Endocrine Society of India's National White Paper on Endocrine Disrupting Chemicals - A Call for Action.

Table 2 summarizes commonly recognized EDCs and their health-related effects. Commonly recognized endocrine disrupting chemicals and their health-related effects ADHD=Attention deficit hyperactivity disorder, AGD=Anogenital distance, AhR=Aryl hydrocarbon receptor, AR=Androgen receptor, BPA=Bisphenol A, BPS=Bisphenol S, DDE=Dichlorodiphenyldichloroethylene, DDT=Dichlorodiphenyltrichloroethane, DEHP=Diethylhexylphthalate, ER=Estrogen receptor, GABA=γ aminobutyric acid, GR=Glucocorticoid receptor, HPG=Hypothalamic-pituitary-gonadal, IQ=Intelligence quotient, IR=Insulin resistance, LBR=Live birth rate, NHL=Non-Hodgkin lymphoma, OPE=Organophosphate esters, PBDE=Polybrominated diphenyl ether, PCB=Polychlorinated biphenyl, PCOS=Polycystic ovary syndrome, PDE4=Phosphodiesterase E4, PFAS=Per- and polyfluoroalkyl substances, PFOA=Perfluorooctanoic acid, POP=Persistent organic pollutant, PTFE=Polytetrafluoroethylene, T2DM=Type 2 diabetes mellitus, TH=Thyroid hormones, TR=Thyroid hormone receptor, PPAR=Proliferator-activated receptor gamma. *PFAS are also called ‘forever chemicals’ as they are highly persistent and bioaccumulate. # POPs include pesticides (DDT, aldrin, dieldrin, endrin, chlordane, lindane, heptachlor), PCBs, PBDEs, PFOA, dioxins, and furans Intrauterine and early life stages are critical windows during which exposure to EDCs can result in epigenetic programming, increasing the risk of noncommunicable diseases later in life. Significant exposure to EDCs during pregnancy (phthalates, PBDEs, PFAS/PFOA, phenols, organochlorines and organophosphates) was documented in the Human Early-Life Exposome project across six European birth cohorts.[ 35 ] A study from Tamil Nadu found high concentrations of parabens, BPA and triclosan in maternal blood and amniotic fluid at term, indicating notable fetal exposure.[ 32 ] Elevated levels of OCPs (e.g. dichlorodiphenyltrichloroethane [DDT], dichlorodiphenyldichloroethylene [DDE] and hexachlorocyclohexane) in maternal blood and placenta were associated with preterm birth and low birth weight in a Delhi-based study.[ 36 ] Maternal exposure to EDCs such as OCPs, polyaromatic hydrocarbons, dioxins, PCBs, and PFAS has also been linked to intrauterine growth restriction, low birth weight and later childhood obesity, with increased body mass index (BMI) and waist circumference.[ 5 33 37 ] Early-life exposure to triclosan has been associated with rapid weight gain and precocious puberty. PFAS have been strongly linked to adiposity, insulin resistance (IR) and fatty liver disease.[ 33 ] Childhood and puberty, marked by rapid endocrine changes, are also sensitive periods. EDCs, especially BPA, phthalates, PFAS, and triclosan have been associated with adverse effects on childhood growth, neurodevelopment and metabolic health.[ 6 11 ] Epidemiological data suggest associations between EDC exposure (BPA, phthalates, PCBs, pesticides) and poorer cognitive performance, lower intelligence quotient, and increased risk of neurodevelopmental disorders, including autism spectrum disorders and attention deficit hyperactivity disorders (ADHD).[ 11 38 ] EDCs (BPA, phthalates, PFAS) also influence pubertal onset, though effects vary with timing, dose and sex. Perinatal exposure may delay thelarche and menarche in girls, while peripubertal exposure is linked to earlier pubarche and menarche. In boys, EDCs may delay the onset or progression of puberty.[ 39 ] Interest in EDCs began in the early 1970s, following the discovery that prenatal exposure to diethylstilbestrol (DES) increased the risk of vaginal and cervical cancer, reproductive tract abnormalities, and reduced fertility in female offspring while it increased the risk of hypospadias, cryptorchidism and testicular hypoplasia in the male offspring.[ 6 40 ] EDCs impact reproductive health through multiple mechanisms, illustrated in Figure 2 , and are linked to a range of reproductive disorders from fetal development to adulthood. Exposure to EDCs may result in reproductive developmental abnormalities, pubertal disorders, reduced fertility, and hormone-sensitive cancers. The effects are often sex-specific with potential long-term and transgenerational consequences. Mechanisms by which endocrine disrupting chemicals affect reproduction EDCs have myriad effects including impaired ovarian development, altered gonadotropin secretion, impaired steroidogenesis, disrupted follicular growth, and reduced uterine receptivity [ Figure 3 ].[ 41 42 ] Growing evidence from animal studies and human data link EDC exposure to abnormal puberty (e.g. early pubarche or thelarche, or precocious puberty), menstrual irregularities, polycystic ovary syndrome (PCOS), endometriosis, fibroids, infertility, preterm birth and other adverse pregnancy outcomes, and early menopause.[ 6 37 41 42 ] Effects of endocrine disrupting chemicals on female reproductive health. BPA = Bisphenol A, DES = Diethylstilbestrol, EDC = Endocrine disrupting chemicals, PCB = Polychlorinated biphenyl, PFAS = Per- and polyfluoroalkyl substances, PFOA = Perfluorooctanoic acid, POP = Persistent organic pollutants, TCDD = Tetrachlorodibenzodioxin In India, few studies have examined these associations. Higher levels of BPA and phthalate esters were reported in women attending an infertility clinic in Mumbai compared with fertile controls.[ 43 ] In women with PCOS, significantly higher levels of BPA were reported from Ahmedabad[ 44 ] while higher levels of OCPs (DDT, endosulfan and heptachlor) correlated with hyperandrogenism, menstrual irregularities and IR in a study from Agra.[ 45 ] Many EDCs possess estrogenic or antiandrogenic properties that disrupt fetal testis development and male genital formation, contributing to testicular dysgenesis syndrome,[ 37 ] as summarized in Table 3 . Perinatal exposure to phthalates, PCBs, DDT/DDE, hexachlorocyclohexane (HCH), dioxins and fungicides has been associated with increased risk of hypospadias and cryptorchidism. A case-control study from Assam found a link between maternal occupational EDC exposure, especially during the first trimester, and risk of hypospadias.[ 46 ] Compounds such as DES, fungicides, herbicides, dioxins and phthalates have been linked to reduced testis weight. In addition, exposure to pesticides, PCBs, PBDEs, dioxins, phthalates, BPA, PFOA, and heavy metals has been linked to impaired sperm quality and reduced fertility.[ 37 ] Effects of endocrine disrupting chemicals on male reproductive health FSH=Follicle stimulating hormone Several EDCs can interfere with hormonal pathways and may induce neoplastic transformation in hormone-sensitive tissues.[ 47 ] EDCs with estrogenic properties have been linked to an increased risk of breast cancer, including DES, DDT/DDE, chlordane, HCH, PCBs, dioxins, PFOA, BPA and triazine herbicides.[ 48 49 50 ] Epidemiological evidence in humans remains limited, partly due to the long latency between exposure and disease onset, and challenges in assessing cumulative exposure. Notably, a higher incidence of breast cancer was reported in women exposed to tetrachlorodibenzodioxin following the Seveso industrial accident in Italy, with increased rates observed after 10, 15 and 20 years. Similar findings were reported following dioxin contamination in Russia.[ 41 ] Data linking EDCs to endometrial and ovarian cancer is limited, but some studies suggest associations with dioxins, PFOA and triazine compounds. In men, several EDCs have been strongly associated with increased prostate cancer risk. These include dioxins, various biocides (e.g. aldrin, dieldrin, atrazine, coumaphos, fonofos, methoxychlor, heptachlor, endosulfan, malathion, phorate, simazine), heavy metals (arsenic, cadmium), BPA, and PCBs.[ 51 ] In addition, certain EDCs such as phthalates, DDE and some fungicides have been linked to testicular germ cell tumors.[ 42 52 ] Several EDCs are increasingly recognized as metabolic disruptors, due to strong evidence linking them to obesity, diabetes and cardiometabolic risk.[ 53 ] Many of these act as obesogens and diabetogens, altering adipocyte biology, energy balance, insulin sensitivity and pancreatic function [ Figure 4 ]. BPA, phthalates, pesticides (DDT, chlorpyrifos, diazinon, parathion, tributyltin), PCBs, PFAS, PBDEs, dioxins, and heavy metals (arsenic, mercury) have been implicated.[ 54 ] They act via several mechanisms - PPAR γ and AhR activation, estrogen and glucocorticoid receptor interference, IR, adipocyte dysfunction, disrupted energy homeostasis, inflammation, gut dysbiosis, and β-cell dysfunction.[ 5 53 54 55 ] BPA, PFAS/PFOA, pesticides and heavy metals have clear diabetogenic potential.[ 5 6 55 ] Mechanisms of effect of metabolic disruptor chemicals. MASLD = Metabolic dysfunction associated steatotic liver disease, OPE = Organophosphate esters, PFAS = Per- and polyfluoroalkyl substances, PBDE = Polybrominated diphenyl ether POPs, being lipophilic, bioaccumulate in adipose tissue and the food chain, posing long-term risk. BPA and phthalates, though less persistent, are widespread and linked to similar effects. The impact is nonmonotonic and depends on timing, dose and life-stage.[ 5 6 ] Some individuals are genetically predisposed due to specific single nucleotide polymorphisms (SNPs).[ 2 ] Studies across in vitro and animal models show that early-life, especially perinatal, exposure increases the risk of adiposity, hyperinsulinemia and glucose intolerance.[ 5 6 55 ] Epidemiological studies in humans including the National Health and Nutrition Examination Survey (US) and cohorts from China, Sweden and the Netherlands, consistently link higher urinary levels of BPA, phthalates and PFOA to obesity, IR and type 2 diabetes (T2D).[ 5 6 ] A Dutch cohort found prenatal PFOA exposure was associated with overweight in female offspring at 20 years, raising concerns about transgenerational effects.[ 56 ] Epidemiological evidence also links BPA, phthalates, PCBs, DDT/DDE, and dioxins to increased T2D risk.[ 55 ] BPA and dioxins have been associated with hypertension, dyslipidemia, and cardiovascular disease, though causality remains unproven.[ 5 ] In a prospective cohort of 12,271 adults from Delhi and Chennai, those in the highest quartile of DDE had twice the risk of developing diabetes.[ 57 ] Another study from Jaipur reported higher serum BPA levels in persons with diabetes, with positive correlations to BMI, waist circumference and leptin levels, and inverse correlation with adiponectin levels.[ 58 ] Urinary bisphenols and parabens were significantly elevated in young Indian women from Guwahati with positive association with BMI and waist-hip ratio.[ 59 ] In Delhi, Tyagi et al . reported contamination of groundwater with HCH, DDT and DDE and higher levels of these EDCs in blood samples from individuals with prediabetes and T2D compared with normoglycemic controls.[ 60 ] They also suggested that postprandial hypertriglyceridemia may increase exposure to lipophilic OCPs such as DDT in another study.[ 61 ] In a study of 300 adults, higher levels of HCH, dieldrin and DDE were associated with IR, glucose levels and increased diabetes risk, independent of BMI.[ 62 ] Tawar et al . found high levels of 18°CPs (including DDT, HCH, heptachlor and endrin) in the visceral fat from people with T2D. There was a correlation with glycemic markers, central adiposity, and endoplasmic reticulum stress.[ 63 ] In a study conducted in 76 children, BPA, BPS, parabens and triclosan were detected in urine samples but only 3,4-dihydroxybenzoic acid was linked to obesity.[ 33 ] Altered epigenetic patterns linked to preeclampsia in the first trimester of pregnancy have been associated with higher urinary phthalate and phenol levels, particularly microRNAs 15a-5p, 142-3p and 185.[ 64 ] In summary, consistent evidence from cellular, animal and human studies supports the role of EDCs in metabolic disorders. EDCs adversely impact bone health by suppressing osteoblastic bone formation more than promoting bone resorption, leading to decreased bone mass and weakened structure. EDCs such as BPA which have estrogenic activity interfere with bone forming effects of estrogen while PFAS activate PPARγ, inhibiting osteoblastic differentiation. EDCs also disrupt calcium-regulating hormones such as parathyroid hormone and calcitonin, leading to abnormal calcium handling.[ 65 ] In addition, compounds such as PCBs and phthalates hinder bone mineralization by disrupting thyroid hormone synthesis and vitamin D metabolism. The perinatal period is particularly vulnerable to BPA exposure, with dose- and sex-dependent effects on embryonic bone development. Low doses retard ossification while higher doses may cause more severe skeletal effects.[ 66 ] Epidemiological studies link PFAS exposure to low bone mineral density (BMD) and increased risk of osteoporosis in both adults and children.[ 67 ] Phthalates have also been increasingly associated with reduced BMD, particularly in postmenopausal women.[ 68 ] Several EDCs (perchlorate, PCBs, triclosan, PBDEs, BPA) have structural similarities with thyroid hormones and may disrupt thyroid hormone synthesis, distribution, metabolism or action, as summarized in Table 4 .[ 69 ] They are linked to increased risk of thyroid dysfunction as well as thyroid cancers.[ 69 ] Effects of endocrine disrupting chemicals on thyroid function BPA=Bisphenol A, PBDE=Polybrominated diphenyl ethers, PCB=Polychlorinated biphenyls, T4=Thyroxine, TBG=Thyroxine binding globulin, TH=Thyroid hormones Flame retardants, bisphenols, phthalates and microplastics have been shown to disrupt hypothalamic-pituitary-adrenal (HPA) axis by affecting steroidogenic pathways leading to altered glucocorticoid secretion in animal studies.[ 70 ] Elevated BPA and phthalate levels were linked to altered glucocorticoid secretion and action in children, adolescents and adults,[ 53 ] including altered cortisol patterns in pregnant women, increased hair cortisol levels in adolescents and a higher risk of nonfunctioning adrenal incidentalomas.[ 70 ] Although these findings are suggestive, further research, especially in humans, is needed to clarify the impact of EDCs on the HPA axis. Some epidemiological studies have reported that prenatal exposure to phthalates, PFAS and phenols may affect HPA-related outcomes by upregulating cortisol production, but findings have been inconsistent.[ 71 ]

Traditionally, the endocrine-disrupting effects of EDCs were attributed mainly to their interaction with nuclear hormone receptors, including estrogen, androgen and thyroid receptors. However, they target a broader range of receptors including peroxisome proliferator-activated receptor gamma (PPARγ), aryl hydrocarbon receptors (AhR), receptors for glucocorticoids, progesterone, follicle stimulating hormone and various neurotransmitters (e.g. dopamine, serotonin, glutamate, γ-aminobutyric acid, and nicotinic acetylcholine receptors).[ 3 6 11 ] EDCs can also interfere with hormone-binding proteins, hormone metabolism, intracellular enzymes and signal transduction.[ 3 11 ] Figure 1 illustrates key mechanisms of EDC action. Common mechanisms of endocrine disruption by endocrine disrupting chemicals with illustrative examples. DEHP = Diethylhexylphthalate, EDCs = Endocrine disrupting chemicals, PCB = Polychlorinated biphenyl EDCs are linked to a wide range of adverse health effects including neurodevelopmental disorders, reproductive and thyroid dysfunction, obesity, cardiometabolic disease, autoimmune conditions, and hormone-sensitive cancers.[ 3 5 6 ] Developmental exposure during critical “windows of susceptibility” can disrupt epigenetic programing via DNA methylation, histone modification or miRNA regulation, increasing the risk of chronic disease later in life.[ 3 6 11 34 ] These effects may have a long latency period and can even be transgenerational.[ 3 11 ] Importantly, harmful effects are not limited to high-dose occupational exposure; even low-dose routine-level exposure can be detrimental. EDCs may display nonlinear, nonmonotonic dose-response (NMDR) relationships, where lower doses may have unexpected or more potent effects than higher ones.[ 3 6 11 ]

Several international scientific bodies including the WHO, ES, American Public Health Association, American Chemical Society, American College of Obstetricians and Gynecologists and the Royal College of Obstetricians and Gynecologists have emphasized the urgent need to address EDCs. To combat the rising threat of EDCs in India, we propose a multipronged strategy focused on empowerment, awareness, advocacy and research. Healthcare professionals should be equipped with the knowledge and tools to educate patients about sources of EDC exposure, associated health risks, and safer alternatives. The science of EDCs should be integrated into medical and allied healthcare curricula, with emphasis on incorporating environmental and occupational exposure into routine clinical assessments. Practical strategies for clinician engagement are outlined in Figure 5 . Strategies to empower healthcare practitioners There is a pressing need to inform the public about EDC-related health risks and prevention strategies. Tools include brochures, print and social media outreach, and awareness drives in collaboration in schools, communities, and nongovernmental organizations, especially targeting vulnerable populations. The “Reduce, Reuse, Recycle” framework, rooted in the 1970s environmental movement, offers a practical approach to limiting EDC production, use and disposal. The ESI brochure for public awareness on EDCs is provided in Appendix 1 . Regulatory agencies play a vital role in ensuring the safety of chemicals and minimizing exposure to EDCs. Internationally, the European Union’s Registration, Evaluation, Authorization and Restriction of Chemicals (REACH) regulation sets a benchmark by identifying and restricting hazardous chemicals across sectors.[ 4 6 72 73 ] The EU also enforces EDC-related restrictions under the Plant Protection Products Regulation (2009) and Biocidal Products Regulation (2012),[ 73 74 ] while the European Chemicals Agency and European Food Safety Authority provide guidance on EDCs in cosmetics and food, including mandatory labeling of ingredients, allergens and usage instructions. The European Commission additionally assesses the safety of nanomaterials in consumer products.[ 4 73 ] In the United States, the Environmental Protection Agency runs the Endocrine Disruptor Screening Program and enforces the Toxic Substances Control Act to regulate commercial chemicals and prevent EDC contamination.[ 4 6 73 75 ] At the global level, UNEP has proposed testing guidelines focused on EDCs.[ 4 73 ] A two-tiered system using high-throughput screening methods such as gas or liquid chromatography with mass spectrometry and high-performance liquid chromatography, followed by more sensitive assays, has been proposed for identifying suspected and confirmed EDCs.[ 6 76 ] In India, however, regulatory efforts remain fragmented: The Central Pollution Control Board addresses legacy pollutants such as DDT, HCH, aldrin, PCBs, and heavy metals but most EDCs are not routinely monitored. The Chemical (Management and Safety) Rules, modeled on the EU REACH framework, are under development and will require industries to register and notify the government about new and existing chemicals.[ 18 ] The Bureau of Indian Standards has taken steps by introducing BPA-free labeling and banning BPA in baby feeding bottles and food containers for children.[ 18 ] The Central Pollution Control Board addresses legacy pollutants such as DDT, HCH, aldrin, PCBs, and heavy metals but most EDCs are not routinely monitored. The Chemical (Management and Safety) Rules, modeled on the EU REACH framework, are under development and will require industries to register and notify the government about new and existing chemicals.[ 18 ] The Bureau of Indian Standards has taken steps by introducing BPA-free labeling and banning BPA in baby feeding bottles and food containers for children.[ 18 ] Despite these efforts, India still lacks a comprehensive regulatory framework for EDCs. There is an urgent need for structured regulation, routine monitoring, coordinated data collection, inter-agency collaboration, and widespread public awareness.[ 72 ] Figure 6 provides an integrated framework highlighting overlapping responsibilities across occupational, consumer and environmental domains in EDC regulation. Key regulatory and capacity building recommendations from ESI are summarized in Table 5 . Regular biomonitoring for EDCs currently is not recommended outside research settings. Multisectoral interfaces in endocrine disruptor chemicals regulation and public health protection Key regulatory and capacity building recommendations from endocrine society of India WHO=World Health Organization, UNEP=United Nations Environment Programme, EDC=Endocrine disrupting chemical While numerous animal and epidemiological studies have investigated EDCs, significant gaps remain in understanding their effects on human health.[ 77 ] Future research should focus on establishing associations and causal links between exposure and outcomes, particularly for emerging substitute chemicals, such as bisphenol S, which was introduced as a safer alternative to BPA but later shown to have similar endocrine disrupting effects.[ 6 11 ] EDC research is methodologically challenging due to their widespread, low-level presence and complex exposure patterns. Continuous exposure data often need to be categorized (e.g. weekly, daily, never), and varied health outcomes may require advanced statistical methods such as nonparametric analysis, maximum likelihood estimation, or Bayesian techniques.[ 78 79 ] Ethical limitations in human trials and the difficulty of translating animal data further complicate research.[ 78 79 ] In addition, EDCs often involve low-dose effects, NMDR, sensitive windows of exposure, confounders and long latency periods.[ 73 ] The exposome (all the exposures of an individual in a lifetime and how these exposures relate to health) and life course epidemiology approaches integrate frameworks to assess dynamic exposures across multiple domains.[ 79 ] Advancing EDC research requires a multidisciplinary approach, combining basic and translational science, toxicology, endocrinology, epidemiology, healthcare, and public health [ Table 6 ].[ 80 81 ] Future and ongoing research questions in relation to endocrine disrupting chemicals EDC=Endocrine disrupting chemical EDCs have emerged as a pressing concern for human health and environmental safety. This white paper brings together current evidence, Indian data, and global perspectives to highlight the magnitude of the problem and the gaps that remain. ESI urges collective, sustained action through awareness, education, research and regulation. Empowering healthcare professionals and the public with knowledge, encouraging safer industrial and domestic practices, and strengthening national policies are vital steps forward. With coordinated efforts across disciplines and partnerships that bridge science and policy, India can pave the way toward reducing exposure and safeguarding health for generations to come. N.A. There are no conflicts of interest. Artificial intelligence was not used in any form for analysis or writing of this research article.

Individuals and populations are exposed to low doses of multiple chemicals over their lifespan. EDCs are omnipresent and found in a wide range of sources – agricultural, industrial, and domestic. EDC exposure may occur via water, agricultural produce, livestock, packaged and processed food, food containers, personal care products, plastics and other household goods. Table 1 enlists the major sources of EDCs in India. Major sources of endocrine disrupting chemicals in India BPA=Bisphenol A, BPS=Bisphenol S, DDE=Dichlorodiphenyldichloroethylene, DDT=Dichlorodiphenyltrichloroethane, DEET=N,n-diethylmetatoluamide, DEHP=Diethylhexylphthalate, OPE=Organophosphate esters, PBDE=Polybrominated diphenyl ether, PCB=Polychlorinated biphenyl, PFAS=Per- and polyfluoroalkyl substances, PFOA=Perfluorooctanoic acid, PVC=Polyvinylchloride Plastic and plastic-based products remain an important source.[ 9 ] India generates ~9.4 million metric tons of plastic annually, of which 35% and 23% is used in packaging and construction, respectively.[ 10 ] Only 50% is collected and processed; the remaining ends up in landfills and water bodies. At least 40% of plastic is single use.[ 9 ] Behaviors such as online shopping, home delivery and packaged foods, have further increased plastic waste. India is also the third-largest producer of electronic waste, generating 4.1 million metric tons annually.[ 10 ] Ironically, medical devices and other healthcare products also add to the burden of EDCs from plastic additives and pharmaceutical contamination.[ 11 ] As per an estimate, medical products (medical equipment, packaging, tubes, gloves, drape materials, etc.) contribute to 2% of global plastic production and this further surged during the coronavirus disease 2019 pandemic.[ 12 ] Open dumping and burning of waste results in release of toxic byproducts into the environment. There is no comprehensive national data in India, but several small studies have reported alarming levels of EDC exposure from a variety of sources. High concentrations of bisphenols were reported in vegetables, surface water, wastewater and indoor dust, particularly in the agricultural states of Uttar Pradesh, Punjab and Haryana.[ 13 14 ] Organochlorine pesticides (OCPs), polychlorinated biphenyls (PCB), polybrominated diphenyl ethers (PBDE), dioxins and furans were found in several food items, especially dairy and meat, from Delhi and Dehradun.[ 15 ] A nationwide pilot study reported elevated levels of per- and polyfluoroalkyl substances (PFAS) in human hair samples.[ 16 ] Widespread exposure to phthalates has also been reported.[ 17 ] High levels of contamination of the environment with several EDCs are major causes of concern.[ 18 ] Samples of river water and sediment from several Indian rivers including the Yamuna River in Delhi, Mithi River and Thane Creek in Mumbai, Kaveri River, Ganga River and the Sunderban wetlands have been found contaminated with EDCs such as phthalates, bisphenols, pesticides, polyaromatic hydrocarbons, triclosan, parabens, heavy metals, hormones (estrone, estradiol, estriol), and pharmaceutically active compounds (ibuprofen, diclofenac, ketoprofen, etc.).[ 19 20 21 22 23 24 25 ] High concentrations of estrone were also detected in influent wastewater at two wastewater treatment plants in Dehradun.[ 26 ] Many EDCs are “persistent organic pollutants” (POPs) that remain in the environment and accumulate in living organisms. A glaring example of POPs is the Endosulfan Tragedy: endosulfan was widely used as a pesticide on cashew plantations in Kasaragod district of Kerala leading to serious disabilities and eventual ban in 2011.[ 27 ] Exposure during critical developmental periods is particularly concerning. WHO and UNEP surveys (2000–2010) reported high levels of dioxins and furans in human milk samples from India, Europe and Africa.[ 28 ] In Lucknow, OCP levels were notably high in breast milk, especially among vegetarian women.[ 29 ] Elevated levels of PCBs and brominated flame retardants were found in breast milk from mothers living near municipal dumping sites in six locations across India.[ 30 ] High pesticide levels were also detected in bovine milk from Pune,[ 31 ] while in South India, pregnant women and their offspring tested positive for parabens, Bisphenol A (BPA) and triclosan.[ 32 ] In addition, Indian children showed higher urinary concentrations of several EDCs than Chinese children, particularly among those with obesity.[ 33 ]

Endocrine-disrupting chemicals (EDCs) are exogenous chemicals or their mixtures, that can interfere with any aspect of hormone action and consequently have adverse health effects.[ 1 2 3 4 ] EDCs can disrupt endocrine and metabolic function by interacting with various hormone receptors and/or altering their synthesis and degradation.[ 1 3 4 ] They can cause long-term adverse outcomes across multiple systems, including reproductive, cardiometabolic, musculoskeletal, neurodevelopmental and immune systems, as well as increasing the risk of various cancers.[ 1 4 ] EDC exposure in vulnerable populations such as pregnant women, children, and adolescents leading to early life exposure is especially concerning. EDCs which include more than 85,000 natural or synthetic chemicals and/or their breakdown products are widespread, commonly found in the lived environment, and impact nearly everyone.[ 4 5 ] The term EDCs was first coined in 1991 at the Wingspread Conference.[ 1 ] In 2009, the Endocrine Society (ES) published its first Scientific Statement, calling for increased public awareness and policy action regarding EDCs.[ 6 ] This was updated in 2015[ 7 ] and reaffirmed by a recent position statement in 2025.[ 3 ] Recognizing the global threat posed by EDCs, the United Nations Environment Programme (UNEP) and the World Health Organization (WHO) called for the development of an international strategy to address this growing concern in 2012.[ 4 8 ] The ES of India (ESI) recognizes an urgent need to address the challenge of EDCs and advocates the promotion of India-specific research, development of educational resources, public awareness initiatives, and active engagement with policymakers to strengthen regulatory frameworks. With the goal of enhancing understanding of the health impact of EDCs, promoting safer practices and protecting future generations, the ESI National White Paper on EDCs offers a comprehensive overview of endocrine disruptors and provides strategic direction for action.