No abstract

This is the first study in the last 15 years to analyze per-and polyfluoroalkyl substances (PFAS) in breast milk collected from mothers (n = 50) in the United States, and our findings indicate that both legacy and current-use PFAS now contaminate breast milk, exposing nursing infants. Breast milk was analyzed for 39 PFAS, including 9 short-chain and 30 long-chain compounds, and 16 of these PFAS were detected in 4−100% of the samples. The ∑PFAS concentration in breast milk ranged from 52.0 to 1850 pg/mL with a median concentration of 121 pg/mL. Perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) were the most abundant PFAS in these samples (medians 30.4 and 13.9 pg/mL, respectively). Two short-chain PFAS, including perfluoro-n-hexanoic acid (PFHxA, C6) and perfluoro-nheptanoic acid (PFHpA, C7), were detected in most of the samples with median concentrations of 9.69 and 6.10 pg/mL, respectively. Analysis of the available breast milk PFAS data from around the world over the period of 1996−2019 showed that while the levels of the phased-out PFOS and PFOA have been declining with halving times of 8.1 and 17 years, respectively, the detection frequencies of current-use short-chain PFAS have been increasing with a doubling time of 4.1 years.

Organophosphate esters (OPEs) are among the synthetic chemicals found in the highest concentrations in the indoor environment due to their use as flame retardants and plasticizers. In fish and wildlife, metabolites of OPEs have been found to build up in tissues. In this study, 28 triester OPEs (tri-OPEs) and their seven corresponding diester (di-OPE) and three hydroxyl metabolites were measured in breast milk collected from 50 U.S. mothers. Tris­(1-chloro-2-propyl) phosphate, used in foam for insulation and furniture and the target compound with the largest U.S. production volume, was the most abundant tri-OPE (median level of 1.47 ng/mL). Di-n-butyl phosphate (DNBP), the metabolite of tri-n-butyl phosphate (TNBP), which has broad uses in adhesives, plastics, and hydraulic fluids, was the most abundant OPE metabolite (median level of 7.44 ng/mL) detected in these samples. Overall, the Σdi-OPE concentrations (median level of 8.32 ng/mL) were twice as high as the Σtri-OPE concentrations (median of 3.85 ng/mL). The estimated daily intakes of tri- and di-OPEs through lactation were up to 50 times higher than those through diet and dust ingestion. This is the first study to simultaneously determine OPEs and their metabolites in breast milk, and our findings indicate that breastfeeding is a significant source of OPE exposure for infants.

Inhalation of halogenated flame-retardants (HFRs) released from consumer products is an important route of exposure. However, not all airborne HFRs are respirable, and thus interact with vascular membranes within the gas exchange (alveolar) region of the lung. HFRs associated with large (>4 µm), inhalable airborne particulates are trapped on the mucosal lining of the respiratory tract and then are expelled or swallowed. The latter may contribute to internal exposure via desorption from particles in the digestive tract. Exposures may also be underestimated if personal activities that re-suspend particles into the breathing zone are not taken into account. Here, samples were collected using personal air samplers, clipped to the participants’ shirt collars (n = 18). We observed that the larger, inhalable air particulates carried the bulk (>92%) of HFRs. HFRs detected included those removed from commerce (i.e., polybrominated diphenyl ethers (Penta-BDEs: BDE-47, -85, -100, -99, and -153)), their replacements; e.g., 2-ethylhexyl 2,3,4,5-tetrabromobenzoate (TBB or EH-TBB); bis(2-ethylhexyl) 3,4,5,6-tetrabromophthalate (TBPH or BEH-TEBP) and long-produced chlorinated organophosphate-FRs (ClOPFRs): tris(2-chloroethyl)phosphate (TCEP), tris(1-chloro-2-propyl)phosphate (TCPP or TCIPP), and tris(1,3-dichloro-2-propyl)phosphate (TDCPP or TDCIPP). Our findings suggest estimates relying on a single exposure route, i.e., alveolar gas exchange, may not accurately estimate HFR internal dosage, as they ignore contributions from larger inhalable particulates that enter the digestive tract. Consideration of the fate and bioavailability of these larger particulates resulted in higher dosage estimates for HFRs with log Koa < 12 (i.e., Penta-BDEs and ClOPFRs) and lower estimates for those with log Koa > 12 (i.e., TBB and TBPH) compared to the alveolar route exposure alone. Of those HFRs examined, the most significant effect was the lower estimate by 41% for TBPH. The bulk of TBPH uptake from inhaled particles was estimated to be through the digestive tract, with lower bioavailability. We compared inhalation exposure estimates to chronic oral reference doses (RfDs) established by several regulatory agencies. The U.S. Environmental Protection Agency (EPA) RfD levels for several HFRs are considered outdated; however, BDE-99 levels exceeded those suggested by the Dutch National Institute for Public Health and the Environment (RIVM) by up to 26 times. These findings indicate that contributions and bioavailability of respirable and inhalable airborne particulates should both be considered in future risk assessments.