These findings provide novel human biomonitoring evidence linking exposure to phenolic endocrine-disrupting chemicals with systemic metabolic and inflammatory variability in patients with advanced lung cancer.
Abstract
Background and Objectives: Environmental exposure to endocrine-disrupting chemicals (EDCs) is increasingly recognized as a potential contributor to cancer-related biological variability; however, human biomonitoring data in oncology populations remain limited. The present study aimed to assess urinary concentrations of selected phenolic EDCs and their associations with cardiometabolic, hematological, inflammatory, and survival-related parameters in patients with advanced lung cancer. Materials and Methods: A total of 190 patients diagnosed with stage IIIB/IV lung cancer were included in this study. Urinary concentrations of bisphenol A (BPA), bisphenol S (BPS), triclosan (TCS), and resorcinol (RCO) were determined using validated analytical methods. Associations between exposure biomarkers and clinical laboratory parameters were evaluated using sex-stratified statistical analyses and regression models adjusted for age and body mass index. Results: TCS was the most frequently quantified compound (29.47%), followed by BPS (27.37%), RCO (11.58%), and BPA (7.89%). Higher odds of TCS quantification were observed in patients with lung adenocarcinoma and a higher probability of BPA quantification in patients with squamous-cell carcinoma. Sex-specific exposure patterns were observed, with higher BPA and BPS concentrations measured among female patients. Exposure to phenolic EDCs was associated with alterations in kidney function biomarkers, liver enzyme activity, inflammatory cell profiles, and anthropometric indicators. In particular, BPA and BPS showed associations with renal function markers and systemic inflammatory parameters, while TCS exposure was related to reduced leukocyte subpopulations. Survival analysis demonstrates borderline associations for BPA between exposure groups. Conclusions: These findings provide novel human biomonitoring evidence linking exposure to phenolic endocrine-disrupting chemicals with systemic metabolic and inflammatory variability in patients with advanced lung cancer. The observed associations support the biological plausibility that environmental endocrine disruptors may contribute to interindividual heterogeneity in cancer-related physiological responses.
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.
M. Koukakis, Stella Baliou, A. Alegakis et al.· Journal of Xenobiotics· 0 citations
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.
Fei Wang, Chunxiang Li, Linfang Zou et al.· Environment International· 0 citations
This pilot study provides some of the first estimates of PFAS exposure among prostate cancer patients in serum and tap water, showing moderate correlations between tap water and serum concentrations of specific PFAS analytes.
Stefanie A. Joseph, Chidinma Opara, Megan R. Shanahan et al.· medRxiv· 0 citations
Mixture exposure showed a significant positive association with chronic obstructive pulmonary disease risk, and these substances disrupt pulmonary homeostasis through concurrent molecular activation and lipid-metabolic disturbance, evidenced by triglyceride-glucose index mediation.
Yansong Hu, Huanyu Cui, Yakun Wang et al.· BMC Pulmonary Medicine· 0 citations
Findings suggest a strong link between selected paraben and alkylphenol exposure and prior COVID-19 status in blood donors, and the high IMZ levels highlight the need for urgent evaluation of its safety and environmental prevalence.
Wioletta Ratajczak-Wrona, K. Bielawska, J. Wróbel et al.· Life· 0 citations
Background/Objectives: Endocrine-disrupting chemicals (EDCs) interfere with hormonal homeostasis and have been implicated in gynecological malignancy pathogenesis. This narrative review synthesizes current evidence regarding EDC exposure and breast, endometrial, ovarian, and cervical cancers, examining molecular mechanisms, epidemiology, and diagnostic and clinical implications. Methods: We conducted a literature review using PubMed/MEDLINE, Embase, Scopus, and Cochrane databases through April 2026, including systematic reviews, meta-analyses, prospective cohorts, case-control studies, and mechanistic investigations examining EDC-cancer associations. Methodological quality was appraised using the Newcastle-Ottawa Scale and AMSTAR-2, with overall certainty of evidence rated using the GRADE framework. Results: Major EDC classes—bisphenol compounds, phthalates, polychlorinated biphenyls, organochlorine pesticides, and per- and polyfluoroalkyl substances—demonstrate carcinogenic potential through estrogen receptor modulation, epigenetic alterations, oxidative stress, and oncogenic signaling disruption. Breast cancer shows the strongest evidence, with prenatal and early-life DDT/DDE exposure associated with up to a 3.7-fold increased risk. Endometrial cancer demonstrates associations with xenoestrogen mixtures exhibiting non-monotonic dose-responses, whereas ovarian and cervical cancers show emerging but limited associations. Common mechanisms include receptor crosstalk, epigenetic dysregulation with transgenerational effects, oxidative genomic instability, metabolic reprogramming, and cancer stem cell enrichment. Conclusions: Evidence supports EDC contributions to gynecological malignancy through convergent pathways, though causal inference remains constrained by observational epidemiology, long latency periods, and challenges in characterizing real-world mixture exposures. Diagnostic and prevention strategies should integrate EDC exposure into risk-prediction models, leverage multi-omics biomarkers for early detection, and emphasize exposure reduction during critical developmental windows alongside regulatory reform.