Urinary homovanillic acid (HVA) and vanillymandelic acid (VMA) in workers exposed to manganese dust |
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Authors: | Ling Bao Ai Lay Ha Chua Ai Li New Bee Lan Lee Yi Mim Liu Sin Eng Chia Choon Nam Ong |
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Institution: | (1) School of Public Health, Sun Yat-Sen University of Medical Sciences, Guangzhou, China;(2) Present address: Department of Community, Occupational, and Family Medicine, National University of Singapore, Lower Kent Ridge Road, 119074 Singapore |
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Abstract: | The neurotoxicity of manganese (Mn) is well known, however, the neurochemical effect caused by this metal is less well investigated.
In this study, urinary homovanillic acid (HVA) and vanillymandelic acid (VMA), two end products of catecholamine metabolism,
were measured in 39 workers chronically exposed to Mn in a manganese smelting plant. The average duration of Mn exposure was
17.4 yr. Nineteen nonexposed workers were also studied. Concentrations of Mn in serum (MnS) and in urine (MnU) were measured
by Zeeman graphite furnace atomic absorption spectrophotometry (ZAAS), and HVA and VMA determined by high performance liquid
chromatography (HPLC). For Mn-exposed workers, the concentration of MnS was nearly 2.8 times (1.61 ± 0.16 mg/L vs 0.56 ± 0.16
mg/L) and MnU about 4.5 times higher (7.62 ± 0.17 mg/L vs 1.69 ± 0.16 mg/L) than the nonexposed. Although the geometric mean
concentration of HVA in exposed workers was similar to that of the nonexposed (3.09 ± 1.39 mg/g ere. vs 2.99 ± 1.40 mg/g cre.),
the VMA concentration was significantly higher (3.02 ± 1.43 mg/g cre. vs 2.49 ± 1.58 mg/g cre.,p = 0.033). Multiple regression analysis showed that although there were no correlations between any of these parameters with
the duration of exposure to Mn, both HVA and VMA showed significant correlations with increase in MnS and MnU. These data
provide evidence that exposure to Mn was associated with measurable increase in catecholamine metabolites. This finding is
compatible with recent observations in laboratory animals that Mn interferes with neurochemical metabolism. |
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Keywords: | Occupational exposure dopaminergic metabolism catecholamine neurotoxicity neurochemicals |
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