The blood–follicle barrier (BFB) between the blood and follicular fluid (FF) can maintain the microenvironment balance of oocyte. Boron, an exogenous environmental trace element, has been found to possibly play an important role in oocyte maturation. This study aimed to examine the distribution characteristics of boron across the BFB and find the potential effect of boron on FF microenvironment. We analyzed the concentration of boron in paired FF and serum collected from 168 women undergoing in vitro fertilization and embryo transfer in Beijing City and Shandong Province, China. To explore the potential health impact of boron enrichment in oocyte maturation, a global proteomics analysis was conducted to tentatively correlate the protein levels with the boron enrichment. Interestingly, the results showed that the concentration of boron in FF (34.5 ng/mL) was significantly higher than that in serum (22.0 ng/mL), with a median concentration ratio of 1.52. Likewise, the concentrations of boron in FF and serum were positively correlated (r = 0.446), suggesting that boron concentration in serum can represent its concentration in follicular fluid to a large extent.. This is the first time to observe the enrichment of boron in the FF to our knowledge. It is interesting to observe a total of 13 proteins, which mainly belong to immunoglobulin class, were positively correlated with boron concentration in FF. We concluded that boron, as one environmental trace element, was enriched in FF from blood validated by two area in north china, which may be involved in an increased level of immune processes of immunoglobulins.

Sea fish contain omega-3 polyunsaturated fatty acids (omega-3 PUFAs) which have been found to reduce triglyceride (TG) levels. However, sea fish may contain pollutants such as mercury which cause oxidative stress and increase TG levels. Therefore, the relationship between sea fish and TG remains unclear. We aimed to explore whether blood mercury (BHg) can affect the effect of sea fish consumption frequency on TG level among Chinese adults. A total of 10,780 participants were included in this study. BHg levels were measured using inductively coupled plasma mass spectrometry (ICP-MS). The associations of sea fish consumption frequency with BHg and TG levels as well as the association of BHg with TG levels were evaluated using multiple linear regression. Causal mediation analysis was used to evaluate the mediation effect of BHg levels on the association of sea fish consumption frequency with TG levels. The frequency of sea fish consumption showed a negative association with TG level. Compared with the participants who never ate sea fish, the TG level decreased by 0.193 mmol/L in those who ate sea fish once a week or more [β (95%CI): −0.193 (−0.370, −0.015)]. Significant positive associations were observed of BHg with TG levels. With one unit increase of log2-transformed BHg, the change of TG level was 0.030 mmol/L [0.030 (0.009, 0.051)]. The association between sea fish consumption and TG was mediated by log2-transformed BHg [total effect = −0.037 (−0.074, −0.001); indirect effect = 0.009 (0.004, 0.015)], and the proportion mediated by log2-transformed BHg was 24.25%. BHg may reduce the beneficial effect of sea fish consumption frequency on TG levels among Chinese adults. Overall, sea fish consumption has more benefits than harms to TG.

Although cadmium (Cd) is a toxic heavy metal that reportedly causes liver injury, few studies have investigated biomarkers of Cd-induced liver injury. The purpose of this study is to investigate the role of bile acid (BA) in Cd-induced liver injury and determine reliable and sensitive biochemical parameters for the diagnosis of Cd-induced liver injury. In this study, 48 Sprague-Dawley rats were randomly divided into six groups and administered either normal saline or 2.5, 5, 10, 20, and 40 mg/kg/d cadmium chloride for 12 weeks. A total of 403 subjects living in either a control area (n = 135) or Cd polluted area (n = 268) of Dongdagou-Xinglong (DDGXL) cohort were included, a population with long-term low Cd exposure. The BA profiles in rats' liver, serum, caecal contents, faeces, and subjects' serum were detected using high-performance liquid chromatography-tandem mass spectrometry (HPLC–MS/MS). Changes in rats' and subjects' liver injury indices, rats' liver pathological degeneration, and rats' liver and subjects’ blood Cd levels were also measured. Cadmium exposure caused cholestasis and an increase in toxic BAs, leading to liver injury in rats. Among them, glycoursodeoxycholic acid (GUDCA), glycolithocholic acid (GLCA), taurolithocholic acid (TLCA), and taurodeoxycholate acid (TDCA) are expected to be potential biomarkers for the early detect of Cd-induced liver injury. Serum BAs can be used to assess Cd-induced liver injury as a simple, feasible, and suitable method in rats. Serum GUDCA, GLCA, TDCA, and TLCA were verified to be of value to evaluate Cd-induced liver injury and Cd exposure in humans. These findings provided evidence for screening and validation of additional biomarkers for Cd-induced liver injury based on targeted BA metabolomics.

Per- and polyfluoroalkyl substances (PFAS) have become a target of rigorous scientific research due to their ubiquitous nature and adverse health effects. However, there are still gaps in knowledge about their environmental fate and health implications. More attention is needed for remote locations with source exposures. This study focuses on assessing PFAS exposure in Gustavus, a small Alaska community, located near a significant PFAS source from airport operations and fire training sites. Residential water (n = 25) and serum (n = 40) samples were collected from Gustavus residents and analyzed for 39 PFAS compounds. In addition, two water samples were collected from the previously identified PFAS source near the community. Fourteen distinct PFAS were detected in Gustavus water samples, including 6 perfluorinated carboxylic acids (PFCAs), 7 perfluorosulfonic acids (PFSAs), and 1 fluorotelomer sulfonate (FTS). ΣPFAS concentrations in residential drinking water ranged from not detected to 120 ng/L. High ΣPFAS levels were detected in two source samples collected from the Gustavus Department of Transportation (14,600 ng/L) and the Gustavus Airport (228 ng/L), confirming these two locations as a nearby major source of PFAS contamination. Seventeen PFAS were detected in serum and ΣPFAS concentrations ranged from 0.0170 to 13.1 ng/mL (median 0.0823 ng/mL). Perfluorooctanesulfonic acid (PFOS) and perfluorohexanesulfonic acid (PFHxS) were the most abundant PFAS in both water and serum samples and comprised up to 70% of ΣPFAS concentrations in these samples. Spearman's correlation analysis revealed PFAS concentrations in water and sera were significantly and positively correlated (r = 0.495; p = 0.0192). Our results confirm a presence of a significant PFAS source near Gustavus, Alaska and suggest that contaminated drinking water from private wells contributes to the overall PFAS body burden in Gustavus residents.

Paraquat, a widely used herbicide, causes environmental pollution, and liver injury in humans and animals. As a natural compound in fruits, ellagic acid (EA) shows anti-inflammatory and antioxidant effects. This study examines the beneficial effects of dietary EA against the paraquat-induced hepatic injury and further explores the underlying molecular mechanisms using a piglet model. Post-weaning piglets are fed basal diet supplemented with 50 mg/kg, 100 mg/kg, or 200 mg/kg EA for 3 weeks. At week 2, hepatic injury is induced by 4 mg/kg paraquat followed by 7 days recovery. EA supplementation significantly mitigates paraquat-induced hepatic fibrosis, steatosis, and high apoptotic rate. In agreement, EA supplementation reduces serum pro-inflammatory levels, ameliorates inflammatory cells infiltration into hepatic tissue, which are associated with suppressed NF-κB signaling during paraquat exposure. In addition, EA supplementation significantly improves activities of antioxidative enzymes which were correlated with activated Nrf2/Keap 1 signaling during paraquat exposure. Furthermore, EA supplementation restores cecal microbial community during paraquat exposure. The protective effect of EA is strongly linked with increased relative abundance of Lactobacillus reuteri and Lactobacillus amylovorus. Taken together, EA supplementation effectively reduced the occurrence of hepatic oxidative damage and inflammation induced by paraquat through modulating cecal microbial communities, which provides a novel nutritional therapeutic strategy for hepatic injury.

To date, knowledge of internal human exposure to BPA and its analogues (particularly bisphenol S and bisphenol F, etc.) remains limited. In the present study, a method involving dispersive solid-phase extraction and LC/MS was proposed to investigate the contamination levels of 28 precursor bisphenols and 9 major metabolites in serum. The critical variables of preparation method were screened out by Plackett-Burman design and further optimized by central composite design. Left in optimal conditions, a total of 286 samples consisting of 153 males and 133 females were analyzed. The results showed that BPA dominated over all the cases with the highest positive rate (82.2% of all the surveyed people), and totally four metabolites (BPA β-D-glucuronide, BPA monosulfate, BPA bis-(β-D-glucuronide) and BPS monosulfate) were detectable. The occurrence of BPA bis-(β-D-glucuronide) in serum is reported for the first time and its higher positive rate and contamination concentrations suggested that it may be a more important metabolite of BPA than others. Negligible potential risk of health effects to blood donors was observed, since the estimated exposure levels (mean 32.1 ng/kg bw/day, 95th 123.2 ng/kg bw/day) were well below far less than the temporary tolerable reference dose of BPA that recommended by the European Food Safety Authority (4 μg/kg bw/day by). The reference level of BPA for healthy population was determined to be 4.09 μg/L via the percentile method.

Ambient air pollutants are well-known risk factors for childhood asthma and asthma exacerbation. It is unknown whether different air pollutants individually or jointly affect pathophysiological mechanisms of asthma. In this study, we aim to integrate transcriptome and untargeted metabolome to identify dysregulated genetic and metabolic pathways that are associated with exposures to a mixture of ambient and traffic-related air pollutants among adults with asthma history. In this cross-sectional study, 102 young adults with childhood asthma history were enrolled from southern California in 2012. Whole blood transcriptome was measured with 20,869 expression signatures, and serum untargeted metabolomics including 937 metabolites were analyzed by Metabolon, Inc. Participants’ exposures to regional air pollutants (NO₂, O₃, PM₁₀, PM₂.₅) and near-roadway air pollutants averaged at one month and one year before study visit were estimated based on residential addresses. xMWAS network analysis and joint-pathway analysis were performed to identify subnetworks and genetic and metabolic pathways that were associated with exposure to air pollutants adjusted for socio-characteristic covariates. Network analysis found that exposures to air pollutants mixture were connected to 357 gene markers and 92 metabolites. One-year and one-month averaged PM₂.₅ and NO₂ were associated with several amino acids related to serine, glycine, and beta-alanine metabolism. Lower serum levels of carnosine and aspartate, which are involved in the beta-alanine metabolic pathway, as well as choline were also associated with worse asthma control (p < 0.05). One-year and one-month averaged PM₁₀ and one-month averaged O₃ were associated with higher gene expression levels of HSPA5, LGMN, CTSL and HLA-DPB1, which are involved in antigen processing and presentation. These results indicate that exposures to various air pollutants are associated with altered genetic and metabolic pathways that affect anti-oxidative capacity and immune response and can potentially contribute to asthma-related pathophysiology.

Bisphenol A diglycidyl ether (BADGE), bisphenol F diglycidyl ether (BFDGE), and their derivatives are frequently used in food packaging materials. Some toxicological studies have shown that the endocrine-disrupting activities of these compounds are similar to or higher than those of bisphenol A (BPA), which may also adversely affect the growth and development of children and adolescents. Here, we investigated nine bisphenol-diglycidyl ethers (BDGEs) in 181 paired urine and serum samples from children and adolescents from Beijing to determine their partitioning, clearance and exposure levels. The results showed that nine BDGEs were detected in 181 urine and serum samples from children and adolescents from Beijing. Bisphenol A bis(2,3-dihydroxypropyl) glycidyl ether (BADGE·2H₂O) was the primary pollutant. The daily intake of ∑BDGEs was 15.217 ng/kg bw/day among children and adolescents in Beijing. The ranking of BDGEs in terms of renal clearance rate (CLᵣₑₙₐₗ) in this study population was BADGE > BADGE·2H₂O > BFDGE > bisphenol F bis(3-chloro-2-hydroxypropyl) glycidyl ether (BFDGE·2HCl) > bisphenol A (3-chloro-2-hydroxypropyl) (2,3-dihydroxypropyl) glycidyl ether (BADGE·HCl·H₂O). In addition, the serum and urine ratios (S/U ratios) of BFDGE·2HCl, BADGE·2H₂O, BFDGE, BADGE, and BADGE·HCl·H₂O were higher than 1, indicating that these contaminants have a higher enrichment capacity in human blood. To our knowledge, this is the first study on the partitioning and renal clearance rate of BDGEs in paired urine and serum samples from children and adolescents.

Exposure to tobacco smoke during pregnancy has been associated with a series of adverse reproductive outcomes; however, the underlying molecular mechanisms are not well-established. We conducted an untargeted metabolome-wide association study to identify the metabolic perturbations and molecular mechanisms underlying the association between cotinine, a widely used biomarker of tobacco exposure, and adverse birth outcomes. We collected early and late pregnancy urine samples for cotinine measurement and serum samples for high-resolution metabolomics (HRM) profiling from 105 pregnant women from the Atlanta African American Maternal-Child cohort (2014–2016). Maternal metabolome perturbations mediating prenatal tobacco smoke exposure and adverse birth outcomes were assessed by an untargeted HRM workflow using generalized linear models, followed by pathway enrichment analysis and chemical annotation, with a meet-in-the-middle approach. The median maternal urinary cotinine concentrations were 5.93 μg/g creatinine and 3.69 μg/g creatinine in early and late pregnancy, respectively. In total, 16,481 and 13,043 metabolic features were identified in serum samples at each visit from positive and negative electrospray ionization modes, respectively. Twelve metabolic pathways were found to be associated with both cotinine concentrations and adverse birth outcomes during early and late pregnancy, including tryptophan, histidine, urea cycle, arginine, and proline metabolism. We confirmed 47 metabolites associated with cotinine levels, preterm birth, and shorter gestational age, including glutamate, serine, choline, and taurine, which are closely involved in endogenous inflammation, vascular reactivity, and lipid peroxidation processes. The metabolic perturbations associated with cotinine levels were related to inflammation, oxidative stress, placental vascularization, and insulin action, which could contribute to shorter gestations. The findings will support the further understanding of potential internal responses in association with tobacco smoke exposures, especially among African American women who are disproportionately exposed to high tobacco smoke and experience higher rates of adverse birth outcomes.

China has been in a rapid development period in recent decades, the mass production and use of chemical industrial products and pesticides have resulted in a large amount of pollutants in the environment. These pollutants enter the human body through environmental exposure and dietary intake, causing adverse health effects. Although many of them have been banned and restricted in the production and use in China, these pollutants still remain in the human body due to their high persistence and strong bioaccumulation. In this review, we aim to reveal the accumulation levels and profiles, as well as the temporal and spatial distribution of common chemical pollutants including chlorinated paraffins (CPs), polycyclic aromatic hydrocarbons (PAHs), organochlorine pesticides (OCPs), polybrominated diphenyl ethers, organophosphorus flame retardants (OPFRs), new halogenated flame retardants (NHFRs), polychlorinated biphenyls, phthalic acid esters, perfluorinated compounds, bisphenols, organophosphorus pesticides and pyrethroid insecticides in the blood (including whole blood, serum and plasma) of Chinese adults by extracting 93 related studies published from 1990 to 2021. Results have shown that CPs, OCPs and PAHs were the main pollutants in China, the levels of short-chain chlorinated paraffin, p,p'-DDE and phenanthrene in blood even reached 11,060.58, 740.41 and 498.28 ng/g lipid respectively. Under the strict control of pollutants in China, the levels of most pollutants have been on a downward trend except for perfluoro octanoate and perfluoro nonanoate. Besides, OPFRs, NHFRs and PAHs may have a potential upward trend, requiring further research and observation. As for spatial distribution, East China (Bohai Bay and Yangtze River Delta) and South China (Pearl River Delta) were the major polluted regions due to their fast development of industry and agriculture.