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4-Aminodiphenylamine (4-ADPA) is a common additive in rubber tires, known for its antioxidant properties. It plays a crucial role in enhancing tire durability by preventing issues such as drying, cracking, and degradation from prolonged exposure to environmental factors like heat, oxygen, and ozone. However, despite its advantages in extending tire lifespan, the use of 4-ADPA raises significant environmental concerns. As tires wear down, microscopic tire wear particles (TWPs) containing 4-ADPA are released into the environment with substantial leaching, contaminating the waterways. The 4-ADPA leachates pollute and pose a threat to aquatic ecosystems, affecting various forms of marine life. The current study investigates the ecotoxicological effects of 4-ADPA on the aquatic plant Lemna minor (L. minor), focusing on its impact on relative growth and physiological biomarkers. Several parameters were assessed to evaluate ecotoxicity, including frond morphology, fresh biomass, total frond number, chlorophyll content, and starch accumulation. L. minor was grown for 7 and 14 days under controlled laboratory conditions using Hoagland media with varying concentrations of 4-ADPA (10–100 μg/L), while a control group was maintained in media without 4-ADPA. The results indicate that exposure to 4-ADPA led to a dose-dependent reduction in fresh biomass, total frond number, and chlorophyll levels. Lugol’s staining revealed increased starch accumulation in the fronds after exposure to 4-ADPA. The biological effects observed in L. minor following exposure to 4-ADPA, even at environmentally relevant concentrations, demonstrate a significant ecotoxicological impact on aquatic ecosystems. Further research involving additional species and investigating the mechanisms behind 4-ADPA toxicity is recommended to better understand its long-term consequences. 

In utero exposure to per- and polyfluoroalkyl substances (PFAS) presents significant health concerns, primarily through their role in inducing epigenetic modifications that have lasting consequences. This review aims to elucidate the impact of prenatal PFAS exposure on epigenetic mechanisms, including DNA methylation, histone modification, and non-coding RNA regulation, focusing on developmental and long-term health outcomes. The review synthesizes findings from various studies that link PFAS exposure to alterations in DNA methylation in fetal tissues, such as changes in the methylation of genes like IGF2 and MEST, which are linked to disruptions in growth, neurodevelopment, immune function, and metabolic regulation, potentially increasing the risk of diseases such as diabetes and obesity. We also highlight the compound-specific effects of different PFAS, such as PFOS and PFOA, each showing unique impacts on epigenetic profiles, suggesting varied health risks. Special attention is given to hormonal disruption, oxidative stress, and changes in histone-modifying enzymes such as histone acetyltransferases (HATs) and deacetylases (HDACs), which are pathways through which PFAS influence fetal development. Additionally, we discuss PFAS-induced epigenetic changes in placental tissues, which can alter fetal nutrient supply and hormone regulation. Despite accumulating evidence, significant knowledge gaps remain, particularly regarding the persistence of these changes across the lifespan and potential sex-specific susceptibilities. We explore how advancements in epigenome-wide association studies could bridge these gaps, providing a robust framework for linking prenatal environmental exposures to lifetime health outcomes. Future research directions and regulatory strategies are also discussed, emphasizing the need for intervention to protect vulnerable populations from these environmental pollutants. 

The pervasive presence of per- and polyfluoroalkyl substances (PFAS) in the environment and their persistent nature raise significant concerns regarding their impact on human health. This review delves into the obesogenic potential of PFAS, shedding light on their mechanisms of action, epidemiological correlations with obesity and metabolic disorders, and the challenges faced in regulatory frameworks. PFAS, characterized by their carbon-fluorine chains, are ubiquitous in various consumer products, leading to widespread exposure through ingestion of contaminated food and water. Emerging evidence suggests that PFAS may act as endocrine-disrupting chemicals, interfering with lipid metabolism and hormone functions related to obesity. We examine in vitro, in vivo, human, and in silico studies that explore the interaction of PFAS with PPARs and other molecular targets, influencing adipogenesis and lipid homeostasis. Furthermore, the review highlights epidemiological studies investigating the association between maternal PFAS exposure and the risk of obesity in offspring, presenting mixed and inconclusive findings that underscore the complexity of PFAS effects on human health. Presently, there are major challenges in studying PFAS toxicity, including their chemical diversity and the limitations of current regulatory guidelines, potential remediation, and detoxification. This review emphasizes the need for a multidisciplinary approach, combining advanced analytical methods, in silico models, and comprehensive epidemiological studies, to unravel the obesogenic effects of PFAS and inform effective public health strategies.