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Toxicological information

Health surveillance data

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Administrative data

Endpoint:
health surveillance data
Type of information:
experimental study
Adequacy of study:
key study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Non-GLP, non-guideline human study, acceptable for assessment, used as starting point for derivation of the limit value by the SCOEL.

Data source

Reference
Reference Type:
publication
Title:
Biological monitoring of kidney function among workers occupationally exposed to trichloroethylene.
Author:
Green T, Dow J, Ong CN, Ng V, Ong HY, Zhuang ZX, Yang XF, Bloemen L.
Year:
2004
Bibliographic source:
Occup Environ Med. 2004 Apr;61(4):312-7.

Materials and methods

Study type:
biological effect monitoring
Endpoint addressed:
repeated dose toxicity: inhalation
Test guideline
Qualifier:
no guideline available
Principles of method if other than guideline:
Renal dysfunction was monitored in a cross-sectional study of 70 workers currently exposed to trichloroethylene.
GLP compliance:
no

Test material

Constituent 1
Chemical structure
Reference substance name:
Trichloroethylene
EC Number:
201-167-4
EC Name:
Trichloroethylene
Cas Number:
79-01-6
Molecular formula:
C2HCl3
IUPAC Name:
1,1,2-trichloroethene
Constituent 2
Reference substance name:
Trichloroethene
IUPAC Name:
Trichloroethene
Details on test material:
not applicable, epidemiological study

Method

Type of population:
occupational
Ethical approval:
not specified
Details on study design:
Renal dysfunction was monitored in a cross-sectional study of 70 workers currently exposed to trichloroethylene. An age and sex matched control population of 54 individuals was drawn from hospital and administrative staff.

Results and discussion

Results:
The mean exposure to trichloroethylene, estimated from urinary trichloroacetic acid concentrations, was 32 ppm (range 0.5–252 ppm) with an average duration of exposure of 4.1 years (range 1–20 years). Significant differences between the exposed and control populations were found for nephrotoxicity markers N-acetylglucosaminidase (NAG) and albumin, and for the mode of action marker, formic acid.
However, neither NAG nor albumin showed a significant correlation with either the magnitude or duration of exposure to trichloroethylene. There was a significant correlation between urinary formic acid and trichloroacetic acid concentrations. Within the exposed population there were dose dependent increases in urinary methylmalonic acid concentrations and urinary glutathione S-transferase a activity. Although still within the control range, these changes were clearly dose dependent and consistent with one of the proposed mechanisms of trichloroethylene induced kidney toxicity.
Although there was no evidence of kidney toxicity within the population studied, the results suggest that kidney damage could occur at exposure concentrations higher (.250 ppm) than those encountered in this study.

Applicant's summary and conclusion