Environ. Sci. Technol. 2008, 42, 7510–7515
Higher Accumulation of Polybrominated Diphenyl Ethers in Infants Than in Adults L E I S A - M A R E E L . T O M S , * ,† FIONA HARDEN,‡ OLAF PAEPKE,§ PETER HOBSON,| JOHN JAKE RYAN,⊥ AND JOCHEN F. MUELLER† The University of Queensland, National Research Centre for Environmental Toxicology, 39 Kessels Road, Coopers Plains 4108, Australia, School of Life Science, QUT, Gardens Point, Brisbane 4001, Australia, ERGO/Eurofins, Geierstrasse 1, D-22305 Hamburg, Germany, Sullivan and Nicolaides Pathology, Whitmore Street, Taringa 4068, Australia, and Health Canada, Health Products and Food Branch Banting 2203D, Ross Avenue Ottawa, Ontario K1A 0L2 Canada
Received March 14, 2008. Revised manuscript received May 31, 2008. Accepted July 02, 2008.
Pooled serum samples collected from 8132 residents in 2002/ 03 and 2004/05 were analyzed to assess human polybrominated diphenyl ether (PBDE) concentrations from specified strata of the Australian population. The strata were defined by age (0-4 years, 5-15 years, < 16 years, 16-30 years, 31-45 years, 46-60 years, and >60 years); region; and gender. For both time periods, infants and older children had substantially higher PBDE concentrations than adults. For samples collected in 2004/ 05, the mean ( standard deviation ΣPBDE (sum of the homologue groups for the mono-, di-, tri-, tetra-, penta-, hexa-, hepta-, octa-, nona-, and deca-BDEs) concentrations for 0-4 and 5-15 years were 73 ( 7 and 29 ( 7 ng g-1 lipid, respectively, while for all adults >16 years, the mean concentration was lower at 18 ( 5 ng g-1 lipid. A similar trend was observed for the samples collected in 2002/03, with the mean ΣPBDE concentration for children 16 years, 15 ( 5 ng g-1 lipid. No regional or gender specific differences were observed. Measured data were compared with a model that we developed to incorporate the primary known exposure pathways (food, air, dust, breast milk) and clearance (half-life) data. The model was used to predict PBDE concentration trends and indicated that the elevated concentrations in infants were primarily due to maternal transfer and breast milk consumption with inhalation and ingestion of dust making a comparatively lower contribution.
Introduction Polybrominated diphenyl ethers (PBDEs) are emerging environmental pollutants that have been used for over 30 years to reduce the flammability of electrical and electronic products, textiles, and building materials (1). Extensive use of these chemicals, combined with their relatively high * Corresponding author phone: 617 3274 9060; fax: 617 3274 9003; e-mail:
[email protected]. † The University of Queensland. ‡ QUT. § ERGO/Eurofins. | Sullivan and Nicolaides Pathology. ⊥ Health Canada. 7510
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potential for bioconcentration and biomagnification (2, 3), have resulted in their detection in environmental and biological samples worldwide. Definitive health risks in humans have not yet been determined, but in animals liver, thyroid, behavioral, and immune effects have all been reported (4). In comparison to “traditional” persistent organic pollutants (POPs), the exposure modes of PBDEs in humans are less well defined, although dietary sources, inhalation (air/ particulate matter), and dust ingestion have been reported (5-7). Limited investigations of population specific factors such as age or gender report the following: no conclusive relationships between PBDEs and age in adults (8-11); no gender (11-15) or regional (16) differences; similar concentrations in maternal and cord blood (10, 17, 18); and higher PBDE concentrations in children (15, 19, 20). When limited data are available on POPs in humans, researchers have used models to predict chemical concentrations and/or assess exposure based on input and clearance data (21, 22). For PBDEs, data have been modeled to assess exposure pathways and dose estimates in North America (23-25). This study aimed to investigate background concentrations of PBDEs in the Australian population and considered the effect of age, gender, and region. To evaluate the body concentrations, we developed a simple model using PBDE uptake via food, inhalation, and exposure to dust and excretion due to individual PBDE half-lives. The results of the serum analysis were compared with the predicted data. Investigation of these comparisons along with an assessment of the input data used in the model will allow us to focus our further investigations of PBDE sources and exposure pathways in the Australian population.
Methods and Materials Sampling. Deidentified human blood sera was collected and pooled in 2002/03 and 2004/05. The serum samples were obtained from Sullivan and Nicolaides Pathology from surplus stored sera that had been collected as part of routine pathology testing. All samples were stratified according to age, gender, and geographical region. The age groups (years) were as follows: 0-4 (2004/05); >16 (2002/03); 5-15 (2004/ 05); 16-30 (2002/03 and 2004/05); 31-45 (2002/03 and 2004/ 05); 46-60 (2002/03 and 2004/05); and 16 years ΣPBDE concentrations in Australia are lower than concentrations found in the North American (11, 19) population but higher than concentrations found in Europe (14, 15, 26) and Asia (12, 17). Sampling Reproducibility. High variability in concentrations between individual samples has been previously reported where individuals have been found to have PBDE levels in blood 1-2 orders of magnitude greater than median values (27, 28). This observation was not expected to impact results of the replication between pools due to the large number of samples in each pool. The precision in replication data indicated that any elevated individual concentrations or differences due to varying sample volume did not influence the true average of the pool and pooling procedures were uniform. Due to the good agreement between replicates it is also unlikely that contamination of the samples occurred during sampling. For 75% of strata, the ND between replicates for ΣPBDEs (-47, -85, -99, -100, -153, and -154) was 16 years age groups combined (18 ( 5 ng g-1 lipid) (Table 1). In the 2002/03 samples, the 16 years age groups. In the adult pools, subsequent decreases with age were apparent but much smaller. Hence, a decreasing age trend was observed for ΣPBDE concentrations in the Australian population. Developmental, reproductive, and neurotoxic effects as well as permanent effects on learning, activity, and behaviors following PBDE exposure have been reported in animals (33). In humans, PBDE concentrations in breast milk showed an association with congenital cryptorchidism (34) while PBDE concentrations have been associated with lower birthweight and length (35). In addition, it has been suggested that exposure to PBDEs and other contaminants via house dust may disrupt thyroid hormone homeostasis in children (36). Investigation of exposure, body burden, and health outcomes in the young age groups would help to determine if there is cause for concern in relation to elevated PBDE concentrations. The current study investigated the cause of the steep increase in concentration in the younger age groups by developing a model based on our knowledge of current intake and clearance data to allow us to determine whether the early peaks in PBDE concentrations could be predicted. Modeling. Aim of the Model. The aim of the simple model was to evaluate if input and clearance data could be used to predict the measured age distribution and the peak age of maximum PBDE concentrations in the Australian population. Assumptions. By using the concentrations of selected BDE congeners found in human milk samples collected in 2002/ 03 (29) as an infant’s PBDE body burden at birth, we predict the concentrations in a human as s/he grows if exposure remained constant over time at the rate of the PBDE exposure for the mother. The alternative to using PBDE breast milk concentrations as an infant’s body burden was to use serum concentrations from females of child-bearing age (15-30 7512
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and 31-45 years). Breast milk samples were used because the PBDE concentrations are comparable to maternal serum (17, 37) and exposure factors such as parity and lactation period could not be determined from the deidentified serum data. For the development of the model, the following assumptions were made: PBDEs are stored exclusively in body lipids; maternal concentrations equal newborn concentrations (17, 18); all PBDEs ingested via human milk and air were absorbed and retained in the body; and, although there is no data on human resorption of PBDEs, to account for this factor resorption rates of 0.94, 0.78, 0.93, and 0.90 for BDE-47, -99, -100, and -153, respectively, as used in previous PBDE models (23, 25) were used for food and dust intake. An infant was assumed to consume either breast milk or formula from 0-12 months with the addition of food from 6 months until breast milk/formula was ceased at 12 months and food alone was consumed. The model was resolved on a monthly (30 day) basis for the first 24 months due to the large changes in body weight, lipid content, and dietary intake during this time, then on a 3 monthly (90 day) basis for the next 24 months, and then a yearly (365 day) basis from 4 to 65 years. The model was constructed in Microsoft Excel. Input Data. The model was run for the four PBDEs (BDE47, -99, -100, and -153) that are most commonly found at the highest concentration in human samples. Concentrations of PBDEs in breast milk, dust, and air were derived from our own studies (Supporting Information, Table S4) (29, 38). Food and formula data were calculated from a report on PBDEs in food in Australia (Supporting Information, Table S5) (39). Breast milk intake was based on 778 g/day for the first six months followed by a 10% decrease each month until cessation at 12 months (40) using a lipid content of 3.7% (29). We did not include a depuration rate of PBDEs in the breast milk concentration. Food intake data was reported for the following age groups: 2-5 years, 6-12 years, 13-18 years, and >19 years. For young children 36 years age groups, indicating that known input and clearance data were more reflective of exposure. Due to the length of half-lives for these PBDEs (19-78 months (45)), exposure in the older age groups must be constant to cause the stabilization of PBDE concentrations. It should be noted that data on human PBDE halflives is limited, and further assessment of these half-lives in humans is required for accurate risk assessment. The use of pooled samples obtained from both formulaand breast-fed babies may also have resulted in the underestimation of the measured concentrations. In Australia, VOL. 42, NO. 19, 2008 / ENVIRONMENTAL SCIENCE & TECHNOLOGY
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breastfeeding rates decrease from 85% at birth to 45% and 23% at 6 and 12 months, respectively (47), so the pooling of serum from the formula-fed infants would reduce the mean PBDE concentrations in the pools and may have resulted in underestimation of measured values in breast-fed babies. We can also assume that breast-fed babies have even higher concentrations than indicated by the measured data, reinforcing the idea that some input or clearance data is missing for this age group. It should be noted that the World Health Organization recommends breastfeeding in spite of the transient risk posed by POPs in human milk (48). Other potential sources in the young age group, not accounted for in the model, include increased exposure from mouthing and sucking either products, treated with PBDEs or covered in dust contaminated with PBDEs from the indoor environment, or their hands on which PBDEs have recently been shown to be present (49) and from exposure to child-specific products such as car seats, prams, mattresses, and toys which may also be a source of PBDEs. In assessing the predictive value of the model it is also important to consider variation in an individual’s response to PBDE exposure. Overall body burden of PBDEs may be determined by individual metabolic differences that affect rates of retention/sequestration (50) as well as occupational exposure (51), and these factors were not accounted for by the model. This may be particularly evident in children and young adults. In contrast, measured values reflect the overall concentration as a function of an individual’s input, metabolism, and degradation. The sample collection was structured with the aim of obtaining a representative sample of the Australian population. However, due to the use of deidentified samples and pooling, occupational or dietary (including breast milk) exposure were unknown and resulted in the determination of mean concentrations. Hence, the minimum and maximum PBDE concentrations in the population were not determined. Continued monitoring of PBDE exposure as a function of age will further validate the accuracy of this model and enable the identification and perhaps reduction of specific sources and pathways of exposure of PBDEs for infants and young children.
Acknowledgments We thank the staff at Sullivan and Nicolaides Pathology, Eurofins/ERGO, and Health Canada. EnTox is a partnership between Queensland Health and The University of Queensland. This work was part of a consultancy funded by the Australian Government, Department of Environment, Water, Heritage and the Arts (DEWHA). The views and opinions expressed in this publication do not necessarily reflect those of the Australian Government or the Minister for the Department of the Environment, Water, Heritage and the Arts. The authors gratefully acknowledge Lawrence Hearn and Susan Bengtson-Nash for reviewing the manuscript. L.M.L.T. is funded by a UQENTox/SOM joint research scholarship.
Supporting Information Available Full results for all pools as well as details on input data. This material is available free of charge via the Internet at http:// pubs.acs.org.
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