Abstracts/Lung Cancer 12 (1995) 113-160 111

Mainstream (EMS) and Sidestream Smoke (SS) composed of gases and Respirable Suspended Particles (RSP). It is both a highly diluted and an aged mixture the composition of which is ditBcuh to assess. Based mainly on syllogisms it has been hypothesized that exposure to low levels of ETS increases the risk of lung cancer in nonsmokers. There is no question that nonsmokers living in the presence of smokers are exposed to tobacco smoke constituents. But, to conclude on the significance of such an exposure, in terms of increased incidence of lung cancer in non smokers, can only rely on a quantitative biomonitoring of exposure to agents proven to play a causative role in lung carcinogenesis. Nether nicotine nor its metabolites are likely to be precise markers of exposure to such chemicals. Molecular epidemiology offers a promising, but still to be validated, tool to meet such a challenge by measuring proteins and/or DNA adducts in serum or urine samples.

Recent results and opea questions of health hazards by radon with special consideration of the ‘Schnceberger lung disease’ Lawsmann D, Amdt D, Mehnelt WH. Bunde~emndheitsamt, Klinisch- Diagnosttscher Bereich, WaldowaNe II 7, D-10318 Berlin. Wiss Umw 1993;1:75-83. The authors present a summan ‘zing review on the reliable knowledge on health hazards by radon and its, in part biological high-effective daughter products. Some unsolved problems are addressed. Literature data are supplemented by own results regarding the epidemiology of the ‘Schneeberger lung disease’ and the problem of lung fibrosis caused by radon exposure.

Residental radon exposu~ and lung cancer - An epidemiological study of Norwegian municipalities Magrms K, Engeland A, Green BMR Haldorsen T, Muirhead CR, Strand T. Cancer Registty of Nomoy. Inst. for Epidem. Cancer Research, University of Oslo, Oslo. Int J Cancer 1994;58:1-7. The study is based on a collaboration between the Cancer Registry of Norway, the Norwegian Radiation Protection Authority, and National Radiological Pmtection Board (NRPB, UK). The association between indoor radon exposure and lung cancer was studied in 427 municipalities. NRPB detectors were sent to 10,000 householders, and 7,500 of the detectors were returned. Data from a nation-wide survey of smoking habits in 1964-1965 were available. Data onasbestos exposure were also wed in a regression analysis. The reporting to the Cancer Registry of all new cases of cancer is fairly complete, as hospital departments and institutes of pathology are obliged to report all cancer cam. The histologiwl1y confirmed lung cancer cases were groujwd into squamous-cell carcinoma, small-cell carcinoma, adenocarcinoma and other or non-spe&ed histological types. The age-adjusted rate of lung cancer by histological type was the dependent variable in the regression analysis. A consistent increase in incidence of lung cancer was seen with increasing tobacco consumption, but no positive trend could be shown with increasing radon exposure in the descriptive presentation of the data. In the regression analysis, however, the incidence of small-ceU anapmstic lung tumors in females increased significantly with increasing radon exposure. When based on the regression coefficients, the fraction of lung cancers attributable to radon is about 2-4.X However, systematic errors cannot be excluded in an ecological study such as presented here.

Higher lung cancer rates ia young womea than young men: ‘Us- maaia, 1983 to 1992 Dwyer T, Blizzard L, Shugg D, Hill D, Ansari MZ. Menzies Ctr Population Health Res., University of Tasmania, I7 Liverpool Shvet, Hobart, Tm. 7000. Cancer Causes Control 1994;5:351-8. In a background of changing lung cancer rates in the past decade, mean incidence and mortality rates for persons aged 25-44 in Tasmania for the decade 1983 through 1992 were examined using Tasmanian Cancer Registry data. The smoking behavior of Tasmanian adults and schoolchildren was also investigated, using data from a social survey conducted by the Australian Bureau of Statistics and from Bve secondary school smoking surveys. The Tasmanian age-standardized lung cancer incidence rates in 25-44 year olds for the IO-year period were 6.2 per 100,000 females and 3.3 per 100,000 males. Mean rates of incidence were higher for females than for males (P = 0.02). The corresponding mortality rates were 4.2 in females and 2.4 in males f.P = 0.08). The prevalence of smoking by adult Tasmanian women is higher than that for other Australian women (p < 0.05). and their duration of smoking is longer (P < 0.01). Tasmanian schoolgirls have a higher smoking prevalence than Australian mainland schoolgirls (P = 0.01) and higher prevalence than Tasmanian schoolboys (P = 0.01). The data suggest that smoking prevalence among teenagers passed that for males only a decade before the observed excess of female incident cases among 25- 44 year olds in Tasmania.

Cohort mwtaIity aad seated -ontnd study of lung cancer among structural pest conhI workers in Florida (United Statea) Pesatori AC, Sontag JM, Lubin JH, Consoti D, Blair A. National CancerInstitute. Executive Plaza North, Rockville, MD 20892. Cancer &Uses CON01 1994;5:310-8. A previous report on the mortality of this cohort of Florida (United States) pest control workers found the risk of lung cancer was positively associated with the number of years licensed. An additional follow-up (1977-82) of this male cohort confirmed the excess (SMR = 1.4) and the rising risk with increasing number of years licensed (SMR = 2.2 among workers employed more than 20 years). A nested case-control study was undertaken to determine the effects of smoking and the type of pesticide exposure on lung cancer risk. OccupationaI histories and other data were obtained on 65 deceased lung cancer cases, 122 deceased controls, and 172 living controls. Interviews were conducted with next- of-km regardless of the vital status of the subject. Odds ratios (OR) were adjusted by age and smoking. Adjustments for diet and other occupations had no effect on risk estimates arid were not included in the final model. Using information from licensing records, ORs for lung cancer were greater for workers first licensed before age 40 (OR = 2.4,95 percent confidence interval [CT] = 1.0-5.9 with decea%d wntrols) and increased from 1.4 (CI = 0.7-3.0) for subjects licensed lo-19 years to 2.1 (CI = 0.8-5.5) for subjects licensed 20 or more years. Using living controls, an association with duration of employment was observed when years of licensure were lagged five years, but was not observed in unlagged analyses. Using information from the questionnaire, the risk of lung cancer was greater among those who worked as pest control operators than non-pest control workers. Although numbers were typically small, lung cancer risk among pest control operators was associated with reported exposure to carbamates, organophosphates, and phenoyacetic acids and more specifically with diazinon, DDT, carbaryl, arid pmpoxur. These results further suggest that pesticides may play a role in lung cancer risk and underscore the need for research that focuses on specitic chemicals.