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Background An earlier investigation found increased bladder cancer incidence among workers at a rubber chemical manufacturing plant that used o-toluidine, aniline and nitrobenzene. The cohort was expanded to include additional workers (n=1875) and updated through 2007 to assess bladder cancer with improved exposure characterisation. Methods Work histories were updated and exposure categories and ranks were developed for o-toluidine, aniline and nitrobenzene combined. Incident cancers were identified by linkage to six state cancer registries. Residency in time-dependent cancer registry catchment areas was determined. SIR and standardised rate ratios for bladder cancer were calculated by exposure category and cumulative rank quartiles for different lag periods. Cox regression was used to model bladder cancer incidence with estimated cumulative rank, adjusting for confounders. Indirect methods were used to control for smoking. Results Excess bladder cancer was observed compared to the New York State population (SIR=2.87, 95% CI 2.02 to 3.96), with higher elevations among workers definitely exposed (moderate/high) (SIR=3.90, 95% CI 2.57 to 5.68), and in the highest cumulative rank quartile (SIR=6.13, 95% CI 2.80 to 11.6, 10-year lag). Bladder cancer rates increased significantly with estimated cumulative rank (10-year lag). Smoking only accounted for an estimated 8% elevation in bladder cancer incidence. Conclusions Bladder cancer incidence remains elevated in this cohort and significantly associated with estimated cumulative exposure. Results are consistent with earlier findings in this and other cohorts. Despite other concurrent chemical exposures, we consider o-toluidine most likely responsible for the bladder cancer incidence elevation and recommend a re-examination of occupational exposure limits.

Objectives Occupational exposure to chlorinated aliphatic solvents has been associated with an increased cancer risk, including brain cancer. However, many of these solvents remain in active, large-volume use. We evaluated glioma risk from non-farm occupational exposure (ever/never and estimated cumulative exposure) to any of the six chlorinated solvents—carbon tetrachloride, chloroform, methylene chloride, trichloroethylene, tetrachloroethylene or 1,1,1-trichloroethane—among 798 cases and 1175 population-based controls, aged 18–80 years and non-metropolitan residents of Iowa, Michigan, Minnesota and Wisconsin. Methods Solvent use was estimated based on occupation, industry and era, using a bibliographic database of published exposure levels and exposure determinants. Unconditional logistic regression was used to calculate ORs adjusted for frequency matching variables age group and sex, and age and education. Additional analyses were limited to 904 participants who donated blood specimens (excluding controls reporting a previous diagnosis of cancer) genotyped for glutathione- S -transferases GSTP1, GSTM3 and GSTT1 . Individuals with functional GST genes might convert chlorinated solvents crossing the blood–brain barrier into cytotoxic metabolites. Results Both estimated cumulative exposure (ppm-years) and ever exposure to chlorinated solvents were associated with decreased glioma risk and were statistically significant overall and for women. In analyses comparing participants with a high probability of exposure with the unexposed, no associations were statistically significant. Solvent-exposed participants with functional GST genes were not at increased risk of glioma. Conclusions We observed no associations of glioma risk and chlorinated solvent exposure. Large pooled studies are needed to explore the interaction of genetic pathways and environmental and occupational exposures in glioma aetiology.

Introduction In 1991, the US National Institute for Occupational Safety and Health (NIOSH) reported an increased bladder cancer risk in a cohort of 1749 workers potentially exposed to o-toluidine and aniline at a chemical manufacturing plant. As additional information showed that workers in certain departments had been misclassified regarding o-toluidine exposure, we therefore conducted a reanalysis of the data using updated exposure categories. Methods We updated exposure categories based on information ascertained during a plant walkthrough, documents on file at the plant, interviews with current and former employees, and answers provided by company and union officials to specific questions. Bladder cancer incidence was determined through 31 December 1988 and mortality through 31 December 1994. Results Thirteen cases of bladder cancer were observed versus 3.57 expected (New York State rates excluding New York City) (standardised incidence ratio (SIR) 3.64, 95% CI 1.94 to 6.23). Among workers classified as definitely exposed, increasing risks were observed for longer duration of employment (for ≥10 years, standardised rate ratio (SRR) 6.07, 95% CI 0.77 to 48.17) and time since first employment in the exposed departments (for ≥20 years, SRR 3.39, 95% CI 0.40 to 29.03). One bladder cancer death was observed among those definitely exposed. Conclusions These findings are comparable to the results reported earlier by NIOSH, and confirm that workers in this plant have an increased risk of bladder cancer.

Objectives To extend follow-up of cause-specific mortality in workers at seven beryllium processing plants and to estimate associations between mortality risk and beryllium exposure. Methods 9199 workers were followed for mortality from 1940 through 2005. Standardised mortality ratios (SMRs) were estimated based on US population comparisons for lung, nervous system and urinary tract cancers, chronic obstructive pulmonary disease (COPD), chronic kidney disease, and categories containing chronic beryllium disease (CBD) and cor pulmonale. Associations with maximum and cumulative exposure were calculated for a subset of the workers. Results Overall mortality in the cohort compared with the US population was elevated for lung cancer (SMR 1.17; 95% CI 1.08 to 1.28), COPD (SMR 1.23; 95% CI 1.13 to 1.32), and the categories containing CBD (SMR 7.80; 95% CI 6.26 to 9.60) and cor pulmonale (SMR 1.17; 95% CI 1.08 to 1.26). Mortality rates for most diseases of interest increased with time-since-hire. For the category including CBD, rates were substantially elevated compared to the US population across all exposure groups. Workers whose maximum beryllium exposure was $10 mg/m 3 had higher rates of lung cancer, urinary tract cancer, COPD and the category containing cor pulmonale than workers with lower exposure. Significant positive trends with cumulative exposure were observed for nervous system cancers (p¼0.0006) and, when short-term workers were excluded, lung cancer (p¼0.01), urinary tract cancer (p¼0.003) and COPD (p

Objectives Previous studies at a New York State chemical manufacturing plant reported elevated risks of cardiovascular disease among workers. We updated the mortality experience of 1874 workers employed between 1949 and 2006 through December 31, 2007. We investigated exposures to carbon disulfide and shift work and their association with coronary artery disease. Method Jobs with carbon disulfide and shift work exposure (≥1 day) were identified among departments and job titles in specific years. Standardised mortality ratios (SMR) compared mortality to the US population, adjusted for gender, race, age, and calendar year. Internal comparisons used directly standardised rate ratios (SRR). Results Overall, excess deaths were observed for coroanary artery disease (SMR=1.24, 95% CI 1.04–1.48). Most workers exposed to carbon disulfide perfortmed shift work; we evaluated coronary artery disease mortality in groups defined by duration of exposure to these agents. Compared to the US population, statistically significant increases in mortality were observed among workers with both exposures for 90 days or more (SMR=1.36, 95% CI 1.03–1.76), and among workers with fewer than 90 days of both exposures (SMR=1.31, 95% CI 0.65–2.34). Using cutpoints of 4 years (median exposure duration among long-term cases), the results were no longer statistically significant. In internal comparisons, long-term workers exposed to carbon disulfide and shift work for 4 years or more had a near 3-fold increase in coronary artery disease mortality, compared to workers exposed less than 4 years. Conclusions Excess coronary artery disease mortality confirms earlier results, but further investigation is needed to understand risk factors.