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3.1 I), armed servic& personnel (OR = 3.10). agricultural workers (OR = 2.05). driver sales (OR = 2.21). mechanics (OR = 1.72), painters (OR = 1.96). and drivers (OR = 1.88). Industries with significant elevated iungcanccrriskincludedfanning(OR=2.2l),mining (OR=2,98),and primary ferrous metals manufacturing (OR = 2.43). Analyses of white and black men separately revealed that the excess of lung cancer among mechanics is restricted to black males (OR = 4.16). The risk of lung canceramongarmedservices personnel is higheramong blackmen (OR = 10.54) than among white men (OR = 3.06). Five of the occupations observed more often among lung cancer cases have probable exposure to diesel exhaust.

Carcinogenic risk of non-uniform alpha particle irradiation in the lungs: Radon progeny effects at bronchial bifurcations Hofmann W, Crawford-Brown DJ, Menache MG, Martonen TB. Ableilung fur Biophysik, Universitor S&burg. Hellbrunnersrrasse 34, A-5020 Salzburg. Radial Pro1 Dosim 1991;38:91-8.

The combined effect of enhanced deposition and reduced clearance at bronchial bifurcations leads to increased radon progeny doses within branching sites compared with uniformly distributed activity within a given airway generation. A multi-stage carcinogenesis model was used topredicttheprobabilityoflungcancerinductionatdiffcrentsitesofthe bronchial region. For relatively low radon progeny exposures, lung cancer risk is significantly higher in bifurcation zones, particularly at carinal ridges, than along tubular segments. At sufficiently high expo- sures, however, lung cancer risk is highest in the tubular portions of a generation. This suggests that the common assumption of a uniform dose distribution provides realistic risk estimates for high uranium miner exposures, but may underestimate lung cancer risk at low, environmentalexposures. Ifconcomitantexposuretocigarettesmokcis factored intoourriskanalysis mamultiplicative fashion.then theeffect related to risk inhomogeneity becomes even more pronounced.

Relation of bronchioloalveolar carcinoma to tobacco Morabia A, Wynder EL. American Healrh Foundation. 320 E43rd Street, New York, NY 10017. Br Med J 1992;304:541-3.

Objective - To determine whether bronchioloalveolar carcinoma is related to tobacco use. Design - Case-control study. Setting - 11 teaching hospitals of Chicago, Long Island, New York, and Philadel- phia, 1977-89. Subjects - 87 patients with histologically diagnosed bmnchioloalveolar carcinoma (cases) and 286 non-cancer and 297 cancer patients matched to cases on age, sex, race, hospital, and date of admission. Results - 10% of male cases and 25% of female cases had never smoked. Relative risks of bronchioloalveolar carcinoma (as estimated by the relative odds) were greater for subjects who started smoking at a younger age, smoked for a longer time, or smoked more cigarettes per day. Relative risks decreased proportionally to the dura- tion of smoking cessation. Conclusion - Smoking plays an important part in theaetiology of bronchioloalveolar carcinoma but is not the only potential cause because of the large proportion of never smokers among patients with this disease.

Theriskoflungcancerandmesotheliomaafterccssation ofasbestos exposure: A propsective cohort study of shipyard workers Sanden A, Jarvholm B, Larsson S, Thiringer G. Department ofoccupa- tional Medicine, St. Sigfridsgatan 85. S-412 66 Goteborg. Eur Respir J 1992;5:281-5.

A prospective cohort study of 3.3893 shipyard workers, mainly exposed to chrysotile, indicated no increased risk of lung cancer 7-15 yrs after exposure to asbestos had ceased. The shipyard workers, however, liad an increased risk of pleural mesotbeliomas with 11 observed cases versus I .5 expected. An explanation for these observa- tionsmay bethatasbestosmay havediffcrentcarcinogenicmechanisms in causing lung cancer and mesothelioma. A non-increased risk of lung cancer some years after exposure to asbestos has stopped is in accor- dance with asbestos acting as a promotor. The high risk of mesotheli- oma, on the other hand, may indicate that asbestos acts as a complete carcinogen in developing this disease.

Dietary cholesterol, fatty acids, and the risk of lung cancer among men Knekt P, Seppanen R, Jarvinen R, Virtamo J. Hyvonen L, Pukkala E et al. Research lnstirute for Social Security, Social Insurance Institution, Helsinki. Nutr Cancer 1991;16:267-75.

The relation between dietary cholesterol and fatty acids and the incidence of lung cancer was studied among 4,538 Finnish men aged 20-69 years and initially free of cancer. During 20 years of follow-up, 117 lung cancer cases were diagnosed. Cholesterol intake was not associated with lung cancer risk, the age-, smoking-, and energy- adjusted relative risk between the lowest and highest tertiles being 1.0 [95% confidence interval (CI) = 0.6-1.91. The intake of saturated fatty acids was nonsignificantly related with lung cancer incrdence, the relative risk for the lowest compared with the highest tertile being I .6 (Cl = 0.8-3.2). The association was stronger among smokers than among nonsmokers, the relative risks being 2.1 (CI = 1 .O-4.3) and 1.3 (CI = 0.4-4.1). respectively. Therelativerisk among smokers, however, decreased to 1.5 after adjustment for the amount they smoked. In the total cohort, there was a significantly elevated risk of lung cancer among men with a high intake of butter, one of the main sources of saturated fatty acids, the relative risk being 1.9 (CI = 1 .l-3.2). The present data do not confirm previous results suggesting that dietary cholesterol predicts the Occurrence of lung cancer among men. The association between intake bf saturated fatty acids and lung cancer observed in the present study may be partly due to heavy smoking among high consumers of saturated fat.

Epidemiology of passive smoking Uberla K. Institut fur Medirinische Informationsverarbeitung, Biom- etrie tutd Epidemiologic. Ludwig-Maximilians-Universitat, Marcion- inistr. IS. 8oW Munchen 70. Z Hautkr 1991;66(Suppl2):26-9.

Statistical facts on lung cancer arc presented. The study from HIRAYAMA is discussed and its weaknesses are analysed. The results of a re-analyses of his data are presented. There are two cohort studies with divergent results and 21 case control studies. All case control studies have serious weaknesses. A met&analysis shows, that studies with low methodological quality have a higher relative risk (1.79) in comparison to studies with better methodological quality (1.09). Only 3 out of 10 criteria which are generally used to establish a causal connection from epidemiologic studiesarcpartially fulfilled. All epide- miological data can be explained by bias, confounding, misclassifica- tion or chance as well as by accepting the alternative hypotheses. A causal connection between environmental tobacco smoke and lung cancer is a serious hypothesis. Using the. critical view of a scientist one can equally well adhere to the nullhypothesis with good reasons.

Comparison of hvocarhoplatin-containing regimens with standard chemotherapy for small cell lung cancer in a randomised phase II study Postmus PE, Splinter TAW, Palmen FMLHG, Camey DN, Festen J, Burghouts JThW et al. Department of Pulmonary Diseases, University Hospital, Oostersingel59,9?13 EZ Groningen. Eur J Cancer 1992:28:% loo.

The EORTC Lung Cancer Cooperative group performed a random- ised phase II study in patients with small cell lung cancer comparing the standard cyclophosphatnide/doxorubicin/etoposide (CDE) regimen with two regimens containing the new and active cisplatin derivative, carboplatin,4OOmgfm*incombination with ifosfamide,adrug without important myelotoxicity, at a dose of 5 g/m’ (IMP) or the non- myelotoxic drug vincristine twice 2 mg (VP). Of 178 evaluable patients, 63 received CDE 130 limited disease (LD), 33 extensive disease (ED)], 55 received IMP (22 LD, 33 ED) and 60 (26 LD, 34 ED) were treated with VP. The response duration was not statistically different: CDE 31 weeks, IMP 29 weeks and VP 21 weeks. The time to progression after CDE was 28 weeks, IMP 24 weeks and VP 17 weeks. This was significantly shorter afver VP than after CDE (P = O.O17).The 60%