ELSEVIER Lung Cancer 13 (1995) 81-104

Abstracts

LUNG CANCER

-@&

Prevention

Cigarette use and the estimation of lung cancer attributable to radon in the United States Lubm JH. Steindorf K Eprdemtologtc Methods Sectron. Norronol Cancer Instthle, Executrve Plora North, Belhesdo, MD 2&5’92-7368 Radm, Res 1995.141:79-85

Resldenual exposure to radioactive radon and I,P decay produc,s has been estlmaled 10 account for IO-I 2% of all lung cancer deaths in ,he U S I, has been dhiicul, Lo evaluate fully the impact of cigarette smokmg, the most ,mpor,ant cause- of lung cancer. on ,h,s est~male, because factors for patterns of tobacco use have not been included I” the risk models, s,ncc risk models are derived from s,ud,es of underground miners exposed 10 radon and detailed data OD smoking are hmired Lung cancer risk estmxates for exposure 10 radon progeny m smoker and non-smoker popula,ions are ablamed by applying the same nsk model 10 each population group, thereby assummg the jomt effects of smckmg and exposure to radon progeny are mul,,plica,we However. tn mmers, jomt relauve risks (RR) for ,he two exposures are mas, cowsten, wth an mtermedmte relatwnship between mulbphcawe and adduwe. so that the present approach likely results in an ~verestmate of risk m smokers and an underesllmate of r,sk in nonsmokers. Lubin e, al (Nabonal Institutes of Health Publicatmn No 94.3644. 1994) present an ad hoc approach for adJus,ing nsk models lo mcorpora,e smoking status The approach 1s based on the relatwe magnaude of the effects of radon progeny m smokers and nonsmokers and lherefore may no, be apphcable to non-mmer populations if the proporwxn of smokers and ,he RR for smokmg ddTer We show lha, the moddicabon cam be denwd expbcilly by assammg an arithmetic mixture model for the ~omt RR for smokmg and exposure lo radon progeny In thtsway. smokmgparamelers m ,he populalionofmterest (thepropor,mn of smokers and the RR of smckmg) can be used directly to adJust radon

progeny risk models and &lain nsk estimates that are specitic for smokers and nonsmokers Wilh an mlemxdials RR relationship for smokmg and radon progeny, the altnbutable percentage of lung cancer deaths from rwdenual radon may be lwofold grealer in non-smokers lhan m smokers

Mutagen sensitivity as l biological marker of lung cancer risk in African Americans Spiti MR. HN TC. Wu X, Fueger JJ, Amos Cl, Roth IA. Departmenl ofEpidenvo/ogy. Texas Unrv. MD. Anderson Con. Ctr. ISIS Holcombe Boulevanl Houston, TX 77030. Cancer Epidemiol Biomarken Prev l995.4:99-103.

Cigarette snmkmg is the nqor determinant of lung cancer. However, only a fracuon of smokers develops lung cancer; genetically detetined susceptibility fac,ors seem to play an imponant role also. Previous case- control studies have shown that in vitro blmmycin-induced mutagen senwivay is an independent risk factor for head-and-neck cancers. and prehminary data suggest a similar association with lung cancer. However, these shidies were almost exclusively perfomred on Caucasian populations. To test whether ethnic ditfcrcnces in cancer risk are due 10 differences in mutagen sensitivity, we are using the in vitro mutagen sensitivity assay to cnnduc, a case-control study of mutagen sensitivity and lung cancer risk in low-risk (Mexican-American) and high-risk (African-Amencan) groups Here we report the resuhs of our ongomg

study of 209 African-Americans (90 cases and II9 controls) ,n the Houston-Galveston area. Mexican-American data will be reported separately as case am-al incnaur. Predic,ably, all wasures ofclgarene smoking status (mcluding intensity. duration. tar content, depth of inhalation. and fype of agarete) were significant precbc,ors of risk In addition, 55.3% of the cases mre mutagen sensitive (defined as I break/cell). compared with 24.6% of the controls. with an age-. sex-. and smokmg-adjusted odds ratio (OR) of 3.7 (95% confidence limits = 1.4.9.4). Ofintcnn. higherriskswere notedfor former smokers (OR= 5.4) cornoared with current smokers (OR = 3. I) and ewcially for yokger imner smokers (<55 years). By histologic-spexiec anaiysis. mutagen sensiwity was significantly assocmted with risk for adenccarcinoma (OR = 4.8) and squamous cell carcinoma (OR = 8 5) StraUlied analysts showed that there was an mteraction hewzen mutagen sensitiwy and current and former smoking and heavy smoking ( 20 pack-years) that appeared to be greater &an multiplicative. These nsk es,,n,a,es are generally h,gher than those we reported for head-and- neck cancer in Caucasian populations. FurUKr research should focus on lhe cytogewtic and molecular evaluation of whether the break sites arc random or occur at specific sites and on comparisons wilh DNA repair assay systems.

Epidemiology and etiology

~53 and ras gene mutations in lung cancer: Implications for smoking and occupational exposures Huseafvel-Purslainen K. P.&n~aa M. Anmla S. Vainlo H Fmnwhlnsl Occ;,,ot,onol Heollh. Topeh&nkofu J,a4, FIN-00250 Helsvtk~ J Occup Environ Med 1995.37.69-76

This paper rewews mutalional activalion of ras oncogenes and mclm’alm of the ~53 tumor suppressor gene m human lung cancer Wedwxss the frequency. type, and locationofmulalions in these genes m relation to known e,wlogtcal fxtors for lung cancer The mos, nudwd examples of these are exposure 10 ,cbacco smoke. and to radon and asbestos fibers at work. We summarize data from our lalwatoty on K- ras and ~53 mutations in fresh tissue ramples horn pauents wrth resected primary lung carcinoma whose smoking and occupational histones were know. Mast of the tumors exammed were histologxally non-small cell carcmoma (NSCLC). mainly of the squamous cell carcinoma and adenocarcinoma types. We compare the prevalence and nature of mutations ,n the ,wo histolog,cal types of NSCLC

Trends in lung cancer mm-t&y in regions oftbe Czech republic Kuhik A. Reissirova I. f&a. Plicnich Nemoa, Budrnovo 67. IN0 71 Proho 8. Stud P;eumol Phtiseal 1994;54:405-IO.

Regional di&mra in monality from malignant wmours contribute to ,he improvement of understanding the aetiology of hunours and 10 ,heJudgemcn,ofeffciencyof,heirprevention. Analysis ofdewlopmen, of lung cancer tonality in the period of 1983.1992 in eight reawns of the Czech republic has shown cons,deraMe differences between the mdrvidual regwns In both sexes mortality was high in the North Bohemia and West Bohemia. and, on the other band. relatively low m the South Moravia and Ean Bohemia. Prague had a high monahty m women and a low mortahty in men. In the ten-year period 1983-1992