The etiology of breast cancer is not fully understood. Environmental and occupational exposures may contribute to breast cancer risk.
We linked 324 job titles from the 1970 census of 892,591 Finnish women with incidence of breast cancer (23,638 cases) during 1971-1995. We converted job titles to 31 chemical and two ergonomic agents through a measurement-based, period-specific, national job-exposure matrix. Poisson regression models were fit to the data, with adjustment for birth cohort, follow-up period, socioeconomic status, mean number of children, mean age at first delivery, and turnover rate.
For premenopausal breast cancer, medium/high level of occupational exposure to ionizing radiation was associated with a standardized incidence ratio (SIR) of 1.3 (95% confidence interval (CI) 0.7-2.5; trend P = 0.03). For postmenopausal breast cancer, we found on SIR of 1.2 (1.1-1.3) for low level and 1.4 (1.1-1.8) for medium/high level of ionizing radiation (trend P = 0.001); and an SIR 1.3 (1.1-1.7) for medium/high levels of both asbestos and man-made vitreous fibers. Aromatic hydrocarbon solvents showed a significant trend for a modest excess of postmenopausal breast cancer.
Our study indicates that occupational exposure to ionizing radiation may be associated with an increased risk of female breast cancer. High-quality studies on environmental and occupational etiology of breast cancer are needed for further elucidation of risk factors.
OBJECTIVES: This study analyzed cancer incidence among man-made vitreous fiber workers. METHODS: A cancer incidence follow-up was conducted among 3685 rock-slag wool (RSW) and 2611 glass wool (GW) production workers employed for > or =1 year in Denmark, Finland, Norway, or Sweden, and the standardized incidence ratios (SIR) were calculated on the basis of national incidence rates. RESULTS: Overall cancer incidence was close to expectation. Lung cancer incidence was increased among the RSW [SIR 1.08, 95% confidence interval (95% CI) 0.85-1.36] and GW (SIR 1.28, 95% CI 0.91-1.74) workers. For both subcohorts, a trend was suggested for time since first employment (P-value for linear trend 0.1 and 0.2, respectively). Neither subcohort showed an association with employment during the early technological phase, when fiber exposure was high. The incidence of oral, pharyngeal, and laryngeal cancer was increased among the RSW (SIR 1.46, 95% CI 0.99-2.07) and the GW (SIR 1.41, 95% CI 0.80-2.28) subcohorts. Despite a trend in risk for these neoplasms among the GW workers with time since first employment, the lack of a positive relation with other indirect indicators of fiber exposure points against a causal interpretation. No association between RSW or GW exposure and the risk of other neoplasms was suggested. CONCLUSIONS: These lung cancer results are similar to those of a mortality study that included a larger number of factories. For other cancers there was no suggestion of an association with RSW or GW exposure.
We have updated the follow-up of cancer mortality for a cohort study of man-made vitreous fiber production workers from Denmark, Finland, Norway, Sweden, United Kingdom, Germany, and Italy, from 1982 to 1990. In the mortality analysis, 22,002 production workers contributed 489,551 person-years, during which there were 4,521 deaths. Workers with less than 1 year of employment had an increased mortality [standardized mortality ratio (SMR) = 1.45; 95% confidence interval (CI) = 1.37-1.53]. Workers with 1 year or more of employment, contributing 65% of person-years, had an SMR of 1.05 (95% CI = 1.02-1.09). The SMR for lung cancer was 1.34 (95% CI = 1.08-1.63, 97 deaths) among rock/slag wool workers and 1.27 (95% CI = 1.07-1.50, 140 deaths) among glass wool workers. In the latter group, no increase was present when local mortality rates were used. Among rock/slag wool workers, the risk of lung cancer increased with time-since-first-employment and duration of employment. The trend in lung cancer mortality according to technologic phase at first employment was less marked than in the previous follow-up. We obtained similar results from a Poisson regression analysis limited to rock/slag wool workers. Five deaths from pleural mesothelioma were reported, which may not represent an excess. There was no apparent excess for other categories of neoplasm. Tobacco smoking and other factors linked to social class, as well as exposures in other industries, appear unlikely to explain the whole increase in lung cancer mortality among rock/slag wool workers. Limited data on other agents do not indicate an important role of asbestos, slag, or bitumen. These results are not sufficient to conclude that the increased lung cancer risk is the result of exposure to rock/slag wool; however, insofar as respirable fibers were an important component of the ambient pollution of the working environment, they may have contributed to the increased risk.
To assess the risk of cancer among workers of a Moscow (Russia) shoe factory exposed to chloroprene (2-chloro-1,3-butadiene) (CP).
This is a retrospective cohort mortality study among 5,185 shoe manufacturing workers employed between 1940 and 1976, and followed from 1979 through 1993. Exposure to CP was assessed by linking the job history with industrial hygiene data. We calculated standardized mortality ratios (SMR) using the Moscow population as reference, and conducted an internal comparison analysis based on Poisson regression modeling.
For the entire cohort, all-cause mortality was close to expectation and all-cancer mortality was increased. There was an increase in the mortality from liver cancer (SMR = 2.4, 95 percent confidence interval [CI] = 1.1-4.3), kidney cancer (SMR = 1.8, CI = 0.9-3.4), and leukemia (SMR = 1.9, CI = 1.0-3.3). Mortality from liver cancer and leukemia was associated with various indicators of CP exposure. A similar, although less consistent, pattern was found for kidney cancer mortality; while for the remaining neoplasms, no association was suggested with CP exposure.
The association between CP exposure and risk of leukemia may be due to concomitant exposure to benzene. The results for liver cancer point towards a carcinogenic effect of CP.
OBJECTIVES: To study the carcinogenicity of inorganic mercury in humans. METHODS: We studied the mortality from cancer among 6784 male and 265 female workers of four mercury mines and mills in Spain, Slovenia, Italy and the Ukraine. Workers were employed between the beginning of the century and 1990; the follow-up period lasted from the 1950s to the 1990s. We compared the mortality of the workers with national reference rates. RESULTS: Among men, there was no overall excess cancer mortality; an increase was observed in mortality from lung cancer (standardized mortality ratio [SMR] 1.19, 95 percent confidence interval [CI] 1.03-1.38) and liver cancer (SMR 1.64, CI 1.18-2.22). The increase in lung cancer risk was restricted to workers from Slovenia and the Ukraine: no relationship was found with duration of employment or estimated mercu ry exposure. The increase in liver cancer risk was present both among miners and millers and was stronger in workers from Italy and Slovenia: there was a trend with estimated cumulative exposure but not with duration of employment, and the excess was not present in a parallel analysis of cancer incidence among workers from Slovenia. No increase was observed for other types of cancer, including brain and kidney tumours. Among female workers (Ukraine only), three deaths occurred from ovarian cancer, likely representing an excess. CONCLUSIONS: Exposure to inorganic mercury in mines and mills does not seem strongly associated with cancer risk, with the possible exception of liver cancer; the increase in lung cancer may be explained by co-exposure to crystalline silica and radon.
Studies of clinical series of psoriasis patients have suggested an increased risk of nonmelanoma skin cancer and melanoma; the risk of other neoplasms has rarely been studied. In order to assess the incidence of cancer in a nationwide series of psoriasis patients from Sweden, we followed up, for the years 1965-89, 9773 patients with a hospital discharge diagnosis of psoriasis made during 1965-83, who were alive and free from malignancy 1 y after first discharge. We compared their incidence of neoplasms with that of the national population by computing standardized incidence ratios (SIR). We observed a total of 789 neoplasms [SIR 1.37, 95% confidence interval (CI) 1.28, 1.47]. There was an increase in the risk of cancers of the oral cavity and pharynx (SIR 2.80, 95% CI 1.96, 3.87), liver (SIR 1.91, 95% CI 1.28, 2.74), pancreas (SIR 1.56, 95% CI 1.02, 2.23), lung (SIR 2.13, 95% CI 1.71, 2.61), skin (squamous cell carcinoma, SIR 2.46, 95% CI 1.82, 3.27), female breast (SIR 1.27, 95% CI 1.00, 1.58), vulva (SIR 3.24, 95% CI 1.18, 7.06), penis (SIR 4.66, 95% CI 1.50, 10.9), bladder (SIR 1.43, 95% CI 1.03, 1.92), and kidney (SIR 1.56, 95% CI 1.04, 2.25). The risk of malignant melanoma was decreased (SIR 0.32, 95% CI 0.10, 0.74). Despite some limitations (possible diagnostic misclassification, lack of data on treatment, relatively short follow-up), our study provides evidence against an increased risk of melanoma among patients hospitalized for psoriasis. In addition to nonmelanoma skin and genital cancers, patients hospitalized for psoriasis were at increased risk of several malignancies, in particular those associated with alcohol drinking and tobacco smoking.
The carcinogenicity of cigar and pipe smoking is established but the effect of detailed smoking characteristics is less well defined. We examined the effects on cancer incidence of exclusive cigar and pipe smoking, and in combination with cigarettes, among 102395 men from Denmark, Germany, Spain, Sweden and UK in the EPIC cohort. Hazard ratios (HR) and their 95% confidence intervals (CI) for cancer during a median 9 year follow-up from ages 35-70 years were estimated using proportional hazards models. Compared to never smokers, HR of cancers of lung, upper aero-digestive tract and bladder combined was 2.2 (95% CI: 1.3, 3.8) for exclusive cigar smokers (16 cases), 3.0 (2.1, 4.5) for exclusive pipe smokers (33 cases) and 5.3 (4.4, 6.4) for exclusive cigarette smokers (1069 cases). For each smoking type, effects were stronger in current than in ex-smokers, and in inhalers than in non-inhalers. Ever smokers of both cigarettes and cigars (HR 5.7 (4.4, 7.3), 120 cases) and cigarettes and pipes (5.1 (4.1, 6.4), 247 cases) had as high a raised risk as had exclusive cigarette smokers. In these smokers, the magnitude of the raised risk was smaller if they had switched to cigars or pipes only (i.e. quit cigarettes) and had not compensated with greater smoking intensity. Cigar and pipe smoking is not a safe alternative to cigarette smoking. The lower cancer risk of cigar and pipe smokers as compared to cigarette smokers is explained by lesser degree of inhalation and lower smoking intensity. (c) 2010 UICC.
OBJECTIVE: Estimating the risk of bladder cancer from cigar and pipe smoking is complicated by a small number of non-cigarette smokers included in most relevant studies. METHODS: We undertook a pooled analysis of the data on men from six published case-control studies from Denmark, France, Germany, and Spain, to assess the association between pipe and cigar smoking and bladder cancer, and to compare it with the risk from cigarette smoking. Complete history of tobacco smoking was ascertained separately for cigarettes, cigars, and pipe. Odds ratios (ORs) were estimated after adjusting for age, study, and employment in high-risk occupations. RESULTS: The pooled data set comprised 2279 cases and 5268 controls, of whom 88 cases and 253 controls smoked only cigars or pipe. The OR for pure cigarette smoking was 3.5 (95% confidence interval [CI] 2.9-4.2), that for pure pipe smoking was 1.9 (95% CI 1.2-3.1) and that for pure cigar smoking was 2.3 (95% CI 1.6-3.5). The increase in the OR of bladder cancer that was observed with duration of smoking was non-significantly lower for cigars than for cigarettes. CONCLUSION: Our results suggest that smoking of cigars and pipe is carcinogenic to the urinary bladder, although the potency might be lower than for cigarettes.
BACKGROUND: Coffee consumption has been associated with an excess bladder cancer risk, but results from epidemiological studies are inconsistent. This association has been long debated, in part due to the potential confounding by smoking. We examined the risk associated with coffee consumption in nonsmokers in a pooled analysis of ten European bladder cancer case-control studies. METHODS: The pooled data set comprises 564 cases and 2929 hospital or population controls who had never smoked. They were enrolled in ten studies conducted in Denmark, Germany, Greece, France, Italy and Spain. Information on coffee consumption and occupation was re-coded following standard criteria. Unconditional logistic regression was applied adjusting for age, study center, occupation and gender. RESULTS: Seventy-nine percent of the study population reported having drunk coffee, and 2.4% were heavy drinkers, reporting having drunk on average ten or more cups per day. There was no excess risk in ever coffee drinkers (OR = 1.0, 95% CI 0.8-1.3) compared to never drinkers. The risk did not increase monotonically with dose but a statistically significant excess risk was seen for subjects having drunk ten or more cups per day (OR = 1.8, 95% CI 1.0-3.3). This excess was seen in both men and women. There was no evidence of an association of the risk with duration or type of coffee consumption. The pooled results were not dependent on the findings of any specific study, but they depended on the type of controls with an overall excess risk observed only for studies using hospital controls. CONCLUSION: Nonsmokers who are heavy coffee drinkers may have a small excess risk of bladder cancer. Although these results cannot be attributed to confounding by smoking, the possibility of bias in control selection cannot be discarded. On the basis of these results, only a very small proportion of cancers of the bladder among nonsmokers could be attributed to coffee drinking.
Two retrospective cohort studies were conducted to assess the risk of cancer among workers exposed to chloroprene (2-chloro-1,3-butadiene) (CP). One is a study of incidence and mortality among 2314 production workers employed in the CP production plant in Yerevan, Armenia, between 1940 and 1988. The cohort was followed up for cancer incidence for the years 1979-1990 and for cancer mortality for 1979-1988. The second study is a mortality study among 5185 shoe manufacturing workers in Moscow who used polychloroprene latex and glue. Shoe workers were employed between 1940 and 1976, and followed from 1979 through 1993. The standardized incidence ratios (SIR) and standardized mortality ratios (SMR) were calculated using the Armenian and Moscow population as reference. An internal comparison analysis based on Poisson regression modeling was conducted. In the Yerenan cohort, incidence and mortality from all cancers were below expectation, but increased incidence (SIR, 3.27; 95% confidence interval (CI), 1.47-7.27), and mortality (SMR, 3.39; CI, 1.09-10.5) from liver cancer were noted. A dose-response relationship was suggested between the risk of liver cancer and indices of CP exposure. For the entire Moscow cohort, all-cause mortality was close to expectation and all-cancer mortality was increased. There was an increase in the mortality from liver cancer (SMR, 2.4; CI, 1.1-4.3), kidney cancer (SMR, 1.8; CI, 0.9-3.4), and leukemia (SMR, 1.9; CI, 1.0-3.3). Mortality from liver cancer and leukemia was associated with various indicators of CP exposure. A similar, although less consistent, pattern was found for kidney cancer. The association between CP exposure and risk of leukemia may be due to concomitant exposure to benzene. The results for liver cancer point towards a carcinogenic effect of CP.