Overview of the Toxicology of Benzene

Snyder, Robert

doi:10.1080/00984100050166334

Cited by 137 publications

(69 citation statements)

References 45 publications

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“…The frequency of t(14;18) translocation-positive cells, but not the prevalence, was increased with increasing plasma tetrachlorodibenzo-p -dioxin (TCDD), possibly through alteration of immune parameters and immune response by TCDD ( 32 ). As well as depression of the immune system through reduction of B and T lymphocyte numbers, benzene exposure also perturbs their mitogenic responses ( 33 ). Table 1 shows the gender and age characteristics of the population as well as smoking and drinking status.…”

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confidence: 99%

Chromosome Translocations in Workers Exposed to Benzene

McHale

Lan²,

Corso³

et al. 2008

JNCI Monographs

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Epidemiological studies indicate that benzene exposure is associated with an increased risk of human leukemia and lymphoma ( 1 , 2 ). Chromosomal translocations are thought to be initiating events in leukemia and lymphoma, and specific translocations are used as markers of diagnosis, disease progression, and relapse. As benzene is thought to act by producing chromosomal aberrations and altered cell differentiation ( 3 ), we investigated the possibility of using circulating levels of two acute myeloid leukemia (AML) -associated translocations, t(8;21) ( 4 ) and t(15;17) ( 5 ), and a follicular lymphoma -associated translocation, t(14;18) ( 6 ), as biomarkers of early effect for benzene. Evidence for the occurrence of these translocations in normal individuals is limited, with t(8;21) detected in 1 in 496 cord blood samples ( 7 ) and t(15;17) detected in healthy volunteers ( 8 ). As recently reviewed ( 9 ), the prevalence of t(14;18) in peripheral blood lymphocytes of healthy donors is relatively high at ~ 50% (range 8% -80% depending on the polymerase chain reaction (PCR) methodology employed and target cell population) ( 9 -13 ) and rises with smoking ( 14 ), but the correlation between frequency and age remains unclear ( 13 , 15 ). The biological consequences of these aberrations in healthy individuals are yet to be understood. One possibility is that the frequency of translocationpositive cells represents a biomarker of early effect for hematopoietic carcinogens which could correlate with the cumulative risk of developing t(14;18)-related follicular lymphoma and t(8;21)-and t(15;17)-related AML, and perhaps other cancers.The two principal technologies for detection of specifi c chromosome translocations are fl uorescence in situ hybridization (FISH) and real-time PCR. FISH distinguishes individual chromosomes by hybridization with sequence-specifi c, chromosomepainting probes labeled with spectrally nonoverlapping fl uorophores. In real-time quantitative PCR (qPCR), a fl uorescently labeled probe is hybridized to the amplifi cation target, and fl uorescent signal proportional to the input DNA/cDNA is generated during amplifi cation, thereby allowing quantifi cation. qPCR assays the whole peripheral blood mononuclear cell (PBMC) population in G 0 , whereas FISH examines a culture-modifi ed popula tion [consisting of mainly mature T lymphocytes stimulated by the mitogen phytohemagglutinin that have gone through two cell divi sions ( 16 )]. The two methods also generate different estimates of t(14;18) translocation levels with FISH detecting all possible t(14;18) breakpoints and the real-time assay described here only detecting breakpoints occurring in the major breakpoint region (MBR) of the BCL-2 gene. Although it was previously thought that the majority of BCL-2 breakpoints occur in the MBR ( 17 ), it has been shown more recently that many breakpoints occur outside of the MBR and the minor cluster region ( 18 ). The ability of FISH to detect more translocation breakpoints is offset by its lower relative sensit...

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Section: Downloaded Frommentioning

confidence: 99%

Chromosome Translocations in Workers Exposed to Benzene

McHale

Lan²,

Corso³

et al. 2008

JNCI Monographs

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“…A link between benzene exposure and leukemia has been established in some studies (Synder, 2000 andGuenel et al, 2002). The major sources of benzene in ambient air of urban area are motor vehicle exhaust and evaporation loss during handling, distribution and storage of petrol (Leung and Harrison, 1998).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of benzene exposure in adults and urinary s-phenylmercapturic acid in children living in Adelaide, South Australia

Bahramiand

Edwards

2006

Int. J. Environ. Sci. Technol.

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ABSTRACT:Benzene Exposure was evaluated in adults and children living in Adelaide, South Australia by measuring benzene and urinary s-phenylmercapturic acid (SPMA). To determine of benzene exposure in each subject the personal passive samplers was used and samples were analyzed by gas chromatography system equipped to flame ionization detector. The level of SPMA was determined by competitive enzymelinked immunosorbent assay (ELISA) in children. The mean concentration of benzene in Summer and Winter were 1.62±1.43 and 1.36±0.87 ppb respectively. There was a significant difference between exposure to benzene for subjects with less and more than 6 hours activity over days of week (p<0.05). The mean urinary concentrations levels of SPMA adjusted to creatinene for children that living less and more than 200 meters distance from main road were 1.56 and 4.67 µmol/mol creatinene, respectively and the significant difference was seen in two groups (p<0.005). Data shows, that SPMA can be utilized as a biomarker for exposure to benzene in children. Exposure to benzene is more for children that living near to main road compare to other children. Adults have more activity in out side of home has more exposure to benzene than other people.

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“…Proliferative disorders of the hemopoietic system, which most frequently develop in humans exposed to benzene, include chronic myeloid leukemia, acute myeloid leukemia, lymphoblastic leukemia, malignant lymphoma and multiple myeloma. Development of tumors of the hemopoietic system reflects the damage to bone marrow pluripotential stem cells, which leads to anemia, leukopenia or thrombocytopenia and, then, to fully symptomatic aplastic anemia or myeloid leukemia [1,2].…”

Section: Introductionmentioning

confidence: 99%

Influence of acetylsalicylic acid on hematotoxicity of benzene

Kowalówka-Zawieja¹,

Zielińska-Psuja²,

Przystanowicz³

et al. 2013

International Journal of Occupational Medicine and Environmental Health

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Objectives: The aim of the study was to evaluate the influence of acetylsalicylic acid (ASA) on benzene hematotoxicity in rats. Materials and Methods: The study was carried out on rats exposed for 2, 4 and 8 weeks to benzene vapour at a concentration of 1.5 or 4.5 mmol/m 3 of air (5 days per week, 6 hours per day) alone or together with ASA at the doses of 5, 150 or 300 mg/kg body weight (per os). Results: Benzene at a concentration of 4.5 mmol/m 3 caused a slight lymphopenia, granulocytosis and reticulocytosis in blood. In bone marrow traits of megaloblastic renewal, presence of undifferentiated cells and giant forms of granulocytes as well as an increase in myeloperoxidase and decrease in chloroacetate esterase activity and lipids content were noted. ASA (150 and 300 mg/kg b.w.) influenced some of hematological parameters, altered by benzene intoxication. ASA limited the solvent-induced alteration in blood reticulocyte count and in the case of bone marrow in the erythroblasts count. Traits of megaloblastic renewal in bone marrow were less pronounced. Besides, higher activity of myeloperoxidase and the decrease in the level of lipids in granulocytes were noted. Conclusion: Our results suggest that ASA limited the benzene-induced hematotoxicity.

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Overview of the Toxicology of Benzene

Cited by 137 publications

References 45 publications

Chromosome Translocations in Workers Exposed to Benzene

Chromosome Translocations in Workers Exposed to Benzene

Evaluation of benzene exposure in adults and urinary s-phenylmercapturic acid in children living in Adelaide, South Australia

Influence of acetylsalicylic acid on hematotoxicity of benzene

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