The choice of metabolic biomarkers also deserves attention. Rather than relying solely on conventional lipid measures, the study included leptin and adiponectin, two adipokines that reflect adipose tissue function and insulin sensitivity. Leptin is produced proportionally to fat mass and signals satiety to the hypothalamus, but in states of excess adiposity, circulating leptin rises while cellular responsiveness diminishes, a phenomenon known as leptin resistance. Adiponectin, by contrast, is an insulin-sensitizing hormone whose levels tend to fall as visceral fat accumulates. The ratio between these two hormones has been proposed as a sensitive indicator of metabolic dysfunction in children, sometimes detecting disturbances earlier than changes in body mass index or standard lipid panels become apparent. Fructosamine, meanwhile, offers a practical alternative to fasting glucose measurements in studies where blood is drawn without regard to meal timing. Because fructosamine reflects the glycation of serum proteins over the preceding two to three weeks, it provides an integrated picture of recent glycemic control without requiring participants to fast, which is a considerable logistical advantage in pediatric research.

The observation that associations differed by pubertal stage is scientifically meaningful for several reasons. Puberty is characterized by profound hormonal shifts, including rising concentrations of sex steroids and growth hormone, both of which influence lipid metabolism. Growth hormone, for instance, tends to raise LDL cholesterol and lower insulin sensitivity during mid-puberty, while estrogen in girls generally improves lipid profiles by raising HDL cholesterol. These physiological changes create a moving baseline against which any environmental effect must be measured. If a chemical perturbs lipid metabolism, its apparent impact may be amplified, attenuated, or masked depending on the pubertal context in which exposure is assessed. The finding that perfluorononanoic acid and perfluorodecanoic acid were linked to higher triglycerides in peripubertal boys, while perfluorooctane sulfonate showed an inverse association with triglycerides in postpubertal boys, illustrates this complexity. Such direction reversals across developmental stages have been reported in other cohorts and may reflect genuine biological differences in how PFAS interact with maturing endocrine systems, or alternatively may arise from changes in PFAS body burden during puberty, since these chemicals bind to serum proteins and their apparent concentrations can be influenced by shifts in blood volume and body composition as children grow.

The pharmacokinetics of PFAS in children are relevant to interpreting these results. Long-chain PFAS compounds have elimination half-lives in humans that range from several years for perfluorooctane sulfonate to roughly four to five years for some perfluorinated carboxylic acids, and even longer for certain longer-chain analogues. This means that serum levels measured at age 12 partly reflect exposures accumulated over years, and in the case of the longest-lived compounds, may still carry a contribution from prenatal and early-life exposure transferred through the placenta and through breastfeeding. Because the PELAGIE cohort collected cord blood and childhood samples at earlier follow-ups, future analyses from this same population can help disentangle whether metabolic associations at age 12 are driven by concurrent exposure, by earlier life exposure, or by the cumulative burden of both. This is precisely the kind of question that cross-sectional data alone cannot resolve, and it underscores the authors’ call for longitudinal follow-up.

The detection of PFAS in every serum sample examined is consistent with biomonitoring surveys conducted across Europe and North America, which consistently find near-universal presence of perfluorooctane sulfonate, perfluorooctanoic acid, and perfluorohexane sulfonate in blood serum. These three compounds were among the most heavily produced PFAS historically and remain widespread despite phase-outs and restrictions, owing to their extreme persistence, their continued presence in the environment, and in some cases ongoing production in parts of the world where regulations are less stringent. Perfluorooctane sulfonate has been listed under the Stockholm Convention on Persistent Organic Pollutants, and perfluorooctanoic acid has been the subject of international restrictions as well, yet both remain detectable in human serum decades after their peak production. The longer-chain perfluorinated carboxylic acids examined in this study, such as perfluoroundecanoic acid and perfluorodecanoic acid, are less well characterized in the epidemiological literature, partly because they were produced in smaller volumes and measured less frequently in earlier studies. Their emergence as the compounds most consistently associated with lipid markers in this cohort highlights the value of measuring a broader panel of PFAS rather than focusing only on the legacy compounds.

Several mechanisms have been proposed to explain how PFAS might influence lipid metabolism. These compounds activate peroxisome proliferator-activated receptors, a family of nuclear receptors that regulate fatty acid oxidation, adipogenesis, and lipid storage. Experimental studies in rodents and in human cell models have shown that PFAS exposure can alter expression of genes involved in cholesterol synthesis and transport, mitochondrial fatty acid metabolism, and bile acid homeostasis. Some PFAS also interact with other nuclear receptors involved in endocrine signaling, raising the possibility that their metabolic effects are mediated partly through interference with thyroid hormone action, since thyroid status strongly influences lipid profiles in growing children. Whether these mechanisms operate similarly in preadolescents as in adults remains an open question, and the sex-specific patterns observed in this study may reflect differences in hormonal milieu, body composition, or PFAS clearance between boys and girls.

The non-fasting design of the blood collection warrants brief consideration when interpreting the lipid findings. Triglyceride concentrations in particular are sensitive to recent food intake, and non-fasting measurements can introduce variability that fasting protocols would avoid. However, growing consensus in pediatric lipidology supports the use of non-fasting lipid profiles for routine screening, since postprandial changes in total cholesterol, HDL, and LDL are generally modest, and non-fasting sampling reflects the metabolic state in which children spend most of their time. The use of the Friedewald equation to derive LDL cholesterol is standard practice, though it becomes less accurate at very high triglyceride concentrations, a situation unlikely to be common in a healthy cohort of twelve-year-olds.

It is also worth noting the strengths and limitations inherent in the study design. The PELAGIE cohort offers the advantage of detailed prospective data collection from early pregnancy onward, allowing careful adjustment for factors such as maternal characteristics, socioeconomic variables, and child diet and physical activity, all of which can confound associations between chemical exposure and metabolic health. The sample size of 451 children is respectable for a single-region birth cohort, though stratification by both sex and pubertal stage reduces the number of participants in each subgroup analysis, which can limit statistical precision and increase the possibility that some findings reflect chance. Cross-sectional designs, by their nature, cannot establish temporal ordering between exposure and outcome, and reverse causation remains a theoretical concern, since body size and body composition can influence PFAS serum concentrations through dilution and volume of distribution effects. Children with higher adiposity may show lower serum PFAS concentrations per unit of exposure simply because the same body burden is distributed across a larger volume, a phenomenon that has been documented in prior studies and that could bias observed associations in either direction.

From a public health perspective, the study reinforces the rationale for reducing PFAS exposure during childhood, a period when the developing cardiovascular and endocrine systems may be particularly susceptible to chemical perturbation. Regulatory actions in the European Union and elsewhere have increasingly targeted entire classes of PFAS rather than individual compounds, reflecting recognition that the thousands of substances in this chemical family share structural features and persistence. Dietary interventions, such as reducing consumption of food packaged in greaseproof materials, and household measures, such as filtering drinking water where contamination is known, represent practical steps families can take, though the ubiquity of these chemicals means that individual-level avoidance has limits. The findings from this French cohort, together with converging evidence from other populations, support continued biomonitoring and longitudinal research to clarify whether the metabolic associations observed at age twelve translate into measurable cardiovascular risk as these children mature into adolescence and adulthood.

Subject of Research: Association between PFAS exposure and metabolic biomarkers in 12-year-old children

Article Title: PFAS exposure in 12-year-old children and its association with metabolic markers

Article References: Lejeune, N., Rouxel, E., Monfort, C., Tillaut, H., Goxe, C., Rouget, F., Giton, F., Gaudreau, É., Lainé, F., Garlantézec, R., Cordier, S., Chevrier, C., & Warembourg, C. (2026). PFAS exposure in 12-year-old children and its association with metabolic markers. Pediatric Research. https://doi.org/10.1038/s41390-026-05396-4

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05396-4

Keywords: PFAS, children, metabolic markers, cholesterol, puberty, PELAGIE cohort, lipids, environmental health, endocrine disruptors, triglycerides, exposure, year-old

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

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: Toumi, D., Souaf, B., Bayoudh, A., Alibi, S., Spanò, I., Di Bella, G., Alminderej, F. M., Majdoub, H., & Mansour, H. B. (2026). Occurrence, distribution and potential sources of phthalate and non-phthalate plasticizers in maternal and fetal-related biological matrices. Environmental Geochemistry and Health, 48(16), Article 637. 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

Bisphenol A was first synthesized in 1891 as a synthetic estrogen, long before industry discovered its usefulness in polycarbonate plastics and epoxy resins. Today it is produced in quantities of millions of tons per year and appears in food containers, thermal receipts, dental sealants, medical equipment, and personal care products. Because it leaches from these materials at every stage from manufacturing to disposal, humans are exposed continuously through food, dust inhalation, and skin contact. Researchers have detected the compound in serum, urine, breast milk, placental tissue, amniotic fluid, follicular fluid, and umbilical cord blood, confirming that it crosses the placenta and reaches the developing fetus.

The reason bisphenol A interferes with hormones is structural: its two phenolic rings echo the shape of 17β-estradiol, the body’s principal estrogen, allowing it to dock into the same pocket on estrogen receptor alpha. Once bound, the chemical-receptor complex moves into the nucleus, where it can bind to estrogen response elements on DNA and recruit co-activator proteins to switch genes on or off. Depending on dose, tissue, and receptor subtype, bisphenol A can either mimic or block estrogenic signaling, disrupting pathways governing reproduction, immunity, and brain development. When regulators restricted its use, manufacturers turned to structural cousins such as bisphenol S, bisphenol F, and bisphenol AF, but mounting evidence indicates many of these substitutes carry estrogenic or anti-estrogenic activity equal to or exceeding the original.

Testing every new chemical with traditional animal studies is impractical, so computational screening has become a central tool in endocrine risk assessment. In the new study, Satpathy assembled a panel of twenty endocrine-disrupting bisphenols and evaluated how each one binds the ligand-binding domain of human estrogen receptor alpha, using the high-resolution crystal structure PDB 3ERT as the starting point. Missing residues in the crystal structure were rebuilt with homology modeling, and the refined model passed rigorous validation checks, including an ERRAT quality factor above 95 percent and a Ramachandran plot showing no residues in disallowed regions.

The docking protocol itself was put through its paces before any bisphenols were scored. The co-crystallized ligand 4-hydroxytamoxifen was removed and re-docked, reproducing its crystallographic pose with an acceptable deviation, and caffeine was included as a negative control, binding weakly as expected for a compound with no known estrogen receptor affinity. Two independent docking engines, MzDOCK and AutoDock Vina, produced consistent rankings. Against this validated backdrop, one substitute stood out dramatically: bisphenol PH, or BPPH, achieved a docking score of −11.4 kcal/mol, comfortably stronger than 17β-estradiol itself at −9.9 kcal/mol.

Interaction analysis revealed why. All three reference ligands, bisphenol A, bisphenol PH, and estradiol, occupy the canonical estrogen-binding cavity and make contact with the same conserved residues, including Met343, Leu346, Leu387, Met388, Leu391, Arg394, and Phe404. Binding is dominated by hydrophobic contacts, with only a few hydrogen bonds anchoring each ligand. The phenolic hydroxyl groups of estradiol and bisphenol PH both form stable hydrogen bonds with Glu353, an interaction thought to be important for receptor activation, while the bulkier aromatic system of bisphenol PH adds extra hydrophobic and pi-stacking interactions that appear to lock it more firmly into the pocket.

Docking scores alone can mislead, so the study turned to molecular dynamics simulations, which track every atom of the protein-ligand complex as it moves in a bath of water and salt at physiological temperature. Three independent 50-nanosecond simulations of the bisphenol PH complex, run with different random seeds, all showed the same picture: the protein backbone settled quickly, the ligand remained firmly in place, and the hydrogen bonds it formed persisted throughout. An extended 100-nanosecond simulation confirmed that both the unbound receptor and the bisphenol PH complex reached stable equilibrium after roughly 20 nanoseconds, with the ligand maintaining its key contacts for the remainder of the run.

Free-energy calculations using the MM-PBSA method, which combines molecular mechanics energies with a model of solvation, ranked the complexes in the same order as the docking scores. Bisphenol PH showed the strongest predicted binding at +112.38 kJ/mol on the YASARA scale, where larger positive values indicate stronger binding, followed by estradiol at +86.63 kJ/mol and bisphenol A at +72.06 kJ/mol. The convergence of two independent computational approaches on the same ranking strengthens the case that bisphenol PH forms an unusually stable complex with the receptor.

The most striking results concern helix-12, a short helix at the receptor’s C-terminus that acts as the molecular switch for estrogen signaling. When estradiol binds, helix-12 folds closed over the ligand pocket, creating the AF-2 groove where co-activator proteins attach; antagonists displace the helix and block activation. Structural superposition showed that bisphenol PH holds helix-12 in an agonist-like position nearly identical to estradiol, with a helix-specific deviation of just 1.326 angstroms, while bisphenol A shifted the helix considerably more, at 2.187 angstroms. Dynamic cross-correlation analysis then revealed something subtler: estradiol coordinates helix-12 with helix-3 through strong anti-correlated motion, bisphenol PH partially preserves this coupling, and bisphenol A nearly abolishes it, decoupling the helix from the receptor core altogether.

That graded pattern, from full agonist-like coordination through partial mimicry to near-complete decoupling, suggests that bisphenols do not simply act as weak copies of estrogen. Instead, each compound imposes its own dynamic signature on the receptor, potentially altering which co-regulators are recruited and which genes are ultimately expressed. The study’s author notes that computational results are predictive rather than definitive: the simulations cover only the ligand-binding domain, run for at most 100 nanoseconds, and will need microsecond-scale trajectories, mutant-receptor comparisons, and laboratory validation to confirm biological activity. Still, the message for toxicology is clear. Judging endocrine disruptors by static binding affinity alone misses the dynamic story, and the substitutes marketed as safer alternatives may disturb estrogen receptor signaling through mechanistic pathways all their own.

Subject of Research: Computational analysis of how bisphenol A and its analogues bind and allosterically modulate estrogen receptor alpha

Article Title: Structural and dynamic characterization of estrogen receptor-α binding by bisphenol A and its analogues

Article References: Satpathy, R. (2026). Structural and dynamic characterization of estrogen receptor-α binding by bisphenol A and its analogues. Discover Chemistry, 3(1), Article 462. https://doi.org/10.1007/s44371-026-00911-2

Image Credits: AI Generated

DOI: 10.1007/s44371-026-00911-2

Keywords: bisphenol A, estrogen receptor alpha, endocrine disruptors, molecular docking, molecular dynamics simulation, MM-PBSA, helix-12, bisphenol PH, 17β-estradiol, ligand-receptor interaction, allosteric signaling, toxicology

HFPOs were engineered with oxygen atoms inserted into their fluorinated carbon chains, a modification intended to make the molecules more degradable and less persistent than PFOA and PFOS. That promise has not held up. Rodent studies have shown that HFPO-dimer acid, better known as GenX, lingers in blood and liver with extended half-lives and crosses the placenta, while HFPO-trimer acid is absorbed rapidly, excreted slowly and accumulates even more strongly than PFOA. Human biomonitoring has confirmed the concern: residents of North Carolina exposed through contaminated drinking water carry HFPO-DA in their blood, and people living near fluorochemical plants in China have been found with HFPO-TA in their serum at concentrations reaching hundreds of nanograms per milliliter. Animal experiments have linked these compounds to liver mitochondrial disruption, cardiovascular toxicity in zebrafish embryos, damage to the blood-testis barrier and impaired spermatogenesis, but whether they directly compromise human sperm function remained an open question until now.

To answer it, the team obtained semen samples from thirty healthy donors meeting World Health Organization criteria for normal sperm, purified the cells and exposed them to graded concentrations of HFPO-DA, HFPO-TeA and HFPO-TA under physiological conditions. Computer-assisted sperm analysis revealed a consistent pattern: total and progressive motility declined significantly within hours of exposure across all three compounds, and viability dropped at the higher doses. The effects were not limited to gross movement. When the researchers assessed the acrosome reaction, the explosive release of enzymes that allows sperm to penetrate the egg’s outer coat, they found that HFPO-TA suppressed both spontaneous and progesterone-triggered reactions in a dose-dependent manner, while HFPO-TeA and HFPO-DA interfered with the progesterone-induced response. A viscous-medium penetration assay, a standard proxy for the hyperactivated swimming needed to navigate the female reproductive tract, showed sharply reduced penetration capacity, and high-speed imaging of flagellar waveforms revealed blunted beat amplitude and disrupted asymmetric beating patterns characteristic of capacitated sperm.

Transmission electron microscopy then exposed the structural carnage behind these functional failures. Sperm exposed for two hours to mid-range concentrations of the compounds showed swollen and disintegrating acrosomal membranes, misaligned mitochondria in the neck region, fragmented mitochondrial cristae and vacuolization of the mitochondrial sheath that wraps the flagellum. Even more striking, all three HFPOs disorganized the peripheral dense fibers, and HFPO-TeA and HFPO-TA severely scrambled the axoneme itself, the elegant ‘9+2’ array of microtubules that powers flagellar beating. Because mature sperm are transcriptionally silent and carry minimal DNA repair machinery or antioxidant defenses, such structural damage cannot be repaired by the cell; it accumulates until function collapses.

The functional consequences of that damage were quantified with fluorescent probes. Total intracellular reactive oxygen species rose to 150 to 170 percent of control levels after exposure to medium concentrations of HFPO-TeA and HFPO-TA, but the mitochondrial compartment fared far worse: mitochondrial superoxide climbed to 1.7 to 2.0 times control values. Mitochondrial membrane potential, the electrical gradient that drives ATP synthesis, depolarized by a factor of 1.4 to 1.6, and HFPO-TA triggered a 2.1-fold collapse in sperm ATP production. The team then turned to Mitoquinone, or MitoQ, an antioxidant that accumulates specifically inside mitochondria. Pretreating sperm with 100 nanomolar MitoQ significantly blunted the losses in total and progressive motility, reduced both total and mitochondrial ROS, and preserved membrane potential, providing pharmacological proof that mitochondrial oxidative stress sits at the heart of the toxicity.

Calcium emerged as the other half of the story. Using the fluorescent indicator Fluo-4 AM and real-time recording, the researchers observed that HFPO-DA, HFPO-TeA and HFPO-TA each triggered a rapid transient surge of intracellular calcium within seconds of exposure, followed by stabilization near baseline. When sperm were pretreated with NNC 55-0396, a CatSper channel inhibitor, the HFPO-induced calcium peaks were markedly attenuated, identifying the sperm-specific CatSper channel as the gateway for the influx. The parallels with progesterone, the physiological activator of CatSper in the female tract, were unmistakable. HFPO exposure alone produced calcium flux patterns resembling progesterone stimulation, yet pre-exposure to the chemicals suppressed subsequent progesterone-induced calcium responses in a concentration-dependent fashion. When HFPOs and progesterone were co-administered, the combined calcium peaks exceeded those of HFPO alone but fell short of the sum of the individual responses, suggesting the compounds act as partial agonists at CatSper, competing with progesterone and desensitizing sperm to its signal.

Time-resolved imaging revealed the sequence linking calcium to mitochondrial collapse. Cytosolic calcium peaked within roughly twenty seconds of HFPO stimulation, while mitochondrial calcium, tracked with a targeted probe, began rising within about eighty seconds and then accumulated progressively rather than stabilizing. This biphasic pattern, an acute transient followed by sustained overload, indicates that HFPOs first open the CatSper floodgate and that the resulting calcium is then shunted into mitochondria through the mitochondrial calcium uniporter, overwhelming the organelles. Calcium overload in mitochondria is a well-known trigger for excessive ROS generation, membrane depolarization and apoptotic signaling, and the new data place human sperm squarely within that pathological cascade.

To map the molecular fingerprints of each homologue, the team deployed integrated metabolomics and proteomics. Untargeted metabolomic profiling identified hundreds of differentially regulated metabolites per compound and revealed distinct pathway disruptions: HFPO-DA perturbed phenylalanine, amino sugar and sphingolipid metabolism; HFPO-TeA altered alanine, aspartate and glutamate metabolism, primarily through L-aspartic acid; and HFPO-TA skewed glycerophospholipid metabolism and arginine biosynthesis, mainly through glutamic acid. Quantitative proteomics, capturing more than 7,400 proteins, showed that all three compounds converged on calcium signaling, sphingolipid signaling, apoptosis and fatty acid metabolism, while each left its own signature: HFPO-DA uniquely affected nitrogen metabolism and oxidative phosphorylation, HFPO-TeA selectively perturbed carbon metabolism, and HFPO-TA predominantly impacted cell adhesion molecules and the TCA cycle. These compound-specific profiles explain why the three homologues showed divergent toxic potencies despite damaging the same fundamental sperm processes.

The authors are careful to frame the study’s scope. The experimental concentrations, spanning 5 to 500 micromolar for HFPO-DA and 5 to 100 micromolar for HFPO-TA and HFPO-TeA, exceed the highest reported human serum levels by roughly six- to one-thousand-fold, and the in vitro acute exposure model cannot replicate the chronic, low-dose, cumulative exposure typical of real-world contamination. The proposed competitive interaction between HFPOs and progesterone at CatSper also remains inferential until direct binding studies, patch-clamp recordings or molecular docking can be performed. Nevertheless, the mechanistic chain the study establishes, from CatSper-mediated calcium influx to mitochondrial calcium overload, oxidative stress, ATP depletion and loss of motility and fertilization competence, offers a compelling explanation for epidemiological findings linking PFAS body burdens to reduced sperm density, motility and testosterone in populations across Denmark, Italy and China. As HFPOs continue to accumulate in water, wildlife and human blood worldwide, the research adds male fertility to the growing list of health risks posed by the replacements for the forever chemicals they were meant to replace.

Subject of Research: Toxic effects of HFPO perfluoroalkyl substitutes on human sperm calcium signaling and mitochondrial function

Article Title: HFPO homologue exposure impairs human sperm function via calcium dyshomeostasis and mitochondrial dysfunction

Article References: Le, M., Xue, J., Ding, J., Wu, L., Yuan, Y., Zheng, L., Hu, L., & Zhang, D. (2026). HFPO homologue exposure impairs human sperm function via calcium dyshomeostasis and mitochondrial dysfunction. Journal of Advanced Research. https://doi.org/10.1016/j.jare.2026.10.013

Image Credits: AI Generated

DOI: 10.1016/j.jare.2026.10.013

Keywords: PFAS, HFPO, GenX, male fertility, sperm motility, CatSper, calcium signaling, mitochondrial dysfunction, reactive oxygen species, acrosome reaction, reproductive toxicology, endocrine disruptors

The research team, led by Alex da Silva de Freitas of the Universidade Federal Fluminense, set out to test a deceptively simple hypothesis: that rising human activity in the watershed would change both the identity and the concentration of contaminants settling into the lagoon’s sediments between the two sampling campaigns. To do this, they collected surface sediments from the top five centimeters at seven fixed stations during the dry seasons of 2021 and 2023, using a Van Veen grab sampler. Fixing the sampling locations across both years allowed direct comparisons in space and time, a design that many contaminant surveys lack.

The analytical strategy combined two complementary approaches. First, the team extracted contaminants from freeze-dried sediment using methanol, concentrated the extracts by solid-phase extraction, and identified and quantified the target compounds by gas chromatography–mass spectrometry after chemical derivatization to boost volatility and stability. Second, they assessed the biological punch of the extracts using the yeast estrogen screen, a bioassay in which a genetically engineered strain of Saccharomyces cerevisiae carries the human estrogen receptor wired to a reporter system. When estrogenic compounds activate the receptor, the yeast produces an enzyme that turns a colorless substrate red, allowing researchers to express the total estrogenic effect of a sample as 17β-estradiol equivalents.

The chemistry told a clear story. Nine of twelve target compounds were detected across the two campaigns. Bisphenol A, the plasticizer found in polycarbonate plastics and epoxy resins, was the most ubiquitous, appearing in nearly every sample at concentrations ranging from 0.10 to 0.99 nanograms per gram of sediment, with a marked increase between 2021 and 2023. The alkylphenols 4-octylphenol and 4-nonylphenol, byproducts of industrial surfactant degradation, ranged from 0.010 to 0.390 and 0.033 to 0.344 nanograms per gram respectively, signaling sustained or growing inputs. Steroid estrogens and pharmaceuticals showed patchier distributions, with estrone detected at a couple of stations and the lipid-lowering drug gemfibrozil, the painkiller diclofenac, and naproxen appearing in the 2023 campaign.

One station stood out dramatically. Site M7, sampled in 2023, contained nine of the twelve monitored compounds, including the full suite of steroid hormones: estrone, 17β-estradiol, the synthetic contraceptive estrogen ethinylestradiol, and estriol, alongside pharmaceuticals and alkylphenols. The researchers identify M7 as a localized hotspot of mixed contamination, most likely fed by urban wastewater inputs. The presence of ethinylestradiol is particularly notable because this synthetic estrogen, used in oral contraceptives, is among the most potent endocrine disruptors known, exhibiting greater estrogenic activity and toxicity than its natural counterparts even at vanishingly low concentrations.

The biological results, however, were more enigmatic. Estrogenic activity, ranging from 0.01 to 0.18 nanograms of estradiol equivalents per gram, was detected only in samples from station M4 in 2021 and M5 in 2023. Strikingly, the sample that contained both 17β-estradiol and ethinylestradiol showed no measurable estrogenic response in the yeast assay. Even more puzzling, one sample from station M5 in 2021 proved so cytotoxic that yeast cell viability collapsed to just five percent, effectively masking any estrogenic signal that might have been present. This mismatch between chemical detection and biological response is not a failure of the study but a window into the messy reality of environmental toxicology.

The authors attribute these discrepancies to several interacting factors. Compounds bound tightly to sediment organic matter may simply not be bioavailable to the yeast cells, limiting receptor access. Complex environmental mixtures can contain antagonistic substances that suppress estrogen receptor activation or interfere with downstream gene expression, producing non-additive effects that no single-compound analysis would predict. And co-extracted matrix components can inhibit yeast growth outright, as the dramatic cytotoxicity at M5 demonstrated. The lesson, the researchers argue, is that chemical presence alone does not translate into measurable biological activity, and neither chemistry nor bioassays alone can capture the full picture. Only by integrating targeted chemical analysis with effect-based screening can scientists realistically assess the risk posed by contaminant mixtures in sediments.

Sediment texture, surprisingly, offered little explanatory power. Although fine-grained sediments are typically expected to soak up hydrophobic contaminants, micropollutants turned up across samples with widely differing particle-size characteristics, and silt content shifted by more than twenty percentage points at some stations between the two years. Instead, the researchers point to hydrodynamics as the dominant force shaping contaminant distribution. Maricá Lagoon is shallow, averaging just one to two meters deep, and wind-driven waves approaching one meter in height regularly resuspend sediments and redistribute particle-bound pollutants. Silting of the Ponta Negra and Cordeirinho channels restricts tidal exchange with the ocean, lengthening water residence times and favoring the retention of both nutrients and contaminants. Inflows from the Mumbuca River and the Inoã Channel, both conduits for anthropogenic inputs, likely shuttle contaminants across the system and help create localized accumulation zones.

The temporal comparison between 2021 and 2023 reveals a system that is dynamic yet stubbornly contaminated. Compounds like bisphenol A, the alkylphenols, and diclofenac appeared in both campaigns, pointing to continuous inputs and long-term stability in the sedimentary archive rather than one-off pollution events. Meanwhile, the appearance of gemfibrozil and naproxen only in 2023 suggests shifting emission patterns or changing transport and deposition conditions. The persistence of endocrine-active compounds across both years indicates that the lagoon shows little sign of recovery, even as the exact mixture of chemicals continues to evolve with the watershed’s growing population, sand extraction, clay mining, livestock farming, and notoriously limited sewage treatment. According to Brazil’s National Sanitation Information System, only about 55 percent of the population has access to sewage treatment, a gap that is especially acute in the Rio de Janeiro metropolitan region.

Why should anyone beyond Rio de Janeiro care about nanogram-scale contamination in a shallow lagoon? Because sediments act as both sinks and secondary sources. Contaminants that settle into the mud can persist for years, then be remobilized by resuspension and taken up by benthic organisms, entering food webs where chronic exposure to even trace-level mixtures can impair reproduction, development, and physiology in fish and invertebrates. This study also marks the first report of pharmaceutical residues in Maricá Lagoon sediments, establishing a baseline for long-term monitoring. The broader message resonates far beyond Brazil: as urbanization accelerates around tropical coastlines worldwide, restricted-exchange lagoons are quietly archiving our pharmaceutical and industrial footprints. Detecting those archives, and understanding when they translate into real biological harm, will require exactly the kind of dual chemical-plus-bioassay approach this study champions, applied repeatedly over time in the places where people and water most intimately intersect.

Subject of Research: Temporal occurrence of emerging contaminants and estrogenic activity in sediments of a tropical coastal lagoon in Brazil

Article Title: Temporal variability of emerging contaminants and estrogenic activity in sediments of a tropical coastal lagoon

Article References: da Silva de Freitas, A., de Oliveira Santos, A. D., Sanson, A. L., Ferreira dos Santos, R., Teresa Lima do Nascimento, M., Gomes, G., dos Santos Argolo, A., da Cruz Félix, L., Bila, D. M., & Baptista Neto, J. A. (2026). Temporal variability of emerging contaminants and estrogenic activity in sediments of a tropical coastal lagoon. Environmental Monitoring and Assessment, 198(10), Article 1073. https://doi.org/10.1007/s10661-026-15919-5

Image Credits: AI Generated

DOI: 10.1007/s10661-026-15919-5

Keywords: emerging contaminants, endocrine disruptors, bisphenol A, alkylphenols, steroid estrogens, pharmaceuticals, yeast estrogen screen, GC-MS, sediment contamination, coastal lagoon, Maricá Lagoon, Brazil

The research team, led by Anna Nynca of the University of Warmia and Mazury in Olsztyn, together with colleagues from the Polish Academy of Sciences, Jagiellonian University, and the University of Rzeszow, focused on a class of chemicals known as endocrine-active compounds, or EACs. These substances, which include industrial chemicals and pharmaceutical agents, can mimic, block, or otherwise interfere with the body’s hormonal signaling. Because hormones orchestrate nearly every aspect of early reproductive development, scientists have become increasingly concerned that EAC exposure during critical early-life windows may act as a developmental toxicant, quietly rewiring tissues at the molecular level long before any outward symptoms appear.

To probe this question, the researchers turned to the neonatal pig, a species widely regarded as one of the most translationally relevant animal models for human reproductive development. The pig uterus undergoes a process called adenogenesis in the days after birth, in which the glands that will later nourish embryos form and mature within the uterine wall. This developmental program depends on precisely timed hormonal cues, making it exquisitely sensitive to chemical interference. The pig’s reproductive anatomy, hormonal cycles, and genomic architecture all resemble the human situation far more closely than the commonly used rodent models, which is why the team chose it as their experimental platform.

The experimental design was elegant in its simplicity. Newborn female piglets were divided into two feeding groups: one nursed naturally from their mothers, receiving sow’s milk, and the other raised on infant formula. On postnatal day 10, a period when uterine development is in full swing, the researchers collected uterine tissue from both groups. They then sliced the tissue into explants, thin sections that can be kept alive in laboratory culture dishes, and exposed these explants to three different endocrine-active compounds. The explant approach allowed the team to control chemical exposure precisely while keeping the tissue in a near-physiological state, and they confirmed tissue viability across the culture period by measuring lactate dehydrogenase release.

The three compounds represented distinct mechanistic threats. The first, 2-hydroxyflutamide, is an anti-androgen, a substance that blocks the receptors through which male hormones exert their effects. The second, 4-tert-octylphenol, is an industrial chemical used in the production of detergents and plastics, known to mimic estrogen. The third, HPTE, is a metabolite of the banned pesticide methoxychlor and acts as a disruptor of both estrogenic and androgenic signaling. By testing all three against uterine tissue from both feeding groups, the researchers could ask a deceptively simple question: does the same chemical produce the same molecular response in tissue that has been nourished differently?

The answer, revealed through a comprehensive transcriptomic analysis, was a resounding no. Using RNA sequencing, the team mapped the coding genes, long non-coding RNAs, and microRNAs expressed in each tissue sample, comparing treated explants against untreated controls. They found that the feeding regimen consistently shaped uterine responses to all three tested compounds. In the uteri of sow-fed piglets, the transcriptional upheaval triggered by 4-tert-octylphenol and HPTE was markedly attenuated, as if sow’s milk had equipped the tissue with a buffer against chemical disruption. In contrast, uterine tissue from formula-fed piglets displayed far greater transcriptional sensitivity, with many more genes swinging up or down in response to the same chemical challenge.

The affected genes were not random. Functional analysis showed that the dysregulated transcripts clustered around biological processes central to uterine development itself: cell-cycle regulation, morphogenesis, and the organization of cilia, the hair-like cellular projections that play roles in tissue patterning and fluid movement. All three processes are essential to adenogenesis, the gland-forming program underway in the neonatal uterus. This convergence suggests that endocrine-active compounds do not merely perturb isolated genes but strike at the very machinery that builds the reproductive organ, raising the possibility that early exposure could leave lasting structural and functional imprints.

Perhaps the most surprising twist came from the microRNA data. MicroRNAs are short regulatory RNA molecules that fine-tune gene expression after transcription, and their production depends on a processing machinery involving the proteins Drosha, DGCR8, and Dicer, whose abundance the team also measured. While sow-fed tissue showed a muted response at the level of messenger RNA, it exhibited more pronounced microRNA responses to chemical exposure. Notably, the microRNA remodeling induced by HPTE was not prevented by natural feeding, indicating that sow’s milk protects some layers of gene regulation but not others. This layered, diet-dependent pattern of protection suggests that the molecular consequences of early nutrition are far more nuanced than a simple shield-versus-vulnerability model would predict.

The broader implications reach well beyond pig farming. Infant formula is a nutritional staple for millions of human babies, and human infants are simultaneously exposed to endocrine-active compounds through plastics, personal care products, food contaminants, and pharmaceuticals. If early nutrition genuinely modulates the molecular responsiveness of developing reproductive tissue, as this study indicates, then the interplay between infant feeding and environmental chemical exposure deserves far closer scrutiny. The authors emphasize that their results support the hypothesis that feeding regimen and the associated rearing conditions are linked to differences in the molecular responsiveness of neonatal uterine tissue to endocrine challenge, a conclusion that invites parallel investigation in human developmental biology.

The study, funded by the National Science Centre of Poland and conducted under approved ethical protocols, also showcases the power of modern multi-omic approaches, integrating coding transcriptomes, long non-coding RNA profiles, microRNA sequencing, and protein-level validation of the miRNA-processing machinery. As endocrine disruptors continue to permeate the modern environment, research of this kind points toward a compelling and actionable idea: the earliest nutritional choices we make for the youngest members of our species may help determine how resilient their bodies are to the chemical challenges of the world they inherit. The neonatal uterus, it turns out, listens carefully to what it is fed, and its genomic response to toxic insult may be written, at least in part, by the very first meals of life.

Subject of Research: The influence of early neonatal nutrition on transcriptomic and miRNA responses of the developing uterus to endocrine-active compounds in a porcine model

Article Title: Early nutrition modulates transcriptomic responses to endocrine-active compounds in neonatal porcine uterine explants

Article References: Nynca, A., Swigonska, S., Molcan, T., Wojtaszek, M., Grzesiak, M., Koziorowska, A., Koziorowski, M., Slomczynska, M., & Knapczyk-Stwora, K. (2026). Early nutrition modulates transcriptomic responses to endocrine-active compounds in neonatal porcine uterine explants. BMC Genomics. https://doi.org/10.1186/s12864-026-13348-9

Image Credits: AI Generated

DOI: 10.1186/s12864-026-13348-9

Keywords: endocrine disruptors, neonatal nutrition, sow's milk, infant formula, porcine uterus, adenogenesis, transcriptomics, microRNA, developmental toxicology, uterine explants, gene expression, reproductive development

The scale of the problem is staggering. Pharmaceuticals and personal care products, steroid hormones, UV filters from sunscreens, pesticides, industrial chemicals, per- and polyfluoroalkyl substances, microplastics, and artificial sweeteners all slip more or less continuously through conventional wastewater treatment plants, which were simply never designed to catch them. Studies cited in the review document pharmaceutical residues in the Ganges River Basin, contaminants of emerging concern across Kenya’s River Athi Basin, steroid hormones in wastewater streams worldwide, and pesticide residues detected in maternal and umbilical cord blood. The common thread is that these compounds are biologically active at vanishingly small concentrations, are released continuously rather than in discrete spills, and persist long enough to travel far from their sources.

The health and ecological consequences are equally sobering. Endocrine-disrupting chemicals interfere with hormonal signaling and have been linked to reproductive health effects in humans and feminization of fish populations. Antibiotic residues in freshwater ecosystems drive the evolution of antimicrobial resistance, one of the most serious public health threats of the century. Polycyclic aromatic hydrocarbons accumulate in sediments and biota, with documented effects on wildlife and mammalian ovarian function. UV filters such as avobenzone become more toxic in combination with microplastics, as demonstrated in studies on the water flea Daphnia magna. Even mixtures of pharmaceuticals at low individual concentrations can impair the early life stages of fish, a reminder that the risk lies in the cocktail, not just the individual ingredient.

Perhaps the most provocative conclusion of the review is that the world’s failure to remove these contaminants is not a failure of technology per se. Effective removal methods exist. The real problem, the authors argue, is a fundamental mismatch between the properties of the contaminants and the mechanisms of the treatments deployed against them. Adsorption onto activated carbon and membrane filtration can strip contaminants from water with high efficiency, but they do not destroy anything; they merely concentrate the pollutants into spent sorbents and brines, creating secondary waste streams that must themselves be managed. Separation, in other words, is not destruction.

Biological treatment, the backbone of municipal wastewater engineering, fares no better against this class of pollutants. Activated sludge communities and constructed wetlands are remarkably good at degrading ordinary organic matter, but microbial metabolism is selective and slow when confronted with synthetic molecules engineered to resist breakdown, such as certain antibiotics, pesticides, and pharmaceuticals. Degradation kinetics are too sluggish for the hydraulic residence times of real plants, and some compounds pass through essentially untouched. The review notes that even advanced biological strategies, including microalgae-bacteria symbioses and bioaugmentation, remain constrained by this selectivity problem and by the sensitivity of microbial communities to toxic shocks and seasonal variation.

Advanced oxidation processes represent the current state of the art in destructive treatment, generating hydroxyl radicals and sulfate radicals that attack organic molecules with ferocious speed. Ozone-based systems, UV/hydrogen peroxide, UV/persulfate, photocatalysis with titanium dioxide, and electro-Fenton chemistry can all degrade pharmaceuticals, endocrine disruptors, and pesticides within minutes to hours. Yet the review is candid about their limits: high energy demand, incomplete mineralization that leaves behind partially oxidized transformation products sometimes more toxic than the parent compound, sensitivity to the complex matrix of real wastewater, and operational complexity that complicates full-scale deployment. Hybrid systems that couple, for example, ozonation with nanofiltration or photocatalysis with biological polishing can push performance further, but at the price of added cost and engineering intricacy.

Into this landscape the authors introduce cold plasma technology, and here the physics is genuinely distinctive. A cold plasma is a partially ionized gas in which electrons, accelerated by strong electric fields, reach temperatures of tens of thousands of kelvin while the bulk gas remains near ambient temperature. When such a discharge is created in air or oxygen above or within water, energetic electrons collide with gas molecules and dissociate them, generating a rich cocktail of reactive oxygen and nitrogen species: hydroxyl radicals, atomic oxygen, ozone, hydrogen peroxide, nitrate, nitrite, and peroxynitrite, alongside ultraviolet photons and shock waves. Crucially, these oxidants are generated in situ, on demand, without the storage, dosing, and transport of hazardous chemicals. When plasma contacts water directly, through dielectric barrier discharges, pulsed corona discharges, plasma jets, or bubble and falling-film reactor geometries, the reactive species diffuse into the liquid and attack contaminant molecules through oxidation, nitration, and bond cleavage.

The evidence base for plasma water treatment has grown rapidly. Studies compiled in the review report successful plasma degradation of antibiotics including sulfonamides, tetracyclines, fluoroquinolones, and penicillins; pharmaceuticals such as carbamazepine, ibuprofen, diclofenac, paracetamol, and fluoxetine; pesticides including atrazine, chlorpyrifos, endosulfan, and imidacloprid; endocrine disruptors such as bisphenol A; dyes; and UV filters. Reactor engineering matters enormously: water-film and bubble configurations maximize the plasma-liquid interface where chemistry happens, and hybrid plasma-catalytic systems, pairing discharges with titanium dioxide, tungsten oxide, zinc oxide, graphene composites, or activated carbon, exploit plasma-generated species and photons to accelerate photocatalysis and adsorption synergistically. The authors’ own recent work includes a dual-function dielectric barrier discharge bubble system that decouples nitrogen fixation from contaminant degradation, hinting at reactors that could clean water while recovering a nutrient value.

Still, the review refuses to oversell the technology. Energy efficiency remains the central hurdle: plasma systems must compete on energy per order of pollutant removal with ozone and UV-based oxidation, and comparisons published in the literature show plasma-based advanced oxidation can be competitive but is not yet uniformly superior. Reactor scalability from laboratory milliliters to treatment-plant cubic meters per hour is unproven at municipal scale. The field lacks standardized performance metrics, making cross-study comparison difficult, and most demonstrations use ultrapure water spiked with a single contaminant rather than real wastewater, whose organic matter, salts, and suspended solids quench radicals and shield targets. Residual toxicity assessment after treatment, though increasingly reported, needs to become routine. The authors frame these not as disqualifiers but as the research agenda: mechanistic frameworks linking plasma chemistry, reactor design, and plasma-liquid interaction to predictable degradation outcomes.

The bigger picture the review paints is one of process intensification, the engineering philosophy of doing more chemistry in smaller, smarter reactors. Cold plasma’s appeal lies in its versatility: one electrical input yields a spectrum of oxidants capable of broad-spectrum attack on chemically diverse pollutants, tunable by gas composition, power modulation, and reactor geometry, and combinable with catalysis, adsorption, and biological polishing in hybrid trains. As regulatory scrutiny of pharmaceuticals, PFAS, and endocrine disruptors tightens worldwide, and as water reuse becomes a necessity rather than an option, the gap between what conventional plants deliver and what modern chemistry demands will only widen. Whether cold plasma fills that gap will depend on the coming decade of scaling studies, but this assessment makes a compelling case that the fourth state of matter deserves a seat at the table of water treatment’s future.

Subject of Research: Assessment of emerging contaminants in water and the potential of cold plasma technology for their degradation

Article Title: Emerging contaminants in water pathways: sources, impacts, conventional, and cold-plasma-based cleaner technology assessment

Article References: Abdulsalam, M., Kimani, B. G., Ahlawat, K., & Machala, Z. (2026). Emerging contaminants in water pathways: sources, impacts, conventional, and cold-plasma-based cleaner technology assessment. Environmental Science and Pollution Research. https://doi.org/10.1007/s11356-026-38258-x

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38258-x

Keywords: emerging contaminants, cold plasma, water treatment, wastewater, advanced oxidation processes, pharmaceuticals, endocrine disruptors, pesticides, reactive oxygen species, plasma-liquid interaction, process intensification, antimicrobial resistance

The scale of the exposure problem is difficult to overstate. Pharmaceuticals such as antibiotics, anti-inflammatory drugs, antidepressants, antiepileptics, and hormones are deliberately engineered to trigger biological responses at vanishingly small doses, and they retain that potency once they reach rivers, estuaries, and coastal waters. Personal care products—antimicrobials, preservatives, fragrances, surfactants, and ultraviolet filters—pour continuously into domestic and industrial wastewater. Endocrine-disrupting compounds such as bisphenol A, nonylphenol, estradiol, and 17-ethinylestradiol can interfere with hormonal and cell-signaling pathways even at environmental concentrations. Because wastewater treatment plants were never designed to strip out these molecules, effluent-dominated waters carry a chronic chemical burden. In the Red Sea’s sewage-influenced coastal zones, for example, caffeine has been measured at 62 to over 3000 nanograms per liter, with total pharmaceutical and personal care product concentrations exceeding 10 micrograms per liter at the most contaminated sites.

What makes microalgae such powerful sentinels is their biology. With short generation times, enormous surface area-to-volume ratios, and constant immersion in the surrounding water, they absorb and respond to dissolved contaminants faster than almost any other organism. The review’s quantitative tables reveal just how variable—and how alarming—the toxicity can be. In the standard freshwater test species Pseudokirchneriella subcapitata, the antibacterial agent triclosan produced 72-hour growth inhibition at concentrations as low as 0.0018 micromolar, among the lowest thresholds recorded for any contaminant class. Yet in a mixed microalgal consortium, triclosan’s 72-hour toxicity value was 8 milligrams per liter, a difference of several orders of magnitude. Nonylphenol proved dramatically more toxic to the estuarine alga Tetraselmis sp. than chemically related endocrine disruptors, with inhibition concentrations of 0.190 to 0.313 milligrams per liter compared with more than 2 milligrams per liter for bisphenol A and 17-ethinylestradiol.

Perhaps the most technically consequential finding concerns photosynthesis, the machinery that converts light into the chemical energy driving the entire cell. Chlorophyll a emerges as the earliest and most consistent biochemical casualty: antibiotics, non-steroidal anti-inflammatory drugs, antidepressants, and endocrine disruptors all deplete it across a wide range of species. In Microcystis flos-aquae, exposure to the antibiotics florfenicol and thiamphenicol cut chlorophyll content by roughly 46 and 56 percent respectively, signaling profound disruption of the photosynthetic apparatus. The damage extends deep into Photosystem II, the oxygen-producing reaction center most vulnerable to photo-oxidative attack. The antidepressant fluoxetine slashed the maximum quantum yield of Photosystem II—measured as the Fv/Fm ratio—by approximately 81 percent in Raphidocelis subcapitata at just 15 to 30 micrograms per liter. Mechanistically, many of these compounds block electron transfer between the quinone acceptors QA and QB, destabilize the oxygen-evolving complex, and dismantle thylakoid membranes, choking the flow of energy before any visible growth decline appears.

Beneath the photosynthetic damage lies what the review identifies as the central toxicity hub: oxidative stress. Contaminants as structurally different as ibuprofen, clarithromycin, bisphenol A, and nonylphenol converge on the same endpoint—overproduction of reactive oxygen species, including superoxide radicals, hydrogen peroxide, hydroxyl radicals, and singlet oxygen. When electron transport is jammed, absorbed light energy has nowhere to go and leaks into the formation of these destructive molecules. They attack polyunsaturated fatty acids in cell membranes, triggering lipid peroxidation that is tracked by rising levels of malondialdehyde, a standard biomarker. In Scenedesmus obliquus, non-steroidal anti-inflammatory drugs induced exactly this cascade, degrading membranes, bleaching pigments, and collapsing photosynthetic efficiency. Under the microscope, exposed cells show chloroplast swelling, thylakoid disorganization, vacuolization, and mitochondrial abnormalities. At the molecular level, reactive oxygen species oxidize DNA—producing strand breaks and mutations—and oxidize amino acid residues in proteins, including the Photosystem II reaction-center proteins sitting closest to the sites of radical generation.

Microalgae are not passive victims, however. The review catalogs a sophisticated defensive arsenal: enzymatic antioxidants such as superoxide dismutase, catalase, peroxidase, ascorbate peroxidase, and glutathione reductase surge into action upon exposure; non-enzymatic scavengers including carotenoids, glutathione, and phenolic compounds mop up radicals; non-photochemical quenching dissipates excess light energy as heat before it can damage reaction centers; and extracellular polymeric substances bind contaminants before they reach the cell surface. Some species even display hormesis—low doses of ethinylestradiol, ciprofloxacin, sulfamethoxazole, amoxicillin, bezafibrate, tamoxifen, and certain anti-inflammatory drugs actually stimulated growth, apparently by providing an auxiliary carbon source or priming stress-response pathways. But the defenses have hard limits. Under chronic exposure or high concentrations, antioxidant enzymes themselves become oxidized and inactivated, and the cell tips from adaptation into irreversible injury. Repeated dosing with clarithromycin, for instance, produced greater reactive oxygen species accumulation than a single pulse, revealing cumulative damage that standard 72-hour assays completely miss.

That gap between acute testing and chronic reality is one of the review’s sharpest criticisms of the field. A ten-day exposure to carbamazepine at 200 milligrams per liter inhibited growth by 97 percent in Scenedesmus obliquus, yet the same concentration suppressed Chlamydomonas mexicana by only 30 percent, and Spirulina platensis showed just 34 percent inhibition at 100 milligrams per liter. Species identity, exposure duration, and endpoint selection all reshape toxicity rankings, which is why the authors warn against generalizing results from the handful of freshwater chlorophytes—Chlorella vulgaris, Scenedesmus species, and Pseudokirchneriella subcapitata—that dominate the literature. Marine and estuarine microalgae, cyanobacteria, and natural biofilms remain drastically understudied, even though stream biofilm experiments showed diphenhydramine suppressing algal biomass by 18 to 81 percent and photosynthetic performance by up to 99 percent. Single-compound tests compound the problem, since real waters carry mixtures that can act synergistically; co-exposure to pharmaceuticals and microplastics, for example, generates more oxidative damage than either contaminant alone.

The biotechnological implications cut in two directions at once. Contaminant stress often forces microalgae to redirect carbon from cell division into storage lipids, carotenoids, and protective secondary metabolites, creating a growth–metabolite trade-off: biomass yield falls while the content of commercially valuable compounds such as beta-carotene, astaxanthin, lutein, and zeaxanthin rises. Mild stress could therefore be exploited as a production strategy, provided contaminant accumulation in the harvested biomass is carefully monitored, since pharmaceuticals and their transformation products may lodge in cells destined for food, feed, or nutraceutical markets. At the same time, microalgae’s capacity to uptake, biotransform, and degrade these pollutants—mediated partly by cytochrome P450 enzymes—positions them as workhorses for phycoremediation. Pilot thin-layer reactors fed real wastewater laced with antibiotics and analgesics maintained biomass productivity and chlorophyll fluorescence without measurable harm, hinting that resilient algal communities could simultaneously clean water and generate feedstock for biofuels, biofertilizers, and bioplastics within a circular bioeconomy.

The review closes with a three-pronged roadmap for the decade ahead. First, ecotoxicology must embrace ecological realism: chronic multigenerational exposures, environmentally relevant mixtures, and a much broader taxonomic spread that includes marine and estuarine species. Second, omics technologies—genomics, transcriptomics, proteomics, and metabolomics—should be deployed to map the genes and networks governing contaminant uptake, detoxification, and hormesis, enabling the design of tolerant strains through synthetic biology and adaptive laboratory evolution. Third, algal biorefineries should be engineered around circular bioeconomy principles, coupling contaminant removal with nutrient recovery, carbon capture, and biomass valorization, backed by rigorous life-cycle assessments and techno-economic analysis. If those priorities are met, the very organisms now serving as early-warning indicators of chemical pollution could become the foundation of a sustainable technology that turns wastewater from an environmental liability into a resource stream.

Subject of Research: Ecotoxicological effects of pharmaceuticals, personal care products, and endocrine-disrupting compounds on microalgae

Article Title: Ecotoxicological effects of pharmaceuticals, personal care products, and endocrine disruptors on microalgae: a comprehensive review

Article References: Kumar, A., Venmathi Maran, B. A., & Prasad, K. (2026). Ecotoxicological effects of pharmaceuticals, personal care products, and endocrine disruptors on microalgae: a comprehensive review. Blue Biotechnology, 3(1), Article 13. https://doi.org/10.1186/s44315-026-00064-y

Image Credits: AI Generated

DOI: 10.1186/s44315-026-00064-y

Keywords: microalgae, emerging contaminants, pharmaceuticals, personal care products, endocrine disruptors, oxidative stress, photosynthesis, ecotoxicology, phycoremediation, reactive oxygen species, algal biotechnology, wastewater treatment