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PubMed1993

Enhanced mortality and liver damage in virus-infected mice exposed to p-xylene.

This study assessed effects of exposure to p-xylene, a ubiquitous air pollutant, on mice infected with murine cytomegalovirus (MCMV), a mouse model for a common human virus. It was postulated that adverse health effects could occur as a result of (1) enhanced infection due to xylene-induced immune suppression, (2) increased p-xylene toxicity due to viral suppression of cytochrome P-450 (P-450), and/or (3) additive or synergistic effects on liver function due to tissue injury by both p-xylene and MCMV. Mice were exposed to filtered air, 600 or 1200 ppm p-xylene 6 h/d for 4 d and infected with a sublethal dose of MCMV after the first exposure. No deaths occurred among uninfected, p-xylene-exposed mice or infected, air-exposed mice; 34% and 0% mortality occurred respectively in infected mice exposed to 1200 and 600 ppm p-xylene. Virus titers in the liver and splenic natural killer cell activity were unaffected by exposure to 1200 ppm p-xylene. Small but significant increases in serum aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase activities, indicators of liver damage, were observed at 4 d postinfection. p-Xylene exposure had no effect on these serum enzyme activities in uninfected mice, but 1200 ppm potentiated this effect in infected mice. MCMV significantly suppressed and p-xylene significantly increased total P-450 levels in the liver, but there was no significant interaction between the two. Isozymes 1A1, 2B1/B2, and 2E1 were decreased to a similar degree, suggesting that the virus does not target specific isozymes. Enhanced mortality was not due to immune suppression. While p-xylene potentiated liver damage was caused by the virus, the magnitude of serum enzyme activities indicates that this damage was not a likely cause of death. The cause of deaths is unclear, results were consistent with the hypothesis that enhanced mortality was related to enhanced xylene toxicity due to suppression of P-450, although additive or synergistic damage to tissues other than liver cannot be ruled out.

Analysis of Variance↗

PubMed1992

Influence of various mixtures of inhaled toluene and xylene on the biological monitoring of exposure to these solvents in rats.

The present study was undertaken to describe the influence of simultaneous exposure by inhalation to toluene and xylene on some aspects of their respective metabolic disposition. Adult male rats were exposed acutely (5 h) to 75, 150, and 225 ppm of toluene or xylene and to various mixtures of these solvents: toluene (75 ppm) and xylene (225 ppm), toluene (150 ppm) and xylene (150 ppm), toluene (225 ppm) and xylene (75 ppm). Compared with single exposure, simultaneous exposure resulted in lower amounts of excreted hippuric acid (20-30%) and methylhippuric acids (4-40%) in urine over a period of 24 h, even though significant differences were seen only with the toluene (150 ppm) and xylene (150 ppm) combination. In addition, increased concentrations of solvents in blood (toluene, 230%; xylene, 500%) and in brain (toluene, 230%; xylene, 320%) were found during the immediate post-exposure period. Simultaneous exposure also enhanced the pulmonary elimination of both solvents (toluene, 190-240%; xylene, 340-650%). Influence of repeated simultaneous exposure (9 days) was investigated for the toluene (150 ppm) and xylene (150 ppm) combination and the results compared with those of repeated exposure to each solvent administered singly. Under these conditions, repeated simultaneous exposure decreased the excretion of urinary metabolites, but only after the first exposure. On the other hand, simultaneous exposure resulted in significantly higher concentrations of toluene (210%) and xylene (240%) in blood throughout the entire 9-day exposure period. These results strongly suggest mutual metabolic interactions (inhibition) between toluene and xylene that affect the metabolic disposition of both solvents and ultimately the biological monitoring of data of exposure to a combination of solvents in rats.

Administration, Inhalation↗

PubMed2001

Biological monitoring of workers exposed to ethylbenzene and co-exposed to xylene.

OBJECTIVE: Ethylbenzene is an important constituent of widely used solvent mixtures in industry. The objective of the present study was to provide information about biological monitoring of occupational exposure to ethylbenzene, and to review the biological limit values corresponding to the threshold limit value of ethylbenzene. METHODS: A total of 20 male workers who had been exposed to a mixture of ethylbenzene and xylene, through painting and solvent mixing with commercial xylene in a metal industry, were recruited into this study. Environmental and biological monitoring were performed during an entire week. The urinary metabolites monitored were mandelic acid for ethylbenzene and methylhippuric acid for xylene. Correlations were analyzed between urinary metabolites and environmental exposure for ethylbenzene and xylene. The interaction effects of a binary exposure to ethylbenzene and xylene were also investigated using a physiologically based pharmacokinetic (PBPK) model. RESULTS: The average environmental concentration of organic solvents was 12.77 ppm for xylene, and 3.42 ppm for ethylbenzene. A significant correlation (R2 = 0.503) was found between environmental xylene and urinary methylhippuric acid. Urinary level of methylhippuric acid corresponding to 100 ppm of xylene was 1.96 g/g creatinine in the worker study, whereas it was calculated as 1.55 g/g creatinine by the PBPK model. Urinary level of mandelic acid corresponding to 100 ppm of ethylbenzene was found to be 0.7 g/g creatinine. PBPK results showed that the metabolism of ethylbenzene was highly depressed by co-exposure to high concentrations of xylene leading to a non-linear behavior. CONCLUSIONS: At low exposures, both methylhippuric acid and mandelic acid can be used as indicators of commercial xylene exposures. However at higher concentrations mandelic acid cannot be recommended as a biological indicator due to the saturation of mandelic acid produced by the co-exposure to xylene.

Benzene Derivatives↗

PubMed2001

Predicting natural attenuation of xylene in groundwater using a numerical model.

The aquifer beneath an abandoned refinery in the Lower Rhine area, Germany, was contaminated with a number of different mineral oil products. Groundwater sampling in the area around the former xylene plant revealed that a xylene plume had developed in the underlying groundwater, and moreover, that there is strong evidence for in situ microbial xylene degradation with oxygen, nitrate, sulfate and ferric iron as electron acceptors. In order to prevent further xylene spreading, three pumping wells extracting contaminated water were installed downgradient of the spill zone. The numerical reactive transport code Transport Biochemisty Chemistry (TBC) was applied to this situation to quantify the relation of microbial degradation to xylene removal by the pumping wells. It could be shown that the unamended in situ degradation was an appreciable xylene removal process that contributed to about one-third to the total xylene removal (degradation plus extraction). A further objective of the model application was to predict xylene spreading under regional flow conditions, i.e. without operation of the three pumping wells, to consider the possible effects of natural xylene attenuation. To accomplish this, the model calibrated for the situation with operating wells was transferred to the hydraulic situation of regional flow while retaining the parameters of the biochemical model. It turned out that the xylene plume that is expected to develop downgradient of the source area will be limited to an extension of not more than 1000 m. An interesting feature of the simulations results was that xylene degradation under iron-reducing conditions, which was of minor importance for the situation with operating pumping wells, becomes the dominant degradation mechanism under regional flow conditions. Moreover, iron reduction will be the key process in controlling plume evolution. The model application illustrates that multi-species reactive transport models are needed to adequately transfer reactive processes from one hydraulic situation to another, while single species models are not suited for this predictive task.

Forecasting↗

PubMed2004

Inhibition of rat respiratory-tract cytochrome P-450 activity after acute low-level m-xylene inhalation: role in 1-nitronaphthalene toxicity.

The xylenes are commonly used industrial solvents that have been shown to inhibit cytochrome P-450 (CYP450) activities in an organ- and isozyme-specific pattern. This study examined the dose-response and durational effects of m-xylene inhalation on cytochrome P-450 activities in the respiratory tract and liver as well as the effects of these CYP450 alterations on 1-nitronaphthalene (1-NN)-induced respiratory or hepatic toxicity. After m-xylene inhalation exposure there was a dose-related inhibition of all nasal mucosa CYPs examined. At 300 ppm, inhibition was sustained up to 2 days after exposure, but on day 5 all CYP activities were increased. There was also dose-related inhibition of lung CYPs 2B1, 2E1, and 4B1. The activities of these CYPs returned to those of control by day 2 but lung CYP 2B1 was increased 5 days following m-xylene exposure. Hepatic CYP 2E1 activity was increased immediately following m-xylene exposure (300 ppm). CYP 2B1 and CYP 1A2 activities were increased through day 2, all activities returning to control values 5 days postexposure. 1-NN treatment caused severe respiratory toxicity that was prevented by prior m-xylene exposure. Lactate dehydrogenase (LDH) and protein were increased in nasal lavage fluid (NLF) but gamma-glutamyl transferase (GGT) was unchanged. m-Xylene coexposure prevented or ameliorated the increases in LDH and protein but increased GGT. 1-NN-induced increases in bronchoalveolar lavage fluid (BALF) LDH and GGT were attenuated by m-xylene. 1-NN caused pronounced histopathological changes in both respiratory and olfactory regions of the nasal mucosa. Lesions in both regions were characterized by acute epithelial necrosis and exfoliation and suppurative exudate in the airways. These changes were prevented by m-xylene coexposure. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were not changed in animals exposed to 1-NN but were increased by m-xylene coexposure. Low-level m-xylene exposure organ-selectively altered CYP450 isozyme activities and subsequent 1-NN toxicity.

Administration, Inhalation↗

PubMed2003

Biological monitoring of low level occupational xylene exposure and the role of recent exposure.

The correlation between low level time-weighted average (TWA) atmospheric xylene exposure (p.p.m.) and urinary methylhippuric acid (MHA) expressed per gram of creatinine was examined. Subjects were recruited from workplaces that utilized xylene. Ambient monitoring of o-, m- and p-xylene isomers was carried out using passive diffusion vapour monitors. Adjusted (post-shift minus pre-shift) and post-shift urinary levels of xylene metabolites (2-, 3- and 4-MHA) were determined by GC-MS. Twenty subjects were recruited into the study. Total xylene TWA exposures were 3.36 +/- 3.63 p.p.m. (mean +/- SD) with a range of 0.03-14.44 p.p.m. The r(2) values for the regression equations between xylene exposure and individual and total adjusted MHA isomers were 0.390, 0.709, 0.677 and 0.631 for o-, m-, p- and total xylenes, respectively, which was greater than the respective correlations between non-adjusted samples. In conclusion, biological monitoring of occupational xylene exposure at levels <15 p.p.m. using urinary MHA showed a good correlation with atmospheric levels and is a valid complement to ambient monitoring. Even though occupational xylene exposure in the workplaces studied was generally low, MHA was found in the pre-shift urine of all workers and the use of adjusted values showed modest improvements in correlations. Recent exposure prior to sampling, either from occupational or non-occupational sources, should be considered when biological monitoring of xylene is undertaken. Extrapolation of data from this study predicted a MHA concentration in post-shift urine of 1.3 g/g creatinine after exposure to a TWA of 100 p.p.m. xylene.

Adult↗

PubMed1995

Xylene substitutes in frozen sections.

BACKGROUND: Toxic exposure to xylene may occur during routine histopathologic staining procedures. Safer xylene substitutes have been available for over a decade, however, a 1991 survey of 25 Mohs training programs revealed that only 56% were using xylene substitutes. OBJECTIVE: The purpose of this study was to compared xylene to xylene substitutes in the histologic preparation of frozen sections with respect to staining quality, clarity, cellular detail, and tissue distortion. METHODS: Xylene and xylene substitutes were used as the final clearing agent in the routine histologic preparation of fresh frozen horizontal sections. The slides were evaluated by a dermatopathologist and a Mohs surgeon in a blinded manner. RESULTS: No difference between xylene and the xylene substitutes were noted. CONCLUSION: In light of the improved safety profile and efficacy of the xylene substitutes, they should replace xylene in the Mohs laboratory.

Cyclohexenes↗

PubMed1976

XYL, a nonconjugative xylene-degradative plasmid in Pseudomonas Pxy.

Pseudomanas Pxy metabolizes p- or m-xylene through intermediate formation of the corresponding methylbenzyl alcohol and toluic acid via the meta pathway. The strain Pseudomonas Pxy spontaneously loses its ability to grow with xylene or toluate, and the rate of loss of this ability is greatly enhanced by treatment of the cells with mitomycin C. The assay of enzymes involved in xylene degradation in xylene-negative Pxy cells indicates the loss of the entire enzyme complement of the pathway. The genes specifying all the xylene-degradative enzymes, including those of the meta pathway, appear to be borne on a nonconjugative plasmid and can be transferred to xylene-negative Pxy or P. putida strain PpG1 cells only in the presence of a transfer plasmid termed factor K. When transferred to strain PpG1, the xylene-degradative plasmid, termed XYL, coexists stably with factor K, but transduction of XYL is not accompanied by a cotransfer of factor K. XYL appears to be compatible wit- all the other known degradative plasmids in P. putida. The xylene pathway is inducible in wild-type Pxy as well as in Pxy and PpG1 exconjugants, suggesting the cotransfer of regulatory genes along with the plasmid. The enzymes converting xylene to toluate are induced by xylene, methylbenzyl alcohol, or the aldehyde derivatives but not significantly by toluate, whereas catechol dioxygenase and other enzymes are induced by toluates and presumable by xylene as well.

Benzyl Alcohols↗

PubMed1982

Metabolic interaction between m-xylene and ethanol.

Ingestion of a moderate dose of ethanol (0.8 g/kg) by volunteers prior to 4-h inhalation exposure to m-xylene (6.0 or 11.5 mmol/m3) caused marked alterations in xylene kinetics. After ethanol intake the blood xylene level rose about 1.5-2.0-fold and urinary methylhippuric acid excretion declined by about 50% suggesting that ethanol decreased the metabolic clearance of xylene by about one half during xylene inhalation. This effect was noticeable up until a few hours after completed xylene exposure. Urinary excretion of 2,4-xylenol, the minor m-xylene metabolite, was generally not decreased by ethanol and sometimes the reverse seemed to be the case. The disturbance of xylene kinetics can be hypothesized to be caused mainly by ethanol-mediated inhibition of microsomal metabolism. When four volunteers who ingested ethanol prior to m-xylene inhalation at the higher concentration were monitored for blood acetaldehyde, transiently raised levels were found without notable effects on ethanol elimination. This observation may explain why some individuals experienced dizziness and nausea during the combined ethanol-xylene exposure.

Acetaldehyde↗

PubMed1980

Effect of toluene and xylenes on liver glutathione and their urinary excretion as mercapturic acids in the rat.

Administration of toluene and xylenes to rats caused a decrease in liver glutathione concentration. The effect was most pronounced after the administration of o-xylene. 26% of the initial glutathione level was found three hours after treatment with o-xylene (4.0 mmoles/kg). No in vitro conjugation of o-xylene with glutathione was observed, neither spontaneously nor in the presence of 105,000 g supernatant from rat liver homogenate, containing glutathione S-transferases. Thus, a metabolite of o-xylene, which is not formed during incubation with 105,000 g supernatant, reacts with glutathione. A thioether was isolated from urine of rats given o-xylene; the compound was identified as o-methylbenzyl mercapturic acid by GC-MS and NMR. Chromatographic evidence was found for the presence of benzyl mercapturic acid in the urine of toluene-treated rats. The amounts of mercapturic acids excreted in the urine after administration of toluene, p-xylene, m-xylene, and o-xylene were 0.4-0.7,0.6,1.3, and 10-21% of the dose, respectively. These results demonstrate the involvement of a thusfar unknown pathway in the biotransformation of toluene and xylenes.

Acetylcysteine↗

PubMed1991

Urinary methylhippuric acid isomer levels after occupational exposure to a xylene mixture.

The quantitative relationship between exposure to xylene vapor and urinary excretion of methylhippuric acid (MHA) isomers were studied in the second half of a working week. The participants in the study were 121 male workers engaged in dip-coating of metal parts who were predominantly exposed to three xylene isomers. The intensity of exposure measured by diffusive sampling during an 8-h shift was such that the geometric mean vapor concentration was 3.8 ppm for xylenes (0.8 ppm for o-xylene, 2.1 ppm for m-xylene, and 0.9 ppm for p-xylene), 0.8 ppm for toluene, and 0.9 ppm for ethylbenzene. Urine samples were collected at the end of the shift and analyzed for metabolities by HPLC. The statistical analysis showed that there is a linear relationship between the intensity of exposure to xylenes and the concentration of MHA in urine, that the regression line passes very close to the origin, and that the increment in observed (i.e., noncorrected) MHA concentrations as a function of increasing xylene concentration was 17.8 mg x l-1 ppm-1. Further examination on the basis on individual xylene isomers showed that the slopes of the regression lines for o- and m-isomers were similar (i.e., 17.1 and 16.6 mg l-1 ppm-1, respectively), whereas that for p-xylene was larger (21.3 mg l-1 ppm-1).

Air Pollutants, Occupational↗

PubMed1993

Enzyme induction by ethanol consumption affects the pharmacokinetics of inhaled m-xylene only at high levels of exposure.

The experimental study with rats was undertaken to verify the working hypothesis that enzyme induction caused by ethanol consumption affects the kinetics of m-xylene only at a high level of exposure. m-Xylene was administered to ethanol-treated rats either perorally (0.01, 0.02 or 0.1 ml/kg) or by inhalation (50, 100 or 500 ppm each for 6 h) and the concentration of m-xylene in the blood and the urinary excretion of a m-xylene metabolite (m-methyl hippuric acid or m-MHA) were measured with time. The ethanol consumption, which increased the in vitro m-xylene metabolism about 5-fold, had no effect on the metabolism of inhaled m-xylene in vivo until the exposure concentration was raised to 500 ppm. On the other hand, metabolism of m-xylene after oral administration was markedly enhanced at any dose by the consumption, as evidenced by a decrease in the blood concentration of m-xylene together with an increase in the urinary excretion of m-MHA. These findings indicate that enzyme induction does not affect the pharmacokinetics of inhaled m-xylene when its exposure concentration is low. This may be because the hepatic blood flow, rather than the enzyme activity, rate-limits the metabolism of m-xylene, which is highly metabolized in the liver.

Administration, Inhalation↗

PubMed1986

A comparative study of the effects of benzene, toluene, and xylenes on their in vitro metabolism and drug-metabolizing enzymes in rat liver.

Male Sprague-Dawley rats were injected ip with benzene, toluene, or a mixture of xylene isomers at 20 mmol hydrocarbon/kg daily for 3 days. The effects of administration of these hydrocarbons upon their own in vitro metabolism, as well as upon cytochrome P-450, NADPH-cytochrome c reductase, aminopyrine N-demethylase, aniline hydroxylase, glutathione, glutathione S-transferase, and UDPglucuronyltransferase in liver were studied. Each hydrocarbon studied increased its own in vitro metabolism. Benzene had no effect on the metabolism of toluene or xylenes. Toluene and xylenes increased the metabolism of benzene, toluene, and xylenes. Cytochrome P-450 was elevated by toluene and xylenes, but was not affected by benzene. NADPH-cytochrome c reductase was induced by all three hydrocarbons. Aminopyrine N-demethylase and aniline hydroxylase were induced by toluene and xylenes and were not affected by benzene. Glutathione was elevated by benzene, decreased by xylenes, and not affected by toluene. Glutathione S-transferase was induced differentially by these hydrocarbons toward various substrates: toward 1-chloro-2,4-dinitrobenzene by benzene and toluene, toward 1,2-dichloro-4-nitrobenzene by benzene and xylenes, and no effect toward 1,2-epoxy-3-(p-nitrophenoxy)propane by any hydrocarbons. UDPglucuronyltransferase was induced by benzene and toluene when o-aminophenol and phenol were used as the substrate. Xylenes had no effect. Benzene was more effective at inducing conjugation enzymes. Xylenes were more effective at inducing cytochrome P-450 dependent enzymes. Toluene was equipotent at inducing both types of enzymes. The results indicate that the addition of methyl groups to the aromatic ring affects the inductive pattern of these monocyclic aromatic hydrocarbons.

Animals↗

PubMed1992

Effect of p-xylene inhalation on the bioactivation of bromobenzene in rat lung and liver.

It is unclear whether the pneumotoxicity observed with bromobenzene (BB) in phenobarbital-induced rats is related to BB bioactivation in lung, liver or both. To help differentiate pulmonary from hepatic bioactivation, BB was administered alone and in combination with p-xylene, which inhibits pulmonary but induces hepatic cytochromes P450. Exposure to p-xylene alone (3400 ppm for 4 hr) produced no changes in bronchoalveolar lavage fluid (BALF) measurements (gamma-glutamyl transpeptidase, lactate dehydrogenase, protein, white blood cell count) or serum sorbitol dehydrogenase. p-Xylene increased hepatic microsomal benzyloxy- (BROD), pentoxy- (PROD), and ethoxy- (EROD) resorfuin O-dealkylase activities but decreased pulmonary microsomal BROD and PROD. Immunoblot analysis revealed an induction of hepatic but not pulmonary microsomal P450IIB apoprotein. When rats were exposed to p-xylene (2800 ppm) or room air for 4 hr, treated 12 hr later with BB (0.5 ml/kg, ip) or corn oil, and killed after 12 hr, p-xylene increased hepatic P450IIB (27-fold) concomittant with a similar increase in BROD activity. p-Xylene also increased hepatic P450IA apoprotein (3.4-fold) with a complimentary increase in EROD activity. p-Xylene potentiated BB-induced hepatotoxicity. In pulmonary microsomes p-xylene and BB each produced similar decreases in both EROD and BROD activities. The combination of p-xylene and BB had an additive effect on pulmonary P450IA1 reduction. BALF analysis and histopathology revealed no pneumotoxicity with any treatment. p-Xylene potentiation of BB-induced hepatotoxicity without pneumotoxicity suggests that the liver does not produce metabolites of BB which are directly involved in pulmonary damage.

Administration, Inhalation↗

PubMed1992

Sex differences in the bioavailability of soil-adsorbed m-xylene in orally exposed rats.

The bioavailability of soil-adsorbed m-xylene was assessed in male and female rats gavaged with an aqueous suspension of 14C-m-xylene alone or adsorbed to sandy or clay soil. Sex-related differences were observed in the rate and the amount of m-xylene-derived radioactivity absorbed and excreted in the presence of the soils. A higher peak plasma concentration of radioactivity was observed in females following treatment with sandy soil-adsorbed m-xylene. Further, sandy and clay soil-adsorbed chemicals demonstrated significantly longer absorption half-lives (t1/2), while sandy soil produced a shorter elimination t1/2 vs. m-xylene alone in female rats. Increased bioavailability of sandy soil-adsorbed m-xylene in females was evidenced by a significantly increased area under the plasma concentration time curve (AUC). Neither of the soils altered the maximum plasma concentration, the rate at which xylene-derived radioactivity was absorbed or eliminated, or the AUC in male rats. Fat contained the highest tissue concentration of xylene-derived radioactivity in all treatment groups of both sexes. Further, in all male and female treatment groups m-xylene was primarily metabolized and excreted in urine with methyl hippuric acid identified as the main urinary metabolite. Sandy soil slightly delayed urinary excretion in females while both soils increased expired air excretion in males compared to m-xylene alone. Methylhippuric acid was the main urinary metabolite in all groups.

Administration, Oral↗

PubMed1990

Comparison of three sampling and analytical methods for measuring m-xylene in expired air of exposed humans.

Three breath sampling and analytical methods were tested following exposure of 12 subjects for 4 hr to 75 ppm m-xylene in a controlled environmental chamber. Mixed-expired breath was sampled for m-xylene from all 12 subjects with a new stainless steel device that permits continuous mainstream or sidestream sampling of the solvents present. The m-xylene was sampled from the mainstream using charcoal cloth and from the sidestream using Tenax TA. Alveolar breath also was sampled for m-xylene from 6 of these subjects using bags. The carbon dioxide concentrations of the mixed and alveolar samples, obtained from these 6 subjects, were also determined and used to assess the accuracy of the mixed-expired sampling and analytical procedures. Breath sampling was conducted over the immediate 240-min postexposure period. All m-xylene samples were analyzed using gas chromatography with flame ionization detection. Carbon dioxide concentrations were determined with an infrared analyzer. Nonlinear regression analysis was used to model the desaturation of m-xylene via the breath. Overall, the desaturation of m-xylene from all subjects by all methods was best described using three-compartment pharmacokinetic models. The precision of each sampling and analytical method, estimated from the residual variabilities of the desaturation curves were 0.13 for alveolar sampling, 0.14 for mainstream-mixed sampling (12 subjects), and 0.23 for sidestream-mixed sampling (12 subjects). For all 12 subjects, the breath m-xylene concentrations determined by sidestream-mixed sampling averaged 83% of those determined by mainstream-mixed sampling; this bias was significant. For the 6 subjects from whom both mixed-expired and alveolar breath samples were obtained, the average m-xylene desaturation rates determined by both mainstream-mixed and alveolar sampling were comparable but substantially different from those determined by sidestream-mixed sampling. For these subjects, comparison of the average and individual mixed to alveolar ratios of m-xylene and carbon dioxide showed that mainstream-mixed sampling was accurate and that sidestream-mixed sampling was not.

Air Pollutants, Occupational↗

PubMed1994

Anaerobic degradation of toluene and o-xylene by a methanogenic consortium.

Toluene and o-xylene were completely mineralized to stoichiometric amounts of carbon dioxide, methane, and biomass by aquifer-derived microorganisms under strictly anaerobic conditions. The source of the inoculum was creosote-contaminated sediment from Pensacola, Fla. The adaptation periods before the onset of degradation were long (100 to 120 days for toluene degradation and 200 to 255 days for o-xylene). Successive transfers of the toluene- and o-xylene-degrading cultures remained active. Cell density in the cultures progressively increased over 2 to 3 years to stabilize at approximately 10(9) cells per ml. Degradation of toluene and o-xylene in stable mixed methanogenic cultures followed Monod kinetics, with inhibition noted at substrate concentrations above about 700 microM for o-xylene and 1,800 microM for toluene. The cultures degraded toluene or o-xylene but did not degrade m-xylene, p-xylene, benzene, ethylbenzene, or naphthalene. The degradative activity was retained after pasteurization or after starvation for 1 year. Degradation of toluene and o-xylene was inhibited by the alternate electron acceptors oxygen, nitrate, and sulfate. Degradation was also inhibited by the addition of preferred substrates such as acetate, H2, propionate, methanol, acetone, glucose, amino acids, fatty acids, peptone, and yeast extract. These data suggest that the presence of natural organic substrates or contaminants may inhibit anaerobic degradation of pollutants such as toluene and o-xylene at contaminated sites.

Anaerobiosis↗

PubMed1995

m-xylene toxicokinetics in phenobarbital-treated rats: comparison among inhalation exposure, oral administration, and intraperitoneal administration.

Rats, pretreated with phenobarbital (PB) for 3 days (80 mg/kg/day), were challenged with m-xylene orally or intraperitoneally at a small (0.01 ml/kg or 0.081 mmol/kg) or a large (0.10 ml/kg or 0.814 mmol/kg) dose, or by 6-hr inhalation exposure at a low (40 ppm) or a high (400 ppm) concentration. The concentrations of m-xylene and its major metabolite, m-methyl hippuric acid (m-MHA), were measured over time in the blood and urine, respectively. PB treatment, which increased the hepatic metabolism of m-xylene in vitro about sixfold, had a significant effect on the metabolism of inhaled m-xylene (decreased blood m-xylene concentration together with increased urinary excretion of m-MHA) only at a high exposure concentration (400 ppm). On the other hand, the enzyme induction had a significant effect on the metabolism of orally administered m-xylene either at a small (0.081 mmol/kg) or a large (0.814 mmol/kg) dose, due to the first-pass metabolism that plays a great role in this route. When m-xylene was administered intraperitoneally, the effect of enzyme induction was shown only at the large dose, a finding which suggests that intraperitoneal administration is more similar to inhalation exposure than oral administration. However, in agreement with oral administration but in contrast to inhalation exposure, PB treatment increased the urinary excretion of m-MHA only shortly after intraperitoneal administration of m-xylene, with no significant increase occurring in the total amount of m-MHA excreted in the urine, despite the great difference in the blood m-xylene concentration between PB-treated and control rats.

Administration, Inhalation↗