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A liquid chromatography tandem mass spectrometric method for in vivo dose monitoring of diepoxybutane, a metabolite of butadiene.

1,3-Butadiene, a common air pollutant formed in the combustion of organic matter, has been assessed by the U.S. EPA to be a strongly carcinogenic compound. This risk assessment is very uncertain because of the lack of information on the dose of the powerful carcinogenic metabolite diepoxybutane (DEB). This report presents an analytical method for in vivo dose monitoring of a unique marker for DEB. For a large number of alkylating agents in vivo doses are monitored by measurement by gas chromatography/mass spectrometry (GC/MS) of adducts to N-terminal valine in hemoglobin (Hb), using a modified Edman degradation method. This method is applicable to monofunctional epoxides from butadiene. However, in reaction with N-terminal valine, DEB forms an adduct which is ring-closed to a pyrrolidine, N,N-(2,3-dihydroxy-1,4-butadiyl)valine, with a tertiary amino group that prevents detachment of the alkylated valine by the Edman reagent. Therefore a method has been developed based on the analysis by liquid chromatography/electrospray ionization mass spectrometry (LC/ESI-MS) of the N-modified N-terminal peptides enriched after trypsin digestion of globin. In this study Hb samples from mice injected intraperitoneally with (+/-)-DEB were examined qualitatively and quantitatively with regard to the ring-closed adduct. The N-terminal pyrrolidine-heptapeptide was identified in treated mice. The highest adduct levels were obtained in samples from animals given the highest dose of DEB and the adduct levels were below the detection level in control mice.

Alkylation↗

Variability in human sensitivity to 1,3-butadiene: Influence of the allelic variants of the microsomal epoxide hydrolase gene.

The carcinogenic effects of 1,3-butadiene (BD), a chemical widely used in the rubber industry, are thought to be due to its epoxide metabolites. In humans, these epoxides are detoxified predominantly by hydrolysis, a reaction mediated by the microsomal epoxide hydrolase (mEH) enzyme. The mEH gene is polymorphic and the most common mEH coding-region variants detected in human populations are the two amino acid polymorphisms Tyr113His and His139Arg. Polymorphic amino acid substitutions at residues 113 and 139 in the human mEH protein can associate in four distinct combinations: Tyr113/His139, Tyr113/Arg139, His113/His139, and His113/Arg139. In vitro studies have shown that each of these genotypes has a unique mEH protein level that can affect net mEH enzymatic activity. In the current study, we examined the relationships among the genotypes involving these two polymorphisms and the mutagenic responses associated with occupational exposure to BD. We studied 49 nonsmoking workers from two styrene-butadiene rubber facilities in southeast Texas using the autoradiographic HPRT mutant lymphocyte assay as a biomarker of genotoxic effect. We genotyped the study participants simultaneously for both polymorphisms, using a multiplex PCR assay developed in our laboratory, and the subjects were assigned to a specific group based on the predicted mEH activity associated with their genotypes (low, intermediate, and high). In the study population, 67% were exposed to low BD levels of <150 ppb (measured by personal badge dosimeters) and 33% were exposed to >150 ppb (mean 2,244 ppb). In the BD low-exposure group, the mEH genotypes had no significant effect on the HPRT variant (mutant) frequency (Vf). In the high-exposure group (BD > 150 ppb), individuals with genotypes associated with low mEH activity had a significant (P < 0.05) 3-fold increase in HPRT Vf (Vf +/- SEM = 13.95 +/- 2.15 x 10(-6)) compared to high-activity individuals (4.41 +/- 1.19 x 10(-6)), and a 2-fold increase in Vf compared to intermediate-activity individuals (6.44 +/- 2.09 x 10(-6)). Our results indicate that mEH genotypes may play a significant role in human sensitivity to the genotoxic effects of exposure to BD.

Alleles↗

Segmentary effects on the renal proximal tubule due to hexachloro-1,3-butadiene in rats: biomarkers related to gender.

Renal tissue biomarkers (glutamine synthetase and p-aminohippuric acid uptake) were studied in male and female rats after treatment with hexachloro-1,3-butadiene. Reduced glutathione content also was also determined in liver and kidney. Histopathological examination (light microscopy) was then performed. The aim was to define sex differences in nephrotoxic effects caused by the solvent injected i.p. at 50, 100 and 200 mg kg(-1) dose. The rats were sacrificed 24 and 48 h after treatment; after 24 h a significant (P < 0.05) dose-dependent depletion of liver reduced glutathione was observed in male rats only; after 48 h male and female rats showed a significant (P < 0.05) increase at 50 and 100 mg kg(-1) doses. Reduced glutathione in the kidney was increased in male but not in female rats 24 and 48 h after treatment. Glutamine synthetase activity in renal tissue showed a significant (P < 0.05) dose-dependent decrease 24 and 48 h after treatment in both sexes, but is was significantly (P < 0.05) greater in female rats after 48 h. p-Aminohippuric acid uptake in renal cortical slices appeared significantly (P < 0.05) decreased in both sexes at the higher dose 24 h after treatment but this was significantly (P < 0.05) greater in female rats. A further significant (P < 0.05) impairment was observed after 48 h in males treated with a 200 mg kg(-1) dose. In addition, a slight but significant (P < 0.05) loss of p-aminohippuric acid uptake was observed 48 h after treatment with a 100 mg kg(-1) dose in both sexes. Light microscopy showed that the pars recta of the proximal tubule was mainly affected and tubular damage increased according to dose and time, involving the inner medulla and cortex. In conclusion, female rats show a significantly earlier and higher susceptibility of the kidney to toxic effects of hexachloro-1,3-butadiene.

Animals↗

Absence of detectable P450 2E1 in bone marrow of B6C3F1 mice: relevance to butadiene-induced bone marrow toxicity.

The observation that the concentration of butadiene monoepoxide (BMO) is greater in bone marrow than in the blood following inhalation of 1,3-butadiene (BD) by B6C3F1 mice prompted the present investigation into whether cytochrome P450 2E1, the isozyme believed to be involved in the epoxidation of BD, is present in the bone marrow of B6C3F1 mice. The bone marrow of male and female B6C3F1 mice was analyzed by Western blot analysis and immunohistochemistry to determine whether cytochrome P450 2E1 is present, and, if present, in which cell types. Both Western blot and immunohistochemical analyses revealed the apparent absence of P450 2E1 in B6C3F1 mouse bone marrow. This observation suggests that BD is converted to BMO outside of bone marrow and is subsequently concentrated in the bone marrow, or that the conversion of BD to BMO occurs by an alternate enzymatic pathway within the bone marrow.

Animals↗

Toxicology of 1,3-butadiene, chloroprene, and isoprene.

The diene monomers, 1,3-butadiene, chloroprene, and isoprene, respectively, differ only in substitution of a hydrogen, a chlorine, or a methyl group at the second of the four unsaturated carbon atoms in these linear molecules. Literature reviewed in the preceding sections indicates that these chemicals have important uses in synthesis of polymers, which offer significant benefits within modern society. Additionally, studies document that these monomers can increase the tumor formation rate in various organs of rats and mice during chronic cancer bioassays. The extent of tumor formation versus animal exposure to these monomers varies significantly across species, as well among strains within species. These studies approach, but do not resolve, important questions of human risk from inhalation exposure. Each of these diene monomers can be activated to electrophilic epoxide metabolites through microsomal oxidation reactions in mammals. These epoxide metabolites are genotoxic through reactions with nucleic acids. Some of these reactions cause mutations and subsequent cancers, as noted in animal experiments. Significant differences exist among the compounds, particularly in the extent of formation of highly mutagenic diepoxide metabolites, when animals are exposed. These metabolites are detoxified through hydrolysis by epoxide hydrolase enzymes and through conjugation with glutathione with the aid of glutathione S-transferase. Different strains and species perform these reactions with varying efficacy. Mice produce these electrophilic epoxides more rapidly and appear to have less adequate detoxification mechanisms than rats or humans. The weight of evidence from many studies suggests that the balance of activation versus detoxification offers explanation of differing sensitivities of animals to these carcinogenic actions. Other aspects, including molecular biology of the many processes that lead through specific mutations to cancer, are yet to be understood. Melnick and Sills (2001) compared the carcinogenic potentials of these three dienes, along with that of ethylene oxide, which also acts through an epoxide intermediate. From the number of tissue sites where experimental animal tumors were detected, butadiene offers greatest potential for carcinogenicity of these dienes. Chloroprene and then isoprene appear to follow in this order. Comparisons among these chemicals based on responses to external exposures are complicated by differences among studies and of species and tissue susceptibilities. Physiologically based pharmacokinetic models offer promise to overcome these impediments to interpretation. Mechanistic studies at the molecular level offer promise for understanding the relationships among electrophilic metabolites and vital genetic components. Significant improvements in minimization of industrial worker exposures to carcinogenic chemicals have been accomplished after realization that vinyl chloride caused hepatic angiosarcoma in polymer production workers (Creech and Johnson 1974; Falk et al. 1974). Efforts continue to minimize disease, particularly cancer, from exposures to chemicals such as these dienes. Industry has responded to significant challenges that affect the health of workers through efforts that minimize plant exposures and by sponsorship of research, including animal and epidemiological studies. Governmental agencies provide oversight and have developed facilities that accomplish studies of continuing scientific excellence. These entities grapple with differences in perspective, objectives, and interpretation as synthesis of knowledge develops through mutual work. A major challenge remains, however, in assessment of significance of environmental human exposures to these dienes. Such exposure levels are orders of magnitude less than exposures studied in experimental or epidemiological settings, but exposures may persist much longer and may involve unknown but potentially significant sensitivities in the general population. New paradigms likely will be needed for toxicological evaluation of these human exposures, which are ongoing but as yet are not interpreted.

Butadienes↗

Biological activation of 1,3-butadiene to vinyl oxirane by rat liver microsomes and expiration of the reactive metabolite by exposed rats.

When 1,3-butadiene is incubated with rat liver microsomes and NADPH both enantiomers of vinyl oxirane are formed, the amount of epoxide being dependent on incubation time, microsomal protein, and substrate concentration. Inhibition by SKF 525 A or dithiocarb as well as induction by pretreatment with phenobarbital or 20-methylcholanthrene suggest participation of cytochrome P-450 in this reaction. The amount of epoxide is enhanced by addition of 1,1,1-trichloropropene oxide and reduced by glutathione, especially in the presence of hepatic cytosol. When rats are exposed to 1,3-butadiene in a closed chamber (conditions of maximal metabolism) vinyl oxirane is exhaled and can be quantitatively determined from the gas phase. The concurrent exhalation of acetone is consistent with the idea of biologic action of a reactive metabolite.

Acetone↗

Evaluation of DNA damage by alkaline elution technique after inhalation exposure of rats and mice to 1,3-butadiene.

The alkaline filter elution technique was used to evaluate single strand breaks (SSB), DNA-DNA (DDCL) and DNA-protein cross-links (DPCL) in liver and lung of male rats (Sprague-Dawley) and male mice (B6C3F1) after exposure to 2000 ppm 1,3-butadiene (BD) for 7 days (7 h/day and/or to 100, 250, 500, 1000) 2000 ppm BD for 7 h. SSB were detected in liver DNA of both species at 2000 ppm. Cross-links are more pronounced in mouse lung than in mouse liver. Elution rates of lung DNA from mice exposed for 7 h to different concentrations of BD revealed an increase in cross-links between 250 and 500 ppm, and a further increase in cross-links up to 2000 ppm. No such signs of genotoxicity could be observed for the lung of rats. Our data support the involvement of reactive metabolites (epoxybutene and especially diepoxybutane) in butadiene-induced carcinogenesis in the mouse but not to that extent in the rat.

Animals↗

Personal exposure to 1,3-butadiene in a petrochemical plant, assessed by use of diffusive samplers.

OBJECTIVE: This study assessed personal exposure to 1,3-butadiene in a petrochemical plant after the threshold limit value (TLV) had been lowered to 1 part per million (ppm). Air samples were collected from the breathing zone of ten workers by use of diffusive samplers. The number of samples per participant was from three to 18. METHODS: Samples were collected by use of 3M 3500 passive monitors and analysed with a gas chromatograph (GC). Sampling proved to be simple and inexpensive, and laboratory analysis of 1,3-butadiene (BD) permits the analysis of 0.01 ppm in an 8 h sample. RESULTS: Altogether, 117 samples were analysed, of which 32 samples were under the limit of quantification (LOQ), 81 samples were between the LOQ and 1 ppm, and four samples exceeded the TLV. CONCLUSIONS: This study draws a new picture about the exposure level during BD production and how well adherence to the new TLV is being implemented. The data demonstrated that the TLV was rarely exceeded.

Butadienes↗

Genotoxic activity of 1,3-butadiene and nitrogen dioxide and their photochemical reaction products in Drosophila and in the mouse bone marrow micronucleus assay.

The genotoxic activity of a photochemical reaction mixture of 1,3-butadiene and nitrogen dioxide was investigated in vivo in the mouse bone marrow micronucleus assay and the somatic mutation and recombination test in Drosophila (the wing spot test). Butadiene alone was not mutagenic in Drosophila, but induced micronuclei in mice at 10 ppm after 23 h of exposure. Nitrogen dioxide was not genotoxic in either test system. The photochemical reaction products were toxic but probably not mutagenic in Drosophila and not genotoxic in mouse bone marrow. The in vivo results do not confirm earlier in vitro results that demonstrated a strong direct-acting mutagenic activity of the photochemical products in Salmonella.

Animals↗

Effect of short-term inhalation exposure to 1,3-butadiene on murine immune functions.

Interest in 1,3-butadiene (BD) as a potential immunomodulator was prompted by reports of an increased incidence of neoplasia in humans exposed to BD during the manufacture of styrene-butadiene synthetic rubber, and by a recent study which demonstrated a high incidence of thymic lymphomas in B6C3F1 mice. B6C3F1 mice were exposed to 1250 ppm BD by inhalation 6 hr per day, 5 days per week, for 6 or 12 weeks. Immune function assays were selected to evaluate specific humoral and cell-mediated immunity and spontaneous cytotoxicity; lymphoid organ histopathology was also evaluated. A slight decrease in antibody plaque-forming cells (PFC) per spleen was observed in exposed mice, although PFC per 10(6) splenic lymphocytes was normal. Significant extramedullary hematopoiesis and erythroid hyperplasia was observed in spleens from exposed mice, and correlated with a twofold increase in thymidine incorporation in spontaneously proliferating splenocytes. No differences in proliferation to alloantigens were demonstrable between control and BD-exposed splenocytes. Mitogenesis by phytohemagglutinin, Concanavalin A, and lipo polysaccharide was suppressed in splenocytes from exposed mice, but may have been due to the cellular dilution effect of hematopoietic activity. Cytotoxic T-lymphocyte generation was suppressed after a 6-week exposure to BD, but was comparable to controls after 12 weeks of exposure. No differences in spontaneous cytotoxicity were observed between control and exposed mice. Overall, no persistent immunological defects were detectable after inhalation exposure to this tumorigenic agent.

Administration, Inhalation↗

The fate of isoprene inhaled by rats: comparison to butadiene.

Isoprene (2-methyl-1,3-butadiene), a volatile monomer occurring in the natural environment and used in the manufacture of elastomers, is a close chemical relative of the animal carcinogen 1,3-butadiene. To obtain toxicokinetic data for inhaled isoprene, male F344 rats were exposed in groups of 30 to 14C-labeled isoprene vapor at four concentrations from 8 to 8200 ppm. The percentage of the inhaled isoprene that was metabolized decreased with increasing exposure concentration. The percentage of the total metabolites (that is, non-isoprene-retained 14C) excreted in urine and feces or expired was determined as a function of vapor concentration. About 75% of the total metabolites was excreted in urine. This was independent of inhaled isoprene concentration. After exposure to 8200 ppm, a larger percentage of the metabolites was excreted in feces than after exposure to lower concentrations. Using vacuum line techniques, blood metabolite concentrations were determined as functions of both vapor concentration and exposure duration. At one exposure concentration (1480 ppm) metabolites were measured in the nose, lungs, liver, kidney, and fat, as well as in blood. A mutagenic metabolite, isoprene diepoxide, was tentatively identified in all tissues examined. Between 0.0018 and 0.031% of the inhaled 14C label was tentatively identified as this metabolite in blood. The relative amount of the metabolites present in blood was highest for low concentrations of inhaled isoprene and for shorter exposure durations. Body fat appeared to be a reservoir for both isoprene metabolites and isoprene itself. The appearance of metabolites in the respiratory tract after short exposure durations together with low blood concentrations of isoprene indicated that substantial metabolism of inhaled isoprene in the respiratory tract may occur.

Administration, Inhalation↗

Sister-chromatid exchanges induced by 1.3-butadiene and its epoxides in CHO cells.

Sister-chromatid exchanges (SCEs) were analyzed in CHO cells after pulse treatment with 1,3-butadiene, 3,4-epoxy-1-butene (monoepoxybutene) and 1,2:3,4-diepoxybutane (diepoxybutane). A weak dose effect was observed after exposure to 1,3-butadiene but only in the presence of S9 mix. Monoepoxybutene and diepoxybutane were highly effective in inducing SCEs at concentrations of 0.1-1 microM both in the presence and in the absence of S9 mix. At higher concentrations the response was more pronounced without S9 mix.

Animals↗

Assessment of exposure to butadiene in the process industry.

Occupational exposure levels to 1,3-butadiene (BD) are variable but generally below 1 ppm in the European process industry. A preliminary analysis showed that hemoglobin adduct levels of butadiene monoxide (BMO) were increased among the worker groups with higher potential exposure to BD (process work, bomb voiding, repair duties) than among less exposed workers in maintenance and laboratory or control persons. In the same workers no exposure related effects were seen in the cytogenetic parameters studied, i.e. chromosomal aberrations, sister chromatid exchanges or micronuclei in peripheral blood lymphocytes. However, the glutathione-S-transferase polymorphism in the T1 gene might play a role in determining interindividual sensitivity to BD-induced chromosomal aberrations. Chromosomal aberrations (gaps excluded) were significantly (P < 0.05) increased among the workers lacking the GSTT1 gene as compared to the BD workers with the gene, while the other polymorphic GSTM1 gene showed no association with the cytogenetic parameters. More work needs to be done to study the adducts by other active BD metabolites than BMO and the role of the genetic polymorphisms controlling the variability of individual responses.

Butadienes↗

Mortality update of butadiene production workers.

This is a further update of a cohort mortality study of 2795 male workers employed at least 6 months between 1942 and 1994 at a 1,3-butadiene facility. Earlier reports on this cohort found a statistically significant deficit for all causes of death and lower than expected mortality for most leading causes of death. Prior reports noted an excess of deaths from lymphosarcoma primarily in those employed less than 10 years, first employed before 1946, and employed in jobs with the potential for daily exposure to butadiene (BD). There was a nonsignificant elevation for leukemia in persons potentially exposed to BD on an intermittent basis. The purpose of this update was to examine the patterns of mortality with four additional years of follow-up. Persons who had become eligible since the cohort was last updated through 1990 were also added. A total of 1222 deaths were identified, and death certificates were obtained for all but 20 of the deaths (1.6%). The standardized mortality ratio (SMR) for all causes of death is 88 (95% confidence interval (CI) = 83-93), and for all cancer, the SMR is 92 (95% CI = 82-104). There were 42 deaths from lymphohematopoietic cancers (LHC) with 28.6 expected (SMR = 147, 95% CI = 106-198), 9 observed vs. 4.7 expected deaths for lymphosarcoma (SMR = 191, 95% CI = 87-364), 13 observed vs. 11.5 expected deaths for leukemia (SMR = 113, 95% CI = 60-193), and 15 observed vs. 9.9 expected deaths from cancer of other lymphatic tissue (SMR = 152, 95% CI = 85-250). Subcohort analyses showed that the elevated risk of all LHC and its subcategories was restricted to persons who were first employed before 1950. As an adjunct to the SMR analyses, modeling was done using a qualitative cumulative exposure score as a time-dependent explanatory variable for, (1) all LHC (ICD 200-209); (2) lymphosarcoma (ICD 200); (3) lymphosarcoma and other lymphoma (ICD 200, 202); (4) multiple myeloma (ICD 203); and (5) leukemia (ICD 204-207). The cumulative exposure score was not significantly associated with any of these cancers. Cancer risk was found to increase with age for all of the LHC groups analyzed, except for lymphosarcoma. Similarly, cancer risk was found to increase with age-at-hire for all of the LHC groups except for multiple myeloma.

Butadienes↗

Risk assessment of butadiene for the Existing Substances Regulation (ESR) in the European Union.

The European Commission's Existing Substances Regulation (ESR) requires an evaluation of the risks to humans (workers, consumers and the general public) and the environment, posed by selected existing chemical substances. The Regulation focuses initially on high tonnage chemicals, and in this first year of the ESR, the UK undertook to produce the risk assessment document for 1,3-butadiene. This was in recognition of a need to reconsider the regulatory position in the light of new and ongoing research. In particular, the risk assessment was an opportunity to address the current debate over the animal toxicity data, where marked species differences exist, and the relevance of these data for human health. The human health part of the risk assessment of butadiene involves a comparison of health effects against exposures in the three population sectors. In this paper, the approach to risk assessment is exemplified for the occupational exposure setting. The conclusion reached for the human health hazard assessment has been influenced significantly by both the available animal and human data. Species differences in toxicity, in particular with regard to mutagenicity and carcinogenicity, have been considered, along with the mechanistic arguments for these differences and their relevance for human health. In addition, the evidence for health effects in humans is considered. The overall conclusion of the health hazard assessment is that there is concern for genotoxicity and for carcinogenicity, for which a threshold of effect cannot be identified. The occupational exposure assessment indicates that exposure in the workplace is generally well-controlled, of the order of 3-5 ppm or below. The overall conclusion of the risk assessment for the occupational setting is that there is concern for the possibility of genotoxicity and carcinogenicity at the exposure levels which occur in some European workplaces.

Animals↗

Inhalation toxicity and carcinogenicity of isoprene in rats and mice: comparisons with 1,3-butadiene.

As with 1,3-butadiene (BD), inhalation exposure of B6C3F1 mice to isoprene (2-methyl-1,3-butadiene) caused a macrocytic anemia; induced increases in sister chromatid exchanges in bone marrow cells and in levels of micronucleated erythrocytes in peripheral blood; and produced degeneration of the olfactory epithelium, forestomach epithelial hyperplasia, and testicular atrophy. Most notable was the finding that like BD, isoprene induced neoplasms in the liver, lung, Harderian gland, and forestomach of mice. The carcinogenic effects of isoprene were observed after a 26-week exposure (6 h/day, 5 days/week) of male mice to 700 ppm or higher concentrations of isoprene followed by a 26-week recovery period. Unlike BD, isoprene did not induce lymphomas or hemangiosarcomas of the heart in mice under these conditions nor did it induce chromosomal aberrations in mouse bone marrow cells. No toxicological effects were evident in rats exposed for 13 weeks to either isoprene or BD at concentrations up to 7000 ppm or 8000 ppm, respectively. Interstitial cell hyperplasia of the testis was observed in male F344 rats exposed to 7000 ppm isoprene for 26 weeks, and following a 26-week recovery period, there was a marginal increase in benign testicular interstitial cell tumors.

Administration, Inhalation↗

Biological formation of the 1,3-butadiene DNA adducts 7-N-(2-hydroxy-3-buten-1-yl)guanine, 7-N-(1-hydroxy-3-buten-2-yl)guanine and 7-N-(2,3,4-trihydroxy-butyl)guanine.

Male mice (B6C3F1) and male Wistar rats were exposed to [1,4-(14)C] butadiene in a closed all-glass desiccator jar system, and liver DNA was obtained. After acid hydrolysis and HPLC chromatography radioactive 7-N-(1-hydroxy-3-buten-2-yl)guanine and 7-N-(2,3,4-trihydroxybutyl)guanine were identified as radioactive DNA adducts. The same DNA adducts were identified upon incubation of calf thymus DNA, rat liver microsomes, [1,4-(14)C]butadiene and an NADPH-regenerating system. In this system, a third radioactive adduct was found which was identified as 7-N-(2-hydroxy-3-buten-yl)guanine.

Animals↗

The mutagenicity of butadiene towards Salmonella typhimurium.

Gaseous butadiene (BUT) was mutagenic towards S. typhimurium strain TA 1530 when the incubation mixture was supplemented with a NADPH-fortified rat liver microsomal preparation; mutagenicity increased with the dose. A significant mutagenic effect was similarly observed when the petri dishes, containing the bacteria but no metabolic activation system, were incubated in the presence of butadiene, in a desiccator in which plates containing the S-9 rat liver fraction had been placed. This indirect mutagenic effect was attributed to the formation, by the S-9 mix, of volatile intermediate(s) that migrated and induced mutations in neighbouring bacteria.

Animals↗