Per- and polyfluoroalkyl substances (PFASs) have come under increased scrutiny due to concerns about their potential toxicity and prevalence in the environment, particularly drinking water. PFASs are difficult to remove in full-scale water treatment systems because of their physicochemical properties. Here we evaluated the effectiveness of point-of-use (POU) and point-of-entry (POE) residential drinking water filters in removing a suite of three perfluoroalkyl sulfonic acids, seven perfluoroalkyl carboxylic acids, and six per- and polyfluoroalkyl ether acids in homes in central (n = 61) and southeastern (n = 12) North Carolina. POU systems included countertop and pitcher filters, faucet-mounted filters, activated carbon block refrigerator filters, activated carbon block under-sink filters, under-sink dual-stage filters, and under-sink reverse osmosis filters. All under-sink dual-stage and reverse osmosis filters tested showed near complete removal for all PFASs evaluated. In contrast, all other filters containing activated carbon exhibited variable PFAS removal. In these filters, PFAS removal efficiency was dependent on chain length, with long-chain PFASs (∼60–70% removal) being more efficiently removed than short-chain PFASs (∼40% removal). A few whole-house activated carbon POE systems (n = 8) were also evaluated; however, results were variable, and in some cases (four of eight systems), increased PFAS levels were observed in the filtered water.

Over the past few years, human exposure to per- and polyfluoroalkyl substances (PFAS) has garnered increased attention. Research has focused on PFAS exposure via drinking water and diet, and fewer studies have focused on exposure in the indoor environment. To support more research on the latter exposure pathway, we conducted a study to evaluate PFAS in indoor dust. Dust samples from 184 homes in North Carolina and 49 fire stations across the United States and Canada were collected and analyzed for a suite of PFAS using liquid and gas chromatography–mass spectrometry. Fluorotelomer alcohols (FTOHs) and di-polyfluoroalkyl phosphoric acid esters (diPAPs) were the most prevalent PFAS in both fire station and house dust samples, with medians of approximately 100 ng/g dust or greater. Notably, perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorohexane sulfonate, perfluorononanoic acid, and 6:2 diPAP were significantly higher in dust from fire stations than from homes, and 8:2 FTOH was significantly higher in homes than in fire stations. Additionally, when comparing our results to earlier published values, we see that perfluoroalkyl acid levels in residential dust appear to decrease over time, particularly for PFOA and PFOS. These results highlight a need to better understand what factors contribute to PFAS levels in dust and to understand how much dust contributes to overall human PFAS exposure.

Triphenyl phosphate (TPHP) is an unsubstituted aryl phosphate ester used as a flame retardant and plasticizer within the United States. Using zebrafish as a model, the objectives of this study were to rely on (1) mRNA-sequencing to uncover pathways disrupted following embryonic TPHP exposure and (2) high-content screening to identify nuclear receptor ligands that enhance or mitigate TPHP-induced cardiotoxicity. Based on mRNA-sequencing, TPHP exposure from 24 to 72-h postfertilization (hpf) resulted in a concentration-dependent increase in the number of transcripts significantly affected at 72 hpf, and pathway analysis revealed that 5 out of 9 nuclear receptor pathways were associated with the retinoid X receptor (RXR). Based on a screen of 74 unique nuclear receptor ligands as well as follow-up experiments, 2 compounds-ciglitazone (a peroxisome proliferator-activated receptor gamma, or PPARγ, agonist) and fenretinide (a pan-retinoic acid receptor, or RAR, agonist)-reliably mitigated TPHP-induced cardiotoxicity in the absence of effects on TPHP uptake or metabolism. As these data suggested that TPHP may be activating RXR (a heterodimer for both RARs and PPARγ), we coexposed embryos to HX 531-a pan-RXR antagonist-from 24 to 72 hpf and, contrary to our hypothesis, found that coexposure to HX 531 significantly enhanced TPHP-induced cardiotoxicity. Using a luciferase reporter assay, we also found that TPHP did not activate nor inhibit chimeric human RXRα, RXRβ, or RXRγ, suggesting that TPHP does not directly bind nor interact with RXRs. Overall, our data suggest that TPHP may interfere with RXR-dependent pathways involved in cardiac development.

Diphenyl phosphate (DPHP) is an aryl phosphate ester (APE) used as an industrial catalyst and chemical additive and is the primary metabolite of flame retardant APEs, including triphenyl phosphate (TPHP). Minimal DPHP-specific toxicity studies have been published despite ubiquitous exposure within human populations following metabolism of TPHP and other APEs. Therefore, the objective of this study was to determine the potential for DPHP-induced toxicity during embryonic development. Using zebrafish as a model, we found that DPHP significantly increased the distance between the sinus venosus and bulbus arteriosis (SV-BA) at 72 h postfertilization (hpf) following initiation of exposure before and after cardiac looping. Interestingly, pretreatment with D-mannitol mitigated DPHP-induced effects on SV-BA length despite the absence of DPHP effects on pericardial area, suggesting that DPHP-induced cardiac defects are independent of pericardial edema formation. Using mRNA-sequencing, we found that DPHP disrupts pathways related to mitochondrial function and heme biosynthesis; indeed, DPHP significantly decreased hemoglobin levels in situ at 72 hpf following exposure from 24 to 72 hpf. Overall, our findings suggest that, similar to TPHP, DPHP impacts cardiac development, albeit the potency of DPHP is significantly less than TPHP within developing zebrafish.

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