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Biomedical subjects

L Perbellini

Publications and source records attributed to L Perbellini.

At least 73 records · Page 4Linked to original sources

[Proposal for a new method of thermal desorption of solvents from passive personal samplers].

A new thermic desorption method for some organic solvents from the passive dosimeters (Mod. TK 200) is described. The single active carbon leaft after solvent absorption have been put at 200 C into a oven connected with the gas-chromatograph injector. After 10 minutes of "static thermic desorption", the carrier flow (nitrogen), which usually goes through the gas-chromatograph in injector and columns, is diverted into the desorption oven and into the gas-chromatograph injector by means of a manual valve. After 5 seconds the initial route of the carrier is restored and the fraction of the solvents dragged by the carrier is analyzed. Subsequently each active carbon leaf is desorbed several times to study the trend of desorption rate of the solvent from the passive dosimeters. The data obtained from n-hexane, 2-methylpentane, 3-methylpentane, methyl ethyl ketone, cycloexane and trichloroethilene seem to suggest that the "static termic desorption, is an useful method, although further investigations are needed.

Air Pollutants, Occupational↗

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↗

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↗

Purge and Trap analysis of toluene in blood: comparison with the Head Space method.

A procedure for the determination of toluene in blood by the Purge and Trap method is described. The method, which had not been previously employed for the determination of volatile organic substances in biological fluids, has a linear range which extends up to at least 1500 micrograms/L, and gives results in excellent agreement with the conventional Head Space method; the detection limit was not exactly determined, but is estimated to be less than 7.5 micrograms/L, much better than for the Head Space method. Using the Purge and Trap method, we have observed the accumulation of toluene in the blood of experimental subjects as a result of a weekly exposure to toluene.

Environmental Exposure↗

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↗

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↗

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↗

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↗

Biomonitoring of industrial solvent exposures in workers' alveolar air.

Ten different solvents, viz., toluene, styrene, methylethyl ketone, acetone, dimethylformamide, cyclohexane, n-hexane, methylcyclopentane, 2-methylpentane, and 3-methylpentane were determined in environmental air and in the alveolar air of workers during the work shift. As regards all ten solvents studied, alveolar concentration (Ca) and the difference between environmental concentration (Ci) and alveolar concentration (Ci-Ca), were correlated with environmental concentration. According to the slopes of the regression lines, the ratio between alveolar and environmental concentration (Ca/Ci) and the alveolar retention ((Ci-Ca)/Ci) in the case of all ten solvents studied were complementary, i.e., their sum was equal to unity. The solvents with high solubility in blood, i.e., toluene, styrene, methylethyl ketone, acetone, and dimethylformamide showed a Ca/Ci ratio lower than 0.5 and the solvents with low solubility, i.e., cyclohexane, hexane, and their isomers showed a Ca/Ci ratio higher than 0.5. According to the findings which prove that the alveolar concentration of all solvents studied during the work shift is a function of variations in the environmental concentrations it seems reasonable to suggest the use of alveolar tests for monitoring environmental exposure to solvents during the work shift.

Air Pollutants↗

N-N-dimethylformamide concentration in environmental and alveolar air in an artificial leather factory.

N-N-Dimethylformamide was determined every hour during the eight hours of the work shift in the alveolar air of eight workers employed in an artificial leather factory and in the breathing zone of the eight workers. The alveolar ventilation of each worker was measured for 10 minutes during the work shift. Alveolar dimethylformamide concentration (Ca) was correlated with the environmental concentration (Ci) in six of the eight workers. The amount of dimethylformamide retained per litre of ventilated air, calculated as the difference (Ci - Ca), was correlated with environmental concentration in seven of the eight workers. Lung uptake of dimethylformamide per minute was correlated with environmental concentration in all eight workers. The ratios between alveolar and environmental concentration (Ca/Ci x 100) and the lung retention of dimethylformamide, calculated by the formula (1 - Ca/Ci) x 100, were 27.8% and 72.2% respectively. They did not show any correlation with environmental concentration, exposure time, or alveolar ventilation.

Air Pollutants↗