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Exploring the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and the risk of dyslipidemia and possible mediating effects is essential for conducting epidemiological health studies on related lipid disorders. Therefore, our study aimed to elucidate the potential association between PAH exposure and dyslipidemia risk and further identify the mediating effects based on blood cell-based inflammatory biomarkers. This cross-sectional study was conducted on 8380 individuals with complete survey data from the National Health and Nutrition Examination Survey (2001–2016). Multiple models (generalized linear regression model, restricted cubic spline model, Bayesian kernel machine regression, weighted quantiles sum regression) were used to assess the relationship between PAH co-exposure and the dyslipidemia risk and further identify potential mediating effects. Among the 8380 subjects, 2886 (34.44 %) had dyslipidemia. After adjusting for the confounding factors, the adjusted OR and 95% CI for dyslipidemia in the highest quartile of subjects were 1.30 (1.11, 1.51), 1. 22 (1.04, 1.43), 1.21 (1.03, 1.42), 1.29 (1.10, 1.52), 1.18 (1.01, 1.37), and 1.04 (0.89, 1.23) for 1-hydroxynaphthalene, 2-hydroxynaphthalene, 3-hydroxyfluorene, 2-hydroxyfluorene (2-FLU), 1-hydroxyphenanthrene, and 1-hydroxypyrene. The Bayesian kernel machine regression model also showed a positive correlation between PAH mixtures and dyslipidemia, and 2-FLU has the highest contribution. Mediation effect analyses showed that white blood cells and neutrophils were statistically significant in the association between PAHs and dyslipidemia. The present study suggests that individual and mixed PAH exposures may increase the risk of dyslipidemia in adults. Inflammatory biomarkers significantly mediated the relationship between PAH exposure and dyslipidemia. Environmental pollutants and their mechanisms should be more intensively monitored and studied. [Display omitted] • Studies on the combined toxic effects of PAH exposure on dyslipidemia are lacking. • Individual and mixed PAH exposures may increase the risk of dyslipidemia in adults. • Inflammatory biomarkers significantly mediated the relationship between PAH exposure and dyslipidemia. [ABSTRACT FROM AUTHOR]

Di(2-ethylhexyl) phthalate (DEHP) is a commonly used phthalate ester compound, while lead is a persistent and bioaccumulative heavy metal. Both can be exposed to the body through a variety of ways, which may have an impact on the blood system. In this study, we examined the impact of co-exposure to DEHP (0, 10, 100 mg/kg) and Pb (0, 5, 50 mg/kg) on the blood system of male SD rats. The study revealed that continuous exposure to DEHP and Pb for 20 days resulted in a decrease in leukocytes and lymphocytes, while an increase in neutrophils and monocytes. Co-exposure led to a significant decrease in the spleen coefficients. Furthermore, the combined exposure could increase the ratio of bone marrow cells in G1 phase, and decrease the ratio of cells in S phase and G2 phase. Cytokine testing showed that combined exposure affects the secretion of hematopoietic factors and may cause bone marrow cell apoptosis. Single or combined exposure to DEHP and Pb can cause oxidative stress in serum and bone marrow. Overall, these results indicate that the co-exposure of DEHP and Pb adversely affected the blood system of rats, mainly due to the induction of oxidative stress and ultimately affects the secretion of cytokines. The combined effect of the two substances is primarily antagonistic. These results have important implications for the risk assessment of combined pollution and provide valuable theoretical guidance. [Display omitted] • DEHP or Pb can affect blood cell count and cytokine secretion of SD rats. • The combined exposure could increase the ratio of bone marrow cells in G1 phase, decrease the ratio of cells in S phase and G2 phase. • DEHP or Pb can cause oxidative stress in the serum and bone marrow. • The combined effect is mainly antagonism. [ABSTRACT FROM AUTHOR]

Complex interactions have been established between nanoparticles (NPs) and heavy metals in real environments. Herein we used zebrafish embryos to investigate the influence of titanium dioxide NPs (n-TiO 2) on the uptake, bioconcentration, and depuration, and toxicity of Pb. The formation of n-TiO 2 –Pb complexes was confirmed in an exposure suspension. An increase in Pb bioconcentration was observed in zebrafish embryos upon co-exposure to n-TiO 2 and Pb; moreover, n-TiO 2 –Pb complexes could be found in the embryos, indicating the bioavailability of NPs. However, there was no difference in the depuration rates of Pb in the presence of n-TiO 2. Metallothionein (MT) content was significantly increased upon exposure to Pb alone, and the content significantly increased even further upon co-exposure. A downregulation in the expression levels of the neurodevelopment-related genes gfap , syn2α , and elavl3 was observed in the embryos, and we also noted a reduction in the swimming speed of and the total distance traveled by the larvae. To summarize, our results indicate that n-TiO 2 can act as an effective carrier of Pb to enhance its uptake, bioavailability, and toxicity in zebrafish embryos. • n-TiO 2 -Pb complexes were formed in co-exposure suspension. • Bioconcentration and bioavailability of Pb was increased by n-TiO 2 in zebrafish embryos. • Neurotoxicity of Pb was enhanced in the presence of n-TiO 2. [ABSTRACT FROM AUTHOR]

Few studies have investigated the associations between heavy metals and anxiety. The purpose of this study was to examine the associations between single and combined exposure to heavy metals and anxiety. This study employed data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2012. Anxiety was assessed by patients self-reporting the number of anxious days per month. First, we evaluated the associations between 10 heavy metals single exposure and anxiety by multivariable logistic regression. We then selected 5 heavy metals (cadmium, antimony, cobalt, tungsten, and uranium) for further analysis by elastic net regression. Subsequently, principal component analysis (PCA), weighted quantile regression (WQS), and Bayesian kernel machine regression (BKMR) were utilized to evaluate the associations between 5 heavy metals co-exposure and anxiety. This study included 4512 participants, among whom 1206 participants were in an anxiety state. Urinary cadmium and antimony were separately related to an increased risk of anxiety (p for trend <0.01 and < 0.01, respectively). In PCA analysis, PC1 was associated with an increased risk of anxiety (p for trend <0.001). In WQS analysis, the positive WQS index was substantially linked with the risk of anxiety (OR (95%CI): 1.23 (1.04,1.39)). In BKMR analysis, the overall effects of co-exposure to heavy metals were positively connected with anxiety. Our study identified a positive correlation between individual exposure to cadmium and antimony and the risk of anxiety. Additionally, the co-exposure to cadmium, antimony, cobalt, tungsten, and uranium was associated with an increased risk of anxiety. [Display omitted] This is the first general population study on heavy metals and anxiety. We employed four statistical methods for comprehensive verification. Urinary cadmium and antimony were separately related to an increased risk of anxiety. The co-exposure to heavy metals was associated with an increased risk of anxiety. [ABSTRACT FROM AUTHOR]

It has been globally recognized that obesity has become a major public health concern, especially childhood obesity. There is limited information, however, regarding the exposure risk of organic ultraviolet (UV) filters, a kind of emerging contaminant, on childhood obesity. This study would be made on 284 obese and 220 non-obese Chinese children with eight organic UV filters at urinary levels. The eight organic UV filters, including 2-Ethylhexyl 4-aminobenzoate (PABA-E), octisalate (EHS), homosalate (HMS), 2-Ethylhexyl- p -methoxycinnamate (EHMC), benzophenone-3 (BP-3), amiloxate (IAMC), octocrylene (OC) and 4-Methylbenzylidene camphor (4-MBC) were identified in urine samples with detection rates ranged from 35.32% to 100%, among which PABA-E, HMS, IAMC and OC were firstly detected in children' s urine. And the urinary UV filters concentration was associated with genders, living sites, guardian education levels, household income, and dietary factors. Urinary EHMC concentrations and childhood obesity were positively associated for girls [Adjusted OR = 2.642 (95% CI: 1.019, 6.853)], while OC concentrations and childhood obesity were negatively associated for girls [Adjusted OR = 0.022 (95% CI: 0.001, 0.817)]. The results suggest that EHMC exposure may be an environmental obesogen for girls. Moreover, two statistical models were used separately to evaluate the impact of UV filter mixtures on childhood obesity, including the Bayesian kernel machine regression (BKMR) model and the quantile g-computation (qgcomp) model. The negative association between UV filter mixtures and childhood obesity was proposed from both BKMR and qgcomp models. Further experimental and epidemiological studies are called upon to discern the individual and mixture impacts of organic UV filters on childhood obesity. [Display omitted] • Chinese children have been widely exposed to multiple kinds of UV filters. • EHMC exposure could be an environmental pathogenic factor for girls. • OC exposure could be an environmental antagonistic factor for girls. • Co-exposure to organic UV filters was inversely associated with childhood obesity. [ABSTRACT FROM AUTHOR]

Previous studies have suggested that exposure to heavy metals might increase the risk of hyperlipidemia. However, limited research has investigated the association between exposure to mixture of heavy metals and hyperlipidemia risk. To explore the independent and combined effects of heavy metal exposure on hyperlipidemia risk, this study involved 3293 participants from the National Health and Nutrition Examination Survey (NHANES), including 2327 with hyperlipidemia and the remaining without. In the individual metal analysis, the logistic regression model confirmed the positive effects of barium (Ba), cadmium (Cd), mercury (Hg), Lead (Pb), and uranium (U) on hyperlipidemia risk, Ba, Cd, Hg and Pb were further validated in restricted cubic splines (RCS) regression model and identified as positive linear relationships. In the metal mixture analysis, weighted quantile sum (WQS) regression, Bayesian kernel machine regression (BKMR), and quantile-based g computation (qgcomp) models consistently revealed a positive correlation between exposure to metal mixture and hyperlipidemia risk, with Ba, Cd, Hg, Pb, and U having significant positive driving roles in the overall effects. These associations were more prominent in young/middle-aged individuals. Moreover, the BKMR model uncovered some interactions between specific heavy metals. In conclusion, this study offers new evidence supporting the link between combined exposure to multiple heavy metals and hyperlipidemia risk, but considering the limitations of this study, further prospective research is required., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Abstract Trace metal ions such as cadmium (Cd2+) and trace organics typified by 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) are common co-contaminants in the environment and cause toxic effects in aquatic organisms that pose serious health risks. We studied the effects of Cd2+ on the regulation of cytochrome P450 1A1 (cyp1a1) gene-induction by TCDD using zebrafish embryos and larvae and adult zebrafish tissues. Our results showed that TCDD induced the cyp1a1 gene in all developmental stages and tissues of zebrafish, and the induction was higher in females than males. However, for the upstream genes (ahr2 and arnt2b) that mediate cyp1a1 gene induction in the zebrafish liver cell line was not induced by TCDD similar to the pattern of cyp1a1 in all investigated groups. After co-treatment with Cd2+, induction of the aryl hydrocarbon receptor pathway by TCDD was inhibited in the zebrafish larvae and the livers, intestines, kidneys and gills of adult zebrafish, but not in the embryos or brains of adult zebrafish, indicating that the toxicological effects of Cd2+ on TCDD are dependent on the developmental stages and tissue types. The present study confirms that Cd2+ blocks the TCDD-induced cyp1a1 gene in vivo but emphasizes that the effects are specific to the developmental stage, type of tissue and sex. The combined effects of Cd2+ and TCDD must be taken into consideration together with these parameters to accurately predict and assess cadmium and TCDD-induced toxicity in fish and carcinogenesis in animals in general. Graphical abstract Image 1 Highlights • Combined effects of Cd2+ and TCDD on zebrafish were studied in vivo. • Zebrafish embryo, larvae, and adults were investigated. • Inhibitory effects of Cd2+ on TCDD-induced genes in larvae and some adult organs. • Female fish are more sensitive than males to show cyp1a inductions. [ABSTRACT FROM AUTHOR]

It was hypothesized that interactions between emerging contaminants such as decabromodiphenyl ether (BDE-209) and nanoparticles (NPs) such as nano-SiO 2 (nSiO 2 ), can affect contaminant transport in the aquatic environment and its ecotoxicity. This study assessed the influence of nSiO 2 on the uptake of BDE-209 by zebrafish embryo. The distribution of BDE-209 and nSiO 2 on the external chorion and the internal embryo mass ( i.e. , dechorionated embryo) was measured. For single exposure of nSiO 2 to zebrafish embryo, separately, results showed that nSiO 2 accumulation on the chorion surface was higher than that in the dechorionated embryo. The nSiO 2 accumulation on the chorion surface was 129–200 mg-nSiO 2 /g-chorion at 48 h post fertilization, hpf, of exposure time, whereas the equilibrium adsorption of nSiO 2 on the dechorionated embryo was ca. 0.42–0.54 mg-nSiO 2 /g-embryo at 6 hpf. Results showed that the formation of nSiO 2 -BDE-209 associates promoted both extracellular and intracellular uptake of BDE-209 by zebrafish embryo, thereby increasing the bioconcentration of BDE-209 on the chorion surface and in embryo. The results also revealed that the accumulation of BDE-209 on the chorion was remarkably greater than that on the dechorionated embryo at 48 hpf. The uptake of BDE-209 was 17.2 ± 0.45 mg/g-chorion (or 86 ng-BDE-209/chorionated embryo) and 0.37 ± 0.01 mg/g-embryo (or 18.6 ng-BDE-209/dechorionated embryo), respectively, when co-exposure of zebrafish embryos to BDE-209 and nSiO 2 . Results from the SEM and EDS analysis revealed that nSiO 2 already passed through the chorion and adhered to the embryo surface/mass. [ABSTRACT FROM AUTHOR]

Nanoplastics (NPs) are emerging pollutants posing risks to marine biota and human health due to their small size and high bioavailability. However, there are still knowledge gaps regarding effects of co-existing pollutants on NPs toxicity to marine organisms at their respective environmentally relevant concentrations. Herein we investigated developmental toxicity and histopathological alterations caused by co-exposure of polystyrene nanoplastics (PS-NPs) and bisphenol A (BPA) to marine medaka, Oryzias melastigma. Embryos at 6 h post-fertilization were exposed to 50-nm PS-NPs (55 μg/L) or BPA (100 μg/L) or co-exposed to a combination of both. Results showed that PS-NPs exhibited decreased embryonic heart rate, larval body length, and embryonic survival as well as larval deformities such as hemorrhaging and craniofacial abnormality. When co-exposed, BPA mitigated all the adverse developmental effects caused by PS-NPs. PS-NPs also led to an increase in histopathological condition index of liver with early inflammatory responses, while co-exposure of BPA with PS-NPs did not. Our data suggest that the toxicity reduction of PS-NPs in the presence of BPA might result from the decreased bioaccumulation of PS-NPs caused by the interaction between BPA and PS-NPs. This study unveiled the impact of BPA on the toxicity of nanoplastics in marine fish during early developmental stages and highlight the need of more research on the long-term effects of complex mixtures in the marine environment by applying omics approaches to better understand the toxicity mechanism. [Display omitted] • PS-NPs showed a declined waterborne concentration in the presence of BPA. • PS-NPs caused mortality, growth inhibition and deformities of developing medaka. • PS-NPs caused liver inflammatory responses with vacuolation, apoptosis and necrosis. • BPA mitigated the developmental toxicity of PS-NPs. • BPA reduced the liver inflammatory responses caused by PS-NPs. [ABSTRACT FROM AUTHOR]

Microplastics (MPs) have emerged as contaminants of concern because of their ubiquitous presence in almost all aquatic environments. The ecological effects of MPs are complex and depend on multiple factors including their age, size and the ecological matrix. There is an urgent need for multifactorial studies to elucidate their impacts. We measured the effects of virgin and naturally aged MPs, alone, pretreated with cadmium (Cd), or in combination with ionic Cd, on the bioaccumulation of Cd, metallothionein expression, behavior, and histopathology of adult zebrafish (Danio rerio). Zebrafish were exposed to virgin or aged polyethylene MPs (0.1% MPs enriched diets, w/w) or waterborne Cd (50 μg/L) or a combination of the two for 21 days. There was an additive interaction between water-borne Cd and MPs on bioaccumulation in males but not in females. Cd accumulation increased by twofold when water-borne Cd and MPs were combined. Water-borne Cd induced significantly higher levels of metallothionein compared to MPs pre-exposed to Cd. However, Cd-treated MPs caused greater damage to the intestine and liver compared to untreated MPs suggesting that bound Cd could be released or modulate MPs toxicity. We also showed that co-exposure to water-borne Cd and MPs increased anxiety in the zebrafish, compared with water-borne Cd alone, suggesting using microplastics as a vector may increase toxicity. This study demonstrates that MPs can enhance the toxicity of Cd, but further study is needed to elucidate the mechanism. [Display omitted] • Microplastics are contaminants of concern because of their ubiquitous presence in almost all aquatic environments. • Microplastics can act as vectors for transfer of other pollutants into fish. • Exposure to both water-borne and microplastic-bound cadmium led to additive accumulation in male zebrafish. • Water-borne cadmium induced metallothionein more strongly than microplastic bound cadmium. • Microplastic bound cadmium caused similar tissue damage to water-borne cadmium. [ABSTRACT FROM AUTHOR]

Carbon nanotubes are increasingly entering the aquatic environment and may interact with other co-existing contaminants, such as antibiotics. However, whether these interactions may affect their bioavailability in aquatic organisms is the subject of considerable debate. The primary objective of this study was to assess the risks arising from the coexistence of roxithromycin (ROX) and multi-walled carbon nanotubes (MWCNTs) in waters containing natural organic matter (NOM), focusing on the distribution and bioaccumulation of ROX in crucian carp ( Carassius auratus ), and the related biochemical status. There were no significant differences in ROX bioaccumulation in fish following exposure to ROX with and without NOM. However, the further addition of MWCNTs significantly facilitated the bioaccumulation of ROX in the liver (32–80%), gill (15–74%), intestine (51–113%), and bile (15–67%) in different exposure periods. Meanwhile, a 0.3-fold increase in the metabolic enzyme activity and oxidative stress in the liver were markedly accelerated by the co-exposed MWCNTs compared to ROX alone. The findings imply that the ROX adsorbed on MWCNTs may be a higher threat to fish than ROX alone. The high and fast release of ROX from MWCNTs in bile salts and serum albumin may contribute to the enhancement in bioaccumulation and bioactivity of ROX in fish with MWCNTs. [ABSTRACT FROM AUTHOR]

PM 2.5 varies in source and composition over time and space as a complicated mixture. Consequently, the health effects caused by PM 2.5 varies significantly over time and generally exhibit significant regional variations. According to numerous studies, a notable relationship exists between PM 2.5 and the occurrence of many diseases, such as respiratory, cardiovascular, and nervous system diseases, as well as cancer. Therefore, a comprehensive understanding of the effect of PM 2.5 on human health is critical. The toxic effects of various PM 2.5 components, as well as the overall toxicity of PM 2.5 are discussed in this review to provide a foundation for precise PM 2.5 emission control. Furthermore, this review summarizes the synergistic effect of PM 2.5 and other pollutants, which can be used to draft effective policies. [Display omitted] • PM 2.5 exposure causes many human diseases. • The toxicity of PM 2.5 depends on particle composition, source, and size. • Co-exposure to pollutants causes distinct toxicity from single pollutant exposure. [ABSTRACT FROM AUTHOR]

Cloransulam-methyl is a new herbicide and has broad application prospect. However, the effect of cloransulam-methyl on earthworm have yet to be clarified. As more and more titanium dioxide nanoparticles (TiO 2 NPs) enter the soil, cloransulam-methyl and TiO 2 NPs have a risk of co-exposure, but the effect of TiO 2 NPs on cloransulam-methyl toxicity is unknown. In the study, the ecotoxicity of cloransulam-methyl (0.1, 1 mg kg−1) on earthworm and the effect of TiO 2 NPs (10 mg kg−1) on cloransulam-methyl toxicity was investigated after exposure for 28 and 56 d. Exposure tests showed cloransulam-methyl and cloransulam-methyl + TiO 2 NPs promoted the accumulation of reactive oxygen species, malondialdehyde and 8-hydroxydeoxyguanosine, increased the activities of superoxide dismutase and catalase, resulted in lipid peroxidation and DNA damage. Besides, the results at the genetic level showed cloransulam-methyl and cloransulam-methyl + TiO 2 NPs altered the expression of physiologically-related genes, which demonstrated that cloransulam-methyl and cloransulam-methyl + TiO 2 NPs induced oxidative stress and cell apoptosis, and disturbed the normal reproduction in earthworm. The results of comprehensive toxicity comparison indicated cloransulam-methyl and TiO 2 NPs co-exposure has higher toxicity compared to cloransulam single exposure. Our results suggest that TiO 2 NPs can enhance the toxicity of cloransulam-methyl on Eisenia fetida in terms of oxidative stress, cell apoptosis and reproduction aspects. Based on above studies, it is of great importance for evaluating the risk of cloransulam-methyl co-exposure with TiO 2 NPs in soil. [Display omitted] • Cloransulam-methyl induces oxidative stress and cell apoptosis on E. fetida. • Cloransulam-methyl disturbs gene expressions related to reproduction. • The Hsp70 and ANN genes are more sensitive to cloransulam-methyl exposure. • TiO 2 NPs enhances the cloransulam-methyl toxicity on E. fetida. [ABSTRACT FROM AUTHOR]

Air pollution is a serious environmental health problem that has been previously associated with neuropathological disorders. However, current experimental evidence mainly focuses on the adverse effects of a single air pollutant, ignoring the biological responses to the co-existence of these pollutants. In the present study, we co-exposed C57BL/6 J mice to PM 2.5 , SO 2 and NO 2 and explored their neurobehavior, histopathologic abnormalities, apoptosis-related protein expression and mitochondrial dysfunction. The results indicate that co-exposure to PM 2.5 , SO 2 and NO 2 impaired spatial learning and memory and caused abnormal expression of apoptosis-related genes (p53, bax and bcl-2). Additionally, these alterations were related to morphological changes in mitochondria, a reduction of ATP, the elevation of mitochondrial fission proteins and the downregulation of fusion proteins. These findings provide a basis for the understanding of mitochondrial abnormality-related neuropathological dysfunction in response to co-exposure to ambient air pollutants, which suggests an adaptive response to the frangibility of the central nerve system. [ABSTRACT FROM AUTHOR]

Given the severe situation of world-wide particulate matter air pollution, it is urgent to explore the combined effects of particulate matter components on cardiovascular system. Using zebrafish model, this study was aimed to determine whether the low level co-exposure to silica nanoparticles (SiNPs) and benzo[a]pyrene (B[a]P) had a pronounced cardiovascular toxicity than the single exposure to either SiNPs or B[a]P alone. The FTIR and TGA analysis showed that the co-exposure system possessed of high absorption and thermal stability. Embryos exposed to SiNPs or B[a]P alone did not show cardiac toxicity phenotype at the NOAEL level. However, embryos co-exposed to SiNPs and B[a]P exhibited pericardial edema and bradycardia. While ROS generation remained unaffected, the co-exposure induced significant neutrophil-mediated inflammation and caused erythrocyte aggregation in caudal vein of embryos. Microarray analysis and STC analysis were performed to screen the cardiovascular-related differential expression genes and the expression trend of genes in each group. The co-exposure of SiNPs and B[a]P significantly enhanced the expression of proinflammatory and procoagulant genes. Moreover, the co-exposure markedly increased the phosphorylated AP-1/c-Jun and induced TF expression, but not NF-κB p65. This study for the first time demonstrated the inflammatory response and blood hypercoagulable state were triggered by the combination of SiNPs and B[a]P at low level exposure. [ABSTRACT FROM AUTHOR]

The effect of combined exposure to decabromodiphenyl ether (BDE-209) and lead (Pb) on neurodevelopment of zebrafish ( Danio rerio ) larvae was investigated. Zebrafish embryos were exposed to Pb (0, 5, 10, 20 µg/L) and BDE-209 (0, 50, 100, 200 µg/L), either alone or in combination (Mix1: 5 + 50 µg/L, Mix2: 10 + 100 µg/L, Mix3: 20 + 200 µg/L) for up to 144 h post-fertilization. Growth of secondary motoneuron axons and expression of genes related to central nervous system development was significantly inhibited in Mix3 co-exposure group. A significant increase in reactive oxygen species (ROS), lipid peroxidation, DNA damage, and perturbation of the antioxidant system was detected in the Mix3 group compared to single-toxicant treatments or control. Depressed locomotor activity was recorded in the Mix2 and Mix3 groups. Addition of N- acetyl cysteine to Mix3 eliminated excessive ROS, and protected against lipid peroxidation, DNA damage, and locomotor dysfunction. Pb uptake was increased in the presence of BDE-209, but BDE-209 bioconcentration and the ability to metabolize BDE-209 were decreased in the presence of Pb. These results suggest that BDE-209 and Pb have a synergistic disruptive effect on neurodevelopment in zebrafish larvae by enhanced generation of ROS, which is a major factor that contributes to developmental neurotoxicity. [ABSTRACT FROM AUTHOR]

Limited evidence was found in the associations of volatile organic compound (VOC) exposure with bone health indicators. This study aimed to explore the associations of individual and combined metabolites of VOCs (mVOCs) in urine, a representative of the internal exposure level of VOCs, with bone mineral density (BMD), osteoporosis (OP) and fracture, and potential mediators. Data of the National Health Examination and Nutrition Survey 2005–2006 and 2013–2014 was used. Multiple linear and logistic regression modeling were performed to analyze the associations of individual mVOC with bone health indicators. The least absolute shrinkage and selection operator (LASSO) regression was adopted to select mVOCs that were more relevant to bone health indicators for further weight quantile sum (WQS) analysis used for analyzing the associations between multiple VOC co-exposure and bone health indicators. Mediation analysis was used to identify potential mediators. Seventeen mVOC members with detection rate of >50% in urine of all 3478 participants aged ≥20 years (1829 females) were involved. Levels of most mVOCs were higher in women than men. Eight mVOCs were negatively associated with BMDs, and two and four mVOCs were positively associated with OP and fracture risks, respectively. WQS regression revealed decreased femoral neck BMD (β = −0.010 g/cm2, 95% CI: −0.020, −0.0001) and total spine BMD (β = −0.015 g/cm2, 95% CI: −0.028, −0.002) in response to increasing mVOC mixture levels. And alkaline phosphatase (ALP), body mass index (BMI), fasting insulin (FI) and high-density lipoprotein (HDL), were mediators in the associations with proportions of mediating effect ranging from 4.6% to 10.2%. Individual and combined VOC (co-)exposure were associated with reduced BMDs in American adults. ALP, BMI, FI and HDL were demonstrated to be mediators in the association of multiple VOC co-exposure with BMD. [Display omitted] • Individual and multiple VOCs co-exposure were associated with reduced BMD. • BMI, HDL, FI, and ALP mediated the association of VOCs co-exposure with BMD. • LASSO regression was used to select representative VOC and avoid collinearity. • WQS regression was used to explore the VOCs co-exposure and BMD association. [ABSTRACT FROM AUTHOR]

Graphene oxide (GO), a frequently utilized graphene family nanomaterial, is inevitably released into the aquatic environment and interacts with organic pollutants, including perfluorooctane sulfonate (PFOS), a well-known persistent organic pollutant. To determine the adverse effects of GO chronic exposure on PFOS bioaccumulation and toxicity, adult freshwater bivalves, namely Asian clams (Corbicula fluminea) were treated for 28 days with PFOS (500 ng/L) and different concentrations of GO (0.2, 1, 5 mg/L) as PFOS single and GO single exposure groups, as well as PFOS-GO mixture exposure groups. Our results demonstrated that the bioaccumulation of PFOS was significantly enhanced by co-exposure in gills and visceral masses, which was 1.64–2.91 times higher in gills than in visceral masses. Both single, as well as co-exposure, caused a significant reduction in clams' siphoning behavior, compared to the controls. Further, the co-exposure significantly increased the production of reactive oxygen species (ROS), exacerbating malondialdehyde (MDA) content, enhancing superoxide dismutase (SOD) and catalase (CAT), while decreasing glutathione reductase (GR) and glutathione S-transferase (GST) enzymatic activities in clam tissues. And co-exposure significantly altered the expressions of se-gpx , sod , cyp30 , hsp40 , and hsp22 genes (associated with oxidative stress and xenobiotic metabolism) both in gills and visceral masses. Moreover, co-exposure caused significant histopathological changes such as cilia degradation in the gills, expansion of tubule lumens in digestive glands, and oocyte shrinkage in gonads. Finally, the enhanced integrated biomarker response (EIBR) index revealed that co-exposure to 500 ng/L PFOS + 1 mg/L/5 mg/L GO was the most stressful circumstance. Overall, our findings suggested that the presence of GO increased PFOS bioaccumulation in tissues, inducing multifaceted negative implications at molecular and behavioral levels through oxidative stress generation in Asian clams. [Display omitted] • Perfluorooctane sulfonate (PFOS) gills uptake was twice that in visceral mass. • PFOS-graphene oxide (GO) mixture caused more oxidative stress than single exposure. • Co-exposure altered se - gpx, sod , cyp30 , hsp-22 , hsp-40 expressions in both tissues. • Co-exposure caused more histopathological damages than that of single exposure. • Co-exposure with 1 mg/L GO or 5 mg/L GO appeared as most stressful circumstances. [ABSTRACT FROM AUTHOR]

Abstract: Fridericia bulbosa () was proposed as a new test species to assess soil ecotoxicity. The acute toxicity of mercury (Hg) and bromoxynil (BX) on the mortality of Fridericia bulbosa (F. bulbosa) in OECD soil was investigated. The results suggested there were statistically significant differences (p <0.05) between controls and treatments except lower concentration of exposure to single pollutant. BX was more toxic to F. bulbosa than Hg. The 14d LC50 values for F. bulbosa exposed to Hg and BX were 3.87 and 2.41mgkg−1, respectively. The effects of mixtures with single pollutants on earthworms were observed differently. Toxicity of Hg on earthworms was significantly influenced by the concentration of BX. BX was the main contributive factor of the combined toxic effects. It can be proved that F. bulbosa is a suitable bio-indicator to measure the acute toxicity of mixed pollutants in soil and the mortality of earthworms may be considered as a valuable and sensitive biomarker to diagnose adverse effect of Hg or BX in soil environment. [Copyright &y& Elsevier]

This study explored the combined effects of titanium dioxide nanoparticles (nano-TiO 2) and triphenyl phosphate (TPhP) on the neurodevelopment of zebrafish larvae as well as the underlying mechanisms. With this regard, zebrafish embryos were exposed to nano-TiO 2 of 100 μg·L−1, TPhP of 0, 8, 24, 72, and 144 μg·L−1, or their combinations until 120 h post-fertilization (hpf). Results indicated 100 μg·L−1 nano-TiO 2 alone to be nontoxic to zebrafish larvae. However, obvious developmental toxicity manifested as inhibition of surviving rate, heart rate and body length as well as increased malformation was observed in the higher concentrations of TPhP (72 and 144 μg·L−1) alone and the co-exposure groups. Additionally, results suggested that nano-TiO 2 significantly enhanced the bioaccumulation of TPhP in zebtafish larvae, and thus aggravated the abnormities of spontaneous movement and swimming behavior in zebrafish larvae induced by TPhP. Nano-TiO 2 also exacerbated the TPhP-induced inhibition of the axonal growth on the secondary motor neuron, and aggravated the TPhP-induced decrease on expressions of neuron-specific green fluorescent protein (GFP) and neuronal marker genes (ngn1 and elavl3). Further, the content of neurotransmitter serotonin was not altered by TPhP alone exposure, but was decreased significantly in the co-exposure group of 144 μg·L−1 TPhP and nano-TiO 2. Our data indicated that nano-TiO 2 might aggravate the neuron abnormities and serotonin system dysfunction by enhancing the TPhP accumulation, leading to exacerbated abnormal locomotors in zebrafish larvae. [Display omitted] • Nano-TiO 2 aggravated accumulation and developmental toxicity of TPhP in zebrafish larvae. • Nano-TiO 2 aggravated TPhP-induced abnormities of spontaneous movement and swimming behavior in zebrafish larvae. • Nano-TiO 2 enhanced TPhP-induced inhibition of secondary motor neuron axon growth. • Nano-TiO 2 enhanced TPhP-induced decreased expressions of the neuron-specific GFP. • Co-exposure of TPhP and nano-TiO 2 leads to dysfunction of the 5-HT system. [ABSTRACT FROM AUTHOR]

Human beings are extensively and concurrently exposed to multiple volatile organic compounds (VOCs, including some Class I human carcinogens), which may induce oxidative stress in human body. Data on urinary metabolites of VOCs (mVOCs) among young children are limited. No studies have examined their inter-day variability of mVOCs and their associations with oxidative stress biomarkers (OSBs) using repeated urine samples from children. In this study, we measured twenty one mVOCs and three OSBs [8-hydroxy-2′-deoxyguanosine (8-OHdG; for DNA), 8-hydroxyguanosine (8-OHG; for RNA], and 4-hydroxy nonenal mercapturic acid (HNEMA; for lipid)] in 390 urine samples of 130 children (three samples on three consecutive days provided by each participant) aged 0–7 years from September 2018 to January 2019 in Shenzhen, south China, and Wuhan, central China. HPMMA (3-hydroxypropyl-1-methyl mercapturic acid/N-Acetyl-S-(3-hydroxypropyl-1-methyl)- l -cysteine), 3HPMA (3-hydroxypropyl mercapturic acid/N-Acetyl-S-(3-hydroxypropyl)- l -cysteine), and ATCA (2-aminothiazoline-4-carboxylic acid) had higher specific gravity-adjusted median concentrations (1 383, 286, and 273 μg/L, respectively) than the others. Intraclass correlation coefficients of mVOCs ranged from 0.29 to 0.71. After false-discovery rate (FDR, defined as FDR q -value < 0.05) adjustment, linear mixed-effects models revealed that 14 mVOCs were positively associated with 8-OHdG (β range: 0.09–0.37), 11 mVOCs were positively associated with 8-OHG (β range: 0.08–0.30), and 11 mVOCs were positively associated with HNEMA (β range: 0.21–0.70) in urine. Considering the weight of the mVOC index accounted for the associations, based on the weighted quantile sum regression model, parent compounds of DHBMA (3,4-dihydroxybutyl mercapturic acid/N-Acetyl-S-(3,4-dihydroxybutyl)- l -cysteine) and t,t-MA (trans,trans -muconic acid) should be listed as priority VOCs for management to mitigate health risks. For the first time, this study characterized the inter-day variability of urinary mVOCs and their associations with selected OSBs (8-OHdG, 8-OHG, and NHEMA) in young, healthy Chinese children. [Display omitted] • First to characterize the profile of urinary mVOCs in Chinese infants and toddler. • Inter-day variability of the mVOCs among young children was evaluated. • Over ten mVOCs were positively associated with 8-OHdG, 8-OHG, and HNEMA. • DHBMA was the major contributor in elevated 8-OHdG and 8-OHG. • t,t-MA was the major contributor in elevated HNEMA. [ABSTRACT FROM AUTHOR]

Lead (Pb) and cadmium (Cd) are common heavy metals in the environment, exerting detrimental effects on central nervous system. Although increasing evidence demonstrated the Pb and Cd-induced neurotoxicity, the exact epigenetic mechanisms induced by combined exposure (co-exposure) of Pb and Cd are still unclear. In this study, the neurotoxicity of individual exposure and co-exposure to Pb and Cd in vivo (150 ppm and 5 ppm respectively) and in vitro (10 μM and 0.1 μM respectively) was investigated. The results showed that neurite outgrowth was inhibited by either individual or combined exposure to Pb/Cd, whereas the co-exposure aggravated the inhibitory effect in PC12 cells. The results of Morris Water Maze (MWM), Y maze and Golgi-Cox staining showed that either Pb or Cd alone exposure damaged the ability of learning and memory and decreased the dendritic spine density in both the hippocampal CA1 and DG area of Sprague–--Dawley (SD) rats, and that the co-exposure aggravated the damages. Subsequently, histone deacetylase (HDAC) 2 was significantly increased in both hippocampal tissues and PC12 cells co-exposed to Pb and Cd, and the treatment of trichostatin A (TSA) and HDAC2–knocking down construct (shHDAC2) could markedly prevent neurite outgrowth impairment in PC12 cells. In summary, HDAC2 plays essential regulatory roles in neurotoxicity induced by the co-exposure to Pb and Cd, providing a potential molecular target for neurological intervention. • The co-exposure to Pb and Cd aggravated the damage of learning and memory of SD rats. • The co-exposure aggravated the reduction of dendritic spine density. • HDAC2's expression was promoted by co-exposure in vivo and in vitro. • TSA and shHDAC2 rescued the neurite outgrowth deficits caused by Pb and Cd. [ABSTRACT FROM AUTHOR]

Multiple pesticide residues are frequently present in tea leaves and while the majority of residues satisfy Taiwan's current health regulations, there are potential health effects from pesticide exposure that are of great concern for tea drinkers. We undertook a systematic probabilistic risk assessment of 59 pesticides in tea leaves from 1629 tea leaf samples obtained by Taiwan's Food and Drug Administration in two monitoring surveys in 2015. Bayesian statistics used a Markov Chain Monte Carlo approach to estimate posterior distributions of pesticide residues in tea leaves, lifetime average daily doses and hazard quotients (HQs) of evaluated pesticides. We classified 95th percentile values of HQs into three categories: 0 < HQ < 0.5, 0.5 ≤ HQ ≤ 1 and 1 < HQ. The 95th percentiles of HQs for triazophos (3.39), carbofuran (2.04) and endosulfan (1.80) exceeded 1 in the adult population; the HQ for 3-OH carbofuran was 0.97 and was less than 0.5 for the remaining 55 pesticides. The health risk posed by pesticide residues for tea drinkers is negligible, if triazophos, carbofuran, endosulfan, and 3-OH carbofuran residues satisfy regulatory standards. However, five legacy pesticides, DDT, methomyl, carbofuran, dicofol and endosulfan, were identified. To reduce uncertainties, this study combined Bayesian statistics with a mode of action approach for systematic risk assessment of co-exposure to multiple pesticide residues in tea leaf samples. Measuring pesticide transfer rates will improve the quality of future risk assessments concerning residues in tea leaves. Appropriate management of pesticides in Taiwanese tea farms and monitoring of pesticide residues in imported tea is warranted to protect Taiwan's tea drinkers. • The study was conducted for individual and multiple exposure of 59 pesticides in 1629 tea leaf samples. • Uncertainties were reduced by using the Bayesian statistics with Markov Chain Monte Carlo simulation. • The risk assessment incorporated brewing factors of dry tea leaves to better characterize the exposure assessment. • Most pesticide residues in tea leaves pose negligible health risk; triazophos, carbofuran and endosulfan may pose risks. [ABSTRACT FROM AUTHOR]