Prenatal and perinatal exposure to Per- and polyfluoroalkyl substances (PFAS)-contaminated drinking water impacts offspring neurobehavior and development.

Per- and polyfluoroalkyl substances (PFAS) are persistent organic pollutants ubiquitous in the environment and humans. In-utero PFAS exposure is associated with numerous adverse health impacts. However, little is known about how prenatal PFAS mixture exposure affects offspring's neurobehavioral function. This study aims to determine the causal relationship between in-utero PFAS mixture exposure and neurobehavioral changes in Sprague-Dawley rat offspring. Dams were exposed via drinking water to the vehicle (control), an environmentally relevant PFAS mixture, or a high-dose PFAS mixture. The environmentally relevant mixture was formulated to resemble measured tap water levels in Pittsboro, NC, USA (10 PFAS compounds; sum PFAS =758.6 ng/L). The high-dose PFAS load was 3.8 mg/L (5000×), within the range of exposures in the experimental literature. Exposure occurred seven days before mating until birth. Following exposure to PFAS-laden water or the vehicle during fetal development, neurobehavioral toxicity was assessed in male and female offspring with a battery of motor, cognitive, and affective function tests as juveniles, adolescents, and adults. Just before weaning, the environmentally relevant exposure group had smaller anogenital distances compared to the vehicle and high-dose groups on day 17, and males in the environmentally relevant exposure group demonstrated lower weights than the high-dose group on day 21 (p < 0.05). Reflex development delays were seen in negative geotaxis acquisition for both exposure groups compared to vehicle-exposed controls (p = 0.009). Our post-weaning behavioral measures of anxiety, depression, and memory were not found to be affected by maternal PFAS exposure. In adolescence (week five) and adulthood (week eight), the high PFAS dose significantly attenuated typical sex differences in locomotor activity. Maternal exposure to an environmentally relevant PFAS mixture produced developmental delays in the domains of pup weight, anogenital distance, and reflex acquisition for rat offspring. The high-dose PFAS exposure significantly decreased typical sex differences in locomotor activity.

Chemistry of surface water, precipitation, throughfall, leaves, sediment, soil, and air near a gold mining region in Peru.

Artisanal and small-scale gold mining (ASGM) is the primary global source of anthropogenic mercury (Hg) emissions and a large source of landscape change. ASGM occurs throughout the world, including in the Peruvian Amazon. This data set contains measurements of surface water, precipitation, throughfall, leaves, sediment, soil, and air samples from across the Madre de Dios region of Peru, in locations near and remote from ASGM. These data were collected to determine the fate and transport of Hg across the landscape. Samples were collected in 2018 and 2019. Data predominantly included total Hg and methyl Hg concentrations in surface water, precipitation, throughfall, leaves, sediment, soil, and air. Additional water and soil parameters were also measured to better characterize their chemistry. There are no copyright restrictions; please cite this data paper when the data are used in publication.

Amazon forests capture high levels of atmospheric mercury pollution from artisanal gold mining.

Mercury emissions from artisanal and small-scale gold mining throughout the Global South exceed coal combustion as the largest global source of mercury. We examined mercury deposition and storage in an area of the Peruvian Amazon heavily impacted by artisanal gold mining. Intact forests in the Peruvian Amazon near gold mining receive extremely high inputs of mercury and experience elevated total mercury and methylmercury in the atmosphere, canopy foliage, and soils. Here we show for the first time that an intact forest canopy near artisanal gold mining intercepts large amounts of particulate and gaseous mercury, at a rate proportional with total leaf area. We document substantial mercury accumulation in soils, biomass, and resident songbirds in some of the Amazon's most protected and biodiverse areas, raising important questions about how mercury pollution may constrain modern and future conservation efforts in these tropical ecosystems.

Perfluoroalkyl Substance Exposure and the BDNF Pathway in the Placental Trophoblast.

Background: Per- and polyfluoroalkyl substances (PFAS) are persistent organic pollutants that have become globally ubiquitous in humans and the environment. In utero PFAS exposure is associated with neurodevelopmental effects; however, the mechanism is poorly understood. Brain-derived neurotrophic factor (BDNF) signaling is critical to fetal neurodevelopment during pregnancy and maintains important regulatory roles later in life. This study aims to characterize placental BDNF signaling and investigate whether PFAS exposure disrupts the signaling pathway in placental trophoblast cells. Methods: The expression and localization of BDNF receptors-p75NTR and TrkB-in first trimester and term human placentas and trophoblast cells were investigated by immunofluorescence staining. To assess the effects of PFAS exposure on the BDNF pathway, BeWo cells were treated with PFAS mixtures that mimicked blood levels in a highly exposed population and major PFAS compounds in the mixture at 0.01, 0.1, 1, and 10 µM concentrations. Changes in pro-BDNF levels and phosphorylation of TrkB receptors were examined by Western blot. Results: In first trimester human placentas, TrkB and p75NTR receptors were primarily localized to syncytiotrophoblast and cytotrophoblast cells. At term, TrkB and p75NTR receptors were primarily observed in the placental villous stroma. TrkB receptor staining in trophoblasts was reduced at term, while p75NTR receptor staining was negative. TrkB receptors were confined to the nuclear and perinuclear spaces, and phosphorylation occurred at the Tyr816 residue in BeWo cells. Exposure to PFOS, PFOA, PFBS, and the six-PFAS mixture did not significantly affect BDNF levels or activation (phosphorylation) of TrkB. Treating cells with 1 µM and 10 µM of PFNA resulted in increased TrkB phosphorylation compared to unexposed controls, but BDNF levels were unchanged. Conclusions: BDNF receptors are present in different regions of human placental villi, indicating diverse functions of BDNF signaling in placental development. Our findings suggest that the BDNF pathway in placental trophoblast cells is not disrupted by exposures to PFOS, PFOA, PFBS, and a PFAS mixture, but may be affected by PFNA exposures. Further investigation is needed on how PFAS affects other critical signaling pathways during fetal neurodevelopment.