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Biomedical subjects

P Pfäffli

Publications and source records attributed to P Pfäffli.

At least 73 records · Page 4Linked to original sources
PubMed1979

Effects of subacute toluene inhalation on its metabolism and disposition in rat.

Exposure of adult male rats to 300 ppm of toluene for 1 to 15 weeks 6 h daily caused accumulation of the solvent in brain and in perirenal fat. The body solvent content tended to decrease during extended exposure which might be explained by the enhanced activity of drug-metabolizing enzymes in liver. Our findings also indicate that metabolic and functional adaptation takes place in longer exposures to low levels of toluene vapour.

Adipose Tissue↗
PubMed1979

Neurochemical and behavioural effects of long-term intermittent inhalation of xylene vapour and simultaneous ethanol intake.

Two-month-old male Wistar rats were exposed to 300 p.p.m. of xylene vapour with simultaneous ethanol ingestion for 5 to 18 weeks. Neurochemical effects of mere vapour inhalation included an increase in microsomal superoxide dismutase activity in brain at the end of the experiment. Concomitant ethanol ingestion added significantly to the xylene-induced effects by causing increased proteolysis at the 9th and 14th week of exposure whereas cerebral superoxide dismutase failed to increase in these animals. Preening frequency decreased transiently in ethanol and in xylene groups at 6 and 9 to 12 weeks, respectively, whereas increased ambulation occurred only in the xylene--ethanol group after 12 and 14 weeks of exposure. The behavioural effects were therefore different in the combined exposure, and our biochemical and behavioural observations may point at significant interaction of both solvents although the biochemical mechanisms remain largely unexplained.

Adipose Tissue↗
PubMed1979

Styrene and styrene oxide concentrations in the air during the lamination process in the reinforced plastics industry.

Styrene and styrene oxide concentrations were measured during the lamination process in the reinforced plastics industry. The mean concentration of styrene in the personal samples was 130 ppm, the highest value measured being 350 ppm. The average concentration for styrene oxide alone was 0.1 ppm, whereas the corresponding measurement for styrene oxide and its decomposition products combined was 0.7 ppm. In comparison then, the concentrations of styrene oxide and its derivatives were much lower (about 0.5% of the total) than those of styrene.

Air↗
PubMed1979

Effects of intermittent styrene inhalation, ethanol intake and their combination on drug biotransformation in rat liver and kidneys.

The modifying effects of daily ethanol ingestion in the drinking water as a 15 % solution (v/v) on drug biotransformational changes induced by inhalation exposure to styrene (300 ppm or 1260 mg/m3, 6 h daily, 5 d/week, up to 17 weeks) were studied in rat liver and kidney. The drug hydroxylation activities (7-ethoxycoumarin O-deethylase and 2,5-diphenyloxazole hydroxylase) both in liver and in kidneys were increased more by ethanol ingestion than by styrene inhalation. When administered in combination, styrene and ethanol exerted mostly an additive enhancing effect. However, hepatic NADPH-cytochrome c reductase activity was reduced both in styrene and in ethanol-treated rats. Hepatic styrene oxide hydratase activity was virtually unaffected by styrene treatments. The depression of glutathione concentration in liver was greater after styrene-ethanol than after styrene treatment alone. The hepatic UDPglucuronosyltransferase activity was enhanced slightly both in styrene and in styrene-ethanol rats. The binding affinity of styrene towards cytochrome P-450 was increased after styrene inhalation as shown by lowered K8 values. The perirenal fat concentration of styrene showed a rough inverse relationship to the overall monooxygenation activities in liver and kidney. Despite the additively induced enzyme activities in styrene-ethanol-treated rats the accumulation of styrene in fat of these animals was on the whole somewhat greater, suggesting that these two solvents in vivo also have mutual inhibitory effects on biotransformation.

Animals↗
PubMed1978

Effects of long-term turpentine inhalation on rat brain protein metabolism.

Chronic exposure of adult male rats to commercial turpentine resulted in an accumulation of the solvent in perinephric fat and brain. The body solvent content remained virtually stable during 8 weeks. Brain RNA content was below the control range initially and it increased to the control level at the 4th week of exposure. Serum non-specific cholinesterase activity was somewhat below the control range at the first and second week of exposure and it returned to the control level thereafter. The present data are in agreement with the small effects of turpentine exposure on human central nervous system in clinical follow-up studies.

Aerosols↗
PubMed1978

Operating room nurses' psychomotor and driving skills after occupational exposure to halothane and nitrous oxide.

Concentrations of halothane and nitrous oxide were assayed by gas chromatography throughout a working day in three operating theatres and in the end-tidal air of 19 nurses 15 and 60 min after leaving the theatres. Perceptual, psychomotor and driving skills were measured in these nurses and in 11 younger nurses working in the wards of the same hospital. A complicated psychomotor test battery and a driving simulator were used. End-tidal air concentrations of halothane and nitrous oxide were positively correlated with the exposure level of these gases in the operating theatres. Some of the operating room nurses had greater amounts of halothane in their end-tidal air (average 15 to 10 ppm) than student volunteers 4.5 h after 3.5 min of general anaesthesia with a combination of halothanenitrous-oxide oxygen (10 ppm halothane). These volunteers had worse psychomotor and driving performances when measured than controls who had not been anaesthetized. No correlations were found between the concentrations of halothane or nitrous oxide in end-tidal air and psychomotor or driving performance. Despite their higher age and exposure to the operating room environment, the driving skills of the operating room nurses were similar to those of the ward nurses. The results suggest that tolerance to anaesthetic gases develops among operating room personnel. No impairment of driving skills can be expected after daily exposure to halothan and nitrous oxide among long-term employees in operating theatres.

Air Pollutants↗
PubMed1978

Residual nitrous oxide in operating room personnel.

The concentrations of nitrous oxide in the blood and end-tidal air of 10 operating-room nurses were assayed by gas chromatography immediately and 1, 2, 5, and 21 h after 3 hours of exposure to an average of 380 ppm of nitrous oxide in operating-room air. In the second trial the nurses' end-tidal air concentrations of nitrous oxide were assayed on Monday, Wednesday, Friday and Sunday morning, and on Sunday afternoon and evening to reveal a possible accumulation of nitrous oxide during a routine week. After cessation of exposure there was a rapid decrease in the blood concentrations of nitrous oxide during the first hour (from 153 +/- 110 microgram/1 to 48 +/- 20 microgram/l at 1 h; means +/- s.d.), followed by a slower decrease. Small amounts (mean +/- s.d.: 18 +/- 6 microgram/l) of nitrous oxide were still measurable on the following morning 21 h after exposure. At 2 or 5 h after exposure there was an increase in blood and end-tidal air concentrations of nitrous oxide in seven and nine nurses, respectively. The end-tidal air concentrations of nitrous oxide were greater on Wednesday (22 +/- 7 microgram/l) than on Monday morning (8.4 +/- 1.5 microgram/l), but on Friday they were similar to those measured on Monday morning. The concentrations measured on Sunday, i.e. 2 days after exposure, were similar (average 15 microgram/l) to those measured during the week. It is concluded that, after cessation of exposure to nitrous oxide, there is a rapid decrease in the concentrations in blood and end-tidal air, but small amounts of nitrous oxide remain in the body for at least 3 days after cessation of exposure.

Air Pollutants↗
PubMed1978

Biochemical and toxicological effects of combined exposure to 1,1,1-trichloroethane and trichloroethylene on rat liver and brain.

1. Inhalation exposure of adult male rats to a mixture of 1,1,1-trichloroethane (500 p.p.m.) and trichloroethylene (200 p.p.m.) for four days 6 h daily resulted in an accumulation of 1,1,1-trichloroethane in perirenal fat. Further exposure on the fifth day caused a rapid increase in various organ contents of both solvents with secondary depression of brain RNA. 2. The four-day exposure doubled the RNA content of liver and caused a slight decline in the concentrations of glutathione in liver. 3. The amount of cytochrome P-450 in liver was increased, as well as the overall mono-oxygenase activity, measured with styrene as substrate. During continuing treatment on the fifth day, styrene mono-oxygenase activity decreased, the activity after 6 h being only about 50% of that at the beginning of the fifth day of exposure. 4. UDP-glucuronosyl transferase activity (measured in digitonin-activated microsomes) was doubled by the four-day combined exposure to 1,1,1-trichloroethane and trichloroethylene. 5. The changes during the fifth day of exposure, e.g. rapid increase in the concentrations of solvents in organs, the detection of trichloroethylene in tissues and depression of mono-oxygenase activity, obviously also occurred during the exposures on days 1 to 4 and reverted during each post-exposure period.

Animals↗
PubMed1978

Evaluation of occupational exposure to xylene by blood, exhaled air and urine analysis.

Occupational xylene exposure in the breathing zone of 15 painters was measured during three consecutive workdays. The applicability of the use of different biological samples was tested by the monitoring of xylene concentrations in blood and exhaled air, and urinary methylhippuric acid excretion as well. The best relation to the time-weighted average of xylene exposure was obtained for urinary methylhippuric acid concentration at the end of the workday; an amount of 665 mg/g of creatinine corresponded to 50 ppm of xylene. The amount of methylhippuric acid in a morning sample at the end of the work week, on the other hand, correlated to the mean exposure of the three preceding days. Xylene concentrations in exhaled air and blood sampled after the workday correlated poorly to the exposure of the preceding day. The urinary elimination of methylhippuric acid after the finished work week showed two distinct phases of excretion, with different biological half-times (1.9-5.3 h for the first 10 h after exposure and 16.5-48.4 h for the next two days).

Adult↗
PubMed1978

Percutaneous absorption of solvent vapors in man.

It is known from industrial experience and experimental studies that percutaneous absorption of concentrated liquid solvents may be considerable and even hazardous if large enough areas of skin are exposed for long periods of time. Percutaneous penetration of xylene, styrene, toluene, 1,1,1-trichloroethane and tetrachloroethylene vapors at ambient air concentrations of 600 ppm for 3.5 h was studied in a dynamic exposure chamber with a restricted number of human volunteers. Although the small number of exposed persons precluded conclusive quantitation of absorption and valid intercompound comparisons, aromatic solvents and tetrachloroethylene appear to penetrate skin much more readily than 1,1,1-trichloroethane. Skin penetrating properties of solvents seem, under the circumstances, to be associated primarily with lipid solubility. It was approximated that percutaneous exposure (total body surface) to 600 ppm of xylene vapor for 3.5 h corresponded to an equally long inhalation exposure of less than 10 ppm. Similar percutaneous exposure to 1,1,1,-trichloroethane corresponded to an inhalation exposure of only 0.6 ppm. Disease-affected skin may display altered permeability characteristics, and one volunteer with atopic dermatitis exhibited a more than three times larger absorption of xylene vapor when compared to subjects with normal skin. It may be concluded that in the work environment percutaneous absorption of solvent vapors from the surrounding air through undamaged skin is likely to be insignificant.

Adult↗
PubMed1978

Thermal degradation products of homopolymer polystyrene in air.

Polystyrene without additional compounds was treated in a laboratory oven at elevated temperatures (200 degrees, 350 degrees, 500 degrees C) under slight air flow (0.7 l/min). The thermal degradation products appearing in different phases (gases, vapors, aerosols) were collected and analyzed by methods of chromatography. Thermogravimetric analysis showed the thermal degradation of the polymer to begin at 270 degrees C in air and stop at 425 degrees C. The main groups of vaporized compounds generated were monoalkyl-substituted aromatic hydrocarbons and their oxidized products, of which styrene monomer and benzaldehyde were the most abundant. Only trace amounts of carbon monoxide and aliphatic compounds (hydrocarbons, aldehydes, and acids) were produced. The aerosol produced, the amount of which increased as the temperature rose, contained mainly fragments of the polymer chain (e.g., dimers and trimers of styrene). The traces of styrene, cumene, and ethylbenzene that appeared at 200 degrees could represent residual compounds in the initial polymer and indicate the beginning of the thermal degradation. If proportional concentrations are kept as a criterion, the important products, from the point of view of industrial hygiene, were styrene, benzaldehyde, styrene oxide, acetophenone, and l-phenylethanol. The large amount of aerosol that appeared may also be of practical importance.

Acids↗
PubMed1978

Effects of thermal degradation products of polystyrene on drug biotransformation and tissue glutathione in rat and mouse.

Rats and mice were exposed to the fumes of oxidative thermal degradation of polystyrene (350 degrees C). A decrease in the reduced glutathione (GSH) in both liver and lung was detected immediately after both the acute (mice, 3 h) and subacute (rats, 3 weeks) exposures were stopped. Later on an elevation in the amount of GSH due to the increased synthesis (rebound effect) could be seen. Cytochrome P-450 content in mouse liver was initially decreased after acute exposure, but the prolonged treatment doubled the amount of the P-450 hemoprotein in liver microsomes. After acute exposure 7-ethoxycoumarin 9-deethylase activity in mouse liver was doubled in 24 h. When the exposures were continued, this enhancement in ethoxycoumarin O-deethylase activity gradually disappeared. O-deethylase activity was also enhanced in rat liver and lung after subacute exposure. The exposures given had no effect on diphenyloxazole hydroxylase, and the effects on the conjugating enzymes (epoxide hydratase, UDPglucuronosyltransferase, glutathione S-transferase)) were insignificant in rat liver.

Animals↗
PubMed1978

Accumulation of styrene monomer and neurochemical effects of long-term inhalation exposure in rats.

A simplified compartment model indicated that fat styrene content might be used as an index of the whole body styrene burden. Intermittent exposure of adult male rats to 300 ppm 5 d a week, 6 h daily for 1 to 11 weeks showed an initial steady increase in the fat styrene content up to the 4th week and an exponential decrease thereafter. This phenomenon might have resulted from the enhancement of styrene oxidation due to the prolonged exposure. The effect of the increased oxidation on the body styrene burden is theoretically doubled after 9.1 weeks of exposure. Neurochemical effects after that time might have resulted from an increased binding of styrene oxide in the cellular macromolecules, e.g., to their sulfhydryl groups. The activity of the metabolite towards the cellular constituents could very well explain the increased proteolysis possibly caused by lysosomal labilization. The present data also lend support to the theory of the importance of metabolic activation to styrene and other solvent toxicity.

Adipose Tissue↗
PubMed1977

Effects of chronic styrene inhalation on rat brain protein metabolism.

Adult male rats were exposed to 7.9 mumol/1 (300 ppm) of styrene for 2--11 weeks 6 h daily excluding Saturdays and Sundays. The exposures caused a marked styrene accumulation in brain and perinephric fat, and the accumulation tended to increase upto the 4th week. The body styrene content decreased thereafter gradually towards the end of the experiment to reach half of the styrene content of the 4th week. Serum creatine kinase activity increased at the initial stage of the exposures while serum non-specific cholinesterase was below the control range at the same time. Earliest biochemical changes were detected at the 9th week of exposure, and they included increased activity of lysosomal acid proteinase. Increased enzyme activity prevailed to the end of the exposures. Simultaneous minor alterions could be detected in spinal cord axonal protein pattern whereas water-soluble protein composition in cerebellum did not change. Biochemical alterations in brain were not accompanied by significant changes in serum enzyme activities. It is concluded that marked metabolic adaptation to inhaled styrene takes place. Serum enzyme determinations may prove valuable in the adaptation period whereas they may not reflect beginning chronically neurotoxic effects.

Acetylcholinesterase↗
PubMed1977

Trichloroethylene and 1,1,1-trichloroethane: effects on brain and liver after five days intermittent inhalation.

The inhalation exposure of adult male rats to 7.9 mumol/l (200 ppm) of trichloroethylene for 4 days 6 h each day led to an accumulation of the solvent in the perirenal fat 17 h after the last exposure. Exposures to 20 mumol/l (500 ppm) of 1,1,1-trichloroethane caused similar accumulation. The latter rats presented no changes in their behaviour in an open-field test whereas the motor behaviour of the animals exposed to trichloroethylene was more active in comparison to controls 1 h after the exposure on the 4th day. Trace effects of trichloroethylene on emotional behaviour of the same rats could be seen 17 h after the last exposure. Further exposures on the 5th day increased brain, liver, lung and blood contents of trichlorethylene and 1,1,1-trichloroethane. A slight decrease in brain RNA content was found in the 1,1,1-trichloroethane exposed rats while RNA decreased significantly after the fifth day of trichloroethylene inhalation. The exposure to 1,1,1-trichloroethane on the 5th day depressed also the microsomal cytochrome P-450 content in liver of rats whereas trichloroethylene increased the hemochrome content slightly at the same time.

Animals↗
PubMed1977

Recovery, psychomotor skills, and simulated driving after brief inhalational anesthesia with halothane or enflurane combined with nitrous oxide and oxygen.

Recovery from anesthesia was assessed in a controlled manner in 34 healthy student volunteers, using a psychomotor test battery 1 and 5 hours and a driving simulator 2, 4.5, and 7 hours after 3.5 minutes of anesthesia with halothane or enflurane combined with nitrous oxide and oxygen. Psychomotor performances remained significantly (P less than 0.05 to P less than 0.001) worse than in an unanesthetized control group for 5 hours after both halothane and enflurane. However, impairment of driving skills 4.5 hours after anesthesia was measurable only after halothane (P less than 0.05). It is concluded that after even brief periods of halothane or enflurane anesthesia patients should not drive or operate machinery for at least 7 hours. The magnitudes and durations of the residual effects of both agents on psychomotor performance were, however, less than those previously found after thiopental, methohexital, or diazepam.

Adult↗
PubMed1977

Biochemical and behavioural effects of inhalation exposure to tetrachlorethylene and dichlormethane.

The exposure of adult male rats to 200 ppm of tetrachlorethylene t hours daily for 4 days resulted in a marked sequestration of solvent in perirenal fat 17 hours after the last exposure period. Similar exposure of similar rats to 500 ppm of dichlormethane led to a lesser accumulation of the solvent in fat as studied at the same time. Further exposures on the fifth day increased promptly the solvent contents of various organs. The exposure to tetrachlorethylene caused a diminished brain RNA content on the fifth day with simultaneous increase in the activity of non-specific cholinesterase. Similar changes in the RNA content were not seen in experiments with dichlormethane while the activity of acid proteinase increased above the control level in brain. Observations on the performance of the same animals in an open-field situation revealed that ambulation was affected in experiments with tetrachlorethylene immediately after exposure while preening pattern was changed after exposure to dichlormethane. Analysis on liver microsomal cytochrome P-450 content displayed slight increases in the hemochrome content in both experiments. The present data indicated that a rather modest exposure to both solvents could cause significant solvent accumulation in the fat and brain with marked effects on rat behaviour and protein metabolism in brain while changes in liver cytochrome P-450 content might not reflect the magnitude of these changes.

Adipose Tissue↗