Partition coefficients of some industrial aliphatic hydrocarbons (C5-C7) in blood and human tissues.

Saline/air, blood/air, olive oil/air, and tissue/air (lung, kidney, liver, brain, muscle, heart, and fat) partition coefficients were determined for nine aliphatic hydrocarbons: n-pentane, 2,2-dimethylbutane, 3-methylpentane, 2-methylpentane, methylcyclopentane, n-hexane, cyclohexane, 3-methylhexane, and n-heptane. Blood/air partition coefficients were found to range between 0.38 (n-pentane) and 1.9 (n-heptane) and the value of the tissue/air partition coefficients rose from n-pentane to n-heptane. The tissue/air partition coefficients were significantly correlated with the blood/air partition coefficients (r = 0.92-0.98). According to the slope of the regression lines, the mean solubility of the nine aliphatic hydrocarbons in the different tissues was higher than in blood by the factors: lung 1.4 (range 1.2-2.1) heart 3.9 (range 0.5-4.5), liver 5.6 (range 5.5-13.5), kidney 5.2 (range 1.6-5.8), brain 6.5 (range 5.8-10.7), muscle 7.6 (range 1.8-8.8), and fat 205 (range 104-254). The blood/air and olive oil/air partition coefficients were significantly correlated with the boiling points and the molecular weights of the aliphatic hydrocarbons studied.

Methyl ethyl ketone exposure in industrial workers. Uptake and kinetics.

Exposure to methyl ethyl ketone (MEK) was studied in workers occupationally exposed in industrial workplaces. Alveolar concentrations of MEK were compared with environmental exposure and with blood MEK concentrations. Urinary excretion of MEK and its metabolite, acetylmethylcarbinol , were compared with environmental exposure. The solubility of MEK was also studied in human body tissues which allowed us to estimate the distribution and kinetics of MEK by means of data computing on a multicompartimental mathematic model. The alveolar MEK concentration was correlated with the environmental MEK concentration and corresponded to 30% of it. Blood MEK concentration was correlated with alveolar MEK concentration and corresponded to 104-116 times the alveolar concentration and 31-35 times the environmental concentration. Urinary MEK excretion was correlated with environmental MEK exposure and the urinary excretion of acetylmethylcarbinol . The mean urinary MEK concentration was 4.8 times the mean environmental MEK concentration. The MEK solubility in the human tissues (brain, kidney, lung, fat, heart, muscles and liver) turned out to be similar to that found in blood (blood/air = 183). The amount of MEK and its metabolite, acetylmethylcarbinol , eliminated by the kidney corresponded together to 0.1% of the alveolar MEK uptake.

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.