In order to investigate the renal function, a cross-sectional study was carried out on four groups of workers significantly exposed to a mixture of alicyclic and aliphatic C5-C7 hydrocarbons, to styrene, to a mixture mostly composed of toluene and xylenes and to chlorinated hydrocarbons, respectively. The study involved 438 workers. Exposure was characterized by means of urinary metabolites, or by means of environmental measures, when biological indicators were not available. The renal function impairment indicators included total proteinuria, albuminuria and urinary excretion of muramidase (E.C. 3.2.1.17) and beta-glucuronidase (E.C. 3.2.1.31). The trend of these parameters provides some evidence of renal damage due to occupational exposure to organic solvents and suggests that the lesions are mild and tubular rather than glomerular.

The lung uptake and excretion of cyclohexane were studied in five workers and three volunteers in a shoe factory. Air samples were collected from the breathing zones with personal samplers, and simultaneous samples of inhaled and alveolar air were collected with the aid of a Rhan-Otis valve. Cyclohexane was absorbed on activated NIOSH approved charcoal tubes. The uptake was calculated from the pulmonary ventilation, the retention coefficient and environmental concentration. Alveolar excretion was monitored during a 6 h post-exposure period. The amount of exhaled cyclohexane was calculated from the decay curve. According to experimental data, the alveolar retention of cyclohexane is about 34% of the inhaled dose. This corresponds to a lung uptake of 23%. The post-exposure alveolar excretion does not exceed 10% of the total uptake. The difference between respiratory uptake and excretion indicates that the amount metabolized may be very large. Nevertheless, the urinary excretion of the main metabolites, cyclohexanol and cyclohexanone, was only about 1% of the absorbed dose.

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.

ABSTRACr Lung uptake and excretion of n-hexane were studied in ten workers in a shoe factory. Simultaneous samples of inhaled and alveolar air were collected with the aid of a Rhan-Otis valve, personal samplers, and charcoal tubes. Alveolar excretion was monitored during a six hour postexposure period. Uptake was calculated from lung ventilation, the retention coefficient, and environmental concentrations. The amount of exhaled n-hexane was calculated from the decay curve. According to the experimental data, alveolar retention was about 25% of the inhaled n-hexane, corresponding to a lung uptake of about 17%. The postexposure alveolar excretion was about 10% of the total uptake. The main metabolites of n-hexane were identified and measured by capillary GC/MS in spot urine samples collected before, at the end, and 15 hours after the same working shift. Urinary concentrations were low, though related to n-hexane in the air. 2,5-Hexanedione in the end of shift samples gave the best estimate of overall exposure. About 3 mg/g creatinine of 2,5-hexanedione would correspond to about 50 ppm of n-hexane in the air (mean daily exposure).The use of n-hexane is widespread in industry. It is an excellent and inexpensive solvent used especially in glues, varnishes, and paints. Many mixtures are commercially available, and the most common among them contain different proportions of n-hexane and its isomers 2-methyl and 3-methyl pentane, cyclohexane, and methyl ethyl ketone. Occupational exposures have been reported to cause peripheral neuropathies in workers'-3; electrophysiological changes have also been found in subjects exposed to relatively low airborne concentrations. 48 The pharmacokinetics of n-hexane has been widely investigated in rats but much less is known for man. Among the published studies there is little agreement about the retention of inhaled n-hexane and about the proportion which is excreted through the lung during the postexposure period. the metabolism of n-hexane in man, with the aim of evaluating more specifically: (a) the respiratory uptake and elimination in workers occupationally exposed under constant model ventilation conditions; (b) the possible relation between n-hexane uptake and urinary excretion of its metabolites; and (c) the usefulness of either alveolar concentration or urinary excretion of n-hexane metabolites for biological monitoring purposes. MethodThe study was performed on 10 young healthy , and the flow rate 1 ml helium per minute. Particular interest was focused on the following metabolites: 2 and 3-hexanol, 2,5-hexanediol, methyl n-butyl ketone, 2,5 hexanedione, y-valerolactone, and 2,5-dimethylfuran. Authentic samples of each substance were obtained from Fluka AG (Buchs, Switzerland). The urinary metabolites were identified on the basis of gas chromatographic retention time, and their mass spectra were compared with those of authentic samples, using a Finnigan MAT 1020 mass spectrometer (Finnigan MAT, Cincinnati, OH, USA). EQUATIONSIntake, uptake, and alveolar excretion were calc...

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