Association of individual and combined exposure to polycyclic aromatic hydrocarbon (PAH) and phthalate (PAE) metabolites with maternal estradiol levels in early pregnancy: A cross-sectional study.

Phthalate acid esters (PAEs) are ubiquitous endocrine-disrupting chemicals with oxidative potential. While diet is a major exposure pathway, especially for high-molecular-weight PAEs, the contribution of specific food categories to internal doses and their subsequent impact on oxidative stress remain inadequately quantified. In this cross-sectional study of 327 adults, we measured 14 urinary monoester metabolites (mPAEs) and linked them with 24 h dietary records and oxidative stress biomarkers. Monoethyl phthalate was the most abundant metabolite (median: 37.8 μg/g creatinine (Cre)), followed by the summed metabolites of di(2-ethylhexyl) phthalate (∑5DEHP, 21.7 μg/g Cre). Redundancy analysis showed that the diet accounted for 33.6% of urinary mPAEs variance, with meat, poultry, protein-rich foods, and staples as major contributors. In mixture-based models, monobenzyl, monobutyl, and mono(2-ethyl-5-hydroxyhexyl) phthalates were identified as key drivers of oxidative damage to DNA (8-oxo-7,8-dihydro-2'-deoxyguanosine), lipids (malondialdehyde), and proteins (dityrosine). Furthermore, nonlinear dose-response patterns were observed, with steeper increases in risk at low-to-moderate exposures. Cumulative risk assessment revealed that 7.3% of individuals exceeded safety thresholds, primarily due to di-n-butyl phthalate and DEHP. Our findings emphasize the value of integrating dietary data in exposure assessment and support incorporating mixture effects and nonlinearity into PAEs risk evaluation and food safety governance.

Phthalates exposure as a risk factor for gestational diabetes mellitus: Integrated evidence from epidemiological and human liver organoids studies.

Transplacental transfer efficiency of environmental chemicals in association with gestational diabetes mellitus

Abstract Background Although Hashimoto’s thyroiditis was recognized over a century ago, its precise cause is still unclear. There are raised concerns that plasticizers like phthalate are related to exacerbation of HT. Aim We investigated the potential link of urinary phthalate to thyroid functions in HT. Patients and methods Our comparative cross-sectional study involved 80 participants, 60 of them had newly diagnosed Hashimoto’s thyroiditis (Group A) who were further subdivided into Group A1: 20 euthyroid patients, Group A2: 20 participants having TSH between 5.1 and 10 mIU/ml and Group A3: 20 subjects who had TSH > 10 mIU/ml. The remaining 20 participants had no autoimmune thyroid disease with negative anti-thyroid antibodies (Group B) and served as control. We measured thyroid stimulating hormone, free thyroxine, free triiodothyronine, thyroid peroxidase antibody and the urinary phthalates: mono (2-ethylhexyl) phthalate, monoethyl phthalate and monobutyl phthalate for all participants. Results In patients with HT collectively (group A) each of the measured urinary phthalates had a positive correlation with thyroid stimulating hormone and a negative correlation with free thyroxine. In the same group mono (2-ethylhexyl) phthalate, monoethyl phthalate and not monobutyl phthalate had a negative correlation with free triiodothyronine. Comparing the subgroups of group A subgroups and group B there was a significant difference in the levels of each of the urinary phthalate markers, all being the highest in group A3. Conclusion Urinary phthalates were significantly related to thyroid hormone levels in Hashimoto’s thyroiditis. This supports the concerns raised around urinary phthalate affecting the severity of Hashimoto’s thyroiditis.

Urinary levels and estimated daily intake of phthalates and phenols in kidney transplanted Norwegian children.

Exposure to Phthalate Metabolite Mixtures as a Risk Factor for Low Muscle Mass: Insights From the National Health and Nutrition Examination Survey (2011-2018).

BackgroundExperimental studies have indicated that phthalate exposure may influence immune function, while other studies suggest that immune responses may impact lung function. However, the epidemiological evidence connecting phthalate exposure, immune response markers, and lung function is limited. This study aims to investigate these associations and explore potential mediation and interaction effects.MethodsData from healthy adults in the Taiwan Biobank (baseline 2008–2015; follow-up 2011–2020) were analyzed (N = 759). At baseline, 10 urinary phthalate metabolites were measured including monoethyl phthalate (MEP) mono（2-ethyl-5-oxy-hexyl）phthalate (MEOHP), mono（2-ethyl-5-hydroxyhexyl）phthalate (MEHHP), and mono（2-ethyl-5-carboxypentyl）phthalate (MECPP). Immune indicators were estimated using DNA methylation data for granulocytes, CD4+ T cells, and CD8+ T cells. Lung function at follow-up was assessed via predicted FVC, FEV₁, and FEV₁/FVC. Generalized linear models and mediation models assessed associations, interactions and mediating effects, respectively.ResultsMEP was positively associated with granulocytes (β = 0.009, 95% CI: 0.002, 0.015), while MEHHP was positively associated with CD4+ T cells (β = 0.030, 95% CI: 0.001, 0.059). MEHHP and MECPP were inversely associated with FEV₁/FVC (β= -0.014, 95% CI: -0.025, -0.003 for MEHHP; β= -0.016, 95% CI: -0.032, -0.001 for MECPP). MEOHP was negatively associated with both predicted FEV₁ (β= -0.027, 95% CI: -0.050, -0.005) and FEV₁/FVC (β= -0.018, 95% CI: -0.033, -0.002). Significant interactions between MEHHP and MEOHP levels and CD8+ T cell levels with FEV₁ and FEV₁/FVC were observed.ConclusionsExposure to specific phthalates or increased levels of certain immune cells may be linked to the risk of impaired lung function. Additionally, the association between phthalate exposure and lung function impairment may be affected by elevated immune responses.Key messages• Phthalate exposure and immune dysregulation may increase the risk of impaired lung function in adults.• Associations between phthalate exposure and lung function may be dependent on immune responses.

Early-life exposure to organic chemicals (OCs) may influence childhood obesity and associated cardiometabolic risk. These conditions have been shown to disproportionately affect minority populations such as Mexican Americans (MAs). However, information on the impact of organic chemicals on cardiometabolic risk in MA children is limited. Therefore, we conducted a pilot study to assess the extent to which exposure to organic chemicals influences cardiometabolic traits (CMTs) in MA children. We recalled 25 children from a previous study and collected 25 primary teeth from them. Chemical analyses of the teeth were performed using established protocols. Target analytes included acetaminophen (APAP); 3,5,6-trichloro-2-pyridinol (TCPy), 2-isopropyl-6-methyl-4-pyrimidinol (IMPy), diethyl phosphate (DEP), N,N-diethyl-m-toluamide (DEET), tris(2-butoxyethyl) phosphate (TBOEP), monoethyl phthalate (MEP), mono-n-butyl phthalate (MnBP), monoisobutyl phthalate (MiBP), monobenzyl phthalate (MBzP), mono-2-ethylhexyl phthalate (MEHP), mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP), mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP). The organic chemicals most frequently detected in the teeth were APAP; the insect repellent DEET; plasticizers MnBP and MiBP; and the plasticizer-derived metabolite MEHP. These five analytes were included in association analyses with selected CMTs. After adjusting for covariate (age, sex, tooth-type) effects, we found significant (p < 0.05) positive correlations between MiBP and the following CMTs: fat mass, fasting insulin, and the homeostasis model of assessment-insulin resistance (HOMA-IR). Both MnBP and MEHP exhibited negative correlation with blood pressure measures and triglycerides, respectively. In addition, APAP showed a strong negative correlation with HDL-C (p = 0.009) and positive association with triglycerides (p < 0.10). These findings suggest a potential role for early-life exposures to organic chemicals in influencing cardiometabolic risk in MA children.

Divergent effects of EDCs on bone maturation: Role of body mass index and puberty.

Associations between urinary phthalate metabolite mixtures, semen quality, and serum reproductive hormone levels in Japanese men seeking fertility treatment.

The mediating role of maternal inflammation on associations between first-trimester plasticizer exposure and personal-social and language in infants.

Association between Phthalate exposure and Reproductive Health in Patients Undergoing Assisted Reproductive Treatment: A Systematic Review and Meta-Analysis.

BackgroundPreterm birth (< 37 weeks gestation) is a leading cause of infant morbidity and mortality, yet the underlying causes remain unknown in many cases. Environmental exposures, including endocrine-disrupting chemicals such as phthalates, have been implicated in preterm birth risk. Phthalates are commonly used as plasticisers in consumer products, resulting in widespread human exposure. While some studies suggest an association between maternal phthalate exposure and reduced gestational length, findings remain inconsistent. This study aimed to investigate the relationship between urinary phthalate metabolite concentrations and gestational length in an Australian pregnancy cohort.MethodsThis prospective cohort study was nested within the Omega-3 to Reduce the Incidence of Prematurity (ORIP) trial. A total of 605 women with singleton pregnancies from South Australia provided urine samples between 22- and 26-weeks’ gestation for phthalate metabolite analysis. Thirteen phthalate metabolites were quantified using liquid chromatography-tandem mass spectrometry. Gestational age at birth was determined from medical records. Linear regression models assessed associations between phthalate concentrations and gestational length, adjusting for maternal characteristics including age, BMI, socioeconomic status, education, smoking, and alcohol consumption.ResultsPhthalate metabolites were detected in > 99% of urine samples, with the highest concentrations observed for mono-ethyl phthalate (MEP), mono-isobutyl phthalate (MiBP), and mono-butyl phthalate (MBP). There was no evidence of an association between phthalate exposure and gestational length in either unadjusted or adjusted analyses. No significant association was found between phthalate exposure and preterm birth risk.ConclusionsDespite widespread phthalate exposure, no clear link was identified between maternal phthalate levels and shortened gestation in this Australian cohort. However, continued surveillance is needed to monitor emerging plasticiser exposures and inform public health policies on maternal and infant health.Trial registration numberAustralian New Zealand Clinical Trials Registry number, ACTRN12613001142729. Date of registration: 27/09/2013.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12884-025-07980-8.

Phthalate exposure is associated with subclinical coronary atherosclerosis: The Aragon Workers' Health Study (AWHS)

Longitudinal analysis of maternal exposure to phthalates and bisphenol A and their impact on infant neurodevelopment and autistic behavior: The potential mediating role of thyroid hormones.

Periconception bisphenol and phthalate concentrations in women and men, time to pregnancy, and risk of miscarriage.

Dietary patterns and exposure to non-persistent endocrine-disrupting chemicals during pregnancy.

Prenatal exposure to mixtures of phthalates and bisphenol A and eczema risk: findings in atopic and non-atopic children from the LiNA birth cohort.

Neonatal exposure to an environmentally relevant phthalate mixture alters ovarian function in mice.