Occupational and environmental medicine · 2011
Vitamin B12 and folate deficiency and elevated plasma total homocysteine in workers with chronic exposure to chromate.
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Wang Tian-Cheng, Jia Guang, Zhang Ji, Ma Yan-Hui, Liu Lan-Zheng, Zhang Ning, Feng Wei-Yue, Zhou Jing-Wen, Song Yan-Shuang, Yan Lei, Du Xian-Mei
Аннотация
OBJECTIVES: Chronic occupational exposure to chromium can result in a broad range of adverse effects including multiple organ damage, genotoxicity and carcinogenesis. However, the metabolic consequences of chromium exposure have not been fully investigated. This study was designed to examine vitamin B12, folate and homocysteine metabolic changes in workers chronically exposed to chromate. The potential association between metabolic alteration and renal impairment induced by chromate exposure was also assessed.
METHODS: The level of chromium exposure was evaluated by measuring chromium concentrations in red blood cells (RBC-Cr) and urine (U-Cr). Renal impairment was assessed with serum cystatin C (Cys-C) and urinary β2-microglobulin (β2M). Serum vitamin B(12), folate and plasma total homocysteine (tHcy) were measured and correlations analysed.
RESULTS: Significant increases in RBC-Cr, U-Cr, serum Cys-C, plasma tHcy and urinary β2M concentrations were observed in workers chronically exposed to chromate compared to controls. In the exposed workers, serum vitamin B12 and folate levels were decreased and significantly inversely correlated with RBC-Cr concentrations, and increased plasma tHcy concentrations were mirrored by decreased serum vitamin B12 and folate levels. Elevated plasma tHcy concentrations were positively related to serum Cys-C concentrations.
CONCLUSIONS: Hyperhomocysteinemia in chronically exposed workers was primarily induced by vitamin B12 and folate deficiency. This metabolic change might be associated with renal dysfunction in chromate processing workers after long term exposure.
METHODS: The level of chromium exposure was evaluated by measuring chromium concentrations in red blood cells (RBC-Cr) and urine (U-Cr). Renal impairment was assessed with serum cystatin C (Cys-C) and urinary β2-microglobulin (β2M). Serum vitamin B(12), folate and plasma total homocysteine (tHcy) were measured and correlations analysed.
RESULTS: Significant increases in RBC-Cr, U-Cr, serum Cys-C, plasma tHcy and urinary β2M concentrations were observed in workers chronically exposed to chromate compared to controls. In the exposed workers, serum vitamin B12 and folate levels were decreased and significantly inversely correlated with RBC-Cr concentrations, and increased plasma tHcy concentrations were mirrored by decreased serum vitamin B12 and folate levels. Elevated plasma tHcy concentrations were positively related to serum Cys-C concentrations.
CONCLUSIONS: Hyperhomocysteinemia in chronically exposed workers was primarily induced by vitamin B12 and folate deficiency. This metabolic change might be associated with renal dysfunction in chromate processing workers after long term exposure.