A New Approach Refined Probabilistic Health Risk Assessment of Shaoguan Smelter Based on Microenvironment - Guangdong Province, China, 2021.

Introduction: This study introduces a novel method for developing an advanced exposure conceptual model tailored for health risk assessment, focusing on microenvironments. Methods: The research was conducted at a major smelter in China to assess the health risks associated with trace metals (TMs) pollutants in the facility and the surrounding soil. Results: Deterministic risk assessment indicated that cobalt, cadmium, antimony, manganese, arsenic, plumbum, and mercury (Co, Cd, Sb, Mn, As, Pb, and Hg) necessitated further evaluation through probabilistic risk assessment to assess potential health risks to residents. The 95% quantile concentrations of other TMs were found to be within acceptable health risk limits. For the probabilistic risk assessment, exposure parameters such as body weight, respiration rate, and exposure duration were collected using a questionnaire. This targeted assessment of the residential microenvironment revealed it as the site of the highest carcinogenic (CR) and non-carcinogenic risks (NCR), with values ranging from 2.84×10-5 to 6.7×10-5 and 1.59 to 5.57, respectively. Conclusion: The primary contaminants posing the greatest health risks in residential and industrial areas have been identified as As, Pb, and Mn. The probabilistic health risk model, which focuses on microenvironmental factors, yields more precise results and offers a valuable tool for managing soil health risks.

Typical emerging contaminants in sewage treatment plant effluent, and related watersheds in the Pearl River Basin: Ecological risks and source identification.

Emerging contaminants pose a potential risk to aquatic ecosystems in the Pearl River Basin, China, owing to the high population density and active industry. This study investigated samples from eight sewage treatment plants, and five surface water bodies of related watersheds. To screen the risk of emerging contaminants (ECs), and clarify their sources, this study calculated the risk quotient of detected chemical and performed source identification/apportionment using the positive matrix factorization method. In total, 149 organic pollutants were identified. Pharmaceuticals showed significant concentrations in sewage treatment plant samples (120.87 ng/L), compared with surface water samples (1.13 ng/L). The ecological risk assessment identified three chemicals with a heightened risk to aquatic organisms: fipronil sulfide, caffeine, and roxithromycin. Four principal sources of contaminants were identified: pharmaceutical wastewater, domestic sewage, medical effluent, and agricultural runoff. Pharmaceutical wastewater was the primary contributor (60.4 %), to the cumulative EC concentration and to ECs in sewage treatment plant effluent. Agricultural drainage was the main source of ECs in surface water. This study provides a strategy to obtain comprehensive information on the aquatic risks and potential sources of EC species in areas affected by artificial activities, which is of substantial importance to pollutant management and control.

Residual distribution and risk assessment of neonicotinoids in urban green space soils of the pearl river delta, South China: A socioeconomic analysis.

Urban green spaces are the soil component in cities that interacts most closely with humans. This study investigated the residues of seven neonicotinoids (NEOs) in soils from urban green spaces within the Pearl River Delta (PRD) region and analyzed the correlation between the residue characteristics and the region's economic development. Notably, we introduced the Nemerow Index method, a comprehensive approach, to quantify the overall pollution level of NEOs in the soil of urban park green spaces and utilized this to assess the cumulative exposure probability risks for different populations in this scenario. We found that: (1) The soil of urban park green spaces exhibited varying degrees of NEOs contamination (Σ7NEOs: N.D.-137.31; 6.25 µg/kg), with imidacloprid and clothianidin constituting the highest proportions (89.46 % and 83.60 %); (2) The residual levels of NEOs in Children's Park were significantly higher than those in community parks within Guangzhou, with an average value of 13.30 µg/kg compared to 3.30 µg/kg; (3) The residual characteristics of NEOs exhibited a positive correlation with regional economic development; specifically, the per capita GDP well correlated with IMIRPF, a summation of seven NEOs in imidacloprid equivalents via relative potency factors (R2 =0.86). Regions with higher economic development typically exhibited elevated IMIRPF levels; (4) The fitted cumulative probability distributions for average daily exposure doses revealed that children's exposure was an order of magnitude higher than adults'. Despite this, the exposure risks for both groups remained within acceptable limits.

Tracing semi-quantitatively the absorption and removal of organic pollutants in human hair based on secondary ion mass spectrometry.

Human hair has become a promising non-invasive matrix in assessing exposure to environmental organic pollutants (OPs). However, exogenous contaminants, which were absorbed into the hair via sweat, sebum, and air particles/dust, could contribute to OP levels in hair and interfere with the precise exposure assessment. So far, the microscopic mechanisms underlying the absorption of exogenous OPs into hair remain inadequately understood. This study focused on the in-situ investigation of the diffusion processes of exogenous OPs into the hair structure using secondary ion mass spectrometry (SIMS) and isotopic tracer techniques. Results showed that the relative signal intensities of deuterium-labeled tris(1,3-dichloro-2-propyl) phosphate (TDCPP), 1-hydroxypyrene (1-OH-Pry), and bisphenol A (BPA) in the hair cortex were notably elevated after a 6-hour exposure. Diffusion coefficients of contaminants were related to their molecular weight, and absorption volumes to their water solubility and molecular structures. Exposure duration and solvent influenced the rate of diffusion and absorption volumes. The distribution of deuterium-labeled molecules in exposed hair samples after washing with two different solvents (acetone or water) was similar to that before washing. Our findings revealed the diffusion of OPs in hair cross-sections, indicating exogenous contributions to contaminants that are biologically incorporated into the hair.

Neurotoxicity of tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) through the GABAergic and serotonergic neurotransmission in Caenorhabditis elegans.

Tetrabromobisphenol-A-bis(2,3-dibromopropyl ether) (TBBPA-BDBPE), a novel additive brominated flame retardant, is being developed for use in polyolefin and copolymers. Despite its emerging application, the neurotoxicity and mechanisms of action of TBBPA-BDBPE remain unexplored. Caenorhabditis elegans was utilized as the model organism to study the neurotoxic effects of TBBPA-BDBPE across environmental concentrations ranging from 0 to 100 µg/L. This investigation focused on various toxicological endpoints such as locomotive behavior, neuronal injury, neurotransmitter transmission, and the regulation of nervous system-related gene expression. Acute exposure to TBBPA-BDBPE at concentrations of 10-100 µg/L significantly impaired nematode movement, indicating potential neurotoxicity. In transgenic nematodes, this exposure also caused damage to γ-aminobutyric acid (GABAergic) and serotonergic neurons, along with notable changes in the levels of GABAergic and serotonergic neurotransmitters. Further molecular studies indicated alterations in neurotransmission-related genes (cat-4, mod-1, unc-25, and unc-47). Molecular docking analysis confirmed the binding affinity of TBBPA-BDBPE to key neurotransmission proteins-CAT-4, MOD-1, UNC-25, and UNC-47. These findings demonstrate that TBBPA-BDBPE exerts neurotoxic effects by impacting GABAergic and serotonergic neurotransmission in nematodes. This study provides new insights into the potential environmental risks of TBBPA-BDBPE.

Brominated flame retardants in surface sediment from Western Guangdong, South China: Occurrence, distribution and toxicity in Caenorhabditis elegans.

Sediment is the ultimate sink of environmental pollutants. A total of 128 surface sediment samples were collected from 8 rivers and 3 reservoirs in Maoming City, Guangdong Province. This study assessed the content and distribution of brominated flame retardants in sediments. The acute toxicity effects of tetrabromobisphenol A (TBBPA) and hexabromocyclododecane (HBCDs) in sediments were evaluated using Caenorhabditis elegans as model organisms. The concentration of TBBPA in sediments ranged from not detected (ND) to 12.59 µg/kg and was mainly distributed in the central area, which was affected by the emission of TBBPA from residential and factory. The concentration of HBCDs ranged from ND to 6.31 µg/kg, and the diastereoisomer distribution was consistent, showing a trend close to the South China Sea. The composition pattern of HBCDs in the surface sediments from rivers were 41.73%-62.33%, 7.89%-25.54%, and 18.76%-40.65% for α-, ß-, and γ-HBCD, respectively, and in the sediments from reservoirs were 26.15%-45.52%, 7.44%-19.23%, and 47.04%-61.89% for α-, ß-, and γ-HBCD, respectively. When the sum of concentrations of TBBPA and HBCD in sediments were above high levels, reactive oxygen species in nematodes significantly increased, resulting in an oxidative stress response. Intestinal permeability was also enhanced, causing intestinal damage. In addition, in terms of this study, TBBPA had a greater impact on biotoxicity compared to HBCDs, and more attention should be paid to the toxic effects of the river ecosystem organisms in Maoming City, Guangdong Province. This study can complement the pollution database in the study area and provide basic data for pollution control.

Aged polystyrene microplastics cause reproductive impairment via DNA-damage induced apoptosis in Caenorhabditis elegans.

Although polystyrene microplastics (PS-MPs) could induce toxic effects on environmental organisms, the toxicity of aged PS-MPs with H2O2 on soil organisms remains unclear. Our study utilized Caenorhabditis elegans as model organism to examine the reproductive toxicity of pristine PS-MPs (pPS-MPs) and aged PS-MPs (aPS-MPs) at environmentally relevant concentrations (0.1-100 µg/L). Acute exposure to aPS-MPs could induce greater reproductive impairment compared to pPS-MPs, as evidenced by changes in brood size and egg release. Assessment of gonad development using the number of mitotic cells, length of gonad arm, and relative area of gonad arm as parameters revealed a high reproductive toxicity caused by aPS-MPs exposure. Furthermore, aPS-MPs exposure promoted substantial germline apoptosis. Additionally, exposure to aPS-MPs (100 µg/L) markedly altered the expression of DNA damage-induced apoptosis-related genes (e.g., egl-1, cep-1, clk-2, ced-3, -4, and -9). Alterations in germline apoptosis caused by aPS-MPs were observed in mutants of cep-1, hus-1, egl-1, ced-3, -4, and -9. Consequently, the augmentation of reproductive toxicity resulting from aPS-MPs exposure was attributed to DNA damage-triggered cellular apoptosis. Additionally, the EGL-1-CEP-1-HUS-1-CED-3-CED-4-CED-9 signaling pathway was identified as a key regulator of germline apoptosis in nematodes. Our study provides insights into potential environmental risk of aPS-MPs with H2O2 on environmental organisms.

Exposure to synthesized tribromobisphenol A and critical effects: Metabolic pathways, disease signature, and benchmark dose derivation.

2,2',6-Tribromobisphenol A (Tri-BBPA), the main debrominated congener of tetrabromobisphenol A (TBBPA), is ubiquitous in the environment and human body but with unknown toxicity. Tri-BBPA was synthesized and applied to investigate its sub-chronic exposure effects on 28 organ coefficients and clinical health indicators related to liver function, kidney function, and cardiovascular system function in female mice. Results showed that the liver was the targeted organ of Tri-BBPA exposure. Compared to the control group, the changes in liver coefficient, cholinesterase, total protein, albumin, γ-glutamyl transpeptidase, lactate dehydrogenase, and creatine kinase levels ranged from -61.2 % to 35.5 % in the high-exposed group. Creatine kinase was identified as a critical effect indicator of Tri-BBPA exposure. Using the Bayesian benchmark dose derivation method, a lower reference dose than TBBPA was established for Tri-BBPA (10.6 µg/kg-day). Serum metabolomics revealed that Tri-BBPA exposure may primarily damage the liver by disrupting tryptophan metabolism related to L-alanine, tryptamine, 5-hydroxyindoleacetic acid, and 5-methoxyindoleacetate in liver cells and leading to liver dysfunction. Notably, epilepsy, schizophrenia, early preeclampsia, and late-onset preeclampsia were the top six enriched diseases, suggesting that the nervous system may be particularly affected by Tri-BBPA exposure. Our findings hinted a non-negligible health risk of exposure to debrominated products of TBBPA.

Human molybdenum exposure risk in industrial regions of China: New critical effect indicators and reference dose.

Evidence increasingly suggests molybdenum exposure at environmental levels is still associated with adverse human health, emphasizing the necessity to establish a more protective reference dose (RfD). Herein, we conducted a study measuring 15 urinary metals and 30 clinical health indicators in 2267 participants residing near chemical enterprises across 11 Chinese provinces to investigate their relationships. The kidney and cystatin-C emerged as the most sensitive organ and critical effect indicator of molybdenum exposure, respectively. Odds of cystatin-C-defined chronic kidney disease (CKD) in the highest quantile of molybdenum exposure significantly increased by 133.5% (odds ratio [OR]: 2.34, 95% CI: 1.78, 3.11) and 75.8% (OR: 1.76, 95% CI: 1.24, 2.49) before and after adjusting for urinary 14 metals, respectively. Intriguingly, cystatin-C significantly mediated 15.9-89.5% of molybdenum's impacts on liver and lung function, suggesting nephrotoxicity from molybdenum exposure may trigger hepatotoxicity and pulmonary toxicity. We derived a new RfD for molybdenum exposure (0.87 µg/kg-day) based on cystatin-C-defined estimated glomerular filtration rate by employing Bayesian Benchmark Dose modeling analysis. This RfD is significantly lower than current exposure guidance values (5-30 µg/kg-day). Remarkably, >90% of participants exceeded the new RfD, underscoring the significant health impacts of environmental molybdenum exposure on populations in industrial regions of China.

Placental inflammatory injury induced by chlorinated polyfluorinated ether sulfonate (F-53B) through NLRP3 inflammasome activation.

Chlorinated polyfluorinated ether sulfonate, commercially known as F-53B, has been associated with adverse birth outcomes. However, the reproductive toxicology of F-53B on the placenta remains poorly understood. To address this gap, we examined the impact of F-53B on placental injury and its underlying molecular mechanisms in vivo. Pregnant C57BL/6 J female mice were randomly allocated to three groups: the control group, F-53B 0.8 µg/kg/day group, and F-53B 8 µg/kg/day group. After F-53B exposure through free drinking water from gestational day (GD) 0.5-14.5, the F-53B 8 µg/kg/day group exhibited significant increases in placental weights and distinctive histopathological alterations, including inflammatory cell infiltration, heightened syncytiotrophoblast knots, and a loosened trophoblastic basement membrane. Within the F-53B 8 µg/kg/day group, placental tissue exhibited increased apoptosis, as indicated by increased caspase3 activation. Furthermore, F-53B potentially induced the NF-κB signaling pathway activation through IκB-α phosphorylation. Subsequently, this activation upregulated the expression of inflammatory cytokines and components of the NLRP3 inflammasome, including activated caspase1, IL-1ß, IL-18, and cleaved gasdermin D (GSDMD), ultimately leading to pyroptosis in the mouse placenta. Our findings reveal a pronounced inflammatory injury in the placenta due to F-53B exposure, suggesting potential reproductive toxicity at concentrations relevant to the human population. Further toxicological and epidemiological investigations are warranted to conclusively assess the reproductive health risks posed by F-53B.

Photoaged Nanopolystyrene Affects Neurotransmission to Induce Transgenerational Neurotoxicity in Caenorhabditis elegans.

Nanopolystyrene (NPS), a frequently employed nanoplastic, is an emerging environmental contaminant known to cause neurotoxicity in various organisms. However, the potential for transgenerational neurotoxic effects, especially from photoaged NPS (P-NPS), remains underexplored. This study investigated the aging of virgin NPS (V-NPS) under a xenon lamp to simulate natural sunlight exposure, which altered the physicochemical characteristics of the NPS. The parental generation (P0) of Caenorhabditis elegans was exposed to environmental concentrations (0.1-100 µg/L) of V-NPS and P-NPS, with subsequent offspring (F1-F4 generations) cultured under NPS-free conditions. Exposure to 100 µg/L P-NPS resulted in more pronounced deterioration in locomotion behavior in the P0 generation compared to V-NPS; this deterioration persisted into the F1-F2 generations but returned to normal in the F3-F4 generations. Additionally, maternal exposure to P-NPS damaged dopaminergic, glutamatergic, and serotonergic neurons in subsequent generations. Correspondingly, there was a significant decrease in the levels of dopamine, glutamate, and serotonin, associated with reduced expression of neurotransmission-related genes dat-1, eat-4, and tph-1 in the P0 and F1-F2 generations. Further analysis showed that the effects of P-NPS on locomotion behavior were absent in subsequent generations of eat-4(ad572), tph-1(mg280), and dat-1(ok157) mutants, highlighting the pivotal roles of these genes in mediating P-NPS-induced transgenerational neurotoxicity. These findings emphasize the crucial role of neurotransmission in the transgenerational effects of P-NPS on locomotion behavior, providing new insights into the environmental risks associated with exposure to photoaged nanoplastics.

Low-dose BPA-induced neuronal energy metabolism dysfunction and apoptosis mediated by PINK1/parkin mitophagy pathway in juvenile rats.

Bisphenol A (BPA) is related to neurological disorders involving mitochondrial dysfunction, while the mechanism remains elusive. Therefore, we explored it through in vitro and in vivo experiments. In vitro, hippocampal neurons derived from neonatal rats of different genders were exposed to 1-100 nM and 100 µM BPA, autophagy activator Rapa and inhibitor 3-MA for 7 d. The results suggested that even nanomolar BPA (1-100 nM) disturbed Ca2+ homeostasis and damaged the integrity of mitochondrial cristae in neurons (p < 0.05). Furthermore, BPA increased the number of autophagic lysosomes, LC3II/LC3I ratio, and p62 expression, and decreased parkin expression (p < 0.05), suggesting that the entry of damaged mitochondria into autophagic pathway was prompted, while the autophagic degradation pathway was blocked. This further disrupts neuronal energy metabolism and promotes neuronal apoptosis. However, Rapa attenuated the adverse effects caused by BPA, while 3-MA exacerbated these reactions. In vivo, exposure of juvenile rats to 0.5, 50, 5000 µg/kg‧bw/day BPA during PND 7-21 markedly impaired the structure of hippocampal mitochondria, increased the number of autophagosomes, the rate of neuronal apoptosis, and the expression levels of pro-apoptotic proteins Cyt C, Bax, Bak1, and Caspase3, and decreased the expression of anti-apoptotic protein Bcl2 (p < 0.05). Particularly, male rats are more sensitive to low-dose BPA than females. Overall, environmental-doses BPA can induce the imbalance of energy metabolism in hippocampal neurons via PINK1/parkin mitophagy, thereby inducing their apoptosis. Importantly, this study provides a theoretical basis for attenuating BPA-related neurological diseases.

Enhanced humification of full-scale apple wood and cow manure by promoting lignocellulose degradation via biomass pretreatments.

Agroforestry waste and cow manure pollute the environment, of which, agroforestry waste is difficult to degrade. Compost is an effective way to dispose agroforestry waste; however, the low degradation efficiency of lignocellulose in agroforestry waste affects the process of composting humification. This study investigated lignocellulose degradation and composting humification in full-size apple wood and cow manure composting processes by applying different pretreatments (acidic, alkaline, and high-temperature) to apple wood. Simultaneously, physicochemical characterization and metagenome sequencing were combined to analyze the function of carbohydrate-active enzymes database (CAZy). Therefore, microbial communities and functions were linked during the composting process and the lignocellulose degradation mechanism was elaborated. The results showed that the addition of apple wood increased the compost humus (HS) yield, and pretreatment of apple wood enhanced the lignocellulose degradation during composting processes. In addition, pretreatment improved the physicochemical properties, such as temperature, pH, electric conductivity (EC), ammonium nitrogen (NH4+), and nitrate nitrogen (NO3-) in the compost, of which, acid treated apple wood compost (AcAWC) achieved the highest temperature of 58.4 °C, effectively promoting nitrification with NO3- ultimately reaching 0.127 g/kg. In all composts, microbial networks constructed a high proportion of positively correlated connections, and microorganisms promoted the composting process through cooperation. The proportions of glycosyltransferase (GT) and glycoside hydrolase (GH) promoted the separation and degradation of lignocellulose during composting to form HS. Notably, the adverse effects of the alkali-treated apple wood compost on bacteria were greater. AcAWC showed significant correlations between bacterial and fungal communities and both lignin and hemicellulose, and had more biomarkers associated with lignocellulose degradation and humification. The lignin degradation rate was 24.57 % and the HS yield increased by 27.49 %. Therefore, AcAWC has been confirmed to enhance lignocellulose degradation and promote compost humification by altering the properties of the apple wood and establishing a richer microbial community.

Combined neurotoxicity of aged microplastics and thiamethoxam in the early developmental stages of zebrafish (Daniorerio).

Microplastics (MPs) pollution, together with its consequential effect on aquatic biota, represent a burgeoning environmental concern that has garnered significant scholarly attention. Thiamethoxam (TMX), a prevalently utilized neonicotinoid insecticide, is renowned for its neurotoxic impact and selective action against targeted pests. The aquatic environment serves as a receptacle for numerous pollutants, such as MPs and neonicotinoid insecticides. However, there is currently a lack of comprehensive understanding regarding the toxic effects of co-exposure to aged MPs and neonicotinoid insecticides in aquatic organisms. Therefore, we endeavor to elucidate the deleterious impacts of aged polystyrene (PS) and TMX on zebrafish (Danio rerio) larvae when present at environmentally relevant concentrations, and to reveal the underlying molecular mechanisms driving these effects. Our study showed that exposure to aged PS, TMX, or their combination notably inhibited the heart rate and locomotion of zebrafish larvae, with a pronounced effect observed under combined exposure. Aged PS and TMX were found to diminish the activity of antioxidative enzymes (SOD, CAT, and GST), elevate MDA levels, and disrupt neurotransmitter homeostasis (5-HT, GABA and ACh). Notably, the mixtures exhibited synergistic effects. Moreover, gene expression related to oxidative stress (e.g., gstr1, gpx1a, sod1, cat1, p38a, ho-1, and nrf2b) and neurotransmission (e.g., ache, ChAT, gat1, gabra1, 5ht1b, and 5ht1aa) was significantly altered upon co-exposure to aged PS and TMX in larval zebrafish. In summary, our findings support the harmful effects of aged MPs and the neonicotinoid insecticides they carry on aquatic organisms. Results from this study enhance our understanding of the biological risks of MPs and insecticides, as well as help fill existing knowledge gaps on neonicotinoid insecticides and MPs coexistence toxicity in aquatic environment.

Melanin-mediated accumulation of polycyclic aromatic hydrocarbons in human hair: Insights from biomonitoring and cell exposure studies.

While human hair is widely used to monitor micro-organic contaminants (MOCs), their incorporation mechanisms are poorly understood. Melanin, known to facilitate the accumulation of drugs in hair, hasn't been studied in the field of MOCs. Here, polycyclic aromatic hydrocarbons (PAHs), a class of priority MOCs, were investigated through hair biomonitoring as well as cell exposure experiments. PAH concentrations and melanin contents were measured in black and white hairs from the same individual. The results showed that five dominant PAHs (phenanthrene, fluoranthene, pyrene, benzo[a]anthracene and chrysene) in black hair (0.66 ng/g - 35.1 ng/g) were significantly higher than those in white hair (0.52 ng/g - 29.6 ng/g). Melanin contents in black hair (14.9 - 48.9 ng/g) were markedly higher than in white hair (0.35 - 2.15 ng/g) and were correlated to PAH concentrations, hinting melanin-mediated accumulation of PAHs in hair. The in vitro experiment using murine melanoma cells demonstrates that PAH levels in cells were affected by melanin, suggesting the affinity of melanin to PAHs. Both biomonitoring and cell exposure experiment implicate the pivotal role of melanin in PAH accumulation in hair. Therefore, to ensure the accuracy of hair biomonitoring for MOCs, attention must be paid to the melanin content uniformity.

Leaching kinetics and bioaccumulation potential of additive-derived organophosphate esters in microplastics.

Considerable research has been conducted to evaluate microplastics (MPs) as vehicles for the transfer of hazardous pollutants in organisms. However, little effort has been devoted to the chemical release of hazardous additive-derived pollutants from MPs in gut simulations. This study looked at the leaching kinetics of organophosphate esters (OPFRs) from polypropylene (PP) and polystyrene (PS) MPs in the presence of gut surfactants, specifically sodium taurocholate, at two biologically relevant temperatures for marine organisms. Diffusion coefficients of OPFRs ranged from 1.71 × 10-20 to 4.04 × 10-18 m2 s-1 in PP and 2.91 × 10-18 to 1.51 × 10-15 m2 s-1 in PS. The accumulation factors for OPFRs in biota-plastic and biota-sediment interactions ranged from 1.52 × 10-3-69.1 and 0.02-0.7, respectively. Based on B3LYP/6-31G (d,p) calculations, the biodynamic model analysis revealed a slight increase in the bioaccumulation of OPFRs at a minor dose of 0.05% MPs. However, at higher concentrations (0.5% and 5% MPs), there was a decrease in bioaccumulation compared to the lower concentration for most OPFR compounds. In general, the ingestion of PE MPs notably contributed to the bioaccumulation of OPFRs in lugworms, whereas the contribution of PP and PS MPs was minimal. This could vary among sites exhibiting varying levels of MP concentrations or MPs displaying stronger affinities towards chemicals.

First Insight into Fetal Exposure to Legacy and Emerging Plasticizers Revealed by Infant Hair and Meconium: Occurrence, Biotransformation, and Accumulation.

Epidemiological studies have demonstrated the embryonic and developmental toxicity of plasticizers. Thus, understanding the in utero biotransformation and accumulation of plasticizers is essential to assessing their fate and potential toxicity in early life. In the present study, 311 infant hair samples and 271 paired meconium samples were collected at birth in Guangzhou, China, to characterize fetal exposure to legacy and emerging plasticizers and their metabolites. Results showed that most of the target plasticizers were detected in infant hair, with medians of 9.30, 27.6, and 0.145 ng/g for phthalate esters (PAEs), organic phosphate ester (OPEs), and alternative plasticizers (APs), and 1.44, 0.313, and 0.066 ng/g for the metabolites of PAEs, OPEs, and APs, respectively. Positive correlations between plasticizers and their corresponding primary metabolites, as well as correlations among the oxidative metabolites of bis(2-ethylhexyl) phthalate (DEHP) and 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH), were observed, indicating that infant hair retained the major phase-I metabolism of the target plasticizers. While no positive correlations were found in parent compounds or their primary metabolites between paired infant hair and meconium, significant positive correlations were observed among secondary oxidative metabolites of DEHP and DINCH in hair and meconium, suggesting that the primary metabolites in meconium come from hydrolysis of plasticizers in the fetus but most of the oxidative metabolites come from maternal-fetal transmission. The parent compound/metabolite ratios in infant hair showed a decreasing trend across pregnancy, suggesting in utero accumulation and deposition of plasticizers. To the best of our knowledge, this study is the first to report in utero exposure to both parent compounds and metabolites of plasticizers by using paired infant hair and meconium as noninvasive biomonitoring matrices and provides novel insights into the fetal biotransformation and accumulation of plasticizers across pregnancy.

Photoaged polystyrene microplastics result in neurotoxicity associated with neurotransmission and neurodevelopment in zebrafish larvae (Danio rerio).

Microplastics (MPs) are emerging pollutants widely distributed in the environment, inducing toxic effects in various organisms. However, the neurotoxicity and underlying mechanisms of simulated sunlight-aged MPs have rarely been investigated. In this study, zebrafish (Danio rerio) were exposed to environmentally relevant concentrations (0, 0.1, 1, 10, and 100 µg/L) of virgin polystyrene (V-PS) and aged polystyrene (A-PS) for 120 hpf to evaluate the neurotoxicity. The results demonstrated that simulated sunlight irradiation altered the physicochemical properties (morphology, functional groups, and chemical composition) of V-PS. Exposure to A-PS causes greater toxicity on locomotor ability in larval zebrafish than V-PS. Motor neuron development was disrupted by transgenic (hb9-GFP) zebrafish larvae exposed to A-PS, with significant alterations in neurotransmitter levels (ACh, DA, 5-HT, and GABA) and enzyme activity (AChE, ChAT, and ChE). Further investigation found that exposure to A-PS had a significantly impact on the expression of neurotransmission and neurodevelopment-related genes in zebrafish. These findings suggest that A-PS induces neurotoxicity by its effects on neurotransmission and neurodevelopment. This study highlights the neurotoxic effects and mechanisms of simulated sunlight irradiation of MPs, providing new insights for assessing the ecological risks of photoaged MPs in the environment.

Comprehensive analysis of environmental exposure to hazardous trace elements and lung function: a national cross-sectional study.

BACKGROUND: There is growing interest in the joint effects of hazardous trace elements (HTEs) on lung function deficits, but the data are limited. This is a critical research gap given increased global industrialisation. METHODS: A national cross-sectional study including spirometry was performed among 2112 adults across 11 provinces in China between 2020 and 2021. A total of 27 HTEs were quantified from urine samples. Generalised linear models and quantile-based g-computation were used to explore the individual and joint effects of urinary HTEs on lung function, respectively. RESULTS: Overall, there were negative associations between forced expiratory volume in 1 s (FEV1) and urinary arsenic (As) (z-score coefficient, -0.150; 95% CI, -0.262 to -0.038 per 1 ln-unit increase), barium (Ba) (-0.148, 95% CI: -0.258 to -0.039), cadmium (Cd) (-0.132, 95% CI: -0.236 to -0.028), thallium (Tl) (-0.137, 95% CI: -0.257 to -0.018), strontium (Sr) (-0.147, 95% CI: -0.273 to -0.022) and lead (Pb) (-0.121, 95% CI: -0.219 to -0.023). Similar results were observed for forced vital capacity (FVC) with urinary As, Ba and Pb and FEV1/FVC with titanium (Ti), As, Sr, Cd, Tl and Pb. We found borderline associations between the ln-quartile of joint HTEs and decreased FEV1 (-20 mL, 95% CI: -48 to +8) and FVC (-14 mL, 95% CI: -49 to+2). Ba and Ti were assigned the largest negative weights for FEV1 and FVC within the model, respectively. CONCLUSION: Our study investigating a wide range of HTEs in a highly polluted setting suggests that higher urinary HTE concentrations are associated with lower lung function, especially for emerging Ti and Ba, which need to be monitored or regulated to improve lung health.

Chronic neurotoxicity of Tetrabromobisphenol A: Induction of oxidative stress and damage to neurons in Caenorhabditis elegans.

Tetrachlorobisphenol A (TCBPA) has been used as an alternative flame retardant in various fields. However, the long-term effects of TCBPA on the nervous system remain unclear. Thus, Caenorhabditis elegans (L4 larvae) were selected as a model animal to investigate the neurotoxic effects and underlying mechanisms after 10 d of TCBPA exposure. Exposure to TCBPA (0.01-100 µg/L) decreased locomotive behavior in a concentration-dependent manner. In addition, reactive oxygen species (ROS) formation and lipofuscin accumulation were significantly increased, and the expression of sod-3 was upregulated in the exposed nematodes, indicating that TCBPA exposure induced oxidative damage. Furthermore, 100 µg/L TCBPA exposure caused a reduction in dopamine and serotonin levels, and damage in dopaminergic and serotoninergic neurons, which was further confirmed by the downregulated expression of related genes (e.g., dop-1, dop-3, cat-1, and mod-1). Molecular docking analysis demonstrated the potential of TCBPA to bind to the neurotransmitter receptor proteins DOP-1, DOP-3, and MOD-1. These results indicate that chronic exposure to TCBPA induces neurotoxic effects on locomotive behavior, which is associated with oxidative stress and damage to dopaminergic and serotoninergic neurons.