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Cumulative arsenic exposure and lung cancer in smelter workers: A dose-response study
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increase in [Ca*+](i), whilecausing both cell types to undergo squamous differentiation. When treated with 8% calcium-free fetal bovine serum, a serum-sensitive subclone of BEAS-2B cells exhibited a higherelevaLion of [Ca”](i) than a serum-resislant (i.e.. not stimulated to differentiate by serum) subclone. However, a serum component involved in the induction of squamous differentiation, transforming growth factor type U, did not increase [Ca’+](i) in either normal cells or BEAS-2B cells. 12. 0-TeIradecanoylphorbol-13-acetale, an exogenous inducer of squamous differentiation and activator of protein kinase C, did nol increase [Ca2+](i), but did atlenaute serum-induced elevation of [Ca2+](i). These results suggest that while an increase in [Ca2’](i) is associated with serum-induced squamous differentiation, a cytosolic ionized calcium signal is not required for the initiation of the squamous differentiation pathway induced by either transforming growth factor type B or 12-0-tetradecanoylphorbol-13.acetate.
Death risk due to cancer of the respiratory apparatus in chromate production workers. De Marco R, Bemardinelli L, Mangione MP. Istin& di Scienre SanitarieApplicate, CattedradiBiome?riaeStatisticaMedica,271OOPavia. Med Lav 1988;79:368-76. The paper reports Ihe results of a retrospective cohort study aimed al assessing the risk of death due to respiratory cancer in the workers of a chromate prod&on plant. A total of 981 subjects had been employed for varying periods between 1948 and 1985. The study covered workers with more than one year of cumulative exposure, for whom the risk period starts 10 years after beginning of exposure (latency period). Among the eligible subjects 20 cases of respiratory tract cancer were observed: 14 locared in the lung, 3 in the pleura,and 3 in Ihe larynx. The observed deaths were compaxd with the expected deaths on the basis of the mortality rates for Italy. The SMR was statistically significant for tumours of the pleura (SMR = 30) and the lung (SMR = 2.12). Although no dose-response relationship was observed for pleural turnours, for lung (urnours analysis of SMR’s, according to both duration and intensity of exposure, revealed a considerable excess risk (SMR = 4.20) in the factory deparlmenls where exposure to hevavalent chromium was greatest and in the group of subjects who had worked in the factory for more than 10 years.
Smoking, occupational exposure to rubber, and lung cancer. Zhang Z-F, Yu S-Z, Li W-X, Choi BCK. Depanmenl ofEpidemiology, School ofPublic Health, Shanghai Medical University, Shanghai. Br I Ind Med 1989;46:12-5. A cohort of 1624 employees (957 men, 667 women) in a rubber factory in Shanghai have been followed up since 1972 and their 12 year mortality experience is presented. The relative risk of lung cancer for smokers was 8.5 for men and 11.4 for women and for rubber workers exposed to curing agents or talc powder 3.2 for men and 4.6 for women. Cumulative arsenic exposure and lung cancer in smelter workers: A dose-response study. Jarup L, Pershagen G, Wall S. Departmenr ofEnvironmental Hygiene, Karolinskalnstitute, Karolinska Hospital, S-104 01 Stockholm. Am. J Ind Mcd 1989;15:31-41. The cause-specific mortality was followed through 1981 in a cohort of 3,916 male Swedish smelter workers employed for at least 3 months from 1928 through 1967. Arsenic levels in the air of all workplaces wIthin the smelterwereestimated for threedifferent time periods. Using this exposure matrix and detailed information of the work history, cumulative arsenic exposure could be computed for each worker. Standardized mortality ratios (SMRs) were calculated for several dose categories using age-specific mortality rates from the county where the smelter was situated. A positive dose-response relationship was found betweencumultativearsenicexposureandlungcancermortalitywithan overall SMR of 372 (304450, 95% confidence interval). The lung cancer mortality was related to the estimated average intensity of exposure to arsenic but not to the duration. No positive dose-response relationship was found between arsenic and ischemic heart disease or cerebrovascular disease. There was also no evident dose-response rcladonship between estimated exposure to sulfur dioxide and lung cancer.
Multistage modelling of lung cancer mortality in asbestos textile workers. Pearce N. Department of Community Health, Wellington School of Medicine, Wellington Hospital. Wellington. Int J Epidemiol 1988:17:747-52. The Armitage-Doll multistage model of cancer is applied to data from a cohort study of lung cancer in 1261 while male workers from one asbestos textile manufacturing plant. Threeapproachesare used: induction time analysis; analysis of Ihe relationship of the excess incidence rate to age ar first exposure and time since first exposure; and direct fitting of the Armitage-Doll model. Poisson regression was used for all analyses. The induction time analysis was conducted using Rothman’s ‘wmdow of exposure’ method. This suggested that the increase in rate ratio was primarily due to exposure occurring 15-24 years previously, whereas there was litde effect from exposures occurring O-14 or 25+ years previously. The excess Incidence rate increased both with age at first exposure and time sinced first exposure. suggesting that asbestos acted at a stage intermediate between the first and penultimate stages. Direct fitting of the Armitage-Doll model suggested that the best fit was obtained by assummg that asbestos acts at stage 3.4 or 5 of a six-stage process. Most analyses of the type presented here are unable to determine at which stage a carcinogen acts, due to the small numbers of cancer death occurring in typical occupational cohorts. Furthermore, there is reason to doubt the validity of the Armitage-Doll model. However, such analyses can at least suggest whether a carcinogen appears to act at an early, intermediate or late stage, and the general statistical methods applied here will retain their usefulness as further models are developed and larger data sets become available.
Smoking-adjusted mcldence of lung cancer among Swedish men in different occupations. Carstensen JM, Pershagen G, Eklund G. Department of Cancer Epidemiology, Radiumhemmet. Karolinska University Hospital, S-104 01 Stockholm. Int J Epidemiol 198&17:753-S. The Swedish Cancer-Environment Register was used to study the relation between occupation and lung cancer risk during the period 1961-79 in 1.6 million men aged 30-64 years in 1960. By adding information concerning smoking habits from a sample of 1% of the Swedish population, smoking-adjusted standardized incidence ratios (SIR) wereestimated for different occupational categories according to the population census of 1960. Smoking-adjusted excess risks (p
Lung cancer risk from environmental exposure to radon daughters. ICRP publication 50. Jacobi W. GSF, Institut fur Strahlenschutz. D-8042 Munich-Neuherberg. Radial. POOL Dosim. 1988;24:19-22. A summary of the recently published ICRP Task Group report on the lung cancer risk from environmental exposure to radon daughters is given. The attributable risk has been estimated proceeding from the excess lung cancer rate observed among Rn exposed miners and among the atomic bomb survivors, taking into account appropriate correction factors. Different types of approaches are outlined, using absolute and relative risk projection models and assuming a linear exposure-risk relationship at low exposure levels. The main emphasis IS given to a proportional hazard model which has been adapted to account for these epidemiological data. The results of surveys yield, for most counuies a population-averaged mean value of IO-25 Bq m 3 for the equdibrium equivalent 2*2Rnconcentration m houses. Assuming a chronic lifetime exposure al this mean indoor level the risk analysis indicates that about 3-15% of the total observed lung cancer rate among populations might be associated with the environmental exposure to radon daughters. The proportional hazard model leads to the suggestion that this relative
increase in [Ca*+](i), whilecausing both cell types to undergo squamous differentiation. When treated with 8% calcium-free fetal bovine serum, a serum-sensitive subclone of BEAS-2B cells exhibited a higherelevaLion of [Ca”](i) than a serum-resislant (i.e.. not stimulated to differentiate by serum) subclone. However, a serum component involved in the induction of squamous differentiation, transforming growth factor type U, did not increase [Ca’+](i) in either normal cells or BEAS-2B cells. 12. 0-TeIradecanoylphorbol-13-acetale, an exogenous inducer of squamous differentiation and activator of protein kinase C, did nol increase [Ca2+](i), but did atlenaute serum-induced elevation of [Ca2+](i). These results suggest that while an increase in [Ca2’](i) is associated with serum-induced squamous differentiation, a cytosolic ionized calcium signal is not required for the initiation of the squamous differentiation pathway induced by either transforming growth factor type B or 12-0-tetradecanoylphorbol-13.acetate.
Death risk due to cancer of the respiratory apparatus in chromate production workers. De Marco R, Bemardinelli L, Mangione MP. Istin& di Scienre SanitarieApplicate, CattedradiBiome?riaeStatisticaMedica,271OOPavia. Med Lav 1988;79:368-76. The paper reports Ihe results of a retrospective cohort study aimed al assessing the risk of death due to respiratory cancer in the workers of a chromate prod&on plant. A total of 981 subjects had been employed for varying periods between 1948 and 1985. The study covered workers with more than one year of cumulative exposure, for whom the risk period starts 10 years after beginning of exposure (latency period). Among the eligible subjects 20 cases of respiratory tract cancer were observed: 14 locared in the lung, 3 in the pleura,and 3 in Ihe larynx. The observed deaths were compaxd with the expected deaths on the basis of the mortality rates for Italy. The SMR was statistically significant for tumours of the pleura (SMR = 30) and the lung (SMR = 2.12). Although no dose-response relationship was observed for pleural turnours, for lung (urnours analysis of SMR’s, according to both duration and intensity of exposure, revealed a considerable excess risk (SMR = 4.20) in the factory deparlmenls where exposure to hevavalent chromium was greatest and in the group of subjects who had worked in the factory for more than 10 years.
Smoking, occupational exposure to rubber, and lung cancer. Zhang Z-F, Yu S-Z, Li W-X, Choi BCK. Depanmenl ofEpidemiology, School ofPublic Health, Shanghai Medical University, Shanghai. Br I Ind Med 1989;46:12-5. A cohort of 1624 employees (957 men, 667 women) in a rubber factory in Shanghai have been followed up since 1972 and their 12 year mortality experience is presented. The relative risk of lung cancer for smokers was 8.5 for men and 11.4 for women and for rubber workers exposed to curing agents or talc powder 3.2 for men and 4.6 for women. Cumulative arsenic exposure and lung cancer in smelter workers: A dose-response study. Jarup L, Pershagen G, Wall S. Departmenr ofEnvironmental Hygiene, Karolinskalnstitute, Karolinska Hospital, S-104 01 Stockholm. Am. J Ind Mcd 1989;15:31-41. The cause-specific mortality was followed through 1981 in a cohort of 3,916 male Swedish smelter workers employed for at least 3 months from 1928 through 1967. Arsenic levels in the air of all workplaces wIthin the smelterwereestimated for threedifferent time periods. Using this exposure matrix and detailed information of the work history, cumulative arsenic exposure could be computed for each worker. Standardized mortality ratios (SMRs) were calculated for several dose categories using age-specific mortality rates from the county where the smelter was situated. A positive dose-response relationship was found betweencumultativearsenicexposureandlungcancermortalitywithan overall SMR of 372 (304450, 95% confidence interval). The lung cancer mortality was related to the estimated average intensity of exposure to arsenic but not to the duration. No positive dose-response relationship was found between arsenic and ischemic heart disease or cerebrovascular disease. There was also no evident dose-response rcladonship between estimated exposure to sulfur dioxide and lung cancer.
Multistage modelling of lung cancer mortality in asbestos textile workers. Pearce N. Department of Community Health, Wellington School of Medicine, Wellington Hospital. Wellington. Int J Epidemiol 1988:17:747-52. The Armitage-Doll multistage model of cancer is applied to data from a cohort study of lung cancer in 1261 while male workers from one asbestos textile manufacturing plant. Threeapproachesare used: induction time analysis; analysis of Ihe relationship of the excess incidence rate to age ar first exposure and time since first exposure; and direct fitting of the Armitage-Doll model. Poisson regression was used for all analyses. The induction time analysis was conducted using Rothman’s ‘wmdow of exposure’ method. This suggested that the increase in rate ratio was primarily due to exposure occurring 15-24 years previously, whereas there was litde effect from exposures occurring O-14 or 25+ years previously. The excess Incidence rate increased both with age at first exposure and time sinced first exposure. suggesting that asbestos acted at a stage intermediate between the first and penultimate stages. Direct fitting of the Armitage-Doll model suggested that the best fit was obtained by assummg that asbestos acts at stage 3.4 or 5 of a six-stage process. Most analyses of the type presented here are unable to determine at which stage a carcinogen acts, due to the small numbers of cancer death occurring in typical occupational cohorts. Furthermore, there is reason to doubt the validity of the Armitage-Doll model. However, such analyses can at least suggest whether a carcinogen appears to act at an early, intermediate or late stage, and the general statistical methods applied here will retain their usefulness as further models are developed and larger data sets become available.
Smoking-adjusted mcldence of lung cancer among Swedish men in different occupations. Carstensen JM, Pershagen G, Eklund G. Department of Cancer Epidemiology, Radiumhemmet. Karolinska University Hospital, S-104 01 Stockholm. Int J Epidemiol 198&17:753-S. The Swedish Cancer-Environment Register was used to study the relation between occupation and lung cancer risk during the period 1961-79 in 1.6 million men aged 30-64 years in 1960. By adding information concerning smoking habits from a sample of 1% of the Swedish population, smoking-adjusted standardized incidence ratios (SIR) wereestimated for different occupational categories according to the population census of 1960. Smoking-adjusted excess risks (p
Lung cancer risk from environmental exposure to radon daughters. ICRP publication 50. Jacobi W. GSF, Institut fur Strahlenschutz. D-8042 Munich-Neuherberg. Radial. POOL Dosim. 1988;24:19-22. A summary of the recently published ICRP Task Group report on the lung cancer risk from environmental exposure to radon daughters is given. The attributable risk has been estimated proceeding from the excess lung cancer rate observed among Rn exposed miners and among the atomic bomb survivors, taking into account appropriate correction factors. Different types of approaches are outlined, using absolute and relative risk projection models and assuming a linear exposure-risk relationship at low exposure levels. The main emphasis IS given to a proportional hazard model which has been adapted to account for these epidemiological data. The results of surveys yield, for most counuies a population-averaged mean value of IO-25 Bq m 3 for the equdibrium equivalent 2*2Rnconcentration m houses. Assuming a chronic lifetime exposure al this mean indoor level the risk analysis indicates that about 3-15% of the total observed lung cancer rate among populations might be associated with the environmental exposure to radon daughters. The proportional hazard model leads to the suggestion that this relative