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ToxSci Advance Access originally published online on August 6, 2007
Toxicological Sciences 2007 100(1):224-237; doi:10.1093/toxsci/kfm199
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© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

An Adaptable Internal Dose Model for Risk Assessment of Dietary and Soil Dioxin Exposures in Young Children

Brent D. Kerger*,1, Hon-Wing Leung{dagger}, Paul K. Scott{ddagger} and Dennis J. Paustenbach§

* Health Science Resource Integration, Tallahassee, Florida 32309 {dagger} Private Consultant, Philadelphia, Pennsylvania 19103 {ddagger} ChemRisk, Pittsburgh, Pennsylvania 15222 § ChemRisk, San Francisco, California 94105

1 To whom correspondence should be addressed at 2976 Wellington Circle West, Tallahassee, FL 32309. Fax: (850) 906-9777. E-mail: brentkerger{at}att.net.

Received March 8, 2007; accepted July 25, 2007


  Abstract

An adaptable model is presented for assessing the blood lipid concentrations of polychlorodibenzodioxins and polychlorodibenzofurans (PCDD/Fs) from dietary (breast milk, formula, milk, and other foods) and soil pathway exposures (soil ingestion and dermal contact) utilizing age-specific exposure and intake estimates for young children. The approach includes a simple one-compartment (adipose volume) toxicokinetic model that incorporates empirical data on age-dependent half-lives and bioavailability of PCDD/F congeners, child body size and intake rates, and recent data on breast milk and food dioxin levels. Users can enter site-specific soil concentration data on 2,3,7,8-chlorinated PCDD/F congeners for specific assessment of body burden changes from soil pathways in combination with background dietary exposures from birth through age 7 years. The model produces a profile of the estimated PCDD/F concentration in blood lipid (in World Health Organization 1998 dioxin toxic equivalents) versus time for a child from birth through age 7 years. The peak and time-weighted average (TWA) internal dose (defined as blood lipid dioxin toxic equivalents) for a variety of specific child exposure assumptions can then be compared to safe internal dose benchmarks for risk assessment purposes, similar to an approach taken by United States Environmental Protection Agency for assessing child lead exposures. We conclude that this adaptable toxicokinetic model can provide a more comprehensive assessment of potential health risks of PCDD/Fs to children because it integrates recent empirical findings on PCDD/F kinetics in humans and allows users to assess contributions from varied dietary and site-specific environmental exposure assumptions.

Key Words: dioxins; furans; childhood; diet; soil; toxicokinetic model.


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