Previous Lung Disease and Risk of Lung Cancer among Men and Women Nonsmokers

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1 American Journal of Epidemiology Copyright 1999 by The Johns Hopkins University School of Hygiene and Public Health All rights reserved Vol. 149,. 1 Printed in U.S.A. Previous Lung Disease and Risk of Lung Cancer among Men and Women nsmokers Susan T. Mayne, 1 Joan Buenconsejo, 1 and DwightT. Janerich 2 From 1982 to 1984, the authors conducted a population-based case-control study of lung cancer in men and women nonsmokers in New York State. In-person interviews were completed for 437 lung cancer cases (197 never smokers, 240 former smokers) and 437 matched population controls. Cases and controls were asked to report any history of physician-diagnosed nonmalignant lung disease; cases were more likely than controls to report such a history. Statistically significant associations were found for emphysema (odds ratio (OR) = 1.94, 95% confidence interval (Cl) ), chronic bronchitis (OR = 1.73, 95% Cl ), and the combined endpoint of emphysema, chronic bronchitis, or asthma (OR = 1.82, 95% Cl ). After adjustment for active and passive tobacco smoke exposure, emphysema, chronic bronchitis, and asthma (each condition and the combined endpoint) were significantly associated with lung cancer risk. The risk was more marked for squamous cell carcinomas and for subjects who were diagnosed at older ages, and it remained significant when surrogate interviews were excluded. These results are consistent with the hypothesis that certain prior lung conditions increase the risk of lung cancer in men and women nonsmokers. Am J Epidemiol 1999;149: asthma; bronchitis; case-control studies; emphysema; lung diseases; lung neoplasms A number of nonmalignant lung conditions, such as chronic bronchitis, emphysema, asthma, pneumonia, tuberculosis, silicosis, and asbestosis, have been associated with an increased risk of lung cancer (1-9). Some of these conditions, such as emphysema and chronic bronchitis, are strongly associated with tobacco smoking, with an obvious potential for residual confounding. The problem of residual confounding by active smoking can be overcome by studying previous lung diseases as a risk factor for lung cancer in nonsmokers. While it is difficult to assemble a case group of nonsmokers with lung cancer, a few studies of nonsmokers, particularly women, have been done. For example, Wu et al. (1) reported that in the United States, women lifetime nonsmokers with lung cancer had a statistically significant excess of any previous lung disease, asthma, and chronic bronchitis compared with a control group of women nonsmokers. Alavanja et al. (2) also studied US women who were nonsmokers and found significant risks for asthma and pneu- Received for publication December 9, 1997, and accepted for publication May 5, Abbreviations: Cl, confidence interval; OR, odds ratio. 1 Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, CT. 2 Foundation for Blood Research, Portland, ME. Reprint requests to Dr. Susan T. Mayne, Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College Street, New Haven, CT monia among lifetime nonsmokers and for emphysema and tuberculosis among former smokers. We completed a population-based case-control study of lung cancer in men and women nonsmokers in the United States; some of the findings have been published previously (10, 11). This study provided a unique opportunity to examine risk factors for lung cancer in a relatively large number of men and women nonsmokers. Moreover, as these data were originally obtained primarily to evaluate passive smoke exposure as a risk factor for lung cancer in nonsmokers, this study enabled us to consider the confounding effects of environmental tobacco smoke, as well as a number of other potential confounders, when examining the association between previous lung disease and lung cancer risk. This report summarizes the major findings of our evaluation of previous lung diseases as a risk factor for lung cancer in men and women nonsmokers. MATERIALS AND METHODS A population-based, individually matched casecontrol study of lung cancer in nonsmokers was conducted in New York State from 1982 to The data collection methods have been described previously (10, 11). The procedures used were approved by the Institutional Review Board of the New York State Department of Health. Informed consent was obtained from all participants. 13

2 14 Mayne et al. The study area comprised eight Standard Metropolitan Statistical Areas (23 counties) of upstate New York. A special system to enable rapid ascertainment of lung cancer cases was established in this region so that diagnosed patients could be identified and interviewed as soon as possible. Patients were typically identified via the medical records department, the pathology department, or the tumor registry at the institutions in this region. To be included as a case in the study, a patient had to reside in the 23-county region, be aged years, have never smoked more than 100 cigarettes (nonsmokers), or have smoked at some time but not more than 100 cigarettes in the 10 years prior to diagnosis (former smokers). Cases also must have been given a diagnosis of primary lung cancer between July 1, 1982, and December 31, Initial diagnoses were confirmed by clinical records and by reexamination of pathologic specimens. Slides or blocks of tissue were available for all but five cases. All materials were reviewed by investigators, who were masked with respect to the patient's initial diagnosis, smoking history, and other risk factors. Interviews were conducted with 76 percent of the eligible patients or their closest available relatives or friends (surrogates). One population control was selected for each case. Controls were selected randomly from the New York State Department of Motor Vehicles' file of licensed drivers. For each case, six potential controls were identified on the basis of age (±5 years), sex, and county of residence. Potential controls were called and screened for smoking status. The first potential control whose smoking status matched that of the case and who agreed to participate in the study was included. On average, two potential controls had to be contacted to obtain one who matched the case and was willing to participate. The field staff conducted face-to-face interviews in the homes of all cases and controls. Information was collected by using a precoded questionnaire that took approximately 1 hour to complete. Cases and controls were interviewed in the same manner and with the same questionnaire. attempt was made to mask interviewers to case-control status because of the often-obvious evidence of disease among lung cancer patients. Despite efforts to identify and interview all cases rapidly, surrogate interviews were needed for approximately one third of all cases. When a surrogate respondent was used for the case, a surrogate respondent was also used for the matched control (with the exception of nine matched controls for whom surrogate control interviews were not matched for surrogate case interviews). Thus, cases and controls were matched for sex, age, smoking history, county of residence, and interview type (self or surrogate). Cases and controls were asked whether a physician had ever told them that they had ever had certain lung conditions. If they answered yes, they were asked to report the number of times that they had been told, the year in which the condition was first diagnosed, the year in which they were first hospitalized for the condition, the number of times that they were hospitalized for the condition, and whether they received medication for the condition. Descriptive statistics were first used to characterize the study population. Case-control differences in variables associated with prior lung diseases (number of events, number of years since first hospitalization, etc.) were evaluated by using either the Student's t test or the Wilcoxon's test as appropriate to test statistical significance. Odds ratios for prior lung diseases were then estimated by conditional logistic regression, as described by Holford et al. (12). This method is based on the linear logistic model described by Cornfield et al. (13) and takes into account pairwise matching in case-control studies. To determine whether the relation between prior lung diseases and lung cancer risk differed according to interview type, smoking status, sex, age, or histologic type, the relevant case-control pairs from each subgroup were examined separately, and odds ratios were calculated as described previously. The attributable risk percentage for the population was calculated as described by Kelsey et al. (14). To address the issue of confounding, several potential confounders (interview type, smoking history, sex, county of residence, and age) were matched and thus were not included in the logistic models. A variety of measures of prior active smoking among the former smokers were evaluated for potential confounding, including the number of cigarettes smoked per day, years of smoking, pack-years of exposure, and years since quitting. Only the first measure was found to differ by case-control status and to affect the risk estimates; therefore, it was included in multivariate models. Passive smoke exposure was quantified as described previously (10) and was included in multivariate models. Similarly, dietary variables were quantified as described previously (11) and were included in multivariate models. Education was dichotomized for adjustment on the basis of tree-based regression analyses (15). All other adjustment variables were modeled as continuous variables. The final multivariate models included the following potential confounders: tobaccorelated variables (cigarettes per day, lifetime passive smoke exposure), dietary variables (frequency of consumption of fresh fruit and vegetables, whole milk, and supplemental vitamin E), and education. Am J Epidemiol Vol. 149,. 1, 1999

3 Previous Lung Disease and Lung Cancer Risk 15 It is conceivable that the cases might have had early symptoms of lung cancer that could have been diagnosed incorrectly as prior lung disease, which could artificially increase the magnitude of any association between prior lung diseases and lung cancer risk. To examine this possibility, we reran the analyses by restricting the data set to those previous lung diseases that were first diagnosed more than 5 years before the date of interview. RESULTS i b C\j h-; CO CO C\J CM n1 V4J «CO o ^ The sociodemographic characteristics of the 437 case-control pairs included in this analysis are summarized in table 1. Of the cases, approximately one half were female and 45 percent were never smokers. Adenocarcinoma was the predominant (51 percent) histologic type among the cases. This distribution of lung cancer by histologic type in nonsmokers differed from the overall distribution in the early 1980s, when squamous cell carcinoma was predominant (16). The duration of smoking and the number of years since quitting were similar for cases and controls who were former smokers, although among those who had smoked previously, the intensity of smoking was significantly greater among the cases than the controls (mean number of cigarettes per day, 28.2 vs. 23.7). As shown in table 2, cases were more likely than their matched controls to report a history of physiciandiagnosed nonmalignant lung diseases. Odds ratios were elevated for all conditions about which they were queried except for punctured lung, reported by only two cases and four controls, and for influenza, reported by 86 cases and 86 controls. Physician-diagnosed emphysema (odds ratio (OR) = 1.94, p = 0.02) and chronic bronchitis (OR = 1.73, p = 0.02) were significantly associated with lung cancer risk. Physiciandiagnosed asthma also notably increased lung cancer risk (OR = 1.85), although this effect was not statistically significant in univariate analyses (p = 0.07). A total of 21 percent of cases (90/437) but only 12 percent of controls (54/437) reported a history of emphysema, chronic bronchitis, or asthma (OR = 1.82, p = 0.001). When all prior lung conditions were considered together, a greater proportion of cases than of controls reported being affected (54 vs. 49 percent). Data on the risk associated with a history of emphysema, chronic bronchitis, or asthma, by sex, smoking status, age, interview type, and histology, are shown in table 3. The odds ratios indicate that in men, chronic bronchitis was associated with a larger risk (OR = 2.08) than either emphysema (OR = 1.53) or asthma (OR = 1.43). However, in women, the converse was true; emphysema (OR = 4.00) and asthma (OR = 2.33) were associated with greater risk than chronic bronchi- % <n 6 fl m 2 < g. 31 CO CD s: cq cq oi r^ CM C\J < V m < <o T- ii cu ii o II. -2 II S "g-sto csw CD CO O loo O o 1 a oo Am J Epidemiol Vol. 149,. 1, 1999

4 16 Mayne et al. TABLE 2. Previous nonmalignant lung diseases and risk of lung cancer among men and women nonsmokers, New York Lung Cancer Study, Condition Cases (no.) Controls (no.) Odds ratio* 95% confidence interval P value Tuberculosis Pneumonia Emphysema Influenza Chronic bronchitis Asthma Punctured lung Bulbar polio Lung infection Any prior lung condition Emphysema, chronic bronchitis, or asthma Any prior lung conditionf * Crude odds ratio from conditional logistic regression analyses, t Excluding emphysema, chronic bronchitis, or asthma. tis (OR = 1.50). Among never smokers (many of whom were women), emphysema increased risk threefold. Asthma was not an important risk factor in never smokers (OR = 1.10) but was associated with substantial risk in former smokers (OR = 4.33). All three conditions were more important risk factors for lung cancer diagnosed at older versus younger ages, and all three were significantly associated with lung cancer risk when analyses were restricted to those pairs interviewed in person. Both emphysema and chronic bronchitis more than doubled the risk of squamous cell cancers (p < 0.05) but contributed little toward the risk of adenocarcinomas in this study population. Since the intensity of smoking among cases who were former smokers was greater than that of their matched controls, some of these associations could be due to residual confounding by active smoking. Also, exposure to environmental tobacco smoke during childhood increases the frequency of physician-diagnosed bronchitis (17), and exposures during adulthood reduce pulmonary function (17). Therefore, multivariate analyses were done to generate risk estimates, and Am J Epidemiol Vol. 149,. 1, 1999

5 Previous Lung Disease and Lung Cancer Risk 17 TABLE 3. History of emphysema, chronic bronchitis, or asthma and risk of lung cancer among men and women nonsmokers, New York Lung Cancer Study, Emphysema Sex Male Female Smoking status Former smoker Never smoker Age at interview (years) >70 <70 Interview type Self Proxy Histology Squamous Adenocarcinoma Other Chronic bronchitis Sex Male Female Smoking status Former smoker Never smoker Age at interview (years) >70 <70 Interview type Self Proxy Histology Squamous Adenocarcinoma Other Asthma Sex Male Female Smoking status Former smoker Never smoker Age at interview (years) >70 <70 Interview type Self Proxy Histology Squamous Adenocarcinoma Other Pairs* (no.) Odds ratiot % confidence interval ^ ^ * One population control was selected for each case. t Crude odds ratio from conditional logistic regression analyses. P value we took into account these and other potential confounding variables. As shown in table 4, emphysema, chronic bronchitis, and asthma were all significantly associated with lung cancer risk following adjustment for active and passive tobacco smoke exposure (model 1) but were no longer significant after additional adjustment for dietary variables and education. The TABLE 4. Multivariate analysis of history of emphysema, chronic bronchitis, or asthma and risk of lung cancer among men and women nonsmokers, New York Lung Cancer Study, Pairs* (no.) Odds ratiot 95% confidence interval P value Emphysema Univariate Model 1f Model 2% Model Model 4H Chronic bronchitis Univariate Model Model Model Model Asthma Univariate Model Model Model Model Emphysema, chronic bronchitis, or asthma Univariate Model Model Model Model * One population control was selected for each case. t Adjusted for smoking-related variables (cigarettes smoked/day, lifetime passive smoke exposure). % Adjusted for dietary variables (frequency of consumption of fresh fruits and vegetables, whole milk, and vitamin E supplements). Adjusted for smoking-related variables and dietary variables. H Adjusted for smoking-related variables, dietary variables, and educational level (<15 years vs. >15 years). three conditions combined remained statistically significant in all models except the final one (model 4). The loss of significance after adjustment may partially reflect a loss of statistical power (a decrease in the number of pairs with informative data); however, the point estimates for chronic bronchitis and emphysema, but not for asthma, were reduced after adjustment. Cases and controls who reported having a given lung condition were queried about the number of events, the year in which they were first diagnosed with the condition, the year in which they were first hospitalized for the condition, the number of hospitalizations for the condition, and whether medication was given for the condition. The reports from cases and controls with a given lung condition were similar for these variables, and only two of the case-control comparisons were statistically significant. First, cases were significantly older at first hospitalization for pneumonia than were controls (median 55.5 years vs years, p = ). Second, the proportion of cases and controls with a given lung condition who received medication for that condition was similar for all conditions except emphysema (28 percent of cases vs. 58 Am J Epidemiol Vol. 149,. 1, 1999

6 18 Mayne et al. percent of controls received medication for that condition, p = 0.035). We also performed analyses in which we eliminated data on previous lung diseases that reportedly were first diagnosed less than or equal to 5 years before the date of interview. As the 5-year cutpoint is entirely arbitrary, these results should be interpreted cautiously. netheless, this analytic approach should provide a more conservative estimate of effect. The numbers of cases and controls with a given lung condition diagnosed more than 5 years before the date of interview were as follows: asthma, 19 cases versus 14 controls (OR = 1.41, 95 percent CI ); emphysema, 24 cases versus 15 controls (OR = 1.60, 95 percent CI ); and chronic bronchitis, 39 cases versus 26 controls (OR = 1.54, 95 percent CI ). DISCUSSION This study adds to the evidence that certain previous nonmalignant lung diseases are a risk factor for lung cancer. As this study was done with nonsmokers and included assessment of potential confounding by both active and passive smoking, it would seem that the associations observed are not likely to be attributable to tobacco smoke exposure. When all lung diseases were considered together, a history of any previous lung disease increased the odds of lung cancer by 23 percent (nonsignificant). The point estimates indicate that three conditions emphysema, chronic bronchitis, and asthma increased lung cancer risk by percent. This increased risk was statistically significant for all three conditions after taking into account smoking history (former smokers) and passive smoke exposure (table 4, model 1). Further adjustment for dietary variables (models 2 and 3) and for education (model 4) reduced the magnitude of the risk associated with emphysema and chronic bronchitis, but adjustment did not reduce the risk associated with asthma. However, in this situation the appropriateness of adjustment for diet and education, a proxy for socioeconomic status, is debatable, given that these variables may well be part of the causal path (i.e., dietary factors are associated with airways obstruction (18-19)). Thus, models 2-4 are included for the sake of completeness. However, perhaps model 1 is the most appropriate and the one most comparable with other reports on this topic, most of which did not adjust for dietary variables and only some of which adjusted for education. In the control population, the prevalence of asthma (3.4 percent) and emphysema (4.4 percent) was relatively low and was in the range reported in other studies (summarized by Wu et al. (1)). The prevalence of chronic bronchitis was somewhat higher (7.6 percent) and was also in the range reported in other studies (1). Given the relatively low prevalence of asthma and emphysema and the similar risk conferred by these conditions and by chronic bronchitis, the three conditions were grouped together in univariate and multivariate analyses to increase statistical power. There is a considerable diagnostic overlap for asthma, bronchitis, and chronic obstructive pulmonary disease, making a combined endpoint logical. However, as this grouping was not a priori, results pertaining to the combined grouping should be interpreted cautiously. Results indicate that having any of these three conditions increases the risk of lung cancer by 82 percent (p = (table 2)). Specifics of selected prior lung conditions are described below. In the full population, in women, in those older than age 70 years at the time of interview, and for squamous cell cancers, previous emphysema emerged as a significant risk factor for lung cancer. Others have also reported that the effect of emphysema is stronger in older subjects (5). In our study, emphysema was unassociated with the risk of adenocarcinoma of the lung (OR = 1.14); this finding is consistent with reports by others (2, 6, 8). The observation that cases with emphysema were significantly less likely to be given medication for the condition than were controls with emphysema may in part reflect the lower educational (table 1) and income status (data not shown) of cases versus controls in this study. Chronic bronchitis emerged as a significant risk factor for lung cancer in the full population, in men, in former smokers, in those older than age 70 years at the time of interview, and for squamous cell carcinomas. The finding that the risk was greater for older subjects is consistent with findings from other reports (1,5), as is the lack of risk for adenocarcinomas (2, 6, 8). Some studies have reported that asthma is associated with a reduced risk of lung cancer (5), whereas others have found that asthma increases the risk (1, 2). Some studies of smokers suggest effect modification by sex, with asthma increasing lung cancer risk among men but not among women (20, 21). Some of the inconsistencies may derive from the fact that asthmatics may voluntarily abstain from using tobacco, ultimately showing a lower incidence of lung cancer than the general population. Thus, they would appear to be protected when compared with the general population. However, when compared with a control population of nonsmokers, the risk becomes evident. The finding that asthma was less strongly associated with adenocarcinoma is consistent with findings from other studies of nonsmokers (2). Asthma has become increasingly common among American youth, raising the question of whether life- Am J Epidemiol Vol. 149,. 1, 1999

7 Previous Lung Disease and Lung Cancer Risk 19 long asthma increases the risk of lung cancer in nonsmokers. In this study, cases with asthma were more likely to be diagnosed at older ages than were controls with asthma (age 31 vs. 18 years, p = 0.13), suggesting that latency of disease is not an important risk factor. Cases were also older at first hospitalization (age 46 vs. 21 years, p = 0.19). These differences, while nonsignificant, run counter to those expected, suggesting that the risk associated with asthma should be interpreted with caution. This study found that none of the other lung conditions significantly increased the risk of lung cancer. For example, a history of tuberculosis increased the risk only slightly (OR =1.2 (table 2)) and nonsignificantly (p = 0.67). However, others have found that a history of tuberculosis is significantly associated with lung cancer risk (22). The lack of effect observed in our study may reflect the low (2.3 percent) prevalence of tuberculosis in our control population. How might asthma, emphysema, and chronic bronchitis increase the risk of lung cancer? First-degree relatives of patients with lung cancer or chronic obstructive pulmonary disease have been shown to have significantly higher age-, sex-, race-, and smokingadjusted rates of impaired pulmonary function (23) that might enable an increase in circulating toxins and carcinogens. This might explain our finding that former smokers with asthma, but not never smokers with asthma, were at a markedly increased risk of lung cancer due to impaired clearance of tobacco carcinogens. Alternatively, pulmonary diseases cause tissue damage, which results in the release of peptide growth factors from injured cells and inflammatory cells (24). Inflammatory cells also produce interleukins, interferons, and a host of other molecules that control cell proliferation (24). Cell proliferation (mitogenesis) increases mutagenesis (25), and a proliferative state might form a microenvironment favoring clonal expansion of preneoplastic foci (24, 25). If the association between certain prior lung conditions and lung cancer risk is causal, and if our risk estimates reflect the true magnitude of the associations, then attributable risk calculations indicate that asthma may account for 2.8 percent, emphysema for 4.0 percent, chronic bronchitis for 5.3 percent, all three conditions combined for 9.2 percent, and any prior lung condition for 10.1 percent of the lung cancer cases in nonsmokers. These attributable risks are relatively low, not unexpected given the low prevalence in the control population, coupled with risk estimates of <2.0 for all conditions in the full population. The strength of this study lies in the fact that we were able to analyze data on a relatively large number of lung cancer cases who were nonsmokers. Also, the population-based study design is an important strength. Detailed histories of tobacco smoke exposure were obtained, and cases were carefully classified by histologic type. However, the exposure of interest (previous lung conditions) was based on self-report; no effort was made to abstract medical records of these cases to confirm previous diagnoses of nonmalignant lung conditions. Thus, recall bias is of concern, but the increased risks associated with only some of these conditions but not all argue against a strong influence of recall bias in these data. Also, it is conceivable that some of the excess in prior lung diseases among the cases may in fact reflect preclinical lung cancer. Results of analyses excluding events first diagnosed within 5 years of the date of interview (an arbitrary cutpoint) show a reduction in the risk estimates; nonetheless, the excess risk in cases relative to controls was not eliminated when this more conservative analytical approach was used. Another limitation is that smoking status was based on self-report; no objective marker such as cotinine was used. Thus, it is possible that cases and controls who truly were smokers were misclassified as nonsmokers. In conclusion, this population-based case-control study of lung cancer in nonsmokers suggests that previous lung disease, specifically emphysema, chronic bronchitis, and possibly asthma, may increase the risk of lung cancer. These associations remained significant following adjustment for prior active smoking and previous exposure to passive smoking, adding further weight to the suggestions of others that these associations are not due to residual confounding by tobacco. ACKNOWLEDGMENTS Supported by grant R01 CA from the National Institutes of Health and by institutional funds from the Yale Cancer Center in New Haven, Connecticut. REFERENCES 1. Wu AH, Fontham ETH, Reynolds P, et al. Previous lung disease and risk of lung cancer among lifetime nonsmoking women in the United States. Am J Epidemiol 1995,141: Alavanja MCR, Brownson RC, Boice JD Jr, et al. Preexisting lung disease and lung cancer among nonsmoking women. Am J Epidemiol 1992;136: Wu AH, Henderson BE, Pike MC, et al. Smoking and other risk factors for lung cancer in women. J Natl Cancer Inst 1985;74: Samet JM, Humble CG, Pathak DR. Personal and family history of respiratory disease and lung cancer risk. Am Rev RespirDis 1986;134: Am J Epidemiol Vol. 149,. 1, 1999

8 20 Mayne et al. 5. Osann KE. Lung cancer in women: the importance of smoking, family history of cancer, and medical history of respiratory disease. Cancer Res 1991;51: Gao Y-T, Blot WJ, Zheng W, et al. Lung cancer among Chinese women. Int J Cancer 1987;40: Wu AH, Yu MC, Thomas DC, et al. Personal and family history of lung disease as risk factors for adenocarcinoma of the lung. Cancer Res 1988;48: Wu-Williams AH, Dai XD, Blot W, et al. Lung cancer among women in north-east China. Br J Cancer 1990;62: Blot WJ, Fraumeni JF Jr. Cancers of the lung and pleura. In: Schottenfeld D, Fraumeni JF Jr, eds. Cancer epidemiology and prevention. 2nd ed. New York, NY: Oxford University Press, 1996: Janerich DT, Thompson WD, Varela LR, et al. Lung cancer and exposure to tobacco smoke in the household. N Engl J Med 1990;323: Mayne ST, Janerich DT, Greenwald P, et al. Dietary betacarotene and lung cancer risk in nonsmokers. J Natl Cancer Inst 1994;86: Holford TR, White C, Kelsey JL. Multivariate analysis for matched case-control studies. Am J Epidemiol 1978; 107: Cornfield J, Gordon T, Smith W. Quantal response curves for experimentally uncontrolled variables. Bull Int Statist Inst 1961;38: Kelsey JL, Thompson WD, Evans AS. Methods in observational epidemiology. New York, NY: Oxford University Press, Zhang H, Bracken MB. Tree-based risk factor analysis for preterm delivery and small-for-gestational-age birth. Am J Epidemiol 1995;141: Devesa SS, Shaw GL, Blot WJ. Changing patterns of lung cancer incidence by histological type. Cancer Epidemiol Biomarkers Prev 1991 ;1: US Department of Health and Human Services. The health consequences of involuntary smoking: a report of the Surgeon General. Rockville, MD: US Department of Health and Human Services, Office on Smoking and Health, (DHHS publication no. (CDC) ). 18. Morabia A, Sorenson A, Kumanyika SK, et al. Vitamin A, smoking and airway obstruction. Am Rev Respir Dis 1989;140: Schwartz J, Weiss ST. Relationship between dietary vitamin C intake and pulmonary function in the First National Health and Nutrition Examination Survey (NHANES I). Am J Clin Nutr 1994;59: Vena JE, Bona JR, Byers TE, et al. Allergy-related diseases and cancer: an inverse association. Am J Epidemiol 1985;122: Reynolds P, Kaplan GA. Asthma and cancer. (Letter). Am J Epidemiol 1987; 125:539^ Zheng W, Blot WJ, Liao ML, et al. Lung cancer and prior tuberculosis infection in Shanghai. Br J Cancer 1987;56: Cohen B, Diamond EL, Graves CG, et al. A common familial component in lung cancer and chronic obstructive pulmonary disease. Lancet 1977;2: Sporn MB, Roberts AB. Peptide growth factors and inflammation, tissue repair, and cancer. J Clin Invest 1986;78: Ames BN, Gold LS. Too many rodent carcinogens: mitogenesis increases mutagenesis. Science 1990;249:970-l. Am J Epidemiol Vol. 149,. 1, 1999

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