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INTRODUCTION  The preceding chapter addressed the topic of hazard identification and concluded that environmental tobacco smoke (ETS) exposure is causally associated with lung cancer. If an effect is large enough to detect in epidemiologic studies investigating the consequences of ETS exposure at common exposure levels, the individual risk associated with exposure is considered to be high compared with most environmental contaminants assessed. Of course, the number of lung cancer deaths attributable to ETS exposure for a whole population, such as the United States, depends on the number of persons exposed as well as the individual risk. Studies of cotinine/creatinine concentrations in nonsmokers indicate that ETS is virtually ubiquitous. For example, in urinary bioassays of 663 nonsmokers, Cummings et al. (1990) found that over 90% had detectable levels of cotinine. Among the 161 subjects who reported no recent exposure to ETS, the prevalence of detectable cotinine was still about 80%. Although the average cotinine level for all those tested may be below the average for subjects exposed to spousal ETS, as studied in this report, it indicates uptake of ETS to some extent by a large majority of nonsmokers (see also Chapter 3). Consequently, exposure to ETS is a public health issue that needs to be considered from a national perspective. This chapter derives U.S. lung cancer mortality estimates for female and male neversmokers and longterm (5+ years) former smokers. Section 6.2 discusses prior approaches to estimating U.S. population risk. Section 6.3 presents this report's estimates. First, the parameters and formulae used are defined (Section 6.3.2), and then lung cancer mortality estimates are calculated from two different data sets and confidence and sources of uncertainty in the estimates are discussed. Section 6.3.3 derives estimates based on the combined relative risk estimates of the 11 U.S. studies from Chapter 5. Section 6.3.4 bases its estimates on the data from the single largest U.S. study, that of Fontham et al. (1991). Finally, Section 6.3.5 discusses the sensitivity of the estimates to changes in various parameter values. ETSattributable lung cancer mortality rates (LCMR) for each of the individual studies from Chapter 5 are presented in Appendix C. 6.2. PRIOR APPROACHES TO ESTIMATION OF POPULATION RISK Several authors have estimated the population risk of lung cancer from exposure to ETS. Two approaches have been used almost exclusively. One approach analyzes the overall epidemiologic evidence available from casecontrol and cohort studies, as done in this report; the other estimates a doseresponse relationship for ETS exposure extrapolated from active smoking, based on "cigaretteequivalents" determined from a surrogate measure of exposure common to passive and active smoking. A recent review of risk assessment methodologies in passive smoking may be found in Repace and Lowrey (1990). 6.2.1. Examples Using Epidemiologic Data The National Research Council report (NRC, 1986) is a good example of the epidemiologic approach. An overall estimate of relative risk (RR) of lung cancer for neversmokers exposed to both spousal smoking and background ETS versus those exposed only to background ETS is obtained by statistical summary across all available studies. Two "corrections" are then made to the estimate of RR to correct for the two sources of systematic bias. The first correction accounts for expected upward bias from former smokers and current smokers who may be misclassified as neversmokers; this correction results in a decrease in the RR estimate. The second correction is an upward adjustment to the RR taking into account the risk from background exposure to ETS (experienced by a neversmoker whether married to a smoker or not) to obtain estimates of the excess lung cancer risk from all sources of ETS exposure (spousal smoking and background ETS) relative to the risk in an ETSfree environment. Population risk can then be characterized by estimating the annual number of lung cancer deaths among neversmokers attributable to all sources of ETS exposure. This calculation requires the final corrected estimates of RR (one for background ETS only and one for background plus spousal smoking), the annual number of lung cancer deaths (LCDs) from all causes in the population assessed (e.g., neversmokers of age 35 and over), and the proportion of that population exposed to spousal smoking. The entire population is assumed to be exposed to some average background level of ETS; although, in fact, the population contains some individuals with high exposure and others with virtually no exposure. The NRC report combines data for female and male neversmokers to obtain an overall observed RR estimate of 1.34 (95% confidence interval [C.I.] = 1.18, 1.53), but this estimate is most heavily influenced by the abundant female data. (The female data alone generate a combined RR estimate of 1.32 [95% C.I. = 1.18, 1.52], while the male data produce an RR estimate of 1.62 [95% C.I. = 0.99, 2.64].) To adjust for potential misclassification bias, the NRC uses the construct of Wald and coworkers. The technical details of the adjustment are contained in Wald et al. (1986) and to a lesser degree in the NRC report. After correcting the overall observed RR estimate of 1.34 downward for an expected positive (upward) bias from smoker misclassification, the NRC concludes that the relative risk is about 1.25, and probably lies between 1.15 and 1.35. Correction for background sources (i.e., nonspousal sources of ETS) increases the NRC estimate of RR for an "exposed" person (i.e., exposed to ETS from spousal smoking) to 1.42 (range of 1.24 to 1.61); the change is due only to implicit redefinition of RR to mean risk relative to zeroETS exposure instead of relative to nonspousal sources of ETS. Under this redefinition, the RR for an "unexposed" person (i.e., unexposed to spousal ETS) versus a truly unexposed person (i.e., in a zeroETS environment) becomes 1.14 (range of 1.08 to 1.21). The NRC report further estimates that about 21% of the lung cancers in nonsmoking women and 20% in nonsmoking men may be attributable to exposure to ETS (NRC, 1986, Appendix C); these estimates, however, are based on RRs corrected for background ETS but not for smoker misclassification. Applying these percentages to estimates of 6,500 LCDs in neversmoking women and 3,000 LCDs in neversmoking men in 1988 (American Cancer Society, personal communication), the number attributable to ETS exposure is 1,365 and 600, respectively, for a total of about 2,000 LCDs among neversmokers of both sexes. Robins (NRC, 1986, Appendix D [included in the NRC report but neither endorsed nor rejected by the committee]) explores three approaches to assessment of lung cancer risk from exposure to ETS, each with attendant assumptions clearly stated. A related article by Robins et al. (1989) contains most of the same information. Method 1 is based solely on evaluation of the epidemiologic data applying two assumptions: (1) correction of relative risk for background exposure to ETS independent of age, and (2) the excess relative risk in a nonsmoker is proportional to the lifetime dose of ETS. In this method, Robins uses a weighted average RR of 1.3. After correcting this RR for background ETS exposure, ageadjusted populationattributable risks are calculated for females and males separately. Adjusting Robins' results to 6,500 annual LCDs in female neversmokers and 3,000 LCDs in male neversmokers, for comparison purposes, yields estimates of 1,870 female LCDs and 470 male LCDs attributable to ETS. Method 2 uses an overall relative risk value based on epidemiologic data, but also makes some assumptions to appeal to results of Day and Brown (1980) and Brown and Chu (1987) on lung cancer risk in active smokers. Again, adjusting Robins' estimates to 6,500 female LCDs and 3,000 male LCDs, the range of excess LCDs attributable to ETS is 1,650 to 2,990 for neversmoking females and 420 to 1,120 for neversmoking males. Method 3 is a "cigaretteequivalents" approach and is discussed in Section 6.2.2. The Centers for Disease Control (CDC) has published an estimate of 3,825 (2,495 female and 1,330 male) deaths in nonsmokers from lung cancer attributable to passive smoking for the year 1988 (CDC, 1991a), with reference to the NRC report of 1986. Those figures are the midrange of values for males and females from method 2 of Robins in Appendix D of the NRC report (NRC, 1986). Blot and Fraumeni (1986) published a review and discussion of the available epidemiologic studies about the same time that the reports of the Surgeon General and NRC appeared. The set of studies considered by Blot and Fraumeni are almost identical to those included in the NRC report, except for omission of one cohort study (Gillis et al., 1984), and inclusion of Wu et al. (1985), the casecontrol study excluded by the NRC because the raw data were unpublished. An overall relative risk estimate calculated from the raw data for females yields 1.3 (95% C.I. = 1.1, 1.5). When the results are combined for highexposure categories, the overall relative risk estimate is 1.7 (1.4, 2.1). Wells (1988) provides a quantitative risk assessment that includes several epidemiologic studies subsequent to the NRC and Surgeon General's reports of 1986 (NRC, 1986; U.S. DHHS, 1986). Like the NRC report, the epidemiologic data for both women and men are considered, for which Wells provides separate estimates of overall relative risk and attributable risk. Wells calculates an overall relative risk of 1.44 (95% C.I. = 1.26, 1.66) for females and 2.1 (1.3, 3.2) for males. Following the general approach of Wald et al. (1986), the misclassification percentage for eversmokers is assumed to be 5% (compared to 7% for Wald et al.). Rates are corrected for background exposure to ETS, except in studies from Greece, Japan, and Hong Kong, where the older nonsmoking women are assumed to experience very little exposure to ETS outside the home. A refinement in the estimation of populationattributable risk is provided by adjusting for age at death (which also appears in the calculations of Robins, NRC, Appendix D). The calculation of populationattributable risk applies to former smokers as well as neversmokers, which is a departure from Wald et al. and the NRC report. The annual number of LCDs attributable to ETS in the United States is estimated to be 1,232 (females) and 2,499 (males) for a total of 3,731. About 3,000, however, is thought to be the best current estimate (Wells, 1988). (In addition to the estimates of ETSattributable LCDs, Wells uses the epidemiological approach to derive estimates of ETSattributable deaths from other cancers11,000and from heart disease32,000.) Saracci and Riboli (1989), of the International Agency for Research on Cancer (IARC), review the evidence from the 3 cohort studies and 11 of the casecontrol studies (Table 41). The authors follow the example of the NRC and Wald et al. with respect to the exclusion of studies, and add only one additional casecontrol study (Humble et al., 1987). The overall observed relative risk for the studies, 1.35 (95% C.I. = 1.20, 1.53), is about the same as that reported by the NRC, 1.34 (1.18, 1.53). It is not reported how the overall relative risk was calculated. Repace and Lowrey (1985) suggest two methods to quantify lung cancer risk associated with ETS. One method is based on epidemiologic data, but, unlike the previous examples, Repace and Lowrey use a study comparing SeventhDay Adventists (SDAs) (Phillips et al., 1980a,b) with a demographically and educationally matched group of nonSDAs who are also neversmokers to obtain estimates of the relative risk of lung cancer mortality, in what they describe as a "phenomenological" approach. The SDA/nonSDA comparison provides a basis for assessing lung cancer risk from ETS in a broader environment, particularly outside the home, than the other epidemiologic studies. It also serves as an independent source of data and an alternative approach for comparison. Information regarding the number of agespecific LCDs and personyears at risk for the two cohorts is obtained from the study. The basis for comparison of the two groups is the premise that the nonSDA cohort is more likely to be exposed to ETS than the SDA group due to differences in lifestyle. Relatively few SDAs smoke, so an SDA neversmoker is probably less likely to be exposed at home by a smoking spouse, in the workplace, or elsewhere, if associations are predominantly with other SDAs. One of the virtues of this novel approach is that it contributes to the variety of evidence for evaluation and provides a new perspective on the topic. Phillips et al. (1980 a,b) reported that the nonSDA cohort experienced an average LCMR equal to 2.4 times that of the SDA cohort. Using 1974 U.S. Life Tables, Repace and Lowrey calculate the difference in LCMR for the two cohorts by 5year age intervals and then apply this value to an estimated 62 million neversmokers in the United States in 1979 to obtain the number of LCDs attributable to ETS annually. The result, 4,665, corresponds to a risk rate of about 7.4 LCDs per 100,000 personyears. In an average lifespan of 75 years, that value equates to 5.5 deaths per 1,000 people exposed. The second method described by Repace and Lowrey is a "cigaretteequivalents" approach and is discussed in Section 6.2.2. Wigle et al. (1987) apply the epidemiologic evidence from the SDA/nonSDA study (Phillips et al., 1980a,b) to obtain estimates of the number of LCDs in neversmokers due to ETS in the population of Canada. The estimated number of deaths from lung cancer attributable to passive smoking is calculated separately for males and females, using agespecific population figures for Canada and the agespecific rates of death from lung cancer attributable to ETS estimated by Repace and Lowrey (1985). A total of 50 to 60 LCDs per year is attributed to spousal smoking alone, with 90% of them in women. Overall, involuntary exposure to tobacco smoke at home, work, and elsewhere may cause about 330 LCDs annually. 6.2.2. Examples Based on CigaretteEquivalents The cigaretteequivalents approach assumes that the doseresponse curve for lung cancer risk from active smoking also applies to passive smoking, after extrapolation of the curve to lower doses and conversion of ETS exposure into an "equivalent" exposure from active smoking, determined from a surrogate measure of exposure common to passive and active smoking. Relative cotinine concentrations in body fluids (urine, blood, or saliva) of smokers versus nonsmokers and tobacco smoke particulates in sidestream smoke (SS) and mainstream smoke (MS) have commonly been used for this purpose. The lung cancer risk of ETS is assumed to equal the risk from active smoking at the rate determined by the cigaretteequivalents. For example, suppose the average cotinine concentration in exposed neversmokers is 1% of the average value found in people who smoke 30 cigarettes per day. The lung cancer risk for a smoker of (0.01)30 = 0.3 cigarettes per day is estimated by lowdose extrapolation from a doseresponse curve for active smoking, and that value is used to describe the lung cancer risk for ETS exposure. This general explanation describes the nature of the approach; however, authors vary in their constructed solutions and level of detail. The basic assumption of cigaretteequivalents procedures is that the lung cancer risks in passive and active smokers are equivalently indexed by the common measure of exposure to tobacco smoke, i.e., a common value of the surrogate measure of exposure in an active and a passive smoker would imply the same lung cancer risk in both. This assumption may not be tenable, however, as MS and SS differ in the relative composition of carcinogens and other components identified in tobacco smoke and in their physicochemical properties in general; the lung and systemic distribution of chemical agents common to MS and SS are affected by their relative distribution between the vapor and particle phases, which differs between MS and SS and changes with SS as it ages. Active and passive smoking also differ in characteristics of intake; for example, intermittent (possibly deep) puffing in contrast to normal (shallow) inhalation, which may affect deposition and systemic distribution of various tobacco smoke components as well (see Sections 3.2 and 3.3.2). Several authors have taken issue with the validity of the cigaretteequivalents approach. For example, Hoffmann et al. (1989), in discussing the longer clearance times of cotinine from passive smokers than from active smokers, conclude that "the differences in the elimination time of cotinine from urine preclude a direct extrapolation of cigaretteequivalents to smoke uptake by involuntary smokers." A recent consensus report of an IARC panel of experts (Saracci, 1989) states, "Lacking knowledge of which substances are responsible for the wellestablished carcinogenic effect of MS, it is impossible to accurately gauge the degree of its similarity to ETS in respect to carcinogenic potential." The Surgeon General's report devotes a threepage section to the concept of cigaretteequivalents, quantitatively demonstrating how they can vary as a measure of exposure (U.S. DHHS, 1986). It concludes that "these limitations make extrapolation from atmospheric measures to cigaretteequivalents units of disease risk a complex and potentially meaningless process." (On a lesser note, it has generally been assumed that the doseresponse relationship for active smokers is reasonably well characterized. Recent literature raises some questions on this issue [Moolgavkar et al., 1989; Gaffney and Altshuler, 1988; Freedman and Navidi, 1987a,b; Whittemore, 1988].)Citing cigaretteequivalents calculated in other sources, Vutuc (1984) assumes a range of 0.1 to 1.0 cigarettes per day for ETS exposure. Relative risks for nonsmokers are calculated for 10year age intervals (40 to 80) based on the reported relationships of dose, time, and lung cancer incidence in Doll and Peto (1978). Relative risks for smokers of 0.1 to 1.0 cigarettes per day give a range in relative risk from 1.03 to 1.36. The author concludes that "as it applies to passive smokers, this range of exposures may be neglected because it has no major effect on lung cancer incidence." Vutuc assumes that his figures apply to both males and females. If an exposure fraction of 75% is assumed for both males and females, the range of relative risks given correspond to a range for populationattributable risk. If the number of LCDs among neversmokers in the United States in 1988 is about 6,500 females and 3,000 males (personal communication from the American Cancer Society), then the number of LCDs in neversmokers attributable to ETS is estimated to range from 240 to 2,020 (140 to 1,380 for females alone). So Vutuc's figures are consistent with several hundred excess LCDs among neversmokers in the United States. These estimates are from our extension of Vutuc's analysis, however, and are not the claim of the author. Repace and Lowrey (1985) describe a cigaretteequivalents approach as an alternative to their "phenomenological" approach discussed in Section 6.2.1. One objective is to provide an assessment of exposure to ETS from all sources that is more inclusive and quantitative than might be available from studies based on spousal smoking. They consider exposure to ETS both at home and in the workplace, using a probabilityweighted average of exposure to respirable suspended particulates (RSP) in the two environments. Exposure values are derived from their basic equilibrium model relating ambient concentration of particulates to the number of burning cigarettes per unit volume of air space and to the air change rate. From 1982 statistics of lung cancer mortality rates among smokers and their own previous estimates of daily tar intake by smokers, the authors calculate a lung cancer risk for active smokers of 5.8 ' 10é6 LCDs/year per mg tar/day per smoker of lung cancer age. The essential assumption linking lung cancer risk in passive and active smokers is that inhaled tobacco tar poses the same risk to either on a per unit basis. Extrapolation of risk from exposure levels for active smokers to values calculated for passive smokers is accomplished by assuming that doseresponse follows the onehit model for carcinogenesis. An estimated 555 LCDs per year in U.S. nonsmokers (neversmokers and former smokers) are attributed to ETS exposure (for 1980). The ratio of total LCDs in 1988 to 1980 is approximately 1.37 (Repace, 1989). With that population adjustment factor, the approximate number of LCDs attributable to ETS among nonsmokers is closer to 760 for 1988 (including former smokers). Method 3 of Robins (NRC, 1986, Appendix Dagain, included in the NRC report but not specifically endorsed by the committee) extrapolates from data on active smoking, along with several assumptions. Applying his results to 6,500 females and 3,000 males, the range of excess LCDs in neversmokers due to ETS is 550 to 2,940 for females and 153 to 1,090 for males. Russell and coworkers (1986) use data on urinary nicotine concentrations in smokers and nonsmokers to estimate exposure and risk from passive smoking. The risk of premature death from passive smoking is presumed to be in the same ratio to premature death in active smokers as the ratio of concentrations of urinary nicotine in passive to active smokers (about 0.007). Calculations are made using vital statistics for Great Britain and then extrapolated to the United States. The latter estimate, 4,000+ deaths per year due to passive smoking, is for all causes of death, not just LCDs. Arundel et al. (1987) attributes only five LCDs among female neversmokers to ETS exposure. The corresponding figure for males is seven (both figures are adjusted to 6,500 females and 3,000 males). The expected lung cancer risk for neversmokers is estimated by downward extrapolation of the lung cancer risk per mg of particulate ETS exposure for current smokers. The authors' premise is that the lung carcinogenicity of ETS is entirely attributable to the particulate phase of ETS, and the consequent risk in passive smoking is comparable to active smoking on a per mg basis of particulate ETS retained in the lung. If the vapor phase of ETS were also considered, the number of LCDs attributable to ETS would likely increase (e.g., see Wells, 1991). X` hp x (#%'0*,.8135@8: RR(dE) > 1 (see Section 8.3). The method used here is based on several assumptions: (1) that body cotinine levels in neversmokers are linearly related to ETS exposure; (2) that current ETS exposure is representative of past exposures; and (3) that the excess risk of lung cancer in nonsmokers exposed to ETS is linearly related to the dose absorbed. Estimates of RR(dE) for female neversmokers were derived in Chapter 5, where they were corrected for smoker misclassification bias; these are redefined in Section 6.3.2 as RR2. The relative risk estimates are then adjusted to be applicable to different baseline exposure groups in order to calculate population risks for neversmoking women. In order to extend the analyses to female former smokers and male never and former smokers, the relative risks are converted to excess or additive risks. The use of additive risks is more appropriate for these groups because of the different baseline lung cancer mortality rates by sex and smoking status (former vs. never). More specifically, estimates of ETSattributable population mortality are calculated from female lung cancer mortality rates, which are themselves derived from summary relative risk estimates either from the 11 U.S. studies combined (Section 6.3.3) or from the Fontham et al. (1991) study alone (Section 6.3.4), along with other parameter estimates from prominent sources (Section 6.3.2). The LCMRs in this instance are defined as the number of LCDs in 1985 per 100,000 of the population at risk. The LCMR in U.S. women under age 35 is minuscule, so only persons of age 35 and above are considered at risk. Although these LCMRs are expressed as a mortality rate per 100,000 of the population at risk, as derived they are applicable only to the entire population at risk and not to any fraction thereof that might, for example, have a different average exposure or age distribution. The LCMR for the subpopulation and exposure scenario to which the epidemiologic studies apply most directlyneversmoking females exposed to spousal ETSis estimated first. That estimate is then incremented to include exposure to nonspousal ETS for all neversmoking females. For the ETSattributable population mortality estimates, these LCMRs are applied to neversmoking males and former smokers at risk, as well as to the females at risk for which the rates were specifically derived. The most reliable component of the total estimate constructed for the United States is the estimate for the female neversmokers exposed to spousal ETS. The other components require additional assumptions, which are described. As the number of assumptions increases, so does the uncertainty of the estimates. Thus, the total estimate of lung cancer risk to U.S. nonsmokers of both sexes is composed of component estimates of varying degrees of certainty. One might argue that smokers are among those most heavily exposed to ETS, since they are in close proximity to sidestream smoke (the main component of ETS) from their own cigarettes and are also more likely than neversmokers to be exposed to ETS from other smokers. The purpose of this report, however, is to address respiratory health risks from ETS exposure in nonsmokers. In current smokers, the added risk from passive smoking is relatively insignificant compared to the selfinflicted risk from active smoking. 6.3.2. Parameters and Formulae for Attributable Risk Several parameters and formulae are needed to calculate attributable risk. These are presented in Table 61, with the derivations explained below. The size of the target population, in this case the number of women in the United States of age 35+ in 1985, is denoted by N, with N = N1 + N2, where N1 = the number of eversmokers and N2 = the number of neversmokers. The total number of LCDs from all sources, T, is apportioned into components from four attributable sources: (1) nontobaccosmokerelated causes, the background causes that would persist in an environment free of tobacco smoke; (2) background ETS, which refers to all ETS exposure other than that from spousal smoking; (3) spousal ETS; and (4) eversmoking. The risk from nontobaccosmokerelated causes (source 1) is a baseline risk (discussed below) assumed to apply equally to the entire target population (neversmokers and eversmokers alike). The eversmoking component of attributable risk (source 4) refers to the incremental risk above the baseline in eversmokers (this report does not partition the incremental risk in eversmokers further into components due to background ETS and spousal ETS, except for longterm [5+ years] former smokers). The background ETS component (source 2) is the incremental risk above the baseline in all neversmokers from exposure to nonspousal sources of  '3  X,  1  1 yX` hp x (#%'0*,.8135@8:x6y ,  Table 61. Definition and estimates of relative risk of lung cancer for 11 U.S. studies combined for various exposure sources and baselines; population parameter definitions and estimates used to calculate U.S. populationattributable risk estimates for ETS h ddxX( ddxX( h "p p " DENOMINATORăNUMERATOR of relative risk"    "(Baseline)!All persons9Neversmokers 9ETS exposure%PCurrent and former smokers"  "t Source of exposureNontobaccosmoke sources of exposure0Background ETS?Background ETS and spousal ETSd&QActive smoking"@@"#[nt]h1[nt]+[ETSB]@[nt]+[ETSB]+[ETSS]%P[nt]+[ETS]+[ACT]"P P "|[nt]$1t2RR03 = 1.34 BRR02 = 1.591ă&SRR01 = 13.8"P P "d[nt]+[ETSB]$5$BRR2 = 1.192ă&SRR11 = 10.3"H    H    "R [nt]+[ETSB]+[ETSS]$5 E&SRR1 = 9.263ă  X` hp x (#%'0*,.8135@8: RR2 > 1. (For the values used in this report, this relation is true. See also the discussion in Section 8.3.) Under these assumptions, RR02 = 1 + ZdN (from Section 6.3.1), or ` `   RR02 = (Z 1)/( Z/RR2 1).-pp27  <xxA(62) Determination of a value for Z from data on cotinine concentrations (or cotinine/creatinine) is discussed below. The conversion of RR1 to the same zeroETS baseline risk as RR02 follows from multiplying expression (61) by RR02/RR2, i.e., ` `   RR01 = RR1(P2RR02 + (1 P2)RR02/RR2).7  <xxA(63) X` hp x (#%'0*,.8135@8:x6y , X` Uhp x (#%'0*,.8135@8:Y  ddx >Y .@@@@@@@P@@@@@@@P. Lung cancer mortality2   .@@@@@@@@P@@@@@@@@P.(1)(2)(3)(4)(5).@@@@@@@@P@@@@@@@@P..EEEEEEEUEEEEEEEU.Smoking status3Exposed to spousal ETSNumber at risk (in millions)Nontobaccosmokerelated causes4Background ETSSpousal ETSEversmokingTotal.@@.NSNo12.921,220 (3.2) 410 (1.1).@@..@@.NSYes19.381,830 (4.8) 620 (1.6) 470 (1.2).@@..@@.ES25.692,420 (6.4)31,0305 (81.7).@@..H H .Total58.005,470 (14.4) 1,030 (2.7) 470 (1.2)31,030 (81.7)38,000  1Percentage of grand total (38,000) in parentheses. 2The nonblank entries in the table are the product of an individual's attributable risk of lung cancer from nontobacco smokerelated causes (expression 69 (38,000/58,000,000)), the number at risk in column (1), and the following columnspecific XC` Uhp x (#%'0*,.8135@8:x6y , X` /p x (#%'0*,.8135@8:x6y , X` hp x (#%'0*,.8135@8:x6y , X`  p x (#%'0*,.8135@8: