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PubMed1998

Particle-bound benzene from diesel engine exhaust.

OBJECTIVES: The large surface area of the carbon core of diesel exhaust particles may contribute to the adsorption or condensation of such volatile carcinogenic organic compounds as benzene. The attention of this study focused on determining the distribution of benzene between the gas and particulate phases in the breathing zone of bus garage workers. METHODS: Benzene and suspended particulate matter were evaluated jointly in the air of a municipal bus garage. Personal passive monitors were used for benzene sampling in the breathing zone of the workers. Active samplers were used for sampling diesel exhaust particles and the benzene associated with them. The benzene levels were measured by gas chromatography. RESULTS: Diesel engine exhaust from buses was the main source of air pollution caused by benzene and particles in this study. The concentration of benzene in the gas and particulate phases showed a wide range of variation, depending on the distance of the workplace from the operating diesel engine. Benzene present in the breathing zone of the workers was distributed between the gas and particulate phases. The amounts of benzene associated with particles were significantly lower in summer than in winter. CONCLUSIONS: The particulate matter of diesel exhaust contains benzene in amounts comparable to the concentrations of carcinogenic polycyclic aromatic hydrocarbons (PAH) and the usually found nitro-PAH. The concentration of benzene in the gas phase and in the suspended particulate matter of air can serve as an additional indicator of exposure to diesel exhaust and its carcinogenicity.

Analysis of Variance↗
PubMed1988

Carcinogenicity of benzene, toluene and xylene: epidemiological and experimental evidence.

Benzene. The evidence for carcinogenicity of benzene in humans was evaluated by the IARC in 1982 as follows: "It is established that human exposure to commercial benzene or benzene-containing mixtures can cause damage to the haematopoietic system, including pancytopenia. The relationship between benzene exposure and the development of acute myelogenous leukaemia has been established in epidemiological studies. "Reports linking exposure to benzene with other malignancies were considered to be inadequate for evaluation. "There is sufficient evidence that benzene is carcinogenic to man." This evaluation now warrants some elaboration and updating. While the epidemiological evidence concerning benzene carcinogenicity is strongest for acute myelocytic leukaemia, there is some limited evidence of increased risks of chronic myeloid and chronic lymphocytic leukaemia. In addition, recent studies have suggested an increased risk of multiple myeloma, while others indicate a dose-related increase for total lymphatic and haematopoietic neoplasms. Corroborative evidence for such a generalized effect comes from experimental studies showing that exposure to benzene depresses all lympho-haematopoietic cell lines. While only limited evidence of benzene carcinogenicity in experimental animals exists, the recent findings of the National Toxicology Program (NTP, 1984) in the U.S.A. and Maltoni et al. (1985) strongly indicate that benzene is an experimental carcinogen. Toluene and xylene. While no direct human evidence is available, there is recent evidence of carcinogenicity of toluene and xylene at high concentrations in experimental animals. It should also be noted that any future epidemiological observations of cancer risks associated with toluene or xylene would have to take account of the suspected effects of benzene impurities.

Animals↗
PubMedDate not supplied

Temporal variability of benzene exposures for residents in several New Jersey homes with attached garages or tobacco smoke.

The U.S. Environmental Protection Agency's (EPA) previous TEAM studies of personal exposure to VOCs for 700 residents in several U.S. cities found that indoor air concentrations were often higher than outdoor levels. Several potential sources of benzene exposure were identified, including environmental tobacco smoke and materials or activities associated with attached garages. Indoor, personal, and outdoor monitoring was conducted at eleven New Jersey homes over multiple 12-hr monitoring periods. One study objective was to assess the impact of attached garages on human exposure to benzene and the variability of benzene exposure across time. Benzene was also measured in several homes inhabited by smokers and in homes without known combustion sources for comparative purposes. At homes with a garage or environmental tobacco smoke, mean indoor and personal benzene concentrations were two to five times higher than outdoor levels at all but one home. Mean personal exposures ranged from 8 to 31 micrograms/m3. Indoor/outdoor ratios were calculated and ranged from 0.8 to 11. Benzene levels in the four garages ranged from 3 to 196 micrograms/m3 and usually were higher than either indoor living areas or personal levels. Multi-zone air exchange rates were measured, and benzene source strengths in each zone were estimated. Garage source strength estimates for benzene ranged from 310 to 52,000 micrograms/h. The mass transfer of benzene from sources in the garage to home living areas was also large in three of the homes, ranging from 730 to 26,000 micrograms/h. Materials or activities in the garage were a source of benzene exposure for the residents in these three homes. Large temporal variations (factors of 2 to 30) were observed in indoor and personal benzene concentrations, indoor/outdoor ratios, and source strengths over the six or ten monitoring periods at each home. Changes in outdoor air benzene levels were an underlying factor in changing exposure levels, with indoor sources further elevating indoor air levels and personal exposures.

Air Pollution, Indoor↗
PubMedDate not supplied

Gas chromatographic/mass spectrometric determination of benzene in nonstick cookware and microwave susceptors and its migration into foods on cooking.

Benzene in poly(tetrafluoroethylene) (PTFE) coatings of nonstick cookware was determined by heating a small amount of coating in a sealed vial. Gas chromatography/mass spectrometry (GC/MS) was used to analyze the vial headspace for benzene. A small survey (26 samples) of retail nonstick cookware detected benzene ranging from 2 to 50 micrograms/dm2 in 7 samples. Nonstick frying pans with various polymer coatings were obtained directly from 1 manufacturer. Benzene (6-30 micrograms/dm2) was detected in a number of these samples and was attributed to the use of a phenylmethyl silicone ingredient that contained benzene at 360 mg/kg. To determine the possible transfer of benzene from these coatings during normal use, several foods (puddings, cakes, and roast potatoes) were prepared in previously unused cookware. The foods were analyzed by using static headspace GC/MS. Benzene was not detected in any of these foods at a limit of detection of 2 micrograms/kg. In related studies, the determination of benzene release from microwave susceptors was performed by heating the materials in a sealed system at 190 degrees C for 4 min. Benzene release above 1 microgram/dm2 was not detected in 24 samples of susceptors. However, 1 specially supplied sample of non-metallized susceptor released 10 micrograms/dm2 benzene when heated above normal anticipated temperatures of usage (to 220 degrees C). Foods such as french fries and pizza when cooked according to the manufacturer's instructions in susceptors contained no benzene with a limit of detection of 2 micrograms/kg. Even under abuse conditions of susceptors, the transfer of benzene to foods remained below this limit.

Benzene↗
PubMed2005

Vibrational spectroscopy of Ni+ (benzene)n complexes in the gas phase.

Ni+ (benzene)n (n = 1-6) and Ni+ (benzene)n Ar(1,2) (n = 1,2) are produced by laser vaporization in a pulsed nozzle cluster source. The clusters are mass selected and studied by infrared laser photodissociation spectroscopy in a reflectron time-of-flight mass spectrometer. The excitation laser is an OPO/OPA system that produces tunable IR in the C-H stretching region of benzene. Photodissociation of Ni+ (benzene)n complexes occurs by the elimination of intact neutral benzene molecules, while Ni+ (benzene)n Ar(1,2) complexes lose Ar. This process is enhanced on resonances, and the vibrational spectrum is obtained by monitoring the fragment yield versus the infrared wavelength. Vibrational bands in the 2700-3300 cm(-1) region are characteristic of the benzene molecular moiety with systematic shifts caused by the metal bonding. A dramatic change in the IR spectrum is seen at n = 3 and is attributed to the presence of external benzene molecules acting as solvent molecules in the cluster. The results of previous theoretical calculations are employed to investigate the structures, energetics, and vibrational frequencies of these complexes. The mono-benzene complex is found to have a C2v structure, with benzene distorted by the metal pi-bonding. The di-benzene complex is found to have a D2h structure, with both benzenes distorted. The comparison between experiment and theory provides intriguing new insight into the bonding in these prototypical pi-bonded organometallic complexes.

Journal Article↗
PubMed2005

Computer simulation investigation of the water-benzene interface in a broad range of thermodynamic States from ambient to supercritical conditions.

The dependence of the properties of the water-benzene system on the thermodynamic conditions in a broad range of temperatures and pressures has been investigated by computer simulation methods. For this purpose, Monte Carlo simulations have been performed at 23 different thermodynamic states, ranging from ambient to supercritical conditions. The density profiles of the water and benzene molecules have been determined at each of the thermodynamic states investigated. Information on the dependence of the mutual solubility of the two components in each other as well as of the width of the interface on the temperature and pressure has been extracted from these profiles. The width of the interface has been found to increase with increasing temperature up to a certain point, where it diverges. The temperature of this divergence corresponds to the mixing of the two phases. The determination of the critical mixing temperature at various pressures allowed us to estimate the upper critical curve, separating the two-phase and one-phase liquid systems, of the phase diagram of the simulated water-benzene system. In analyzing the preferential orientation of the interfacial molecules relative to the interface, it has been found that the main orientational preference of the benzene molecules is to lie parallel with the plane of the interface, and the water molecules penetrated deepest into the benzene phase prefer to stay perpendicular to the interface, pointing by one of their O-H bonds almost straight toward the benzene phase, whereas the waters located at the aqueous side of the interface are preferentially aligned parallel with the interfacial plane. Although the strength of the observed orientational preferences decreases rapidly with increasing temperature, the preferred orientations themselves are found to be independent of the thermodynamic conditions. Remains of the orientational preferences of the molecules are found to be present up to temperatures as high as 650 K. The analysis of the relative orientation of the neighboring water-benzene pairs has revealed that the radius of the first hydration shell of the benzene molecules is independent of the thermodynamic conditions, even if the system consists of one single phase. It has been found that the nearest water neighbors of the benzene molecules are preferentially located above and below the benzene ring, whereas more distant water neighbors, belonging still to the first hydration shell, prefer to stay within the plane of the benzene molecule. In the two-phase systems the dipole vector of the nearest waters has been found to be preferentially perpendicular to the vector pointing from the center of the benzene molecule to the water O atom.

Journal Article↗
PubMed2005

Reactions of benzene oxide with thiols including glutathione.

S-Phenylmercapturic acid is a minor metabolite of benzene used as a biomarker for human benzene exposures. The reaction of intracellular glutathione with benzene oxide-oxepin, the initial metabolite of benzene, is presumed to give 1-(S-glutathionyl)-cyclohexa-3,5-dien-2-ol, which undergoes dehydration to S-phenylglutathione, the precursor of S-phenylmercapturic acid. To validate the proposed route to S-phenylglutathione, reactions of benzene oxide-oxepin with glutathione and other sulfur nucleophiles have been studied. The reaction of benzene oxide with an excess of aqueous sodium sulfide, followed by acetylation, gave bis-(6-trans-5-acetoxycyclohexa-1,3-dienyl)sulfide, the structure of which was proved by X-ray crystallography. Reactions of benzene oxide-oxepin in a 95:5 (v/v) mixture of phosphate buffer in D2O with (CD3)2SO were monitored by 1H NMR spectroscopy. In the absence of glutathione, the half-life of benzene oxide-oxepin was ca. 34 min at 25 degrees C and pD 7.0. The half-life was not affected in the range of 2-15 mM glutathione in the presence and absence of a commercial sample of human glutathione S-transferase (at pH 7.0, 8.0, 8.5, or 10.0). The adduct 1-(S-glutathionyl)-cyclohexa-3,5-diene-2-ol was identified in these reaction mixtures, especially at higher pH, by mass spectrometry and by its acid-catalyzed decomposition to S-phenylglutathione. Incubation of benzene oxide with N-acetyl-L-cysteine at 37 degrees C and pH 10.0 and subsequent mass spectrometric analysis of the mixture showed formation of pre-S-phenylmercapturic acid and the dehydration product, S-phenylmercapturic acid. The data validate the premise that benzene oxide-oxepin can be captured by glutathione to give (1R,2R)- and/or (1S,2S)-1-(S-glutathionyl)-cyclohexa-3,5-dien-2-ol, which dehydrate to S-phenylglutathione. The capture is a relatively inefficient process at pH 7 that is accelerated at higher pH. These studies account for the observation that the metabolism of benzene is dominated by the formation of phenol. The pathway leading to S-phenylmercapturic acid is necessarily minor on account of the low efficiency of benzene oxide capture by glutathione at pH 7 vs spontaneous rearrangement to phenol.

Cyclohexanes↗
PubMed2006

The presumptive detection of benzene in water in the presence of phenol with an active membrane-UV photo-ionisation differential mobility spectrometer.

Studies with a new technique, active membrane-differential mobility spectrometry, with aqueous standards of benzene and phenol are described. The atmospheric pressure photo-ionisation chemistries of benzene and phenol in the presence of oxygen are similar in that benzene forms phenol radicals that subsequently react to yield diphenylether and 4-phenoxyphenol products. Further phenol sequesters charge from benzene ions leading to a significant loss of sensitivity. This is an important consideration in the development of screening techniques for the presence of benzene in environmental water samples. This challenge was addressed by including a pre-separation stage prior to photo-ionisation, and a 10 cm long polydimethylsiloxane active membrane inlet using nitrogen as a carrier gas was used to sample, concentrate and deliver low resolution separations to the 10.6 eV UV-ionisation region of a differential mobility spectrometer. Acetone was also proposed as a charge carrier for the UV photo-ionisation source; to promote phenol protonation and inhibit charge sequestration from benzene. The responses of the system to aqueous standards of benzene and phenol with and without acetone doping at 10.2 mg m(-3) were evaluated and four to five-fold increases in sensitivity were obtained with acetone doping. With a sampling time of 60 s and a total measurement cycle of 180 s it was possible to obtain quantitative responses to single standards over the concentration range 6 to 177 microg cm(-3) with linear correlations with R(2) values ranging from 0.97 to 0.99. The effects of the heating rate of the membrane and the dispersion field strength of the differential mobility spectrometer on sensitivity and the differentiation of benzene from phenol responses were optimised, leading to a configuration where a voltage heating programme of 4.75 V s(-1) was applied to a 124 microm stainless steel wire heating element within the active membrane, and a dispersion field strength of 22 kV cm(-1) was used to test a mixture of benzene (14 microg cm(-3)) and phenol (6 microg cm(-3)) in water. The presence of benzene was identified through the presence of a peak corresponding to a benzene response, V(C) = -9 V FWHM = 1 V, that followed the thermal desorption profile of benzene.

Journal Article↗
PubMed2001

Physiologically based pharmacokinetic modeling of benzene metabolism in mice through extrapolation from in vitro to in vivo.

Benzene (C6H6) is a highly flammable, colorless liquid. Ubiquitous exposures result from its presence in gasoline vapors, cigarette smoke, and industrial processes. Benzene increases the incidence of leukemia in humans when they are exposed to high doses for extended periods; however, leukemia risks in humans at low exposures are uncertain. The exposure-dose-response relationship of benzene in humans is expected to be nonlinear because benzene undergoes a series of metabolic transformations, detoxifying and activating, in the liver, resulting in multiple metabolites that exert toxic effects on the bone marrow. We developed a physiologically based pharmacokinetic model for the uptake and elimination of benzene in mice to relate the concentration of inhaled and orally administered benzene to the tissue doses of benzene and its key metabolites, benzene oxide, phe nol, and hydroquinone. As many parameter values as possible were taken from the literature; in particular, metabolic parameters obtained from in vitro studies with mouse liver were used since comparable parameters are also available for humans. Parameters estimated by fitting the model to published data were first-order rate constants for pathways lacking in vitro data and the concentrations of microsomal and cytosolic protein, which effectively alter overall enzyme activity. The model was constrained by using the in vitro metabolic parameters (maximum velocities, first-order rate constants, and saturation parameters), and data from multiple laboratories and experiments were used. Despite these constraints and sources of variability, the model simulations matched the data reasonably well in most cases, showing that in vitro metabolic constants can be successfully extrapolated to predict in vivo data for benzene metabolism and dosimetry. Therefore in vitro metabolic constants for humans can subsequently be extrapolated to predict the dosimetry of benzene and its metabolites in humans. This will allow us to better estimate the risks of adverse effects from low-level benzene exposures.

Administration, Inhalation↗
PubMed2001

Development of a novel bioreactor system for treatment of gaseous benzene.

A novel, continuous bioreactor system combining a bubble column (absorption section) and a two-phase bioreactor (degradation section) has been designed to treat a gas stream containing benzene. The bubble column contained hexadecane as an absorbent for benzene, and was systemically chosen considering physical, biological, environmental, operational, and economic factors. This solvent has infinite solubility for benzene and very low volatility. After absorbing benzene in the bubble column, the hexadecane served as the organic phase of the two-phase partitioning bioreactor, transferring benzene into the aqueous phase where it was degraded by Alcaligenes xylosoxidans Y234. The hexadecane was then continuously recirculated back to the absorber section for the removal of additional benzene. All mass transfer and biodegradation characteristics in this system were investigated prior to operation of the integrated unit, and these included: the mass transfer rate of benzene in the absorption column; the mass transfer rate of benzene from the organic phase into the aqueous phase in the two-phase bioreactor; the stripping rate of benzene out of the two-phase bioreactor, etc. All of these parameters were incorporated into model equations, which were used to investigate the effects of operating conditions on the performance of the system. Finally, two experiments were conducted to show the feasibility of this system. Based on an aqueous bioreactor volume of 1 L, when the inlet gas flow and gaseous benzene concentration were 120 L/h and 4.2 mg/L, respectively, the benzene removal efficiency was 75% at steady state. This process is believed to be very practical for the treatment of high concentrations of gaseous pollutants, and represents an alternative to the use of biofilters.

Alcaligenes↗
PubMed2003

Utility of a routine medical surveillance program with benzene exposed workers.

BACKGROUND: A medical surveillance program of benzene-exposed workers has to be established in such a way as to observe early signs of benzene-induced cytopenia, pancytopenia, or leukemia. This study evaluates the utility of routine medical survey applied to benzene-exposed workers by analyzing the hematological, immunological, and cytogenetic assay results. METHODS: The results of a previous study of hematological, immunological, and cytogenetic assays in benzene-exposed workers (up to 15 ppm) are used to discuss medical surveillance program by defining the relationship between various benzene exposure concentrations and toxic endpoints. RESULTS: Exposure to benzene concentration lower than 5 ppm does not produce any abnormal hematological measurements. For benzene cumulative exposure above 100 (ppm-years), some blood indices [mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), band neutrophils] show significant differences in comparison to the control group. The incidence of dicentric chromosomes was higher and the level of B-lymphocytes was lower even with workers exposed to 5 ppm of benzene; correlation with exposure indicators was not found. CONCLUSIONS: The results suggest that peripheral blood indices, although not sensitive enough, are still the most suitable parameters in a health surveillance program applied to benzene-exposed workers. B-lymphocytes could be a promising indicator of the benzene-induced damage. Cytogenetic tests did not prove to be suitable. Further investigation of useful screening tests for health surveillance program of benzene-exposed workers is still required.

Adult↗
PubMed2002

Kinetics of benzene biotransformation under microaerophilic and oxygen-limited conditions.

A special microbial consortium adapted to degrade petroleum hydrocarbons at limited availability of oxygen, transformed benzene, a highly toxic and carcinogenic contaminant of groundwater and soil, at low initial dissolved oxygen (DO) concentrations of 0.05-2 mg/L. The employed initial concentrations of dissolved oxygen were considerably lower than the previously reported values. Under these conditions, the overall transformation of benzene ranged from 34% +/- 1.7% to 100%, considerably higher than the theoretical predictions for complete mineralization of benzene based on the requirement of 3.08 mg oxygen/mg benzene. Unlike biotransformation that proceeded at the lowest examined DO concentration of 0.05 mg/L, the mineralization of benzene, defined by its conversion to CO(2) and water, required a minimum DO concentration of 0.2 mg/L. The mineralization of benzene under microaerophilic conditions (DO < 2 mg/L), ranged from 0.83% +/- 0.06% to 89% +/- 1.3%, which was less than the theoretical predictions at any given initial DO concentration. The regulatory effects of dissolved oxygen concentration or its partial pressure on the activities of enzymes catalyzing the biotransformation of aromatic hydrocarbons was postulated to account for the reduced mineralization of benzene. The ratio between the transformed benzene and the consumed oxygen increased with the decrease of initial DO concentration, reaching a value of 2.8, considerably higher than the theoretical value of 0.33 obtained for a complete aerobic oxidation of benzene. Phenol was the major and the most stable intermediate metabolite during the biotransformation of benzene at low concentrations of DO. While benzene transformation stopped after the depletion of oxygen in the experimental system, phenol continued to accumulate under strictly anaerobic conditions, indicating its formation from an alternative carbon source, possibly biomass.

Aerobiosis↗
PubMed1997

Benzene-induced hematotoxicity and bone marrow compensation in B6C3F1 mice.

Long-term inhalation exposure of benzene has been shown to cause hematotoxicity and an increased incidence of acute myelogenous leukemia in humans. The progression of benzene-induced hematotoxicity and the features of the toxicity that may play a major role in the leukemogenesis are not known. We report the hematological consequences of benzene inhalation in B6C3F1 mice exposed to 1, 5, 10, 100, and 200 ppm benzene for 6 hr/day, 5 days/week for 1, 2, 4, or 8 weeks and a recovery group. There were no significant effects on hematopoietic parameters from exposure to 10 ppm benzene or less. Exposure of mice to 100 and 200 ppm benzene reduced the number of total bone marrow cells, progenitor cells, differentiating hematopoietic cells, and most blood parameters. Replication of primitive progenitor cells in the bone marrow was increased during the exposure period as a compensation for the cytotoxicity induced by 100 and 200 ppm benzene. In mice exposed to 200 ppm benzene, the primitive progenitor cells maintained an increased percentage of cells in S-phase through 25 days of recovery compared with controls. The increased replication of primitive progenitor cells in concert with the reported genotoxicity induced by benzene provides the components necessary for producing an increased incidence of lymphoma in mice. Furthermore, we propose this mode of action as a biologically plausible mechanism for benzene-induced leukemia in humans exposed to high concentrations of benzene.

Animals↗
PubMed2001

Pharmacokinetic studies in Tg.AC and FVB mice administered [14C] benzene either by oral gavage or intradermal injection.

Chronic benzene toxicity has been demonstrated to result in either aplastic anemia or acute myelogenous leukemia, a form of granulocytic leukemia, in exposed people (Snyder and Kalf, Crit. Rev. Toxicol. 24, 177-209, 1994). Aplastic anemia has been demonstrated in animal models following benzene exposure but, heretofore, it has not been possible to replicate benzene-induced granulocytic leukemia in animals. The Tg.AC mouse appears to be the first animal model in which a granulocytic leukemia was produced by treatment with benzene (Tennant et al., The Use of Short- and Medium-Term Tests for Carcinogenic Hazard Evaluation, 1999; French and Saulnier, J. Toxicol. Environ. Health 61, 377-379, 2000). Leukemia was observed in Tg.AC mice to which benzene was administered dermally. Neither orally dosed Tg.AC mice or mice of the parental FVB strain treated by either route of exposure developed leukemia. It is well established that benzene metabolism is required to produce benzene toxicity. To determine whether metabolic differences arising from differences in route of exposure or strain of mouse directed the development of leukemia, the pharmacokinetics of benzene were compared between the two strains and between the two routes of administration. Regardless of the route of exposure or the strain of mouse, seven major metabolites plus unmetabolized benzene were detected in most samples at most time points. Few differences were observed between the two strains following either route of administration. These results suggest that the genetic modification in the Tg.AC mouse, i.e., insertion of the v-Ha-ras construct into the genome, did not disrupt any major pathways involved in determining the pharmacokinetics of benzene. Two significant differences were observed between the two routes of exposure: first, benzene was absorbed more slowly after intradermal injection than after oral gavage, and second, the intradermally dosed mice produced more conjugates of hydroquinone than did the orally dosed mice. These differences in metabolism may be involved in the previously observed differences in hematotoxicity between the two routes of exposure.

Administration, Oral↗
PubMed1994

Concentrations of benzene in blood and S-phenylmercapturic and t,t-muconic acid in urine in car mechanics.

Different parameters of biological monitoring were applied to 26 benzene-exposed car mechanics. Twenty car mechanics worked in a work environment with probably high benzene exposures (exposed workers); six car mechanics primarily involved in work organization were classified as non-exposed. The maximum air benzene concentration at the work places of exposed mechanics was 13 mg/m3 (mean 2.6 mg/m3). Elevated benzene exposure was associated with job tasks involving work on fuel injections, petrol tanks, cylinder blocks, gasoline pipes, fuel filters, fuel pumps and valves. The mean blood benzene level in the exposed workers was 3.3 micrograms/l (range 0.7-13.6 micrograms/l). Phenol proved to be an inadequate monitoring parameter within the exposure ranges investigated. The muconic and S-phenylmercapturic acid concentrations in urine showed a marked increase during the work shift. Both also showed significant correlations with benzene concentrations in air or in blood. The best correlations between the benzene air level and the mercapturic and muconic acid concentrations in urine were found at the end of the work shift (phenylmercapturic acid concentration: r = 0.81, P < 0.0001; muconic acid concentration: r = 0.54, P < 0.05). In conclusion, the concentrations of benzene in blood and mercapturic and muconic acid in urine proved to be good parameters for monitoring benzene exposure at the workplace even at benzene air levels below the current exposure limits. Today working as a car mechanic seems to be one of the occupations typically associated with benzene exposure.

Acetylcysteine↗
PubMed1992

S-phenylcysteine formation in hemoglobin as a biological exposure index to benzene.

Benzene is metabolized to intermediates that bind to hemoglobin, forming adducts. These hemoglobin adducts may be usable as biomarkers of exposure. In this paper, we describe the development of a gas chromatography/mass spectroscopy assay for quantitating the binding of the benzene metabolite, benzene oxide, to cysteine groups in hemoglobin. We used this assay to study the hemoglobin adduct, S-phenylcysteine (SPC), in the blood of rats and mice exposed to benzene either by inhalation or by gavage. We were able to detect SPC in the hemoglobin of exposed rats and mice, to show the linearity of the exposure dose-response relationship, and to establish the sensitivity limits of this assay. For the same exposure regime, rats showed considerably higher levels of SPC than did mice. As yet, we have not been able to detect SPC in the globin of humans occupationally exposed to benzene. We attempted to determine whether the SPC found in hemoglobin originated from the metabolism of benzene within or outside of the red blood cell. We hypothesized that the greatest red blood cell metabolism would be associated with peripheral reticulocytes, which retain high metabolic capacity. After exposing rats to benzene, we isolated the red blood cells and used discontinuous Percoll gradients to fractionate them into age groups. No differences in SPC levels were found among any of the fractions, suggesting that the SPC found in globin originates from the metabolism of benzene to benzene oxide in a location external to the red blood cell. To our knowledge, this is the first demonstration of the nonenzymatic binding of the benzene metabolite, benzene oxide, to protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Benzene degradation coupled with chlorate reduction in a soil column study.

Perchlorate and chlorate are electron acceptors that during reduction result in the formation of molecular oxygen. The produced oxygen can be used for activation of anaerobic persistent pollutants, like benzene. In this study chlorate was tested as potential electron acceptor to stimulate benzene degradation in anoxic polluted soil column. A chlorate amended benzene polluted soil column was operated over a period of 500 days. Benzene was immediately degraded in the column after start up, and benzene removal recovered completely after omission of chlorate or a too high influent chlorate concentration (22 mM). Mass balance calculations showed that per mole of benzene five mole of chlorate were reduced. At the end of the experiment higher loading rates were applied to measure the maximal benzene degradation rate in this system; a breakthrough of benzene was not observed. The average benzene degradation rate over this period was 31 micromol l(-1) h(-1) with a maximal of 78 micromol l(-1) h(-1). The high degradation rate and the necessity of chlorate indicate that oxygen produced during chlorate reduction indeed is used for the activation of benzene. This is the first column study where benzene biodegradation at a high rate coupled with anaerobic chlorate reduction is observed.

Anaerobiosis↗
PubMed1981

Modulation of benzene-induced lymphocytopenia in the rat by 2,4,5,2',4',5'-hexachlorobiphenyl and 3,4,3',4'-tetrachlorobiphenyl.

Repeated administration of benzene (440 mg/kg/day, s.c.) to 6-week-old male Fischer-344 rats resulted in a progressive decline in the number of circulating lymphocytes. Pretreatment of these animals with 2,4,5,2',4',5'-hexachlorobiphenyl (HCB) or 3,4,3',4'-tetrachlorobiphenyl (TCB) protected against benzene toxicity for as long as 7 days, but not after 10 days of repeated dosing. Representative phase I (mixed-function oxidase) and phase II (conjugating) enzyme activities were measured to determine whether the altered susceptibility to benzene toxicity in TCB- and HCB-pretreated rats could be correlated with changes in the profile of hepatic oxidative and detoxification pathways. Measurement of 7-ethoxycoumarin O-deethylase and benzphetamine N-demethylase activities indicated that the loss of protection by HCB or TCB against benzene toxicity after 7 days was not associated with changes in the activities of hepatic mixed-function oxidases inducible by 3-methylcholanthrene or phenobarbital. The time course for the stimulation by TCB and return to control values, of UDP-glucuronosyl transferase activity, a potential route for the elimination of benzene metabolites, mirrored the time course for the protection against toxicity. Epoxide hydratase activity was induced 2- to 3-fold by HCB. Although stimulation of this pathway could result in a decreased concentration of phenol, this activity did not decline with the loss of protection. Hepatic 10 000 X g supernatant fractions, prepared from livers of rats given TCB, were incubated with a non-saturating concentration of [14C] benzene (equivalent to 19 nmol/mg wet wt. tissue). Under these conditions the metabolism of benzene was depressed (40% of control) 2 days after pretreatment; after 14 days, the metabolism of benzene returned to control values. This pattern correlated temporarily with the protection against lymphocytopenia. The data indicate that the protection against benzene toxicity in rats pretreated with HCB or TCB is not necessarily related to the capacity of these compounds to induce phase I activities. In rats pretreated with TCB, the data suggest that decreasing the concentration of primary benzene metabolites, either by inhibiting the hepatic metabolism of benzene or increasing hepatic conjugation activity is an important factor modulating toxicity.

Animals↗