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Contaminated water and food are the main sources of documented per- and polyfluoroalkyl substances (PFAS) exposure in humans. However, other sources may contribute to the overall PFAS intake. While several studies documented the presence of PFAS in consumer products, PFAS evaluation in dental products has been limited to floss and tape to date. This study estimated PFAS exposures from a convenience sample of leave-in dental products (night guards and whitening trays), which remain in contact with the mouth for longer durations than previously evaluated dental products. This analysis evaluated whether consumer usage of these dental products meaningfully contributes to oral exposure of PFAS. Leaching of PFAS upon disposal of products was also considered. Out of 24 PFAS measured, perfluorobutanoic acid (PFBA; 3.24–4.17 ng/product or 0.67–0.83 ng/g) and perfluorooctanesulfonic acid (PFOS; 7.25–16.45 ng/product or 1.2–2.3 ng/g) were detected in night guards, and no PFAS were detected in whitening trays. Non-targeted analysis showed additional possible PFAS, which could not be characterized. The findings showed that PFOS and/or PFBA present in night guards were unlikely to pose a health concern. From an ecological perspective, the dental products examined were shown to constitute a negligible contribution to environmental PFAS. In conclusion, the examined dental products do not represent a significant source of exposure to PFAS for humans or the environment. The study demonstrates how risk assessment can be integrated by the industry into product stewardship programs to evaluate the potential health and environmental impacts of chemicals in consumer products. [ABSTRACT FROM AUTHOR]

2‐Amino‐2‐methyl‐1‐propanol (AMP™) is a widely used pH stabilizer in personal care products (PCPs); thus, the safety implications of dermal AMP exposure remain of interest. We have previously reported that exposure to AMP in PCPs when used as intended is not anticipated to result in an increased risk of hepatotoxicity (primarily steatosis and altered phospholipid homeostasis). The current study focuses on AMP in PCP's potential for developmental and reproductive toxicity (DART) in humans, based on data from animal studies. Animal studies suggest that exposure to AMP can result in post‐implantation loss. However, such effects occur at maternally toxic doses, posing a challenge for determining appropriate hazard classifications in the context of relevant consumer use scenarios. Our assessment concluded that human exposure to AMP in PCPs is not anticipated to result in DART at non‐maternally toxic doses. Further, mode of action (MOA) analysis elucidated the potential biological pathways underlying DART effects observed in high‐dose animal studies, such that perturbation of uterine choline synthesis was the most well‐supported MOA hypothesis. Downstream uterine effects might reflect choline‐dependent changes in epigenetic control of pathways important for implantation maintenance and uterine cell energetics. Since AMP‐induced post‐implantation loss occurs at doses higher than pathology related to liver toxicity, maintaining AMP exposures from exceeding the onset dose for maternal liver effects will also be protective of DART effects. Furthermore, dermal exposure to AMP expected from the use of PCPs is highly unlikely to result in toxicologically significant systemic AMP concentrations; thus, DART is not anticipated. Animal studies suggest that exposure to 2‐amino‐2‐methyl‐1‐propanol [AMP™; a pH stabilizer in personal care products (PCPs)] can result in post‐implantation loss. Our evaluation indicated that perturbation of uterine choline synthesis was the most likely hypothesis for developmental and reproductive toxicity (DART). Importantly, we showed that DART was not anticipated following exposure to non‐maternally toxic doses, since dermal exposure in humans from PCPs was unlikely to yield toxicologically significant systemic AMP concentrations. [ABSTRACT FROM AUTHOR]

Per‐ and poly‐fluoroalkyl substances (PFAS) are ubiquitous in the environment and are detected in wildlife and humans. With respect to human exposure, studies have shown that ingestion is the primary route of exposure; however, in certain settings, exposure via inhalation could also be a significant source of exposure. While many studies examined toxicity of PFAS via ingestion, limited information is available for PFAS toxicity via the inhalation route, translating into a lack of exposure guidelines. Consequently, this article examined whether route‐to‐route extrapolation to derive guidelines for inhalation exposure is appropriate for PFAS. Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) were used as exemplary PFAS given the abundance of toxicity data for these two compounds. Our evaluation determined that available toxicity and toxicokinetic data support route‐to‐route extrapolation for PFAS in order to derive inhalation‐based standards. Results from this analysis suggest that an air concentration of 7.0 × 10−5 mg/m3 (or 0.07 μg/m3) would be an appropriate RfC for PFOA and PFOS assuming the 2016 EPA RfD of 0.00002 mg/kg‐day, whereas use of the interim RfDs proposed in 2022 of 1.5 × 10−9 and 7.9 × 10−9 mg/kg would yield much lower RfCs of 5.25 × 10−9 and 2.77 × 10−8 mg/m3 (or 5.25 × 10−6 and 2.77 × 10−5 μg/m3) for PFOA and PFOS, respectively. [ABSTRACT FROM AUTHOR]

2‐Amino‐2‐methyl‐1‐propanol (AMP™) is widely used as a neutralizer/pH stabilizer in personal care products (PCPs); however, the potential health implications of dermal AMP exposure remain to be fully elucidated. Consequently, an in‐depth analysis was performed to determine if PCPs containing AMP pose an elevated risk in humans under the intended use conditions. Animal studies have shown that at high doses, oral AMP exposure could lead to liver steatosis; thus, this study focused on hepatotoxicity. Our assessment revealed that the derived margin of exposure (MoE) values for AMP‐containing PCPs were above 100, indicating that dermal exposure to AMP is unlikely to present an elevated risk of hepatotoxicity. Further, mode of action (MOA) analysis was conducted to elucidate the potential mechanisms underlying the observed hepatotoxicity in animal studies. Our analysis proposed that AMP interferes with the CDP‐choline pathway in hepatocytes via the inhibition of one or more enzymes integral to the pathway and/or the replacement of choline in the assembly of the phospholipid unit. Ultimately, these events halt the lipid export via very low‐density lipoproteins, which can subsequently develop into fatty liver accompanied by hepatotoxicity and other pathological changes if AMP exposure persists at sufficiently high doses. MOA analysis corroborated that dermal exposure to AMP expected from use of PCPs is highly unlikely to result in toxicologically significant systemic concentrations of AMP and thus hepatotoxicity. We concluded that dermal exposure to AMP in PCPs is not anticipated to result in an increased risk of hepatotoxicity. 2‐Amino‐2‐methylpropanol (AMP™) is widely used as a neutralizer/pH stabilizer in personal care products. An in‐depth analysis was performed using existing data to determine if personal care products containing AMP pose an elevated risk for liver effects in humans under the intended use conditions. Dermal exposure to AMP expected from use of personal care products is highly unlikely to result in toxicologically significant systemic concentrations of AMP and thus is not anticipated to result in an increased risk of hepatotoxicity. [ABSTRACT FROM AUTHOR]

To mitigate the spread of COVID-19, face masks, including fabric face coverings, have been encouraged or mandated. To meet demand, traditional clothes-making fabrics have been redirected to face covering manufacture. It has been reported that phthalates may be present in textiles, posing a health risk consideration for the industry; however, the potential presence of and exposure to phthalates in fabric face coverings have not been evaluated. Consequently, this study 1) estimated the concentrations of phthalates in fabric face coverings, 2) estimated the potential consumer exposures, and compared them to health guidance values (HGVs), and 3) advised on voluntary phthalate testing in textiles and/or face coverings. Precautionary upper-bound phthalate mass in face coverings was estimated from phthalate concentrations in clothing articles. Exposure to phthalates was predicted to occur predominantly via inhalation and direct dermal contact; however, for both routes, the doses were below HGVs, indicating that, based on the limited materials characterized in the literature, a health risk was unlikely. Further, the limit of 0.1% (w/w) set for individual or sum of phthalates in child care articles in the U.S. and other countries was deemed protective for children and adult face coverings. We conclude that the establishment of industry-wide voluntary phthalate quality specifications and test data for commercial face coverings or textiles used to manufacture them is advisable to substantiate product safety given the limited data. [ABSTRACT FROM AUTHOR]

Engineered nanomaterials (ENMs) are increasingly incorporated into a variety of commercial applications and consumer products; however, ENMs may possess cytotoxic properties due to their small size. This study assessed the effects of two commonly used ENMs, zinc oxide nanoparticles (ZnONPs) and silver nanoparticles (AgNPs), in the model eukaryote Saccharomyces cerevisiae. A collection of ≈4600 S. cerevisiae deletion mutant strains was used to deduce the genes, whose absence makes S. cerevisiae more prone to the cytotoxic effects of ZnONPs or AgNPs. We demonstrate that S. cerevisiae strains that lack genes involved in transmembrane and membrane transport, cellular ion homeostasis, and cell wall organization or biogenesis exhibited the highest sensitivity to ZnONPs. In contrast, strains that lack genes involved in transcription and RNA processing, cellular respiration, and endocytosis and vesicular transport exhibited the highest sensitivity to AgNPs. Secondary assays confirmed that ZnONPs affected cell wall function and integrity, whereas AgNPs exposure decreased transcription, reduced endocytosis, and led to a dysfunctional electron transport system. This study supports the use of S. cerevisiae Gene Deletion Array as an effective high-throughput technique to determine cellular targets of ENM toxicity. [ABSTRACT FROM AUTHOR]

The effects of chronic social stress on hepatic glycogenmetabolism were examined in rainbow trout Oncorhynchus mykiss by com- paring hepatocyte glucose production, liver glycogen phosphory-lase (GP) activity, and liver β-adrenergic receptors in dominant, subordinate, control, fasted, and cortisol-treated fish. Hepatocyte glucose production in subordinate fish was approximately half that of dominant fish, reflecting hepatocyte glycogen stores in subordinate trout that were just 16% of those in dominant fish. Fasting and/or chronic elevation of cortisol likely contributed to these differences based on similarities among subordinate, fasted, and cortisol-treated fish. However, calculation of the "glycogen gap"--the difference between glycogen stores used and glucose produced--suggested an enhanced gluconeogenic potential in sub-ordinate fish that was not present in fasted or cortisol-treated trout. Subordinate, fasted, and cortisol-treated trout also exhibited similar GP activities (both total activity and that of the active or a form), and these activities were in all cases significantly lower than those in control trout, perhaps reflecting an attempt to protect liver glycogen stores or a modified capacity to activate GP. Dominant trout exhibited the lowest GP activities (20%-24% of the values in control trout). Low GP activities, presumably in conjunction with incoming energy from feeding, allowed dominant fish to achieve the highest liver glycogen concentrations (double the value in control trout). Liver membrane β-adrenoceptor numbers (assessed as the number of ³H-CGP binding sites) were significantly lower in subordinate than in dominant trout, although this difference did not translate into attenuated adrenergic responsiveness in hepatocyte glucose production in vitro. Transcriptional regulation, likely as a result of fasting, was indicated by significantly lower β2-adrenoceptor relative mRNA levels in subordinate and fasted trout. Collectively, the data indicate that social status shapes liver metabolism and in particular glycogen metabolism, favoring accumulation of glycogen reserves from incoming energy in dominant fish and reliance on onboard fuels in subordinate fish. [ABSTRACT FROM AUTHOR]

The article discusses the use of β-blockers drug as endocrine disruptors and its possible effects on aquatic organisms. It says that wide use of β-adrenergic blockers or β-blockers drug which have been used as treatment for treat hypertension have led to its existence in the aquatic environment, mainly from sewage affluents. Moreover, the adrenergic system of a mammal is compared to fish and to the homologous octapaminerguc system of mollusks which is an aquatic invertebrate. Comparison shows that the function and structure of the systems are associated to the molecular similarities of octapaminergic receptors, andrenoreceptors, and catecholamine molecules, creating a possible endocrine-disrupting β-blockers. It suggests endocrine-disrupting effects of β-blockers.