Trichloroethylene exposure in vapour degreasing and the urinary excretion of N-acetyl-β-d-glucosaminidase

Abstract

In order to elucidate the potential nephrotoxicity of low level occupational exposure to trichloroethylene (TRI), urine analysis of the tubular enzyme N-acetyl-beta-D-glucosaminidase (U-NAG) was included in a cross-sectional study of metal degreasers in central Sweden. Eighty-six percent of 8-h TRI in air measurements were well below 50 mg/m3. Normal levels of NAG were found in morning urine samples from 29 workers compared to a historical reference group. A weak positive correlation (r = 0.48; P < 0.01) was observed between U-NAG activity and the concentration of the TRI metabolite trichloroacetic acid in urine but not with other estimates of recent or long-term exposure. In conclusion, TRI does not seem to be nephrotoxic at low exposure levels.

Potential Health Effects of Occupational Chlorinated Solvent Exposure

“…Studies of liver and kidney proteins in urine or somatic mutations have been done in RCC case–case, RCC case–control, and cross‐sectional exposed‐referent populations. Statistically significant findings of “urinary protein patterns indicative of kidney damage” or of somatic mutations could not be related causally to TCE exposure in cases or to clinical effects among TCE‐exposed workers 24,26–29,31,40 . A weak relationship was seen between levels of urinary N ‐acetyl‐β‐gluoosaminidase and concurrent hours per week exposed to TCE 101 .…”

“…Exposure to chlorinated solvents has been associated with kidney and liver damage in case reports for 80 years and has been studied more systematically for about 20 years 22,23 . Case–control and cross‐sectional exposed‐referent studies have examined somatic cell mutations and kidney proteins in the urine of individuals exposed and unexposed to chlorinated solvents; however, differences between solvent‐exposed and ‐unexposed individuals in levels of various proteins in the urine have not been related to clinical signs of kidney damage 24–40 …”

“…22,23 Case-control and cross-sectional exposed-referent studies have examined somatic cell mutations and kidney proteins in the urine of individuals exposed and unexposed to chlorinated solvents; however, differences between solvent-exposed and -unexposed individuals in levels of various proteins in the urine have not been related to clinical signs of kidney damage. [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40] Although inhalation is the main route of occupational exposure to chlorinated solvents, there is very little literature on short-or long-term effects on the respiratory system. Elevated SMRs for respiratory disease mortality not associated with duration of employment have been seen in cohort studies, [41][42][43] but lung cancer has not been associated with solvent exposure.…”

“…Statistically significant findings of "urinary protein patterns indicative of kidney damage" or of somatic mutations could not be related causally to TCE exposure in cases or to clinical effects among TCE-exposed workers. 24,[26][27][28][29]31,40 A weak relationship was seen between levels of urinary N-acetyl-␤-gluoosaminidase and concurrent hours per week exposed to TCE. 101 Bolt et al 24 recently studied excretion of ␣ 1 -microglobulin among RCC cases and controls, with some cases and some controls having been exposed to TCE.…”

Health evaluation of trichloroethylene in indoor air

“…Nach Exposition gegenüber 33-55 mg Trichlorethen/m 3 zeigten sich bei den Beschäftig-ten keine nephrotoxischen Effekte [29].…”