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