RESUMO
BACKGROUND: A cohort of 3,607 workers employed in three DuPont titanium dioxide production facilities was followed from 1935 through 2006. METHODS: Combined and plant-specific cohort mortality was compared with the overall US population and other DuPont employees. The relationships between selected causes of death and annual cumulative exposures to titanium dioxide and chloride were investigated using Poisson regression methods to examine trends with increasing exposure. RESULTS: Among the 833 deaths, no causes of deaths were statistically significantly elevated either overall or plant-specific when compared to the US population. Compared to DuPont workers, statistically significantly elevated SMRs for all causes, all cancers, and lung cancers were found driven by the workers at the oldest plant. Comparing increasing exposure groups to the lowest group, disease risk did not increase with exposure. CONCLUSIONS: There was no indication of a positive association between occupational exposure and death from all causes, all cancers, lung cancers, non-malignant respiratory disease, or all heart disease.
Assuntos
Poluentes Ocupacionais do Ar/efeitos adversos , Indústria Química , Doenças Profissionais/mortalidade , Exposição Ocupacional/efeitos adversos , Titânio/efeitos adversos , Adulto , Idoso , Causas de Morte , Delaware , Feminino , Seguimentos , Cardiopatias/induzido quimicamente , Cardiopatias/mortalidade , Humanos , Masculino , Pessoa de Meia-Idade , Mississippi , Modelos Estatísticos , Neoplasias/induzido quimicamente , Neoplasias/mortalidade , Doenças Profissionais/induzido quimicamente , Exposição Ocupacional/análise , Distribuição de Poisson , Análise de Regressão , Doenças Respiratórias/induzido quimicamente , Doenças Respiratórias/mortalidade , Tennessee , Fatores de TempoRESUMO
OBJECTIVES: Beryllium sensitisation (BeS) and chronic beryllium disease (CBD) are caused by exposure to beryllium with susceptibility affected by at least one well-studied genetic host factor, a glutamic acid residue at position 69 (E69) of the HLA-DPß chain (DPßE69). However, the nature of the relationship between exposure and carriage of the DPßE69 genotype has not been well studied. The goal of this study was to determine the relationship between DPßE69 and exposure in BeS and CBD. METHODS: Current and former workers (n=181) from a US nuclear weapons production facility, the Y-12 National Security Complex (Oak Ridge, Tennessee, USA), were enrolled in a case-control study including 35 individuals with BeS and 19 with CBD. HLA-DPB1 genotypes were determined by PCR-SSP. Beryllium exposures were assessed through worker interviews and industrial hygiene assessment of work tasks. RESULTS: After removing the confounding effect of potential beryllium exposure at another facility, multivariate models showed a sixfold (OR 6.06, 95% CI 1.96 to 18.7) increased odds for BeS and CBD combined among DPßE69 carriers and a fourfold (OR 3.98, 95% CI 1.43 to 11.0) increased odds for those exposed over an assigned lifetime-weighted average exposure of 0.1 µg/m(3). Those with both risk factors had higher increased odds (OR 24.1, 95% CI 4.77 to 122). CONCLUSION: DPßE69 carriage and high exposure to beryllium appear to contribute individually to the development of BeS and CBD. Among workers at a beryllium-using facility, the magnitude of risk associated with either elevated beryllium exposure or carriage of DPßE69 alone appears to be similar.
Assuntos
Beriliose/genética , Berílio/toxicidade , Cadeias beta de HLA-DP/genética , Exposição Ocupacional/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Casos e Controles , Feminino , Cadeias beta de HLA-DP/imunologia , Humanos , Indústrias , Masculino , Pessoa de Meia-Idade , Armas Nucleares , Fatores de RiscoRESUMO
A chemical exposure assessment was conducted for a cohort mortality study of 6157 chemical laboratory workers employed between 1943 and 1998 at four Department of Energy sites in Oak Ridge, Tennessee, and Aiken, South Carolina. Previous studies of chemical laboratory workers have included members within professional societies where exposure assessment was either limited or not feasible, or chemical processing employees where laboratory and production workers were combined. Because sufficient industrial hygiene records were unavailable for all four sites, weighted duration of employment was used as a surrogate for the magnitude of exposure. Potential exposure indices were calculated for each worker using number of days employed and weighting factors for frequency of contact and year of employment. A total of 591 unique laboratory job titles indicative of a chemical laboratory worker were collapsed into 18 general job title categories. Through discussions with current and retired workers, along with examination of historical organizational charts and job descriptions, the percentage of time with activities involving the direct handling of chemicals in the laboratory was estimated for each job title category. Scaled weighting factors of 1, 0.6, 0.3, and 0.05 were assigned to the job title categories representing 100%, 60%, 30%, and 5% of daily activities handling chemicals, respectively. Based on limited industrial hygiene monitoring data, personal radiation monitoring records, and professional judgment, weighting factors that declined 4% annually were applied to each year to account for improvements in laboratory technique, advancements in instrumentation, improvement in engineering controls, and increased safety awareness through time. The study cohort was separated into three categories of chemical exposures based on department level information: (1) inorganic, (2) mixed inorganic and organic, and (3) unknown. Potential exposure indices ranged from 0.15 to 6824.5 with a median value of 377.5 and a mean equal to 884.2. This exposure assessment method is useful for epidemiologic analyses when quantitative exposure data are absent or insufficient.