Risk of lung cancer from environmental exposures to tobacco smoke

Epidemiologic evidence on the relation between environmental tobacco smoke and cancer is reviewed. The labeling of tobacco smoke as an environmental cause of lung cancer has been challenged based on allegations of bias in the epidemiologic data. However, tobacco smoke has been shown to increase the risk of lung cancer down to the lowest exposure levels. Environmental tobacco smoke contains the same carcinogenic compounds as those found in the tobacco smoke inhaled directly by the smoker. Nonsmokers environmentally exposed have elevated levels of tobacco smoke byproducts in biological samples. These observations alone are sufficient to identify tobacco smoke as an environmental carcinogen. The epidemiologic studies showing that environmental exposure to tobacco smoke is associated weakly but consistently with increased risk of lung cancer. While these epidemiologic studies have been challenged, it does not appear that the observed epidemiologic associations are due to misclassification or confounding. Indeed, the epidemiologic results, particularly among the studies with superior data collection methods and better control of bias and confounding, find consistent associations between environmental tobacco smoke and lung cancer. This paper summarizes the evidence that environmental exposure to tobacco smoke increases the risk of lung cancer, and considers the criticisms of the epidemiologic evidence which have been raised.     

Risk factors for lung cancer among nonsmoking women

To evaluate risk factors for lung cancer in nonsmoking women, we used data of a case-control study conducted between 1991 and 1996 in Germany. A total of 234 female histologically confirmed lung cancer patients and 535 population controls who had never smoked more than 400 cigarettes in their lifetime were personally interviewed with respect to occupation, exposure to environmental tobacco smoke (ETS), family history of cancer, prior physician-diagnosed lung diseases or cancer and diet. One-year radon measurements in the last dwelling were performed. Odds ratios (OR) adjusted for age and region and 95% confidence intervals (CI) were calculated via logistic regression. When cumulative duration of exposure to ETS in hours was considered, the OR for high compared to not or low ETS exposed women was 2.62 (CI:1.35-5.06) for occupational exposure and OR=1.67 (CI:0.86-3.25) for spousal exposure, exhibiting a significant trend for ETS at work. Working more than 10 years in jobs or industries with known or suspected lung carcinogens was associated with OR=2.0 (CI:0.99-4.0). An elevated risk due to prior lung diseases was present for pneumonia (OR=1.6; CI:1.07-2.40) and tuberculosis (OR=1.6; CI:0.77-3.37). No significant increase in risk with increasing residential radon levels or with the presence of a family history of lung cancer was apparent. Protective effects were observed for high vs. low consumption of fresh vegetables (OR=0.5; CI:0.25-0.82) and cheese (OR=0.3, CI:0.21-0.55). ETS at work, occupational hazards and previous pneumonia may be risk factors for lung cancer in nonsmoking women, while a diet rich in fresh vegetables and cheese seems to be protective.     

Cancer in the offspring of parents with lung cancer

Despite several studies on the role of passive smoking in the development of childhood cancer, particularly leukaemia, lymphomas and brain cancer, no definitive answer has yet been provided. The aim of the cohort study reported here was to analyse the incidence of cancer in the offspring of young lung cancer patients on the basis of the assumption that all of the offspring were exposed passively to smoke. The files of the Danish Cancer Registry provided 3348 cases of lung cancer patients born after 1935, and their offspring (n = 6417) were identified through the Danish Population Register. The files of the offspring were then linked with the files of the Danish Cancer Registry and the numbers of cancers observed in the offspring were compared with those expected from national age-specific and calender-time-specific rates. A total of 135 333 person-years was the basis for analysis. Twenty-six cancers were observed, with 30.3 expected, yielding a standardised incidence ratio (SIR) of 0.9 (90% confidence interval (CI), 0.6–1.2). There was no excess of brain tumours, leukaemias or lymphomas. Stratification for sex of the lung cancer patients revealed a non-significantly increased risk for both non-Hodgkin’s lymphoma (three cases; SIR = 3.4; 90% CI: 0.9–8.7) and Hodgkin’s disease (three cases; SIR = 2.6; 90% CI: 0.7–6.6) in the offspring of female lung cancer patients. These results suggest that there is little evidence of an excess cancer risk in childhood, whether due to passive smoking or to as yet unidentified genetic factors, among the offspring of people who develop lung cancer. However, the results are limited by the fact that exposure was only assessed indirectly, with no measurement of actual cigarette consumption made.     

Interaction between environmental tobacco smoke and arsenic methylation ability on the risk of bladder cancer

Objective: Arsenic exposure and environmental tobacco smoke (ETS) have been suspected to be associated with bladder cancer risk. We hypothesize that interaction between ETS and the ability to methylate arsenic, a detoxification pathway, modifies the risk of bladder cancer.Methods: From January 1996 to December 1999, we identified 41 newly diagnosed bladder cancer patients and 202 fracture and cataract patients at the National Cheng-Kung University (NCKU) Medical Center. The levels of urinary arsenic species [As(III), As(V), MMA(V), and DMA(V)] were determined in all subjects.Results: We found significant interaction between ETS and secondary methylation index (SMI) on the risk of bladder cancer (p=0.02). Among non-smokers with a high primary methylation index (PMI), the risk of bladder cancer was lower in subjects exposed to ETS (OR, 0.37; 95% CI, 0.14–0.96) than in subjects without exposure to ETS. Among non-smokers without ETS, the risk of bladder cancer was 4.7 times higher in subjects with a low SMI (95% CI, 1.30–16.81) than in subjects with a high SMI.Conclusions: Ability to methylate arsenic plays an important role in reducing the risk of bladder cancer attributable to the continuation of arsenic exposure from drinking water and from ETS exposure.     

Lifetime residential and workplace exposure to environmental tobacco smoke and lung cancer in never-smoking women, Canada 1994-97

Although the risk of lung cancer among never-smokers living with a spouse who smokes has been extensively studied, the impact of lifetime residential and workplace environmental tobacco smoke has received less attention. As part of a large population-based case-control study of lung cancer, we collected lifetime residential and occupational passive smoking information from 71 women with lung cancer and 761 healthy control subjects, all of whom reported being lifetime nonsmokers. The adjusted odds ratio (OR) for lung cancer associated with residential passive exposure only was 1.21 (95% confidence interval [CI] 0.5-2.8). Although more years of and more intense residential passive smoke exposure tended to be associated with higher risk estimates, no clear dose-response relationship was evident. The OR for women with passive exposure as a child and as an adult was 1.63 (95% CI 0.8-3.5) and for those only exposed as an adult 1.20 (95%CI 0.5-3.0). Exposure to environmental tobacco smoke only in the workplace was associated with an adjusted OR of 1.27 (95% CI 0.4-4.0). Risks associated with increasing occupational exposure year tertiles were 1.24, 1.71 and 1.71. Total smoker-years of residential and occupational exposure combined resulted in a statistically significant trend (linear test for trend p = 0.05) with ORs for tertiles of exposure of 0.83, 1.54 and 1.82. Our results are consistent with the literature suggesting that long-term, regular exposure to either residential or occupational environmental tobacco smoke is associated with increased lung cancer risk in never-smoking women.     

Previous cancer and radiotherapy as risk factors for lung cancer in lifetime nonsmokers

A history of previous primary cancer and of radiotherapy were investigated as risk factors for lung cancer in lifetime nonsmokers in a hospital-based case-control study. By design, subjects with a previous tobacco-related primary (of the lung, larynx, oropharynx, esophagus, kidney, bladder, or pancreas) were excluded. Information was available on 30 male and 47 female lung cancer cases and 87 male and 132 female controls, all lifetime nonsmokers, interviewed in hospitals in four United States cities between 1985 and 1990. In males, neither a history of a previous primary nor a history of radiotherapy was associated significantly with lung cancer; however, the numbers of exposed cases were small. In females, after adjustment for age, education, hospital, lifetime environmental tobacco-smoke exposure, and body mass index, both a history of a reproductive primary and a history of radiotherapy were associated significantly with lung cancer (odds ratio [OR]=4.9,95 percent confidence interval [CI]=1.4–17.7, and OR=4.4, CI=1.3–15.1, respectively). Due to a high correlation between a history of a reproductive primary and a history of radiotherapy in the cases, it was not possible to estimate the effect of one exposure independent of the other. These results are consistent with the possibility that endocrine factors may play a role in some lung cancers in women.Dr Kabat is with Albert Einstein College of Medicine, Bronx, NY, USA. At the time of this work, the author was in the Division of Epidemiology, American Health Foundation, New York, NY, USA. Address correspondence to Dr Kabat, Department of Epidemiology and Social Medicine, Albert Einstein College of Medicine, Belfer Building, Rm 1302, 1300 Morris Park Avenue, Bronx, NY 10461-1602, USA. This work was supported by US National Cancer Institute Program Project grant CA32617 and Center grant CA17613.     

A European validation study of smoking and environmental tobacco smoke exposure in nonsmoking lung cancer cases and controls

Objectives: The purpose of this study was to validate, in a case-control study, the reporting by lung cancer cases and controls of their own lifetime smoking habits and of the smoking habit of the spouse. Methods: In a multicenter (Sweden, Spain, Italy) case-control study of environmental tobacco smoke (ETS) and lung cancer, subjects were screened by repeated probing to exclude regular smokers of one cigarette/day or more for one year or more, and to quantify any occasional smoking. We then performed a short validation interview with next-of-kin in three centers. Results: Only five of 408 index subjects who had never smoked regularly (1.7 percent) were reported by next-of-kin to be former regular smokers. These subjects had a cumulative lifetime consumption of cigarettes below 1.1 pack years. Among 351 subjects with quantitative smoking information from both sources who reported ever smoking 400 cigarettes or less (the definition of never-smoker used in the multicenter ETS study), nine subjects (2.6 percent) had smoked more than this amount occasionally according to next-of-kin. Misclassification was not higher for cases than controls. Relative risks for lung cancer associated with indicators of ETS exposure were not substantially altered by excluding the nine possibly misclassified subjects. The reports from 223 pairs of index subjects and next-of kin regarding the cumulative amount smoked by the spouse agreed quite well (Spearman's rank correlation 0.75 for reported smokers, 0.92 for all subjects). Only one index subject failed to report a spouse who had smoked regularly (99 percent sensitivity). Conclusions: Smoking status and exposure to spousal ETS as reported by lung cancer cases and controls agreed strongly with reports by next-of-kin. Overall, our results suggest that bias from smoker misclassification is likely to be insignificant, and they contribute to the evidence linking exposure to ETS with an increased risk of lung cancer.     

A cohort study of tobacco use,diet, occupation,and lung cancer mortality

In 1966, a cohort of White males aged 35 or over, who were policy-holders with the Lutheran Brotherhood Insurance Society (United States), completed a mail questionnaire on tobacco use, diet, and demographic characteristics. During the 20 years of follow-up, 219 lung cancer deaths occurred. Besides the strong relationship with cigarette smoking, we observed an effect on lung cancer risk among current users of cigars or pipes who were nonsmokers of cigarettes (relative risk [RR]=3.5, 95 percent confidence interval[CI]=1.0–12.6) or who were past/occasional users of cigarettes (RR=2.7, CI=1.4–5.3). In addition, elevated risks (from 1.5 to 2.6) of lung cancer were found among craftsmen and laborers, with the highest risks among subjects who worked in the mining or manufacturing industry. No association between current (as of 1966) use of beer or hard liquor and lung cancer was observed, although past users were at elevated risk. An inverse association between lung cancer and intake of fruits was observed, and risks of lung cancer were lower among persons in the highest dietary intake quintiles of vitamins A and C. Except for oranges, however, none of the inverse associations with fruits or dietary nutrients had statistically significant trends. The findings from this cohort study add to the evidence of an adverse effect of cigar/pipe smoking and possibly protective effect of dietary factors on lung cancer risk.     

Risk modification by CYP1A1 and GSTM1 polymorphisms in the association of environmental tobacco smoke and lung cancer: a case-control study in Japanese nonsmoking women

Genetic backgrounds may modify the association of environmental tobacco smoke (ETS) with lung cancer risk. Polymorphisms of both the activating and detoxifying enzymes, cytochrome P4501A1 (CYP1A1) and glutathione-S-transferase M1 (GSTM1), may be important as genetic factors. We conducted a multicenter case-control study in Japanese nonsmoking women. Cases were women aged 30-89 years and newly diagnosed as having lung cancer from November 1997 to March 2001 in 4 study areas. We also recruited age-matched (5-year strata) and hospital-matched nonsmoking controls. A total of 158 cases and 259 hospital controls supplied blood for genotyping. Detailed information on ETS exposure from husbands and that in other situations and on potential confounders was collected by interview. Odds ratios (ORs) were estimated by using conditional logistic models. We found no increase in the risk of lung cancer for CYP1A1 Msp I genotypes. For the GSTM1 null genotype vs. nonnull genotype, the OR was 1.37 [95% confidence interval (CI) 0.90-2.09], which indicated a somewhat increased risk for the GSTM1 null genotype. A gene-environment interaction was suggested, with combined GSTM1 null genotype and high-dose ETS exposure (>/=40 pack-years by husbands) conferring significantly higher risk (OR = 2.27, 95% CI 1.13-4.57) compared to the GSTM1 nonnull genotype and low-dose ETS exposure (<40 pack-years). Our results do not support a major role of Msp I polymorphism of the CYP1A1 gene as a risk factor for lung cancer among nonsmoking women. In contrast, the GSTM1 null genotype posed an increased, although not significant, risk among them. Additional studies are warranted to confirm the ETS-GSTM1 polymorphism interaction suggested in our present study.     

美国肿瘤预防控制概况

恶性肿瘤是美国中老年人死亡的主要原因。2007年美国癌症死亡人数为56万,占全部死亡人数的23%。预计2011年美国新发癌症病例将达到160万,有57万人死于癌症。但大多数的癌症可以通过干预措施得以预防,比如控烟、改善饮食习惯、加强体育锻炼和控制肥胖。同时早期诊断也是美国控制恶性肿瘤的工作重点。定期进行癌症筛查,能够实现癌症的早期诊断,降低癌症患者的死亡率,延长生存期,提高生命质量。     

Cigarette smoking,use of other tobacco products and stomach cancer mortality in US adults: The Cancer Prevention Study II

Cigarette smoking is associated with increased risk of stomach cancer in many studies but there are limited data on this relationship in women and on risk associated with use of tobacco products other than cigarettes. We examined stomach cancer death rates in relation to cigarette smoking in women and use of cigarette, cigar, pipe, or smokeless tobacco in men in a nationwide prospective mortality study in the United States (US). Cohort follow-up from 1982-96 identified 996 and 509 stomach cancer deaths among 467,788 men and 588,053 women, respectively. Cox proportional hazards models were fitted to estimate rate ratios (RR) and 95% confidence intervals (CI) using non-users of tobacco as the referent group. Multivariate-adjusted RRs were the highest for men who currently smoked cigars (RR = 2.29, 95% CI = 1.49-3.51) or cigarettes (RR = 2.16, 95% CI = 1.75-2.67) and both increased with smoking duration. Women who currently (RR = 1.49, 95% CI = 1.18-1.88) or formerly (RR = 1.36, 95% CI = 1.08-1.71) smoked cigarettes were at significantly increased risk, as were men who formerly smoked cigarettes (RR = 1.55, 95% CI = 1.28-1.88), or currently (RR = 1.81, 95% CI = 1.40-2.35) or formerly (RR: 1.57, 95% CI = 1.22-2.03) used more than one type of tobacco. Men who reported a history of chronic indigestion or gastroduodenal ulcer had substantially higher mortality rates associated with current cigarette (RR = 3.45, 95% CI = 2.05-5.80) or cigar (RR = 8.93, 95% CI = 4.02-19.90) smoking, as did men who were current aspirin users. If causal, the estimated proportion of stomach cancer deaths attributable to tobacco use would be 28% in US men and 14% in women. We conclude that prolonged use of tobacco products is associated with increased stomach cancer mortality in men and women. The accumulated evidence from this and other studies support reconsidering stomach cancer as a tobacco-related cancer.     

Strain-dependent differences in susceptibility to lung cancer in inbred mice exposed to mainstream cigarette smoke

It is becoming increasingly clear that genetic susceptibility is an important host factor determining the effects of exposure to a number of airborne particles and gases. Although numerous studies have identified a genetic component for spontaneous pulmonary tumor development and for chemically induced lung cancer (e.g., urethane) in mice, a systematic examination of murine inter-strain differences in response to cigarette smoke inhalation has not been conducted. We addressed this research gap by examining the strain distribution pattern of lung cancer in nine inbred strains of mice exposed to 258 mg/m³ mainstream cigarette smoke for 5 months followed by 4 months of rest. Lung tumors were enumerated on fixed lungs visualized at low magnification and on serial step sections examined microscopically. With the low magnification examination, we observed statistically significant increases in the number of lung tumors in cigarette smoke-exposed A/J and the genetically-related A/HeJ mice (p < 0.05). While fewer tumors were identified by the microscopic enumeration method, it confirmed that significant increases in lung tumors occurred only in A/J and A/HeJ mice exposed to cigarette smoke (p < 0.05). Thus, as predicted by epidemiologic studies and animal experiments using chemically induced lung cancer models, these findings suggest that genetic host factors play a significant role in the pulmonary tumorigenic response of mice to mainstream cigarette smoke.     

Never smokers and lung cancer risk: a case-control study of epidemiological factors

We performed an analysis of potential epidemiological risk factors for lung cancer using data from 280 cases and 242 hospital-based controls, all lifetime never smokers (those who had smoked <100 cigarettes in their lifetimes) and frequency matched on age, gender and ethnicity. The data on demographic characteristics, medical history of respiratory diseases (asthma, emphysema, pneumonia and hay fever), weight and height, family history, female characteristics and environmental tobacco smoke (ETS) and dust exposure were derived from personal interviews. We performed a logistic regression analysis of these variables adjusting for age, gender, ethnicity, income and years of education. Exposure to ETS (OR = 2.08, 95% CI [1.25-3.43]) and dusts (OR = 2.43, 95% CI [1.53-3.88]) were associated with significantly increased risk. In the analysis for joint effects, exposure to both ETS and dusts conferred a higher risk (OR = 3.25, 95% CI [1.58-6.70]) than exposure to either alone. Family history of any cancer with onset before age 50 in at least 1 first degree relative was a significant risk predictor (OR = 1.70, 95% CI [1.10-2.64]). Individuals with a self-reported physician-diagnosed history of hay fever, but not asthma, had a decreased lung cancer risk (OR = 0.57, 95% CI [0.35-0.92]). In the multivariate analysis, exposure to ETS and dusts, and family history of cancer with onset before age 50 were significant risk factors, while a history of hay fever (occurring without asthma) was significantly protective.     

Smoking and Passive Smoking in Relation to Lung Cancer in Women

in a population based case-control study the association between female lung cancer and some possible etiological agents was investigated; 210 incident cases in Stockholm county, Sweden, and 209 age-matched population controls were interviewed about their exposure experiences according to a structured questionnaire. A strong association between smoking habits and lung cancer risk was found for all histological subgroups. Relative risks for those who had smoked daily during at least one year ranged between 3.1 for adenocarcinoma to 33.7 for small cell carcinoma in a comparison with never-smokers. All histological types showed strong dose-response relationships for average daily cigarette consumption, duration of smoking, and cumulative smoking. there was no consistent effect of parental smoking on the lung cancer risk in smokers. Only 38 cases had never been regular smokers and the risk estimates for exposure to environmental tobacco smoke were inconclusive. the high relative risks of small cell and squamous cell carcinoma associated with smokmg may have implications for risk assessments regarding passive smoking.     

Lung cancer trends in young adults: an early indicator of progress in tobacco control (United States)

Objective: Tobacco smoking is known to increase lung cancer occurrence beginning in young adulthood, although age-specific rates have not been used to monitor the early consequences of tobacco control efforts in the United States. We evaluated state trends in lung cancer death rates among young adults in relation to an index of state tobacco control activities and conventional indices of current smoking and cessation. Methods: We calculated lung cancer death rates in young adults (age 30–39 years) over two time intervals from 1990–1994 through 1995–1999 in states with at least 25 deaths per interval. We measured the correlation of an index of state tobacco control in 1992–1993 with absolute rates and with total percent change during the two time intervals. Results: Both lung cancer death rates during the recent time interval (1995–1999) and the change in these rates from 1990–1994 correlated strongly and inversely with the index of state tobacco control efforts measured in 1992–1993. Lung cancer death rates decreased in states with high tobacco control efforts, but increased in states with low tobacco control efforts. Tobacco control indices were strongly and positively correlated with cessation of smoking by age 30–39 years. Conclusions: Lung cancer death rates among young adults are strongly and inversely correlated with recent indices of tobacco control. Future monitoring of the effectiveness of statewide comprehensive tobacco control programs should assess trends in lung cancer rates in young adults as well as youth and adult smoking prevalence.     

Ataxia-telangiectasia mutated expression is associated with tobacco smoke exposure in esophageal cancer tissues and benzo[a]pyrene diol epoxide in cell lines

Esophageal cancer is a substantial health problem because of its usually late stage at diagnosis and poor prognosis. Tobacco smoking and alcohol use are the most important risk factors in the development of esophageal squamous cell carcinoma (SCC). Our previous study demonstrated the binding of benzo[a]pyrene diol epoxide (BPDE), a carcinogen present in tobacco smoke and environmental pollution, to the ataxia-telangiectasia mutated (ATM) gene. To understand how this binding affects the alteration of ATM expression and to identify biomarkers for the detection of esophageal cancer, we analyzed ATM mRNA expression in tissue specimens from patients with esophageal SCC and premalignant lesions using in situ hybridization. We then performed in vitro experiments to verify and extend our ex vivo observations. We found that ATM expression was increased in esophageal SCC and its premalignant lesions when compared with normal tissues and that increased ATM expression was associated with tobacco smoke exposure and tumor de-differentiation. Moreover, BPDE induced ATM expression in esophageal SCC cell lines in a time-dependent manner. In summary, the BPDE in tobacco smoke may be responsible for increased ATM expression in premalignant and malignant esophageal tissues. Our findings suggest that the ATM gene should be further evaluated as a biomarker for the early detection of esophageal cancer and tobacco use in patients.     

Population-density and county-level variation in breast cancer mortality rates among white women residing in the Northeastern and Southern United States

OBJECTIVE: We assessed the contribution of variation in risk factor prevalence to population-density and county-level variation in breast cancer mortality rates. METHODS: In 1995 we collected risk factor information in a telephone interview of a random digit dialed sample of: (1) 1241 women from counties in the upper and lower tertiles of population density as of 1970 in the Northeast and South of the United States (Design A); (2) 2492 women from counties in the upper and lower tertiles of 1970-1979 breast cancer mortality rates in the four populations from Design A, and; (3) 276 women in Nassau County in New York State. We calculated 1990-94 mortality ratios (MRs) adjusted for breast cancer risk factors. RESULTS: The high/low population-density fully-adjusted MRs in women > or = 55 years were 1.01 (95% CI 0.9-1.2) and 1.00 (95% CI 0.8-1.2). The fully-adjusted MRs for high versus low mortality counties ranged from 0.95 (95% CI 0.8-1.2) to 1.29 (95% CI 1.0-1.6) in women > or = 55 years. CONCLUSIONS: Differences in risk factor prevalence explained higher rates in high-density versus low-density areas in older women. Modest elevations in the adjusted high/low breast cancer MRs among older women in certain groups of counties may reflect unidentified risk factors but more likely are due to chance.     

Attributable risk of lung cancer in lifetime nonsmokers and long-term ex-smokers (Missouri,United States)

A population-based, case-control study of incident lung cancer among women in Missouri (United States) who were lifetime nonsmokers and long-term ex-smokers was conducted between 1986 and 1992. The study included 618 lung cancer cases and 1,402 population-based, age matched controls. Information on lung-cancer risk factors was obtained by interviewing cases, next-of-kin of cases (36 percent and 64 percent of the cases, respectively) and controls. Year-long radon measurements also were sought in every dwelling occupied for the previous five to 30 years. Population attributable risks (PAR) for specific risk factors were computed for all subjects, for lifetime nonsmokers, for long-term ex-smokers, by histologic cell type (i.e., adenocarcinoma cf nonadenocarcinoma) and for direct interviews with case (for living cases) and for next-of-kin interviews (for dead cases or cases too ill to complete an interview). The mean age at lung cancer diagnosis was 71 years, and nearly 50 percent of the lung cancers were histologically confirmed adenocarcinomas. Almost 40 percent of all lung cancers among lifetime nonsmokers and almost 50 percent of lung cancers among all subjects could be explained by the risk factors under study. Dietary intake of saturated fat and nonmalignant lung disease were the two leading identified risk factors for lung cancer among the lifetime nonsmokers, followed by environmental tobacco smoke, and occupational exposures to known carcinogens. A small nonsignificant risk was found for study subjects exposed to median domestic radon concentration of 4 pCi/l (25-year time-weight average). Since only a small fraction of the population is exposed at this level, it is estimated that the PAR for domestic radon was less than two percent in Missouri. The risk for saturated fat intake was similar for lifetime nonsmokers, ex-somkers, adenocarcinoma cases, and nonadenocarcinoma cases; however, the increased risk was much more pronounced for next-of-kin interviews (PAR=31 percent) than for interviews with the study subjects (PAR = nine percent). A similar pattern of PAR was identified among ex-smokers but, in this group, the lingering effect of a history of smoking was also very important. Along with saturated fat intake (PAR=20 percent), the combined effect of previous active and passive smoking even after 15 years of cessation of active smoking was responsible for more lung cancer than any other risk factor under study (PAR=59 percent).Drs Alavanja, Benicbou, Swanson, and Boice are with the Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD, USA. Dr Brownson is with the Department of Community Health, Saint Louis University School of Public Health, St Louis, MO, USA. Address correspondence to Dr Alavanja, Epidemiology and Biostatistics Program, National Cancer Institute, EPN/543, 6130 Executive Blvd, Bethesda, MD 20892, USA.     

Environmental tobacco smoke and lung cancer risk in nonsmoking women.

BACKGROUND: Exposure to environmental tobacco smoke (passive smoking) has been suggested to be a cause of lung cancer, although early epidemiologic studies have produced inconsistent results. PURPOSE: We conducted an epidemiologic case-control study to assess the relationship between exposure to environmental tobacco smoke and lung cancer risk among women who have never smoked (i.e., having smoked for a total of less than 6 months or having smoked less than 100 cigarettes in their lifetimes). METHODS: Case patients (n = 210) were women with histologically confirmed primary carcinomas of the lung who were lifetime nonsmokers. They were identified through hospital tumor registries and the Florida Cancer Data System of the Statewide Cancer Registry. Community-based control women (n = 301) were also lifetime nonsmokers and were identified through random-digit dialing. Details on childhood and adulthood exposures to environmental tobacco smoke were ascertained through interviews with the study participants themselves or with surrogate respondents. Risks were calculated in terms of smoke-years, defined as the sum of the reported years of exposure to cigarette smoke from each smoker in the household. RESULTS: The risk of lung cancer more than doubled for women who reported 40 or more smoke-years of household exposure during adulthood (odds ratio [OR] = 2.4; 95% confidence interval [CI] = 1.1-5.3) or 22 or more smoke-years of exposure during childhood and adolescence (OR = 2.4; 95% CI = 1.1-5.4). Risks were highest for non-adenocarcinoma lung cancers, although modest elevations in risk were also observed for adenocarcinomas. When a surrogate respondent other than the patient's husband provided information on exposure, the risk estimates were considerably lower. CONCLUSION: These findings suggest that long-term exposure to environmental tobacco smoke increases the risk of lung cancer in women who have never smoked.     

Clinico-pathological features and survival of lung cancer patients in Paris, France

We studied the clinico-pathological features of 750 lung cancers identified in Paris, France, during 1988. An internal comparison was performed between adenocarcinomas and other subtypes. Survival of 502 patients was studied. 85% of patients were males; 93% were smokers or ex-smokers. Squamous cell carcinomas, adenocarcinomas, small cell carcinomas and large cell cancers accounted for 51, 22, 15 and 12% of all cases, respectively. Differences were found for the distribution of histological subtyping according to sex (P = 0.001) and smoking status (P = 0.0001) with a greater proportion of adenocarcinomas for women and non-smokers. Median overall survival was less than one year. In multiple regression analysis, small cell lung cancer patients appeared to have a worse prognosis than other histological subtypes. This study describes patients who were treated in community practice and might be more representative of the real clinico-pathological profile of this disease in France.