The review, led by an international team synthesizing studies from Science Direct and Google Scholar using the keywords plastic, microplastic, and additives, examines how these synthetic materials fragment and release their chemical cargo into some of the world’s most productive ecosystems. The authors frame plastic pollution not merely as a visible nuisance but as a vector for endocrine disruptors and mutagens capable of affecting future generations, making systematic scientific approaches essential for remediation and sustainable environmental management.

The scale of the problem is staggering. Roughly 60 percent of all plastics ever produced have been discarded, largely because of limited recyclability and inadequate waste management. Global plastic production has grown explosively since the mid-twentieth century, and the very properties that make thermoplastics and thermosets so useful, their malleability and persistence, also make them permanent contaminants. Once in the environment, plastics are broken down by photo-oxidation, physical abrasion, climatic changes, chemical reactions, and biological interactions, generating microplastics smaller than 0.5 millimeters while simultaneously releasing covalently bonded additives into surrounding water and sediment.

Microplastics pose a dual threat, according to the review. First, they act as vectors, carrying hazardous chemicals attached to their surfaces. Second, they are intrinsic pollution sources in their own right, leaching additives as they weather. The synergistic toxicity is amplified when microplastics interact with pesticides, pharmaceuticals, and trace metals in the same environment. Because many additives are small molecules with low boiling points, they migrate rapidly between environmental phases through chemisorption and physisorption mechanisms, and their release kinetics depend on polymer character, additive content, environmental conditions, and the size and shape of the particles themselves.

The consequences ripple through food webs. The migration of microplastic particles and their additives across trophic levels has been linked to genetic disorders, prenatal effects, and impaired cognitive functions in exposed organisms. Advanced research methodologies, including particle diffusion and aqueous boundary layer diffusion models, are now being deployed to understand how additives detach and travel, though the authors caution that most laboratory findings need to be validated under real-world environmental conditions, where changing contexts complicate predictions.

Estuaries are particularly vulnerable because of their position at the interface of freshwater and marine systems. Riverine inflow, mangrove debris, coastal influx, urban runoff, and dense human activity make these environments highly productive and depositional. Since the majority of the world’s population lives near coasts, estuarine contamination translates directly into human exposure risk. The review documents an extensive catalog of plastic chemicals in coastal systems worldwide, including benzotriazole UV stabilizers in marine products, phthalates and polybrominated diphenyl ethers in the Yangtze estuary, phthalate esters in the Pearl River Delta, tris (butoxy ethyl) phosphate in Nanyang Lake estuary, organophosphate esters in the benthic compartments of the Loire estuary, and phenolic compounds in the Bay of Bengal coastal waters.

Sediments emerge as the critical sink in this pollution story. They serve as the ultimate repository for organic carbon, inorganic particles, and synthetic materials, facilitating the integration of organic matter into the geological carbon cycle. When physical, chemical, and biological processes combine, substantial quantities of external synthetic materials sink through the water column and are retained in bed sediment, where they acquire distinctive biochemical compositions. The concentrations recorded vary enormously across the globe, from 0.04 to 0.99 microplastics per cubic meter in the Tamar River in England to 5,720 plus or minus 2,580 items per kilogram in the Kallar Kahar wetland in Pakistan, with intermediate values such as 851 plus or minus 177 items per kilogram in Pearl River Estuary sediments and 1,260 particles per kilogram in the Azhikkal estuary of the Arabian Sea.

The biological toll in estuarine habitats is already measurable. Fragmented microplastics and their additives interfere with water availability, sediment characteristics, benthos survival rates, and fish health in intertidal ecosystems. The review highlights unresolved questions about sinking capacity in aquaculture systems, changes in biotic metabolism, pore water dynamics, habitat destruction, productivity reduction, and mutation, all of which require more elaborate investigation. In low-lying aquatic systems, contamination is modulated by tidal effects, salinity gradients, acidic content, chlorophyll concentrations, and biotic interactions, factors that vary seasonally and geographically.

The authors propose that the combined signature of microplastics and plastic-derived chemicals could function as an ecological contamination marker for estuarine systems, a diagnostic tool that integrates both the physical particles and their chemical payloads. This dual approach could allow managers to detect pollution earlier and more comprehensively than particle counting alone, since additives persist and accumulate in water, sediment, and biotic material even as plastics fragment into ever smaller, harder-to-detect pieces.

Looking forward, the review calls for long-term environmental monitoring of the interaction between microplastics and plastic additives, standardized conceptual frameworks for assessing individual parametric effects, and better protocols for evaluating nano-plastic particles. Climatic variations, interactive reactions, and the degradation mechanisms of macro-plastics remain major topics of discussion in the global scientific community. Ultimately, the authors argue that effective policy implementation and new legal regulations are essential for sustainable development practices, because without governance changes, the chemical legacy of decades of plastic production will continue to settle into the sediments of the world’s estuaries, where it may persist for generations.

Subject of Research: Plastic-derived chemical additives and microplastic contamination in estuarine ecosystems

Article Title: Review on plastic-derived chemical pollutants in estuarine ecosystems: Assessing the scale of microplastic contamination

Article References: Nisari, A. R., & Renjith, K. R. (2026). Review on plastic-derived chemical pollutants in estuarine ecosystems: Assessing the scale of microplastic contamination. Estuarine Management and Technologies, 3, 113-121. https://doi.org/10.3897/emt.3.183953

Image Credits: AI Generated

DOI: 10.3897/emt.3.183953

Keywords: microplastics, plastic additives, estuaries, endocrine disruptors, sediment contamination, phthalates, flame retardants, marine pollution, food web transfer, environmental monitoring, Review, plastic-derived

Phthalates are a class of synthetic chemicals used to make rigid plastics flexible and durable, and they are found in an enormous range of everyday products, including food packaging, medical devices, vinyl flooring, and children’s toys. Over the past two decades, a growing body of epidemiological and laboratory evidence has linked phthalate exposure to an increased risk of premature birth, infertility, and other health concerns, prompting manufacturers to seek alternatives. DINCH emerged as one of the most prominent of these substitutes and has been marketed as a plasticizer with a more favorable safety profile. The new study suggests, however, that the assumption of safety may deserve closer scrutiny, because higher maternal DINCH levels were consistently associated with reduced newborn size, a marker that clinicians consider an important early indicator of lifelong health risk.

The scale of the association was quantified precisely by the research team. Every tenfold increase in exposure to DINCH corresponded to a 27-gram reduction in newborn birth weight. While 27 grams may appear modest in isolation, the researchers emphasize that even small differences in birth size can matter significantly at the population level. Fetal growth problems can raise the risk of heart disease, learning difficulties, obesity, and other conditions that echo into adolescence and adulthood, a phenomenon known as the developmental origins of health and disease. Lead author Leonardo Trasande, MD, MPP, the Jim G. Hendrick, MD, Professor of Pediatrics at NYU Grossman School of Medicine, noted that a chemical promoted as a safer replacement for phthalates and other plasticizers may affect how babies grow in the womb, and that even small shifts in birth size can carry consequences across the life course.

The study drew its data from the Environmental Influences on Child Health Outcomes program, a National Institutes of Health initiative that tracks families’ health from pregnancy through childhood. One of the strengths of this cohort is its diversity: participants came from many different racial, ethnic, and economic backgrounds across the United States, making the results more representative of the nation than those of many earlier studies, which often relied on smaller or more homogeneous samples. Urine samples were analyzed for three DINCH breakdown products, the metabolites that the body produces as it processes and excretes the chemical. Some participants provided more than one sample, which allowed the researchers to track exposure across different trimesters of pregnancy, a methodological advance that distinguishes this work from prior analyses.

Indeed, the researchers report that this is the first study to measure DINCH at different times during pregnancy, and the timing of exposure proved to be an important variable. DINCH exposure during the third trimester was more strongly tied to lower birth weight for gestational age than exposure earlier in pregnancy, a pattern that aligns with the biology of late gestation, when fetal growth accelerates rapidly and nutrient and oxygen transfer through the placenta becomes especially critical. The analysis also accounted for other factors known to influence birth size, including the mother’s age, education, and number of previous pregnancies, strengthening the case that the observed associations are not simply artifacts of confounding.

The results revealed notable patterns beyond overall weight. Babies whose mothers had higher levels of DINCH in their urine were more likely to be classified as small for gestational age, a clinical designation applied when a newborn’s weight falls below the 10th percentile for babies born at the same stage of pregnancy. Sex-specific differences emerged as well: boys showed greater differences in birth length, while girls were more likely to be small for their gestational age. Between 50 percent and 70 percent of the pregnant women in the study had measurable levels of a DINCH by-product in their urine, indicating that exposure to this substitute plasticizer is widespread in the American population rather than confined to a narrow subset of consumers.

Mechanistically, laboratory studies in animals and human cells offer clues about how DINCH might influence fetal development. These studies suggest that when DINCH breaks down in the body, its by-products can interfere with hormones that guide fetal development and trigger inflammation that may affect how nutrients and oxygen reach the baby. Together, these effects may contribute to pregnancy complications such as reduced fetal growth, high blood pressure during pregnancy, and early labor. A small analysis of pregnant women undergoing fertility treatment has also linked higher DINCH exposure to an increased chance of preterm birth, although that particular finding was not observed in the current report, leaving the question of preterm delivery open for further investigation.

The study also raised concerns about disparities in exposure and health impacts. Mothers who were Hispanic or who had lower levels of education were more likely to have children affected by DINCH, according to the authors, a pattern consistent with broader evidence that chemical exposures are not evenly distributed across the population and that communities already facing structural disadvantages may bear a disproportionate share of environmental health burdens. Trasande argued that these results underscore the need for stronger oversight of chemicals used in food packaging and other household products, requiring that they be tested before they are introduced to the market rather than after they are connected to health concerns. He pointed to the global plastics treaty now under negotiation at the United Nations as a key opportunity to establish such policies.

The researchers were careful to note an important limitation: the analysis is observational and cannot prove that DINCH exposure directly causes smaller birth size. Observational studies of this kind identify associations within large populations, and while the team controlled for many known determinants of birth size, residual confounding remains a possibility in any study of environmental exposures. Nonetheless, the convergence of human epidemiological data with laboratory evidence of endocrine interference and inflammatory effects strengthens the biological plausibility of the findings and adds DINCH to the growing list of plastic additives whose health profiles warrant reexamination.

Looking ahead, the study authors plan to examine other plasticizers currently being used as alternatives to phthalates and to study in more detail how DINCH may slow fetal growth. Senior author Taylor Etzel, PhD, of Johns Hopkins University led the work alongside Trasande, with contributions from researchers at NYU Langone, RTI International, Northeastern University, Rutgers University, Johns Hopkins, the University of Colorado Anschutz, Emory University, Columbia University, the University of Michigan, Penn State University, the University of California, San Francisco, Dartmouth College, Wayne State University, the University of Washington, the University of Illinois at Urbana Champaign, and the University of North Carolina at Chapel Hill. Funding was provided by the National Institutes of Health’s Environmental Influences on Child Health Outcomes program. In the meantime, Trasande suggested that families concerned about plastic additives can talk with their healthcare providers and consider practical steps that may reduce exposure, while the scientific and policy communities continue to evaluate whether the replacements for yesterday’s problem chemicals are solving the problem or simply relocating it.

Subject of Research: Effects of prenatal exposure to the plasticizer DINCH on fetal growth and birth outcomes

Article Title: Exposure to ‘safer’ plastic additive during pregnancy linked to smaller birth size

Article References: Exposure to ‘safer’ plastic additive during pregnancy linked to smaller birth size. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: DINCH, phthalates, plasticizers, prenatal exposure, birth weight, fetal growth, endocrine disruption, ECHO program, Environment International, NYU Langone, plastics treaty, environmental health

Phthalate esters are among the most widely produced plasticizer families in the world. They are added to polyvinyl chloride and countless consumer goods—food packaging, cosmetics, personal care products, medical devices, floor coverings, and nail polish—to make rigid plastics flexible and durable. Because phthalates are not chemically bound to the polymer matrix, they leach, migrate, and evaporate into food, dust, water, and air. Decades of toxicological work have classified several of them as endocrine-disrupting chemicals, capable of interfering with hormone signaling, reproductive development, and metabolic regulation. Regulatory agencies in the European Union and the United States have restricted a series of the most concerning compounds, including DEHP, DBP, BBP, and DiBP, particularly in toys and childcare articles, prompting industry to pivot toward alternative plasticizers such as terephthalates and adipates.

That pivot is precisely what makes the new data so striking. The most prevalent plasticizer detected across all four maternal and fetal matrices was DEHT, or di(2-ethylhexyl) terephthalate, a structural isomer of the restricted DEHP that is widely promoted as a safer replacement. DEHT recorded the highest geometric mean concentration in urine at 403.7 micrograms per kilogram, followed by placenta at 318.6 micrograms per kilogram, blood at 304.5 micrograms per kilogram, and amniotic fluid at 275.0 micrograms per kilogram. In other words, a chemical introduced to reduce risk is now the dominant plasticizer burden in pregnant women, and it is not staying in the mother. Its presence in amniotic fluid—the liquid bathing the fetus—demonstrates that substitution has not eliminated fetal exposure, it has changed the chemical profile of that exposure.

Among the classical phthalates, the short-chain compounds told their own story. Diisobutyl phthalate (DiBP) showed the highest concentrations in placental tissue, at 195.8 micrograms per kilogram, and in urine, at 226.0 micrograms per kilogram, indicating both substantial body burden and efficient renal clearance. Dimethyl phthalate (DMP) and diethyl phthalate (DEP), lower-molecular-weight esters commonly found in cosmetics, fragrances, and personal care formulations, were mainly detected in amniotic fluid, at 128.2 and 64.8 micrograms per kilogram respectively. The distribution pattern is chemically meaningful: smaller, more water-soluble molecules tend to partition differently across biological membranes than bulkier, lipophilic ones, and their accumulation in amniotic fluid suggests they can traverse the placental barrier and equilibrate within the fetal compartment.

The placenta is often described as a protective shield, but pharmacologically it behaves more like a semi-permeable membrane governed by physicochemical rules. Molecular size, lipophilicity, ionization state, and protein binding all determine whether a compound crosses by passive diffusion, facilitated transport, or is retained. Plasticizers, being moderately lipophilic and of low molecular weight, are well positioned to cross. The Tunisian team’s measurements confirm this: substantial amounts of both phthalate and non-phthalate plasticizers were found on the fetal side of the barrier. Although the renal system contributes significantly to elimination—reflected in the high urinary concentrations of DEHT and DiBP—excretion is evidently not fast enough to prevent transplacental transfer during pregnancy.

The health implications of prenatal exposure are the subject of a growing and sobering literature. Phthalates have been linked in epidemiological and experimental studies to altered reproductive development, preterm delivery, changes in fetal growth parameters, and disruption of placental function-related genes. Research on the placental methylome and transcriptome suggests that phthalate exposure during the first trimester can reprogram gene regulation at a critical developmental window. Experimental work has also documented oxidative damage and suppression of the Wnt/β-catenin signaling pathway in placental tissue following dibutyl phthalate exposure. For the non-phthalate alternatives, the toxicological record is thinner but increasingly concerning; recent in silico and in vitro studies have flagged diisobutyl adipate, one of the compounds detected in this cohort, for potential lipid metabolism-disrupting effects.

Exposure sources for pregnant women are pervasive and difficult to avoid. Phthalates migrate from PVC food packaging into fatty foods, leach from bottled beverages, and contaminate spices, herbs, and dairy products, as previous surveys of Tunisian and Mediterranean markets by some of the same research groups have documented. Cosmetics and personal care products contribute dermal exposure, with DEP in particular a common ingredient of fragranced formulations. Indoor dust carries plasticizers shed from floorings, wall coverings, and consumer goods, while medical devices can deliver direct doses to vulnerable patients. The Monastir cohort, drawn from middle-class households, underscores that this is not an exposure limited to industrial workers or heavily polluted environments—it is a background exposure affecting the general population of expectant mothers.

The study’s analytical approach deserves attention because measuring parent plasticizers in biological matrices is technically demanding. These compounds are rapidly metabolized in the body into monoester metabolites, which are the usual targets of human biomonitoring in urine. Detecting the parent compounds themselves in placenta, amniotic fluid, blood, and urine, at geometric means ranging from tens to hundreds of micrograms per kilogram, provides a snapshot of circulating chemical burden rather than merely of recent excretion. The multi-matrix design is what allows the exposure continuum to be reconstructed: chemicals present in maternal blood and urine, retained in placental tissue, and dissolved in amniotic fluid trace a pathway from external exposure to the fetal environment.

The authors argue that their findings support further evaluation of both phthalates and their substitutes, and the data give that call force. If DEHT, the flagship replacement, now dominates the exposure profile of pregnant women and penetrates the amniotic cavity, then regulatory success measured by the disappearance of restricted phthalates may mask a regrettable substitution problem, in which one hazardous chemical is swapped for another whose safety profile is unproven in humans. The researchers emphasize the need for improved exposure control, especially for vulnerable populations such as pregnant women and developing fetuses. For now, the study stands as a technical warning: the plastic chemistry of modern life does not stop at the placental barrier, and the burden of proof is shifting to the alternatives that industry hoped would close the chapter on phthalate risk.

Subject of Research: Occurrence and placental transfer of phthalate and non-phthalate plasticizers in maternal and fetal biological matrices

Article Title: Occurrence, distribution and potential sources of phthalate and non-phthalate plasticizers in maternal and fetal-related biological matrices

Article References: Occurrence, distribution and potential sources of phthalate and non-phthalate plasticizers in maternal and fetal-related biological matrices. (n.d.). https://doi.org/10.1007/s10653-026-03540-x

Image Credits: AI Generated

DOI: 10.1007/s10653-026-03540-x

Keywords: phthalates, plasticizers, DEHT, endocrine disruptors, prenatal exposure, placental transfer, amniotic fluid, human biomonitoring, GC-MS/MS, Tunisia, pregnancy, non-phthalate alternatives

The review focuses on three notorious families of additives. Bisphenol A, widely used in polycarbonate plastics and epoxy resins, is a well-documented endocrine disruptor linked to neurobehavioral effects and reproductive concerns. Phthalates, such as di-(2-ethylhexyl) phthalate and dibutyl phthalate, keep flexible plastics supple but have been associated with cardiovascular and metabolic harm through adipose tissue dysfunction. Brominated flame retardants, including polybrominated diphenyl ethers, hexabromocyclododecane, and tetrabromobisphenol A, resist fire but persist in the environment for decades, bioaccumulate in wildlife and humans, and have been targeted by international agreements such as the Stockholm Convention.

What makes these compounds especially troublesome is their behavior once released. Most possess high octanol-water partition coefficients, meaning they favor organic matter and fatty tissues over water. They sorb to sediments, concentrate in indoor dust, travel through food webs, and accumulate in fish — sometimes passing from parent to offspring. Detection methods such as gas chromatography-mass spectrometry and liquid chromatography-tandem mass spectrometry now routinely find them in rivers, harbor sediments, landfill leachate, and take-out food containers worldwide. The authors emphasize that risk assessment remains hampered by a lack of standardized protocols and ecotoxicological data for many newer additive alternatives.

Conventional remediation options each carry drawbacks. Chemical oxidation can be energy-intensive and incomplete. Direct photolysis is slow and selective. Thermal degradation risks generating toxic by-products. Microbial remediation, while attractive, often stalls when confronted with the recalcitrant, hydrophobic structures of brominated compounds. Advanced oxidation processes using Fenton chemistry or ozonation improve matters but typically demand continuous chemical inputs and careful pH control, complicating real-world deployment at treatment plants.

Photocatalysis offers a fundamentally different approach. When a semiconductor nanomaterial such as titanium dioxide absorbs photons with sufficient energy, electrons are excited from the valence band to the conduction band, leaving behind holes. These charge carriers migrate to the particle surface and react with water and dissolved oxygen to generate reactive oxygen species — hydroxyl radicals, superoxide anions, and hydrogen peroxide — that attack organic molecules with extraordinary oxidative power. Crucially, the only inputs are light and oxygen, and the target end products are carbon dioxide, water, and simple inorganic species, a process measured as total organic carbon mineralization.

The numbers reported in the review are striking. Titanium dioxide under ultraviolet light degraded more than 95 percent of bisphenol A within 180 minutes, with a pseudo-first-order rate constant of 0.031 per minute. Zinc oxide, active under visible light, achieved 85 percent removal in 240 minutes at a rate constant of 0.025 per minute. Combining the two into TiO2-ZnO composites pushed degradation efficiency to 96 percent, exploiting complementary band structures to separate charge carriers more effectively and suppress the recombination that limits pure catalysts.

Researchers have engineered an impressive arsenal of variations. Doping TiO2 with nitrogen, sulfur, or transition metals extends light absorption into the visible spectrum. Coupling semiconductors with reduced graphene oxide or carbon nanotubes provides conductive pathways that shuttle electrons away before they recombine. Z-scheme and heterojunction architectures — such as Ag/Ag3PO4 bridged to graphitic carbon nitride, or Fe3O4-TiO2 magnetic composites — combine strong oxidation and reduction capability with easy recovery of the catalyst using magnets. For brominated flame retardants, some systems exploit reductive debromination first, stripping bromine atoms before oxidative mineralization, because partial degradation alone can sometimes yield daughter products more toxic than the parent compound.

Green synthesis is emerging as a parallel theme. The authors highlight nanomaterials fabricated using plant-derived reducing agents, including biosynthesized nickel ferrite coated with reduced graphene oxide and phytogenic zinc cobaltite spinel nanoarchitectures that degrade endocrine disruptors under solar irradiation. Such routes avoid the harsh chemicals and high energy demands of conventional sol-gel synthesis, improving the life-cycle profile of the catalysts themselves — a consideration increasingly scrutinized through life cycle assessment studies of solar-driven photocatalytic water treatment.

Significant hurdles remain before laboratory successes translate into riverside infrastructure. Long-term catalyst stability, fouling in real wastewaters rich in dissolved organic matter, and scalability of nanomaterial production all demand answers. Capital and operational expenditures for compound parabolic collector reactors and LED-driven systems must fall. More urgently, the toxicity of degradation by-products needs systematic evaluation, since a catalyst that merely fragments a molecule rather than mineralizing it may swap one hazard for another. The review also calls for standardized risk-assessment frameworks and stronger regulatory coordination under instruments such as REACH and guidance from the European Food Safety Authority.

Still, the trajectory is clear. As analytical chemistry reveals just how pervasive plastic additives have become — in human blood, indoor dust, and the deepest ocean sediments — photocatalysis stands out as a sunlight-powered, low-waste technology capable of destroying rather than merely relocating these contaminants. With continued innovation in visible-light-active materials, careful attention to by-product safety, and pilot-scale validation in real municipal water matrices, engineered nanomaterials may soon become a routine line of defense against the chemical shadow cast by the age of plastic.

Subject of Research: Photocatalytic degradation of hazardous plastic additives using engineered nanomaterials

Article Title: Occurrence, environmental risks, and photocatalytic removal strategies of hazardous plastic additives: current research and future perspectives

Article References: Rani, M., Agarwal, B., & Shanker, U. (2026). Occurrence, environmental risks, and photocatalytic removal strategies of hazardous plastic additives: current research and future perspectives. Environmental Science and Pollution Research. https://doi.org/10.1007/s11356-026-38299-2

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38299-2

Keywords: plastic additives, bisphenol A, phthalates, brominated flame retardants, photocatalysis, titanium dioxide, zinc oxide, engineered nanomaterials, endocrine disruptors, reactive oxygen species, water treatment, environmental pollution

The review, led by Suelen Goulart and colleagues at the Federal University of Santa Catarina in Brazil, followed the PRISMA protocol for systematic reviews, screening 255 articles from the CAPES Periodicals Portal and ultimately including 31 that met strict criteria: original peer-reviewed studies, published in English, using biopsy sampling on live marine mammals to assess environmental contaminants. Because the animals are sampled at sea without capture, restraint, or sedation, biopsies offer something necropsies of stranded animals cannot: a real-time snapshot of contamination in healthy, active populations. Stranded animals, the authors note, are often debilitated or decomposed, underrepresent robust populations, and introduce biases that impede continuous health monitoring. Biopsies also allow effective metabolic quenching, making the samples reliable for metabolomics, and they can be paired with ecological data such as satellite telemetry and stable isotope analysis to build a fuller picture of exposure.

The tissue most often sampled is blubber, which appeared in roughly 74 percent of the studies, followed by skin at about 39 percent. The preference is no accident. Blubber is the energy store and thermal regulator of marine mammals, and it preferentially accumulates lipophilic contaminants, making it the ideal matrix for persistent organic pollutants. Skin, by contrast, is rich in keratin and other proteins with sulfhydryl groups, and it turns out to be the superior target for non-lipophilic inorganic contaminants such as mercury, which bind proteins rather than fats. The choice of tissue, in other words, is dictated by the chemistry of the pollutant being hunted.

Persistent organic pollutants dominated the field: 23 of the 31 studies, or 74.19 percent, focused on them, with polychlorinated biphenyls (PCBs) and dichlorodiphenyltrichloroethanes (DDTs) the most frequently quantified, followed by hexachlorobenzene, polybrominated diphenyl ethers, and chlordanes. Both PCBs and DDTs were banned in the 1970s and 1980s, yet they persist in marine food webs with alarming intensity. In false killer whales from Hawaii, 84 percent of individuals exceeded safety thresholds for total PCBs, with average concentrations reaching 30,000 nanograms per gram lipid weight. In the Gulf of Mexico, bottlenose dolphins showed PCB levels as high as 82,500 nanograms per gram lipid weight and DDTs up to 164,000. Adriatic dolphins carried a DDT metabolite comprising 90 percent of their total DDT burden. The Mediterranean Sea emerged as the single most studied region, accounting for 39.1 percent of the POPs papers, a reflection of its history of industrial contamination, restricted water circulation, and dense coastal urbanization.

The review also reveals a striking biological pattern: in 82.6 percent of the POPs studies, males accumulated higher contaminant loads than females. The explanation lies in maternal offloading. During gestation, pollutants such as PCBs, DDTs, and flame retardants cross the placenta into fetal tissue, and after birth, calves receive further doses through milk, often reaching concentrations that exceed maternal levels. Females effectively shed their toxic burdens with each reproductive cycle, while males have no such outlet. Juveniles, too, showed elevated contamination, with humpback whale calves in the Gulf of Maine reaching 12,000 nanograms per gram lipid weight of PCBs, suggesting that accumulation begins well before sexual maturity and that developing bodies are especially vulnerable.

Trophic position proved to be a powerful predictor of exposure. Apex predators carried 10 to 40 times higher concentrations than species feeding lower in the food web. Killer whales in the Canadian Arctic accumulated total POPs of 216,000 nanograms per gram lipid weight, and sperm whales in the Mediterranean reached 22,849 nanograms per gram of PCBs, while krill-feeding fin whales in the same basin carried only 572. The reason is biomagnification: killer whales prey on contaminated seals and cetaceans, sperm whales consume lipid-rich squid, and each step up the chain concentrates the chemicals further. Filter-feeding humpback whales showed moderate contamination except in pollution hotspots such as the Mediterranean, where they reached 10,477 nanograms per gram of DDTs.

The health consequences documented in the review are severe. Concentrations above 9,000 nanograms per gram lipid weight are considered a critical threshold for immunosuppression in aquatic mammals, and 65.2 percent of the POPs studies reported levels exceeding known toxicity thresholds. Populations of long-finned pilot whales and Cuvier’s beaked whales in the Mediterranean, bottlenose dolphins in the Atlantic, Gulf of Mexico, and Indian Ocean, and false killer whales in Hawaii all surpassed the 17,000 nanogram threshold associated with reproductive impairment. At the molecular level, more than half of the POPs studies documented disrupted detoxification, endocrine, and neurological systems. In one innovative study, researchers cultured skin fibroblasts from biopsy samples of Norwegian killer whales and exposed them to a mixture of the ten most abundant pollutants at environmentally relevant concentrations, observing significant downregulation of the detoxification gene CYP1A1 and deregulation of lipid metabolism pathways. In Florida dolphins, high DDT levels were associated with reduced testosterone in males and suppressed cortisol in females, impairing reproduction and stress responses.

Inorganic contaminants received far less attention, with only eight studies, yet the findings were no less concerning. Mercury appeared in six of the eight papers, and the Mediterranean pilot whales carried the highest concentrations recorded, at 33,028 nanograms per gram. Resident bottlenose dolphins in Ecuador’s Gulf of Guayaquil all exceeded immunotoxic mercury thresholds. In Australia, stranded Burrunan dolphins from industrialized regions carried blubber mercury levels nearly three times higher than live individuals from less impacted waters, with hepatic concentrations reaching 840,000 nanograms per gram, evidence that long-term dietary accumulation eventually overwhelms the body’s detoxification capacity. The review also highlights chromium-induced genotoxicity in fin whale skin cells, which showed dose-dependent cytotoxicity and DNA damage in laboratory exposures. Perhaps most striking is how little is known about emerging contaminants: only two studies examined phthalates, yet the plasticizer DEHP was detected in every sample from three cetacean species, reaching an extreme outlier of 4,697 nanograms per gram in a bottlenose dolphin near Madeira.

Geographically, the science is strikingly lopsided. North America accounted for 38.1 percent of the continental study occurrences and Europe 28.6 percent, while Africa and South America contributed just 7.1 percent each and Antarctica and Australia 4.8 percent each. Cetaceans, particularly bottlenose dolphins, which appeared in 11 of the 31 studies, dominated the literature, while pinnipeds were nearly absent, largely because sampling seals requires capture, restraint, or sedation, making the procedure far more stressful than a remote dart. The authors argue that this bias leaves regions facing intense plastic disposal and chemical contamination, including Brazil’s so-called Blue Amazon and the coasts of Uruguay and Argentina, dangerously under-monitored, a concern amplified by recent regulatory shifts such as Brazil’s new pesticide law, which replaces stringent danger criteria with more flexible risk assessments.

The review closes with a call to action that extends well beyond marine mammalogy. The authors urge standardization of collection, storage, and analytical protocols, noting that differences in chromatographic methods have produced discrepancies in PCB measurements of up to 40 percent between studies, and they propose global biobanks and certified reference materials modeled on the United States National Institute of Standards and Technology. They advocate integrating biopsies with multi-omics approaches, stable isotope analysis, satellite telemetry, and machine learning to map pollution hotspots and identify resilient populations. Framed within the One Health paradigm, the message is that the contaminants accumulating in whale blubber and dolphin skin are the same ones moving through the seafood that coastal and Arctic communities depend on. In a warming ocean where climate change may remobilize legacy pollutants, the small dart sample retrieved from the wake of a diving whale may prove to be one of the most important early-warning systems humanity has for the health of the sea, and of itself.

Subject of Research: Biopsy-based contaminant monitoring in free-ranging marine mammals as a measure of ocean health

Article Title: Assessing oceans’ health through biopsy sampling in free-ranging marine mammals: a systematic review (2014–2024)

Article References: Goulart, S., Galani, G., Lima, L. F. D., Piccinin, I. N. L., Valente, F. D. S., Nunes, A., Renault-Braga, E. P., & Maraschin, M. (2026). Assessing oceans’ health through biopsy sampling in free-ranging marine mammals: a systematic review (2014–2024). Environmental Science and Pollution Research, 33(28), 14055-14085. https://doi.org/10.1007/s11356-026-38163-3

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38163-3

Keywords: marine mammals, biopsy sampling, persistent organic pollutants, PCBs, DDTs, mercury, phthalates, cetaceans, ocean health, ecotoxicology, One Health, pollution monitoring

The chemicals in question are ubiquitous in modern life. Phthalates, which make plastics flexible, appear in food packaging, pharmaceuticals, dietary supplements, and personal care products. Phenols, including bisphenol A, bisphenol S, parabens, benzophenone-3, and triclosan, are found in everything from water bottles and receipt paper to cosmetics and antibacterial soaps. Because these substances are metabolized and excreted within hours to days, they are classified as non-persistent, yet the near-constant stream of exposure means biomonitoring studies routinely detect them in more than 90 percent of pregnant women in the United States. That combination of ubiquity and biological transience is precisely what makes studying their health effects so challenging.

The scientific rationale for concern is grounded in developmental biology. During embryonic and fetal development, organogenesis and tissue differentiation are exquisitely sensitive to hormonal signals, and endocrine-disrupting chemicals can interfere with the hormonal regulation of metabolism and energy balance. Phthalates, for example, can activate nuclear hormone receptors, particularly peroxisome proliferator-activated receptors, which govern adipogenesis, lipid metabolism, and energy storage. Activation of PPAR-gamma in the developing fetus may promote adipocyte differentiation and alter the production of adipokines such as leptin and adiponectin, potentially predisposing offspring to altered adiposity trajectories after birth. Some phthalates also exhibit anti-androgenic and weakly estrogenic activity, disrupting hormone signaling in utero, and previous research has linked prenatal phthalate exposure to altered steroid hormone profiles in humans as well as adverse metabolic outcomes in animal models.

To interrogate these questions at scale, the research team, led by Dorothy Nakiwala of the University of Colorado Anschutz Medical Campus, drew on 586 mother-child pairs from three ECHO cohort sites: the PROTECT Study in Puerto Rico, which recruited between 2010 and 2018; the Healthy Start Study in Colorado, recruited from 2009 to 2014; and the Illinois Kids Development Study, recruited from 2013 to 2018. All births occurred between 2009 and 2020. Maternal urine samples collected during pregnancy were shipped frozen to the Centers for Disease Control and Prevention, where concentrations of the phenol and phthalate metabolites were quantified using established laboratory methods. Children’s weight and height were measured primarily during clinic visits, and body mass index was converted to sex- and age-specific z-scores using the CDC 2000 growth charts, with assessments occurring between ages two and five at a mean age of 3.96 years.

The methodological architecture of the study is where it distinguishes itself from much of the prior literature. Rather than relying on a single statistical approach, the researchers triangulated their findings using covariate-adjusted single-pollutant linear regression alongside two complementary mixture methods: Bayesian Weighted Quantile Sum regression and Bayesian Kernel Machine Regression. The BWQS approach collapses multiple correlated exposures into a single weighted index under the assumption of a monotonic dose-response relationship, while BKMR uses a kernel function to flexibly model non-linear and interactive exposure-response patterns without imposing such assumptions. Models were adjusted for child sex and age, maternal age at delivery, pre-pregnancy BMI, parity, maternal race, maternal education, and study site, with covariate selection guided by a directed acyclic graph. Exposures were modeled both as continuous, log-transformed variables and as tertile categories to allow detection of threshold effects.

The headline result was null. When the entire 23-chemical mixture was evaluated, neither BWQS nor BKMR identified a statistically significant association with childhood BMI z-scores. The BWQS posterior mean estimate for a one-tertile increase in the mixture index was −0.06, with a credible interval spanning zero, and sex-stratified estimates of −0.24 for boys and 0.03 for girls were similarly inconclusive. The BKMR overall risk function, comparing joint increases in all exposures from the 25th to the 75th percentile against the 25th percentile, showed a non-significant, non-linear relationship with wide uncertainty intervals. There was also no evidence of interactions among pollutants, meaning the effect of any single chemical did not change appreciably as levels of the others rose.

The single-pollutant analyses, however, told a subtler story. When exposures were treated as continuous variables, no significant associations emerged. But when chemicals were categorized into tertiles, non-monotonic patterns appeared. Mono-benzyl phthalate, a metabolite of benzyl butyl phthalate, showed an inverse association: children whose mothers fell in the highest exposure tertile had BMI z-scores 0.33 lower than those in the lowest tertile, with a 95 percent confidence interval of −0.60 to −0.06. Mono-ethyl phthalate, a metabolite of diethyl phthalate, showed the opposite tendency, with the second tertile associated with a BMI z-score 0.27 higher than the first. Most strikingly, among boys only, mono-n-butyl phthalate in the second tertile was associated with a BMI z-score 0.45 higher than the first tertile, a non-monotonic pattern in which the third tertile showed no significant elevation. Among girls, the mono-ethyl phthalate pattern mirrored the pooled results but did not reach statistical significance.

The researchers are careful to contextualize these effect sizes. A shift of 0.1 to 0.2 standard deviations in BMI z-score may not be clinically meaningful for an individual child, but at the population level, even modest average shifts can increase the proportion of children classified as overweight or obese. Given that prenatal exposure to phenols and phthalates is essentially universal, small average effects could translate into a meaningful public health burden. The inverse association with mono-benzyl phthalate, meanwhile, aligns with at least one prior study, and one hypothesis holds that certain phthalates may impair growth by selectively disrupting muscle development rather than promoting fat accumulation, which could explain why phthalate exposure sometimes correlates with lower rather than higher BMI. The positive associations with mono-ethyl phthalate and mono-n-butyl phthalate, both low molecular weight phthalates found in pharmaceuticals, supplements, and personal care products, echo earlier reports linking prenatal mono-ethyl phthalate exposure to higher BMI trajectories from ages two to fourteen.

The consistency of the null mixture findings with previous research is itself informative. Studies using BKMR by Güil-Oumrait and colleagues, Berger and colleagues, and Ouidir and colleagues similarly reported no significant associations between prenatal phenol-phthalate mixtures and BMI z-scores at ages ten, five, and three, respectively, while cumulative-exposure studies using weighted quantile sum approaches by Svensson and Montazeri and their teams also found null results. One plausible explanation lies in exposure misclassification: because these chemicals clear the body so rapidly, spot urine samples may not adequately represent exposure across an entire pregnancy, and random misclassification typically biases results toward the null. The authors also note that BMI, their primary outcome, reflects overall body size without distinguishing fat from lean mass, potentially masking specific adiposity pathways, and that residual confounding by dietary behaviors associated with packaged and processed food consumption cannot be excluded.

Looking forward, the study’s authors argue that future research should prioritize repeated biomonitoring throughout pregnancy to better characterize exposures that fluctuate substantially over time, along with adequate statistical power to evaluate sex-specific effects, longitudinal follow-up, and direct measures of body composition. They also emphasize that postnatal and concurrent childhood exposures deserve attention, particularly given the short biological half-lives of these compounds. For now, the message is one of calibrated caution: the strongest evidence to date finds no cumulative effect of prenatal phenol-phthalate mixtures on early childhood BMI, but suggestive non-monotonic and sex-specific signals for individual chemicals underscore that the obesogen hypothesis, and the chemistry of everyday products that underpins it, remains a question science has not yet closed.

Subject of Research: Prenatal exposure to endocrine-disrupting phenols and phthalates and early childhood body mass index

Article Title: Prenatal exposure to nonpersistent endocrine disruptors and early childhood BMI: single pollutant and mixture analyses from the ECHO Program

Article References: Nakiwala, D., Perng, W., Barrett, E. S., Niu, Z., Alshawabkeh, A. N., Meeker, J. D., Dabelea, D., Starling, A. P., for the ECHO Cohort Consortium, Smith, P. B., Newby, L. K., Adair, L., Jacobson, L. P., Catellier, D., McGrath, M., Douglas, C., Duggal, P., Knapp, E., Kress, A., … Smith, L. M. (2026). Prenatal exposure to nonpersistent endocrine disruptors and early childhood BMI: single pollutant and mixture analyses from the ECHO Program. Pediatric Research. https://doi.org/10.1038/s41390-026-05466-7

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05466-7

Keywords: endocrine-disrupting chemicals, phthalates, phenols, prenatal exposure, childhood obesity, BMI z-score, ECHO Program, chemical mixtures, BKMR, BWQS, developmental programming, biomonitoring

Non-persistent chemicals are those that do not linger in the body for months or years, unlike legacy pollutants such as persistent organic pollutants or heavy metals. Instead, they are metabolized and excreted within minutes, hours, or days. This category includes an enormous range of compounds that pregnant women encounter daily: phthalates from food packaging and personal care products, parabens from cosmetics, benzophenones from sunscreens, bisphenols from plastics, antimicrobials from soaps, pesticide residues, flame retardant metabolites, polycyclic aromatic hydrocarbons from combustion sources, melamine derivatives, and aromatic amines from tobacco smoke and dyes. Because these chemicals clear the body so rapidly, urinary biomarkers essentially reflect very recent exposure. Whether a single measurement can stand in for exposure over an entire pregnancy depends entirely on how stable an individual’s concentrations remain over months of gestation.

The research team, led by Giehae Choi of Johns Hopkins University together with colleagues from institutions across the United States, tackled this question by analyzing three urine samples collected at different time points during pregnancy from 90 participants at three ECHO Cohort sites: New York, Illinois, and Puerto Rico. The scale of the chemical analysis was remarkable. The laboratory measured 154 analytes representing 163 chemicals across 12 chemical classes, using liquid chromatography-tandem mass spectrometry methods at the Wadsworth Center Human Health Exposure Analysis Resource laboratory. Of these, 84 analytes were detected in at least 20 percent of samples at a given site, providing sufficient data for variability analysis.

The central statistical tool was the intraclass correlation coefficient, or ICC, which quantifies how reliably a single measurement represents a person’s typical level across repeated measurements. ICCs range from 0 to 1, with values approaching 1 indicating that concentrations are highly stable within an individual over time, and values near 0 indicating that measurements are essentially unpredictable from one time point to the next. The team calculated ICCs for 58 analytes with detection frequencies above 60 percent, using log2-transformed concentrations standardized for urinary dilution by specific gravity. They also computed kappa statistics for 56 analytes with more moderate detection rates, assessing whether the mere presence or absence of a chemical above the detection limit was consistent across the three pregnancy samples.

The results were strikingly heterogeneous. ICCs ranged from −0.12 to 0.91, and the pattern of high versus low reliability differed substantially by cohort site for most chemicals. Only two analytes bucked this trend: benzophenone-1 and propyl paraben showed consistently high ICCs above 0.5 at all three sites, indicating stable exposure throughout pregnancy, while bisphenol F showed consistently low ICCs below 0.1 everywhere. Beyond these exceptions, the site-specific patterns were revealing. All parabens showed high reliability in Illinois but lower reliability in Puerto Rico and New York. Benzophenones were more stable in New York. Antimicrobials were more stable in Puerto Rico. Most phthalate and polycyclic aromatic hydrocarbon metabolites were moderately to highly reliable in Illinois but less so in Puerto Rico, while most aromatic amines showed the opposite pattern, with moderate to high reliability in New York but lower reliability in Illinois.

One of the study’s most technically insightful contributions was its analysis of how concentration levels relative to detection limits shape reliability estimates. The researchers hypothesized that measurement error exerts a proportionally greater influence when concentrations sit close to the limit of detection, obscuring the true rank-ordering of individuals. They therefore calculated the ratio of each analyte’s site-specific median concentration to its detection limit. Chemicals with median concentrations more than 50 times the detection limit tended to show greater stability across pregnancy, with notable exceptions among certain phthalate metabolites. This exception is itself informative: high concentrations paired with low ICCs suggest that exposure to the source products occurs sporadically but intensely, rather than continuously. Conversely, chemicals with median concentrations within tenfold of the detection limit generally showed lower ICCs, indicating that low-level measurements may reflect recent, sporadic exposures rather than a chronic exposure state. Benzophenone-8 provided a fascinating exception, maintaining moderate ICCs despite low concentrations, which the authors interpret as evidence of near-continuous low-level exposure.

The consistently high ICCs for benzophenone-1 deserve particular attention given the widespread use of benzophenones as ultraviolet filters in sunscreens, cosmetics, and personal care products, as well as their use as UV stabilizers in food packaging. Because these compounds do not bioaccumulate and have short biological half-lives, stable urinary concentrations can only mean that exposure itself is nearly continuous throughout pregnancy. Benzophenone-1 may appear more stable than benzophenone-3 partly because it is a major metabolite of benzophenone-3, integrating exposure from multiple sources, and because only a small fraction of benzophenone-3 is excreted unchanged in urine. The finding that benzophenone-3 was stable in Puerto Rico and New York but not Illinois may reflect seasonal differences in sunscreen use, a reminder that exposure context shapes biomarker reliability.

The site-specific differences also point to the influence of demographic, geographic, and behavioral factors on exposure chronicity. The New York site, where a majority of participants were classified in the high cotinine category suggesting substantial tobacco smoke exposure, showed moderate to high ICCs for aromatic amines such as aniline, which is found in tobacco smoke. Continuous exposure to tobacco through active or passive smoking could plausibly explain this stability. Similarly, moderate ICCs for melamine analogs like ammelide in New York may reflect ongoing exposure through contaminated foodstuffs and water. These observations suggest that individual, cultural, and structural factors, rather than pure physiology alone, determine whether a person’s chemical exposures remain constant or fluctuate across the months of gestation.

The practical consequences for environmental epidemiology are substantial. For the majority of non-persistent chemicals examined, a single pregnancy urine sample appears to represent exposure near the time of collection rather than exposure across the entire pregnancy. This matters enormously because different gestational windows carry different vulnerabilities: organogenesis in the first trimester, neurodevelopment throughout gestation, and fetal growth in later trimesters may each be sensitive to chemical exposures at distinct time points. If researchers link a single third-trimester measurement to a birth outcome and interpret it as reflecting first-trimester exposure, they risk substantial exposure misclassification, typically biasing estimated health associations toward the null. The authors note that simulation work suggests a chemical with an ICC below 0.2 would require more than 35 samples per person to keep this bias below 10 percent, an approach that is neither affordable nor practical for most studies.

Fortunately, the study outlines realistic alternatives. Researchers can incorporate validation sub-studies with repeated measurements and apply measurement error correction techniques such as regression calibration or simulation extrapolation. They can time urine collection to align with known critical windows of developmental susceptibility rather than defaulting to arbitrary collection schedules. They can collect multiple samples and pool them within each subject, which reduces assay costs while improving the representation of typical exposure. Or they can turn to alternative biospecimens such as hair, which integrates exposure over longer periods. The study also provides some of the first evidence on within-pregnancy stability for understudied chemical classes, including halogenated phenols such as the carcinogen pentachlorophenol, melamine and its analogs, and aromatic amines, filling critical gaps in the exposure science literature. As chemical production and consumer patterns evolve, the authors caution that reliability estimates from earlier studies may not transfer to current exposures, making ongoing characterization of biomarker variability an essential, not optional, component of rigorous environmental health research. For now, the message is clear: when it comes to non-persistent chemicals in pregnancy, one sample tells you where a woman was this week, not where she has been for nine months.

Subject of Research: Intra-individual variability of urinary non-persistent chemical biomarkers measured at three time points during pregnancy

Article Title: Intra-individual variability of urinary non-persistent chemical concentrations during pregnancy in the ECHO Cohort

Article References: Choi, G., Xun, X., Bennett, D. H., Meeker, J. D., Sathyanarayana, S., Schantz, S. L., Trasande, L., Watkins, D. J., Pellizzari, E., Li, W., Kannan, K., Woodruff, T. J., Buckley, J. P., & for the ECHO Cohort Consortium (2026). Intra-individual variability of urinary non-persistent chemical concentrations during pregnancy in the ECHO Cohort. Journal of Exposure Science & Environmental Epidemiology. https://doi.org/10.1038/s41370-026-00979-z

Image Credits: AI Generated

DOI: 10.1038/s41370-026-00979-z

Keywords: ECHO Cohort, pregnancy, non-persistent chemicals, urinary biomarkers, intraclass correlation, phthalates, parabens, benzophenones, exposure assessment, environmental epidemiology, aromatic amines, melamine

The review, led by Maria Camila Amaya and colleagues, followed the established Joanna Briggs Institute methodology and the PRISMA-ScR reporting guidelines, the gold standards for transparent evidence synthesis. The team searched multiple scientific databases for studies published between 2015 and 2025, applying predefined inclusion and exclusion criteria to every candidate paper. From an initial pool of 223 articles, only 27 survived the rigorous selection process, a winnowing that reflects both the novelty of the field and the uneven quality of the available evidence. The extracted data were synthesized in a standardized matrix, allowing the researchers to map where the evidence is strong, where it is thin, and where it is entirely absent.

Perhaps the most eye-catching finding concerns the sheer scale of particle release during ordinary bottle feeding. Previous work, prominently a study published in Nature Food, documented that polypropylene feeding bottles can shed millions of microplastic particles per liter during formula preparation, particularly when hot water is used to sterilize and mix the contents. Polypropylene is the workhorse plastic of baby bottles, prized for its durability and heat resistance, but those same properties do not prevent mechanical and thermal stress from liberating microscopic fragments directly into the liquid an infant drinks. For a baby consuming several bottles a day, the review notes, this can translate into exposure to high daily particle levels from a single, routine source.

The chemical side of the contamination story is equally concerning. The studies included in the review identified bisphenols, phthalates, and other endocrine-disrupting chemicals in infant formula, baby food, and their packaging materials. These compounds are not exotic contaminants; they are integral components or additives of the plastics that surround our food. Bisphenol A, even where restricted, has been partly replaced by structural cousins that may migrate from polyester-phenol coatings and multilayer plastic pouches. Phthalate esters have been quantified in powdered formula from multiple countries, and organophosphate flame retardants have been detected in baby foods, with infants showing notably high exposure linked to plastic baby products.

What makes early-life exposure to these chemicals so consequential is the biology of the developing endocrine system. Endocrine-disrupting chemicals can interfere with thyroid hormones, oestrogenic signaling, and metabolic regulation, and decades of toxicological research have established that such interference can produce effects at very low doses, sometimes following non-monotonic dose-response curves in which lower exposures are not necessarily safer. The Endocrine Society’s scientific statements have repeatedly warned that critical developmental windows, including gestation and infancy, are periods when hormonal disruption can reprogram tissues with consequences that may not become apparent for years. The review’s authors emphasize that infants, with their higher relative food intake per body weight and immature detoxification systems, sit squarely within these vulnerable windows.

The evidence on health effects, while still limited, points in a coherent direction. Studies reviewed by the team reported alterations in the intestinal microbiota of infants exposed to microplastics via baby bottles, including changes in short-chain fatty acid profiles, which are key metabolic messengers produced by gut bacteria. Other work documented shifts in immune-related biomarkers and responses; one longitudinal cohort linked plasticiser exposure to measurable changes in infant immune parameters, and separate research associated phthalate exposure with altered gut microbiota composition and modified IgM vaccine responses in human newborns. Experimental studies in rodents have shown developmental and reproductive toxicity from polystyrene microplastics, and lactational exposure at infant-equivalent doses induced transgenerational reproductive toxicity in female mice, findings that, while not directly transferable to humans, underscore the biological plausibility of harm.

The contamination pathway begins even before birth. The review highlights evidence of prenatal exposure, building on landmark studies that detected microplastics in human placental tissue and in maternal and foetal samples, as well as microplastics identified in human breast milk. This means that the bottle and the formula are not the first exposure an infant encounters; they are an additional layer on top of a body burden that may already exist at delivery. Human biomonitoring studies have found microplastics in stool samples, lung tissue, and blood, confirming that these particles circulate through the body rather than passing through inertly. In vitro work adds a mechanistic dimension: polystyrene microplastics have been shown to compromise intestinal barrier function and interfere with protein digestion, and polypropylene particles can affect the digestion of cow’s milk proteins, the very proteins that form the nutritional backbone of standard formula.

Complicating the scientific picture is the difficulty of measuring contamination accurately. One study included in the review raised the possibility that plastic additives can generate false positive errors in microplastic detection within infant feeding bottles, a reminder that analytical methods in this young field are still being refined. Detection limits, particle identification techniques, and the distinction between micro- and nanoplastics all vary across studies, which helps explain why the authors repeatedly characterize the evidence base as limited. Most of the health findings derive from experimental, animal, or observational studies rather than from the longitudinal human cohorts that would be needed to establish definitive cause-and-effect relationships in infants.

That evidentiary gap is precisely what the review’s authors identify as both a problem and a call to action. The absence of strict regulations specifically governing microplastics and endocrine disruptors in infant formula and feeding equipment, combined with the scarcity of long-term studies tracking exposed children over time, reinforces what they describe as an urgent need to advance public policies controlling these agents and to promote health education that helps families reduce exposure. Regulatory frameworks for food contact materials were largely built before the era of microplastic science, and they typically assess chemicals one at a time rather than the complex mixtures that migrate from real-world packaging.

For parents, the review does not prescribe panic, but it does suggest that precaution is reasonable while the science matures. Practical steps highlighted in the broader literature include minimizing the heating of plastic feeding bottles, considering alternative materials where feasible, and following preparation guidelines that reduce particle shedding. The larger burden, the authors argue, lies with manufacturers and regulators: if millions of particles per liter can be released during ordinary formula preparation, and if endocrine-active chemicals are consistently detected in the products and packaging designed for the most vulnerable consumers, then the current regulatory silence on these contaminants in infant nutrition is increasingly difficult to justify. As microplastic research moves from environmental oceans into pediatric wards, this scoping review makes clear that the question is no longer whether infants are exposed, but how much, with what consequences, and what society is prepared to do about it.

Subject of Research: Microplastic and endocrine-disrupting chemical contamination of infant formula and its potential early-life health effects

Article Title: Microplastic and endocrine disruptor contamination in infant formula and early health effects: scoping review

Article References: Amaya, M. C., Rodriguez, S. D. B., Burgos, J. S., & Rincon, E. H. H. (2026). Microplastic and endocrine disruptor contamination in infant formula and early health effects: scoping review. Environmental Science and Pollution Research, 33(30), 15285-15297. https://doi.org/10.1007/s11356-026-38153-5

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38153-5

Keywords: microplastics, infant formula, endocrine disruptors, baby bottles, plastic pollution, environmental health, pediatrics, gut microbiota, bisphenols, phthalates, child development, public health

Xenoestrogens earn their name from their structural resemblance to endogenous estrogens, the natural hormones that guide far more than reproduction. In the brain, estrogen signaling shapes neuronal differentiation, synaptic plasticity, neurotransmitter release, and the organization of sexually dimorphic circuits. Because xenoestrogens can bind estrogen receptors and hijack these pathways, they can mimic, amplify, or scramble hormonal instructions at concentrations far below those traditionally used in toxicological testing. The review emphasizes that these compounds frequently display non-monotonic dose-response curves, meaning that low doses can produce effects that are different, or even opposite, to those seen at high doses. That property upends a foundational assumption of classical toxicology, which has long held that the dose makes the poison.

The chemicals in question are everywhere. Bisphenol A, or BPA, leaches from plastic containers, food-can linings, and thermal receipts. Phthalates, added to plastics to make them flexible and durable, shed from personal care products, building materials, and countless household items. Polychlorinated biphenyls, or PCBs, were banned decades ago yet persist in soil, water, and animal tissue, bioaccumulating as they move up the food chain. Natural xenoestrogens such as phytoestrogens, found in certain plants, add a further layer of complexity. The result, the authors note, is chronic, low-dose, real-world exposure to a shifting cocktail of compounds whose combined effects remain poorly understood.

At the molecular level, the review describes several converging mechanisms of harm. BPA and certain PCBs bind estrogen receptors ERα and ERβ, triggering both genomic and rapid non-genomic signaling through pathways such as MAPK and PI3K/AKT, which govern cell proliferation, apoptosis, and differentiation. Xenoestrogens also disrupt the synthesis, transport, and metabolism of endogenous hormones by interfering with the hypothalamic-pituitary-gonadal axis, tilting the hormonal milieu that the developing brain depends on. Beyond receptor binding, these compounds perturb calcium signaling and glutamatergic neurotransmission by modulating NMDA receptor expression, a shift that can push neurons toward excitotoxicity and impair the precise wiring of synaptic connections.

Perhaps the most unsettling mechanism is epigenetic. Xenoestrogen exposure can induce aberrant DNA methylation and histone modifications, chemically rewriting the instructions that govern gene expression without changing the underlying DNA sequence. Among the genes affected are BDNF, SHANK3, and RELN, all of which are central to synaptic function and have been implicated in neurodevelopmental disorders such as autism spectrum disorder and attention-deficit/hyperactivity disorder. The downstream consequences include defects in synaptic pruning, neuronal migration, and myelination, the very processes that sculpt a mature, functional brain. Because epigenetic marks can be inherited, the review raises the possibility that today’s exposures may predispose future generations to neurodevelopmental vulnerability, a transgenerational shadow that conventional risk assessments have barely begun to address.

The behavioral evidence spans the laboratory and the wild. In rodent models, perinatal exposure to BPA, PCBs, and the synthetic estrogen diethylstilbestrol disrupts mating behavior by deranging the hypothalamic-pituitary-gonadal axis and altering estrogen and testosterone levels. Male rodents exposed to BPA early in life show reduced mounting and intromission frequencies, while females display altered estrous cyclicity and diminished lordosis responses. The sexually dimorphic nucleus of the preoptic area, normally larger in males, shrinks following early-life exposure to estrogenic disruptors, accompanied by disturbances in dopamine and oxytocin signaling that underpin sexual and affiliative behavior. In aquatic species, estrogenic pollutants have feminized male fish and amphibians, collapsing courtship behavior and reproductive success, with one landmark study documenting the collapse of an entire fish population after exposure to a synthetic estrogen.

Cognitive and emotional effects are equally well documented. The review links xenoestrogen exposure to impairments in learning, memory, and executive function, with implications for academic and professional performance, and to heightened anxiety, depression, and mood dysregulation, likely reflecting disruption of the limbic system. Social behavior is also affected, with altered social recognition, interaction, and communication observed across studies. Critically, many of these effects are sex-specific. Estrogen receptor subtypes are distributed differently in male and female brains, particularly in the hypothalamus, hippocampus, and amygdala, and male neurodevelopment depends heavily on the aromatization of testosterone into estradiol, creating distinct points of vulnerability. Prenatal BPA exposure, for example, has been associated with hypomethylation of the estrogen receptor alpha gene in the prefrontal cortex of female rodents but not males, correlating with increased anxiety-like behavior in females. The authors call for sex-stratified analyses to become standard practice in this field.

Timing magnifies the danger. The developing brain passes through tightly choreographed windows, spanning prenatal life, infancy, early childhood, and adolescence, when hormonal signals orchestrate the construction of neural circuits. Exposure during these periods can permanently alter brain structure, neuronal connectivity, and neurotransmitter systems, and the review links prenatal and early-childhood exposures to neurodevelopmental disorders, cognitive deficits, and behavioral abnormalities that persist into adulthood. Fetuses and infants are especially susceptible because their detoxification systems are immature and their brains are maximally plastic, while adolescents face risks during the extensive cortical reorganization of that stage. Regulatory frameworks, the authors argue, have lagged badly behind the science. Agencies such as the United States Food and Drug Administration and Environmental Protection Agency have restricted some compounds, and the European Union and World Health Organization have taken steps of their own, but critics contend these measures are insufficient. Most regulations still test chemicals one at a time and at high doses, missing the low-dose and mixture effects that define real-world exposure, and industry-conducted safety assessments raise conflicts of interest. The pattern of regrettable substitution is a case in point: when BPA was phased out, structurally similar analogs such as BPS and BPF moved in, potentially carrying comparable endocrine-disrupting activity. Legacy pollutants like DDT and PCBs continue to circulate decades after their bans.

What can be done? The review outlines a prevention agenda that spans individual action and structural reform. Reducing exposure means choosing products free of known xenoestrogens, improving manufacturing practices, and strengthening waste management. Public education can empower families, clinicians, and policymakers to make informed choices, while targeted interventions, including dietary modifications and environmental remediation, may help protect the most vulnerable. On the research frontier, the authors identify priorities that include characterizing emerging xenoestrogens, deploying sensitive tools such as neuroimaging and epigenetic profiling, testing whether pharmacological or nutritional therapies can mitigate harm, and untangling the synergistic effects of chemical mixtures. They also flag persistent methodological hurdles: non-monotonic dose responses that defy standard modeling, species differences that complicate extrapolation to humans, and the difficulty of sustaining longitudinal studies long enough to capture chronic and transgenerational outcomes. The bottom line, the authors conclude, is that safeguarding the neurological health of current and future generations demands a coordinated, precautionary response, one that combines rigorous independent research, evidence-based policymaking, international collaboration, and honest public engagement with the invisible chemical landscape that now surrounds every developing brain.

Subject of Research: Neurobehavioral and developmental toxicity caused by xenoestrogen endocrine-disrupting chemicals

Article Title: An overview of neurobehavioral and developmental toxicity induced by xenoestrogens

Article References: Shaw, R., Kamath, A. S., & Chaube, R. (2025). An overview of neurobehavioral and developmental toxicity induced by xenoestrogens. Discover Toxicology, 2(1), Article 10. https://doi.org/10.1007/s44339-025-00025-x

Image Credits: AI Generated

DOI: 10.1007/s44339-025-00025-x

Keywords: xenoestrogens, endocrine-disrupting chemicals, bisphenol A, phthalates, PCBs, estrogen receptors, neurodevelopment, epigenetics, developmental toxicity, neurobehavioral effects, brain development, public health

The research, led by Jagadeesh Puvvula of the University of Pennsylvania’s Perelman School of Medicine together with Aimin Chen and collaborators at Brown University, the University of Kentucky, the University of Arkansas for Medical Sciences, the University of Cincinnati, and the U.S. Centers for Disease Control and Prevention, enrolled 75 pregnant individuals who gave birth at the University of Cincinnati Medical Center between August 2014 and September 2017. All participants carried singleton pregnancies, were between 18 and 45 years of age, and were free of major conditions such as diabetes, thyroid disorders, cardiovascular or renal disease, and cancers affecting pregnancy. The cohort was demographically diverse: roughly half of the participants identified as non-Hispanic Black, the median age at delivery was 29 years, and 17 percent reported smoking tobacco during pregnancy. All births were full-term, ranging from 37 to 41 weeks of gestation.

At the delivery visit, the researchers collected 30 milliliters of maternal urine, 10 milliliters of cord blood, and placental tissue from both the maternal and fetal sides of the organ. The urine samples were analyzed for 37 biomarkers spanning four chemical classes: 12 phenols, 13 phthalates, 4 phthalate replacements, and 8 metabolites of polycyclic aromatic hydrocarbons, or PAHs—the compounds formed whenever organic material burns incompletely, whether in vehicle exhaust, grilled food, or tobacco smoke. Phenol and phthalate biomarkers were quantified at the CDC’s National Center for Environmental Health using high-performance liquid chromatography isotope dilution tandem mass spectrometry, while PAH metabolites were measured at NSF International’s Applied Research Center in Ann Arbor, Michigan. Because some chemicals, such as parabens and certain phthalate metabolites, can leach from medical products used during labor and delivery, the team excluded eight biomarkers potentially contaminated by the clinical setting, leaving 29 exposure markers for analysis.

The epigenetic readout relied on the Illumina Infinium HumanMethylation450K BeadChip, an array that interrogates hundreds of thousands of CpG sites—positions in the genome where a cytosine sits next to a guanine and where a methyl group can be attached without altering the underlying DNA sequence. DNA methylation is a cornerstone of epigenetic regulation: it fine-tunes gene activity during development, and shifts in methylation patterns near gene promoters can change how strongly, or whether, a gene is transcribed. After rigorous preprocessing—background correction, dye-bias normalization, beta-mixture quantile normalization, batch-effect removal via an empirical Bayes framework, and exclusion of probes on sex chromosomes or prone to cross-reactivity—the team retained 418,997 CpGs in cord blood mononuclear cells, 415,604 on the fetal side of the placenta, and 412,460 on the maternal side.

A critical technical challenge in methylation studies is that different tissues contain mixtures of cell types, each with its own methylation signature. To disentangle chemistry from cellular composition, the researchers used reference-based deconvolution methods, estimating the proportions of five immune cell types in cord blood—CD8 and CD4 T-lymphocytes, B-cells, natural killer cells, and monocytes—and six cell types in placental tissue, including trophoblasts, syncytiotrophoblast, stromal cells, Hofbauer cells, endothelial cells, and nucleated red blood cells. These estimated proportions were then included as covariates in the statistical models, alongside maternal age, race, education, tobacco use, pre-pregnancy body mass index, and infant sex. Associations were tested with linear regression for 22 biomarkers measured on a continuous scale and with analysis of variance for 7 biomarkers detected in only 20 to 40 percent of participants, with false discovery rate control at a q-value threshold of 0.05 and a genomic inflation factor filter to guard against spurious results.

The headline result was striking in its selectivity. Of the 29 chemical biomarkers assessed, 11—six PAH metabolites, four phthalate-related compounds, and the phenol bisphenol A—showed statistically significant associations with differential CpG methylation in at least one sample type. But when the stricter inflation-factor filter was applied, two compounds emerged as the most consistent signals: 1-hydroxynaphthalene, a metabolite of naphthalene, and mono-3-carboxypropyl phthalate, known as MCPP, a metabolite of certain phthalates. Both were associated with altered methylation in the placenta, and the fetal side of the organ proved the most responsive of the three tissues examined, echoing the placenta’s role as the direct interface between maternal circulation and the developing fetus.

The PAH findings were particularly detailed. Maternal urinary concentrations of 2-hydroxyfluorene were associated with methylation changes at 46 CpG sites on the fetal side of the placenta, many of them hypomethylated and located within 200 base pairs of transcription start sites. Seven of these sites sat in the promoter regions of two genes: ZNF354C, encoding a zinc finger protein, and CCDC63, a coiled-coil domain gene. On the maternal side, 2-hydroxyfluorene and 1-hydroxypyrene were both linked to hypomethylation of CpGs near MFSD2A, a gene that encodes a transporter critical for delivering essential fatty acids across the blood-brain barrier and, in the placenta, for nutrient transfer to the fetus. Twenty-three CpG sites on the fetal side were commonly associated with both PAH metabolites, suggesting a shared mechanistic footprint of combustion-related exposures.

MCPP told a complementary story. Detected-or-not analysis revealed associations with roughly 130 CpGs on the maternal side of the placenta and 69 on the fetal side, with 34 and 15 of those respectively located in transcription start site regions. On the maternal side, four CpGs clustered within 200 base pairs of the promoter of LIG4, a gene essential for DNA ligase IV activity and the non-homologous end-joining pathway that repairs double-strand DNA breaks. On the fetal side, MCPP-associated CpGs mapped near HOOK1, involved in microtubule tethering, and DZIP1, a zinc finger protein implicated in ciliary biology and developmental signaling. Gene set enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes reinforced these themes: CpGs associated with MCPP were enriched for non-homologous end-joining and for neutrophil extracellular trap formation, the latter plausibly connected to a CpG near CSF3, a gene governing granulocyte production.

The pathway analysis for 1-hydroxynaphthalene pointed in a different direction—toward metabolism. On the fetal side of the placenta, enriched pathways included fatty acid biosynthesis, degradation, and metabolism, along with ferroptosis, an iron-dependent form of regulated cell death. Two CpG sites stood out: one near LEPROT/LEPR, the leptin receptor locus long associated with obesity biology, which showed hypomethylation, and one near ACSL5, an acyl-CoA synthetase involved in long-chain fatty acid metabolism, which showed hypermethylation. A sensitivity analysis restricted to the 500 CpGs with the lowest q-values similarly flagged fatty acid metabolism on the maternal side. The authors note that these lipid-related signals align with broader literature linking PAH exposure to metabolic syndrome, cardiovascular conditions, and systemic inflammation, and with prior work showing that prenatal PAH exposure alters methylation of ACSL3 in cord blood, a proposed biomarker for childhood asthma risk.

The researchers are careful to frame the study as exploratory. The sample was modest, exposures were measured at a single delivery-visit time point that may not capture the full gestational window, and the strongly correlated biomarkers within chemical classes raise multicollinearity concerns. The older 450K array also covers fewer type-II probes than newer EPIC platforms, though the authors argue this may have limited false positives given the sample size. No KEGG pathway survived correction at a q-value below 0.1, and the team emphasizes that replication in larger cohorts is essential before drawing clinical conclusions. Still, the study’s contribution is clear: by profiling methylation in both placental sides and cord blood mononuclear cells against a wide panel of phenols, phthalates, and PAHs, it offers a mechanistic bridge between the ubiquitous chemical exposures of modern pregnancy and the developmental programming of newborn health—and it suggests that the placenta, far from being a passive barrier, records an epigenetic diary of the chemical world the mother inhabits. The methylation data have been deposited in NCBI’s Gene Expression Omnibus under accession GSE269983, and the authors call for multi-omics studies integrating exposome, epigenetic, transcriptomic, and phenotype data to fully map the biological pathways at play.

Subject of Research: Associations between gestational exposure to environmental chemicals and DNA methylation changes in the placenta and cord blood mononuclear cells

Article Title: Gestational exposure to environmental chemicals and epigenetic alterations in the placenta and cord blood mononuclear cells

Article References: Puvvula, J., Braun, J. M., DeFranco, E. A., Ho, S.-M., Leung, Y.-K., Huang, S., Zhang, X., Vuong, A. M., Kim, S. S., Percy, Z., Calafat, A. M., Botelho, J. C., & Chen, A. (2024). Gestational exposure to environmental chemicals and epigenetic alterations in the placenta and cord blood mononuclear cells. Epigenetics Communications, 4(1), Article 4. https://doi.org/10.1186/s43682-024-00027-7

Image Credits: AI Generated

DOI: 10.1186/s43682-024-00027-7

Keywords: epigenetics, DNA methylation, placenta, cord blood, phthalates, polycyclic aromatic hydrocarbons, bisphenol A, endocrine disruptors, pregnancy, environmental health, gene enrichment, birth outcomes