Benzene and lymphohematopoietic malignancies in humans†

Hayes, Richard B.; Yin, Shu; Dosemeci, Mustafa; Linet, Martha S.

doi:10.1002/ajim.1078

Cited by 112 publications

(55 citation statements)

References 76 publications

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“…Benzene exposure is a well-known cause of AML,4 38 but for CML, there is no consistent evidence to date 39 40. Most cohort studies have not found CML in benzene-exposed workers, while the more suggestive evidence comes from population-based case–control studies 39.…”

Section: Discussionmentioning

confidence: 99%

Occupation and risk of lymphoid and myeloid leukaemia in the European Prospective Investigation into Cancer and Nutrition (EPIC)

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Occupation and risk of lymphoid and myeloid leukaemia in the European Prospective Investigation into Cancer and Nutrition (EPIC)

et al. 2013

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“…In contrast to the findings among rubber hydrochloride workers, the NCI-CAPM study showed excess risk at relatively low levels of exposure (<10 ppm average and <40 ppm-years cumulative) but found a relatively modest dose-response effect, with proportionally smaller increases in risk at increasing levels of exposure. The study also reported that workers with 10 or more years of benzene exposure had a relative risk (RR) of developing non-Hodgkin lymphoma (NHL) of 4.2 [95% confidence interval (CI) 1.1–15.9] and an excess risk of myelodysplastic syndromes (MDS) (36, 37, 104). This study considerably expanded the health effects associated with benzene beyond AML and suggested benzene produced effects at levels lower than previously thought.…”

Section: Traditional Epidemiological Studies Of the Carcinogenic Effementioning

confidence: 99%

Advances in Understanding Benzene Health Effects and Susceptibility

Smith

2010

Annu. Rev. Public Health

332

247

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Benzene is a ubiquitous chemical in our environment that causes acute leukemia and probably other hematological cancers. Evidence for an association with childhood leukemia is growing. Exposure to benzene can lead to multiple alterations that contribute to the leukemogenic process, indicating a multimodal mechanism of action. Research is needed to elucidate the different roles of multiple metabolites in benzene toxicity and the pathways that lead to their formation. Studies to date have identified a number of polymorphisms in candidate genes that confer susceptibility to benzene hematotoxicity. However, a genome-wide study is needed to truly assess the role of genetic variation in susceptibility. Benzene affects the blood-forming system at low levels of occupational exposure, and there is no evidence of a threshold. There is probably no safe level of exposure to benzene, and all exposures constitute some risk in a linear, if not supralinear, and additive fashion.

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“…Benzene, an important industrial chemical and universal environmental pollutant, is an established human leukemogen, 8 which causes MDS and AML 9 and probably causes non-Hodgkin’s lymphoma. 10 Benzene is known to induce cytogenetic changes through its active metabolites including hydroquinone (HQ), but the characteristic alterations have not been fully characterized.…”

Section: Introductionmentioning

confidence: 99%

A comparison of the cytogenetic alterations and global DNA hypomethylation induced by the benzene metabolite, hydroquinone, with those induced by melphalan and etoposide

Z¹,

Zhang²,

Peng³

et al. 2010

Leukemia

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Specific cytogenetic alterations and changes in DNA methylation are involved in leukemogenesis. Benzene, an established human leukemogen, is known to induce cytogenetic changes through its active metabolites including hydroquinone (HQ), but the specific alterations have not been fully characterized. Global DNA hypomethylation was reported in a population exposed to benzene, but has not been confirmed in vitro. In this study, we examined cytogenetic changes in chromosomes 5, 7, 8, 11 and 21, and global DNA methylation in human TK6 lymphoblastoid cells treated with HQ for 48 h, and compared the HQ-induced alterations with those induced by two well-known leukemogens, melphalan, an alkylating agent, and etoposide, a DNA topoisomerase II inhibitor. We found that rather than inducing cytogenetic alterations distinct from those induced by melphalan and etoposide, HQ induced alterations characteristic of each agent. HQ induced global DNA hypomethylation at a level intermediate to melphalan (no effect) and etoposide (potent effect). These results suggest that HQ may act similar to an alkylating agent and also similar to a DNA topoisomerase II inhibitor in living cells, both of which may be potential mechanisms of benzene toxicity. In addition to cytogenetic changes, global DNA hypomethylation may be another mechanism underlying the leukemogenicity of benzene.

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Benzene and lymphohematopoietic malignancies in humans†

Cited by 112 publications

References 76 publications

Occupation and risk of lymphoid and myeloid leukaemia in the European Prospective Investigation into Cancer and Nutrition (EPIC)

Occupation and risk of lymphoid and myeloid leukaemia in the European Prospective Investigation into Cancer and Nutrition (EPIC)

Advances in Understanding Benzene Health Effects and Susceptibility

A comparison of the cytogenetic alterations and global DNA hypomethylation induced by the benzene metabolite, hydroquinone, with those induced by melphalan and etoposide

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