Abstracts/ Lung Cancer 12 (1995) 113-160 115

Smoking of hand-rolled cigarettes as a risk factor for small cell lung cancer in men: A case-control study fmm Uruguay De Stefani E, Fierro L, Leninaga MT, Balbi JC, Ronco A, Mc.ndilahatsu M. Registm National de Cancec Ministerio de S&d Publica, Institute National de Oncologia, 8 de Octubre 3265, Montevideo. Lung Cancer (Ireland) 1994;11:191-9. During the time period January 1989-December 1992, a case-control study involving 476 cases of lung cancer and 561 controls was carried out at the Institute NacionaI de Oncologia, Montevideo, Uruguay, in order to analyze the patterns of risk of the different cell types of lung cancer! associated with smoking manufactured and hand-rolled cigarettes. Lifelong smokers of hand-rolled cigarettes displayed a non- significant 30% increased risk, compared with smokers of commercial cigarettes, for all types of lung cancer combined. The analysis for cell- type disclosed a fourfold increase in the risk of small cell lung carcinoma associated with lifelong smoking of hand-rolled products, The possibilities of a chance finding and of misclassification of the disease appears to be an unlikely explanation of this strong and rather specific association.

Risk factors for lung cancer in Rio de Janeim, Brazil: A case-control study Suzuki I, Hamada GS, Zambonic Mh4, De Biasi Cordeiro P, Watanabe S, Tsugane S. EpidemiologyDivision, Nat. Cancer CenterRes. institute, 5-l-l Tsukji, Chuo-ku, T&w 104. LungCancer(IreIand) 1994;11:179- 90. The association between the risk of lung cancer and tobacco smoking, dietary factors and occupationaI exposures was examined in a hospital- based case-control study. The study involved 123 consecutive cases and 123 controls, matched by age (i 13). sex, and race. In this first study of lung cancer risk in Brazil, we found that tobacco smoking is the strongest risk factor with an odds ratio (OR) for current and former smokers of 22 (CI, 6.5-76) and 7.7 (CI, 2.2-27), respectively. An OR of 2.8 (CI, 1.0-7.7) was found for users of black tobacco (in the form of hand- rolled cigarettes) in combination with conventional cigarettes, after adjustment for life-time consumption of any kind of tobacco; users of conventional cigarettes only were considered as a reference group. Cessation of smoking had an important infhtence in reducing the lung cancer risk, whereas early initiation of smoking inc}eased the risk. Among dietary factors, frequent consumption of meat (P < 0.01) and pasta (P = 0.02) were positively associated with lung cancer risk after adjusting for smoking and income. No association was found with pn/ yellow vegetables or fruits. We were unable to detect any sign&ant association related to occupational exposures. This study wntirmed the association of lung cancer with smoking as the most important predictor of risk. It also indicates the increase in risk associated with the use of black tobacco in combination with conventional cigarettes,

A casc-cootml study of diet and lung cancer in Kerala, South lndia . Sankaranarayanan R, Wgkae C, Duffy SW, PW G, Day NE, Nair MK. Division of Cancer Epidemiology, Regional Cancer Centre, Trivandrum. 695 011 Kerala. Int J Cancer 1994;58:644-9. A total of 281 male lung-cancer patients were identiflcd from the hospital cancer registry in the Regional Cancer Centre in Trivandrum. The controls were selected from the visitors and patients’ bystanders in the hospital. The recruitment of cases and controls started in 1990, and the present study used the casea registered in the first year. The questionnaire administered to cases and controls wllected information on tobacco smoking and alcohol habits. Dietary data were wllected using a food frequency questionnaire and were analyzed by multiple logistic

regression producing odds ratio estimates of the relative risk and deviance chi-squared tests of significance. Analysis was done on the computer package, EGRET. AI1 models included age, education, religion and smoking to adjust for the effect of confounding. Green vegetables and bananas were found to have a protective association with lung cancer. The odds ratio associated with the highest quartile of vegetable consumption compared with the lowest was 0.32 (95% confidence interval 0.13, 0.78). Forward stepwise regression analysis indicated pumpkins and onions as the most consistently significant protective factors. Animal protein foods and dairy products were found to have a predisposing effect on lung cancer in this study. The expected influence of smoking on lung cancer (a considerable increase in risk among smokers) provided evidence of the reliability of the data. In conclusion the results from this study show that diet has a role in lung cancer aetiology, although the association is weak compared to the effects of smoking.

A study of autopsied lung cancer cases among retired workers of the Okuno-jima poison gas factory Macda A, Awaya Y, Iham Y, Yoshkla Y, Ishioka S, InamIzu T et al. SecondDept. ofInternalMedicine, Hiroshima Univ. School ofMedicine, Naka-ku, Himshima 730. Lung Cancer (Japan) 1994;34:525-30. We studied 45 autopsied lung cancer patients, who had been involved in manufacturing poison gas at Okuno-jima in Hiroshima Prefecture, Japan, during World War II. Ah patients, Including 3 with double cancers in the lung, were male and were autopsied between 1952 and 1990. The lung cancer mortality rate up to 1977 among retired workers at this factory was significantly higher than that among the general population of Hiroshima Prefecture, after adjusting the background mortality rate for sex, age, and year. We divided the subjects into two groups: group 1 consisted of 26 who died before 1978 and group II of 19 who died during or after 1978. The group I subjects demonstrated 2 characteristic features: 1) 58% of the tumors (I5 of 26) occurred in the trachea or main bronchi and 2) 45% of the tumors (14 of 31) were squamous cell carcinomas, 29% (9) were small-cell carcinomas, 16% (5) were large-cell carcinomas, and only 7% (2) were adenocarcinomas. These clinical features are compatible with the characteristics of occupational lung cancer and were not observed in the group II cases.

Human evidence: Lung cancer mortality risk fmm chrysotile eqmsurc Hughes JM. Ann Occup Hyg 1994;38:555-60. The linear, no-threshold model is wmmonIy used for estimating lifetime lung cancer risk from asbestos exposures. Studies of chrysotile workers have observed shallow slopes for the exposure-response relationship for miners/millers, friction products manufacturing workers and asbestoscement (primarily chtysotile) workers but a steeper slope (approximately 16 times higher) for textile workers. For chrysotile exposures in buildings, where short fibres constitute the great majority of the fibres, the shallow slope is judged more appropriate. Using this slope the data regarding exposure levels to building occupants and maintenance workers, the annualized risks of lung cancer would be approximately 0.01 and 0.6 per million for these groups, respectively. Using the higher slope would result in risks 16 times higher, still considerably lower than those commonly accepted. Contrary to the model’s assumption of increased risk for any amount of exposure, a number of studies have demonstrated evidence that lung cancer risk is not associated with years exposed to low exposure levels. Moreover, the accumulating evidence that asbestos-inducing lung cancer may require lung fibrosis suggests a practical threshold since detectable lung fibrosis

116 Abstracts/Lung Cancer 12 (1995) II3-160

will not result from environmental exposure levels. Evidence suggests that the relative risk to non-smokers may be slightly higher than to smokers (by a factor of 1.8). However, ifthis is true, this has little effect on risk assessment due to the low absolute risk in non-smokers. Tremolite has been associated with an increased risk of lung cancer in a study of vermiculite miners; the slope of the exposure-response relationship was similar to that for crocidolite miners and much higher than that of chrysotile miners. In spite of a recent report indicating that asbestos- associated lung cancer risk may be limited only to adenocarcinomas, the bulk of the evidence fails to con&m this.

Lung cancer mortaIity among asbestos textile workers: A review and update Dement JM, Brown DP Ann Occup Hyg 1994;38:525-32. In an update of the mortality of the cohorr of 1200 South Carolina textile workers, ofwhom almost halfdied, there were 185 excess deaths (SMR= 1.44) which included71 cardiovasctdardis (SMR= 1.37), 43 non-maIignant reapiratotydiseases (SMR= 2.25) and41 hmgcancers (SMR = 2.25). Only two definite mesotheliomas were observed. Other possible cases may have occurred but no confirmatory pathology was available. Strong exposure-response relationships have found for lung cancer and for non-malignant respiratory diseases. The data suggest a doubling of the lung cancer risk at an exposure of approximately 30 fibre years, Mortality from pnetmtoconiosis and other respiratoty diseases was elevated at even the lowest cumulative exposure category (< 2 f ml- ’ years). A nested case-control analysis failed to demonstrum a sign&ant role for mineral oil exposure in the etiology of lung cancer. Differences in airborne fibre sizes may be important in explaining different lung cancer and pneumoconiosis risks in various industries, In particuhar, the data on airborne fibres in textile manufacturing industries suggested 1 l-27%were longer than 5 imcompared to2J%for mining and milling.

Case-cont~ study of residential radon and lung cancer io Winnipeg, Manitoba, Canada Letourneau EG, Krewski D, Choi NW, Goddard MJ, McGregor RG, Zielinski JM et al. Radiation Ptvtection Buwau, 775 BtvokfeIdRoad. Orrawa, Ont. KIA ICI. Am J Epidemiol 1994;140:310-39. A case-control study of lung cancer in relation to exposure to radon in homes in Winnipeg, Manitoba, Canada, was conducted during 1983- 1990. In total, 738 individuals with histologically conIirmed incident cases of lung cancer were interviewed, along with 738 controls matched on age (*5 years) and sex. Radon dosimeters were placed in all residences in which the study subjects had reported living within the Winnipeg metropolitan area for at least 1 year. Radon dosimetry was done by means of integrated alpha-track measurements over a l-year period. In the homes monitored, the average level of radon-222 was about 120 becquerels (I&)/m’ in the bedroom area and 200 Bq/mr in the basement. AIIer adjusting for cigarette smoking and education, no increase in the relative risk for any of the histologic types of lung cancer observed among the cases was detected in relation to cumulative exposure to radon.

Genetic component of lung cancer: Cohort study of twins Braun MM, Caporaso NE, Page WF, Hoover RN. Epidemiology/ Biostatistics Ptvgram, National Cancer Institute. National Institutes o/Health, 6130 Executive Boulevanl, RockviNe, MD 20852. Laneet 1994;344:440-3. Epidemiological and molecular epidemiological findings suggest that inherited predisposition may be a component of lung cancer risk and

an important modulator of the carcinogenic effects of cigarette smoke. We have carried out a genetic analysis of lung cancer mortality on the National Academy of Sciences/National Research Council Twin Registry. The registry is composed of 15924 male twin pairs who were bomintheUSAbctween1917and1927andwhoservedinthearmed forces during World War II. As evidence for a genetic effect on lung cancer, we required concordance for lung cancer death to be greater among monoaygotic than among dixygotic twin pairs. No genetic effect on lung cancer mortality was observed. The ratio of observed to expected concordance among monozygotic twins did not exceed that among dizygotic twins (overall rate ratio 0.75 [95% CI 0.35-1.61). even though monozygotic twin pairs are more likely to be concordant for smoking than dizygotic twin pairs in this population. A cohort analysis (accounting for age, sex, race, and smoking intensity) of lung cancer mortality found no lung cancer deaths during 300 person-years of follow- up (obsetved to expected ratio 0 [O-4.09]) among 47 monozygotic twin smokers whose smoking twins had died of lung cancer, even though smoking histories were very similar within twin pairs. In our study, there is little ifany et&t of inherited predisposition on development of lung cancer. Genetic factors are not likely to be strongly predictive of lung cancer risk in most male smokers older than 50, the age group in which the vast majority of cases occur.

Contribution of cadmium ia cigarettes to lung cancer: An evaluation of risk assessment methodologies Hertz-Picciotto I, Hu S-W. Deportment ofEpidemiology University of North Carolina, Chapel Hill, NC 27599-7400. Arch Environ Health I994;49:297-302. This investigation concerned the use of quantitative risk assessment for edmating cancer mortality at low-level exposures. We empirically tested whether extrapolating by linear no-threshold models predicted imphmsible risks at low-level exposures. Cadmium in cigarette smoke was the low-level exposure, and extrapolation was based on potencies estimated from an occupational study and a rodent cancer bioassay. Inhaled cadmium in mainstream and sidestream smoke was estimated from published laboratory experiments. Smoking-specific lung cancer and a&cause mortality rates were esthnated Born large pcpuIation-based stndies. The mortality rates, amount of inhaled cadmium, and potency values were used to construct life tables for calculating lifetime lung cancer risk with and without a contribution from cadmium in cigarette smoke. The epidemiologic data predicted that 1 to 18 hmg cancer deaths per 10 000 smokers may be attributable to inhaled cadmium in cigarette smoke, or approximately 0.2% to 1.6% of smoking-induced lung cancer deaths. Upper 95% bounds on these figures are 7 to 95 lung cancer deaths or 1.6% to 8.8% of smoking-related deaths. The rodent data predicted that 80 to 416 lung cancer deaths per 10 000 smokers (95% upper bounds: 136- 707) or 13% to 47O% (23-81%) of smoking-induced lung cancer mortality maybe attributable to cadmium in cigarette smoke. Linear extrapolation from human data appears to provide plausible estimates of risk at low doses, Considering the large number of carcinogens present in cigarette smoke, the extrapolation from rodents appears to overestimate human risks. Whether this discrepancy results from differences in potency for cadmium chloride aerosol as opposed to cadmium in particulate form, or from humans having greater sensitivity to cadmium’s carcinogenic effect, or both, remains unclear.

Correlating exposure to enviroamental tobacco smoke exposure with increased incidence of lung cancer in IIOII smokers: Js cotinine a vaIid marker? Roberfroid MB. Dept. of Pharmaceutical Sciences, Universite Catholique de Louvain, B-I200 Brussels. Cancer J. 1994;7:108-14. Environmental Tobacco Smoke (BTS) is a complex mixture of Exhaled