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The use of biomonitoring data in exposure and human health risk assessment: benzene case study.

Arnold SM, Angerer J, Boogaard PJ, Hughes MF, O'Lone RB, Robison SH, Schnatter AR - Crit. Rev. Toxicol. (2013)

Bottom Line: The available data for benzene satisfied most of the Common Criteria and allowed for a risk-based evaluation of the benzene biomonitoring data.Smokers clearly have higher levels of benzene exposure, and biomarker levels of benzene for non-smokers are generally consistent with ambient air monitoring results.While some biomarkers of benzene are specific indicators of exposure, the interpretation of benzene biomonitoring levels in a health-risk context are complicated by issues associated with short half-lives and gaps in knowledge regarding the relationship between the biomarkers and subsequent toxic effects.

View Article: PubMed Central - PubMed

Affiliation: The Dow Chemical Company, Midland, MI 48674, USA. smarnold@dow.com

ABSTRACT
Abstract A framework of "Common Criteria" (i.e. a series of questions) has been developed to inform the use and evaluation of biomonitoring data in the context of human exposure and risk assessment. The data-rich chemical benzene was selected for use in a case study to assess whether refinement of the Common Criteria framework was necessary, and to gain additional perspective on approaches for integrating biomonitoring data into a risk-based context. The available data for benzene satisfied most of the Common Criteria and allowed for a risk-based evaluation of the benzene biomonitoring data. In general, biomarker (blood benzene, urinary benzene and urinary S-phenylmercapturic acid) central tendency (i.e. mean, median and geometric mean) concentrations for non-smokers are at or below the predicted blood or urine concentrations that would correspond to exposure at the US Environmental Protection Agency reference concentration (30 µg/m(3)), but greater than blood or urine concentrations relating to the air concentration at the 1 × 10(-5) excess cancer risk (2.9 µg/m(3)). Smokers clearly have higher levels of benzene exposure, and biomarker levels of benzene for non-smokers are generally consistent with ambient air monitoring results. While some biomarkers of benzene are specific indicators of exposure, the interpretation of benzene biomonitoring levels in a health-risk context are complicated by issues associated with short half-lives and gaps in knowledge regarding the relationship between the biomarkers and subsequent toxic effects.

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A schematic of liver metabolism of benzene. From Boogaard (2009); reproduced with permission of John Wiley & Sons Ltd. EH, epoxide hydrolase; GSH, glutathione; GST, glutathione-S-transferase; DHDH, dihydrodiol dehydrogenase; MPO, myeloperoxidase; NQO1, NADPH quinone oxidoreductase 1.
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f2: A schematic of liver metabolism of benzene. From Boogaard (2009); reproduced with permission of John Wiley & Sons Ltd. EH, epoxide hydrolase; GSH, glutathione; GST, glutathione-S-transferase; DHDH, dihydrodiol dehydrogenase; MPO, myeloperoxidase; NQO1, NADPH quinone oxidoreductase 1.

Mentions: The metabolism of benzene has been extensively studied in humans and laboratory animals (ATSDR, 2007; Lovern et al., 2001; Monks et al., 2010; Snyder, 2004). These include in vivo studies to identify metabolites of benzene as well as in vitro studies to better understand the mechanism of its metabolism. The mouse, rat and non-human primates share the same Phases I and II pathways of benzene metabolism with humans (Henderson, 1996). However, there are species differences in the capacity of these pathways to metabolize benzene which results in differences in the fractional distribution of metabolites formed. These metabolites have potentially different toxicological potency. A scheme of the metabolic pathways of benzene and its metabolites is shown in Figure 2Figure 2.


The use of biomonitoring data in exposure and human health risk assessment: benzene case study.

Arnold SM, Angerer J, Boogaard PJ, Hughes MF, O'Lone RB, Robison SH, Schnatter AR - Crit. Rev. Toxicol. (2013)

A schematic of liver metabolism of benzene. From Boogaard (2009); reproduced with permission of John Wiley & Sons Ltd. EH, epoxide hydrolase; GSH, glutathione; GST, glutathione-S-transferase; DHDH, dihydrodiol dehydrogenase; MPO, myeloperoxidase; NQO1, NADPH quinone oxidoreductase 1.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3585443&req=5

f2: A schematic of liver metabolism of benzene. From Boogaard (2009); reproduced with permission of John Wiley & Sons Ltd. EH, epoxide hydrolase; GSH, glutathione; GST, glutathione-S-transferase; DHDH, dihydrodiol dehydrogenase; MPO, myeloperoxidase; NQO1, NADPH quinone oxidoreductase 1.
Mentions: The metabolism of benzene has been extensively studied in humans and laboratory animals (ATSDR, 2007; Lovern et al., 2001; Monks et al., 2010; Snyder, 2004). These include in vivo studies to identify metabolites of benzene as well as in vitro studies to better understand the mechanism of its metabolism. The mouse, rat and non-human primates share the same Phases I and II pathways of benzene metabolism with humans (Henderson, 1996). However, there are species differences in the capacity of these pathways to metabolize benzene which results in differences in the fractional distribution of metabolites formed. These metabolites have potentially different toxicological potency. A scheme of the metabolic pathways of benzene and its metabolites is shown in Figure 2Figure 2.

Bottom Line: The available data for benzene satisfied most of the Common Criteria and allowed for a risk-based evaluation of the benzene biomonitoring data.Smokers clearly have higher levels of benzene exposure, and biomarker levels of benzene for non-smokers are generally consistent with ambient air monitoring results.While some biomarkers of benzene are specific indicators of exposure, the interpretation of benzene biomonitoring levels in a health-risk context are complicated by issues associated with short half-lives and gaps in knowledge regarding the relationship between the biomarkers and subsequent toxic effects.

View Article: PubMed Central - PubMed

Affiliation: The Dow Chemical Company, Midland, MI 48674, USA. smarnold@dow.com

ABSTRACT
Abstract A framework of "Common Criteria" (i.e. a series of questions) has been developed to inform the use and evaluation of biomonitoring data in the context of human exposure and risk assessment. The data-rich chemical benzene was selected for use in a case study to assess whether refinement of the Common Criteria framework was necessary, and to gain additional perspective on approaches for integrating biomonitoring data into a risk-based context. The available data for benzene satisfied most of the Common Criteria and allowed for a risk-based evaluation of the benzene biomonitoring data. In general, biomarker (blood benzene, urinary benzene and urinary S-phenylmercapturic acid) central tendency (i.e. mean, median and geometric mean) concentrations for non-smokers are at or below the predicted blood or urine concentrations that would correspond to exposure at the US Environmental Protection Agency reference concentration (30 µg/m(3)), but greater than blood or urine concentrations relating to the air concentration at the 1 × 10(-5) excess cancer risk (2.9 µg/m(3)). Smokers clearly have higher levels of benzene exposure, and biomarker levels of benzene for non-smokers are generally consistent with ambient air monitoring results. While some biomarkers of benzene are specific indicators of exposure, the interpretation of benzene biomonitoring levels in a health-risk context are complicated by issues associated with short half-lives and gaps in knowledge regarding the relationship between the biomarkers and subsequent toxic effects.

Show MeSH
Related in: MedlinePlus