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Biomedical subjects

F Brugnone

Publications and source records attributed to F Brugnone.

At least 55 records · Page 3Linked to original sources
PubMed1983

Occupational styrene exposure: environmental and biological monitoring.

Occupational exposure to styrene was studied by environmental and biological monitoring in 22 workers employed in a fiberglass reinforced plastic factory. The mean environmental styrene concentration in individual workplaces ranged from 120 to 684 microliter/l. Blood styrene, which was tested at the end of the work shift, ranged from 450 to 3700 micrograms/l. Urinary mandelic and phenylglyoxylic acid, which were determined at the end of the work shift, ranged from 133 to 2100 and from 107 to 685 mg/l, respectively. Environmental styrene exposure was better correlated with styrenemia than with mandelicuria and phenylglyoxylicuria considered either individually or together. The ratio between environmental and blood styrene showed that styrenemia was, on average, 3.3-4.9 times higher than environmental styrene concentration.

Air↗
PubMed1983

Decline of blood and alveolar toluene concentration following two accidental human poisonings.

In two workers admitted to hospital because of a coma due to an accidental occupational exposure to a mixture of solvents, the level of toluene was respectively 823-1122 micrograms/l in the blood and 53-38 micrograms/l in the alveolar air on the second day of admission (36 h after the accidental exposure). On the fifth day, 112 h after exposure, the toluene level was 120-45 micrograms/l in the blood and 3-1 micrograms/l in the alveolar air. The urinary excretion of o-cresol, calculated as a toluene equivalent, was 0.8-0.9 mg on the second day and 1.7-1.6 mg on the third day. Urinary hippuric acid, as a toluene equivalent, was 1.7-1.4 g on the second day and 1.3-0.7 g on the third day. A half-life of between 19 and 21 h was calculated for toluene both in the blood and in the alveolar air.

Accidents, Occupational↗
PubMed1983

Isopropanol exposure: environmental and biological monitoring in a printing works.

Occupational exposure to isopropanol was studied in 12 workers by testing environmental air, alveolar air, venous blood, and urine during their work shift. Isopropanol, which ranged in environmental air between 7 and 645 mg/m3, was detected in alveolar air, where it ranged between 4 and 437 mg/m3, but not in blood or in urine. Alveolar isopropanol concentration (Ca) was significantly correlated with environmental isopropanol concentration (Ci) at any time of exposure. The value of the arithmetical Ca/ci ratio was 0.418 (SD 0.101). Acetone, which is a metabolite of isopropanol, was found in alveolar air, blood, and urine in concentrations that were higher during exposure than before. Alveolar and blood acetone concentrations were highly correlated with alveolar isopropanol concentrations at any time during exposure. Acetone ranged between 0.76 and 15.6 mg/l in blood, between 4 and 93 micrograms/l in alveolar air, and between 0.85 and 53.7 mg/l in urine. Alveolar (Ca) and blood (Cb) acetone concentrations were highly correlated (r = 0.67), with a Cb/Ca ratio of 101. Alveolar isopropanol uptake ranged between 0.03 and 6.8 mg/min and was highly correlated with environmental isopropanol concentration (r = 0.92). During exposure, acetone eliminated by the lungs ranged between 20 and 273 mg in seven hours and in urine between 0.3 and 9.6 mg in seven hours. Acetonuria was higher the next morning than at the end of exposure.

1-Propanol↗
PubMed1982

Urinary excretion of n-hexane metabolites. A comparative study in rat, rabbit and monkey.

Exposure to n-hexane, a component of many industrial solvent mixtures, is known to cause polyneuropathy in man. The concentration of metabolites in urine following exposure may be useful in biological monitoring. In a comparative study experimental animals (rat, rabbit and monkey) were subjected to single inhalatory treatments of 6, 12 and 24 h with 5,000 ppm of pure n-hexane. At the end of the treatments and at intervals thereafter, urine, and in rats also blood, were collected and analyzed for n-hexane and its metabolites. While the urine of rats contained 2-hexanol, 3-hexanol, methyl n-butyl ketone, 2,5-dimethylfuran, y-valerolactone and 2,5-hexanedione, rabbit and monkey urine were found to contain only 2-hexanedione, rabbit and monkey urine were to contain only 2-hexanol, 3-hexanol, methyl n-butyl ketone and 2,5-hexanedione. Within 72 h of the end of exposure, the principal metabolite was 2,5-dimethylfuran in rats and 2-hexanol in rabbits and monkeys. In all three species the excretion rates of methyl n-butyl ketone, 3-hexanol and 2-hexanol peaked several hours earlier than 2,5-hexanedione (and gamma-valerolactone and 2,5-dimethylfuran in rats). In all species 2,5-hexanedione was still detectable in urine 60 h following exposure. n-Hexane metabolites in rat blood were 2-hexanol, methyl-n-butyl ketone, 2,5-dimethylfuran and 2,4-hexanedione. The first two, as well as n-hexane itself, were found in maximum concentration immediately after termination of exposure, while 2,5-dimethylfuran and 2,5-hexanedione, with the longer exposure times, peaked some hours later. The data from urine collected at the end of exposure were compared with those obtained in a parallel study in humans occupationally exposed to a mixture of hexane isomers. Humans chronically exposed to 10-140 ppm n-hexane had 2,5-hexanedione concentrations in urine ranging from 0.4 to 21.7 mg/l, i.e., in the same proportion as rats exposed once for 6 or 12 h to 5,000 ppm.

Animals↗
PubMed1982

Biomonitoring of occupational toluene exposure.

Toluene exposure was studied in 20 workers employed in painting and hand-finishing in an art furniture factory. Toluene was determined in the environmental air of places of work and in the alveolar air and blood of the workers. Hippuric acid and cresols were also tested in the workers' urine. Blood and urine tests were carried out before the work shift on Monday and Friday morning and at the end of the work shift on Friday afternoon. The other tests were performed on Friday afternoon only. Alveolar toluene concentrations, which were significantly correlated with environmental toluene concentrations (r = 0.6230; P less than 0.01), corresponded to 19.4% of the toluene concentration in the atmosphere. Blood toluene was also found in painters on Monday morning and was significantly correlated with the other parameters. On Friday afternoon it was three times higher than the environmental toluene concentration. Urinary o-Cresol was highly correlated with toluene in the atmosphere, in blood and with hippuric acid in urine. On the basis of the slope of the regression line the ratio between urinary o-Cresol and blood toluene concentration was 0.99. At the end of the work shift urinary hippuric acid concentration was highly correlated with o-Cresoluria and with toluene in blood and in the atmosphere.

Air Pollutants↗
PubMed1981

Measurement of the urinary metabolites of N-hexane, cyclohexane and their isomers by gas chromatography.

A gas chromatographic method for analyzing the urinary metabolites of n-hexane (2-hexanol, 2,5-hexanedione, 2,5-dimethylfuran and gamma-valerolactone), of 2-methylpentane (2-methyl-2-pentanol), of 3-methylpentane (3-methyl-2-pentanol), and of cyclohexane (cyclohexanol) was developed. Processing of urine and the gas chromatographic conditions are described. The recovery rate of all hexane metabolites, except 2,5-dimethylfuran, ranged between 92 and 100%. The variation coefficient of metabolites determination was between 1.5 and 5%, apart from 2.5-dimethylfuran determination for which the variation coefficient was 15%. The detection limits ranged between 0.2 and 0.7 mg/l and between 0.05 and 0.1 mg/l when a packed or capillary column was used. Results obtained from a packed and capillary column are discussed.

Biotransformation↗
PubMed1981

Urinary excretion of the metabolites of n-hexane and its isomers during occupational exposure.

Environmental exposure to commercial hexane (n-hexane, 2-methylpentane, and 3-methylpentane) was tested in several work places in five shoe factories by taking three grap-air samples during the afternoon shift. Individual exposure ranges were 32-500 mg/m3 for n-hexane, 11-250 mg/m3 for 2-methylpentane, and 10-204 mg/m3 for 3-methylpentane. The metabolites of commercial hexane in the urine of 41 workers were measured at the end of the work shift. 2-Hexanol, 2,5-hexanedione, 2,5-dimethylfuran, and gamma-valerolactone were found as n-hexane metabolites and 2-methyl-2-pentanol and 3-methyl-2-pentanol as 2-methylpentane and 3-methylpentane metabolites. The presence of metabolites in the urine was correlated with occupational exposure to solvents. n-Hexane exposure was correlated more positively with 2-hexanol and 2,5-hexanedione than with 2,5-dimethylfuran and gamma-valerolactone. A good correlation was also found between total n-hexane metabolites and n-hexane exposure. 2-Methyl-2-pentanol and 3-methyl-2-pentanol were highly correlated with 2-methylpentane and 3-methylpentane exposure. The results suggest that the urinary excretion of hexane metabolites may be used for monitoring occupational exposure to n-hexane and its isomers.

Air↗
PubMed1981

Experimental neurotoxicity and urinary metabolites of the C5-C7 aliphatic hydrocarbons used as glue solvents in shoe manufacture.

Rats were intermittently exposed (9 to 10 h/d, 5 to 6 d/week) to controlled concentrations of single analytical grad solvents in ambient air. After periods ranging from 7 to 30 weeks the animals were perfused with glutaraldehyde and samples of nerves were processed for light microscopy of sections and of teased fibers. Animals treated with n-hexane at 5000 ppm (14 weeks) or 2500 ppm (30 weeks) developed the typical giant axonal degeneration already described in rats treated continuously with 400 to 600 ppm of the same solvent for 7 weeks or more. No such alterations were found in rats subjected to the following intermittent respiratory treatments: n-hexane 500 ppm (30 weeks) or 1500 ppm (14 weeks), cyclohexane 1500 or 2500 (30 weeks), n-pentane 3000 ppm (30 weeks), n-heptane 1500 ppm (30 weeks), 2-methylpentane 1500 ppm (14 weeks), and 3-methylpentane 1500 ppm (14 weeks). The following metabolites were found in the urine of rats according to treatment (in parenthesis): 2-methyl-2-pentanol (2-methylpentane); 3-methyl-2-pentanol and 3-methyl-3-pentanol (3-methylpentane), 2-hexanol, 3-hexanol, gamma-valerolactone, 2,5-dimethylfuran, and 2,5-hexanedione (n-hexane). 2-Hexanol was found to be the main urinary metabolite of n-hexane, while 2,5-hexanedione was present only in a lesser proportion. This feature of rat metabolism suggests that in this species 2,5-hexanedione reaches an effective level at its site of action during intermittent respiratory treatment with n-hexane with difficulty and explains the high concentrations necessary to cause polyneuropathy in rats subjected to this treatment.

Adhesives↗
PubMed1981

Neurotoxic metabolites of "commercial hexane" in the urine of shoe factory workers.

Urinary metabolites were tested in 41 shoe-factory workers exposed to a mixture of 10 solvents among which "commercial hexane" was the prevailing component. Cyclohexanol, 2-methyl-2-pentanol, 3-methyl-2-pentanol, and trichloroethanol were determined in connection with exposure to cyclohexane, 2-methylpentane, 3-methylpentane, and trichloroethylene, respectively. 2-Hexanol, 2,5-hexanedione, 2,5-dimethylfuran, and gamma-valerolactone were all determined in connection with n-hexane exposure only. 2,5-Hexanedione was the principal n-hexane metabolite found in the workers' urine. This finding of the experimentally proven neurotoxin 2,5-hexanedione in the urine of shoe-factory workers exposed to "commercial hexane" is consistent with the idea that this compound is responsible for the development of neuropathy in this group of individuals.

Air Pollutants↗