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Delayed and competitively inhibited excretion of urinary hippuric acid in field workers coexposed to toluene, ethyl benzene, and xylene.

Research paper by I F IF Mao, F K FK Chang, M L ML Chen

Indexed on: 16 Jun '07Published on: 16 Jun '07Published in: Archives of Environmental Contamination and Toxicology



Abstract

The purpose of this study was to investigate whether the metabolic suppression of hippuric acid (HA) occurs in field workers coexposed to toluene, xylene and ethyl benzene. Eleven male spray painters were recruited into this study and monitored for 2 weeks using a repeated-measures study design. The sampling was conducted for 3 consecutive working days each week. Toluene, ethyl benzene, and xylene in the air were collected using 3M 3500 organic vapor monitors. Urine samples were collected before and after work shift, and urinary HA, methyl hippuric acid, mandelic acid, and phenylgloxylic acid concentrations were determined. In the first week, toluene concentrations were 2.66 +/- 0.95 (mean +/- SE) ppm, whereas ethyl benzene and xylene concentrations were 27.84 +/- 3.61 and 72.63 +/- 13.37 ppm, respectively, for all subjects. Pre-work shift HA concentrations were 230.23 +/- 37.31 mg/g creatinine, whereas pre-work shift HA concentrations were 137.81 +/- 14.15 mg/g creatinine. Mean urinary HA concentration was significantly greater in the pre-work shift samples than in the pre-work shift samples (p = 0.043). In the second week, toluene concentrations were much lower (0.28 ppm), whereas ethyl benzene and xylene were 47.12 +/- 8.98 and 23.88 +/- 4.09 ppm, respectively, for all subjects. Pre-work shift HA concentrations were 351.98 +/- 116.23 mg/g creatinine, whereas pre-work shift HA concentrations were 951.82 +/- 116.23 mg/g creatinine. Mean urinary HA concentration was significantly greater in the pre-work shift samples than in the pre-work shift samples (p <0.01); a significant correlation (r = 0.565; p = 0.002) was found between pre-work shift urinary HA levels and ethyl benzene exposure. This study showed that urinary HA peak was delayed to next morning for workers coexposed to toluene, ethyl benzene, and xylene; xylene and ethyl benzene probably played competitive inhibitors for metabolism of toluene. The study also presumed that urinary HA became the major metabolite of ethyl benzene at the end of work shift, when the exposure concentrations of ethyl benzene were 2.0 times those of xylene.