ArticleEnvironment international2026
Exposure to bisphenols and phthalates and arterial stiffness in women of reproductive age: a New York City cohort analysis.
Article in Environment international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeThis study aimed to examine associations of bisphenol and phthalate exposure with arterial stiffness among women of reproductive age.
methodsParticipants include 637 adult women enrolled in the New York University Children's Health and Environment Study (NYU CHES), a prospective pregnancy cohort. The concentrations of eight bisphenols and 22 phthalate metabolites were quantified in up to three spot urine samples. Primary outcomes included brachial artery distensibility (BrachD) and carotid-femoral pulse wave velocity (cfPWV) as measures of peripheral and central arterial stiffness, respectively, along with blood pressure assessed at repeated study visits up to seven years from exposure measures. Associations between averaged, log2-transformed, creatinine-standardized chemical concentrations and subclinical vascular outcomes of interest were examined using linear mixed-effects models.
resultsIn covariate-adjusted models, a doubling of bisphenol A was positively associated with BrachD (0.09%/mmHg, 95% confidence interval [CI] = 0.02, 0.16), a doubling of bisphenol S was negatively associated with mean arterial pressure (MAP) (-0.52 mmHg, 95% CI = -0.98, -0.05), a doubling of di(2-ethylhexyl) phthalate (DEHP) metabolites was negatively associated with diastolic blood pressure (DBP) (-0.81 mmHg, 95% CI = -1.38, -0.23) and MAP (-0.83 mmHg, 95% CI = -1.45, -0.21), and a doubling of antiandrogenic phthalate metabolites was associated with 0.62 mmHg lower DBP (95% CI = -1.22, -0.03) and 0.66 mmHg lower MAP (95% CI = -1.30, -0.02).
conclusionThese findings suggest that routine exposure to bisphenols and DEHP may be associated with vasorelaxation, potentially related to these chemicals' estrogenic and/or antiandrogenic effects.
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