Search Results (892)

Early life is a critical window for immune system development, during which the gut microbiome shapes innate immunity, antigen presentation, and adaptive immune maturation. Disruptions in microbial colonization—driven by factors such as cesarean delivery, antibiotic exposure, and formula feeding—deplete beneficial early-life taxa (e.g., Bifidobacterium, Bacteroides, and Enterococcus) and impair key microbial functions, including short-chain fatty acid (SCFA) production by these keystone species, alongside regulatory T cell induction. These dysbiosis patterns are associated with an increased risk of pediatric autoimmune diseases, notably type 1 diabetes, inflammatory bowel disease, celiac disease, and juvenile idiopathic arthritis. This review synthesizes current evidence on how the early-life microbiota influences immune maturation, with potential effects on the development of autoimmune diseases later in life. We specifically focus on human observational and intervention studies, where treatments with probiotics, synbiotics, vaginal microbial transfer, or maternal fecal microbiota transplantations have been shown to partially restore a disrupted microbiome. While restoration of the gut microbiome composition and function is the main reported outcome of these studies, to date, no reports have disclosed direct prevention of autoimmune disease development by targeting the early-life gut microbiome. In this regard, a better understanding of the early-life microbiome–immune axis is essential for developing targeted preventive strategies. Future research must prioritize longitudinal evaluation of autoimmune outcomes after microbiome modulation to reduce the burden of chronic immune-mediated diseases. Full article

Low social status leads to chronic social stress that predicts risk for physical and mental illness, especially when it starts early in life. To examine the longitudinal effects of low social status on the immune system, this study assessed the effects of low social status on developmental secretory patterns of pro- and anti-inflammatory markers under baseline conditions, as well as in response to an immune challenge (lipopolysaccharide (LPS)-induced activation of pro- and anti-inflammatory cytokines) in a translational rhesus monkey model of lifelong social subordination stress. Baseline blood samples were collected in 27 socially housed female rhesus monkeys (13 dominants, DOM, and 14 subordinates, SUB) during infancy (6 months), the juvenile pre-pubertal period (16 months), and adulthood (9–10 years) to examine the longitudinal effects of social status on inflammatory markers in unstimulated versus LPS-stimulated conditions mimicking exposure to bacterial infection. Basal levels of the stress hormone cortisol in blood were measured to examine associations between inflammation and activity of the hypothalamic–pituitary–adrenal (HPA) axis throughout the life span. Basal peripheral levels of inflammatory markers (e.g., IL-6) increased across development in both SUB and DOM animals with no significant differences. Basal cortisol levels were significantly higher in infancy as compared to adulthood, but no significant effects of social rank were detected. However, in adulthood, SUB animals showed a cytokine-specific immune response to ex vivo LPS stimulation with significantly higher secretions of IL-1β, IL-2, and IL-10 compared to DOM animals, whereas IL-8 response to LPS was lower in SUB animals than in DOMs. This cytokine-specific response to an immune challenge that mimics bacterial infection could reflect dysregulated immune cells that may have short-term adaptation, but at the cost of longer-term risks for low-grade chronic inflammation and accelerated immune aging for socially subordinate female macaques. Full article

Background and Objectives: Lung cancer in never-smokers (LCINS) has become a major global health concern, ranking as the fifth leading cause of cancer-related mortality. Unlike smoking-related lung cancer, LCINS arises from complex interactions between environmental carcinogens and distinct genomic alterations. This review summarizes current evidence on environmental risks, molecular features, and therapeutic progress shaping lung cancer management. Methods: A narrative review was conducted to examine risk factors for lung cancer in non-smokers. Studies reporting driver mutations in never-smokers and smokers were identified across major lung cancer histological subtypes, including small-cell lung cancer (SCLC), lung adenocarcinoma (LUAD), squamous cell carcinoma (SCC), and large-cell carcinoma (LCC). In addition, PubMed was searched for phase III trials and studies on targeted therapies related to driver mutations published between 2016 and 2025. Results: Environmental factors such as cooking oil fumes, radon, asbestos, arsenic, and fine particulate matter (PM_2.5) are strongly associated with LCINS through oxidative stress, DNA damage, and chronic inflammation. EGFR, PIK3CA, OS9, MET, and STK11 mutations are characteristic of never-smokers, in contrast to TP53 mutations, which are more common in smokers. Recent advances in targeted therapy and immunotherapy have improved survival and quality of life, emphasizing the importance of molecular profiling for treatment selection. Conclusions: LCINS represents a distinct clinical and molecular entity shaped by complex interactions between environmental exposures and genetic susceptibility. Genetic alterations promote tumor immune evasion, facilitating cancer development and progression. Continued advances in air quality control, molecular diagnostics, and precision therapies are essential for prevention, early detection, and reduction of the global disease burden. Full article

Background/Objectives: Pediatric cancer survivors frequently experience neuromuscular sequelae related to chemotherapy-induced neurotoxicity. Agents such as vincristine, methotrexate, and platinum compounds can lead to persistent gait alterations and sensorimotor deficits that impair mobility and quality of life. This study aimed to objectively assess gait in pediatric cancer survivors after the completion of oncological pharmacological treatment to identify specific spatiotemporal, kinematic, and kinetic alterations and characterize neuromechanical patterns associated with neurotoxic exposure. Methods: A cross-sectional observational study was conducted including pediatric cancer survivors (6–18 years) who had completed chemotherapy and age- and sex-matched healthy controls. Gait was analyzed using a Vicon^®3D motion capture system, with reflective markers placed on standardized anatomical landmarks. Spatiotemporal, kinematic, and kinetic variables were compared between groups using parametric tests and statistical parametric mapping (SPM) with Holm–Bonferroni correction (α = 0.05). Results: Pediatric cancer survivors showed slower gait velocity (Mean Difference (MD) = 0.17, p = 0.018, Confidence Interval CI95% = 0.04; 0.4), shorter step (MD = 0.1, p = 0.015, CI95% = 0.01; 0.19) and stride length (MD = 0.17, p = 0.018, CI95% = 0.03; 0.31), as well as reduced single support time (MD = 0.1, p = 0.043, CI95% = 0.01; 0.19), along with significant alterations in pelvic, hip, knee, and ankle kinematics compared with controls. Increased pelvic elevation (MD = 0.92, p = 0.018, CI95% = 0.25; 1.58), reduced hip extension during stance (MD = −2.99, p = 0.039, CI95% = −5.19; −0.74), knee hyperextension in mid-stance (MD = −3.84, p < 0.001, CI95% = −6.18; −0.72), and limited ankle dorsiflexion (MAS MD = −4.04, p < 0.001, CI95% = −6.79; −0.86, LAS MD = −3.16, p < 0.001) and plantarflexor moments in terminal stance (MAS MD = −149.65, p = 0.018, CI95% = −259.35; −48.25, LAS MD = −191.81, p = 0.008, CI95% = −323.81; −57.31) were observed. Ground reaction force peaks during loading response (MAS MD = −16.86, p < 0.001, CI95% = −26.12; −0.72 LAS MD = −11.74, p = 0.001, CI95% = −19.68; −3.94) and foot-off (MAS MD = 10.38, p = 0.015, CI95% = 0.41; 20.53, LAS MD = 11.88, p = 0.01, CI95% = 3.15; 22.38) were also reduced. Conclusions: Children who have completed chemotherapy present measurable gait deviations reflecting persistent neuromechanical impairment, likely linked to chemotherapy-induced neurotoxicity and deconditioning. Instrumented gait analysis allows early detection of these alterations and may support the design of targeted rehabilitation strategies to optimize functional recovery and long-term quality of life in pediatric cancer survivors. Full article

Pervasive microplastics (MPs) and per- and polyfluoroalkyl substances (PFAS) frequently co-occur across aquatic and terrestrial environments due to shared sources, transport pathways, and persistence, yet their interaction-driven effects on environmental fate, bioavailability, and toxicity remain incompletely resolved. This review critically synthesizes current knowledge on the environmental co-occurrence of MPs and PFAS, the physicochemical mechanisms governing their interactions, and the resulting ecological and toxicological consequences across aquatic, terrestrial, and biological systems. Emphasis is placed on sorption and desorption processes; environmental modifiers such as pH, salinity, dissolved organic matter (DOM), and aging; and biological responses under combined exposure scenarios. Across laboratory and field studies, MPs–PFAS co-exposure is frequently associated with altered PFAS partitioning and enhanced organismal uptake, with reported bioaccumulation increases of up to ~2.5-fold relative to PFAS-only exposures. These changes are often accompanied by amplified oxidative stress, immune dysregulation, metabolic disturbance, and reproductive impairment, particularly in aquatic invertebrates and early life stages of fish. Evidence further indicates that the magnitude and direction of combined effects depend on polymer type, particle size, surface aging, and biological context, underscoring the highly system-specific nature of MPs–PFAS interactions. By integrating findings from environmental monitoring, laboratory toxicology, and mechanistic and modeling studies, this review identifies key knowledge gaps related to nanoplastics detection, environmentally realistic exposure conditions, sorption reversibility, and mixture toxicity assessment. Collectively, these insights highlight limitations in current single-contaminant risk frameworks and underscore the importance of incorporating MPs-mediated PFAS transport and bioavailability into exposure assessment and regulatory evaluation. Full article

Lipid raft-associated gangliosides facilitate the early stages of SARS-CoV-2 entry by triggering the exposure of the receptor-binding domain (RBD) within the trimeric spike protein, which is initially sequestered. A broad range of in silico, cryoelectron microscopy and physicochemical approaches indicate that the RBD becomes accessible after a ganglioside-induced conformational rearrangement originating in the N-terminal domain (NTD) of one protomer and propagating to the neighboring RBD. We previously identified a triad of amino acids, Q134-F135-N137, as a strictly conserved element on the NTD. In the present review, we integrate a series of structural and experimental data revealing that this triad may act as a conformational transducer connected to a chain of residues that are capable of transmitting an internal conformational wave within the NTD. This wave is generated at the triad level after physical interactions with lipid raft gangliosides of the host cell membrane. It propagates inside the NTD and collides with the RBD of a neighboring protomer, triggering its unmasking. We also identify a chain of aromatic residues that are capable of controlling electron transfer through the NTD, leading us to hypothesize the existence of a dual conformational/quantum wave. In conclusion, the complete conservation of the Q134-F135-N137 triad despite six years of extensive NTD remodeling underscores its critical role in the viral life cycle. This triad represents a potential Achilles’ heel within the hyper-variable NTD, offering a stable target for therapeutic or vaccinal interventions to disrupt the conformational wave and prevent infection. These possibilities are discussed. Full article

Background: Gestational diabetes mellitus (GDM) is a frequent pregnancy pathology with poor maternal and fetal outcomes and risk of type 2 diabetes in later life. Despite known risk factors, such as obesity, age, and familial history, new data suggest that environmental exposure to agents, such as pesticides, can play a role in the etiogenesis of GDM. Objective: The epidemiologic, experimental, and mechanistic evidence between pesticide exposure and GDM risk is summarized here, and we concentrate on recent research (2000–2025). Methods: We conducted a literature search in PubMed, Embase, and the Cochrane Library for studies published from January 2000 to December 2025 using combinations of the terms “fertilizers”, “herbicides”, and “pesticides” with “diabetes mellitus” and “gestational diabetes”. After deduplication, 12 unique studies met inclusion criteria for qualitative synthesis (GDM endpoint or pregnancy glycemia with pesticide exposure). Results: Occupational and agricultural exposure to pesticides during first pregnancy was determined to be associated with a significantly increased risk of GDM through various epidemiologic studies. New studies have implicated new classes of pesticides, including pyrethroids and neonicotinoids, with higher GDM risk with first-trimester exposure. Experimental studies suggest that pesticides provide potential endocrine-disrupting chemicals that can induce insulin resistance through disruption of hormonal signaling, oxidative stress, inflammation, β-cell toxicity, and epigenetic modifications. However, significant limitations exist. Most of the evidence is observational, measurement of exposure is often indirect, and confounding factors are difficult to exclude. Notably, low dietary and residential exposure is not well studied, and dose–response relationships are undefined. Conclusions: New data indicate that pesticide exposure during early pregnancy and occupational exposure may increase the risk of GDM. Prospective cohort studies using biomonitoring, chemical mixture exposure, and geographic variation in pesticide exposure should be the focus of future research. Due to potential public health implications, preventive strategies to ensure the quality of nutrition and to reduce maternal exposure to pesticides during pregnancy are rational. Full article

The excessive and inappropriate use of the internet by children and young people increases their exposure to risky situations, especially since the COVID-19 pandemic. This study analyzes risky situations on social media among children and adolescents. The objective of this work was to identify the risks associated with the use of social media. A comparative analysis of five clustering algorithms was applied to a dataset developed by eBiz Latin America in collaboration with La Salle University of Arequipa and the Institute of Christian Schools of the De La Salle Brothers of the Bolivia-Peru district. Among the results, it was shown that children around 11 years old display a high prevalence of digital risk behaviors such as adding strangers, followed by pretending to be someone else; adults around 43 years old exhibit a tendency to follow strangers and, even more so, to take photographs without permission; adolescents with an average age of 11 show a heavy use of YouTube, TikTok, and Instagram. It is concluded that among digital risks in children and adults, the clusters highlight shared vulnerabilities, such as the addition of strangers and exposure to requests for personal data, which persist throughout the life stages but intensify in early adulthood. These findings emphasize the urgency of preventive policies addressing generational differences in social network use to promote proactive responses to digital harassment. Full article

Post-dialysis fatigue is one of the most frequent and limiting symptoms among patients undergoing hemodialysis (HD), characterized by intense physical exhaustion that may persist beyond the treatment session. Sleep disturbances frequently coexist with fatigue and may contribute to overall symptom burden. Nutritional status has been identified as a potential determinant of fatigue severity. Understanding these relationships may help identify associated factors and guide multidisciplinary interventions. Objectives: To assess the prevalence and intensity of fatigue in patients receiving HD, to describe the burden of sleep disturbances, and to analyze their association with nutritional status and various clinical, dialytic, and sociodemographic variables. Methods: A cross-sectional descriptive study was conducted between November and December 2024 in adults with chronic kidney disease undergoing maintenance HD. Fatigue and sleep disturbances were assessed using brief patient-reported outcome items adapted from PROMIS item bank concepts and analyzed as separate subscales. Nutritional status was evaluated using the Mini Nutritional Assessment–Short Form (MNA-SF). Sociodemographic, clinical, dialytic, and laboratory variables were collected. Statistical analyses were performed using SPSS v29, applying association and correlation tests (p ≤ 0.05). Results: A total of 729 patients were included (67.1% men), with a mean age of 67.7 ± 14.5 years. Clinically relevant fatigue was reported by approximately 50% of participants, with around 20% presenting severe fatigue. Sleep disturbances affected nearly 60% of patients, with severe impairment reported in approximately 30%. Regarding nutritional status, 61.9% had normal nutrition, 33.2% were at risk of malnutrition, and 4.9% were malnourished. Fatigue was significantly associated with female sex (p < 0.001), longer time on hemodialysis (p < 0.001), greater weekly dialysis exposure (p = 0.012), and poorer nutritional status (p = 0.003). The absence of residual urine output showed a borderline association with fatigue (p = 0.059) but was significantly associated with sleep disturbances (p = 0.002). Sleep disturbance scores were also significantly associated with lower levels of albumin, total proteins, and transferrin. No associations were observed between fatigue and age, BMI, comorbidity, ultrafiltration rate, or biochemical parameters. Conclusions: Fatigue is a highly prevalent and clinically relevant symptom in patients undergoing HD and is closely associated with nutritional status and dialysis-related factors. Sleep disturbances are also highly prevalent and may act as an important modulating factor, potentially amplifying fatigue, particularly in patients with greater biological vulnerability or loss of residual kidney function. The systematic use of patient-reported outcome measures (PROMs) to assess fatigue and sleep, together with nutritional evaluation, may facilitate the early identification of vulnerable patients and guide targeted strategies to reduce symptom burden and improve quality of life. Full article

Background/Objectives: Gestational exposure to a high-fat diet (HFD) reprograms hypothalamic orexigenic circuits prenatally. However, whether astrocytes, critical modulators of this system, are also imprinted by HFD in the fetal brain remains unknown. We investigated the impact of HFD on the prenatal neuroglial architecture of the lateral hypothalamic area (LHA). Methods: Female Wistar rats were fed a control or a 60% fat diet for 12 weeks. Upon reaching obesity (Lee index ≥ 310), dams were mated. Fetuses were harvested via cesarean section at term, and their brains were processed for immunohistochemistry and morphometry to assess cell proliferation, orexin neuron density, and astrocytic reactivity in the LHA. Results: HFD significantly increased cell proliferation and orexinergic neuron density, and induced early signs of astrocyte reactivity in the fetal LHA. These findings reveal that both neuronal and glial components of the LHA orexigenic axis are structurally reprogrammed before birth. Conclusions: This study provides the first evidence that HFD simultaneously alters neuronal and glial developmental trajectories in the fetal hypothalamus. The concurrent programming of astrocytes and orexigenic neurons suggests a prenatal origin for neuroinflammatory susceptibility, reframing obesity as a neurodevelopmental disorder shaped by early life nutritional environments. Full article

Atopic eczema and asthma frequently co-occur, forming a distinct complex phenotype that likely arises from shared genetic pathways and early-life environmental influences. We aimed to investigate whether variants in TNS1 and NRXN1—previously identified in a genome-wide interaction study—influence susceptibility to atopic eczema and the asthma–eczema phenotype and whether early-life environmental tobacco smoke (ETS) exposure modifies these genetic effects. A total of 188 Caucasian children under 2 years at recruitment were prospectively followed up to 6 years of age. Eligibility of all participants for the study or control group was based on a questionnaire and a physician-confirmed diagnosis of eczema and asthma. Early-life ETS exposure was assessed by parental questionnaire. All participants were genotyped for TNS1 and NRXN1 SNPs. The TNS1 rs918949 [T] allele was associated with the combined asthma–eczema phenotype but not with eczema alone. Synergistic gene–environment interactions were identified for both TNS1 and NRXN1, with the highest risk of the combined asthma–eczema phenotype observed among ETS-exposed carriers of risk alleles. Our findings provide the first independent replication of evidence suggesting that TNS1 and NRXN1 may contribute to the asthma–eczema comorbidity through mechanisms that could be substantially modified by early-life ETS exposure. Full article

Background/Objectives: The renin–angiotensin–aldosterone system (RAAS) is pivotal for neonatal circulation and renal adaptation; however, postnatal changes in serum renin and aldosterone immediately after birth remain unclear. This study aimed to establish postnatal changes in these hormones at birth and over the first week of life. Methods: We retrospectively analyzed 374 neonates admitted to Kobe University Hospital between October 2020 and September 2023, with serum renin and aldosterone measured on days 0 and 5 of life. Exclusion criteria were multiple congenital anomalies, severe asphyxia, major peripartum hemorrhage, and in utero exposure to angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers. Hormone levels were compared between term and preterm infants, and correlations with gestational age were assessed. Results: Serum renin concentrations were higher on day 0 than on day 5 (median 99.9 pg/mL [2.6–773.3] vs. 19.9 pg/mL [0.6–2304], p < 0.0001), and aldosterone concentrations similarly decreased (714 pg/mL [6.9–6334] vs. 551 pg/mL [0–11,930], p < 0.0001). At birth, renin and aldosterone levels did not differ significantly between groups. By day 5, both renin (32.8 pg/mL [0.6–2304] vs. 14.5 pg/mL [0.6–208]) and aldosterone (689 pg/mL [4–11,930] vs. 471 pg/mL [13–4697]) concentrations were significantly higher in preterm than in term neonates (p < 0.0001). Conclusions: This study describes early postnatal changes in renin and aldosterone, with higher concentrations at birth than on day 5 and persistently elevated levels in preterm infants. These findings indicate increased RAAS activity in preterm neonates and suggest a greater vulnerability to fluid, electrolyte, and blood pressure instability during early life. Full article

Background/Objectives: Food protein-induced allergic proctocolitis (FPIAP) is a non-IgE-mediated gastrointestinal food allergy. Although tolerance to the culprit food is usually achieved within the first year of life, late acquisition occurs and remains poorly predictable. This study aimed to analyze clinical characteristics and explore factors that may potentially function as predictors of late tolerance acquisition to cow’s milk (CM). Methods: We conducted a cross-sectional study at two Italian pediatric clinics (2020–2024), including infants diagnosed with FPIAP. Clinical, dietary, and immunological variables; onset and duration of rectal bleeding (visible blood in the stools); and time to CM tolerance were analyzed. Late tolerance was defined as acquisition after 19 months according to the distribution of tolerance achievement in our population. Statistical analyses included χ², Mann–Whitney U, Spearman’s correlation, and logistic regression. Results: Ninety-four infants were included (median age at onset 2.9 months [IQR 1.9–4.7]); 58 (62%) were exclusively breastfed and 18 (19%) were born preterm (<37 completed weeks of gestation). CM was the culprit food in all cases; tolerance was achieved in all infants at a median age of 12 months. Family history of atopy and atopic dermatitis were reported in 44% and 19% of infants, respectively. Late CM tolerance was associated with preterm birth, fortification of human milk, early antibiotic exposure, growth faltering, and recurrent infections. Logistic regression identified family history of atopy (OR 5.4 [95% CI 1.2–25.4]; p = 0.031), atopic dermatitis (OR 8.2 [1.7–40.7]; p = 0.010), rectal bleeding >18 days before elimination diet (OR 5.9 [1.3–27.7]; p = 0.023), and IgE sensitization (OR 6.4 [1.2–35.0]; p = 0.034) as factors that may potentially function as predictors of late tolerance acquisition to CM. Conclusions: Identification of factors that may potentially function as predictors of late tolerance acquisition to CM in infants with FPIAP may help providing a personalized clinical management for these patients. Full article

Microplastics represent an emerging threat to aquatic environments and organisms, as they infiltrate water systems, are ingested by marine species, and cause physical harm, endocrine disruption, and bioaccumulation up the food chain, potentially impacting biodiversity and human health. Aquatic ecosystems face considerable harm from microplastic pollution because fish in the early developmental stages, including embryos, larvae, and juveniles, are more susceptible due to their immature physiological and detoxification systems. This review aims to comprehensively explore the impacts of microplastics on the early life stages of fish. Aquatic environments receive primary and secondary MPs from urban runoff and industrial waste, together with degraded plastics, which affect fish embryos and larvae via direct ingestion, surface adhesion, and trophic transmission pathways. The physical impact of MPs causes digestive tract blockages that reduce hatching success and create developmental problems in fish organs, but chemical toxicity develops from plasticizers, heavy metal leaching, and pollutant adsorption, which causes oxidative stress, endocrine disruption, and metabolic dysfunction. Survival rates decrease because exposure causes fish to perform poorly during swimming activities and make limited efforts to avoid predators. The small dimensions and high chemical reactivity of MPs increase their bioavailability, which promotes tissue penetration and leads to accumulation at different levels of the food chain. This comprehensive review emphasizes that we need to establish uniform detection protocols, long-term exposure research, and effective strategies to control MP pollution. The resolution of these difficulties remains essential for protecting fish populations, as well as for protecting biodiversity and minimizing seafood contamination risks to human health. Full article

This study investigates chlorine-induced aging of high-density polyethylene (HDPE) through a 3 × 3 factorial matrix combining three temperatures (20, 40, 60 °C) and three chlorine concentrations (5, 10, 20 ppm) over 45 days. Tensile tests revealed progressive embrittlement, with elongation at break decreasing sharply under severe aging; samples exposed to 60 °C and 20 ppm exhibited premature brittle failure despite peak stresses remaining near ~22 MPa. XRD results showed a reduction in crystallinity from 67.07% (reference) to 61.06–61.31% under the most aggressive conditions, accompanied by a decrease in crystallite size from 5.60 nm to 2.10–2.50 nm. FTIR analysis confirmed oxidation through increased carbonyl absorption at 1716 cm⁻¹ and new bands at 1608–1635 cm⁻¹. TGA revealed substantial thermal deterioration, with T5% falling from 450 °C (reference) to 327 °C at 60 °C/20 ppm, along with an additional degradation peak at 398 °C. DSC showed a melting temperature decrease from 136.32 °C to 131.67 °C and an increase in crystallinity from 41.07% (unexposed sample) to 59.19% (60 °C/20 ppm). Statistical analysis of the results established that degradation is governed by different dominant factors depending on the measured property: Chlorine concentration was found to be the dominant factor for XRD crystallinity and thermal decomposition T5%, confirming that surface structural damage and early molecular weight loss are driven primarily by chlorine-induced oxidation. Conversely, DSC crystallinity was governed primarily by temperature, reflecting thermally driven molecular reorganization within the bulk material. Overall, chlorine exposure, amplified by temperature, accelerates chemical oxidation, structural degradation, and mechanical embrittlement, reducing the long-term reliability of HDPE in chlorinated water systems. The findings provide critical data for predicting the service life and informing material selection for HDPE components used in high-temperature or high-chlorine water distribution systems. Full article