186 Abstracts/Lung Cancer 13 (1995) 185-232

role of chest radiographs in the early detection of lung cancer would be appropriate. A consensus conference would be a suitable forum to reexamine fully the existing data on lung cancer screening and to formulate specific guidelines for early detection strategies in individuals at high risk for lung cancer,

Attributable risk ofhmg cancer in lifetime nonsmokers and long- term ex-smokers (Missouri, United States) Alavanja MCR, Brownson RC, Benichou J, Swanson C, Boice JD Jr. Epidemiology/Biostatistics Program. National Cancer Institute. EPN/ 543, 6130 Executive Boulevard Bethesda. MD 20892. Cancer Causes Control 1995;6:209-16.

A population-based, casecontrol 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 6 18 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-smokers. adenocarcinoma cases, and nonadenocarcinoma cases; however, the increased risk was much more pronounced for next-of-kin interviews (PAR = 3 I 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 I5 years of cessation of active smoking was responsible for more lung cancer than any other risk factor under study (PAR = 59 percent).

Environmental tobacco smoke: Science vs. rhetoric Jinot J, Bayard S. U.S. Envimnmental Pmtection Agency, Washington, DC. Risk Anal 1995;15:91-6.

After an extensive review and analysis of the scientific evidence on the respiratory health effects of passive smoking, the U.S. Environmental Protection Agency concluded that environmental tobacco smoke causes lung cancer in adult nonsmokers and increases the risk of a variety of noncancer respiratory disorders, especially in children. This article is a response to claims in Dr. Gio Gori’s article ‘Policy Against Science: The Case of Environmental Tobacco Smoke,’ appearing in the same issue of this journal, that such conclusions are unwarranted. This response focuses only on the respiratory health effects of environmental tobacco smoke.

Policy against science: The case of environmental tobacco smoke Gori GB. Health Policy Centeez Bethesda, MD. Risk Anal 1995;15:15- 22.

The grounds for official policy claims that environmental tobacco smoke is a major health risk remain speculative. In scientific terms, the evidence is compatible with either a slight increase or a decrease of risks, but is impotent to certify either conclusion. OfliciaJ advocacy of unproven hypotheses presented as valid scientific conclusions raises serious ethical questions, and threatens the credibility of risk assessment as a legitimate policy instrument.

Current status of retinoid chemoprevention of lung cancer Benner SE, Lippman SM. Hong WK. Department of Medicme, Universi& of North Carolina. Chapel Hill, NC. Oncology (USA) 1995;9:205-10.

Clinical trials have suggested that retinoid chemoprevention prevents the development of second primary tumors following head and neck or non-small-cell lung cancer. The findings of these initial studies are now being evaluated in large multi-institution chemoprevention trials. If successful, these ongoing trials will establish the clinical role of retinoids in lung cancer prevention. The findings of these trials may also lead to strategies for primary lung cancer prevention. Until the results of these studies become available, however, lung cancer chemoprevention remains an experimental approach. The recent unexpected findings of increased lung cancer incidence in abets-carotene study in Finnish smokers stresses the importance of establishing the efficacy of chemoprevention agents in carefully conducted clinical trials.

Epidemiology and etiology

Previous lung disease and risk of lung cancer among lifetime nonsmoking women in the United States Wu AH, Fontham ETH, Reynolds P, Greenberg RS, Buftler P, Liff J et al. University ofSouthern California. PMB 8300, 142OSon Pablo Sttvet, LosAngeles, CA 90033. Am J Epidemiol 1995;141:1023-32.

The authors conducted a population-based case-control study of lung cancer in nonsmoking women in Eve metropolitan areas of the United States between December I, 1985, and November 30, 1990. In-person interviews were conducted with 412 lung cancer cases and 1,253 population controls, yielding information on history of nonmalignant lung diseases that were diagnosed by a physician. When lung cancer cases were compared with controls, history of any previous lung disease was associated with a significant increased risk of lung cancer (adjusted odds ratio (AOR) = 1.56,95% confidence interval (CI) 1.2-2.0). Several lung diseases, including asthma, chronic bronchitis, pneumonia, and tuberculosis, were reported more often by lung cancer cases than by controls, and the difference was statistically significant for asthma (AOR = 1.67, 95% Cl 1.1-2.5) and chronic bronchitis (AOR = 1.60, 95% CI 1. I- 2.4). Since significant increased risks were observed for asthma and tuberculosis diagnosed before age 2 1 years, it is unlikely that reported prior lung diseases were prediagnostic manifestations of lung cancers. The increased risks associated with previous lung disease were observed for adenocarcinomas and other carcinomas of the lung; the point estimates were generally higher for the latter category. The risks associated with previous lung diseases remained unchanged after adjustment for potential confounders, including environmental tobacco smoke exposure during childhood and adult life and dietary factors.