The setting is Ronneby, a municipality of roughly 28,000 inhabitants in southern Sweden. For decades, aqueous film-forming foam, or AFFF, used in firefighting training at a nearby military airbase seeped into the groundwater that fed one of the town’s two water treatment plants. When the contamination was finally discovered in 2013, total PFAS concentrations in the water exceeded 10,000 nanograms per liter, dominated by perfluorooctane sulfonic acid (PFOS) and perfluorohexane sulfonic acid (PFHxS), with perfluorooctanoic acid (PFOA) also present. Retrospective analyses of archived newborn blood spots suggest the exposure began as early as 1985 and climbed steadily until around 2005 to 2007. The contaminated supply was shut off on December 16, 2013, but by then, some residents carried serum PFAS concentrations up to a hundred times higher than those seen in the general Swedish population.

That unusual exposure gradient is precisely what made Ronneby valuable to researchers. Most previous studies of PFAS and reproductive hormones have been conducted in populations with only background exposure, and their findings have been inconsistent. Regulatory bodies, including the European Food Safety Authority and the US National Academies of Sciences, have judged the evidence linking PFAS to reproductive hormone alterations insufficient. By studying children whose bodies span a range of exposures from background levels to extreme contamination, the Swedish team could probe exposure-response relationships that background-level studies simply cannot resolve.

The researchers drew on biobanked serum samples collected between 2014 and 2016 from participants in the Ronneby PFAS Biomarker Cohort, aged 5 to 20 years. The final study group comprised 87 girls and 84 boys aged 5 to 11, and 117 boys aged 12 to 20; girls aged 12 and older were excluded because menstrual cyclicity and contraceptive use would have introduced unmanageable variability. About 23 percent of participants came from nearby Karlshamn, where drinking water PFAS levels were below 5 nanograms per liter, providing a reference group. Serum concentrations of PFOS, PFHxS, and PFOA were measured by liquid chromatography-tandem mass spectrometry, and the sum of these three compounds served as the primary exposure measure. Hormones, including follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, sex hormone-binding globulin (SHBG), and total testosterone, were quantified with electrochemiluminescence immunoassays at an accredited clinical laboratory.

The exposure levels were striking. Among the younger children from Ronneby, median combined serum concentrations of the three PFAS exceeded 90 nanograms per milliliter, and among adolescent boys the median reached 173 nanograms per milliliter, with some individuals above 600. For context, the European Food Safety Authority considers a serum level of about 6 nanograms per milliliter to be the threshold below which the tolerable weekly intake of PFAS is assumed to be maintained. PFOS and PFHxS were strongly correlated with one another, reflecting their shared source in the contaminated water, and roughly one quarter of participants were classified as prenatally exposed based on residential records from the year of their birth.

The hormone findings split cleanly along developmental lines. Among children aged 5 to 11, higher PFAS concentrations were associated with elevated prolactin in both sexes, an association that held in the continuous models for girls and boys alike. Boys in this younger group also showed lower FSH as exposure increased, while boys in the medium exposure category had higher SHBG. When the researchers formally tested for sex differences, however, the interaction terms were not statistically significant, meaning they could not conclude that boys and girls responded differently. Among adolescent boys aged 12 to 20, the pattern shifted: higher PFAS levels were associated with lower LH, lower total testosterone, and a lower free androgen index, a calculated measure of bioavailable testosterone that combines testosterone and SHBG. In the categorical analysis, the reduction in LH was most evident in the medium-high exposure group, while testosterone and the androgen index declined across the higher exposure categories.

These results align closely with findings from other highly exposed populations. In the C8 Health Project in the Mid-Ohio Valley, where drinking water was contaminated by PFAS production facilities, higher PFOA and PFOS concentrations were linked to delayed puberty and lower testosterone in both boys and girls. More recently, adolescents living near a 3M chemical plant in Belgium showed similar patterns, with higher PFHxS and PFOA associated with lower LH and testosterone and higher SHBG in teenage boys. The convergence of evidence across three independent contamination hotspots on two continents strengthens the case that the associations are not statistical artifacts, though the observational design still cannot prove causation.

The prolactin finding is particularly intriguing because it is comparatively rare in the PFAS literature. Positive relationships between fluorochemical exposure and prolactin were reported in occupational studies in the 1990s, but few modern studies have examined the question. Prolactin is best known for its role in lactation, but it also feeds back on the hypothalamic-pituitary-gonadal axis, and pathological hyperprolactinemia in adults can suppress gonadotropin release and reduce sex steroid production. The Ronneby team is careful to note that their data do not demonstrate a prolactin-mediated suppression of the hormonal axis, since prolactin was elevated in young children but not in adolescent boys, in whom LH and testosterone were instead reduced. The hormone-specific associations may reflect other mechanisms or differing susceptibility across developmental stages, and experimental studies suggest PFAS may impair testosterone production by disrupting steroidogenesis in the Leydig cells of the testes, though exact mechanisms remain uncertain.

The study has limitations worth weighing. Blood samples were drawn at varying times of day, and hormones such as testosterone and LH follow circadian rhythms that peak in the early morning, introducing variability that likely attenuated the observed effect estimates rather than creating spurious ones. Immunoassay-based sex steroid measurements are less sensitive than mass spectrometry, particularly at the low concentrations typical of children, and most estradiol values fell below the laboratory’s reporting limit and could not be analyzed. The researchers also could not disentangle prenatal from postnatal exposure, because the contamination was already pervasive by the mid-1980s and the two exposure routes are highly correlated in this cohort. Sensitivity analyses adjusting for body mass index produced similar estimates for most hormones.

The clinical significance of the hormonal differences remains uncertain. Testosterone concentrations in the exposed adolescents were still within age-appropriate reference ranges, and pediatric reference intervals for prolactin are lacking, making interpretation difficult. What the study does establish is that real-world, AFFF-driven PFAS contamination, the same scenario now unfolding around airports, military bases, and industrial sites worldwide, is associated with detectable alterations in the hormonal regulation of children at multiple levels of the endocrine system. With legacy PFAS persisting in the environment despite regulatory restrictions and being replaced by newer compounds whose health effects are poorly characterized, the researchers call for longitudinal follow-up of highly exposed populations, more sensitive hormone measurement methods, and standardized sampling to determine whether these early hormonal shifts translate into delayed puberty or long-term reproductive consequences.

Subject of Research: Associations between serum PFAS concentrations and reproductive hormone levels in highly exposed children and adolescents

Article Title: Serum PFAS Concentrations and Reproductive Hormones in Highly Exposed Children and Adolescents

Article References: Hammarstrand, S., Andersson, E., Colldén, H., Lindh, C., Nielsen, C., Jakobsson, K., & Andersson, E. M. (2026). Serum PFAS Concentrations and Reproductive Hormones in Highly Exposed Children and Adolescents. Environmental Advances, Article 100764. https://doi.org/10.1016/j.envadv.2026.100764

Image Credits: AI Generated

DOI: 10.1016/j.envadv.2026.100764

Keywords: PFAS, endocrine disruption, puberty, reproductive hormones, testosterone, prolactin, drinking water contamination, firefighting foam, Ronneby, children's health, HPG axis, environmental epidemiology

The scale of the problem the program addresses is considerable. According to the Australian Institute of Health and Welfare data cited by the research team, only one in four Australian children currently achieve the recommended amount of moderate-to-vigorous physical activity, and only one in three meet screen time guidelines. These shortfalls matter because regular vigorous movement in childhood is linked to healthier cardiovascular and metabolic profiles, better bone development, improved mental wellbeing and stronger academic engagement. Conversely, excessive recreational screen time is associated with poorer sleep, higher sedentary behaviour and reduced opportunities for social and motor skill development. With so few children meeting national recommendations, researchers have increasingly looked beyond the traditional targets of school physical education and family routines toward the environments where children actually spend their time.

Outside school hours care represents one of the largest of those environments. Professor Carol Maher of Adelaide University’s School of Allied Health and Human Performance, the study’s lead researcher, noted that more than 500,000 Australian children spend time in OSHC every week, creating what she described as a real opportunity for children to be more active. Earlier work by her team had revealed enormous variation between services in how active children were during care, with children spending around 60 percent of their time in after-school care inactive. That variation was itself a clue: if some services managed to keep children moving while others did not, then the difference likely lay in modifiable factors such as staff behaviour, the activities on offer and the policies governing the service, rather than in the children themselves.

Activated OSHC was designed around precisely that insight. The program is an evidence-based initiative codesigned by Adelaide University together with the OSHC sector, in collaboration with government and child health experts. Rather than placing responsibility entirely on children and parents, it targets the environment surrounding the child: how staff are trained, what activities are available and what policies the service has in place. Delivered as self-paced online training leading to formal accreditation, the program provides practical tips for creating an active environment, concrete strategies for reducing screen time, and techniques for encouraging participation from all children regardless of age or ability. A central component helps each service develop a physical activity and screen time policy aligned with the Australian guidelines for outside school hours care, embedding healthy practice into institutional structure rather than leaving it to individual staff initiative.

The trial involved almost 200 OSHC services collectively caring for approximately 10,000 children across Australia, making it one of the largest evaluations of its kind in this setting. The results among services that completed the full program were striking. Those services had more than seven times the odds of meeting recommended physical activity and screen time targets before and after school compared with services that had not completed accreditation. Children attending accredited services showed significantly greater increases, of 23 percent, in moderate-to-vigorous physical activity during before-school care. Staff at these services were three times as likely to demonstrate behaviours that actively promote physical activity, indicating that the program changed adult practice as well as child outcomes.

From a technical standpoint, these effect sizes are notable for a relatively light-touch, scalable intervention. Online, self-paced training can be disseminated nationally at low marginal cost, and the accreditation model gives services a clear benchmark aligned with existing Australian guidelines. The finding that before-school care showed measurable gains in moderate-to-vigorous activity is particularly interesting, since morning sessions are shorter and often dominated by quiet supervision, yet they appear highly amenable to change when staff are equipped with appropriate strategies. The tripling of positive staff behaviours suggests a mechanism: trained educators model and prompt activity more consistently, and children respond to the environment they are offered. In intervention science, this pattern of environmental change preceding behavioural change in children is exactly what theory would predict.

However, the study also delivers a sobering counterpoint about implementation. While 80 percent of intervention services registered for the program, fewer than half completed all the training and policy requirements needed for accreditation. Across all intervention services, including those that did not finish, there was no significant improvement in overall guideline adherence or in children’s physical activity. In other words, simply making a program available was not enough to shift outcomes. This null result for the intervention-as-offered is arguably as important as the positive results for completers, because it quantifies the gap between reach and effectiveness. Busy OSHC services juggle staffing constraints, variable educator qualifications and demanding operational schedules, and accreditation demands sustained effort across training modules and policy development.

Professor Maher framed this contrast as one of the biggest challenges facing health programs generally: turning good intentions into lasting change. She emphasised that making a program available is only part of the solution, and that services need time and practical support to put changes into practice and sustain them. Yet she also pointed to the promise in the completers’ results, noting that although fewer than half of the services finished accreditation, those that did showed meaningful improvements in staff practices, their environment and children’s activity. The challenge now, she said, is helping more services get there. This reframing of the problem, from designing an effective intervention to designing effective implementation support, reflects a broader shift in implementation science toward studying how evidence-based programs are adopted, adapted and maintained in real-world conditions.

The research team’s next steps follow directly from that logic. Future work will explore different ways of helping more services successfully implement the program, including additional implementation support and peer learning approaches, in which services that have completed accreditation mentor those still working through it. The team also plans to investigate whether the program can be successfully replicated internationally, a question with significant implications given that outside school hours care and similar before- and after-school models exist in many countries facing the same childhood inactivity trends. If the Australian results translate, the OSHC setting could become a globally relevant lever for population-level physical activity promotion.

The study was funded by the Australian Government’s Medical Research Future Fund and the National Health and Medical Research Council, and the authors reported no conflicts of interest. Its publication in JAMA Network Open places a rigorous evaluation of a practical, policy-aligned intervention before an international clinical and public health audience. For parents, educators and policymakers, the central message is twofold. The hours around the school day, long treated as logistical filler, are a genuine opportunity to close the gap between the one in four children who move enough and the national guidelines designed for all of them. And closing that gap depends less on exhorting individual children to be active than on training staff, shaping environments and embedding policies that make movement the easy, default choice in the places children already are.

Subject of Research: Evaluating an online training and accreditation program to increase physical activity and reduce screen time in Australian outside school hours care services

Article Title: Keeping kids moving beyond the school bell

Article References: Keeping kids moving beyond the school bell. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: physical activity, outside school hours care, children's health, screen time, Activated OSHC, Adelaide University, JAMA Network Open, implementation science, accreditation, public health, Australia, childhood obesity prevention

Chavez is also a member of the NCI-Designated Cancer Center and the Center for Data Science and Artificial Intelligence at Sanford Burnham Prebys, positions that place him at the intersection of cancer biology and computational science. He was named a recipient in the Children’s Health Innovation Award category, which recognizes highly innovative, mission-critical projects that accelerate children’s health innovation using advanced cloud services. Beyond the funding and computing credits, the award includes implementation support from technical specialists, a component that can prove decisive when translating a research prototype into a system that clinicians can actually rely on at the bedside. Proposals were evaluated on several criteria, including the innovative and unique nature of the project, its impact on mission-critical goals, and the presence of clearly defined outcomes and milestones.

The award arrives at a moment when the volume of data generated for a single pediatric cancer patient has grown far beyond what any individual clinician can synthesize. Modern molecular diagnostics can sequence a child’s tumor, profile its epigenetic landscape, measure gene expression, and test drug responses in laboratory models, all alongside conventional clinical records, imaging reports, and treatment histories. Each of these data streams carries clues about what might work for that specific child, but the information typically lives in separate systems, uses different technical vocabularies, and demands different kinds of expertise to interpret. Molecular tumor boards, the multidisciplinary committees that convene to weigh this evidence, do remarkable work, yet assembling and reviewing the full picture can take time that children with aggressive cancers may not have.

Chavez and his team plan to address this bottleneck with a system called Leitstern, a German word for a star that provides orientation. The name captures the project’s ambition: rather than replacing clinical judgment, the system is intended to serve as a guiding reference point amid a sea of data. Leitstern will bring together molecular, clinical, and functional data from individual patients and connect that information with knowledge drawn from scientific literature, drug databases, and clinical trial registries. In practice, this means the system could link a specific mutation found in a child’s tumor to published studies of targeted drugs, to records of how similar tumors have responded, and to open clinical trials that might be appropriate to consider.

What distinguishes the technical approach is its use of specialized AI agents, software components designed to analyze different types of data and generate evidence-based treatment hypotheses for clinicians to review. This agent-based architecture reflects a broader shift in applied artificial intelligence, away from a single monolithic model and toward coordinated systems in which each component handles the data type it is best suited to interpret. One agent may focus on genomic alterations, another on functional screening results, another on matching findings to trial eligibility criteria. Their outputs converge into treatment hypotheses that remain, crucially, advisory: the final decisions rest with the clinicians who review them.

Transparency and privacy are built into the design from the start. Patient data will be de-identified before it enters the system, and Leitstern is being engineered so that every recommendation can be traced back to its underlying sources. In a clinical domain where a single suggestion can alter the course of a child’s treatment, this kind of traceability is not a luxury but a requirement. Clinicians need to see not only what the system proposes but why, which evidence supports the proposal, and how strong that evidence is. By making the chain of reasoning inspectable, the team aims to build the trust that any clinical decision-support tool must earn before it can change practice.

The project also comes with unusually concrete evaluation goals, developed by Chavez together with graduate student Christopher Brown. The team will compare the system’s recommendations with decisions previously made by molecular tumor boards, providing a direct benchmark against expert human judgment. They will assess the reproducibility of its results, an essential quality for any tool intended for clinical settings, and measure how quickly it can produce reports, with a target of completing analyses in less than 24 hours. The team further aims for 100 percent traceability of the system’s predictions back to their supporting evidence. Eventually, the researchers plan to test the system prospectively, analyzing new cases before they are reviewed by a tumor board and then comparing the system’s findings with the board’s recommendations, a study design that offers a rigorous, real-time test of the technology’s value.

For Chavez, the motivation is fundamentally about time. Children with cancer can generate an enormous amount of complex clinical, molecular, and functional data, and the goal, he explained, is to bring that information together in a way that helps clinicians identify potential treatment options more quickly. For children with aggressive cancers, he noted, time is critical, and reducing delays in identifying treatment options can make a meaningful difference. With Leitstern, the team wants to use AI to help make sense of that complexity while ensuring that every recommendation can be traced back to the evidence that supports it. That framing, acceleration without sacrificing accountability, captures the central tension in bringing artificial intelligence into clinical medicine.

The recognition also reflects a deliberate strategy by AWS to direct cloud resources toward pediatric health. By focusing on children’s health, the company seeks to bring more attention to the wide variety of causes and care organizations dedicated to helping children live longer, healthier lives through the strategic use of cloud technology. Rick Buettner, Global Director of Nonprofits at AWS, said that this year’s Children’s Health Innovation Award recipients are doing extraordinary work to improve the lives of children, from the everyday moments to the life-changing ones. He pointed to projects ranging from using cloud technology to improve bus routes for special needs students to leveraging AI to answer pediatric health questions without subjecting minors to lengthy clinical studies, describing these organizations as reimagining what is possible for children and saying AWS is honored to support nonprofits whose work is creating lasting, meaningful change.

The Imagine Grant program, launched in 2018, has since awarded more than 21 million dollars in unrestricted funding, AWS cloud computing credits, and technical expertise to more than 170 nonprofit organizations worldwide. For Sanford Burnham Prebys, an independent not-for-profit biomedical research institute whose research spans six centers, including its NCI-designated Cancer Center, with expertise in cardiovascular, neurologic, and metabolic diseases, data science and artificial intelligence, and therapeutic discovery, the award extends an existing strength in computational biology into one of its most consequential applications. If Leitstern meets its milestones, delivering reproducible, fully traceable treatment hypotheses in under a day, the project could offer a template for how cloud-based AI systems support precision oncology for children, where the stakes are highest and every hour of delay matters.

Subject of Research: AI-powered clinical decision support for personalized pediatric cancer treatment

Article Title: Lukas Chavez from Sanford Burnham Prebys named recipient of 2026 AWS Children’s Health Innovation Award

Article References: Lukas Chavez from Sanford Burnham Prebys named recipient of 2026 AWS Children’s Health Innovation Award. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: pediatric cancer, artificial intelligence, precision oncology, AWS Imagine Grant, Sanford Burnham Prebys, molecular tumor boards, cloud computing, clinical decision support, Lukas Chavez, Leitstern, data science, children's health

The Academy did not stop at advising families to avoid raw dairy. It renewed its call for a ban on the sale and distribution of raw milk and raw milk products, including raw cheeses, arguing that their consumption increases the risk of life-threatening infections. The policy statement also directly confronts one of the most persistent marketing claims surrounding raw milk: that it offers superior health benefits compared with pasteurized products. According to the Academy, those claims are not supported by scientific evidence. Pasteurization, a process of heating and then cooling milk that has been in use for more than a century, dramatically reduces the risk of infection without stripping away the nutritional value that families rely on from dairy.

The numbers behind the Academy’s concern are striking. Lead author Adam J. Ratner, MD, MPH, FAAP, noted that nearly half of illnesses caused by raw dairy consumption occur in people under the age of 20, and that a significant share of those cases are in children under 5. These illnesses, he emphasized, can be severe and can lead to life-threatening complications. The vulnerability of young children is not incidental: their immune systems are still developing, their body weight is small relative to the dose of pathogen they may ingest, and complications such as severe dehydration from diarrheal illness or kidney failure from certain strains of E. coli can escalate quickly in pediatric patients.

Unpasteurized milk is a well-documented carrier of some of the most dangerous foodborne pathogens known to medicine. The policy statement lists Listeria, E. coli, Salmonella, Campylobacter, and Brucella among the serious organisms transmitted through raw dairy. Each of these bacteria can cause hospitalization, life-threatening illness, miscarriage, or death, and the risks are concentrated in young children, pregnant people, and individuals with weakened immune systems. Listeria monocytogenes is particularly formidable because it can grow even at refrigerator temperatures, meaning contaminated dairy stored properly in a home kitchen can still become more dangerous over time. Salmonella and Campylobacter are among the most common causes of bacterial gastroenteritis worldwide, while Shiga toxin-producing E. coli can trigger hemolytic uremic syndrome, a condition that destroys red blood cells and can cause kidney failure in children.

Pregnant people face especially high stakes from foodborne infection. The policy statement notes that the incidence of listeriosis is estimated to be 12 to 14 times higher during pregnancy than in the general population, a reflection of the immune changes that pregnancy induces. Listeria infection during pregnancy can result in miscarriage, stillbirth, premature delivery, or severe illness in newborns, outcomes that make even a low probability of contamination unacceptable from a public health standpoint. Because Listeria can cross the placenta, a mother may experience mild or even unnoticed symptoms while the fetus suffers devastating consequences. This asymmetry between maternal illness and fetal harm is a central reason obstetric and pediatric guidelines consistently single out unpasteurized dairy as a food to avoid entirely during pregnancy.

The most consequential update in the new statement concerns H5N1, the highly pathogenic avian influenza virus that has swept through poultry populations globally and, beginning with the 2024 United States dairy cattle outbreak, demonstrated an ability to infect cows. The Academy highlights emerging evidence that H5N1 may represent a new and potentially serious risk associated with raw milk. Research indicates the virus can be transmitted from infected dairy cattle into milk, where it can reach high concentrations and remain detectable in refrigerated raw milk for up to five weeks. That persistence is unusual and troubling: a virus surviving for more than a month in a chilled, nutrient-rich medium has ample opportunity to reach consumers, especially in distribution chains that lack pathogen testing.

During the 2024 U.S. dairy outbreak, infectious H5N1 virus was detected in nearly one-quarter of raw milk samples in affected areas. To date, there are no confirmed human cases of H5N1 infection resulting from the consumption of raw milk, and the Academy is careful to state this. Nevertheless, it characterizes the virus as a credible, emerging threat. The distinction between documented transmission and credible risk is important in virology: influenza viruses are capable of crossing species barriers, and the mammary gland infections observed in dairy cattle established a novel route by which a respiratory pathogen of birds could contaminate a staple food. Pasteurization, which inactivates influenza viruses effectively, closes that route for conventional dairy, but no such barrier exists for raw products.

The regulatory landscape in the United States remains fragmented. Despite the well-documented health risks, the sale and distribution of raw milk products remain legal in at least 27 states. Raw milk is defined as milk obtained from cows, goats, or sheep that has not undergone pasteurization, the heating process designed to eliminate harmful bacteria and other pathogens. Federal law prohibits the interstate sale of raw milk for human consumption, but intrastate sales fall under state jurisdiction, producing a patchwork in which a family’s exposure to raw dairy risk depends largely on geography. The Academy’s renewed call for a ban on sale and distribution is aimed squarely at this patchwork, arguing that voluntary warnings have not eliminated a preventable source of severe illness.

The scientific case for pasteurization rests on both microbiology and nutrition. The process typically involves heating milk to a temperature sufficient to inactivate vegetative bacterial pathogens and enveloped viruses, followed by rapid cooling to slow the growth of any surviving organisms. Decades of comparative studies have found no meaningful nutritional deficit in pasteurized milk relative to raw milk; the proteins, calcium, and vitamins that make dairy a dietary staple survive the treatment essentially intact. What pasteurization removes is the microbial load, including organisms that may be present even in milk from healthy-appearing animals, since udder infections and fecal contamination during milking can introduce pathogens without any visible sign. Co-author Mark R. Corkins, MD, FAAP, addressed the perception gap directly, saying that parents may choose raw milk because they have heard it is healthier or more natural, but that the scientific evidence tells a different story. Pasteurized dairy products, he said, provide the same essential nutrients without exposing children and families to preventable infections from dangerous bacteria and viruses, and for infants, children, and pregnant people they are clearly the safest choice.

The policy statement was developed through the Academy’s standard process, in which statements written by medical experts reflect the latest available evidence and undergo several rounds of peer review before approval by the AAP Board of Directors and publication in Pediatrics. It will be featured during a presentation on October 5 at the AAP 2026 National Conference and Exhibition in San Diego, where Dr. Ratner is scheduled to discuss the policy during a Meet the Red Book session at the San Diego Convention Center. For families navigating conflicting claims about raw dairy, the Academy has also published a consumer-facing resource, “Raw Milk: What Parents Need to Know About the Risk,” through its HealthyChildren.org platform. The core message of the updated guidance is unambiguous: whatever the appeal of raw milk on the shelf, the pathogens it can carry, from Listeria and E. coli to a potentially pandemic-capable influenza virus, are preventable hazards, and pasteurization remains one of the most effective and time-tested public health interventions in the food supply.

Subject of Research: Health risks of unpasteurized (raw) milk and dairy products for children and pregnant people, including emerging H5N1 avian influenza contamination

Article Title: American Academy of Pediatrics warns of dangers in consuming raw milk, dairy products

Article References: American Academy of Pediatrics warns of dangers in consuming raw milk, dairy products. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: raw milk, pasteurization, American Academy of Pediatrics, H5N1 avian influenza, foodborne illness, Listeria, E. coli, Salmonella, pregnancy, children's health, dairy cattle, public health policy

The research, published in the journal Environmental Geochemistry and Health by Chirarat Arpornwichanop of Chulalongkorn University and the Thai Ministry of Public Health, together with Nares Chuersuwan of Suranaree University of Technology, tackles a fundamental blind spot in air pollution policy. Conventional regulation of PM2.5 is based entirely on mass, meaning the total weight of fine particles in a given volume of air. But as the authors point out, a mass-based standard cannot identify which specific elements within those particles actually determine toxicological priority. Two days with identical PM2.5 concentrations could carry very different burdens of arsenic, cadmium, or antimony, and therefore pose very different hazards to a developing child.

To address this gap, the team conducted what they describe as a fixed-site secondary-data study, evaluating scenario-based pediatric life-stage exposure using a single ambient dataset of PM2.5-bound elements combined with exposure parameters drawn from the published literature. The elemental data came from selected 24-hour filter-sampling days between December 2020 and September 2021, generated under a Thai government research project on the sources of fine particulate matter in Bangkok and nearby provinces, supported by the National Research Council of Thailand. Because the sampling days were selected rather than continuous, the researchers applied seasonal weighting to construct annual outdoor concentration inputs that reflected the pronounced seasonal cycle of air quality in the region, which includes severe haze episodes during the dry season.

What makes the study methodologically distinctive is the way it layers multiple realistic assumptions on top of the raw outdoor concentrations. Children do not spend their lives outdoors, and particles do not pass unimpeded into buildings. The researchers therefore combined the seasonally weighted outdoor inputs with estimates of indoor penetration of particles, time-activity patterns describing how much time children spend in different microenvironments, and respiratory deposition calculations that account for how much of the inhaled particulate mass actually settles in the airways. Respiratory deposition varies substantially with age, because the anatomy and breathing patterns of an infant differ dramatically from those of a school-age child, which is precisely why the analysis was resolved by life stage rather than treating children as a single homogeneous group.

The study then introduced an additional layer of biological realism: solubility in simulated lung fluid, or SLF. Not every metal deposited in the respiratory tract is equally available to the body. Elements that dissolve readily in the fluid lining the lungs can enter the bloodstream and tissues more easily, while insoluble fractions may persist in the airways or be cleared mechanically. By adjusting the exposure profiles according to SLF solubility assumptions derived from the bioaccessibility literature, the researchers created a more refined picture of which elements are genuinely bioavailable after inhalation, rather than simply present on the particles.

For the noncancer analysis, the team prioritized element-specific respiratory-deposited intake, followed by a profile adjusted for SLF solubility. To rank the elements in an exploratory within-study comparison, they employed comparative priority quotients, or CPQs, a mixed-benchmark approach that allows different elements to be compared against appropriate toxicity reference values. The results of the mass-based and toxicity-based rankings diverged in a striking and instructive way. The annual concentrations and respiratory-deposited intake profiles were dominated by aluminum, iron, boron, and zinc, elements that are abundant in crustal dust and urban particulate matter but comparatively low in toxicity. Yet when the CPQ ranking was applied under the selected solubility and toxicity-reference assumptions, the priorities shifted decisively toward arsenic, cadmium, and antimony, three elements with well-documented toxicological concerns even at low concentrations.

This divergence between abundance and hazard sits at the heart of the study’s message. A monitoring framework that tracks only total PM2.5 mass, or even total metal mass, would naturally emphasize the abundant crustal elements while potentially underweighting the trace toxicants that drive risk. Arsenic and cadmium are recognized carcinogens, and antimony has raised concern in recent air quality assessments, so their prominence in the priority ranking, despite their low concentrations, underscores why element-specific screening matters for protecting children’s health. The approach demonstrates that the identity of the elements, not merely the quantity of particles, should inform which sources and control measures receive priority.

The researchers also modeled lifetime cancer risk, the primary estimate resting on chromium expressed as a hexavalent chromium equivalent, together with arsenic and cadmium. Because the speciation of chromium in the sampled particles, that is, the proportion present in the more toxic hexavalent form rather than trivalent chromium, was not directly determined, the team ran the estimate across a bounding range of assumptions. The modeled lifetime cancer risk ranged from 1.11 times ten to the minus sixth power at zero percent hexavalent chromium to 2.78 times ten to the minus fifth power at one hundred percent hexavalent chromium. A corresponding conservative sensitivity analysis that included nickel ranged from 1.22 times ten to the minus sixth to 2.79 times ten to the minus fifth. These figures span the range commonly used in regulatory screening to judge whether risk warrants closer attention, and the wide spread illustrates how strongly the chromium speciation assumption influences the outcome, a point the authors handle with deliberate transparency.

Crucially, the authors are careful to frame what their results can and cannot support. The analysis supports within-model prioritization at a single fixed site; it does not represent measured child exposure, and it does not constitute a province-wide risk assessment. The exposure scenarios were constructed from literature-derived parameters rather than direct measurement of individual children, and the elemental dataset originated from selected sampling days at one monitoring location rather than a dense network spanning Nonthaburi. This honesty about scope is a model of responsible risk communication in a field where modeled estimates are too often presented as measured realities. The study is best understood as a screening exercise, a way of identifying which elements and which life stages deserve targeted follow-up with more refined data.

Even within those limits, the implications reach well beyond one province in Thailand. Rapidly urbanizing regions across Southeast and South Asia face seasonal PM2.5 episodes that routinely exceed international guidelines, and pediatric populations bear the long-term consequences of early-life exposure. The life-stage-resolved framework applied here, combining seasonal weighting, indoor-outdoor dynamics, age-specific respiratory deposition, lung-fluid solubility, and mixed-benchmark priority ranking, offers a transferable template for other cities that possess elemental composition data but lack the resources for full-scale personal exposure studies. As monitoring networks expand and analytical techniques for particle speciation improve, the gap between what regulators measure and what toxicologists worry about can begin to close. For the children of Nonthaburi and millions like them across Asia’s megacities, the air they breathe may finally be judged not just by how much of it there is, but by what, precisely, is riding on those invisible particles.

Subject of Research: Life-stage-resolved screening of pediatric inhalation exposure to PM2.5-bound elements in Nonthaburi, Greater Bangkok, Thailand

Article Title: Life-stage-resolved screening of inhalation exposure to PM2.5-bound elements in Nonthaburi, Greater Bangkok, Thailand

Article References: Arpornwichanop, C., & Chuersuwan, N. (2026). Life-stage-resolved screening of inhalation exposure to PM2.5-bound elements in Nonthaburi, Greater Bangkok, Thailand. Environmental Geochemistry and Health, 48(14), Article 565. https://doi.org/10.1007/s10653-026-03455-7

Image Credits: AI Generated

DOI: 10.1007/s10653-026-03455-7

Keywords: PM2.5, heavy metals, children's health, air pollution, inhalation exposure, respiratory deposition, simulated lung fluid, cancer risk, Thailand, Bangkok, risk assessment, environmental health

The research team, led by Lawal Zubairu of the Sino-French Institute of Nuclear Engineering and Technology at Sun Yat-sen University, together with colleagues at the Nigeria Atomic Energy Commission’s training institute, collected thirty soil samples from across the Rafin Gora mining area. Back at the laboratory of the National Animal Production Research Institute in Zaria, the samples were digested and analyzed by flame atomic absorption spectrophotometry, a workhorse technique that atomizes the sample in a flame and measures how much light each metal absorbs, allowing precise quantification of cadmium, cobalt, chromium, copper, manganese, nickel, lead, arsenic, and zinc. The team then ran the numbers through a battery of established pollution indices and the United States Environmental Protection Agency’s human health risk models.

The pollution indices tell a story of contamination that is real but patchy. The contamination factor, which compares the concentration of each metal in a sample to its background level, revealed that cadmium, arsenic, and zinc showed localized enrichment—meaning that at certain sampling points, human activity had clearly elevated these metals above natural levels. The geoaccumulation index, a logarithmic scale introduced by Müller in 1969 to grade pollution intensity in sediments, classified more than ninety percent of the samples as unpolluted. Yet the pollution load index, which integrates the contamination factors of all measured metals into a single site-level value, exceeded one at most locations, a threshold that signals overall anthropogenic influence rather than purely geological origin.

Ecologically, the news is relatively reassuring. The ecological risk index, originally developed by Hakanson in 1980 for aquatic pollution control, weighs each metal’s toxicity and abundance to estimate the potential harm to ecosystems. Across all sampling locations at Rafin Gora, this index indicated low ecological risk. In other words, the soil ecosystem itself is not yet in crisis. But ecological risk and human health risk are not the same thing, and it is on the human side of the ledger that the study’s most consequential findings emerge.

Using the USEPA’s risk assessment framework, the researchers calculated chronic daily intake values for each metal through three exposure pathways: ingestion of soil particles, inhalation of dust, and dermal contact with soil. The result was unambiguous. Ingestion dominated as the exposure route, and children absorbed doses five to ten times higher than adults. This is not surprising to exposure scientists: children play on the ground, put dusty hands and objects in their mouths, and ingest far more soil per kilogram of body weight than adults do. In a mining village where tailings and crushed ore are scattered across living spaces, that behavioral difference translates directly into a chemical dose difference.

When the researchers summed the hazard quotients—the ratio of each metal’s estimated intake to its reference dose, the level below which no adverse effect is expected—into a hazard index, the values came out at 0.026 for adults and 0.139 for children. Both sit below unity, the conventional line separating acceptable from unacceptable non-carcinogenic risk. Within those totals, however, chromium and arsenic contributed the largest shares of both the hazard quotient and the intake, marking them as the metals that matter most at this site. Cadmium, lead, and the others, despite their fearsome reputations, played comparatively minor roles in the overall risk picture at Rafin Gora.

The carcinogenic risk calculation is where the study acquires its edge. Arsenic and chromium are both recognized human carcinogens, and the USEPA models assign them slope factors that convert chronic intake into a lifetime probability of cancer. The total carcinogenic risk came to 3.66 × 10⁻⁶ for adults and 6.79 × 10⁻⁶ for children. To put those numbers in context: the widely used acceptable upper limit for regulatory purposes is 1 × 10⁻⁴, or one additional cancer case per ten thousand people, and both values fall comfortably below it. But the threshold of negligible risk is conventionally set at 1 × 10⁻⁶, one in a million, and both values—particularly the children’s figure, nearly seven times that level—exceed it. The authors conclude that locally enriched arsenic and chromium drive a non-negligible cancer risk, especially for children.

The Rafin Gora findings resonate with a broader and often tragic pattern across Nigeria’s artisanal gold mining belt. Artisanal and small-scale gold mining is a lifeline for millions of people in West Africa, but it frequently proceeds without environmental safeguards, leaving crushed ore, tailings, and contaminated dust in intimate contact with communities. Previous Nigerian studies have documented heavy metal contamination around artisanal sites in Zamfara, Niger, Osun, and Nasarawa states, and the 2010 Zamfara lead poisoning epidemic—which killed hundreds of children and was traced to lead-rich ores processed inside village compounds—remains one of the starkest demonstrations of what unregulated ore processing can do. The Rafin Gora study adds a carefully quantified data point to this regional picture, showing that even where acute poisoning is absent, chronic low-level exposure can quietly accumulate statistical risk.

Methodologically, the study also illustrates both the power and the limits of standard risk assessment. The USEPA models rely on default exposure assumptions—soil ingestion rates, body weights, exposure frequencies—that are drawn largely from Western datasets and may not perfectly match the realities of rural Nigerian life. Moreover, total metal concentration is not the same as bioavailable metal: only the fraction of a metal that dissolves in the gut can actually be absorbed, and that fraction varies with the metal’s chemical form, or speciation. The authors explicitly recommend that future work incorporate bioaccessibility testing and speciation analysis, which would refine the risk estimates and could either temper or sharpen the current conclusions. They also call for practical mitigation at the site itself, including dust suppression to cut the dominant ingestion and inhalation pathways, and soil remediation to remove or immobilize the enriched arsenic and chromium.

For the people of Rafin Gora, the message of this research is neither panic nor complacency. The soils of the mining area are, by the standard indices, mostly unpolluted, the ecological risk is low, and the non-cancer hazard indices sit safely below regulatory thresholds. Yet the same measurements reveal pockets of arsenic and chromium enrichment that push lifetime cancer risk above the level scientists consider negligible, with children bearing the heaviest burden. In communities where gold mining is both livelihood and hazard, that combination argues for targeted, inexpensive interventions—wetting down dusty paths, keeping children’s play areas clear of tailings, remediating the worst hotspots—rather than wholesale abandonment of the mines. It is a reminder that in environmental health, the dose and the exposed population matter as much as the poison, and that careful measurement is the first step toward protecting the most vulnerable.

Subject of Research: Heavy metal contamination and human health risk assessment in soils of an artisanal gold mining area in Katsina State, Nigeria

Article Title: Health risk assessment of heavy metals exposure in soil at Rafin Gora artisanal gold mining area, Nigeria

Article References: Zubairu, L., Mingliang, K., Xueqing, Y., & Raza, K. (2026). Health risk assessment of heavy metals exposure in soil at Rafin Gora artisanal gold mining area, Nigeria. Environmental Science and Pollution Research, 33(30), 15865-15882. https://doi.org/10.1007/s11356-026-38155-3

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38155-3

Keywords: heavy metals, artisanal gold mining, soil pollution, health risk assessment, arsenic, chromium, Nigeria, children's health, carcinogenic risk, USEPA models, environmental pollution, Katsina State

That finding comes from a team led by Ju-Hyeok Kwon and Byong-Hun Jeon at Hanyang University, working with colleagues at institutions across South Korea and the United States, in a study published in the journal Environmental Geochemistry and Health. The researchers set out to compare two of the most influential health risk assessment frameworks applied to fluoride-contaminated land: the United States Environmental Protection Agency’s Risk Assessment Guidance for Superfund, known as RAGS, and South Korea’s own soil-contamination risk assessment guidelines, abbreviated KRAG. Their motivation was practical. South Korea applies a residential soil fluoride standard of 800 milligrams per kilogram, but in some regions fluoride levels are elevated naturally, by geology rather than industry, and it has been unclear how those soil concentrations translate into actual health risk when people are exposed not just through soil but through drinking water and food grown in contaminated ground.

The core problem the study addresses is what risk assessors call multimedia exposure. A regulatory standard written for soil implicitly assumes that soil is the main pathway by which a contaminant reaches the human body, through accidental ingestion of dust and dirt, inhalation of particles, and skin contact. Fluoride does not respect that boundary. It dissolves into groundwater that supplies wells, and it is taken up by crops, accumulating in rice, vegetables, and other staples. Previous studies in India’s Punjab and West Bengal regions, in Iran’s Isfahan province, and in China’s northwest have documented that crop and water intake can dominate total fluoride exposure in affected communities. A soil-only standard, in other words, may capture only a slice of the real dose, and the slice it captures depends heavily on the mathematical assumptions baked into the assessment framework.

To test how much those assumptions matter, the researchers constructed exposure scenarios spanning realistic contamination ranges: soil fluoride concentrations from 200 to 4,000 milligrams per kilogram, water concentrations from 0.5 to 2.5 milligrams per liter, and crop concentrations from 5 to 40 milligrams per kilogram. They then ran these scenarios through both frameworks, calculating a metric called the hazard index, or HI, which compares estimated fluoride intake against a reference dose considered safe. An HI above one signals potential non-cancer health effects, such as dental or skeletal fluorosis. The two frameworks differ in the parameters they assign to exposure, including how much soil children are assumed to swallow, how much water different age groups drink relative to their body weight, and how exposure frequency and duration are defined. Those parameter differences, the study shows, are enough to change the risk verdict entirely.

The results were striking. Under the U.S. EPA’s RAGS framework, children exhibited the highest hazard index for fluoride, reaching a value of 9.116 in the most demanding scenarios, well above the threshold of concern. This reflects a well-known feature of child exposure: children eat and drink more per unit of body weight than adults, and their habits, hand-to-mouth contact, playing in dirt, put them in closer contact with contaminated soil and dust. But when the same scenarios were evaluated under the Korean KRAG guidelines, the hazard index estimates came out lower, and in some scenarios the framework produced a counterintuitive result: children appeared to face lower calculated risk than adults. For a regulatory tool whose purpose is to protect the most vulnerable, that inversion is a red flag, and the authors treat it as evidence that KRAG’s parameterization may understate child-specific exposure through water and food.

To understand exactly where the two frameworks diverge, the team turned to an increasingly popular tool in environmental science: explainable machine learning. Rather than using algorithms as a black box to predict risk, they applied explainable artificial intelligence to dissect the calculations themselves, identifying which input parameters drove the discrepancies between RAGS and KRAG estimates. The analysis pinpointed the parameterization inconsistencies, the differing assumptions about intake rates, body weights, and exposure pathways, that produced the divergent outcomes. This kind of forensic use of explainable AI is part of a broader trend; other recent studies have used machine learning to predict high-fluoride groundwater across the Yellow River Basin and elsewhere. Here, the technique serves a regulatory purpose, showing guideline developers precisely which knobs in the risk equation matter most and where refinement would be most consequential.

As a bridge between the two systems, the researchers proposed a modified approach they call RAGS-K, which applies Korean exposure parameters within the RAGS calculation structure. Under the examined scenarios, RAGS-K yielded higher hazard index estimates than KRAG, suggesting that the Korean framework’s lower estimates stem less from its calculation architecture than from the specific parameter values it assigns. The hybrid also preserved the multimedia structure of RAGS, which explicitly accounts for water and crop intake alongside soil and dust. The implication is that a country can adopt a more complete, child-protective risk calculation without wholesale adoption of foreign guidance; the parameters can be localized while the structure captures all relevant exposure routes.

Perhaps the most consequential finding is about where the risk actually comes from. Across the scenarios, intake from water and crops dominated the calculated child risk and was the main driver of the gap between adult and child hazard estimates. Soil ingestion, the pathway that soil standards are built around, played a comparatively minor role. That means a child drinking fluoride-rich well water and eating vegetables from a contaminated garden may exceed safe intake thresholds even where soil fluoride sits comfortably below the 800 milligram per kilogram regulatory limit. Conversely, remediating soil alone may do little to reduce total exposure if the water and food pathways remain open. The authors argue this supports a shift toward media-integrated risk assessment and management, in which soil, water, and agricultural pathways are evaluated together rather than by separate regulatory silos.

The study arrives amid a growing global literature on fluoride risk. Reviews have catalogued the mechanisms of fluoride toxicity, from enamel mottling to skeletal fluorosis, and field studies in Ethiopia’s Rift Valley have linked groundwater fluoride to dental fluorosis in children, measured through urinary fluoride levels. Remediation research, from granular ferric hydroxide filters to zirconium oxide-impregnated chitosan beads and electrokinetic soil treatment, offers engineering tools for contaminated sites. What has been missing, the Korean team contends, is a rigorous comparison of the regulatory lenses through which those risks are judged. Their work provides exactly that, and its message travels well beyond Korea. Any nation drafting or revising soil standards for fluoride, or for contaminants with similar multimedia behavior, faces the same structural question: a standard calibrated to one exposure pathway, with one set of behavioral assumptions, may silently misjudge risk when the real exposure comes from the dinner table and the kitchen tap. For the children of fluoride-endemic regions, the difference between frameworks is not a matter of statistical nuance. It may be the difference between a risk that is flagged and one that is missed.

Subject of Research: Comparative health risk assessment of fluoride-contaminated soil, water, and food using U.S. EPA and Korean regulatory frameworks

Article Title: Comparative evaluation of regulatory health risk assessment frameworks for fluoride-contaminated environments

Article References: Kwon, J.-H., Choi, K.-W., Park, W.-M., Cho, D.-W., Kumar, R., Lee, S., Choi, J., Chang, S. W., Kim, K.-Y., Ahn, Y., & Jeon, B.-H. (2026). Comparative evaluation of regulatory health risk assessment frameworks for fluoride-contaminated environments. Environmental Geochemistry and Health, 48(14), Article 580. https://doi.org/10.1007/s10653-026-03475-3

Image Credits: AI Generated

DOI: 10.1007/s10653-026-03475-3

Keywords: fluoride, soil contamination, health risk assessment, RAGS, KRAG, hazard index, groundwater, multimedia exposure, explainable machine learning, children's health, South Korea, environmental regulation

The study, led by Aimuanmwosa Frank Eghomwanre and Michael Ovbare Akharame of the Department of Environmental Management and Toxicology, was designed to fill a conspicuous gap. While indoor air quality in European and North American schools has been extensively catalogued, comparable data from tropical African cities remain scarce, a deficit compounded by weak monitoring infrastructure and limited policy attention across the region. To address this, the team deployed a mixed-methods approach that combined objective environmental monitoring with subjective health assessment over ten weeks. The spatial and temporal dimensions mattered: measurements were taken across multiple schools and throughout the school day, allowing the researchers to track how pollutant levels shifted with occupancy, activity and weather, rather than relying on single snapshots that can miss the peaks that matter most for exposure.

The numbers they recorded are sobering. Concentrations of fine particulate matter, known as PM2.5 because the particles are 2.5 micrometres or smaller in diameter, ranged from 11.2 to 81.4 micrograms per cubic metre of air. Coarse particulate matter, PM10, spanned 20.1 to 138.6 micrograms per cubic metre. For context, the World Health Organization’s 2021 global air quality guidelines recommend annual mean PM2.5 levels of just 5 micrograms per cubic metre, with short-term limits far below the upper readings observed in these classrooms. At the top end of the measured range, students were breathing air carrying more than sixteen times the WHO’s annual guideline concentration of the finest, most penetrating particles. Carbon dioxide, a reliable proxy for ventilation adequacy in occupied rooms, peaked at an average of 729.3 parts per million with a standard deviation of 28.4 ppm, a level that signals crowding and insufficient fresh-air exchange even though it remained below some occupational thresholds.

Thermal conditions added a second layer of discomfort. The researchers calculated the temperature-humidity index, or THI, a composite measure that combines air temperature and relative humidity to gauge heat stress on the human body. Values across the classrooms ranged from 28.3 to 30.1, a band the study characterises as indicating severe heat discomfort. In tropical climates, high humidity compounds heat load by impairing the evaporation of sweat, the body’s primary cooling mechanism. Previous research has shown that overheated classrooms impair cognitive performance and concentration, and the Nigerian findings suggest that thermal stress and air pollution are not separate problems but intertwined features of the same poorly regulated built environment. Hot, still air also favours the resuspension of settled dust, meaning that physical discomfort and particulate exposure can reinforce one another.

To translate these exposures into health terms, the team applied the hazard quotient framework of the United States Environmental Protection Agency, a standard method for estimating non-carcinogenic risk from inhalation. The hazard quotient compares an estimated daily intake with a reference concentration considered safe over a lifetime; values below one are conventionally interpreted as indicating no immediate chronic risk. For both PM2.5 and PM10, every hazard quotient calculated in the study fell below unity. On paper, then, the students of Benin City are not on course for the chronic, cumulative respiratory damage that regulatory frameworks are designed to prevent. Yet the questionnaire data told a very different story, and it is this discrepancy that gives the study its urgency.

Using questionnaires adapted from the British Medical Research Council’s respiratory symptom instrument, the researchers found that 58.2 percent of students reported coughing, 32.5 percent reported phlegm production, and 26.7 percent reported chest pain. These are not trivial figures. Acute respiratory irritation, it turns out, frequently manifests at exposure levels well below the chronic thresholds embedded in the hazard quotient methodology. The explanation lies in the biology of the airways: fine particles deposit deep in the bronchial tree and trigger inflammation, mucus secretion and cough reflexes within hours or days of exposure, long before any cumulative dose approaches the levels associated with chronic disease. A hazard quotient built on long-term averaging can therefore coexist with a school population that is coughing through every lesson.

The multivariate analysis sharpened the picture considerably. Elevated particulate matter exposure was strongly associated with increased risk of coughing, an association that held at the p < 0.001 level, and significantly increased the odds of chest pain, with a crude odds ratio of 2.74 and a p-value of 0.001. In practical terms, students in the more heavily polluted classrooms faced nearly triple the odds of reporting chest pain compared with their peers in cleaner environments, before adjustment for other factors. Coughing, the most prevalent symptom, tracked particulate levels most tightly of all, consistent with the established physiology of PM2.5, which provokes airway irritation and reflex coughing as the lungs attempt to clear deposited particles.

Perhaps the most unexpected finding concerned sanitation. After adjusting for confounders including age, sex and socio-economic status, poor sanitation emerged as the strongest predictor of phlegm production, with an adjusted odds ratio of 5.54 and a 95 percent confidence interval of 1.35 to 22.80, significant at p = 0.018. Students in schools with inadequate sanitation faced more than five times the odds of producing phlegm compared with those in better-maintained institutions. This result echoes a growing body of evidence linking dampness, mould and poor building maintenance to respiratory symptoms in children, and it underscores that classroom air is shaped by more than outdoor pollution: the condition of the building itself, from its toilets to its ventilation openings, is a health determinant in its own right.

The broader context makes these findings more consequential. Sub-Saharan Africa’s urban populations are expanding rapidly, and school infrastructure has struggled to keep pace, with classrooms often crowded, naturally ventilated only through windows that may be closed against dust or traffic fumes, and sited near unpaved roads or open waste. Nigeria’s own national environmental air quality regulations exist on paper, but enforcement in school settings is minimal, and the country’s air quality monitoring network remains sparse. Studies from Addis Ababa and other African cities have similarly documented fine particulate levels exceeding WHO guidelines, suggesting that Benin City is not an outlier but a case study in a regional pattern. Children are particularly vulnerable because they breathe more air per unit of body weight than adults, their airways are still developing, and they have little control over the environments in which they spend their days.

What the Benin City study ultimately delivers is a methodological warning wrapped in a public health finding. Risk assessment tools built around chronic exposure thresholds, however rigorous, can systematically understate the lived experience of children in tropical schools, where acute symptoms flourish at concentrations regulators would deem acceptable on paper. The authors argue that particulate matter control and sanitation improvement should be treated as immediate priorities rather than long-term aspirations, and their data give school administrators and policymakers concrete targets: better ventilation to curb carbon dioxide buildup, dust suppression to cut particulate loads, and basic sanitation upgrades that could more than halve the burden of phlegm-producing respiratory illness. For the students of Benin City, and for millions like them across the tropics, the air in the classroom is not a background condition but an active determinant of health, and the evidence now shows that waiting for chronic thresholds to be crossed before acting would mean waiting far too long.

Subject of Research: Classroom air quality, thermal comfort and respiratory health risks among schoolchildren in urban Nigeria

Article Title: Spatio-temporal assessment of classroom air quality and thermal comfort as determinants of respiratory health risks in urban pre-tertiary institutions

Article References: Eghomwanre, A. F., & Akharame, M. O. (2026). Spatio-temporal assessment of classroom air quality and thermal comfort as determinants of respiratory health risks in urban pre-tertiary institutions. Environmental Science and Pollution Research. https://doi.org/10.1007/s11356-026-38254-1

Image Credits: AI Generated

DOI: 10.1007/s11356-026-38254-1

Keywords: indoor air quality, particulate matter, PM2.5, respiratory symptoms, thermal comfort, school health, Nigeria, carbon dioxide, sanitation, hazard quotient, children's health, tropical cities

The study, published in the Journal of Activity, Sedentary and Sleep Behaviors, was led by Aaron Miatke and colleagues at the University of South Australia as part of the Life on Holidays project, a longitudinal cohort study that followed children from twenty-four primary schools in Adelaide between February 2019 and December 2022. The researchers recruited 381 children in Grade 4, drawn from neighbourhoods spanning low, middle and high socio-economic strata, and equipped them with wrist-worn GENEActiv accelerometers that recorded movement around the clock for seven consecutive days at each of five measurement timepoints. Unlike conventional studies that measure only waking hours, this design captured the full daily cycle of sleep, sedentary behaviour, light activity and moderate-to-vigorous activity, allowing the team to model the entire twenty-four-hour day as a single, interconnected system.

That modelling approach, known as compositional data analysis, or CoDA, is what gives the study its statistical teeth. The central insight of CoDA is deceptively simple: a day is a fixed budget of twenty-four hours, so any increase in one behaviour must come at the expense of another. Traditional statistics that treat sleep, sitting and exercise as independent variables ignore this zero-sum reality and can produce misleading conclusions. To handle the problem, the researchers transformed their four-part time-use composition into isometric log-ratio coordinates, a mathematical technique that expresses each behaviour relative to the geometric mean of the others. They then built linear mixed-effects models that accounted for the clustering of children within schools, repeated measurements within children, and covariates including sex, age and socio-economic status. Crucially, they ran the analysis twice: once as a cross-sectional snapshot at baseline, and once longitudinally, using the actual annualised rates of change in body fat, body mass index and cardio-respiratory fitness across three distinct periods, the first school year, the intervening summer holidays, and the second school year.

The cross-sectional results looked reassuringly familiar. At baseline, children who spent more time in moderate-to-vigorous physical activity had lower body mass index z-scores, lower percentages of body fat measured by bioelectrical impedance, and higher estimated maximal oxygen uptake from the twenty-metre shuttle run test, all statistically significant at p less than 0.01. Time spent in light physical activity showed the opposite pattern, unfavourably associated with every outcome, while sedentary behaviour was linked to higher body fat and longer sleep to lower body fat. In other words, the snapshot data replicated the picture painted by most previous research: the whole menu of daily behaviours appeared to matter.

Then came the twist. When the researchers switched to the longitudinal models, which tracked empirical changes in each child’s body over two years rather than comparing children to one another at a single moment, almost all of those associations evaporated. Sleep, sedentary behaviour and light activity lost their statistical significance entirely. Only moderate-to-vigorous physical activity remained a significant predictor of change, and even its association with body fat percentage only approached conventional significance at p equal to 0.06 before the sensitivity analyses sharpened the picture. The overall time-use composition was significantly associated with changes in cardio-respiratory fitness, and the composition explained roughly six percent of the variance in fitness change, but a mere 0.3 percent of the variance in body mass index change and two percent in body fat change.

The isotemporal substitution models, which estimate what would happen if a child traded minutes of one behaviour for another while holding everything else constant, quantified the stakes. Adding thirty minutes per day of moderate-to-vigorous activity at the expense of light activity was associated in cross-sectional models with a reduction in body fat percentage of 2.65 points and a gain of 1.23 millilitres per kilogram per minute in estimated VO2max. In the longitudinal models, the same thirty-minute reallocation from light activity was linked to a faster decline in body fat percentage, a rate of change 0.60 percentage points more favourable per year, and to a VO2max trajectory 0.91 units higher, with similar gains whether the traded-away time came from sleep, sitting or light movement. Notably, the asymmetry ran both ways: the researchers found that the detrimental association of losing moderate-to-vigorous activity was consistently larger than the benefit of gaining it, a warning that declines in activity, such as those seen during weekends, holidays and the transition into adolescence, may exact a disproportionate toll.

Perhaps the most striking discovery came from the sensitivity analyses, which split the moderate-to-vigorous category into its moderate and vigorous components. When vigorous physical activity stood alone, it was significantly and favourably associated with changes in both body fat percentage and VO2max over time, while moderate activity alone lost significance for every outcome. The dose-response comparison was dramatic: just ten minutes per day of additional vigorous activity, swapped for sedentary time, produced an estimated improvement in fitness trajectory of 0.53 units, identical to the improvement produced by thirty minutes per day of additional moderate activity. On a minute-for-minute basis, vigorous exercise was roughly three times as potent for cardio-respiratory fitness. For body fat, only reallocations toward vigorous activity, not moderate activity, reached significance in the longitudinal models.

The authors are careful about interpretation. They suggest that lower-intensity behaviours may simply not provide sufficient physiological stimulus to drive measurable change, whereas moderate-to-vigorous activity carries higher energy expenditure and greater cardiorespiratory demand, provoking the adaptations that improve fitness and body composition. They also note that cardio-respiratory fitness may respond faster to activity changes than adiposity, which is heavily influenced by diet, and that body mass index, which cannot distinguish fat from muscle and bone, may be a blunt instrument in growing children. The study has limitations worth acknowledging: the COVID-19 pandemic disrupted data collection, children from lower socio-economic areas were under-represented among completers, diet and pubertal development were not directly measured, and no winter data were collected, leaving seasonal effects unexplored.

For a world grappling with more than 340 million children affected by obesity and a generation whose fitness is measurably lower than their parents’, the message is both sobering and actionable. Simply cutting screen time or encouraging gentle movement, the study suggests, is unlikely to move the needle on its own. The real leverage lies in getting children breathing hard, whether through sport, sprinting games or active play, and in protecting the vigorous activity they already do. Even ten minutes a day of genuine huff-and-puff exertion, the data indicate, may be worth more than half an hour of anything gentler, a finding that could reshape physical activity guidelines and school programmes alike.

Subject of Research: Associations between 24-hour time use and adiposity and cardio-respiratory fitness in school-aged children

Article Title: Cross-sectional and longitudinal associations between sleep, sedentary behaviour and physical activity with adiposity and cardio-respiratory fitness in school-aged children: a compositional data analysis

Article References: Miatke, A., Olds, T., Maher, C., Fraysse, F., & Dumuid, D. (2025). Cross-sectional and longitudinal associations between sleep, sedentary behaviour and physical activity with adiposity and cardio-respiratory fitness in school-aged children: a compositional data analysis. Journal of Activity, Sedentary and Sleep Behaviors, 4(1), Article 11. https://doi.org/10.1186/s44167-025-00082-y

Image Credits: AI Generated

DOI: 10.1186/s44167-025-00082-y

Keywords: physical activity, children's health, compositional data analysis, adiposity, cardio-respiratory fitness, MVPA, vigorous exercise, sedentary behaviour, sleep, accelerometry, childhood obesity, longitudinal study

The timing of the argument is significant. Climate change is already reshaping the environmental exposures most fundamental to human health, including heat stress, air pollution, altered patterns of allergens, and water insecurity. At the same time, chronic inflammatory skin conditions appear to be rising among children in many regions of the world. Climate-health research, however, has concentrated overwhelmingly on cardiopulmonary and heat-related outcomes, such as respiratory disease, cardiovascular strain, and heat stroke. Conditions that unfold through slower developmental pathways, particularly those affecting the immune systems of fetuses, infants, and young children, have received comparatively little attention. Veliah’s article seeks to redirect some of that attention toward the earliest chapters of human development, when biological systems are most pliable and most vulnerable to permanent reprogramming.

The biological logic behind the proposal draws on several converging fields: developmental immunology, maternal-fetal health, environmental exposure science, and dermatology. During pregnancy and the first years of life, the immune system does not simply mature on a fixed genetic schedule. It is calibrated by the environment, learning which threats to respond to and which to tolerate. Prenatal and early-life exposures, the article argues, may influence immune programming, placental signaling, skin barrier development, and inflammatory responses in ways that persist for decades. A mother’s exposure to extreme heat, airborne particulates, shifting allergen loads, or unreliable water supplies does not stop at the placental boundary; signals generated by such stressors can travel through maternal physiology and reach the developing fetus, potentially biasing the trajectory of its immune system toward inflammatory reactivity.

The skin occupies a unique position in this framework because it is simultaneously a physical barrier and an active immune organ. It is the tissue that confronts the external environment most directly, absorbing ultraviolet radiation, temperature swings, humidity changes, pollutants, and microbial communities. Unlike the lungs or the heart, whose distress may only become measurable through clinical testing, the skin broadcasts its state outward. Redness, dryness, itching, and eczematous lesions are visible to parents, teachers, and clinicians without any diagnostic equipment. This visibility is precisely what makes inflammatory skin conditions attractive as potential sentinel indicators. If the skin registers cumulative environmental stress earlier than internal organs, then rising rates of childhood eczema in a given population could function as an early-warning signal, flagging environmental degradation before it manifests as asthma, cardiovascular disease, or other harder-to-detect outcomes.

Veliah is careful to frame the relationship as complex, multifactorial, and incompletely understood rather than as a simple causal chain. Eczema, or atopic dermatitis, is known to arise from interactions among genetic predisposition, skin barrier defects, immune dysregulation, microbial imbalances, and environmental triggers. Disentangling the specific contribution of climate-related exposures from these overlapping factors is a formidable scientific challenge. Heat, for example, can affect the skin both directly, by altering sweat production and barrier function, and indirectly, by changing the abundance of dust mites, molds, and pollen that provoke allergic sensitization. Air pollution can damage the skin barrier and prime immune cells toward inflammatory responses, while water insecurity can compromise hygiene practices and expose children to irritants and pathogens. Each pathway is plausible; none is yet firmly quantified.

The concept of sensitive developmental windows is central to the argument. Immunologists have long recognized that exposures occurring during specific periods of prenatal and early postnatal life can have disproportionate and long-lasting effects compared with the same exposures later in childhood or adulthood. The placenta itself is an active signaling organ that responds to maternal stress, and disruptions to placental function can alter nutrient delivery, hormone exposure, and immune messaging to the fetus. Skin barrier development also follows a defined developmental timetable in infancy, and interference during this period, whether through dehydration, pollutant contact, or inflammatory activation, may establish patterns of immune reactivity that persist. In this view, climate change is not merely an environmental hazard that adults must endure; it is a force that can become biologically embedded in the next generation before those children can make any choices about the world they inhabit.

The surveillance implications of the framework may be its most practical contribution. Environmental health monitoring traditionally relies on expensive instrumentation: air quality stations, satellite measurements, water testing laboratories, and meteorological networks. These tools are essential, but they are unevenly distributed, particularly in low- and middle-income countries where climate impacts are often most severe. Childhood eczema, by contrast, is diagnosable through simple clinical examination and is already recorded in many health systems. If researchers can establish reliable associations between climate-related environmental stress and inflammatory skin outcomes, pediatric skin clinics and community health records could become a distributed sensing network, offering granular, real-time evidence of how environmental change is affecting vulnerable populations. Such an approach would be especially valuable in regions where formal environmental monitoring infrastructure is thin but health workers are present.

The framework also opens new directions for maternal and child health research. If prenatal heat exposure, air pollution, or water insecurity measurably alters immune programming and skin barrier development, then interventions targeted at pregnant women and infants, such as cooling shelters, air filtration, improved water access, and barrier-protective skin care, could yield benefits that extend far beyond dermatology. Preventing early immune misprogramming could reduce the lifetime burden of allergic and inflammatory disease. Conversely, if the hypothesis proves incorrect or only weakly supported, the research it inspires would still clarify how early-life environmental exposures shape immune development, a question of fundamental importance regardless of outcome.

It is worth emphasizing what the article does not claim. As a Perspective, it presents no new experimental data, no cohort study, and no clinical trial. It explicitly avoids proposing direct causation between climate change and eczema, instead offering a conceptual scaffold intended to encourage discussion and further research. The author declares no competing interests and received no specific funding for the work, and the article notes that a large language model was used to assist with language refinement and formatting, while all scientific content and interpretations were developed and verified by the author. This transparency matters for readers weighing how much weight to give the proposal: it is a well-reasoned call for investigation, not a demonstrated finding.

Even so, the core idea has an arresting quality that may explain its appeal beyond specialist circles. Climate change is often described in abstract units, degrees of warming, parts per million of carbon dioxide, hectares of lost forest. Veliah’s framework translates those abstractions into something a parent can see on a child’s arms. If the rising tide of childhood eczema in heat-stressed, polluted, and water-insecure regions is partly a biological echo of environmental disruption, then the skin becomes a document on which the climate crisis writes its earliest legible notes. Testing that idea rigorously will require longitudinal birth cohorts that track environmental exposures and skin outcomes together, interdisciplinary collaboration across dermatology, immunology, and climate science, and sustained attention to the populations least responsible for emissions yet most exposed to their consequences. The article’s publication is a starting point for that effort, and its central question, whether a rash can be a climate signal, is now formally on the research agenda.

Subject of Research: The role of early-life inflammatory skin conditions as indicators of climate change-related environmental stress

Article Title: Inflammatory skin conditions as early-life indicators of climate change related environmental stress

Article References: Veliah, G. (2026). Inflammatory skin conditions as early-life indicators of climate change related environmental stress. Discover Social Science and Health. https://doi.org/10.1007/s44155-026-00475-7

Image Credits: AI Generated

DOI: 10.1007/s44155-026-00475-7

Keywords: climate change, eczema, dermatology, environmental health, immune development, skin barrier, children's health, air pollution, heat stress, maternal-fetal health, inflammation, public health