Cigarette smoking and lung cancer in New Mexico. Samet IM, Wiggins CL, Humble CG, Pathak DR. Deparrmenf of Medicine. University ofNew Mexico Medical Center. Albuquerque. NM 87131. Am Rev Respir Dis 1988;137:1110-3.

We have used population-based data for the state of New Mexico to calculate cigarette-smoking-specific incidence rates for lung cancer, cumulative incidence rates for lung cancer, and estimates of the proportion of lung cancer cases attributable to smoking. For white New Mexicans, the incidence of lung cancer increased with age and was markedly higher in smokers than in nonsmokers. From 25 through 84 yr ofage,thecumulativeincidenceoflungcancerwas0.9%innonsmoking malesand0.5% in nonsmoking females. The cumulative incidence rates were much higher for smokers; for males who smoked 20 or more cigarettes daily from age 25, the cumulative risk of lung cancer through age 84 was 3 1.7%. For females with the same cigarette smoking history, the estimate of cumulative incidence through age 84 years was 15.3%. The population-attributable risks for lung cancer associated with ciga- rette smoking were 89.5% for males and 85.5% for females.

Analysis of excess lung cancer risk in short-term employees. Lamm SH, Levine MS, Starr JA, Tirey SL. Epi&mio/ogy and Occupu- tional Health, Inc., Washington, DC 20007. Am J Epidemiol 1988;127: 1202-9.

An excess of lung cancer found in a cohort of 741 New York State tremolitic talc workers observed from 1947 through 1978 has been shown paradoxically to be concentrated in short-term workers. Review of past work histories suggests that the excess of lung cancer in these short-term workers may be accounted for by prior exposures rather than by exposures at the employment under investigation. This finding has significant implications in view of the developing practice of including short-term workers inoccupational cohort studies in contrast to the more traditional practice of excluding short-term workers. The traditional practice was based on the assumption that the inclusion of short-term workers with little exposure, and thus little risk, might dilute an otherwise apparent association between mortality and exposure. This study suggests that in certain instances the inclusion of short-term workers may magnify rathcrthan dilute the estimation of risk, reflecting the presence of confounding variables.

Cigarette smoking and male lung cancer in an area of very high incidence. II. Report of a general population cohort study in the West of Scotland. Gillis CR, Hole DJ, Hawthorne VM. West of Scotland Cancer Surveil- lance Unit, Ruchill Hospital, Glasgow G20 9NB. J Epidemiol Commun Health 1988;42:44-8.

A general population cohort of 7055 men aged 45-64 and resident in Renfrew and Paisley, two urban burghs in the West of Scotland, has been followed for 101 years. Analysisofthecigarettesmokingandlungcancer (incidence and mortality) relation has been undertaken in order to establish whether unusual results found in a case-control study of cigarettesmokingandlungcancerin LheadjacentcityofGlasgowcould be confirmed. Lung cancer incidence and mortality rates increased markedly for exposure categories up to an average consumption of 15- 24 cigarettes per day. Above this level the rates increased only margin- ally. Exuressing these rates relative to that estimated for the never-

Cigarette smoking and male lung cancer in an area of very high incidence. I. Report of a case-control study in the West of Scotland. Gillis CR, Hole DJ, Boyle P. West ofScotland Cancer Surveillance Unit, Ruchill Hospital, Glasgow G20 9NB. J Epidemiol Commun Health. 1988; 42:38-43.

Altogether 656 male lung cancer cases and 13 12 age and sex matched controls were interviewed between 1976 and 1981 in a case-control study of cigarette smoking habits and lung cancer in Glasgow and the West of Scotland, an area with the highest recorded incidence in the world. The relative risk of lung cancer increased significantly for smokers whose consumption was below 20cigarettes per day but did not rise significantly in those who smoked more than 20 cigarettes per day. Other smoking characteristics such as inhalation and tar yields ofbrands smoked did not explain this finding. Additionally, the relative risks observed at all levels of cigarette consumption were low in comparison with those in the published literature. By constructing an index of cigarette exposure which included the tar yields of brands smoked, an assessment of the risk of lung cancer in relation to tar exposure independent of amount smoked was derived. Only in smokers of less than 15 cigarettes per day was there a statistically significant reduction in risk of lung cancer associated with lower levels of tar yield.

Never smoker lung cancer risks from exposure to particulate tobacco smoke. Arundel A, Sterling T, Weinkam J. Faculty ofApplied Sciences, School of Computing Science, Simon Fraser University. Burnaby, EC VSA I S6. Environ Int 1987;13:409-26.

The average particulate environmental tobacco smoke (ETS) expo- sure of never and current smokers and the average lung cancer mortality rate for current smokers is estimated from empirical data. These estimates are used in a linear downward extrapolation of the lung cancer risk/mgofparticulate ETS exposure for current smokers tocalculate the average lung cancer risk for never smokers and the number of never smoker lung cancer deaths (LCD) in the U.S. in 1980 from exposure to particulate ETS. The estimated average daily inhaled particulate ETS exposure for never smokers is 0.62 mg/day for men and 0.28 mg/day for women. The average never smoker is estimated to retain 11% of the inhaled exposure, for a daily retained exposure of 0.07 mg for men and 0.03 mg for women. Other estimates are: a daily retained exposure for current smokers of 3 IO mg for men and 249 mg for women, a smoking- attributable lung cancer risk for current smokers in 1980 of 284 LCD/ lCO,OOO men and 121 LCD/100,000 women, and an annual retained- exposure lung cancer risk for never smokers of 0.64 LCD/lOO,OOO men and 0.015 LCD/lOO,OCKl women. These risks and exposures estimate I2 lung cancer deaths among never smokers from exposure to particulate ETS: 8 among the 11.96 million male never smokers and 4 among the 28.85 million female never smokers in the U.S. in 1980. Conversely, between 655 and 3,610 never smoker lung cancer deaths are estimated from methods based on the average lung cancer risk observed in epidemiological studies of exposure to ETS. Three possible reasons for the discrepancy between the exposure and risk-based estimates are discussed: the excess risks observed in epidemiological studies are due to bias, the relationship between exposure and risk is supralinear, or sidestream tobacco smoke is substantially more carcinogenic than an equivalent exposure to mainsucam smoke. . . _

smoked group and comparing them with the relative risks estimated in thecasecontrol studyrevealedasimilarity in termsofboththe shapeand the level of the dose-response relation. Comparison of the lung cancer rates found in this cohort with those observed in other cohort studies in the literature (UK doctors, US Veterans, and American Cancer Society volunteers) suggested that the West of Scotland rates were substantially higher at all levels of cigarette exposure.

A case-referent study investigating the relationship between expo- sure to silica dust and lung cancer. Mastrangelo G. Zambon P, Simonato L, Rizzi P. Center of Environ- mentalCarcinogenesis. UniversityofPadova,I-35100Padova. IntArch Ckcup Environ Health 1988$X:299-302.

A case-referent study was carried out to investigate the relationship

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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.