A F Filipsson1. 1. Department of Toxicology, National Institute of Occupational Health, Solna, Sweden.
Abstract
OBJECTIVES: This study describes the toxicokinetics, pulmonary function, and subjective ratings of discomfort in volunteers experimentally exposed to turpentine vapour (a mixture of monoterpenes). The results were compared with similar exposure to single monoterpenes to look in the toxicokinetics and acute effects for signs of interactions between the monoterpenes. METHODS: Eight male volunteers were exposed to 450 mg/m3 turpentine by inhalation (2 h, 50 W) in an exposure chamber. RESULTS: The mean relative uptakes of alpha-pinene, beta-pinene, and 3-carene were 62%, 66%, and 68% respectively, of the amount supplied. Between 2% and 5% of the net uptake was excreted unchanged in the expired air after the end of exposure. The mean blood clearance 21 hours after exposure (CL21h) of alpha-pinene, beta-pinene and 3-carene, were 0.8, 0.5, and 0.4 l.kg-1.h-1, respectively. The mean half lives (t1/2) of the last phase of alpha-pinene, beta-pinene, and 3-carene averaged 32, 25, and 42 hours, respectively. The t1/2s agreed with previously calculated half lives from single exposures. The total blood clearance CL21h of 3-carene found in this turpentine study was lower, and CL4h of 3-carene was significantly lower than the values obtained from similar exposure to pure 3-carene. The subjects attending both exposure to turpentine and to pure alpha-pinene at 450 mg/m3 had lower CL4h during the exposure to turpentine, when they experienced more discomfort of the throat or the airways (F = 5.7, P = 0.048) than during exposure to control concentrations. After experimental exposure to turpentine an increase in airway resistance was found that differed significantly from results of exposure to 3-carene at 10 mg/m3 (P = 0.021) or 450 mg/m3 (P = 0.047). CONCLUSIONS: Toxicokinetics and acute effects show small, if any, interactions between alpha-pinene, beta-pinene, and 3-carene. The subjects experienced discomfort in the throat and airways during exposure to turpentine and airway resistance was increased after the end of exposure.
OBJECTIVES: This study describes the toxicokinetics, pulmonary function, and subjective ratings of discomfort in volunteers experimentally exposed to turpentine vapour (a mixture of monoterpenes). The results were compared with similar exposure to single monoterpenes to look in the toxicokinetics and acute effects for signs of interactions between the monoterpenes. METHODS: Eight male volunteers were exposed to 450 mg/m3 turpentine by inhalation (2 h, 50 W) in an exposure chamber. RESULTS: The mean relative uptakes of alpha-pinene, beta-pinene, and 3-carene were 62%, 66%, and 68% respectively, of the amount supplied. Between 2% and 5% of the net uptake was excreted unchanged in the expired air after the end of exposure. The mean blood clearance 21 hours after exposure (CL21h) of alpha-pinene, beta-pinene and 3-carene, were 0.8, 0.5, and 0.4 l.kg-1.h-1, respectively. The mean half lives (t1/2) of the last phase of alpha-pinene, beta-pinene, and 3-carene averaged 32, 25, and 42 hours, respectively. The t1/2s agreed with previously calculated half lives from single exposures. The total blood clearance CL21h of 3-carene found in this turpentine study was lower, and CL4h of 3-carene was significantly lower than the values obtained from similar exposure to pure 3-carene. The subjects attending both exposure to turpentine and to pure alpha-pinene at 450 mg/m3 had lower CL4h during the exposure to turpentine, when they experienced more discomfort of the throat or the airways (F = 5.7, P = 0.048) than during exposure to control concentrations. After experimental exposure to turpentine an increase in airway resistance was found that differed significantly from results of exposure to 3-carene at 10 mg/m3 (P = 0.021) or 450 mg/m3 (P = 0.047). CONCLUSIONS: Toxicokinetics and acute effects show small, if any, interactions between alpha-pinene, beta-pinene, and 3-carene. The subjects experienced discomfort in the throat and airways during exposure to turpentine and airway resistance was increased after the end of exposure.
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