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

Biological monitoring of fluctuating occupational exposures to styrene

Nine workers occupationally exposed to styrene producing refrigerator lorries were analyzed. The styrene exposure was monitored 8 hours a day, for 5 days a week, for 1 week. We collected from workers a urine sample before and after each work shift. Moreover, alveolar air samples were obtained at the end of all work shifts. On Thursday afternoon and on Friday morning blood samples were taken from workers. The relationship between styrene exposure and biological data is reported and discussed. Alveolar, urinary and blood concentrations of styrene were comparable, suggesting similar kinetics. Biological styrene concentrations were significantly correlated with the mean daily environmental concentrations, but higher correlation coefficients were found with afternoon exposures. A narrow linear relationship between alveolar (Y) and urinary (X) styrene concentrations was found (Y = 0.359; r = 0.8579; n = 45; p less than 0.001). Urinary concentrations of mandelic acid (Y) confirmed a good relationship with the mean styrene exposure (X) (Y = 2.7 x +169; r = 0.4677 n = 45; p less than 0.01)

Reference values for blood toluene in the occupationally nonexposed general population

Blood toluene was measured by gas chromatography--mass spectrometry in 232 occupationally nonexposed subjects, consisting of 126 rural and 106 urban workers, and 37 chemical workers. Mean blood toluene was significantly lower in rural (698 ng/l) and urban workers (984 ng/l) than in chemical workers (2789 ng/l). Blood toluene was not significantly different between the rural and urban workers or among the urban workers with different jobs. Smokers had significantly higher levels (median 606 ng/l) than nonsmokers (median 424 ng/l). Subjects who had smoked at least one cigarette in the last 2 h before blood sampling had significantly higher blood toluene (median 1170 ng/l) than those who had not smoked during this time (median 693 ng/l), for whom the level was not significantly different from that in nonsmokers. Blood toluene in the total population was less than 2863 ng/l in 95% cases

Blood acetone concentration in "normal people" and in exposed workers 16 h after the end of the workshift

Acetone levels were measured by gas chromatography mass spectrometry (GC-MS) in environmental and alveolar air, blood and urine of 89 non-occupationally exposed subjects and in three groups of workers exposed to acetone or isopropanol. Acetone was detected in all samples from non-exposed subjects, with mean values of 840 micrograms/l in blood (Cb), 842 micrograms/l in urine (Cu), 715 mg/l in alveolar air (Ca) and 154 ng/l in environmental air (Ci). The ninety-fifty percentiles were 2069 micrograms/l in Cb, 2206 micrograms/l in Cu and 1675 ng/l in Ca. The blood/air partition coefficient of acetone was 597. Correlations were found in Cb, Cu and Ca. In specimens sampled at the end of the workshift from subjects occupationally exposed to acetone, a correlation was found in the blood, urine, alveolar and environmental air concentrations. The blood/air partition coefficient of acetone was 146. On average, the blood acetone levels of workers were 56 times higher than the environmental exposure level, and the concentration of acetone in alveolar air was 27% more than that found in inspiratory air. The half-life for acetone in blood was 5.8 h in the interval of 16 h between the end of the workshift and the morning after. The morning after a workshift with a mean acetone exposure of 336 micrograms/l, blood and urinary levels were 3.5 mg/l and 13 mg/l, respectively, which were still higher than those found in "normal" subjects. It can be concluded that endogenous production of acetone and environmental exposure to acetone or isopropanol do not affect the reliability of biological monitoring of exposed workers, even 16 h after low exposure

Reference values for blood benzene in the occupationally unexposed general population

Blood benzene was determined by gas chromatography-mass spectrometry in 431 "normal" subjects, subdivided into 155 rural subjects and 276 urban subjects. Blood benzene (mean value 262 ng/l) was significantly lower in rural (200 ng/l) than in urban (296 ng/l) workers, as well as differing significantly between 293 non-smokers and 138 smokers (205 ng/l and 381 ng/l, respectively). Among non-smokers, values were significantly higher (307 ng/l) in 76 chemical workers. In the total study population, in 95% of cases blood benzene was less than 718 ng/l, the 95th percentile being 514 ng/l in non-smokers vs 901 ng/l in smokers and 576 ng/l in rural vs 822 ng/l in urban subjects. Within each population subgroup, the difference between non-smokers and smokers was statistically significant, except among office workers (non-smokers 234 ng/l, smokers 304 ng/l). Blood benzene (y) was directly proportional to the number of cigarettes smoked (x) (y = 201 + 12x; r = 0.44; n = 431), and inversely proportional to the interval between the last cigarette and the time at which the blood samples was taken (z) (log y = 6.167-0.0015z; r = -0.461; n = 135). The blood half-life of benzene was about 8h. The multiple correlation between blood benzene (Cb), number of cigarettes per day (x) and time since the last cigarette (z) is: Cb = 417 + 7.2x - 0.41z (n = 135; R = 0.20; P less than 0.00001)