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Year : 2002  |  Volume : 4  |  Issue : 16  |  Page : 71--77

Effects of occupational exposure to mercury or chlorinated hydrocarbons on the auditory pathway

1 Keren Ha-Yesod 15 st.,Givat-Shmuel 51905, Israel
2 The Ear Nose and Throat Department, Tel Aviv Medical Center, Sackler School of Medicine, Tel-Aviv University, Israel
3 Kupat-Holim Hakelalit, Occupational Department, Holon, Israel
4 The Israel National Insurance, Jerusalem, Israel
5 The Biostatistics Department, Beilinson Medical center, Petah-Tikva, Israel

Correspondence Address:
Moshe Shlomo
Keren Ha-Yesod 15 st.,Givat-Shmuel 51905
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Source of Support: None, Conflict of Interest: None

PMID: 12537844

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The purpose of this study was to examine the effects of industrial exposure to mercury and chlorinated hydrocarbons (CH) on the auditory pathway. To this effect, auditory brainstem responses (ABR) were recorded from 40 workers exposed to mercury, 37 workers exposed to CH and from a control group of 36 subjects that were never exposed to neurotoxic substances. The interpeak latency (IPL) of waves I-III, III-V and I-V were measured. The mean duration of exposure to mercury and CH was 15.5 (+6.4) and 15.8 (+7.2) years respectively. The air sample monitoring of mercury was 0.008 mg/m3 (0.32 of the Threshold Limit Value - TLV® as published by ACGIH 2000). The mean average air sample monitoring was found to be 98 ppm for TCE, 12.7 ppm for PCE and 14.4 ppm for TCA which is respectively between 0.28 - 0.51 of the TLV® of CH. The mean blood mercury (B-Hg) levels were found to be 0.5mgr% (+0.3mgr%), which is 0.13 of the upper range of the permitted biologic exposure index (BEI) published by the ACGIH 2000. The mean urine samples levels of trichloroacetic acid were between 0.11-0.2 of the permitted BEI for the CH workers. The percent of workers exposed to mercury and CH workers with abnormal prolongation of IPL I-III was higher than the control group (42.5% and 33.8% vs. 18.0% respectively p<0.02). These results are consistent with other studies and show that ABR may provide a sensitive tool for detecting subclinical central neurotoxicity caused by CH and mercury


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