Occupational exposure to cobalt is not associated with incipient signs of dilated cardiomyopathy in a Belgian refinery.

BACKGROUND: Excessive absorption of cobalt has been associated with cases of dilated cardiomyopathy in the past, but it is unclear whether occupationally exposed populations are at risk. OBJECTIVE: To assess the possible relationship between occupational exposure to cobalt and incipient signs of dilated cardiomyopathy. METHODS: A cross-sectional survey was conducted in a cobalt production facility in Belgium constituting one of the largest occupational populations worldwide (n=256 male workers). Exposure to cobalt was assessed by measuring urinary cobalt concentration (µg/gcreat), reflecting recent exposure, and by computing an integrated exposure index (µg/gcreat×years), reflecting long-term exposure. The effect on the myocardium was investigated by echocardiography and electrocardiography, and dose-effect relations with cobalt exposure were traced by multiple regression analysis. RESULTS: No dose-effect relationship between exposure to cobalt and parameters reflecting dilated cardiomyopathy was found in a population of workers characterised by a median recent cobalturia of 4 µg/gcreat and a median long-term cobalturia of 100 µg/gcreat×years. A reduction in the dimensions of the left ventricular internal cavity was associated with recent exposure to cobalt. CONCLUSIONS: Occupational exposure to cobalt does not appear associated with incipient signs of dilated cardiomyopathy within the gradient of exposure recorded in this population.

Occupational exposure to indium: what does biomonitoring tell us?

BACKGROUND: The industrial uses of indium, a rare metal with no known physiological role in humans, have increased dramatically over the past 15 years. The results of animal toxicity studies showing pulmonary and systemic effects as well as some reports in workers have created a growing concern about the possible occurrence of toxic effects in exposed workers. Validated biomarkers to assess exposure to indium are not available. OBJECTIVES: This work aimed at investigating the kinetics of indium in urine (In-U) and plasma (In-Pl) in workers manufacturing In ingots and mainly exposed to hardly water-soluble In compounds. All nine workers from the In department of a large metallurgical concern participated in the study as well as 5 retired workers and 20 controls. METHODS: Personal breathing zone air was collected throughout the work shift on Monday and Friday. Blood and urine samples were collected, before and after the shift, on the same day as the air sampling and on preshift the next Monday after a non-working week-end. Moreover, rats were given either InCl(3) by intraperitoneal injection or In(2)O(3) by pharyngeal aspiration, In was followed in plasma during 120 days and measured in tissues 120 days after exposure. RESULTS: Higher In-Pl and In-U concentrations were found in both current (range 0.32-12.61 µg/L plasma; 0.22-3.50 µg/g creat) and former (0.03-4.38 µg/L plasma; 0.02-0.69 µg/g creat) workers compared with controls (<0.03 µg/L plasma; <0.02 µg/g creat). Both biological parameters were highly correlated but no correlation was found between In-air (10-1030 µg/m(3)) and In-Pl or In-U. Normalizing In-U by the urinary creatinine concentration reduced the inter- (from 90% to 70%) and intra-individual variability (from 54% to 35%). In-Pl remained remarkably stable along the working week (inter- and intra-individual variability: 89% and 10%, respectively). Neither In-U nor In-Pl significantly increased during the day or the week. A week-end without occupational exposure was not sufficient to reach the background In-Pl and In-U levels measured in controls. The results of the experimental investigations confirmed the hypothesis that inhalation of hardly soluble In compounds may cause accumulation of In in the body leading to a prolonged "endogenous exposure" from both a lung depot of "insoluble" particles that are progressively absorbed and from a retention depot in other internal organs. CONCLUSION: This study shows that in workers exposed to hardly soluble In compounds, In-U and In-Pl are very sensitive to detect exposure and mainly reflect long-term exposure. In-Pl levels are particularly stable for a given individual. In-U might be more influenced than In-Pl by recent exposure. Both parameters remained high years after withdrawal from exposure, indicating a possible endogenous exposure and a prolonged risk of pulmonary and systemic diseases even after work exposure has ceased.

Lung function changes in workers exposed to cobalt compounds: a 13-year follow-up.

The objective of the study was to examine the influence of cobalt exposure on lung function changes in workers from a cobalt-producing plant in a health monitoring program implemented between 1988 and 2001. A total of 122 male workers with at least 4 (median = 6) lung function tests (FEV(1) and FVC) during the follow-up period were assessed longitudinally. Cobalt exposure significantly decreased over the follow-up period, as reflected by the measurements in air and urine. The possible association of spirometric changes with cobalt exposure was examined by a random coefficients model, taking into account other potential influential variables, such as smoking, age, previous respiratory illness, exposure to other lung toxicants, or the presence of glutamate in position 69 in the HLA-DP beta-chain, an HLA polymorphism possibly associated with hard-metal-induced lung diseases. The main finding of the follow-up study was that cobalt exposure contributed to a decline in FEV(1) over time, and only in association with smoking. No influence of glutamate in position 69 in the HLA-DP beta-chain polymorphism was detected. Although the amplitude of the additional FEV(1) decrement associated with smoking exposure was relatively small (< 20%) compared with the expected decline in a non-cobalt-exposed smoker, the results indicate that further efforts to reduce cobalt exposure and to encourage workers to quit smoking are still warranted.