Kidney disorders and hematotoxicity of organic solvent exposure

Scandinavian Journal of Work, Environment & Health (Impact Factor: 3.45). 02/1985; 11 Suppl 1:83-90.
Source: PubMed


Short-term exposure to certain solvents, such as several halogenated hydrocarbons, petroleum distillates, ethylene glycol, ethylene glycol ethers, and diethylene glycol, may cause renal tubular necrosis. Tubular lesions with metabolic acidosis have been reported in addicts inhaling solvent vapor (eg, toluene). A Goodpasture's syndrome may be induced by acute or subacute exposure to solvents, but its incidence is rare. No adequate proof is yet available that repeated exposure to nonsubstituted organic solvents may lead to the development of different types of chronic glomerulonephritis, but the available epidemiologic data are suggestive of the existence of such an association. Only a few solvents have been reported to act on the hematopoietic system of humans. The hematotoxicity (aplastic anemia, leukemia) of benzene is well established. Some ethylene glycol ethers are also toxic to bone marrow.

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    • "ing a tubular necrosis , a life threatening situation characterized by oliguria and azotemia ( Sato et al . , 1988 ) . A study carried out by Taverner et al . ( 1988 ) showed that acute exposure to organic solvents caused reversible acute interstitial nephritis . A Goodpasture ' s syndrome may be induced by acute or subacute exposure to solvents ( Lauwerys et al . , 1985 ) . Renal tubular acidosis has been associated with toluene or toluene - containing paint sniffing ( Taher et al . , 1974 ) . Toluene sniffing has been implicated in the formation of renal stones ( Kroege et al . , 1980 ) , protei - nuria ( Streicher et al . , 1981 ) , and hepato - renal damage ( O ' Brien et al . , 1971 ) . Some studie"
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    No preview · Article · Jan 1987 · American Journal of Industrial Medicine
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    ABSTRACT: We examined sensitive biochemical and immunological markers of kidney function and damage in 53 male oil refinery workers exposed to hydrocarbons and compared their results with those of a control group of 61 age-matched nonexposed males. The mean duration of employment of exposed males was 11 years. The current levels of exposure to a variety of aliphatic and aromatic hydrocarbons, as determined by personal monitoring, were well below the current threshold limit values. No difference was found in the urinary tubular parameters beta-N-acetyl-D-glucosaminidase, beta 2-microglobulin (beta 2-m) and retinol-binding protein. Similar serum beta 2-m levels indicated no impairment of the glomerular filtration rate in the exposed workers. The levels of circulating immune complexes were also identical in both groups. The mean albuminuria was slightly higher (p less than .005) in the exposed group in a quantitative assay but was not dipstick-detectable. The mean urinary excretion of a renal antigen was also higher (p less than .05) in the exposed group and correlated with the excretion of albumin. Finally, slightly higher titers of anti-laminin antibodies were found in five exposed employees, but this was not accompanied by an increased albuminuria. We conclude that chronic low-level hydrocarbon exposure in these refinery workers does not lead to clinically significant renal abnormalities. Nevertheless, some findings are consistent with the possible role of hydrocarbon exposure in the induction of renal disturbances.
    No preview · Article · Jan 1987 · American Journal of Industrial Medicine
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