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 raw materials could hardly be more mundane. Post-consumer PVC pipes were collected from a construction site at the university’s Department of Chemical Engineering in Nakhon Nayok, washed, dried at 30 °C for 48 hours, and ground into roughly one-centimeter particles. The cling film waste, supplied by a local retailer, contained 30 weight percent of the plasticizer DINCH, a detail that proved crucial: in earlier work by the same group, blending flexible and rigid PVC at a 50:50 ratio raised elongation at break from 25.3 percent for neat recycled rigid PVC to 206 percent, while lowering the glass transition temperature by 34.9 °C. That flexibility is exactly what a brittle recycled matrix needs. Teak sawdust from Ayutthaya was oven-dried, ground, and sieved to an average particle size of 197 micrometers, with a bulk density of 0.27 g/cm³ and moisture content of just 1.46 percent.

To create the cellular structure, the team turned to azodicarbonamide, a widely used chemical blowing agent known as AC. Thermogravimetric analysis showed that AC decomposes sharply between 190 and 200 °C in a single exothermic step, releasing roughly 240 milliliters of gas per gram, composed mainly of nitrogen (65 percent), carbon monoxide (24 percent), carbon dioxide (5 percent) and ammonia (5 percent). That decomposition window sits almost perfectly inside the molding temperature of 195 ± 5 °C used in the study, and well below the composite’s major degradation stage, which occurs between 314.5 and 318.0 °C. This thermal matching meant the blowing agent could generate gas efficiently without triggering significant thermal damage to the PVC matrix or the wood filler, a prerequisite for producing sound foam.

Processing followed a melt compounding and closed-mold foaming route. The PVC pipe particles, cling film and sawdust were blended on a two-roll mill at 165–180 °C, then compression molded. For the foamed versions, AC was added at loadings of 0.5, 1, 3 and 5 weight percent, and the mold was preheated at 120 °C for five minutes before ramping to the foaming temperature. A tightly controlled ten-minute cycle—three minutes for filling and compression, five for foam expansion and cell growth, and two for cooling—kept expansion in check and ensured dimensional uniformity. The closed mold restricted runaway expansion, producing specimens with a characteristic skin–core structure: a denser surface layer surrounding a porous interior.

The foaming results revealed a classic optimum. Density fell steadily as AC content rose, reaching its lowest value at 3 weight percent, where gas generation, melt viscosity and cell stabilization appeared perfectly balanced. Cell density, the number of cells per unit volume, peaked at the same loading, while average cell size shrank from 40.38 micrometers at 0.5 percent AC to just 24.16 micrometers at 3 percent, accompanied by the narrowest, most uniform cell size distribution. Scanning electron microscopy of cryo-fractured, gold-coated specimens showed no surface openings up to 3 percent AC, indicating gas was effectively retained. At 5 percent, however, excessive gas evolution ruptured cells and opened escape pathways, causing cell coalescence, surface defects and a slight rebound in density—a vivid demonstration that more blowing agent is not always better.

Mechanically, the story was one of trade-offs and clever accounting. The unfoamed composite, with a flexural modulus of 2.71 GPa and flexural strength of 54.1 MPa, predictably outperformed the foams in absolute terms, since voids act as stress concentrators and reduce the load-bearing cross-section. Flexural properties fell to their lowest values at 3 percent AC (1.85 GPa and 32.90 MPa), and notched Izod impact strength dropped from 20.82 J/m for the unfoamed material to 13.33 J/m. But when properties were normalized by density, the picture reversed. Specific tensile modulus rose from 1.51 to 1.57 GPa·cm³/g, specific flexural modulus climbed from 2.04 to 2.23 GPa·cm³/g at 3 percent AC, and specific impact strength reached its maximum of 18.05 J·cm³/(m·g) at 5 percent AC. In stiffness- and strength-to-weight terms, the foams matched or beat the solid material—an essential criterion for lightweight construction.

Dynamic mechanical analysis added an unexpected bonus: superior vibration damping. All foamed composites showed tan δ values between 0.61 and 0.64, comfortably above the 0.3 threshold generally considered effective damping and approaching the 0.5 level classified as excellent, whereas the unfoamed composite managed only 0.43. The cellular architecture dissipates mechanical energy through cell-wall bending, friction at cell junctions, interfacial sliding and heterogeneous strain within the porous structure. The 3 percent AC formulation, with its maximum cell density and minimum density, delivered the greatest damping capacity. Glass transition temperatures of the foams, determined from tan δ peaks, ranged from 76.9 to 78.6 °C, slightly above the unfoamed material’s 70.8 °C, suggesting that cellular constraints subtly restrict segmental mobility of the PVC chains.

Thermal and moisture behavior rounded out the assessment. Differential scanning calorimetry confirmed the amorphous nature of the PVC matrix, with no melting peak and no change in transition pattern upon foaming, while the cling film’s plasticizer evidently acted as an internal plasticizing phase that eased foam formation. Thermogravimetry showed initial degradation temperatures declined modestly with AC content, from 240.2 °C for the unfoamed composite to 218.4 °C at 5 percent, but the major degradation temperatures remained essentially unchanged, and char residues of 26.5 to 27.9 percent matched the unfoamed value of 26.2 percent. Water absorption rose with the development of the cellular structure, peaking at 3 percent AC, yet thickness swelling after 60 days of immersion stayed between 3.88 and 7.07 percent—far below the 16.8 to 19.8 percent typical of particleboard and medium-density fiberboard after just 24 hours, thanks to the continuous polymer barrier around the wood particles.

The authors propose a three-stage deformation mechanism to explain how the foams fail under tension: an initial elastic stage in which spherical cells elongate into ellipses, a second stage of microcrack initiation at cell-wall junctions and wood–matrix interfaces, and a final stage of interfacial debonding, crack coalescence and cell collapse leading to fracture. Interestingly, at 5 percent AC, tensile and flexural properties partially recovered, apparently because over-foaming under the constrained mold caused localized densification and thicker cell walls that carried disproportionate load. The team is careful to note that a full life-cycle assessment, including recyclability and end-of-life management, remains future work. Still, the demonstration stands: three waste streams that would otherwise burden landfills can be merged into a single, foamed, dimensionally stable building material whose best formulation—3 weight percent AC—balances low density, fine uniform cells, strong density-normalized mechanics, excellent damping and good moisture resistance. It is a compelling case that the future of sustainable construction may be hiding in the demolition skip and the kitchen drawer.

Subject of Research: Upcycling mixed PVC waste streams and wood sawdust into foamed wood–plastic composites

Article Title: Toward sustainable wood–plastic composite foams fabricated via ternary blending of upcycled rigid poly(vinyl chloride) pipe, waste cling film and wood sawdust

Article References: Sukkaneewat, B., Sanetuntikul, J., Naknaen, P., Jansri, E., & Petchwattana, N. (2026). Toward sustainable wood–plastic composite foams fabricated via ternary blending of upcycled rigid poly(vinyl chloride) pipe, waste cling film and wood sawdust. Cleaner Engineering and Technology, 35, Article 101298. https://doi.org/10.1016/j.clet.2026.101298

Image Credits: AI Generated

DOI: 10.1016/j.clet.2026.101298

Keywords: wood-plastic composites, recycled PVC, cling film waste, polymer foams, chemical blowing agent, azodicarbonamide, circular economy, upcycling, wood sawdust, plasticizers, damping, sustainable building materials

The study focused on Madin-Darby Bovine Kidney cells, a widely used laboratory model of renal epithelial tissue. The choice of a bovine kidney line is not incidental. Livestock are chronically exposed to phthalates through contaminated feed, water, and environmental matrices, and renal epithelial cells represent a plausible first line of contact for circulating plasticizer metabolites. What the researchers found was a stark, concentration-dependent pattern of cellular injury that unfolded across multiple independent assays, each interrogating a different layer of genomic integrity.

The first layer was simple survival. Using the MTT assay, a colorimetric test in which metabolically active cells convert a yellow tetrazolium compound into purple formazan crystals, the team exposed MDBK cells to DBP concentrations ranging from 5 to 200 micromolar. Cell viability declined in a dose-dependent fashion, and the concentration that killed half the cells, the LC50, came out at 50 micromolar after 24 hours of exposure. That figure anchored the rest of the experimental design: the researchers selected 25, 50, and 75 micromolar as their working concentrations, spanning a range from sublethal stress to severe toxicity, to probe what happens to cells that survive a phthalate encounter.

What happens, it turns out, is a cascade of genetic damage. The alkaline comet assay, a single-cell gel electrophoresis technique that untangles DNA and allows broken strands to migrate out of the cell nucleus like the tail of a comet, revealed significant, dose-dependent increases in the DNA damage index and in the percentage of tail DNA. In parallel, the genomic instability index climbed with rising DBP concentration. These are not subtle statistical whispers; the damage signals rose consistently across the concentration range, and at the highest dose of 75 micromolar, the genotoxic response was comparable to that of the positive control group, the benchmark of maximal damage against which test chemicals are judged.

Chromosomal-level injury told the same story. In the cytokinesis-block micronucleus assay, cells are trapped at the point of division with cytochalasin B, and any chromosome fragments or whole chromosomes left behind during mitosis appear as micronuclei, tiny satellite nuclei outside the main nucleus. DBP-treated cells showed significant increases in micronucleus frequency and in the proportion of binucleated cells, alongside a rise in cytostasis, the halting of cell division. Meanwhile, the cytokinesis-block proliferation index, a measure of how many rounds of nuclear division cells manage to complete, fell as DBP concentration rose. Together, these results indicate that the chemical does not merely nick DNA; it leaves behind chromosomal debris that cells carry into division while simultaneously slowing the very process of proliferation.

Perhaps the most intriguing finding lies in the transcriptional response. Quantitative real-time PCR revealed that two DNA damage-associated genes, OGG1 and HPRT1, were both significantly upregulated in exposed cells. OGG1, which encodes a glycosylase that excises oxidized guanine bases, one of the most common lesions produced by oxidative stress, was elevated 5.33-fold. HPRT1, involved in the salvage pathway of purine nucleotide synthesis and long used as a sentinel of genotoxic stress, rose 6.57-fold. Crucially, higher DBP concentrations drove greater gene expression, suggesting a graded molecular alarm that tracks the dose of exposure.

The upregulation of repair genes is a double-edged signal. On one hand, it demonstrates that the cells recognized the damage and attempted to mount a repair response, a hallmark of activated DNA damage signaling. On the other hand, sustained elevation of repair machinery is itself an indicator of overwhelming or persistent genotoxic stress, and the concurrent rise in micronuclei and cytostasis suggests that the repair effort was not fully keeping pace with the injury. The authors interpret this coordinated pattern as evidence that DBP induces cellular stress and DNA damage while altering the expression of the genes tasked with fixing it, a combination that could erode genomic stability over time.

The broader context makes these results resonate. DBP is frequently detected not only in PVC consumer products but also in environmental matrices, meaning that humans, wildlife, and livestock encounter it continuously through ingestion, inhalation, and dermal contact. As an endocrine-disrupting chemical, it has already been implicated in reproductive and developmental toxicity, and regulatory frameworks in several jurisdictions have restricted its use in toys, cosmetics, and food-contact materials. What this study adds is mechanistic evidence from a renal epithelial model that DBP can act directly on the genome, independent of its hormonal effects, and that the damage is accompanied by transcriptional perturbation of the repair apparatus itself.

There are, of course, important caveats in translating a cell-culture experiment to whole organisms. The concentrations used here, particularly the 50 micromolar LC50, reflect acute exposure in vitro, and the actual internal doses experienced by animals or humans depend on absorption, metabolism, and excretion, processes that the cell line does not capture. MDBK cells, while a robust epithelial model, are bovine rather than human, and species differences in phthalate metabolism could shift the toxic threshold. Nonetheless, the internal consistency of the data, with cytotoxicity, comet-based strand breakage, micronucleus formation, proliferation arrest, and gene expression changes all pointing in the same direction across a coherent dose range, lends the findings considerable weight.

The authors conclude that DBP induces concentration-dependent cyto-genotoxicity and transcriptional alterations in MDBK cells, and they frame the result as an argument for developing safer plasticizer alternatives. As phthalates continue to leach from the built environment into water, food, and tissue, studies like this one sharpen the scientific case for that transition. The genetic alarm bells rung by OGG1 and HPRT1 in these kidney cells are a reminder that the cost of convenience chemistry is not always visible on the label, and that the molecules holding our plastics together may be prying apart something far more delicate inside our cells.

Subject of Research: Cyto-genotoxic effects of the plasticizer dibutyl phthalate in bovine kidney epithelial cells

Article Title: The cyto-genotoxic potential of dibutyl phthalate promotes DNA damage and cellular stress with altered DNA repair gene expression in Madin-Darby Bovine Kidney (MDBK) cells

Article References: Ali, M. M., Ullah, A., Firyal, S., Akhtar, R., Awan, F., Ataya, F. S., Mehmood, H., Raza, S., Majeed, K. A., & Fouad, D. (2026). The cyto-genotoxic potential of dibutyl phthalate promotes DNA damage and cellular stress with altered DNA repair gene expression in Madin-Darby Bovine Kidney (MDBK) cells. BMC Pharmacology and Toxicology. https://doi.org/10.1186/s40360-026-01239-4

Image Credits: AI Generated

DOI: 10.1186/s40360-026-01239-4

Keywords: dibutyl phthalate, phthalates, genotoxicity, DNA damage, MDBK cells, comet assay, micronucleus, OGG1, HPRT1, endocrine disruptors, plasticizers, genomic instability