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.

lnnocente Franchini, MD1 MUTT1 A, VESCOVI PP, FALZOI M, ARFINI G, VALENTI G. FRANCHINI I. Neuroendocrine effects of styrene on occupationally exposed workers. Scand J Work Environ Health 10 (1984) 225-228. The serum levels of prolactin (PRL), human growth hormone (HGH), thyroid-stimulating hormone (TSH), and the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured in 30 females exposed to about 130 (range 65-300) ppm of styrene in the air and in 30 agematched referents to show whether styrene exposure influences the dopaminergic tuberoinfundibular system (TIDA). The exposed subjects' serum levels of PRL were more than double the reference values and were significantly related to the urinary excretion of styrene metabolites, ie, to the sum of mandelic acid (MA) and phenylglyoxylic acid (PGA) in the "next-morning" urine spot sample. Such a relationship still proved to be statistically significant after the removal of the effects of age and duration of exposure with the method of partial correlation. The serum concentrations of HGH in the exposed workers were also higher than in the reference group. Though within the reference levels, the TSH values of the exposed subjects were significantly related to the urinary excretion of MA and PGA. These results are consistent with the dose-dependent depletion in tuberoinfundibular dopamine after experimental styrene exposure of rabbits.

No abstract

The regional distribution of dopamine, norepinephrine and homovanillic acid was assessed in adult male rabbits exposed to styrene vapours. The turnover of dopamine and norepinephrine was also measured in several brain regions by the decay in endogenous catecholamines after inhibition of tyrosine hydroxylase by alpha-methyl-p-tyrosine. Styrene exposure produced a marked and dose-dependent decrease in striatal and tuberoinfundibular dopamine, associated with a consistent increase in homovanillic acid content in the same regions. Norepinephrine levels were unaffected by styrene exposure. The observed increase in catabolism of dopamine cannot be explained by the turnover time, which was not significantly different in the exposed as compared to the control rabbits. Competition of a styrene metabolite with dopamine for the vesicular storage capacity or a selective destruction of dopaminergic terminals are suggested as the possible mechanisms for styrene neurotoxicity.

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...