Bisphenol A (BPA) is a representative endocrine disrupting compound used in a vast array of consumer products, and are being frequently substituted by its analogues, bisphenol S (BPS) and bisphenol F (BPF). We aimed to examine the association between urinary bisphenol levels with obesity and lipid profiles in the general population to comprehensively evaluate its potential of metabolic disturbance. A representative sample of 1046 US adults from the National Health and Nutrition Examination Survey (2013–2016) and 3268 Korean adults from the Korean National Environmental Health Survey (2015–2017) was analyzed. We examined the exposure levels of bisphenols and determined their associations with obesity, high-density lipoprotein cholesterol (HDL-C) and triglyceride (TG) levels, and hypercholesterolemia prevalence through multiple linear, and binary/ordinal logistic regression models. In both populations, high BPA levels (lowest tertile vs. 2nd, 3rd tertiles) showed corresponding associations with lipid profile and obesity. BPA levels were associated with decreased HDL-C levels (Q3: β = −0.053, p = 0.08 (US); Q2: β = −0.030, p-0.03), increased TG levels (Q3: β = 0.121, p = 0.029 (US); Q3: β = 0.089, p = 0.021, and higher odds for obesity (Q3: OR = 1.58, 95% CI: 1.06, 2.35 (US); Q3: OR = 1.41, 95% CI: 1.11, 1.78). Higher BPS levels were positively associated with obesity status, especially in US men (Q2: OR = 1.84, 95% CI: 1.15, 2.96) and Korean women (Q3: OR = 1.27, 95% CI: 0.99, 1.64). A significant decrease in HDL-C (Q3: β = −0.088, p = 0.01) and elevated odds for obesity at higher BPF levels (Q3: OR = 1.60, 95% CI: 1.00, 2.56) was observed in US women. The findings of our study indicate that BPA and its analogues, BPS and BPF, are associated with lipid metabolism disorders in addition to obesity in adults. Given the increase in exposure to BPA alternatives, continuous biomonitoring, and further investigation of their health effects through prospective cohort studies are warranted.

Assessments of antimony (Sb) and arsenic (As) contamination in sediments are reported on a wide range of different particle size fractions, including <63 μm, < 180 μm and <2 mm. Guidelines vary between jurisdictions which limits comparative assessment between contamination events and complicates ecotoxicity assessment, and almost no information exists on Sb size distribution in contaminated sediments. This study quantified and compared the size distribution of Sb and As in 11 sediments (and 2 floodplain soils) collected along 320 km of waterway contaminated by historic mining activity. Sediment particle size distribution was the primary determinant of total metalloid load in size fractions across the varying substrates of the waterway. Minerals and sorption complexes influenced metalloid particle distribution but relative importance depended on location. Arsenic concentrations were greatest in the fine <63 μm fraction across all the different river environments (7.3–189 mg kg⁻¹, or 1–26% of total sample As), attributed to fine-grained primary arsenopyrite and/or sorption of As(V) to fine solid-phases. The Sb particle size concentrations were greatest in mid-size fractions (205–903 mg kg⁻¹) in the upper catchment and up to 100 km downstream to the mid-catchment as a result of remnant Sb minerals. Antimony concentrations in the lower catchment were greatest in the <63 μm fraction (8.8–12.1 mg kg⁻¹), reflecting the increasing importance of sorption for Sb particle associations. This work demonstrates the importance of particle size analysed for assessment of sediment quality, and provides support for analysis of at least the <250 μm fraction for Sb and As when comparing pollutant distribution in events impacted by primary contamination. Analysis of the <63 μm fraction, however, provides good representation in well-dispersed contaminated sediments.

The removal of excessive ammonium from water is vital for preventing eutrophication of surface water and ensuring drinking water safety. Several studies have explored the use of biochar for removing ammonium from water. However, the efficacy of pristine biochar is generally weak, and various biochar modification approaches have been proposed to enhance adsorption capacity. In this study, biochar obtained from giant reed stalks (300, 500, 700 °C) was modified by sulfonation, and the ammonium adsorption capabilities of both giant reed biochars (RBCs) and sulfonated reed biochars (SRBCs) were assessed. The ammonium adsorption rates of SRBCs were much faster than RBCs, with equilibrium times of ∼2 h and ∼8 h for SRBCs and RBCs, respectively. The Langmuir maximum adsorption capacities of SRBCs were 4.20–5.19 mg N/g for SRBCs, significantly greater than RBCs (1.09–1.92 mg N/g). Physical-chemical characterization methods confirmed the increased levels of carboxylic and sulfonic groups on sulfonated biochar. The reaction of ammonium with these O-containing functional groups was the primary mechanism for the enhancement of ammonium adsorption by SRBCs. To conclude, sulfonation significantly improved the adsorption performance of biochar, suggesting its potential application for ammonium mitigation in water.

Various modern products have metallic nanoparticles (MNPs) embedded to enhance products performance. Technological advances enable nowadays even multiple hybrid nanoparticles. Consequently, the future co-release of multiple MNPs will inevitably result in the presence of MNP mixtures in the environment. An important question is if the responses of mixtures of MNPs can be dealt with in a similar way as with the responses of biota to mixtures of metal salts. Moreover, natural organic matter (NOM) is an important parameter affecting the behavior and effect of MNPs. Herein, we determined the joint toxicity and accumulation of copper nanoparticles (CuNPs) and zinc oxide nanoparticles (ZnONPs) in Daphnia magna in the absence and presence of Suwannee River natural organic matter (SR-NOM), compared to the joint toxicity and accumulation of corresponding metal salts. The results of toxicity testing showed that the joint toxicity of CuNPs + ZnONPs was greater than the single toxicity of CuNPs or ZnONPs. The joint toxic action of CuNPs + ZnONPs was additive or more-than-additive for D. magna. A similar pattern was found in the toxicity of the mixtures of Cu- and Zn-salts from the literature data. The presence of SR-NOM had no significant impact on the joint toxicity of CuNPs + ZnONPs. The calculated component-specific contribution to overall toxicity indicated that SR-NOM increased the relative contribution of dissolved ions released from the MNPs to the toxicity of the binary mixtures at high-effect concentrations of individual MNPs. Moreover, dissolved Zn-ions released from the ZnONPs were found to dominate the joint toxicity of CuNPs + ZnONPs in the presence of SR-NOM. Furthermore, the results of the accumulation experiment displayed that the presence of SR-NOM significantly enhanced the accumulation of either CuNPs or ZnONPs in D. magna exposed to the MNP mixtures.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) is frequently detected in the environment due to the abundance of its use. These levels might be hazardous to human health and ecosystems. Phthalates have been associated with neurological disorders, yet whether chronic DEHP exposure plays a role in Parkinson's disease (PD) or its underlying mechanisms is unknown. We investigated the effects of chronic DEHP exposure less than an environmentally-relevant dose on PD hallmarks, using Caenorhabditis elegans as a model. We show that developmental stage and exposure timing influence DEHP-induced dopaminergic neuron degeneration. In addition, in response to chronic DEHP exposure at 5 mg/L, mitochondrial fragmentation became significantly elevated, reactive oxygen species (ROS) levels increased, and ATP levels decreased, suggesting that mitochondrial dysfunction occurs. Furthermore, the data show that mitochondrial complex I (nuo-1 and gas-1) and complex II (mev-1) are involved in DEHP-induced dopaminergic neuron toxicity. These results suggest that chronic exposure to DEHP at levels less than an environmentally-relevant dose causes dopaminergic neuron degeneration through mitochondrial dysfunction involving mitochondrial complex I and II. Considering the high level of genetic conservation between C. elegans and mammals, chronic DEHP exposure might elevate the risk of developing PD in humans.

Environmental heavy metal exposure has been considered to be the risk factor for neurodevelopmental disorders in children. However, the available data on the associations between multiple metals exposure and the risk of dyslexia in China are limited. The purpose of our study was to examine the associations between urinary metal concentrations and Chinese dyslexia risk. A total of 56 Chinese dyslexics and 60 typically developing children were recruited. The urinary concentration of 13 metals were measured by inductively coupled plasma-mass spectrometer (ICP-MS). Binary logistic regression and the Probit extension of Bayesian kernel machine regression (BKMR-P) were used to explore the associations between multiple metal exposure and the risk of Chinese dyslexia. Our results indicated that Co, Zn and Pb were significantly associated with Chinese dyslexia in the multiple-metal exposure model. After adjusting the covariates, a positive association was observed between Pb and the risk of Chinese dyslexia, with the odds ratio (OR) in the highest quartiles of 6.81 (95%CI: 1.07–43.19; p–trend = 0.024). Co and Zn were negatively associated with the risk of Chinese dyslexia. Compared to the lowest quartile, the ORs of Co and Zn in the highest quartile are 0.13 (95%CI: 0.02–0.72; p–trend = 0.026) and 0.18 (95%CI: 0.04–0.88; p–trend = 0.038), respectively. In addition, BKMR-P analysis indicated that with the cumulative level across Co, Zn and Pb increased, the risk of Chinese dyslexia gradually declined and then rebounded, albeit non-significantly, and Pb was the major contributor in this association. In general, the urinary concentrations of Co, Zn and Pb were significantly associated with Chinese dyslexia. More prospective studies are needed to confirm the health effects of multiple metals exposure in children with Chinese dyslexia.

Pollution from vehicle tires has received world-wide research attention due to its ubiquity and toxicity. In this study, we measured various tire-derived contaminants semi-quantitatively in archived extracts of passive air samplers deployed in 18 major cities that comprise the Global Atmospheric Passive Sampling (GAPS) Network (GAPS-Megacities). Analysis was done on archived samples, which represent one-time weighted passive air samples from each of the 18 monitoring sites. The target analytes included cyclic amines, benzotriazoles, benzothiazoles, and p-phenylenediamine (PPD) derivatives. Of the analyzed tire-derived contaminants, diphenylguanidine was the most frequently detected analyte across the globe, with estimated concentrations ranging from 45.0 pg/m³ in Beijing, China to 199 pg/m³ in Kolkata, India. The estimated concentrations of 6PPD-quinone and total benzothiazoles (including benzothiazole, 2-methylthio-benzothiazole, 2-methyl-benzothiazole, 2-hydroxy-benzothiazole) peaked in the Latin American and the Caribbean region at 1 pg/m³ and 100 pg/m³, respectively. In addition, other known tire-derived compounds, such as hexa(methoxymethyl)melamine, phenylguanidine, and various transformation products of 6PPD, were also monitored and characterized semi-quantitatively or qualitatively. This study presents some of the earliest data on airborne concentrations of chemicals associated with tire-wear and shows that passive sampling is a viable techniquefor monitoring airborne tire-wear contamination. Due to the presence of many tire-derived contaminants in urban air across the globe as highlighted by this study, there is a need to determine the associated exposure and toxicity of these chemicals to humans.

Second generation anticoagulant rodenticides (SGARs) are widely used to control rodents around the world. However, contamination by SGARs is detectable in many non-target species, particularly carnivorous mammals or birds-of-prey that hunt or scavenge on poisoned rodents. The SGAR trophic transfer pathway via rodents and their predators/scavengers appears widespread, but little is known of other pathways of SGAR contamination in non-target wildlife. This is despite the detection of SGARs in predators that do not eat rodents, such as specialist bird-eating hawks. We used a Bayesian modelling framework to examine the extent and spatio-temporal trends of SGAR contamination in the livers of 259 Eurasian Sparrowhawks, a specialist bird-eating raptor, in regions of Britain during 1995–2015. SGARs, predominantly difenacoum, were detected in 81% of birds, with highest concentrations in males and adults. SGAR concentrations in birds were lowest in Scotland and higher or increasing in other regions of Britain, which had a greater arable or urban land cover where SGARs may be widely deployed for rodent control. However, there was no overall trend for Britain, and 97% of SGAR residues in Eurasian Sparrowhawks were below 100 ng/g (wet weight), which is a potential threshold for lethal effects. The results have potential implications for the population decline of Eurasian Sparrowhawks in Britain. Fundamentally, the results indicate an extensive and persistent contamination of the avian trophic transfer pathway on a national scale, where bird-eating raptors and, by extension, their prey appear to be widely exposed to SGARs. Consequently, these findings have implications for wildlife contamination worldwide, wherever these common rodenticides are deployed, as widespread exposure of non-target species can apparently occur via multiple trophic transfer pathways involving birds as well as rodents.