Plastics are a growing environmental and health threat. Microplastics (MPs, <5 mm) and nanoplastics (NPs, <1 μm) are pervasive environmental contaminants increasingly detected within human tissues, including placenta, cord blood, breast milk, and infant stool, highlighting chronic early-life exposure. Children represent a uniquely vulnerable population due to higher intake relative to body mass, immature detoxification and immune systems, and rapid organogenesis. MPs and NPs (MNPs) can traverse biological barriers, accumulate in multiple organs, and disrupt key developmental processes through oxidative stress, inflammation, barrier dysfunction, and microbiome dysbiosis. Evidence from in vitro, animal and human studies indicates systemic impacts across gastrointestinal, pulmonary, endocrine, reproductive, immune, and central nervous systems, including impaired intestinal barrier function, dysbiosis, metabolic dysregulation, altered lung morphogenesis, endocrine disruption, reproductive abnormalities, immune dysregulation, and neurocognitive deficits. In addition, many chemicals associated with plastics pose risks to human health due to their toxicity and ability to leach into the surrounding area. This review compiles current knowledge on the physicochemical properties, exposure pathways, and system-specific effects of MNPs and the additives associated with plastics in pediatric populations. It also discusses the need for comprehensive policies to reduce plastic pollution. IMPACT: The increased prevalence of microplastics and nanoplastics pose a threat to children's health. Microplastics and nanoplastics have been found in many organs including the placenta. Children are particularly vulnerable to the effects of microplastics and nanoplastics. The mechanism by which they increase health risks in children are discussed.

Artificial intelligence (AI) in environmental health science is revolutionizing data analysis and problem-solving approaches. These technologies facilitate the prediction of environmental exposures and disease outcomes and enable the identification of causal relationships for subsequent hypothesis testing. AI techniques improve pollution research through the analysis of satellite imagery and the modeling of pollutant dispersion, while AI advances chemical safety evaluations in toxicology by examining extensive datasets. AI is instrumental in addressing pressing environmental challenges, including remediation of polluted sites and ensuring equitable healthcare applications to mitigate biases. The expanding availability of large-scale environmental, geospatial, and health outcome databases offers unprecedented opportunities for innovative applications. Their predictive capabilities are essential in disaster management, enabling real-time analysis and optimizing resource deployment amid climate-related crises. AI-driven approaches play a critical role in carbon capture and waste management efforts aimed at reducing environmental impact. Furthermore, AI can elucidate complex relationships between the exposome-defined as the totality of exposures throughout an individual's life-and health outcomes, facilitating preventative strategies. This review examines the capabilities and limitations of AI in environmental health and safety, providing insights into its judicious and effective use for environmental management and healthcare.

The frequency and severity of heat waves are expected to worsen with climate change. Exposure to extreme heat, or prolonged unusually high temperatures, are associated with increased morbidity and mortality. The fetus, infant, and young child are more sensitive to higher temperatures than older children and most adults given that they are rapidly developing. During pregnancy, exposure to extreme heat may result in dehydration, inflammation, and reduced blood flow in the placenta potentially triggering preterm birth and increased rates of stillbirth and low birth weight infants. Young children experience a range of immediate health effects from heat, including disruptions in their sleep and learning, and exacerbations of asthma. Long-term impacts include lower cognitive function, reduced ability to concentrate, and adverse outcomes in mental and behavioral health. It is possible to protect children by taking steps to reduce the potential long-term harm of increasing exposure to extreme heat, such as implementing early warning systems, establishing community cooling centers, and expanding support programs to provide cooling systems to homes. Further, adapting existing infrastructure to withstand increased heat through increasing shade as well as the use of cool pavements or cool/green roofs in early care centers and other places children spend time may be efficient ways of mitigating the developmental effects of extreme heat. Finally, preventing future temperature increases by addressing the root causes behind our rapidly heating planet by decreasing use of fossil fuel and investing in renewable energy sources are ultimately needed to ensure healthy child development.

Natural disasters (including heatwaves, wildfires, hurricanes, floods, earthquakes and volcanic eruptions) significantly impact respiratory health, posing heightened risks to vulnerable populations such as individuals with pre-existing conditions, children, and the elderly. This review explores the complex relationship between natural catastrophes and respiratory health, emphasising the roles of chemical pollutants, biocontaminants and meteorological factors. Epidemiological evidence highlights alarming trends, including increased asthma exacerbations, COPD hospitalisations and respiratory infections following these events. During heatwaves, elevated ozone levels and emissions from power generation for air conditioning exacerbate respiratory conditions, while fine and ultrafine particulate matter, particularly during dust storms and wildfires, emerge as a major contributor to respiratory morbidity and mortality. Volcanic eruptions release hazardous gases, corrosive minerals and plumes of particles and dust into the atmosphere, which exacerbate symptoms in individuals with pre-existing respiratory conditions. Thunderstorms often increase airborne pollen and mould concentrations, triggering episodes of thunderstorm asthma. Earthquake-damaged buildings are significant sources of dust, worsening respiratory symptoms among affected populations. Floods are the origin of mould proliferation, responsible for asthma and other respiratory diseases. First responders, such as firefighters, face acute and potentially chronic respiratory issues due to prolonged exposure to chemical pollutants and biocontaminants during rescue operations. Marginalised communities disproportionately bear the brunt of these health impacts due to systemic vulnerabilities and limited adaptive capacities. This review underscores the escalating respiratory health threats posed by natural disasters amid ongoing climate change. An integrated approach is needed to address these challenges through improved understanding, targeted interventions, and proactive measures to mitigate risks.

INTRODUCTION:Per- and Polyfluoroalkyl Substances (PFAS) are widely used chemicals, notably in nonstick coatings, fire-fighting foams and equipment, and surfactants. These chemicals degrade slowly and accumulate in tissues and the environment, being detected in water, air, wildlife, and soil across the world. Initial studies have shown that these chemicals are associated with harmful health effects, but research in this area remains limited, especially in sinonasal diseases. METHODS:The National Health and Nutrition Examination Survey (NHANES) 2011-2014 was used to analyze the association between PFAS and taste and smell survey among adults (age ≥ 40) with complete data (n = 1911). The survey included self-reported sinonasal symptoms. Multivariable logistic regression adjusted for covariates was used to describe the relationship between serum PFAS concentrations and sinonasal health. Bayesian kernel machine regression (BKMR) was performed to consider the diverse chemical properties of PFAS and how real-life exposures involve multiple types of PFAS. RESULTS:The logistic regression model found that serum PFAS levels were not significantly associated with sinonasal health outcomes, except serum Me-PFOSA-AcOH (OR: 1.164; 95% CI: 1.020-1.308), which significantly increased the likelihood of reporting frequent nasal congestion in the past 12 months. The BKMR model identified exposure-response relationships on olfaction of Me-FPOSA-AcOH and PFHxS becoming more pronounced as the concentration of PFNA within the mixture increased. CONCLUSION:Our results explore potential relationships between PFAS and adverse sinonasal health effects. Exposure to Me-PFOSA-AcOH may be related to frequent nasal congestion, while other PFAS may have complex, mixture-dependent effects on olfaction.

Abstract The exposome is the measure of all the exposures of an individual in a lifetime and how those exposures relate to health. Exposomics is the emerging field of research to measure and study the totality of the exposome. Exposomics can assist with molecular medicine by furthering our understanding of how the exposome influences cellular and molecular processes such as gene expression, epigenetic modifications, metabolic pathways, and immune responses. These molecular alterations can aid as biomarkers for the diagnosis, disease prediction, early detection, and treatment and offering new avenues for personalized medicine. Advances in high throughput omics and other technologies as well as increased computational analytics is enabling comprehensive measurement and sophisticated analysis of the exposome to elucidate their cumulative and combined impacts on health, which can enable individuals, communities, and policymakers to create programs, policies, and protections that promote healthier environments and people. This review provides an overview of the potential role of exposomics in molecular medicine, covering its history, methodologies, current research and applications, and future directions.

Food allergies (FAs) are adverse immune reactions to normally innocuous foods. Their prevalence has been increasing in recent decades. They can be IgE-mediated, non-IgE mediated, or mixed. Of these, the mechanisms underlying IgE-mediated FA are the best understood and this has assisted in the development of therapeutics. Currently there are two approved drugs for the treatment of FA, Palforzia and Omalizumab. Palfornia is a characterized peanut product used as immunotherapy for peanut allergy. Immunotherapy, involves exposure of the patient to small but increasing doses of the allergen and slowly builds immune tolerance to the allergen and increases a patient’s allergic threshold. Omalizumab, a biologic, is an anti-IgE antibody which binds to IgE and prevents release of proinflammatory allergenic mediators on exposure to allergen. Other biologics, investigational vaccines, nanoparticles, Janus Kinase and Bruton’s tyrosine kinase inhibitors, or DARPins are also being evaluated as potential therapeutics. Oral food challenges (OFC) are the gold standard for the diagnosis for FA. However, they are time-consuming and involve risk of anaphylaxis; therefore, alternative diagnostic methods are being evaluated. This review will discuss how the immune system mediates an allergic response to specific foods, as well as FA risk factors, diagnosis, prevention, and treatments for FA.

Climate change is not just jeopardizing the health of our planet but is also increasingly affecting our immune health. There is an expanding body of evidence that climate-related exposures such as air pollution, heat, wildfires, extreme weather events, and biodiversity loss significantly disrupt the functioning of the human immune system. These exposures manifest in a broad range of stimuli, including antigens, allergens, heat stress, pollutants, microbiota changes, and other toxic substances. Such exposures pose a direct and indirect threat to our body's primary line of defense, the epithelial barrier, affecting its physical integrity and functional efficacy. Furthermore, these climate-related environmental stressors can hyperstimulate the innate immune system and influence adaptive immunity—notably, in terms of developing and preserving immune tolerance. The loss or failure of immune tolerance can instigate a wide spectrum of noncommunicable diseases such as autoimmune conditions, allergy, respiratory illnesses, metabolic diseases, obesity, and others. As new evidence unfolds, there is a need for additional research in climate change and immunology that covers diverse environments in different global settings and uses modern biologic and epidemiologic tools.

People who suffer from asthma can have difficulty breathing after they are exposed to normally harmless substances in the air, such as pollen, dust, smoke, and pet dander. Some people experience a worsening of their asthma symptoms after a thunderstorm, and data tell us that climate change is making asthma more of a problem. But how do weather and climate events make it hard for some people to breathe? Asthma happens when the body’s immune system mistakes airborne particles for dangerous invaders and tries to fight them. It seems that climate change is increasing the amounts of air pollution, pollen, and mold in the air. The more of these triggers people breathe in, the greater the risk of asthma. In this article, we will explain how asthma happens, how climate change is making it worse, and what we can all do to help.

Introduction Increased greenhouse gas emissions since the industrial age have led to higher global temperatures and frequency and severity of climate events, such as heat waves, wildfires, floods, and storms. These changes are adversely affecting human health and increasing disease risk, including risk of allergic diseases. Further understanding of the environmental factors and the cellular and molecular mechanisms mediating these increases can assist in developing strategies to adapt to and mitigate climate change. Materials and Methods We conducted a scoping review of the literature from 2010 through 2024 using PubMed and Scopus. Results Thunderstorms, dust storms, wildfires, and other climate change factors increase allergies both directly and indirectly through increases in particulate matter, pollen, migration of disease vectors and decreases in biodiversity. The epithelial barrier, hygiene, “old friends,” and biodiversity hypotheses have been put forward to explain the underlying mechanism mediating these increases. Conclusion There is an urgent need to reduce the use of fossil fuels to mitigate climate change and protect planetary and human health. While international accords such as the 2015 Paris Agreement have been signed with the aim of lowering greenhouse gases and limiting future global temperature increases, it is clear that increased efforts are needed to meet these goals. Evidence-based solutions for adapting to the increased prevalence of allergic diseases and cost-benefit analysis of current mitigation strategies for lowering allergic diseases are also needed.

Global warming and climate change have increased the pollen burden and the frequency and intensity of wildfires, sand and dust storms, thunderstorms, and heatwaves—with concomitant increases in air pollution, heat stress, and flooding. These environmental stressors alter the human exposome and trigger complex immune responses. In parallel, pollutants, allergens, and other environmental factors increase the risks of skin and mucosal barrier disruption and microbial dysbiosis, while a loss of biodiversity and reduced exposure to microbial diversity impairs tolerogenic immune development. The resulting immune dysregulation is contributing to an increase in immune-mediated diseases such as asthma and other allergic diseases, autoimmune diseases, and cancer. It is now abundantly clear that multisectoral, multidisciplinary, and transborder efforts based on Planetary Health and One Health approaches (which consider the dependence of human health on the environment and natural ecosystems) are urgently needed to adapt to and mitigate the effects of climate change. Key actions include reducing emissions and improving air quality (through reduced fossil fuel use), providing safe housing (e.g., improving weatherization), improving diets (i.e., quality and diversity) and agricultural practices, and increasing environmental biodiversity and green spaces. There is also a pressing need for collaborative, multidisciplinary research to better understand the pathophysiology of immune diseases in the context of climate change. New data science techniques, biomarkers, and economic models should be used to measure the impact of climate change on immune health and disease, to inform mitigation and adaptation efforts, and to evaluate their effectiveness. Justice, equity, diversity, and inclusion (JEDI) considerations should be integral to these efforts to address disparities in the impact of climate change.

Epigenetic modifications control gene expression and are essential for turning genes on and off to regulate and maintain differentiated cell types. Epigenetics are also modified by a multitude of environmental exposures, including diet and pollutants, allowing an individual’s environment to influence gene expression and resultant phenotypes and clinical outcomes. These epigenetic modifications due to gene–environment interactions can also be transmitted across generations, raising the possibility that environmental influences that occurred in one generation may be transmitted beyond the second generation, exerting a long-lasting effect. In this review, we cover the known mechanisms of epigenetic modification acquisition, reprogramming and persistence, animal models and human studies used to understand multigenerational epigenetic transmission, and examples of environmentally induced epigenetic change and its transmission across generations. We highlight the importance of environmental health not only on the current population but also on future generations that will experience health outcomes transmitted through epigenetic inheritance.

Burning of fossil fuels along with deforestation and ecological disruption have led to the warming of the Earth and climate change. Children are especially vulnerable to adverse health effects of climate change associated changes in the air, soil, and water as their organs are still developing, have a faster breathing rate, higher per pound ingested and inhaled exposures, and greater relative body surface area. To protect this vulnerable population, health care professionals need to play a leading role. In 2015, the American Academy of Pediatrics (AAP) updated their original 2007 Global Climate Change and Children's Health policy statement (again updated in 2024) stating that, "failure to take prompt, substantive action would be an act of injustice to all children." Health care professionals need to educate themselves and their patients of the health risks posed by climate change and incorporate climate change counseling into their practice. They also need to go beyond the framework of the healthcare system and work collaboratively with communities, corporations, and governments to advocate for policies and solutions to mitigate and adapt to climate change. The health and wellbeing of future generations rests upon the actions we take today. IMPACT: Summarizes the adverse effects of increased anthropogenic activity and burning of fossil fuels on planetary and human health Details the increased vulnerability of children to environmental assaults and their long-term effects Provides guidance and resources to health care professionals to empower them to act as advocates for systemic and structural changes that protect children's health.

Increased fossil fuel usage has increased CO2 concentrations leading to global warming and climate change with increased frequency and intensity of extreme weather events such as thunderstorms, wildfires, droughts, heat waves, and others. These changes increase the risk of adverse health effects for all human beings. However, these experiences do not impact everyone equally. Underserved communities, including people of color, the elderly, people living with chronic conditions, and socioeconomically disadvantaged groups have greater vulnerability to the impacts of climate change. These vulnerabilities are a result of multiple factors such as disparities in healthcare, lower educational status, systemic racism, and many others. These social inequities are exacerbated by extreme weather events, which act as threat multipliers increasing disparities in health outcomes. It is clear that without human action, these global temperatures will continue to increase to unbearable levels creating an existential crisis. There is now global consensus that climate change is caused by anthropogenic activity and that actions to mitigate and adapt to climate change are urgently needed. The 2015 Paris Accord was the first truly global commitment that set goals to limit further warming. It also aimed to implement equity in action, founded on the principle of common but differentiated responsibilities. Meeting these goals require individual, community, organizational, national, and global cooperation. Health care professionals, often in the frontline with firsthand knowledge of the health impacts of climate change, can play a key role in advocating for just and equitable climate change adaptation and mitigation.

Abstract Climate change increases ground-level ozone concentrations in ambient air, increasing the risk of new-onset and exacerbation of asthma and chronic obstructive pulmonary disease (COPD). It also increases the frequency and severity of wildfires, thereby raising ambient levels of particulate matter and other air pollutants and increasing respiratory tract irritation and new-onset and exacerbation of asthma and COPD. It increases the duration of the pollen season and the allergenicity of pollen, thereby worsening symptoms of allergic rhinitis and asthma. And it increases the frequency and severity of heavy downpours and floods, increasing the likelihood of indoor moisture and growth of and exposure to mold, as well as increased incidence of fungal respiratory disorders. Prevention of climate-induced respiratory disorders can be achieved by mitigation of greenhouse gases and by preventive measures taken by government agencies and individuals to reduce exposure to ozone, particulate matter, pollen, mold, and excessive heat.

IgE-mediated food allergy (IgE-FA) occurs due to a breakdown in immune tolerance that leads to a detrimental type 2 helper T cell (TH2) adaptive immune response. While the processes governing this loss of tolerance are incompletely understood, several host-related and environmental factors impacting the risk of IgE-FA development have been identified. Mounting evidence supports the role of an impaired epithelial barrier in the development of IgE-FA, with exposure of allergens through damaged skin and gut epithelium leading to the aberrant production of alarmins and activation of TH2-type allergic inflammation. The treatment of IgE-FA has historically been avoidance with acute management of allergic reactions, but advances in allergen-specific immunotherapy and the development of biologics and other novel therapeutics are rapidly changing the landscape of food allergy treatment. Here, we discuss the pathogenesis and immunobiology of IgE-FA in addition to its diagnosis, prognosis, and treatment.

In this review, we provide an overview of food allergy genetics and epigenetics aimed at clinicians and researchers. This includes a brief review of the current understanding of genetic and epigenetic mechanisms, inheritance of food allergy, as well as a discussion of advantages and limitations of the different types of studies in genetic research. We specifically focus on the results of genome-wide association studies in food allergy, which have identified 16 genetic variants that reach genome-wide significance, many of which overlap with other allergic diseases, including asthma, atopic dermatitis, and allergic rhinitis. Identified genes for food allergy are mainly involved in epithelial barrier function (e.g., FLG, SERPINB7) and immune function (e.g., HLA, IL4). Epigenome-wide significant findings at 32 loci are also summarized as well as 14 additional loci with significance at a false discovery of < 1 × 10-4. Integration of epigenetic and genetic data is discussed in the context of disease mechanisms, many of which are shared with other allergic diseases. The potential utility of genetic and epigenetic discoveries is deliberated. In the future, genetic and epigenetic markers may offer ways to predict the presence or absence of clinical IgE-mediated food allergy among sensitized individuals, likelihood of development of natural tolerance, and response to immunotherapy.