1
s3 presence of air pollution accounted for less than 5% of the total variation in intraurban lung cancer mortality. In addition, the interpretation of geographic analysis must be guarded due to the introduction of potential biasdue toaggregation. The hypotbesisthatairpolhttion iscontributory to lung cancer cannot be tested until other, stronger individual risk factors for lung cancer can be better measured and controlled in studies of this association. Geographic pattern of lung cancer in Japan and its environmental correlations. Minowa M, Stone BJ, Blot WJ. Department of Epidemiology, Institute of Public Health, Minato-kv. Tokyo 108. Jpn J Cancer Res, Gann 1988;79:1017-23. Standardized lung cancer mortality ratios, 1969-1978, for basic administrative units of Japan were related to various environmental characteristics by multiple regression analysis. Elevated lung cancer mortality was demonstrated in the areas along the seacoast, particuhuly those with fishing ports, low socioeconomic status, and high level of air pollution. High mortality was also observed in coal mining areas and areas with shipyards. Data on tobacco expenditures provided partial adjustment for the effects of cigarette smoking on these correlations. A comparative epidemiologic study on geographic distributions of cancers of the lung and the large intestine in Japan. Murata M, Takayama K, Fukuma S et al. Division of Epidemiology, Chiba Cance.r Center, Chiba 280. Jpn J Cancer Res, Gann 1988;79: 1005-16. To examine what kinds of factors could have caused the geographic variation observed in lung cancer morbidity in Japan, a correlation study was performed comparing various regional traits. The same study was also conducted on huge intestinal cancer, aiming to distinguish the possible urban factors associated with both cancers. Lung cancer was highly correlated with industrialization-related factors such as localiza- tion of manufacturing industries, automobile traffic and air pollution, whereas colon cancer was correlated with the population density of workers in the tertiary industries such as services, tradeandgovemment. A multiple regression analysis could not detect any single factor with an exceptionally strong influence on either cancer. The present findings suggest that the hazardous environmental condition of urban areas has, to some extent, contributed to the recent increase of lung cancer cases in this country. Lung cancer risks of underground miners: Cohort and case-control studies. Archer VE. Rocky Mountain Center for Occupational and Environ- mentalHealth.DepartmentofFamilyandPreventiveMedicine.Univer- sity of Utah, School of Medicine, Salt Luke City, UT. Yale J Biol Med 1988;61:183-93. All underground mines have higher radon levels than are found in surface air. Ventilation is the primary method of controlling radon levels. Fourteen cohort and seven case-control studies done on under- ground miners are reviewed; they include many types of ore. Only five of the studies deal with more than 100 lung cancer deaths. Variations in the attributable risk are given. Some generalizations can be drawn from thesestudies: thelongerthcfollow-up, thegrcaterisdteattributablerisk, even though the relative risk is reasonably constant. The induction- latent period is quite variable but is shortened by high exposure rates, by cigarette smoking, and by increasing age at start of mining. The predominant histological type of lung cancer among miners changed from small-cell undifferentiated for short follow-up time to epidermoid afterlong follow-uptimcs. Withashort follow-uptime,amultiplicative interaction bctwecn smoking and radiation was indicated but, with long follow-up time, the two factors appear to be simply additive. This difference is probably due to theshortened latentperiod among cigarette smokers, not to synergism. Mortality from lung cancer and chronic obstructive pulmonary disease in New Mexico, 1958-82. Samet JM, Wiggins CL, Key CR, Becker TM. New Mexico Tumor Registry, Cancer Center. University of New Men’co. School of Medi- cine, Albuquerque. NM 87131. Am J Public Health 1988;78: 1182-6. We examined mortality from lung cancer and from chronic obstruc- tive pulmonary disease in Hispanic White., Other White., and Native American residents of New Mexico during the period 1958-82. Age- specific mortality was calculated by combining death certificate data with population estimates based on the 1960.1970, and 1980 censuses that were adjusted for inconsistencies in the designation of race and ethnicity. In Other Whites, age-adjusted mortality rates from lung cancer and from chronic obstructive pulmonary increased disease progressively in males and females. Mortality rates for both diseases also increased in Hispanics during the study period, but the most recent rates for Hispanics were well below those for Other Whites. Age- specific mortality rates for lung cancer declined for more recently born Hispanic women at older ages. In Native Americans, rates for both diseases were low throughout the study period and did not show consistent temporal trends. Examination of the role of cigarette smoke in lung carcinogenesis using multistage models. Gaffncy M, Altshuler B. Department of CIinicaland Scientific Affairs, Pfizer Inc., New York, NY 10017. J Nat1 Cancer Inst 1988;80:925-3 1. The widely used multistage model of Armitage and Doll is fit to the British physician lung cancer data of Doll and Hill under the assumption that cigarette smoke induces the initial and penultimate changes. It is shown that the best fit of this model in continuing smokers gives predictions not in accordance with incidence in ex-smokers and dose- response. A better global lit can be obtained by increasing the number of stages, but this de-emphasizes initiation and is inconsistent with the rise of incidence in nonsmokers. Thus, one should lood to other models. A two-stage model with clonal growth in which smoking initiates normal target cells and promotes the clonal growth of just the smoke- initiated cells is proposed. This model is shown to agree with the Doll andHi dataandthusit hasempiricalplausibilitythatshouldencourage biological studies of clonal growth in carcinogenesis. Long-lasting effects of tobacco smoking on pulmonary drug-me- tabolizing enzymes: A case-control study on lung cancer patients. Petruz/elli S, Canms A.-M, Carrozzi L. CNR Institute of Clinical Physiology, Second Medical Clinic, University of Pisa, Pisa. Cancer Res 1988;48:4695-4700. Lung tissue specimens wcrc taken during surgery from middle-aged men with either lung cancer (LC, n = 54) or a nonneoplastic lung disease (n = 20). Aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin O- deethylase (ECDE), epoxide hydrolase (EH), glutathione S-transferase (GST), and UDP-glucuronosyltransferase (UDPGT) activities and glu- tathionc and malondialdehyde contents were determined in 12,000 x g supcmatant fractions from nontumorous parenchymal tissues. Interin- dividual differences in enzyme activities ranged from 1 I- to 440-fold, and glutathione content varied by 17.fold; the values showed unimedal distributions. AHH, ECDE, EH, and UDPGT activities were signifi- cantly and positively correlated to each other; a significant negative correlation was found between GST and the other enzymes. A relation- ship bctwccn enzyme activity and number of cigarettes smoked (pack- years) was found only for GST. Ignoring detailed smoking histories in the 6-month period prcccding surgery, no difference was found in enzymcactivitiesorglutathionecontentbetweenLCandnonneopiastic lung disease patients or between smokers and nonsmokers. However, when the number of days since stopping smoking was considered, in smokers a significant increase was found for AHH. EH, and UDPGT activities and a significant decrease was found for GST activity, as compared to nonsmokers. LC patients who had smoked until the day

Lung cancer risks of underground miners: Cohort and case-control studies

Embed Size (px)

Citation preview

s3

presence of air pollution accounted for less than 5% of the total variation in intraurban lung cancer mortality. In addition, the interpretation of geographic analysis must be guarded due to the introduction of potential biasdue toaggregation. The hypotbesisthatairpolhttion iscontributory to lung cancer cannot be tested until other, stronger individual risk factors for lung cancer can be better measured and controlled in studies of this association.

Geographic pattern of lung cancer in Japan and its environmental correlations. Minowa M, Stone BJ, Blot WJ. Department of Epidemiology, Institute of Public Health, Minato-kv. Tokyo 108. Jpn J Cancer Res, Gann 1988;79:1017-23.

Standardized lung cancer mortality ratios, 1969-1978, for basic administrative units of Japan were related to various environmental characteristics by multiple regression analysis. Elevated lung cancer mortality was demonstrated in the areas along the seacoast, particuhuly those with fishing ports, low socioeconomic status, and high level of air pollution. High mortality was also observed in coal mining areas and areas with shipyards. Data on tobacco expenditures provided partial adjustment for the effects of cigarette smoking on these correlations.

A comparative epidemiologic study on geographic distributions of cancers of the lung and the large intestine in Japan. Murata M, Takayama K, Fukuma S et al. Division of Epidemiology, Chiba Cance.r Center, Chiba 280. Jpn J Cancer Res, Gann 1988;79: 1005-16.

To examine what kinds of factors could have caused the geographic variation observed in lung cancer morbidity in Japan, a correlation study was performed comparing various regional traits. The same study was also conducted on huge intestinal cancer, aiming to distinguish the possible urban factors associated with both cancers. Lung cancer was highly correlated with industrialization-related factors such as localiza- tion of manufacturing industries, automobile traffic and air pollution, whereas colon cancer was correlated with the population density of workers in the tertiary industries such as services, tradeandgovemment. A multiple regression analysis could not detect any single factor with an exceptionally strong influence on either cancer. The present findings suggest that the hazardous environmental condition of urban areas has, to some extent, contributed to the recent increase of lung cancer cases in this country.

Lung cancer risks of underground miners: Cohort and case-control studies. Archer VE. Rocky Mountain Center for Occupational and Environ- mentalHealth.DepartmentofFamilyandPreventiveMedicine.Univer- sity of Utah, School of Medicine, Salt Luke City, UT. Yale J Biol Med 1988;61:183-93.

All underground mines have higher radon levels than are found in surface air. Ventilation is the primary method of controlling radon levels. Fourteen cohort and seven case-control studies done on under- ground miners are reviewed; they include many types of ore. Only five of the studies deal with more than 100 lung cancer deaths. Variations in the attributable risk are given. Some generalizations can be drawn from thesestudies: thelongerthcfollow-up, thegrcaterisdteattributablerisk, even though the relative risk is reasonably constant. The induction- latent period is quite variable but is shortened by high exposure rates, by cigarette smoking, and by increasing age at start of mining. The predominant histological type of lung cancer among miners changed from small-cell undifferentiated for short follow-up time to epidermoid afterlong follow-uptimcs. Withashort follow-uptime,amultiplicative interaction bctwecn smoking and radiation was indicated but, with long follow-up time, the two factors appear to be simply additive. This difference is probably due to theshortened latentperiod among cigarette smokers, not to synergism.

Mortality from lung cancer and chronic obstructive pulmonary disease in New Mexico, 1958-82. Samet JM, Wiggins CL, Key CR, Becker TM. New Mexico Tumor Registry, Cancer Center. University of New Men’co. School of Medi- cine, Albuquerque. NM 87131. Am J Public Health 1988;78: 1182-6.

We examined mortality from lung cancer and from chronic obstruc- tive pulmonary disease in Hispanic White., Other White., and Native American residents of New Mexico during the period 1958-82. Age- specific mortality was calculated by combining death certificate data with population estimates based on the 1960.1970, and 1980 censuses that were adjusted for inconsistencies in the designation of race and ethnicity. In Other Whites, age-adjusted mortality rates from lung cancer and from chronic obstructive pulmonary increased disease progressively in males and females. Mortality rates for both diseases also increased in Hispanics during the study period, but the most recent rates for Hispanics were well below those for Other Whites. Age- specific mortality rates for lung cancer declined for more recently born Hispanic women at older ages. In Native Americans, rates for both diseases were low throughout the study period and did not show consistent temporal trends.

Examination of the role of cigarette smoke in lung carcinogenesis using multistage models. Gaffncy M, Altshuler B. Department of CIinicaland Scientific Affairs, Pfizer Inc., New York, NY 10017. J Nat1 Cancer Inst 1988;80:925-3 1.

The widely used multistage model of Armitage and Doll is fit to the British physician lung cancer data of Doll and Hill under the assumption that cigarette smoke induces the initial and penultimate changes. It is shown that the best fit of this model in continuing smokers gives predictions not in accordance with incidence in ex-smokers and dose- response. A better global lit can be obtained by increasing the number of stages, but this de-emphasizes initiation and is inconsistent with the rise of incidence in nonsmokers. Thus, one should lood to other models. A two-stage model with clonal growth in which smoking initiates normal target cells and promotes the clonal growth of just the smoke- initiated cells is proposed. This model is shown to agree with the Doll andHi dataandthusit hasempiricalplausibilitythatshouldencourage biological studies of clonal growth in carcinogenesis.

Long-lasting effects of tobacco smoking on pulmonary drug-me- tabolizing enzymes: A case-control study on lung cancer patients. Petruz/elli S, Canms A.-M, Carrozzi L. CNR Institute of Clinical Physiology, Second Medical Clinic, University of Pisa, Pisa. Cancer Res 1988;48:4695-4700.

Lung tissue specimens wcrc taken during surgery from middle-aged men with either lung cancer (LC, n = 54) or a nonneoplastic lung disease (n = 20). Aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin O- deethylase (ECDE), epoxide hydrolase (EH), glutathione S-transferase (GST), and UDP-glucuronosyltransferase (UDPGT) activities and glu- tathionc and malondialdehyde contents were determined in 12,000 x g supcmatant fractions from nontumorous parenchymal tissues. Interin- dividual differences in enzyme activities ranged from 1 I- to 440-fold, and glutathione content varied by 17.fold; the values showed unimedal distributions. AHH, ECDE, EH, and UDPGT activities were signifi- cantly and positively correlated to each other; a significant negative correlation was found between GST and the other enzymes. A relation- ship bctwccn enzyme activity and number of cigarettes smoked (pack- years) was found only for GST. Ignoring detailed smoking histories in the 6-month period prcccding surgery, no difference was found in enzymcactivitiesorglutathionecontentbetweenLCandnonneopiastic lung disease patients or between smokers and nonsmokers. However, when the number of days since stopping smoking was considered, in smokers a significant increase was found for AHH. EH, and UDPGT activities and a significant decrease was found for GST activity, as compared to nonsmokers. LC patients who had smoked until the day