Polybrominated diphenyl ethers, PBDEs, are a class of brominated flame retardants that, like other persistent organic pollutants (POPs), have been found in humans, wildlife, and biota worldwide. Unlike other POPs, however, the key routes of human exposure are not thought to be food and fish, but rather are from their use in household consumer products, and to the high levels of PBDEs found in house dust. The exposure of Americans to PBDEs was systematically evaluated in this study. First, exposure media data on PBDE congeners were compiled. Then, an adult intake dose was derived using exposure factors in combination with these data. The exposure pathways evaluated included food and water ingestion, inhalation, and ingestion and dermal contact to house dust. These intakes were converted to a body burden using a simple pharmacokinetic (PK) model. The predicted body burdens were compared with representative profiles of PBDEs in blood and milk. The adult intake dose of total PBDEs was estimated to be 7.7 ng/kg body weight/day, and children's estimated intakes were higher at 49.3 ng/kg/day for ages 1-5, 14.4 ng/kg/day for 6-11, and 9.1 ng/kg/day for 12-19. The much higher dose for the child age 1-5 was due to the doubling of dust ingestion from 50 to 100 mg/day. The predicted adult body burden of total PBDEs was 33.8 ng/kg lipid weight (lwt), compared to representative measurements in blood and milk at 64.0 and 93.7 ng/g lwt, respectively Most of this apparent underprediction in total concentration was due to an underprediction of the key congener, BDE 47. The value for BDE 47 half-life in the body was identified as the variable most likely in error in this exercise. Other congener predictions compared well with measurements, suggesting general validity with the approach. An important finding from this assessment is that the food intake estimate of about 1.3 ng/kg/day (of the 7.7 ng/kg/day total) cannot explain current US body burdens; exposures to PBDEs in house dust accounted for 82% of the overall estimated intakes.

Background: Phthalates have been found in many personal care and industrial products, but have not previously been reported in food purchased in the United States. Phthalates are ubiquitous synthetic compounds and therefore difficult to measure in foods containing trace levels. Phthalates have been associated with endocrine disruption and developmental alteration.Objectives: Our goals were to report concentrations of phthalates in U.S. food for the first time, specifically, nine phthalates in 72 individual food samples purchased in Albany, New York, and to compare these findings with other countries and estimate dietary phthalate intake.Methods: A convenience sample of commonly consumed foods was purchased from New York supermarkets. Methods were developed to analyze these foods using gas chromatography–mass spectroscopy. Dietary intakes of phthalates were estimated as the product of the food consumption rate and concentration of phthalates in that food.Results: The range of detection frequency of individual phthalates varied from 6% for dicyclohexyl phthalate (DCHP) to 74% for di-2-ethylhexyl phthalate (DEHP). DEHP concentrations were the highest of the phthalates measured in all foods except beef [where di-n-octyl phthalate (DnOP) was the highest phthalate found], with pork having the highest estimated mean concentration of any food group (mean 300 ng/g; maximum, 1,158 ng/g). Estimated mean adult intakes ranged from 0.004 μg/kg/day for dimethyl phthalate (DMP) to 0.673 μg/kg/day for DEHP.Conclusions: Phthalates are widely present in U.S. foods. While estimated intakes for individual phthalates in this study were more than an order of magnitude lower than U.S. Environmental Protection Agency reference doses, cumulative exposure to phthalates is of concern and a more representative survey of U.S. foods is indicated.

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An individual (male, 36 years, 87 kg) ingested two separate doses of di-n-butyl phthalate (DnBP) and diisobutyl phthalate (DiBP) at a rate of ~60 μg/kg. Key monoester and oxidized metabolites were identified and quantified in urine continuously collected until 48 h post-dose. For both DnBP and DiBP, the majority of the dose was excreted in the first 24 h (92.2 % of DnBP, 90.3 % of DiBP), while only <1 % of the dose was excreted in urine on day 2. In each case, the simple monoesters were the major metabolites (MnBP, 84 %; MiBP, 71 %). For DnBP, ~8 % was excreted as various side chain oxidized metabolites. For DiBP, approximately 20 % was excreted mainly as the oxidized side chain metabolite 2OH-MiBP, indicating that the extent of oxidative modification is around 2.5 times higher for DiBP than for DnBP. All DnBP and DiBP metabolites reached peak concentrations between 2 and 4 h post-exposure, followed by a monotonic decline. For DnBP metabolites, the elimination halftime of MnBP was 2.6 h; longer elimination halftimes were estimated for the oxidized metabolites (2.9-6.9 h). For DiBP metabolites, MiBP had the shortest halftime (3.9 h), and the oxidized metabolites had somewhat longer halftimes (4.1 and 4.2 h). Together with the simple monoesters, secondary oxidized metabolites are additional and valuable biomarkers of phthalate exposure. This study provides basic human metabolism and toxicokinetic data for two phthalates that have to be considered human reproductive toxicants and that have been shown to be omnipresent in humans.

To better understand human exposure to perfluorinated compounds (PFCs), a model that assesses exposure to perfluorooctane sulfonate (PFOS) and its precursors from both an intake and a body burden perspective and combines the two with a simple pharmacokinetic (PK) model is demonstrated. Exposure pathways were modeled under "typical" and "contaminated" scenarios, for young children and adults. A range of intakes was also estimated from serum concentrations of PFOS reported in the National Health and Nutrition Examination Survey (NHANES) using a first-order 1-compartment PK model. Total PFOS intakes (medians summed over all pathways) were estimated as: 160 and 2200 ng/day for adults and 50 and 640 ng/day for children under typical and contaminated scenarios, respectively. Food ingestion appears to be the primary route of exposure in the general population. For children, the contribution from dust ingestion is nearly as great as from food ingestion. Pathway-specific contributions span several orders of magnitude and exhibit considerable overlap. PK modeling suggests central tendency PFOS intakes for adults range between 1.6 and 24.2 ng/kg-bw/day, and the forward-based intake estimates are within this range. The favorable comparison reported between the forward-modeled and the back-calculated range of intake predictions lends validity to the proposed framework.

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Bisphenol A (BPA) is a high-volume, synthetic compound found in epoxy resins and plastics used in food packaging. Food is believed to be a major source of BPA intake. In this study, we measured the concentration of BPA in convenience samplings of foodstuffs purchased in Dallas, Texas. Sampling entailed collection of 204 samples of fresh, frozen, and canned foods in two rounds in 2010. BPA was positive in 73% of the canned food samples, while it was found in only 7% of non-canned foods at low concentrations. The results of this food sampling program were used to calculate adult dietary intakes of BPA. A pathway approach combined food intakes, a “canned fraction” parameter which described what portion of total intake of that food came from canned products, and measured food concentrations. Dietary intakes were calculated as 12.6 ng/kg-day, of which 12.4 ng/kg-day was from canned foods. Canned vegetable intakes alone were 11.9 ng/kg-day. This dietary intake was compared to total intakes of BPA estimated from urine measurements of the National Health and Nutrition Examination Survey (NHANES). Total adult central tendency intakes ranged from 30 to 70 ng/kg-day for NHANES cycles between 2005 and 2010. Three possibilities were explored to explain the difference between these two approaches for intake estimation. Not all foods which may have been canned, particularly canned beverages such as soft drinks, were sampled in our food sampling program. Second, non-food pathways of exposure may be important for adults, including thermal paper exposures, and dust and air exposures. Finally, our canned food concentrations may not be adequately representative of canned foods in the United States; they were found to be generally lower compared to canned food concentrations measured in six other worldwide food surveys including three in North America. Our finding that canned food concentrations greatly exceeded non-canned concentrations was consistent with other studies, and underscores the importance of canned foods in the overall exposure of adults of BPA.

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