S6

between lung cancer and exposure to silica dust in an area where a relatively high proportion of the workforce was exposed to silicadust in the past. The cases were 309 lung cancer patients admitted at the Chest Department of the Central Belluno Hospital during the period 1973- 1980, while the 309 controls were patients admitted at the same department for diseases other than lung cancer and bronchitis during the same period. Information on exposure to silica and smoking habits were collected from hospital records. The results show an elevated risk, supported by a clear dose-response, due to smoking. Exposure to silica also appears to increase the risk of lung cancer, but only in presence of sihcosis. The risk estimates tend to increase both with amount of smoking and duration of exposure to silica, with the magnitude of the risk being, however, much smaller for the latter effect. NO clear interaction appears to exist between the two factors. The limitations of the study and the problems in interpreting the results are dku~sed.

Associations between high chromium and nickel concentrations in lung tissue and lung cancer. Kollmeier H, Seemann J, Muller K-M et al. Bundesanstaltfw Arbeifss- chutz, D-4600 Dortmund. Prax Klin Pneumol 1988;42:142-8.

In 72 random autopsies chromium (Cr) and nickel (Ni) were attalysed in lung tissue by means of flameless atomic absorption spectrometry (AAS): 3.37*3.12*gCr/g,O.706*1.01 ??gNi/gdry weight.Tbesubjects examined were residents of Bochum and neighbouring cities. Their Cr and Ni concentrations were 4.8 and 3.3 times higher than those in a previous series from Munster and surrounding areas examined for comparison. Cr and Ni concentrations are 1.5 times higher in men than in women. There were 5 cases of lung cancer (all male) with Cr and Ni concentrations 1.5 and 2.5 times higher than in those with other causes of death. A further case of bronchial carcinoma of a former dental laboratory technician hadextremely highCrandNivalues.Bothtbedata from Bochum and surrounding areas and from Munster showed an age- dependent increase of Cr and Ni in the lung, amounting to 2.3% for chromium and 3.0% for nickel, respectively, per year, and in both data sets as well as in the combined sets the Cr and Ni values showed extremely high correlations (r = < 0.9). Obviously the increase in pulmonary Cr and Ni content is caused by, first of all, a steady low level exposure to air pollution (regional), secondly by certain working places (local), and thirdly by smoking with its uptake of Cr and Ni.

A retrospective cohort study of lung cancer and diesel exhaust exposure in railroad workers. C&hick E, Schenker MB, Munoz A et al. Charming Laboratory, Department of Medicine, Brigham and Women’s Hospital, Boston, MA 02115. Am Rev Respir Dis 1988;137:820-5.

The risk of lung cancer as a result of exposure to diesel exhaust from railroad locomotives assessed in a cohort of 55,407 white male railroad workers 40 to 64 yr of age in 1959 who had started railroad service 10 to20yearsearlier.Thecohortwastraceduntiltheendof 1980,anddeath certificates were obtained for 88% of 19,396 deaths; 1,694 lung cancer cases were identified. Yearly railroad job from 1959 to death or retirement was available from the Railroad Retirement Board, and served as an index of diesel exhaust exposure. Directly standardi rates and a proportional hazards model were used to calculate the relative risk of lung cancer based on work in a job with diesel exhaust exposurebeginningin 1959. Arelativeriskof 1.45 (95%Cl= 1.11.1.89) for lung cancer was obtained in the group of workers 40 to 44 yr of age in 1959, the group with the longest possible duration of diesel exposure. The cohort was selected to minimize the effect of past railroad asbestos exposure, and analysis with workers with possible asbestos exposure excluded resulted in a similarly elevated risk. Workers with 20 yr or more elapsed since 1959, the effective start of diesel exposure for the cohort, had the highest relative risk. These results taken in conjunction with other reported results support the hypothesis that occupational exposure to diesel exhaust results in a small but significantly elevated risk for lung cancer.

Occupation and lung cancer in two industrialized areas of nottbetn Italy. Ronco G, Ciccone G, Mirabelli D, Troia B, Vineis P. Unir of Cancer Epidemiology, Dipartimento di Scienze Biomediche e Oncologia Umana, Main Hospital and Universily of Turin, 10126 Turin. Int J Cancer 1988;41:354-8.

A population-based case-control study on lung cancer was conducted in 2 industrialized areas of northern Italy. Cases (126) were all males whodiedfrom lungcancerbetween 1976and 1980.Controls(384) were a random sample of males dying from other causes during the same period. Jobs held during working life have been analyzed according to a list of occupations already known to be causally associated with lung canger (list A) and a list of occupations suspected of being so (list B). Attributable risk percentages in the population for occupations included in either list A or B were about 36% and 12% in the 2 areas. Welders or workers in industries in which welding is common showedelevatedodds ratios: 2.9 for welders (95% CI 0.9-9.8); 4.9 (1.1-22.9) for structural metal workers; 1 I .4 (2.6-49.9) for workers in structural metal produc- tion. Other job categories associated with lung cancer included: electri- cians and workers in electrical machine production, woodworkers (in fumitweorcabinetmaking, butnotincarpentryorjoinery)andcleaning services. Smoking did not seem to exert a substantial confounding effect. Attributable risk percentages for tobacco smoking were about 78% and 76% in the population of tbe 2 areas.

Maintenance of morphology and tumour marker production in human epidermoid lung carcinoma xenografts. Bak M Jr,Mattem J, Volm M.German CancerResearch Center.lnsirute of Experimental Pathology, D-6900 Heidelberg. In Vivo 1987;1:319- 26.

The histopathology and the expression of various marker substances including cytokeratin, epithelial membrane antigen (EMA) and car- cinoembryonicantigen(CEA)often humanepidermoidlungcarcinoma xenograft lines were compared with the corresponding donor patient tumours. It was found that the histological structure and the tumour markers were maintained by the xenografts. Neoplastic cells were more effectively detected using anti-keratin antibodies as compared to anti- bodies against EMA. CEA immunoreactivity was more common in well differentiated turnours. With the aid of electron microscopy, the known cellular heterogeneity of epidermoid lung carcinomas in man was also confirmed in these xenografts.

Projectionsof lung cancer mortality in the United States: 1985-2025 Brown CC, Kessler LG. Biomefry Branch, Division of Cancer Preven- tionandConwoLNationa1 Cancerlnsiitute, Befhesda,MD20892-4200. J Nat1 Cancer Inst 1988;80:43-51.

Lung cancer has been the leading cause of cancer death in the United States for the largerpartof thiscentury. Increases in smoking prevalence from the 1900s through the 1950s have resulted in more than 100,000 deaths annually. Because of the changes during the last decades in smoking prevalence, the decreasing tar content of cigarettes, and the increasing popularity of low-tar cigarettes, trends in lung cancer are difficult to predict. This article presents an analysis of smoking and lung cancer data using an age-period-cohort model for projecting lung cancer mortality through the year 2025. The projections are based on the initial paramctcrization of the model and on prevention objectives related to smoking behavior established by the National Cancer Institute. It is concluded thattherecenttrendsinlungcancerareunlikely tobeaffected by changes in cigarette composition and consumption in the near term, but increasing the effectiveness of anti-smoking campaigns can have a considerable effect on lung cancer rates in the more distant future.