Environmental Exposure to Endocrine-Disrupting Chemicals and SARS-CoV-2 Infection History Among Blood Donors

Hair-Based Biomonitoring of Phthalate Metabolites and Triclosan in Childhood: Links with Metabolic and Endocrine Disorders

Overall, biomonitoring results indicate group-specific concentration patterns of PMs and TCS among children with T1D, HPRD and OB groups compared to the control group, and this is the first study to assess PM and TCS concentrations in children across clinical groups, using hair matrix.

Multi-Media Exposure, Selective Accumulation and Health Risks of Organochlorine Pesticides in Human Serum under Post-Ban Conditions

Organochlorine pesticides (OCPs), despite being banned, persist in the environment and continue to pose potential risks to human health. This exploratory study investigated the concentrations of multiple OCPs in serum samples from 10 local residents and 52 surrounding environmental samples, including soil (n = 10), air (n = 12), indoor dust (n = 10), and food (n = 20), collected in Taizhou, Zhejiang Province, in 2022. Multiple exposure pathways were quantified, and associated health risks were assessed. The results showed evidence of selective accumulation in humans, with serum ΣOCP concentrations ranging from 107.01 to 552.41 ng/g lipid weight (lw). p,p′-DDE was the predominant compound, accounting for 67.81% of total serum OCPs, while β-HCH showed relatively higher enrichment among HCH congeners. Lower proportions of p,p′-DDT and α-/γ-HCH were observed. Source contributions varied across media: food was the primary contributor to p,p′-DDE exposure, indoor dust and soil contributed more to β-HCH and certain DDT isomers, and the atmosphere showed a higher contribution of methoxychlor. Differences between integrated exposure profiles and serum composition highlighted the potential roles of metabolic transformation and lipid-associated accumulation in shaping internal OCP burdens. Risk assessment indicated that DDT metabolites and β-HCH were the major contributors to potential exposure risks. Overall, this study provides preliminary insights into the environmental–human distribution patterns of OCPs observed in Taizhou under post-ban conditions and highlights that environmental concentrations alone may not fully represent chronic internal exposure. These findings improve the understanding of potential OCP exposure pathways and emphasize the need for larger-scale studies incorporating population characteristics and refined exposure parameters for more comprehensive risk assessment

Metabolomics insights into the association between organochlorine pesticides, synthetic pyrethroids exposure and thyroid cancer risk.

BACKGROUND The association between organochlorine pesticides (OCPs)/synthetic pyrethroids (SPs) and thyroid cancer (TC) remains poorly understood, with metabolic mechanisms unexplored. METHODS We conducted a 1:1 age- and sex-matched case-control study (n = 668). Serum levels of 27 target analytes (19 OCPs and 8 SPs) were quantified; subsequent analyses were restricted to 13 compounds (10 OCPs and 3 SPs) with detection frequencies ≥85%. Eight machine learning (ML) algorithms with Shapley Additive Explanations (SHAP) were used to identify key pollutants in the 334 case-control pairs. Untargeted metabolomics was performed in a subset of 50 age- and sex-matched case-control pairs. Mixture effects were assessed by Bayesian kernel machine regression (BKMR) and weighted quantile sum (WQS) regression. Furthermore, the Latent Unknown Clustering Integrating Multi-Omics Data (LUCID) model was employed to integrate exposure and metabolic data, enabling the identification of TC patient subgroups and the exploration of underlying metabolic mechanisms. RESULTS Participants (mean age 45.2 years, 82.3% female) had serum OCPs at 0.007-0.333 ng/mL and SPs at 0.046-0.095 ng/mL. ML algorithms identified fenpropathrin, β-BHC, cyhalothrin, α-BHC, and p,p'-DDD as the top five contributors to TC. Elevated OCPs/SPs exposure was significantly associated with increased TC risk (WQS: adjusted OR = 1.45, 95%CI = 1.34-2.24, P = 0.019; LUCID: OR = 9.33). Fenpropathrin was the primary contributor (BKMR posterior inclusion probability = 1.00; WQS weight = 67.6%). A total of 45 significant differential metabolites (DMs) were identified (VIP ≥1, P < 0.05, and qualitative level 1). LUCID revealed a distinct TC cluster characterized by upregulated S-sulfo-L-cysteine/adenosine and downregulated 2-hydroxycaprylic acid. CONCLUSION OCPs/SPs mixtures, driven by fenpropathrin, disrupt amino acid/nucleotide metabolism while suppressing organic acid metabolism, representing a potential TC-associated metabolic signature.

Cytokine Concentrations in Workers Exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Carcinogenic and non-carcinogenic health risks associated with heavy metal exposure in commonly consumed marine fish in Egypt

This study aimed to quantify the levels of mercury (Hg), arsenic (As), lead (Pb), and cadmium (Cd) in 250 fish samples, including flathead grey mullet, sardine, and mackerel, collected from local fish markets in Mansoura, Egypt, on ten occasions from August 2023 to March 2024. Unlike previous studies that have primarily focused on metal concentrations, this study assessed both carcinogenic and non-carcinogenic health risks among the general population (57.09 g/day) and high-fish consumers (200 g/day). Metal concentrations were determined using atomic absorption spectrophotometry, with method accuracy validated using certified reference materials (CRMs), yielding recoveries of 95.5–100.6%. The average concentrations of Hg, As, Pb, and Cd (µg/g wet weight) were 0.313, 2.13, 0.194, and 0.018 in flathead grey mullet (As > Hg > Pb > Cd); 0.131, 1.65, 0.472, and 0.021 in sardine (As > Pb > Hg > Cd); and 0.196, 0.98, 0.370, and 0.025 in mackerel (As > Pb > Hg > Cd), respectively. Hg and As concentrations were significantly higher in flathead grey mullet, whereas Pb concentration was highest in sardine and Cd concentration was highest in mackerel. Based on the Maximum Permissible Limits (MPLs) set by the Food and Agriculture Organization (FAO), Egyptian Organization for Standardization and Quality (EOS), and Food Standards Australia New Zealand (FSANZ), the proportion of samples exceeding these limits ranged from 9 to 20% for Hg, 22–56% for As, and 20–58% for Pb. For the general population, only the estimated daily intake (EDI) of Hg in flathead grey mullet was above the Provisional Tolerable Daily Intakes (PTDIs), while EDI of most metals exceeded safety thresholds in high fish consumers. Target Hazard Quotient (THQ) for Hg and As exceeded 1.0, while TTHQ values for flathead grey mullet, sardine, and mackerel were 8.4, 5.7, and 4.35 for the general population and 29.43, 19.84, and 15.26 for high-fish consumers, respectively, indicating potential non-carcinogenic health risks. Furthermore, cancer risk (CR) for As ranged from 1.20E−03 to 9.14E−03, exceeding the acceptable safety threshold of 1.0E−04, whereas Pb and Cd risks remained within safe limits. The relatively high metal concentrations may reflect anthropogenic pollution and other environmental inputs affecting the aquatic ecosystem, highlighting the need for regular monitoring and control of pollution sources to reduce contamination and protect public health.

Chronic Kidney Disease Risk Posed by 1-Ethoxy-2,3-difluoro-4-(trans-4-propylcyclohexyl) Benzene (EDPrB): An AOP of mTOR-Mediated Autophagy Dysregulation.

1-Ethoxy-2,3-difluoro-4-(trans-4-propylcyclohexyl) benzene (EDPrB), a highly polluting fluorinated liquid-crystal monomers (FLCMs), accumulates in the kidneys over the long term. First, our study demonstrates that exposure to EDPrB can induce inflammatory responses and fibrosis in human renal cortical proximal tubule epithelial cells (HK-2), posing a risk of nephrotoxicity. Next, our study investigates the renal injury induced by EDPrB in male Kunming mice after 70-day exposure at 13, 130, and 1300 μg/kg bw/day, using an adverse outcome pathway (AOP) framework. Histopathological observations demonstrate that EDPrB corresponds to an elevated probability of developing chronic kidney disease (CKD). Proteomics and Western blot analysis revealed that mTOR signaling may be the mechanism by which EDPrB induces CKD in mice and causes damage to HK-2 cells. Finally, by treating EDPrB-exposed mice with RAPA, we demonstrated that activation of the mTOR signaling is the molecular initiating event driving EDPrB-induced CKD in mice. This study proposes an AOP framework focused on EDPrB-induced CKD. The molecular initiating event is identified as mTOR activation, followed by autophagy inhibition leading to inflammation and fibrosis as key events, ultimately resulting in CKD as an adverse outcome. This highlights the renal risks of FLCMs and supports stricter environmental release regulations.