Mortality among mine and mill workers exposed to respirable crystalline silica.

BACKGROUND: Millions of workers are potentially exposed to respirable crystalline silica (RCS) which has been associated with several diseases. We updated the mortality experience of a cohort of 2,650 mine and mill workers at four manufacturing facilities to assess cause-specific mortality risks associated with estimated cumulative RCS exposure. METHODS: Study eligibility was defined as any employee who had ≥1 year of service by 2000, with work history experience available from 1945 through 2004. Vital status and cause of death were ascertained from 1945 through 2015. RCS exposure was estimated across plant-, department-, job-, and time-dependent categories using historic industrial hygiene sampling data and professional judgment. Associations between cumulative RCS (mg/m3-years) and cause-specific mortality were examined using Cox proportional hazard regression models. RESULTS: In the exposure-response analysis defined on quartiles of cumulative RCS exposure, no increasing trend (ptrend = 0.37) in lung cancer mortality (n = 116 deaths) was observed (Hazard ratio (HR) = 1.00 (referent), 1.20, 1.85, 0.92). Mortality risk for non-malignant respiratory disease was increased across quartiles (HR = 1.00, 1.35, 1.89, 1.70; ptrend = 0.15), based on 83 deaths. Non-malignant renal disease mortality was increased across quartiles (HR = 1.00, 6.64, 3.79, 3.29; ptrend = 0.11), based on 26 deaths. CONCLUSIONS: After nearly seven decades of follow-up, the exposure-response analyses showed no evidence of a positive trend for lung cancer, and limited evidence of a trend for non-malignant respiratory disease, and non-malignant renal disease mortality as a result of cumulative RCS exposure in this occupational cohort.

Longitudinal assessment of lipid and hepatic clinical parameters in workers involved with the demolition of perfluoroalkyl manufacturing facilities.

OBJECTIVE: To examine in a longitudinal occupational assessment whether changes in serum concentrations of perfluorooctanoic acid (PFOA) and perfluorooctanesulfonate (PFOS) are associated with changes in non-high-density lipoprotein (HDL) cholesterol. METHODS: Baseline and end-of-project PFOA, PFOS, lipid, and hepatic clinical chemistries were measured in 204 workers involved with the demolition of former perfluoroalkyl manufacturing facilities. Analyses were restricted to the 179 workers who did not take lipid-lowering medications. Two thirds had baseline PFOA and PFOS levels similar to the general population. RESULTS: The change in non-HDL cholesterol was not associated with the changes in PFOA or PFOS. An increase in HDL was associated with an increase in PFOA, although the magnitude was small. This increase in HDL resulted in a decrease in the total cholesterol/HDL ratio. CONCLUSION: Adverse associations were not observed between changes in PFOA, PFOS, non-HDL cholesterol, HDL, and hepatic clinical chemistries.

Cohort mortality study of roofing granule mine and mill workers. Part II. Epidemiologic analysis, 1945-2004.

The mortality of 2650 employees (93.4% males) in the mine and mill production of roofing granules at four plants was examined between 1945 and 2004. Hypotheses focused on diseases associated with exposure to silica: nonmalignant respiratory disease, lung cancer, and nonmalignant renal disease. Study eligibility required ≥ 1 year of employment by 2000. Work history and vital status were followed through 2004 with < 1% lost to follow-up. Industrial hygiene sampling data (1871 sampling measurements over a 32-year period) and professional judgment were used to construct 15 respirable crystalline silica exposure categories. A category was assigned to all plant-, department-, and time-dependent standard job titles. Cumulative respirable crystalline silica exposure (mg/m(3)-years) was calculated as the sum of the product of time spent and the average exposure for each plant-, department-, job-, and calendar-year combination. The cohort geometric mean was 0.17 mg/m(3)-years (geometric standard deviation 4.01) and differed by plant. Expected deaths were calculated using U.S. (entire cohort) and regional (each plant) mortality rates. Poisson regression was used for internal comparisons. For the entire cohort, 772 deaths (97.4% males) were identified (standardized mortality ratio 0.95, 95% CI 0.88-1.02). There were 50 deaths from nonmalignant respiratory diseases (1.14, 95% CI 0.85-1.51). Lagging exposure 15 years among the male cohort, the relative risks for nonmalignant respiratory disease were 1.00 (reference), 0.80, 1.94, and 2.03 (p value trend = 0.03) when cumulative exposure was categorized < 0.1, 0.1- < 0.5, 0.5- < 1.0, and ≥ 1.0 mg/m(3)-years, respectively. There was a total of 77 lung cancer deaths (1.11, 95% CI 0.88-1.39). Lagging exposure 15 years, the relative risks for males were 1.00 (reference), 1.83, 1.83, and 1.05 (p value trend = 0.9). There were 16 deaths from nonmalignant renal disease (1.76, 95% CI 1.01-2.86). This exposure-response trend was suggestive but imprecise. The study results are consistent with other cohorts with similar levels of exposure to respirable crystalline silica.