Disparities in Endocrine-Disrupting Chemical Exposures and Thyroid Disorders

Emerging studies suggest that endocrine disrupting chemicals (EDCs) in personal care and other consumer products are linked with various adverse health effects, including respiratory and reproductive effects. Despite Black persons using more personal care products than other demographic groups and having a high asthma burden, little is known regarding their consumer product use patterns and associated EDC exposures. To examine the association between recent exposure to select EDCs with specific consumer products and behaviors in a cohort of 110 predominantly Black children with asthma, ages 8-17 years, living in Baltimore City, Maryland. We quantified concentrations of bisphenol A (BPA), bisphenol S (BPS), bisphenol F, two dichlorophenols, four parabens, triclosan, benzophenone-3, and triclocarban in spot urine samples. Questionnaires were used to capture recent (last 24-h) consumer product use and behaviors. Associations between EDCs and consumer product uses/behaviors were assessed using multivariable linear regression, adjusting for age, gender, race/ethnicity, and caregiver income level. Effect estimates were expressed as geometric mean ratios of biomarker concentrations of product-users vs non-users. Increased concentrations to select EDCs were associated with recent use of air freshener (ratios; BPA: 1.9, 95%CI 1.4-2; BPS 1.7, 95%CI 1-2.97; propyl paraben: 3.0, 95%CI 1.6-5.6), scented candles (methyl paraben: 2.6, 95%CI 1.1-6.1), and scented carpet powder (2,5-dichlorophenol: 2.8, 95%CI 1.2-6.3). Additionally, consuming canned food was associated with some increased biomarker concentrations (ratios: BPA: 1.7, 95%CI 1.2-2.4; BPS: 2.1, 95% CI: 1.2-3.6). These findings add to the body of evidence suggesting that recent use of select consumer products in Black children contributes to exposure of chemicals of concern and could potentially inform exposure mitigation interventions. Findings have broad potential health implications for pediatric populations and Black children who may face exposure and health disparities. Little is known about how children's personal care product use and consumer behaviors affect their exposures to endocrine disrupting chemicals (EDCs). This is particularly true for Black children who often experience a disparate exposure burden to many EDCs. This is a significant knowledge gap among children that are uniquely vulnerable to EDCs as they undergo critical windows of growth and development. Our findings show associations between consumer products and EDC exposures in predominantly Black children in low-income settings. Identifying EDC exposure determinants has broad health implications as many of these chemicals have been associated with adverse health risks.

The relationship between endocrine disrupting chemical (EDC) exposure and Precocious Puberty (PP) was investigated in this pilot study, involving girls with signs of PP (P) and pre-pubertal girls (C). Risk factors for PP were assessed through questionnaires, while 17β-oestradiol (E2) levels and oestrogenic activity were quantified on sera. The oestrogenic activity, expressed as E2 equivalent concentration (EEQ), was applied as EDC exposure biomarker. Questionnaires showed a low EDC knowledge, a high EDC exposure, and a potential relationship between some habits at risk for EDC exposure and PP. EEQs were similar between C and P; however, they were significantly higher in girls living in an urban environment than in girls living in a rural environment, suggesting a potential higher EDC exposure in cities. The results of this pilot study highlighted the need to raise awareness on EDCs and can be considered a starting point to clarify the relationship between EDC exposure and PP.

Exposure to endocrine-disrupting chemicals in utero and thyroid cancer risk in offspring

Purpose: This study aimed to identify the relationships between fatigue, psychosocial stress, and behavior of infertile males that reduces endocrine-disrupting chemical (EDC) exposure and to provide baseline data needed for nursing intervention. Methods: A total of 110 infertile males were recruited from a special fertility hospital in Gwangju city in Korea. The participants were administered a self-reported questionnaire. Results: The mean scores were as follows: for fatigue, 59.1 out of 133; for psychosocial stress, 20.3 out of 54; and for behavior that reduced EDC exposure, 52.6 out of 85. Fatigue and psychosocial stress had a positive correlation(r=0.68, p<0.001), behavior that reduces EDC exposure was negatively correlated with fatigue and psychosocial stress(r=-0.54, p<0.001; r=-0.61, p<0.001) Conclusion: Fatigue and stress were higher in infertile males. Our findings suggest that a nursing intervention program should focus on reducing fatigue and stress in infertile males and induce behaviors that decrease EDC exposure.

Long-term impacts of endocrine-disrupting chemicals exposure on kidney function: A community-based cohort study

Purpose of ReviewPregnancy can be seen as a “stress test” with complications predicting later-life cardiovascular disease risk. Here, we review the growing epidemiological literature evaluating environmental endocrine-disrupting chemical (EDC) exposure in pregnancy in relation to two important cardiovascular disease risk factors, hypertensive disorders of pregnancy and maternal obesity.Recent FindingsOverall, evidence of EDC-maternal cardiometabolic associations was mixed. The most consistent associations were observed for phenols and maternal obesity, as well as for perfluoroalkyl substances (PFASs) with hypertensive disorders. Research on polybrominated flame retardants and maternal cardiometabolic outcomes is limited, but suggestive.SummaryAlthough numerous studies evaluated pregnancy outcomes, few evaluated the postpartum period or assessed chemical mixtures. Overall, there is a need to better understand whether pregnancy exposure to these chemicals could contribute to adverse cardiometabolic health outcomes in women, particularly given that cardiovascular disease is the leading cause of death in women.

Preeclampsia (PE) is a critical complication of pregnancy that affects 3% to 5% of all pregnancies and has been linked to aberrant placentation, causing severe maternal and fetal illness and death. This systematic review aims to elucidate the association of in-utero endocrine-disrupting chemical (EDC) exposure and microRNAs and their imprinted genes from prenatal and maternal circulation of PE patients. Databases such as PubMed, PubMed Central, ScienceDirect, the Comparative Toxicogenomics Database (CTD), ProQuest, EBSCOhost, and Google Scholar were utilized to search for articles that investigate the relationships between selected EDCs and epigenetic events such as DNA methylation and microRNAs that are associated with PE. A total of 29 studies were included in the database search. Altered expression of microRNAs (miR-15a-5p, miR-142-3p, and miR-185) in the placenta of PE patients was positively associated with the urinary concentration of phthalates and phenols in the development of the disease in the first trimester. EDCs such as phenols, phthalates, perfluoroalkyl substances (PFOAs), polybrominated diphenyl ethers (PBDEs), and organochlorine phosphates (OCPs) have been reported to be associated with hypertensive disorders in pregnancy. miRNA-31, miRNA-144, miRNA-145, miRNA-210, placental specific clusters (C14MC, and C19MC) may be used as possible targets for PE because of their potential roles in the onset and progression of PE. Prenatal EDC exposure, including exposure to BPA, showed association with signaling pathways including estrogen, sFlt-1/PlGF, ErbB, MAPK/ERK, and cholesterol mechanisms with placental hemodynamics. Even low EDC exposures leave altered epigenetic marks throughout gestation, which might cause PE complications.

In this review, the authors summarize findings from recent literature (published work between 2015 and 2019) as it pertains to how endocrine-disrupting chemical (EDC) exposure affects reproduction and fecundity in rodents. Many studies within recent literature have reported the effects of EDCs on sociosexual choice, ultrasonic vocalizations, sexual behavior, and fecundity. However, a handful of studies investigating the same endpoints report no effects. EDCs are difficult chemicals to study due to their complex nature. Many factors can mitigate or dampen their observable effects. Authors summarize and discuss presented results and possible sources of inconsistency. Both historic and current literature illuminate that reproductive endpoints are affected by EDC exposure, and thus, further exploration of this topic is both warranted and essential.

DNA damage resulting from human endocrine disrupting chemical exposure: Genotoxicity, detection and dietary phytochemical intervention

BackgroundPolybrominated diphenyl ethers (PBDEs) and organophosphate esters (OPEs) are commonly used as flame retardants. Limited research exists on socioeconomic and racial/ethnic disparities in exposure to these compounds and their impact on executive functioning (EF) in early childhood. The present study examined independent and joint effects of income and race/ethnicity on flame retardant exposure in early childhood and investigated associations between flame retardant exposure and children’s EF.MethodsThis cross-sectional study used data from 349 preschool children recruited in Oregon. Children wore silicone wristband samplers for seven days, with exposures to 41 flame retardant compounds analyzed by gas chromatography mass spectrometry. We focused on exposure to 6 compounds (BDE 47, BDE 99, BDE100, TCPP, TDCPP, TPP) and two composite indices (ΣPBDE, ΣOPE). Wilcoxon rank-sum tests examined exposure differences by race/ethnicity and income (low income = below federal poverty level). Multiple linear regression models, nested within classrooms, assessed the association between PBDE and OPE exposure and EF, measured by the Head-Toes-Knees-Shoulders-Revised (HTKS-R) and Dimensional Change Card Sort (DCCS) tasks.ResultsChildren were 5.1 years old (SD = 0.3), 29.9% were from underserved racial/ethnic backgrounds, and 27.8% of families were low income. Compared with higher income families, children from low income families were exposed to 83.4% greater ΣPBDE exposures and 36% greater TDCPP exposures. There was no evidence of racial/ethnic disparities in PBDE or OPE exposures. Controlling for age, sex, income, race/ethnicity, and disability or cognitive delay, neither PBDE nor OPE exposures were consistently related to EF, but children from lower income families scored 28.6% lower on the HTKS-R, and children from underserved races/ethnicities scored 25.9% lower on the HTKS-R.ConclusionsOur findings highlight persistent income disparities in PBDE exposures at a pivotal point in children’s development, and reveal similar disparities in TDCPP exposures. Furthermore, socioeconomic disadvantage was more strongly associated with reduced EF than either PBDE or OPFR exposures. These findings underscore the need to address structural social inequities, and also highlight the need for greater representation of children from underserved backgrounds in research that seeks to characterize chemical and social exposures within neighborhood and preschool environments.

An inadvertent issue of human retina exposure to endocrine disrupting chemicals: A safety assessment

Environmental agencies have identified a growing number of environmental contaminants that have endocrine disrupting activity, and these can become a major public health problem. It is suggested that endocrine disruptors could account for the higher-than-expected increase in the prevalence of some non-communicable diseases, such as obesity, diabetes, thyroid diseases, and some cancers. Several endocrine Disrupting Chemicals (EDCs), such as pesticides, bisphenol A, phthalates, dioxins, and phytoestrogens, can interact with the female reproductive system and lead to endocrine disruption. Initially, it was assumed that EDCs exert their effects by binding to hormone receptors and transcription factors, but it is currently known that they may also alter the expression of enzymes involved in the synthesis or catabolism of steroids. Biomonitoring studies have identified these compounds in adults, children, pregnant women, and fetuses. Among the diseases of the female reproductive tract associated with EDCs exposure are the following: precocious puberty, polycystic ovary syndrome, and premature ovarian failure. The different populations of the world are exposed to a great number of chemicals through different routes of infection; despite the various available studies, there is still much doubt regarding the additive effect of a mixture of EDCs with similar mechanisms of action.

Phenotypes and mechanisms of epigenetic transgenerational inheritance due to prenatal exposure of endocrine disrupting chemicals

Endocrine-disrupting chemicals (EDCs) are environmental contaminants that disrupt hormonal regulation by mimicking, inhibiting, or modifying endocrine signaling pathways. EDCs are commonly present in plastics, pesticides, industrial byproducts, and personal care products and pose substantial health risks, particularly to vulnerable groups such as infants and children. Early-life exposure is especially concerning due to the developing detoxification systems, the immaturity of the blood–brain barrier, and the ongoing organ differentiation, making these periods highly susceptible to EDCs’ harmful effects. Moreover, exposure during critical developmental periods, such as sex differentiation and neurodevelopment, can lead to significant long-term developmental impairments that persist into later life.Perinatal and childhood exposure to EDCs has been linked to various adverse health outcomes, including neurodevelopmental delays, impairments in reproductive health, obesity, type 2 diabetes, thyroid dysfunction, and even a heightened risk of certain malignancies. These effects are mediated through various mechanisms, including direct modulation of hormone receptors, disruption of genetic regulation, and interference with endocrine feedback systems. Alterations in endocrine signaling, particularly disruptions in thyroid hormone homeostasis, may also indirectly impair cognitive development, increasing the risk of attention disorders and intellectual impairment.Although regulatory measures to reduce EDC exposure are crucial, current restrictions remain insufficient. Moreover, as new EDCs emerge, ongoing research is essential to understand their risks and develop effective strategies to minimize their potential harm. Protecting future generations requires a proactive approach that combines public health awareness, strong regulations, and ongoing scientific research. This review highlights the potential risks of EDCs exposure in children and highlights the significance of multidisciplinary research and policy efforts.

Endocrine-disrupting chemicals (EDCs) are exogenous compounds that interfere with hormone action, and growing evidence suggests that human exposure to certain EDCs may increase the risk of obesity, type 2 diabetes mellitus (T2DM), and cardiovascular disease (CVD). To clarify the impact of EDC exposure on cardiometabolic health, we conducted a review of the literature (2005–2025) to identify both human epidemiological studies and animal mechanistic studies. In this narrative review, we primarily summarize the existing human epidemiological evidence on the cardiometabolic effects of EDCs, while also considering mechanistic insights, including selected animal studies, to illustrate biological plausibility. Key findings indicate that EDC exposures are consistently associated with elevated risks of cardiometabolic conditions. Notably, prenatal and early-life EDC exposures appear to increase susceptibility to obesity, impaired glucose metabolism, and cardiovascular dysfunction later in life, while adult exposures are linked to a higher incidence of metabolic syndrome, type 2 diabetes, and related cardiovascular complications. In conclusion, this review underscores EDC exposure as a significant environmental risk factor for cardiometabolic disease. Accordingly, strengthening regulatory policies to reduce human exposure to these chemicals—alongside further research into underlying mechanisms—may be crucial for improving cardiometabolic health outcomes.