyperresponsiveness and ETS exposure as they relate to the development of asthma. The respective roles of antenatal and postnatal exposure to ETS in the pathophysiologic changes associated with asthma and other res- piratory illnesses are in need of further investigation. Behavioral research also is needed to better understand the factors that lead to the initiation of smoking in adolescents, espe- cially young women, and to the maintenance of smoking in preg- nant women and mothers. Additionally, there is a need to develop more effective interventions to achieve sustained pre- and post- natal smoking cessation in pregnant women and mothers, espe- cially those whose children are at higher risk of developing asthma due to their family history, socioeconomic status, and place of residence. Since ETS exposure of children at greatest risk for adverse asthma outcomes (especially low-income and minor- ity children of African-American ancestry) may come from other caregivers as well as the mother or parents (i.e., other family mem- bers with whom the mother and child live and from day care pro- viders), interventions must be developed that will be effective in reducing the child's exposure from all sources. The effectiveness of ETS exposure reduction interventions in actually improving asthma outcomes should be evaluated as well.

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EXPOSURE TO ENVIRONMENTAL TOBACCO SMOKE REFERENCES 291 Abell TD, Baker LC, Ramsey CN Jr. 1991. The effects of maternal smoking on infant birth weight. Family Medicine 23~2~:103-107. AHCPR (Agency for Health Care Policy and Research). 1996. Smoking Cessation: Clinical Practice Guideline (No. 18~. DHHS Publication No. (AHCPR) 96-0892. U.S. Department of Health and Human Services, Public Health Service. Washington, DC. Anderson HR, Cook DG. 1997. Health effects of passive smoke. 2. Passive smoking and sudden infant death syndrome. Review of the epidemiological evidence. Thorax 52~11~:1003-1009. [Published erratum appears in Thorax 1999. 54(4):365-366.] Asmussen I. 1979. Fetal cardiovascular system as influenced by maternal smoking. Clinical Cardiology 2~4~:246-256. Bek K, Tomac N. Delibas A, Tuna F. Tezic HT, Sungur M. 1999. Department of Pediatric Allergy, Dr Sami Ulus Children's Hospital, Ankara, Turkey. Postgraduate Medicine Journal 75~884~:339-341. Benowitz NL, Jacob P III. 1994. Metabolism of nicotine to Cotinine studied by a dual stable isotope method. Clinical Pharmacology Therapeutics 56~5~:483- 493. Benowitz JL, Kuyt F. Jacob P III, Jones RT, Osman AL. 1983. Cotinine disposition and effects. Clinical Pharmacology Therapeutics 34~5~:604-611. Benowitz NL. 1996. Cotinine as a biomarker of environmental tobacco smoke exposure. Epidemiologic Reviews 18~2~:188-204. Benowitz NL. 1999. Biomarkers of environmental tobacco smoke exposure. Environmental Health Perspectives 107(Suppl 2~:349-355. Bruvold WH. 1993. A meta-analysis of adolescent smoking prevention programs. American Journal of Public Health 83~6~:872-880. Bulterys M. 1993. Passive tobacco exposure and sudden infant death syndrome. Pediatrics 92~3~:505-506. California EPA (California Environmental Protection Agency). 1997. Health Effects of Exposure to Environmental Tobacco Smoke. Office of Environmental Health Hazard Assessment. Sacramento, CA. CDC (Centers for Disease Control and Prevention). 1989. Reducing the Health Consequences of Smoking: 25 Years of Progress A Report of the Surgeon General. U.S. Department of Health and Human Services, Public Health Service, CDC, DHHS publication no. (CDC) 89-8411. Washington, DC. CDC. 1997. Cigarette smoking among adults United States, 1995. Morbidity and Mortality Weekly Report 46~51~:1217-1220. CDC. 1998. Tobacco Use Among U.S. Racial/Ethnic Minority Groups African Americans, American Indians and Alaska Natives, Asian American and Pacific Islanders, and Hispanics: A Report of the Surgeon General. U.S. Department of Health and Human Services, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health. Atlanta, GA.

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