January 26–27, 2026
Virtual Workshop

The Division of Lung Diseases at the National Heart, Lung, and Blood Institute (NHLBI) hosted a 2-day virtual workshop titled, “Lung as the Gateway for Environmental Exposures in Pulmonary and Cardiovascular Disease” on January 26–27, 2026. Planning for the workshop was a collaborative effort among NHLBI, the National Institute of Environmental Health Sciences (NIEHS), the National Institute of Allergy and Infectious Diseases (NIAID), and the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). Attendees included basic scientists, primary care physicians, pediatricians, pulmonologists, epidemiologists, toxicologists, implementation scientists, data scientists, other interdisciplinary researchers, and community representatives. Presenters discussed the unique role of the lung as the interface with the environment, and the pulmonary and cardiovascular consequences of inhalational and heat exposures to identify critical research gaps, challenges, and opportunities to advance research and interventions to mitigate potential health effects.

Workshop Objectives

• Describe mechanistic research to understand the pathogenesis of specific pulmonary and cardiovascular diseases following inhaled environmental exposures such as natural disasters and health emergencies (e.g., extreme temperatures, hurricanes, and wildfires).
• Discuss current research tools (e.g., multi-omic approaches, novel biomarkers, and personal monitors and imaging to assess individual exposures).
• Review epidemiologic studies on the links between environmental exposures and human heart and lung diseases, and discuss methods for data integration (e.g., novel big data/machine learning approaches).
• Consider implementation science research, including studies on pharmacological and dietary interventions that may reduce susceptibility to specific pulmonary and cardiovascular diseases following inhaled exposures.

Agenda

The agenda for this workshop can be viewed here.

Program Book

For more information, view the workshop program book.

Videocast

• DAY 1: MONDAY JANUARY 26, 2026, from 9 AM – 2:30 PM ET:
  https://videocast.nih.gov/watch/4e3f476c-17e8-11f1-9f14-124f0a52e769
• DAY 2: TUESDAY JANIARY 27, 2026, from 10 AM – 4 PM ET:
  https://videocast.nih.gov/watch/764a07c0-17f1-11f1-9f14-124f0a52e769

Summary

Introduction to Lung as a Sensory Organ

The human lung is the first line of defense against inhaled exposures, and it works with other body systems to serve as both a sensory and an immune organ. Particles that enter the human body through respiratory airways accumulate and penetrate the lung tissue over time. Environmental exposures, in the perinatal period and during childhood and adolescence, have been shown to affect lung development and function adversely and to increase the risk of respiratory symptoms. Additionally, inhaled exposures throughout the lifespan diminish the lung’s regenerative potential through various mechanisms (e.g., oxidative stress and DNA damage) and worsen pulmonary health conditions (e.g., asthma and chronic obstructive pulmonary disease [COPD]). More frequent and intense natural disasters and extreme weather events increase environmental exposures that affect pulmonary and cardiometabolic health, highlighting a need to prioritize research on the lung as the gateway for these impacts.

Keynote Addresses

Impact of Natural Disasters and Extreme Weather Events on Pulmonary Health

Natural disasters and extreme weather events (e.g., wildfires, drought and desertification, volcanic eruptions, dust storms, and earthquakes) are increasing in frequency and intensity. Research indicates that these events are associated with elevated exposures (e.g., wildfire smoke and increased mold after storms) that adversely affect pulmonary and cardiovascular health. Exposures are linked with acute respiratory problems, exacerbations in chronic lung conditions (e.g., COPD and asthma), and increased healthcare utilization, among other outcomes. Health effects of exposures may occur through multiple mechanisms, including mucociliary and epithelial barrier dysfunction, inflammation, cellular and immune dysfunction, airway remodeling, and epigenetic changes. Preventive and mitigation actions (e.g., public health planning, community engagement, and increased implementation of interventions) are needed to reduce the adverse effects of natural disasters and extreme weather events on health.

Genome-wide Gene-Air Pollution Interaction Analysis of Lung Function in 300,000 Individuals

Lung function is a strong predictor of COPD, respiratory disease, and cardiovascular mortality independent of other relevant factors. A genome-wide association study in approximately 300,000 unrelated European individuals from the UK Biobank examined whether the effects of air pollution on lung function depend on genetics. The analysis identified seven new genome-wide interaction signals. There was an up to 440 ml lower lung function (as measured by FEV1) for certain genotypes when exposed to mean levels of outdoor air pollution. This is approximately equivalent to nine years of average normal loss of lung function in adults. However, only a small number of interaction signals were identified, the results were not consistent across gene-air pollution metrics, there was no association with genetic risk scores, and the findings are yet to be replicated. Alternative methodological approaches may yield useful insights into the relationships among exposure to air pollution, genetics, and lung function. The study highlights the importance of investigating potential vulnerability factors, as the findings may affect policy formulation and opportunities for individual protection. Examining gene-air pollution interactions with measures of longitudinal lung function in a large dataset would be valuable.

Ambient Air Pollution and Early-Life Lung Function

Air pollution is ubiquitous, and exposure during pregnancy is associated with reduced lung function in children, which can affect the trajectory for adult lung health and risk for comorbidities. While the underlying biological mechanisms linking PM to health outcomes remain unclear, evidence points to oxidative stress as a central mechanism. The oxidative potential (OP) of particulate matter (PM), which measures the capacity of PM to generate reactive oxygen species and trigger oxidative stress, integrates both physical and chemical properties of PM and their health consequences. Recent studies suggest that oxidative potential of PM may be a more accurate predictor than mass concentration for respiratory health outcomes. The OP of PM varies according to the type of environment (e.g., urban, rural, or industrial) and emission sources. Research indicates that oxidative stress is three times higher in urban areas with heavy road traffic than in rural regions. Studies are tracking the pulmonary health effects of exposure to OP of PM during early life.

Low-Cost Environmental Air Pollution Sensors for Personal Exposure Assessment and Exposure Assessment in Epidemiologic Studies

Low-cost sensors are available to measure exposure to air pollution components (e.g., PM, trace gases, and volatile organic compounds) and physical exposures (such as temperature, humidity, and heat). The methodological complexity and burden level of measurement on researchers and study participants varies, with individual measures being the most difficult. Although regulating agencies distribute monitors to measure ambient exposures, their placement varies greatly across the United States. Importantly, concentrations of indoor exposures often exceed those measured outdoors. Low-cost sensors in the home offer many advantages—such as improving feasibility, enabling long-term measures, and permitting more homes to be monitored. However, placement within the home can influence readings, and sensors require calibration. Personal exposures are measured by carried instruments, but this may be a burden. Passive samplers (e.g., silicone wristbands) reduce the burden of personal exposure measures. Sensor applications include determining the health effects of ambient pollution, improving indoor air quality and extreme temperature exposures (e.g., in homes and schools), research, and public health promotion.

Panel Discussions:

The four panels that followed the Keynote Address were as follows: (1) cardiopulmonary effects of environmental exposures, (2) mechanisms of inhaled environmental exposures and cardiopulmonary health, (3) tools and technologies for environmental exposures research, and (4) interventions to mitigate cardiopulmonary effects of environmental exposures. A discussion followed each panel.

Panel 1: Cardiopulmonary Effects of Environmental Exposures

Discussions highlighted the epidemiological evidence documenting associations between prenatal exposure to ambient air pollutants on early childhood lung functioning and how these links are influenced by biological sex. Such exposures may affect lung growth and respiratory health across the lifespan; these effects may be mitigated by intervention. Some populations may be particularly susceptible to the negative effects of environmental exposures on pulmonary health—including people with dysanapsis (a common condition in which an individual’s airways are proportionally smaller than their lungs), patients with fibrotic interstitial lung disease, and children with asthma. Sex differences have been documented in both exposure to air pollutants and pulmonary diseases, and evidence is emerging that the interaction between the two—including biological responses—may also vary between males and females. A relatively recent area of research is how the lung microbiome (diverse inhaled microorganisms integral to respiratory health and immune function) interacts with other lung exposures to modify risk of disease and might be harnessed to mitigate negative effects.

Panel 2: Mechanisms of Inhaled Environmental Exposures and Cardiopulmonary Health

Wildfires emit fine particulate matter (PM2.5), which can be up to 10 times more toxic than PM from other sources, as well as harmful gases (e.g., carbon monoxide, volatile organic and inorganic compounds, and nitrogen oxides). Studies have documented a concentration-related increase in mortality risk (particularly cardiovascular and pulmonary mortality) attributable to wildfire-associated PM2.5. Exposure to wildfire smoke also is associated with adverse respiratory outcomes, such as exacerbations of asthma and COPD, and increased risk of lower respiratory infections. Environmental exposures increase allergies and asthma through various mechanisms, including activating the inflammatory pathway (e.g., immunoglobulin E production) and inducing oxidative stress. Cadmium—a component of cigarette smoke, wildfire suppressants, and fossil fuel combustion—is a key airborne toxicant that contributes to chronic lung diseases, including COPD and emphysema. Research indicates that cadmium disrupts inflammation resolution and prolongs tissue damage.

Evidence shows that the nucleotide-binding oligomerization domain-like receptor, or NOD-like receptor, NLRX1 plays an important role in the cellular response to the inhalation of ozone and co-exposure to a type of PM (ultrafine carbon black) suggesting that NLRX1 agonism is a viable strategy to counter air pollution–induced pulmonary inflammation and injury. Air pollution exposure also is associated with significant adverse cardiometabolic health effects and related mortality (e.g., atherosclerosis and ischemic events). PM exposure alters gut microbiota, activating the gastrointestinal-vascular pathway and producing negative metabolic effects and mitochondrial dysfunction.

Many people around the globe are exposed daily to household air pollution from the burning of solid fuels on inefficient cookstoves. In the Ghana Randomized Air Pollution and Health Study, researchers randomly assigned pregnant women to clean-fuel stoves (using liquefied petroleum gas) or traditional stoves (control group) during early pregnancy and through the child’s first year of life. Longitudinal follow-up found that air pollution exposures were lower among participants randomized to the clean-fuel stoves compared with the control group during the intervention period. Additionally, children in the intervention group had better lung function and lower diastolic blood pressure compared to those in the control group at age four years.

Extreme heat exposure—which is associated with exacerbations of COPD, asthma, and interstitial lung disease, as well as the clinical consequences of heart failure, arrhythmias, and ischemia—is increasing in the United States. Factors linked to susceptibility include age, comorbidities, less access to air conditioning, poor housing conditions, and limited green space. High nighttime temperatures may contribute to adverse health effects in cities with urban heat islands. Environmental precision medicine—facilitated by high-resolution geographic data—offers an opportunity to identify those at highest risk and deliver interventions at scale to prevent adverse health outcomes.

Panel 3: Tools and Technologies for Environmental Exposures Research

A range of human-relevant preclinical tools are available to study inhaled environmental exposures and model human diseases (e.g., organ-on-chip, robotics that simulate respiration, organoids, and three-dimensional bioprinting). Although these tools have challenges—as they do not replicate organ-organ crosstalk and model organ systems—they can contribute to the understanding of the effect of environmental exposures on human health and complement other research approaches.

Geospatial context is essential for understanding how place, time, and human mobility shape pulmonary and cardiovascular risk related to environmental exposures. Geospatial artificial intelligence (AI) enables the integration of multiscale environmental exposures with clinical, genomic, and real-world health data. Key resources supporting this research include the Geospatial Analytical Research Knowledgebase, as well as satellite and remote sensing products. By combining quartz tube combustion systems with computational modeling, researchers can identify relationships between groups of chemicals in wildfire exposure mixtures and biological responses to discover plausible mechanisms that drive biological responses. Statistical and machine learning approaches can improve the prediction of disease trajectories. For example, the progression of cystic fibrosis (CF) is strongly influenced by exposure to air pollution. By integrating clinical predictors and environmental risk factors—particularly hyper-local exposures—researchers improved the prediction of lung function declines among young people with CF.

Panel 4: Interventions to Mitigate Cardiopulmonary Effects of Environmental Exposures

Increasing evidence suggests that diet and nutrition influence resilience to the pro-inflammatory, pro-oxidant effects of air pollution exposures on respiratory health. Nutritional characteristics such as antioxidant capacity (fruits and vegetables), inflammation-resolving abilities (omega-3 fatty acids from fish), and positive effects on the gut microbiome (fiber) are among the purported mechanisms. Exposure to air pollution (e.g., PM2.5) is associated with disrupted gut microbiota. Human studies suggest that microbiome-related intervention strategies (e.g., pre- and probiotics) may mitigate the negative consequences of pollutant exposures. However, more research is needed on how the gut microbiome may affect the response of the lung or lower respiratory tract compartments to air pollution.

The use of air purifiers (such as a high-efficiency particulate air [HEPA] filters) to reduce indoor air pollution is one type of intervention that may improve cardiovascular health. An ongoing randomized controlled trial (RCT) is examining whether air purifiers can improve cardiovascular outcomes among patients with heart failure in three cities in India. Research indicates that the use of HEPA filters significantly reduces indoor levels of PM2.5 and nitrogen dioxide. Researchers found that among people with COPD, use of HEPA filters was associated with reduced rescue medication use and fewer symptom exacerbations.

The physical environments of buildings—such as natural and mechanical ventilation, central heating and air conditioning systems, and use of air cleaners—affect indoor air quality. The operation and performance of air cleaning systems and behaviors affecting their use is important for attaining better indoor air quality. Nevertheless, the application of well-established building engineering principles can also improve indoor air quality. For example, it is important to minimize indoor emissions, protect against outdoor pollution, keep buildings dry, and ventilate well. Some environmental and policy actions that affect outdoor air quality—such as the Clean Air Act of 1970, emission-control measures, urban land use policies, and building codes—are associated with improvements in respiratory health. For example, the Clean Air Act reduced PM2.5 and contributed to better child lung function and growth, as well as the extension of the average life expectancy in the United States.

Community Perspectives: Patients

People with chronic lung conditions and their families face challenges—such as daily breathing work and multiple medical procedures and hospital stays. For families that live in areas affected by wildfires and evacuation orders, that extant stress is exacerbated. Medications may require refrigeration, and some respiratory-support equipment is not portable—making evacuation-related decision-making difficult in the absence of clear guidance from authorities. Families may experience constant mental and emotional exhaustion. They may not always feel seen and heard at medical appointments, which tend to be brief. Organizations that support patients can help researchers and care professionals better engage with individuals who have chronic lung conditions and their families.

Research Gaps and Opportunities

• Establish interdisciplinary research teams to address the effects of environmental exposures on cardiopulmonary health, other organs, and systemic tissues.
• Study the acute and long-term effects of complex pollution mixtures (beyond PM), other environmental (e.g., extreme weather events and airborne allergens) and occupational exposures (e.g., inhalants), and their interactions on health and in specific health conditions through mechanistic research, –omics approaches, and other methodologies.
• Determine how environmental exposures influence disease programming, systemic manifestations, progression, and outcomes across the lifespan.
• Examine the relationships between air pollutants and lung and airway microbes, as well as the influence of the gut microbiome on pulmonary functioning and health.
• Study effective interventions for air pollutant exposures.
• Investigate sex differences and the mechanisms underlying observed sex differences in response to exposures across the lifespan.
• Develop, test, and conduct implementation science on real-world interventions that aim to prevent and mitigate the health effects of environmental exposures and extreme weather. Evaluate the cost-effectiveness of interventions.
• Study the longitudinal effects of recurrent environmental exposures (e.g., health consequences of wildfire smoke exposure both in wildland firefighters and the public), as well as their underlying mechanisms.
• Adopt a targeted approach to gene-environment interactions focused on precise exposure, occupation, diet, and genes that are involved in mechanisms (e.g., oxidative stress response) to identify susceptible subgroups.
• Expand pollution metrics beyond concentration of PM2.5 to identify differential toxicity by source.
• Investigate biomarkers of various environmental exposures linked with specific adverse health effects and cardiopulmonary conditions.
• Identify biological targets for medications to mitigate the pulmonary impact of environment-related exposures—particularly air pollution, molds, and pollens.
• Develop, test, and conduct implementation science on small scale, affordable, and practical exposure assessment tools (e.g., sensors) that capture local variability in indoor and outdoor environmental exposures (volatile organic compounds, ultrafine particles, and metals). Improve sensor accuracy, specificity, and energy requirements.
• Integrate open-source data on multiple exposures, biomarkers, -omics, health outcomes and other factors to advance statistical learning, machine learning, and AI modeling approaches. Advance data and model harmonization, as well as clinical risk prediction methods based on hyper-local exposure data.
• Conduct clinical trials and intervention studies that consider both indoor and outdoor exposures and evaluate nutritional/food delivery interventions and their impact on the health effects of environmental exposures.
• Advance exposure science by investing in research that leverages relevant data from longitudinal cohorts, methodological improvements, and expanding the use of tools and technologies for environmental exposures research. Electronic health record data and wearable technology (and integration of both) may provide opportunities to deliver interventions to protect individuals at highest risk.

Conclusion

Throughout the workshop, speakers highlighted the role of the lung as a sensory organ and the effects of environmental exposures, natural disasters, and extreme weather events on cardiopulmonary health. Environmental exposures—particularly during the prenatal, postnatal, and early childhood periods—are associated with poorer lung function and set individuals on a trajectory for adverse health outcomes (e.g., chronic pulmonary conditions) with sex-specific effects. Underlying mechanisms may include inflammation, oxidative stress, DNA damage, gene-environment interactions, effects on microbiota, and epigenetic changes. Patients with chronic pulmonary conditions (e.g., asthma and COPD) are susceptible to the negative effects of ongoing environmental exposures. Low-cost sensors and state-of-the-art tools and technologies—such as organs-on-chip, robotics, and AI modeling of geospatial data—offer research opportunities to advance the understanding of environmental exposures and cardiopulmonary health. Interventions to mitigate the adverse health effects from indoor and outdoor air pollution exposures include switching to cleaner fuels in cook stoves, use of air purifiers, improving building engineering principles, and implementing air pollution reduction policies.

Disclaimer: The findings, knowledge gaps, and opportunities described here represent a summary of individual opinions and ideas expressed during the workshop. The summary does not represent a consensus opinion or directive made to or by NHLBI or NIH.

Participants

Workshop Co-chairs

Nadia Hansel, M.D., M.P.H., Johns Hopkins University 
Mary Rice, M.D., M.P.H., Harvard Medical School
Emily Brigham, M.D., M.H.S., University of British Columbia, Canada

NIH Committee Members

NHLBI

Beena G. Sood, M.D., M.S. (Co-chair)
Marishka K. Brown, Ph.D.
Regina Bures, Ph.D.
Stephanie Davis, Ph.D.
Marisol Espinoza-Pintucci, Ph.D.
Michelle M. Freemer, M.D., M.P.H.
Marrah Lachowicz-Scroggins, Ph.D., M.F.S., GCCP
Joy Liu, M.D.
Qing Lu, Ph.D.
Mary Masterson, Ph.D., M.S.
Gustavo Matute-Bello, M.D.
Lisa Postow, Ph.D.

NIEHS

Jacqui Marzec, M.S. (Co-chair)
Srikanth Nadadur, Ph.D. (Co-chair)
Ashlinn K. Quinn, Ph.D.

NIAID

Taylor Poor, M.D., Ph.D. (Co-chair)
Patrice M. Becker, M.D.
Alkis Togias, M.D.

NICHD

Cinnamon Dixon, D.O., M.P.H.

Speakers and Moderators

Jésus A. Araujo, M.D., Ph.D., M.Sc., David Geffen School of Medicine at University of California, Los Angeles
John R. Balmes, M.D., University of California, Berkeley School of Public Health 
Hasan Bayram, M.D., Koc University Hospital, Turkey 
Kambez Benam, D.Phil., University of Pittsburgh
Emily Brigham, M.D., M.H.S., University of British Columbia, Canada
Christopher Carlsten, M.D., M.P.H., University of British Columbia, Canada
Ulrike Gehring, Ph.D., Utrecht University, Netherlands
Gillian C. Goobie, M.D., Ph.D., University of British Columbia, Canada 
Nadia Hansel, M.D., M.P.H., Johns Hopkins School of Medicine
Anna Hansell, M.P.H., Ph.D., MRCP, FFPH, University of Leicester, United Kingdom
Yvonne Huang, M.D., University of Michigan
Salik Hussain, D.V.M., Ph.D., Health Sciences, West Virginia University 
Ilona Jaspers, Ph.D., University of North Carolina School of Medicine
Kirsten Koehler, Ph.D., Johns Hopkins University
Alison Lee, M.D., M.S., Icahn School of Medicine at Mount Sinai
Jacqui Marzec, M.S., NIEHS
Gustavo Matute-Bello, M.D., NHLBI
Meredith McCormack, M.D., M.H.S., Johns Hopkins University
Srikanth Nadadur, Ph.D., NIEHS
Kari C. Nadeau, M.D., Ph.D., Harvard T.H. Chan School of Public Health
Taylor Poor, M.D., Ph.D., NIAID
Meghan E. Rebuli, Ph.D., University of North Carolina School of Medicine
Stacie Reveles, Cystic Fibrosis Research Institute
Mary B. Rice, M.D., M.P.H., Harvard Medical School
Coralynn Sack, M.D., M.P.H., University of Washington
Chi-Ren Shyu, Ph.D., University of Missouri Institute of Data Science and Informatics
Valérie Siroux, Ph.D., Inserm, France 
Beena G. Sood, M.D., M.S., NHLBI
Brent Stephens, Ph.D., Illinois Institute of Technology
Ranu Surolia, Ph.D., The University of Alabama at Birmingham
Rhonda D. Szczesniak, Ph.D., University of Cincinnati
Rajesh Vedanthan, M.D., M.P.H., New York University Grossman School of Medicine
Rosalind Wright, M.D., M.P.H., Icahn School of Medicine at Mount Sinai