Organophosphate Pesticide Metabolites and Mortality in U.S. Adults: Age-Modified Dose–Response Associations from a National Cohort Study

Urinary organophosphate metabolites, DNA methylation aging, and heart disease mortality in middle-aged and older adults: an exploratory cohort study with in vitro evidence of biological plausibility

Higher urinary DETP was associated with greater heart disease mortality in middle-aged and older adults, and in vitro experiments provided hypothesis-generating support—most directly for inflammatory signaling—rather than confirmation of the epidemiological pathway.

Residential pesticide exposure, mortality risk, and the potential mediating role of urinary metabolites: evidence from a nationally representative cohort

Associations of prenatal exposure to organophosphate flame retardants and organophosphorus pesticides with cardiac structure in 4-year-old children: Evidence from the Shanghai Birth Cohort.

Prenatal exposure to OPFRs and OPPs was associated with smaller left ventricular structural measures in early childhood, mainly reflected by lower left ventricular volume and mass, with OPFRs emerging as main contributors and stronger associations among girls.

Organophosphate Flame Retardants Exposure Disrupts Serum Lipid Metabolism and Induces Hepatotoxicity: Evidence from the Population and Mouse Model.

TDCIPP exposure induced hepatotoxicity in mice, and may induce hepatic lipid toxicity in mice, indicating that the non-cancer risk of BDCIPP should be of concern.

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.

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