Insights into PBDE Uptake, Body Burden, and Elimination Gained from Australian Age–Concentration Trends Observed Shortly after Peak Exposure

Abstract

BackgroundPopulation pharmacokinetic models combined with multiple sets of age–concentration biomonitoring data facilitate back-calculation of chemical uptake rates from biomonitoring data.ObjectivesWe back-calculated uptake rates of PBDEs for the Australian population from multiple biomonitoring surveys (top-down) and compared them with uptake rates calculated from dietary intake estimates of PBDEs and PBDE concentrations in dust (bottom-up).MethodsUsing three sets of PBDE elimination half-lives, we applied a population pharmacokinetic model to the PBDE biomonitoring data measured between 2002–2003 and 2010–2011 to derive the top-down uptake rates of four key PBDE congeners and six age groups. For the bottom-up approach, we used PBDE concentrations measured around 2005.ResultsTop-down uptake rates of Σ4BDE (the sum of BDEs 47, 99, 100, and 153) varied from 7.9 to 19 ng/kg/day for toddlers and from 1.2 to 3.0 ng/kg/day for adults; in most cases, they were—for all age groups—higher than the bottom-up uptake rates. The discrepancy was largest for toddlers with factors up to 7–15 depending on the congener. Despite different elimination half-lives of the four congeners, the age–concentration trends showed no increase in concentration with age and were similar for all congeners.ConclusionsIn the bottom-up approach, PBDE uptake is underestimated; currently known pathways are not sufficient to explain measured PBDE concentrations, especially in young children. Although PBDE exposure of toddlers has declined in the past years, pre- and postnatal exposure to PBDEs has remained almost constant because the mothers’ PBDE body burden has not yet decreased substantially.CitationGyalpo T, Toms LM, Mueller JF, Harden FA, Scheringer M, Hungerbühler K. 2015. Insights into PBDE uptake, body burden, and elimination gained from Australian age–concentration trends observed shortly after peak exposure. Environ Health Perspect 123:978–984; http://dx.doi.org/10.1289/ehp.1408960

Assessing exposure of young Australian children to toxicants in the home environment using a web-based questionnaire

“…This finding may be attributable to decreasing PBDE intake via breast milk combined with the effect of dilution of internal PBDE body burdens as the child grows. In contrast, a previous study conducted in Australia in 2006Australia in -2007 on pooled serum samples demonstrated that peak PBDE exposure occurs between the ages of two and three years, however, it must be noted that this study was conducted a decade prior to the current study, during which time serum PBDE concentrations from young Australian children have been rapidly declining (113,347).…”

“…Although the concentrations of some c-octaBDE and c-pentaBDE congeners in human serum and breast milk samples are decreasing, human exposure to PBDEs, particularly c-decaBDE, will continue to occur for decades to come, due to their continued presence in homes and the environment (345,346). Despite ubiquitous human exposure to PDBEs, there are still many data gaps about how exposure to these chemicals occurs, particularly for young children (347). While several studies elsewhere have assessed PBDE exposure pathways in children through a combined biomonitoring-survey approach to assess potential exposure pathways, the data internationally with regards to BDE-209 are limited, with no such data available in Australia (120,126,171,(348)(349)(350).…”

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“…Sometimes such studies confirm the elimination half-lives from earlier studies (Ritter et al 2009;Bu et al 2015;Wood et al, 2016b) while at other times they reveal inconsistencies in the data. Specifically, neither for North America (Ritter et al 2009;Wong et al 2013) nor for Australia (Gyalpo et al 2015) was it possible to reconcile contaminant intake estimates (accounting for both dietary and dust intakes), measured body burdens, and reported elimination half-lives for PBDEs. In both cases, the intake D r a f t estimates were judged to be too low, suggesting the existence of an unrecognized exposure pathway.…”

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“…Exposure assessments undertaken by modeling existing intake data underestimate the serum concentrations of these chemicals in children Gyalpo et al 2015). Estimates from applying models suggested there is a level of inconsistency between measured and modeled POP data in infants suggesting that intake in infants…”

“…While pharmacokinetic modeling considering absorption, metabolism and excretion were not considered here, the reason for this disparity may be that food intake is not the dominant exposure route for infants and toddlers and rather placental transfer, breastfeeding and dust ingestion are important (Gyalpo et al 2015).…”