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Lung cancer, smoking, and employment in foundries. Becher H, Jedrychowski W, Flak E, Gomola K, Wahrendorf J. Germon Cancer Research Center, Institute ofEpidemiology and Biometry, D- 6900 Heidelberg. Scand J Work Environ Health 1989;15:3842.

A case-referent study on lung cancer was conducted in Cracow, Poland. Men dying of lung cancer within a 6-year period (1980-1985) formed the case group. The reference series was selected fmm death registers and was frequency-matched with the cases by sex and age. Deaths due to other respiratory diseases were excluded. Information on the occupation, smoking habits, and residency of 901 cases and 875 referents was collected from their next-of-km. The combined effect of smoking and industrial exposure, in particular employment in steel or iron foundries, was investigated by multivariate analyses and was very well fitted by a multiplicative model. Foundry employment, in particu- lar in the younger age (~70 years) group, occupational exposure to known carcinogens in other industries for more than 20 years, and smoking were found to be risk factors.

Comparison of smoking-related risk factors among black and white males. Sterling TD, Weinkam JJ. Faculty of Applied Sciences, School of Computing Science, Simon Fraser University. Burnaby. BC V5A 1.76. Am J hid Med 1989;15:319-33.

The lung cancer risk factors of smoking prevalence, amount smoked, andagestarted tosmokewerecomparedforblacksandwhites,usingthe 1970 and 1979/80 National Health Interview Survey (NHIS) survey data. For both survey years, proportionally more blacks were never smokers and fewer were ever smokers (although more were current and fewer former smokers). The average adult black smoker smoked approximately 65% of the number of cigarettes smoked by the average white adult. Blacks started smoking later than whites for almost all occupational categories. Thus, it could be argued that whites had higher smoking-associated risk factors than did blacks. At the same time, a much greater proportion of blacks than whites were in the types of occupation where they would have been exposed to occupational hazards.Thesharpriseinandrhelargerincidenceoflungcanceramong blacks compared to whites may not be due to differences m black and white smoking, but more likely are a reflection of occupational differ- ences.

Respiratory cancer in chrysotile textile and mining industries: exposure inferences from lung analysis. Sebastien P, McDonald JC, McDonald AD, Case B, Harley R. School ofOccupationalHealth,McGill University,Montreal. QueH3AIA3. Br J Ind Med 1989;46: 180-7.

In an attempt to explain the much greater risk of respiratory cancer at the same cumulative exposure in asbestos textile workers in Char- leston, South Carolina, than in Quebec miners and millers, both exposed to chrysotile from the same source, 161 lung tissue samples taken at necropsy from dead cohort members were analysed by transmission electron microscopy. Altogether 1828 chrysotile and 3270 tremolite fibres were identified; in both cohorts tremolite predominated and fibre dimensions were closely similar. Lung fibre concentrations were ana- lysed statistically (a) in 32 paired subjects matched for duration of employment and time from last employment to deatb and (h) in 136 subjects stratified by the same time variables. Both analyses indicated that die Quebec/Charleston ratios for chrysotile fibre concentration in lung tissue were even higher than the corresponding ratios of estimated exposure intensity (mpcf). After allowance for the fact that regression analyses suggested that the proportion of tremolite in dust was probably 2.5 times higher in Thetford Mines, Quebec, than in Charleston, the results from both matched pair and stratification analyses of tremolite fibre concentrations in lung were almost the sameas for chrysotile. It is concluded that neither fibre dimensional differences nor errors in estimation of exposure can explain me higher risks of lung cancer observed in asbestos textile workers. The possible co-carcinogenic role of mineral oil used in the past in asbestos textile plants to control dust provides an alternative hypothesis deserving consideration.

Lung cancer in the meat industry. Coggon D, Pannett B, Pippard EC, Winter PD. MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, Southampton SO9 4XY. Br J Ind Med 1989;46:188-91.

Routine statistics of occupational mortality and incidence of cancer have consistently shown high rates of lung cancer in butchers. Possible explanations include infection by carcinogenic papilloma viruses, exposure to polycyclic aromatic hydrocarbons and nitrites in the pres- ervation of meat, or a confounding effect of tobacco. To explore these possibilities, we have examined the mortality of 1610 men employedat three British companies processing pork, beef, lamb, bacon, and other meat products. The overall death rate was less than in the national population (27 1 deaths observed, 3 10 expected) but mere was an excess of deaths fromcancer(87 observed, 80 expected), and in particular from lung cancer (42 observed, 32 expected). The risk of lung cancer was concentrated in subjects exposed to recently slaughtered meat, espe- cially after an interval of 10 or more years. These findings increase suspicions of a risk of lung cancer in butchers, although further information is neededabout smoking habits in the meat industry. If there is a hazard infection by a papilloma virus would seem the most likely cause.

Basic biology

Methylationstatusofepidermalgrowth factorreceptorgenein lung carcinoma cells. Gamou S, Shimosato Y, Merlino GT, Shimizu N. Department of Molecular Btology. Keio University School of Medicine, Shinjukuku, Tokyo 160. Jpn J Cancer Res 1988;79:989-95.

The methylation status of the epidermal growth factor receptor (EGFR) gene was compared in cell lines from four major types of lung carcmoma, small cell lung carcinoma (SCLC), large cell lung carci- noma, squamous cell carcinoma and adenocarcinoma, in order to examine whether DNA memylation isresponsible for the suppression of EGFR gene in SCLC cells. Southern blot analysis revealed that the structural region of the EGFR gene is methylated in various degrees regardless of the expression of EGF receptor on the surface. An 8- kilobase EcoRI fragment which contains the EGFR gene promoter region is readily digested with various metbylation-sensitive restriction enzymes in all types of cells, indicating that die EGFR gene 5’region is barely methylated. Thus, a mechanism other than DNA methylation appears to control EGFR gene expression and the lack of EGFR gene

expression in SCLC cells may be caused by a paucity of some transcrip tion regulatory factor(s).

CytolyticresponsetohumanTcellsagainstallogeneicsmallcelllung carcinoma treated with interferon gamma. WeynantsP,WautersP,CouliePG,VanDenEyndeB,SymannM,Boon T. Brussels Branch. Ludwig Institute for Cancer Research, B-1200 Brussels. Cancer Immunol Immunother 1988;21:228-32.

Human lymphocytes stimulated in vitro by allogeneic small cell lung carcinoma cell lines did not show any significant cytolytic activity against the stimulatory tumor cells. However, a high level of lysis was observed when both stimulator and target small cell lung carcinoma cells were pretreated with interferon gamma, which increased consid- erably the expression of major histocompatibility class I molecules by these cells. The demonstration that small cell lung carcinoma cells can be lysed by cytolytic T lymphocytes, suggests that it will be feasible to study the autologous T cell response of patients against this tumor.