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Biomedical subjects

P Pfäffli

Publications and source records attributed to P Pfäffli.

At least 37 records · Page 2Linked to original sources
PubMed1991

Styrene revisited--exposure assessment and risk estimation in reinforced plastics industry.

A survey performed in 32 workshops in reinforced plastics industry showed the mean TWA 8 h concentration of styrene in personal air to be 43 ppm (range 5-182 ppm) among laminators and 11 ppm (range 1-133 ppm) among other workers. The biological measurement of urinary mandelic acid + phenylglyoxylic acid showed mean values of 2.4 mmol/l among laminators without respirators and 1.3 mmol/l when respirators were used. No effects of work related exposure were detected in the cytogenetic parameters, chromosome aberrations, sister chromatid exchanges or micronuclei analyzed in peripheral blood lymphocytes. Grading of the exposure on the basis of lamination method, years of exposure, daily laminating time, air styrene concentration and urinary mandelic acid among laminators, neither revealed any dose dependency.

Air Pollutants, Occupational↗
PubMed1990

Air impurities in the PVC plastics processing industry.

Polyvinylchloride (PVC) is a common thermoplastic and one which often contains plasticizers. The most important plasticizer is di-2-ethylhexylphthalate (DEHP). Hygienic conditions in the PVC processing industry were surveyed by measuring the air concentrations of hydrogen chloride, DEHP and phthalic anhydride (PA) in different conditions of actual processing. Methods of sampling and analysis were developed and tested for these measurements. As measured at nine plants hydrogen chloride concentrations, which indicate the degradation of the polymer chain, ranged from less than 0.03 to 0.3 mg m-3. The mean concentrations of DEHP ranged from less than 0.02 to 0.5 mg m-3 and the highest single value was 1.1 mg m-3, which is about 20% of the current hygienic standard. Trace concentrations of PA--a sensitizer which is a degradation product of DEHP--ranged from less than 0.02 to 5 microns m-3 at six plants. The results show that the PVC polymer was efficiently stabilized in normal processing conditions (usually 150-200 degrees C), but that plasticizers, which are not chemically bonded to the polymer, may volatilize more easily.

Air Pollutants, Occupational↗
PubMed1988

Kinetics of methyl ethyl ketone in man: absorption, distribution and elimination in inhalation exposure.

The kinetics of inhaled methyl ethyl ketone (MEK) in human volunteers was studied in an exposure chamber. Relative pulmonary uptake was about 53% throughout a 4-h exposure period at 200 ppm. Blood MEK concentration rose steadily until the end of exposure. Repeated bicycle exercise increased the overall blood MEK level markedly in comparison to sedentary activity, with transient peaks in association with cycling; thus blood MEK concentration depended both on the rate of uptake and the amount taken up. Only 3% of the absorbed dose was excreted unchanged by exhalation. A well-known metabolite of MEK, 2,3-butanediol, was detected in the urine with maximum rates of excretion at about 6 to 12 h from the beginning of exposure. About 2% of the MEK dose taken up by the lungs was excreted in the urine as 2,3-butanediol. The main part of inhaled MEK is supposedly metabolized in the intermediary metabolism. Elimination of MEK in blood appeared to exhibit two phases: the initial alpha-phase (T1/2 = 30 min; kel alpha = 0.023) over the first post-exposure hour, followed by the terminal beta-phase (T1/2 = 81 min; kel beta = 0.009).

Administration, Inhalation↗
PubMed1988

Coexposure of man to m-xylene and methyl ethyl ketone. Kinetics and metabolism.

In a study of the kinetics and metabolic interaction of xylene and methyl ethyl ketone (MEK) eight male volunteers were exposed to m-xylene (100 ppm) and MEK (200 ppm). The exposures to the two compounds were carried out both separately and in combination. Respiratory uptake and blood concentration, as well as urinary metabolites (methyl hippuric acid and 2,3-butanediol), were monitored. Coexposure to xylene and MEK resulted in inhibited xylene metabolism. The xylene concentration in blood increased significantly, and the urinary excretion of methyl hippuric acid decreased. The combined exposure did not cause any change in the concentration of MEK in the blood or the excretion of 2,3-butanediol in the urine. Exposure to MEK 20 h before the m-xylene exposure had no detectable effect on the kinetics of m-xylene.

Adult↗
PubMed1987

Ventilation and organic solvent exposure during car washing.

Spray finishing operations often involve cleaning with solvents. White spirit is widely used as a solvent in car washes in Finland. The purpose of the present study was to determine the levels of solvent exposure of car washers and to evaluate the effectiveness of ventilation systems in car washing facilities. The study covered 11 car washes. Airborne solvent concentrations were measured both in workers' breathing zones and at stationary sampling sites. The solvent concentration in the breathing zones ranged from 5 to 465 mg/m3 during the washing of automobiles and from 45 to 685 mg/m3 during the washing of heavy vehicles. Brief concentration peaks up to 4,500 mg/m3 were detected. The flow rate of ventilation air ranged from 0.3 to 3.9 m3/s. The greatest reduction in solvent concentration in the workers' breathing zones was attained with a ventilation design where the supply air jets blew directly into the work zone.

Air Pollutants↗
PubMed1986

Phthalic acid excretion as an indicator of exposure to phthalic anhydride in the work atmosphere.

The concentration of phthalic acid was determined in the urine of nine subjects occupationally exposed to phthalic anhydride. For the determination, the urine samples were acidified, extracted with dimethyl ether, esterified with boron trifluoride/methanol and measured by electron capture gas chromatography. Environmental air samples were collected in Tenax tubes, eluted with methyl-t-butyl ether and assayed by electron capture gas chromatography. Significant correlations were found between the concentration in urine samples (range: 0.3-14.0 mumol/mmol creatinine), collected at different times of the day, and the time-weighed average atmospheric concentrations (range: 0.03-10.5 mg/m3). No conjugation of phthalic acid in the urine was observed. The detection limit for urine samples (10 ml) was 0.05 mumol/l) and that for air samples 0.4 microgram/m3. The method has potential for biological monitoring of workers exposed to phthalic anhydride. It was found that at atmospheric anhydride concentrations of about 30% of the hygienic reference value (6 mg/m3), which is applied in many market economies, a body-burden was caused which was not eliminated overnight.

Body Burden↗
PubMed1986

Blood levels and half-life of methylmethacrylate after tourniquet release during knee arthroplasty.

The blood levels and the half-life of monomeric methylmethacrylate after tourniquet release were studied in nine patients with osteoarthrosis or rheumatoid arthritis of the knee joint, treated with the Townley prosthesis under spinal anesthesia. Several ventricular extrasystoles were monitored in one patient with high blood levels of monomeric methylmethacrylate (119.80 micrograms/ml). The blood levels of monomeric methylmethacrylate ranged between 0.10 and 1.44 microgram/ml in the rest of the patients. The half-life of monomeric methylmethacrylate in vivo was 47-55 min.

Aged↗
PubMed1986

Biochemical effects and monitoring of exposure of rats to 4-methylcyclohexyl-1,6-dicarboxylic acid anhydride vapour.

Male Wistar rats exposed to 5, 10 or 20 p.p.m. 4-methylcyclohexyl-1,6-dicarboxylic acid anhydride vapour for 2-11 weeks showed dose-dependent blood anhydride concentrations. The maximum concentrations were found after two weeks. At five exposure weeks, they were smaller but they did not decrease further thereafter. The change was coincident with increased epoxide hydrase activity in liver. The excretion of 4-methylcyclohexyl-1,6-dicarboxylic acid was detected in the urine. The excretion was linearly related to the exposure in specimens collected during the 10th and 11th week. Brain acetylcholinesterase activity was transiently inhibited by the exposure at the two higher doses while decreased enzyme activity in the isolated spinal cord axons was only found after 11 weeks. This change was simultaneous with increased creatine kinase activity in the cerebellar homogenate. In the occupational setting, acetylcholinesterase activity might only be significantly inhibited in lungs because of the low exposure levels.

Acetylcholinesterase↗
PubMed1985

Biochemical effects of methyl tertiary-butyl ether in extended vapour exposure of rats.

Male Wistar rats exposed to 50, 100 or 300 ppm methyl tertiary-butyl ether vapour for 2-15 weeks, 6 h daily, 5 days a week, showed a dose-dependent blood ether concentration after 2 weeks' exposure. Blood concentrations of tertiary-butanol, were also dose dependent indicating metabolic breakdown of the ether in vivo. The blood ether concentrations decreased after 6 weeks of exposure at the 50 ppm dose level and remained unaffected at higher doses while tertiary-butanol concentrations increased after 6 weeks with all doses, and began to decrease thereafter. Exposure caused a transient increase in UDP-glucuronosyltransferase activities in liver and kidney microsomes, almost no effects on hepatic cytochrome P-450 concentrations and a minor induction of kidney microsomal cytochrome P-450 content. Exposure produced almost no effect on brain succinate dehydrogenase, creatine kinase or acetylcholinesterase activities, while early inhibition of muscle creatine kinase activity was noted, accompanied by increased activity at the end of exposure.

Adipose Tissue↗
PubMed1985

Methylmethacrylate blood levels in patients with femoral neck fracture.

The blood levels of monomeric methylmethacrylate were measured in 20 patients with fracture of the femoral neck, treated with a Thompson prosthesis under spinal anesthesia. Monomeric methylmethacrylate was detected in the blood stream in all patients; the maximum levels (mean 6.44 micrograms/ml, range 0.05-31.89 micrograms/ml) were measured 30 s after insertion of the Thompson prosthesis. A moderate drop in systolic blood pressure and a marked reduction of arterial oxygen tension was noted after cementation and insertion of the prosthesis; the mean maximum drops were 10.1 mm Hg (range 0-32 mm Hg) and 6.1 mm Hg (range 0-13.5 mm Hg) No dose-dependent correlation could be established between the levels of monomeric methylmethacrylate and the drop in arterial blood pressure or arterial oxygen tension.

Aged↗
PubMed1985

Blood and brain n-pentanol in inhalation exposure.

Male Wistar rats exposed to 100, 300 or 600 p.p.m. n-pentanol vapour for 7 to 14 weeks during five days weekly and 6 hrs daily showed a dose-dependent blood n-pentanol concentration. The brain n-pentanol content was linearly related to the blood pentanol concentrations although this relationship changed after 14 weeks because the brain n-pentanol was significantly smaller than the respective values at 7 weeks. Valeraldehyde, the primary metabolite of n-pentanol, was only found in the brain at the highest vapour dose level. The liver n-pentanol dehydrogenase and 7-ethoxycoumarin O-deethylase activities remained unchanged while kidney ethoxycoumarin deethylase activity was enhanced in a dose-dependent manner at both time points. Brain and muscle acetylcholinesterase activities were increased by the exposure dose-dependently after 7 weeks although this effect ameliorated after 14 weeks. Moderate n-pentanol vapour exposure seems to cause metabolic and functional adaptation in its target organs.

Acetylcholinesterase↗
PubMed1985

Chromosome damage induced by vinyl acetate through in vitro formation of acetaldehyde in human lymphocytes and Chinese hamster ovary cells.

A 48-h treatment with vinyl acetate (0.05-1 mM) induced a drastic increase in sister chromatid exchanges (SCEs) and (in first division cells) structural chromosome aberrations in cultured human lymphocytes. The effects were more pronounced in cultures of isolated lymphocytes than in whole-blood cultures. A distinct dose-dependent induction of SCEs similarly occurred in Chinese hamster ovary cells after a 24-h vinyl acetate treatment (0.125-1 mM). A pulse treatment of Chinese hamster ovary cells for 4 h also yielded a clear increase in SCEs, but at higher concentrations (0.3-5 mM). The presence of rat liver S9 mix enhanced the SCE-inducing effect of vinyl acetate in Chinese hamster ovary cells. Gas chromatographic analysis of human whole-blood lymphocyte cultures treated for 10 s-20 min with vinyl acetate (5.4 mM) revealed a rapid degradation of vinyl acetate and formation of acetaldehyde. During the 20-min observation period, no degradation of vinyl acetate or formation of acetaldehyde were observed in complete culture medium without blood, which suggested that the reaction was enzymatic. Acetaldehyde induced SCEs in human whole-blood lymphocyte cultures at concentrations (0.125-2 mM) comparable to those used for vinyl acetate. The results indicate that vinyl acetate induces chromosome damage in cell cultures through enzyme-mediated hydrolysis to acetaldehyde.

Acetaldehyde↗
PubMed1984

Comparison of local neurotoxicity of three white spirit formulations by percutaneous exposure of rat tail nerve.

A recently developed technique was used to compare the local neurotoxicity of three white spirit (crude oil distillates) formulations. They differed in aliphatic and aromatic hydrocarbon concentrations. Formulations I and II contained over 10% n-nonane, whereas its concentration was negligible in formulation III with 17% aromatics. Formulation I contained no aromatics. Formulation I and II caused local axonopathy by neurophysiological and morphological criteria after 6 weeks of daily 3-h exposures for 5 days a week. No neurophysiological changes were caused by formulation III while morphological analysis revealed infrequent demyelinative foci after 6 weeks. Rats exposed to formulation II with 1% trimethylbenzene isomers showed urinary excretion of dimethylbenzoic acid isomers not detected in other rats thus providing a method for the biological monitoring of exposure.

Animals↗