ATSDR evaluation of health effects of benzene and relevance to public health

Wilbur, Sharon; Wohlers, David; Paikoff, Sari J.; Keith, L. Samuel; Faroon, Obaid

doi:10.1177/0748233708090910

Cited by 53 publications

(27 citation statements)

References 542 publications

(1,222 reference statements)

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“…When inhalation exposure levels are converted into oral administration levels, 60 ppm is equivalent to 30 mg benzene/kg-b.w./day (conversion conditions are as follows: respiratory volume, 20 m 3 /day; absorptivity, 50%; body weight, 70 kg) [26]. Benzene toxicity depends on the amount absorbed and not the site of absorption [26], [27]. Therefore, in the present study, 0, 10, 30, 100, and 300 mg/kg-b.w.…”

Section: Methodsmentioning

confidence: 99%

Assessment of Benzene-Induced Hematotoxicity Using a Human-Like Hematopoietic Lineage in NOD/Shi-scid/IL-2Rγnull Mice

et al. 2012

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Despite recent advancements, it is still difficult to evaluate in vivo responses to toxicants in humans. Development of a system that can mimic the in vivo responses of human cells will enable more accurate health risk assessments. A surrogate human hematopoietic lineage can be established in NOD/Shi-scid/IL-2Rγnull (NOG) mice by transplanting human hematopoietic stem/progenitor cells (Hu-NOG mice). Here, we first evaluated the toxic response of human-like hematopoietic lineage in NOG mice to a representative toxic agent, benzene. Flow cytometric analysis showed that benzene caused a significant decrease in the number of human hematopoietic stem/progenitor cells in the bone marrow and the number of human leukocytes in the peripheral blood and hematopoietic organs. Next, we established chimeric mice by transplanting C57BL/6 mouse-derived bone marrow cells into NOG mice (Mo-NOG mice). A comparison of the degree of benzene-induced hematotoxicity in donor-derived hematopoietic lineage cells within Mo-NOG mice indicated that the toxic response of Hu-NOG mice reflected interspecies differences in susceptibilities to benzene. Responses to the toxic effects of benzene were greater in lymphoid cells than in myeloid cells in Mo-NOG and Hu-NOG mice. These findings suggested that Hu-NOG mice may be a powerful in vivo tool for assessing hematotoxicity in humans, while accounting for interspecies differences.

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Section: Methodsmentioning

confidence: 99%

Assessment of Benzene-Induced Hematotoxicity Using a Human-Like Hematopoietic Lineage in NOD/Shi-scid/IL-2Rγnull Mice

et al. 2012

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“…For reviews, see recent articles in References 10, 48, and 120. The consensus clearly shows that benzene causes AML/ANLL and MDS, even at relatively low doses, and that AML often arises secondary to MDS.…”

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 has been shown to cause human and animal reproductive toxicity [127–128]. Chromosome abnormalities, specifically aneuploidies (numerical chromosomal changes), were detected in the sperm of male workers occupationally exposed to benzene levels above [129–132] and below [133] 1 ppm, the current U.S.…”

Section: Potential Mechanisms Of Actionmentioning

confidence: 99%

Reproductive and developmental toxicity of formaldehyde: A systematic review

Duong

Steinmaus

McHale

et al. 2011

Mutation Research/Reviews in Mutation Research

257

180

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Formaldehyde, the recently classified carcinogen and ubiquitous environmental contaminant, has long been suspected of causing adverse reproductive and developmental effects, but previous reviews were inconclusive, due in part, to limitations in the design of many of the human population studies. In the current review, we systematically evaluated evidence of an association between formaldehyde exposure and adverse reproductive and developmental effects, in human populations and in vivo animal studies, in the peer-reviewed literature. The mostly retrospective human studies provided evidence of an association of maternal exposure with adverse reproductive and developmental effects. Further assessment of this association by meta-analysis revealed an increased risk of spontaneous abortion (1.76, 95% CI 1.20–2.59, p=0.002) and of all adverse pregnancy outcomes combined (1.54, 95% CI 1.27–1.88, p<0.001), in formaldehyde-exposed women, although differential recall, selection bias, or confounding cannot be ruled out. Evaluation of the animal studies including all routes of exposure, doses and dosing regimens studied, suggested positive associations between formaldehyde exposure and reproductive toxicity, mostly in males. Potential mechanisms underlying formaldehyde-induced reproductive and developmental toxicities, including chromosome and DNA damage (genotoxicity), oxidative stress, altered level and/or function of enzymes, hormones and proteins, apoptosis, toxicogenomic and epigenomic effects (such as DNA methylation), were identified. To clarify these associations, well-designed molecular epidemiologic studies, that include quantitative exposure assessment and diminish confounding factors, should examine both reproductive and developmental outcomes associated with exposure in males and females. Together with mechanistic and animal studies, this will allow us to better understand the systemic effect of formaldehyde exposure.

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ATSDR evaluation of health effects of benzene and relevance to public health

Cited by 53 publications

References 542 publications

Assessment of Benzene-Induced Hematotoxicity Using a Human-Like Hematopoietic Lineage in NOD/Shi-scid/IL-2Rγnull Mice

Assessment of Benzene-Induced Hematotoxicity Using a Human-Like Hematopoietic Lineage in NOD/Shi-scid/IL-2Rγnull Mice

Advances in Understanding Benzene Health Effects and Susceptibility

Reproductive and developmental toxicity of formaldehyde: A systematic review

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