Prevention

Declining lung cancer rates among young men and women in the United States: A cohort analysis Devesa SS, Blot WJ, Fraumeni JF Jr. Division of Cancer Etiology, Nnfionnl Cancer Institule, Bethesda. MD 20892. J Natl Cancer Inst 1989;81:1568-71.

Although overall age-adjusted rates of mortality from lung cancer in tbe United States continue to rise, rates at ages below 45 years have begun to decline. In this report we’show that the decrease is greatest among white men, with a 29% drop between the mid-1970s and mid- 1980s. but a decrease also occurred among black men and white and black women. Cohort analyses revealed that the rates of lung cancer peaked among men born around 1925.1930 and among women born around 1935-1940, and have declined thereafter. If these trends con- tinue, overall lung cancer mortality rates will start to decline in the 1990s among men and after the year 2000 among women.

Dietary factors and risk of lung cancer: Results from a case-control study, Toronto, 1981-1985 lain M, Burch JD, Howe GR,Risch HA, Miller AB. NCICEpidemi&y Unit, McMurrich Building, Universi?v of Toronto, 12 Queen’s Park Crescent West. Toronto. Ont. M5S lA8. Int J Cancer 1990;45:287-93.

Associations between dietary factors and risk of lung cancer are reported from a study of 839 cases and 772 population-based controls interviewed in metropolitan Toronto between 1981 and 1985. Increased consumption of vegetables is associated with a decreased relative risk of 0.60 (95% confidence limits = 0.40 to 0.88) for those in the highest compared with the lowest quartile. Cholesterol intake is associated with increased risk, but this is restricted to those in the highest quartile for whom the relative risk is 1.58 (95% confidence limits = 1.05 to 2.38) compared with those in the lowest quartile. The results of this study suggest that dietary factors may affect the risk of lung cancer, but identification of the specific constituents involved will require further research.

Screening for lung cancer in the middle-aged Bemdt R, Nischan P, Ebeling K. Clinic for Oncology, Departmenr of Medicine (Churite). Humboldt University, Schumanns~rasse 20-21. DDR-1040 Berlin. Int J Cancer 1990;45:229-30.

A screening programme for lung diseases has been in operation in the German Democratic Republic for more than 3 decades. The programme is based on biennial chest X-rays (70 x 70 mm posterior-anterior) of the population 40 years of age or over. With respect to lung cancer the results show that, for the population under 60 years of age, the adjusted relative risk of dying from lung cancer among subjects who took part in the last screening round compared with subjects who did not but were screened at least once during the preceding IO-year period was 0.93 (95% confidence interval 0.65-1.33).

Smoking, air pollution, and the high rates of lung cancer in Shen- yang, China XuZ-Y,BlotWJ,XiaoH-Petal.Div~slonofCancerE~io~ogy, National CancerInstitrue, Bethesda, MD. J Nat1 Cancer Inst 1989;81:18oQ-6.

A case-control study involving interviews with 1,249 patients with lung cancer and 1,345 population-based controls was conducted in Shenyang, an industrial city in northeastern China, where mortality rates are high among men and women. Cigarette smoking was found to be the principal cause of lung cancer in this population, accounting for 55% of the lung cancers in males and 37% in females. The attributable risk percentage among females is high compared to elsewhere in China, largely because of higher prevalence of smoking among women. After adjustment for smoking, there were also significant increases in lung cancer risk associated with several measures of exposure to air pollut- ants. Risks were twice as high among those who reported smoky outdoor environments, and increased in proportion to years of sleeping

on beds heated by coal-burning stoves (kang), and to an overall index of indoor air pollution. Threefold increases in lung cancer risk were found among men who worked in the nonferrous smelting industry, where heavy exposures to inorganic arsenic have been reported. The associa- tions with both smoking and indoor air pollution were stronger for squamous cell and small cell carcinomas than for adenocarcinoma of the lung. Risks due to smoking or air pollution were not altered by adjustment for consumption of fresh vegetables or sources of beta carotene or retinal, prior chronic lung diseases, or education level. The findings suggest that smoking and environmental pollution combine to account for the elevated rates of lung cancer mortality in Shenyang.

Epidemiology and etiology

Assessing indoor air pollution exposure and lung cancer risk in Xuan Wei, China ChapmanRS,MumfordJL,HeX,HarrisDB.YangR. Jiang W. Human Studies Division, Health Effects Research Laboratory, Environmenlal Protection Agency, Research Triangle Park. NC 27711. J Am Coll Toxic01 1989;8:941-8.

This report presents the risk-assessment-related aspects of a multidis- ciplinary study of indoor coal smoke pollution and lung cancer in Xuan Wei County, Yunnan Province, China. Xuan Wei presents a unique natural experiment in environmental carcinogenesis because lung can- cer mortality rates and indoor pollution exposures vary widely within the County. Current evidence links lung cancer with domestic burning of ‘smoky coal’, as opposed to ‘smokeless coal’ and wood. Efforts to determine the most carcinogenic components of smoky coal pollution are in progress, as are efforts to develop a quantitative relationship of pollution dose with lung cancer response in Xuan Wei. Seine available evidence suggests that the composition of indoor pollution does not vary greatly throughout Xuan Wei, and thus that lung cancer risk is a function of overall pollution exposure. Other evidenci suggests that different Xuan Wei fuels exhibit different carcinogenic potencies. On- site and laboratory studies are being conducted to differentiate between these possibilities.

ated with a high lung cancer rate in Xuan Wei, China Mumford JL, Chapman RS, Harris DB et al. U.S. Environmental Proteclion Agency, Research Triangle Park. NC 27711. Environ Int 1989;15:315-20.

Residents of Xuan Wei County in%hina have unusuallp high lung cancermonalitythatcannotbeatuibu~totobaccouseoroccupational exposure. They are exposed to smoke from unvented, open pit coal or wood fires (often used for cooking and heating). The variation in lung cancer rates among communes within the county suggests that indoor combustion of smoky coal may be the prime determinant of Iling cancer. To characterize the air in Xuan Wei homes, samples of air particles and semivolatile organic compounds were collected from homes located in two communes; one commune has a high tad of lung cancer, and the other has a low rate. Samples collected in the commune tihere the lung cancer rate is high and where smoky coal is the predominant fuel contained high concentrations of small particles with high organic content; organic extracts of these samples were mutagenic. Sam$ea from homes in the wood-burning commune, which hasa lowrateoflung cancer,consisledmosUyoflargerpaniclesoflowerorg~icconlentand mutagenicity. The smoky coal sample was a mouse skin carcinogen and’ was a more potent initiator of skin tumors in comptiison to the wood or smokeless coal sample.

Mechanisms of smoking-induced lung injury Idell S, Garcia JGN. Deparment of Medicine. University of Tern Health Center al Tyler, Tyler, 7X 75710. Semin Re~pi Med l989;lO:gS- 55.

A considerable body of evidence has been and continues to be

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accumulated that supports involvement of proteolytic enzymes and oxidants in the pathogenesis of smoking-induced lung injury. Still at issue are the host factors that modulate the effects of smoking in the individual subject It remains unclear why a large proportion of smokers are protected fmm the deleterious effect of tobacco exposure. A potential problem with the pmtease-antipmtease hypothesis is that its focus may be too narrow. Whereas it appears that the balance between proteolytic enzymes and their inhibitors is important in determining the integrity of pulmonary structure and function, the role of other intlam- matory pathways in the pathogenesis of smoking-induced lung injury remains to be elucidated. Furthermore, lung injury contingent on the effects of pmteolytic enzymes or oxidants may be signiticandy influ- enced by either genetic or environmental factors. As recently reviewed, clarification of important protective mechanisms that modulate the

effects of cigarette smoking may await the application of biochemical and molecular methodology to traditional epidemiologic analyses of smoking-relateddisease. Current information derived from clinical and experimental studies provides a reasonable explanation for the apparent link between smoking and chronic obstructive pulmonary disease. However, elucidation of the truly important effecters of lung injury present incigarette smokeand thedefensesagainsttheseagentsremains the major challenge for future investigation.

Lung cancer in women

Loewen GM, Roman0 CF. Respiramy Care and Sraff Physician, Pulmonary Division, Deparmenr of Inrernal Medicine. House of rhe GoodSammkn, Watertown, NY 13601. J Fsyctit Dtugs 198%21:319- 21.

In 1983, lung cancer exceeded breast cancer as the leading cause of death in American women. Between 1950 and 1985 there was a 500% increase in lung cancer deaths in women, and this trend is not expected to improve in the next decade. There is no corresponding increase in the overall incidence of lung cancer in the general population of the United States. Cigarette smoking is clearly the primary risk factor in this group and the role of passive smoking remains controversial. Various other etiologic factors, including a shift in occupational exposure, may play a minor role in the development of lung cancer in women. The risk of lung cancer in smokers does not return to that of nonsmokers until 15 years after smoking cessation. If the incidence of smoking in American women was reduced to pm-1950 levels, it is estimated that lung cancer in women would once again become a rare finding after the year 2000.

Changes in patterns of cigarette smoking and lung cancer risk: Results of a case-control study Benhamou E, Benhamou S, Auquier A, Flamant R. Deparremenl de Starisdque Medicale, Ins&w Gustave Roussy. 94805 Villeju$ Br J Cancer 1989;60:601-4.

Data from a case-control study on lung cancer were used to evaluate how changes in ciganztte habits, mainly smoking cessation, switch from non-tiltertofilterbrands,fmmdarktolighttobacco,orfrom handrolled to manufactured cigarettes, and reduction in daily consumption influ- ence lung cancer risk. The results presented concern all males, exclu- sive cigarette smokers. involved in the study, i.e. 1,057 histologically confirmed lung cancer and 1,503 matched controls. The general de- crease in lung cancer risk with the years since cessation was also found in each subgroup of cigarette exposure defined by duration of smoking, daily consumption and type of cigarettes smoked. Among smokers who had given up smoking from less than 10 years earlier, the lung cancer risks were two-fold higher for those who had stopped smoking for coughing or health reasons than for those who had stopped smoking for reasons other than health problems. A decrease in lung cancer risk, although not significant, was found in people who switched from non- tiiter brands to filter brands and fmm dark to light tobacco and in smokers who reduced their daily consumption of cigarettes by more than 25% as compared to smokers who had not changed habits.

Cell type specific, receptor-mediated modulation of growth kinetics in human lung cancer cell lines by nicotine and tobacco-related nitrosamines Schuller HM. Experimenral Oncology Laborarory. Deparnnenr of Pa- thobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37901-1071. Biochem Pharmacol 1989;38:3439-42.

The objective of this study was to investigate a potential involvement of nicotinic cholinergic receptors in the mediation of cell type specific biological effects of nicotine and the two tobacco-related nitrosamines N-nitrosodiethylamine (DEN) and 4-(methylnitmsamino)-I-(3-pyridyl)- I-butanone (NNK) on human lung cells. Three well differentiated human lung cancer cell lines that have been reported previously to possess ultrastructural and biochemical features of normal pulmonary neuroendocrine cells, Clara cells and alveolar type II cells, respectively, were used for these experiments. The effects of nicotine, DEN, and NNK on cell proliferation and its modulation by establishedantagonisu of nicotinic and muscarinic cholinergic receptors were studied. In the neuroendocrine cell line, nicotine and the two nitrosamines caused a strong stimulation of cell proliferation that was inhibited by antagonists of nicotine cholinergic receptors. In the cell lines with features of Clara cells and alveolar type II cells, nitocine did not stimulate cell prolifera- tion. Both nitmsamines stimulated cell proliferation in the cell line with Clara cell features. This effect was not changed by pre-exposure to cholinergic antagonists. The data suggest a selective uptake of nicotine and the two nitmsamines via nicotinic cholinergic receptors in pulmo- nary neuroendocrine cells.

Transformation of lung cells from inhalation of radon daughters in dwellings: a preliminary study Al-Affan IAM, Haque AKMM. Departmem of Physical Sciences and Scienrifc Computing. South Bank Polyrechnic. London SE1 OAA. Int J Radiit Biol 1989;56:413-22.

There is now world-wide concern for the quantification of lung

cancer risk due to indoor radon, but the recent estimates are based on epidemiological studies of miners alone. The present attempt is a preliminary study of thealteration oflung stem cellls irradiated by alpha particles emitted by radon daughters. Local energy deposited has been calculated for alpha particles, emitted from radon daughters lining the mucous layer in the respiratory tracts. This calculation has then been followed by dose evaluation and estimation of transformation of lung cells as a function of age. Mean life span of the stem cells was varied between 5 and 45 years to simulate living conditions in different environments.Thecumulativefractionoftransformedcellsafter4Oand 70 years has been calculated for radonconcentzation in the range 23-230 Bq/m’. Increase of the fraction of transformed cells with radon concen- tration was exponential. It has been assumed that causes other than radiation increase the rate of cell death of mature and stem lung cells, and hence the turnover of stem cells to replace them. It is concluded that the rate of transformation of cells is small for low radon concentration even late in age for non-polluted environments. For radon concentra- tions of 50 and 100 Bq/m3 the fractions of transformed cells are 0.2 and 6 per cent, respectively for an exposure time of 70 years.

Analyses of chromium and nickel in human pulmonary tissue. Investigations in lung cancer patients and a control population under special consideration of medical expertise aspects Raithel HJ, Schaller KH, Akslen LA, Myking AO, Morkve 0, Gulsvik A. Insrilule of Occupational and Social Medicine, University of Er- langen-Nwemberg, D-8520 Erlangen. Int Arch Occup Environ Health 1989;61:507-12.

After inhalative occupational exposure to certain compounds con- taining nickel and chromium (mostly over many years), an accumula- tion of these metals may occur in the lung tissue. ‘Ihis is of particular importance, both from a toxicological point of view and with regard to expert reports, since certain nickel and chromium compounds may