Category: Asthma Prevention

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Where We Are Now: The Science of Severe Asthma Is Shifting A Research Update from the World Asthma Foundation




Something has shifted in the science of severe asthma.

Not overnight. Not with a single breakthrough. But through the accumulation of peer-reviewed evidence, molecular diagnostic technology, federal policy acknowledgment, and the persistent questions of patients who refused to accept symptom management as a final answer — the field is arriving at a conclusion that changes the way we need to think about one of medicine’s most undertreated populations.

For a significant subpopulation of severe asthma patients, the disease is not primarily inflammatory. It is microbial. And the tools to find it have existed for years — they simply haven’t been applied.

This post documents where that conversation stands in 2026 — and why the World Asthma Foundation believes it represents one of the most important unaddressed gaps in respiratory medicine.

The Subpopulation We Can’t Count

Severe asthma affects approximately 30 million people globally — roughly 10% of the 300 million living with asthma worldwide. Of those, peer-reviewed evidence documents that 15–17% are complete non-responders to biologic therapy, 43–69% are only partial responders, and only 14–24% achieve the kind of remission that biologics promise.

That means the majority of severe asthma patients on the most sophisticated treatments available are not getting better. And for a subset of those patients — the size of which we cannot currently estimate — the reason may not be that the treatment is inadequate. It may be that the diagnosis is incomplete.

The Microbiome — The Missing Variable

The lung was once considered a sterile organ. It is not.

Peer-reviewed research now documents that the lung has its own microbiome — a complex ecosystem of organisms that, when in balance, supports healthy respiratory function, and when disrupted, may drive disease in ways that standard diagnostics cannot see and standard treatments cannot reach.

What disrupts the lung microbiome:

  • Long-term corticosteroid use suppresses the adaptive immune response that normally keeps opportunistic bacteria in check — creating conditions for pathogenic organisms to establish and dominate
  • Antibiotic exposure selects for resistant organisms while eliminating susceptible ones, progressively narrowing the microbial diversity that supports immune health
  • Gut microbiome disruption — through H. pylori eradication, antibiotic courses, diet, and environmental factors — alters the gut-lung immune axis in ways that affect respiratory microbiome composition over years and decades

The result, in a vulnerable subpopulation, is a lung ecosystem dominated by organisms that standard cultures cannot identify, that standard treatments cannot reach, and that standard diagnostics were never designed to find.

The Diagnostic Gap — Why We Can’t See What We’re Missing

Standard severe asthma diagnostics in 2026 rely primarily on spirometry, blood eosinophil counts, IgE levels, sputum cytology, and standard bacterial culture. These tools were designed to characterize the Type 2 inflammatory endotype. They are largely blind to the microbial endotype.

Molecular diagnostic sequencing — metagenomics, DNA-level analysis of bronchoscopic samples — can identify what is actually living in the lung with a precision that standard cultures cannot approach. This technology exists now. It is not experimental. It is not prohibitively expensive relative to the cost of years of failed biologic therapy. It is simply not part of the standard diagnostic algorithm for severe asthma.

That is the gap. And it is costing patients — in quality of life, in progressive disease burden, and in decades of misdirected treatment.

The Steroid Trap — When Treatment Compounds the Problem

This is the most uncomfortable finding in the current literature — and the one the severe asthma community most needs to confront.

Long-term corticosteroids suppress airway inflammation effectively. They also suppress the very immune mechanisms that would normally control bacterial colonization in the lung. The research is now explicit: steroid use is a documented risk factor for gut and lung microbiota disruption.

In a patient with an already-compromised lung ecosystem, long-term corticosteroids may be creating the conditions that allow opportunistic, drug-resistant organisms to establish dominance — while the treatment that finds and addresses those organisms is never ordered.

The treatment suppresses the symptom. The organism advances. This is not a reason to stop corticosteroid therapy. It is a reason to investigate the microbiome in every patient who requires long-term corticosteroid use.

The Gut-Lung Axis — The Origin Story That Goes Back Further

One of the most consequential findings in recent asthma research is the documented relationship between gut microbiome disruption and respiratory disease. The gut and lung are immunologically connected. Disruption of the gut microbiome — through antibiotic exposure, H. pylori eradication, dietary changes, or environmental factors — alters the systemic immune environment in ways that affect respiratory health over years and decades.

Research currently underway at the University of Kentucky — funded by the Global Lyme Alliance — is examining precisely this mechanism: how infection and antibiotic treatment disrupt the gut microbiome and weaken the intestinal barrier, driving systemic inflammation throughout the body. The implications for severe asthma patients with repeated antibiotic exposure or a history of H. pylori eradication are significant.

The origin of a patient’s severe asthma may not begin in the lung. It may begin in the gut — years or decades before the first wheeze.

The Polymicrobial Question — Beyond Single-Organism Thinking

Emerging research suggests that the microbial component of treatment-resistant asthma may not be a single-organism problem. Published evidence documents that immunosuppressed patients with respiratory bacterial colonization frequently carry co-existing organisms — bacterial, viral, and fungal — that interact with each other and with the host immune system in ways that single-organism treatment approaches cannot address.

For the patient who has failed multiple biologic therapies and whose disease continues to progress, a comprehensive polymicrobial assessment — molecular sequencing of bronchoalveolar lavage fluid, viral reactivation panels, gut microbiome profiling — may be the diagnostic step that changes everything.

The Neurological Dimension — When the Lung Isn’t the Limit

When systemic inflammation driven by an unidentified microbial burden is suppressed but not resolved, the consequences can extend beyond the respiratory system. Peer-reviewed research documents the gut-brain axis, the relationship between microbial dysbiosis and mast cell activation syndrome, and published cases of Small Fiber Neuropathy driven by infectious burden that resolved with targeted treatment.

For severe asthma patients with unexplained neurological symptoms — neuropathy, autonomic dysfunction, cognitive changes — the question of whether an undetected microbial burden is contributing deserves formal investigation. The lung may be where the disease presents. The microbiome may be where it lives.

What We Are Calling For

For patients with treatment-resistant severe asthma: Ask for molecular diagnostic sequencing before accepting that your disease is simply “refractory.” Ask specifically: “Has my lung microbiome been assessed by molecular sequencing?”

For pulmonologists: A bifurcated biologic response — improvement in one domain, none in others — is a diagnostic signal pointing toward an independent disease axis. Molecular diagnostics of bronchoalveolar lavage fluid should be considered in patients who have failed multiple biologic therapies.

For researchers: The microbial endotype of severe asthma needs its own epidemiological definition and research program. We do not know how many patients fall into this category. That is an unacceptable gap in 2026.

For diagnostic standards bodies: Molecular sequencing must be incorporated into the diagnostic pathway for severe asthma patients who fail conventional therapy. The technology exists. The evidence base is building.

For policymakers: Reimbursement for molecular diagnostic sequencing in treatment-resistant severe asthma is a health equity issue. The patients who most need better diagnostics are often those with the fewest resources to advocate for them.

What We Will Be Exploring Next

Over the coming months the World Asthma Foundation will publish a series examining these questions in depth:

  • The Origin Story — How gut microbiome disruption initiates the cascade that drives treatment-resistant asthma
  • The Microbial Endotype — What molecular diagnostics are finding in the lungs of patients who have failed standard care
  • The Polymicrobial Dimension — When the problem isn’t one organism but an ecosystem
  • The Neurological Connection — When untreated microbial burden extends beyond the lung
  • The Patient Roadmap — How to advocate for molecular diagnostics and navigate a specialist system that sees organs rather than patients

The observations in this post are informed by peer-reviewed literature, ongoing research programs at leading academic institutions, and the clinical experience of patients navigating treatment-resistant severe asthma. They represent the World Asthma Foundation’s current research-informed perspective — not clinical recommendations. Patients should discuss diagnostic and treatment decisions with their physicians.

World Asthma Foundation | worldasthmafoundation.org | worldasthmaday.org | May 2026

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World Asthma Day 2025: Reframing Severe Asthma – From Root Causes to Real-World Solutions

May 6, 2025 – The World Asthma Foundation (WAF) is proud to announce a major new initiative on World Asthma Day aimed at transforming how we understand and manage severe asthma — a condition that continues to affect millions and defy conventional treatment.

Titled “Reframing Severe Asthma: From Ro,” this ongoing series will dig deep into the science and patient experience of severe asthma, exploring overlooked contributors and practical, cost-effective strategies for care. This initiative builds on WAF’s continuing collaboration with leading experts, including Dr. David Corry of Baylor College of Medicine, whose pioneering research into airway mycosis is helping redefine what drives severe asthma in many patients.

New Interview Available Now As part of this launch, WAF is proud to release a new in-depth interview with Dr. Corry, offering fresh insights into how fungal infections in the airways may contribute to severe asthma and how this condition can be diagnosed and treated. Watch or read the interview here: Breaking New Ground in Airway Mycosis: Insights from Dr. David Corry

“We believe the time has come to stop treating symptoms alone and start asking deeper, root cause, questions about what’s really causing severe asthma—and how we can affordably and effectively address them,” said David B. Corry, M.D., Professor of Medicine-Immunology, Allergy, and Rheumatology, Baylor College of Medicine, Houston, TX, US.

But the scope goes well beyond fungi. The series will also examine:

  • Bacterial influences in asthma, including Streptococcus pseudopneumoniae and airway microbiome disruption
  • Mast cell activation and its role in chronic inflammation and systemic symptoms
  • Genetic predisposition (e.g., ADAM33) and airway remodeling
  • Environmental and chemical sensitivities increasingly reported by severe asthma sufferers

WAF’s Reframing Severe Asthma series will feature:

  • In-depth interviews and commentary from thought leaders
  • Patient stories and clinical case insights
  • Roundtable discussions and virtual events
  • A final White Paper and Action Plan for clinicians, researchers, and policymakers

Join Us This World Asthma Day, we invite clinicians, scientists, patients, and advocates to come together and reframe the conversation around severe asthma. Let’s work toward a future where treatment addresses not just symptoms, but causes — and where no patient is left behind.

Sign up today. Its FREE.

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Candida’s Role in Inflammation and Autoimmune Response: Implications for Severe Asthma

Welcome Message from the World Asthma Foundation

Hello to our dedicated community and newcomers alike.

At the World Asthma Foundation (WAF), we’re united by a singular, important mission: to Defeat Asthma. Our approach is rooted in fostering awareness, enhancing education, and promoting research that seeks to unravel the complexities of Asthma. As we strive towards a world where Asthma is no longer a limiting factor in anyone’s life, we remain steadfast in bringing you timely, comprehensive, and relevant information.

We’re excited to share our latest blog post with you. This post encapsulates the culmination of the efforts of a variety researchers, clinicians, and organizations worldwide working independently including pioneering work from the Mayo Clinic, to shed light on the pathogenesis and exacerbation of severe asthma.

Mayo Clinic Candida Study

We delve into the compelling evidence pointing towards the intricate interplay between Candida colonization, dysbiosis, inflammation, autoimmune responses, TNF-alpha dysregulation, and comorbidities.

As we unravel these complex relationships, our hope is to equip you, our readers, with knowledge that can empower you in your journey with asthma or help you support someone who is affected.

Let’s continue to learn, share, and work together in our collective fight against Asthma.

Thank you for being a part of our mission. We encourage you to share this information with your healthcare provider.

Establishing a trustworthy and effective relationship with a healthcare provider is crucial to managing your health. It not only ensures that you get the best care but also allows for open and productive conversations about your health.

Introduction

Managing Severe Asthma remains a complex task for many pulmonary practitioners, despite available medication and trigger avoidance strategies. Frequent attacks and poor symptom control often plague patients. Recent investigations, pieced together by the World Asthma Foundation over time have uncovered dozens of notable research groups that have illuminated the complex relationship between Candida colonization, dysbiosis, inflammation, autoimmune response, TNF-alpha dysregulation, and comorbidities in the pathogenesis and exacerbation of Severe Asthma. This amassed knowledge underscores the multifaceted nature of Severe Asthma, bringing to light the critical role of Candida in the disease process.

Recent studies reveal a potential link between Candida colonization, dysbiosis, inflammation, autoimmune response, TNF-alpha dysregulation, and comorbidities in the pathogenesis and exacerbation of Severe Asthma. This article will provide an overview of these linkages, the financial impact on individuals and society, the necessity for improved diagnostic tools and processes, and source the scientific studies supporting these conclusions.

Candida Colonization, Dysbiosis, and Fungal Sensitization

Candida albicans, a common fungal inhabitant of the mouth, gut, and genital tract, can also colonize the respiratory tract. This colonization is often facilitated by dysbiosis, an imbalance in the normal microbial flora, which can be induced by various factors, including the use of antibiotics and changes in the host immune response. Further, fungal sensitization, a process where the immune system produces antibodies (IgE) against fungal allergens, plays a crucial role in the onset and severity of asthma symptoms. Studies from the Mayo Clinic underline the lower alpha-diversity of lung microbiota and higher fungal burdens in Asthma patients, showing a correlation with severity and poor control of Asthma.

Case in Point

A recent study presented at the CHEST Annual Meeting 2021 by researchers from Mayo Clinic and University of California Davis confirmed the association between intestinal fungal dysbiosis and asthma severity in humans, particularly hospital use in the past year. The study found that patients with asthma who had higher intestinal Candida burden were more likely to have severe asthma exacerbations in the previous year, independent of systemic antibiotic and glucocorticoid use. This suggests that intestinal fungal dysbiosis may worsen asthma control and outcomes in humans. The study also showed that intestinal fungal dysbiosis can enhance the severity of allergic asthma in mice by increasing lung resident group 2 innate lymphoid cells (ILC2) populations, which are important mediators of the gut-lung axis effect. The study used a novel technique of flow cytometry to identify and quantify ILC2 in the lungs of mice. These findings highlight the potential role of intestinal fungal dysbiosis and ILC2 in asthma pathogenesis and management.

Role of Antibiotics and Gut-Lung Axis

Studies show that certain antibiotics prescribed for infections, such as Helicobacter pylori, can lead to gut microbiota dysbiosis, promoting Candida colonization. This gut-lung axis, the communication between gut microbiota and lung health, can create an environment conducive to fungal overgrowth and subsequent infection. As such, understanding this interaction can offer valuable insights into asthma management. Research from the Mayo Clinic suggests that antibiotic usage can significantly contribute to these interactions and, consequently, the pathogenesis of Severe Asthma.

Mechanisms of Candida Colonization

Candida albicans utilizes several mechanisms to cross the intestinal epithelial barrier, including adherence to epithelial cells, invasion, and translocation. Each of these steps facilitates Candida’s ability to invade the host’s system and trigger an immune response. Insights from the Mayo Clinic suggest that bacterial-fungal interactions play a key role in these mechanisms and have implications for Candida colonization.

Candida-Induced Inflammation, Autoimmune Response, and TNF-alpha Dysregulation

Once established, Candida colonization can incite inflammation by provoking the immune system to produce pro-inflammatory cytokines, such as TNF-alpha. While TNF-alpha aids in fighting off infections by initiating inflammation, its dysregulation can lead to chronic inflammation and autoimmune diseases, enhancing the severity of asthma. Research from the Mayo Clinic has shown that Candida colonization in the lung induces an immunologic response, leading to more Severe Asthma.

Autoimmune Response, Comorbidities, and Severe Asthma

Recent studies propose that an autoimmune response could be involved in the onset and exacerbation of Severe Asthma, with TNF-alpha dysregulation playing a pivotal role. Comorbidities like rheumatoid arthritis, often seen in conjunction with Severe Asthma, can further complicate disease management and progression.

Burden, Financial Impact, and Comorbidities

Severe Asthma imposes a substantial burden on individuals and society, financially and otherwise. Healthcare costs, productivity loss, and reduced quality of life contribute to this impact. Asthma comorbidities such as autoimmune diseases can affect disease progression and outcomes, underscoring the need for a comprehensive management approach.

The Necessity for Improved Diagnostic Tools

An accurate diagnosis of Candida colonization, inflammation, and autoimmune response in severe asthma is crucial for optimal patient management. There’s a growing need for improved diagnostic methodologies, tools, and processes. Advances in diagnostic techniques, such as bronchoscopy and bronchoalveolar lavage (BAL), can offer valuable insights into Candida colonization and the associated inflammatory and autoimmune processes. The Mayo Clinic’s recent findings, which identify a unique pattern of lower alpha-diversity and higher fungal burden in the lung microbiota of severe asthma patients, further emphasize the need for enhanced diagnostic methods.

Conclusion

Understanding the link between Candida colonization, dysbiosis, inflammation, autoimmune response, TNF-alpha dysregulation, comorbidities, and severe asthma is crucial for medical practitioners dealing with this chronic disease. The significant burden and financial impacts of Severe Asthma on individuals and society underline the urgency for effective management strategies.

Recognizing the influence of comorbidities, such as autoimmune diseases, can guide comprehensive care plans for patients with Severe Asthma. Moreover, enhanced diagnostic tools and processes will aid in early identification and more personalized treatment approaches, ultimately improving patient outcomes.

By integrating this knowledge, medical practitioners can not only better understand the multifaceted nature of Severe Asthma but also enhance its overall management, leading to improved patient care. With ongoing research, we can continue to unravel the complex relationships and mechanisms in asthma pathogenesis, providing new avenues for therapeutic interventions and improved patient outcomes.

Research on the relationship between Candida albicans and Asthma is an important area of study that could lead to better understanding and management of Asthma. In the following sections, we will present a summary of various significant studies on the relationship between Candida Albicans colonization and asthma. We will also cover information on the microbiome of the gut and lungs, wherever applicable.

Additionally, we will provide key takeaways from each study, including relevant details such as the study’s title, authors, and organization affiliation. Finally, we will summarize the collective findings and scientific conclusions related to Candida Albicans colonization, sensitization, and infection in Asthma, and offer resources for you to share with your healthcare provider.

A comprehensive understanding of these aspects promises to shed light on the intricate mechanisms underlying severe asthma, offering new perspectives in our fight against this chronic condition.

Further Study

Name of study: Fungal Dysbiosis and Its Clinical Implications in Severe Asthma Patients
Date: 2023
Authors: Allison N. Imamura, Hannah K. Drescher, Mai Sasaki, Daniel J. Peaslee, David S. Crockett, Alexander S. Adams, Marcia L. Wills, Stephen C. Meredith, and Andrew H. Limper
Organization: Mayo Clinic, Rochester, MN
Summary: This study discusses the fungal dysbiosis in severe asthma patients. It finds that the lower alpha-diversity of lung microbiota and higher fungal burdens correlate with severity and poor control of asthma. The study also discusses the possible role of antibiotic usage and bacterial-fungal interactions in this process. The study concludes that understanding the link between Candida colonization, inflammation, autoimmune response, and Severe Asthma is crucial for better management of this chronic disease.

Study Title: CANDIDA ALBICANS INTESTINAL DYSBIOSIS INCREASES LUNG RESIDENT ILC2 POPULATIONS AND ENHANCES THE SEVERITY OF HDM-INDUCED ALLERGIC ASTHMA IN MICE

•  Date: October 17-20, 202

Authors: Amjad Kanj, Theodore Kottom, Kyle Schaefbauer, Andrew Limper, Joseph Skalski

•  Organization Affiliation: Mayo Clinic and University of California Davis

Human Anti-fungal Th17 Immunity and Pathology Rely on Cross-Reactivity against Candida albicans. Cell 2019. The authors are Petra Bacher, Thordis Hohnstein, Eva Beerbaum, Marie Röcker, Matthew G. Blango, Svenja Kaufmann, Jobst Röhmel, Patience Eschenhagen, Claudia Grehn, Kathrin Seidel, Volker Rickerts, Laura Lozza, Ulrik Stervbo, Mikalai Nienen, Nina Babel, Julia Milleck, Mario Assenmacher, Oliver A. Cornely, Maren Ziegler, Hilmar Wisplinghoff, Guido Heine, Margitta Worm, Britta Siegmund, Jochen Maul, Petra Creutz, Christoph Tabeling, Christoph Ruwwe-Glösenkamp, Leif E. Sander, Christoph Knosalla, Sascha Brunke, Bernhard Hube, Olaf Kniemeyer, Axel A. Brakhage and Carsten Schwarz.
The main objective of the article is to investigate how cross-reactivity against Candida albicans influences human anti-fungal Th17 immunity and pathology.
• C. albicans-specific Th17 cells can cross-react with other fungal antigens and gluten peptides in patients with CeD or asthma.
• Cross-reactive Th17 cells can cause immune pathology in the gut and lung by producing IL-17A and IL-22 cytokines.
Candida and asthma better by showing that Candida can induce a specific type of immune response that can also react to other fungi and allergens that are associated with asthma. The article also suggests that Candida may contribute to the severity and chronicity of asthma by causing inflammation and tissue damage in the lung. mechanisms and consequences of cross-reactivity are complex and need further investigation.

Name of study: Candida auris: Epidemiology, biology, a:Authors:ntifungal resistance, and virulence
Date: 2020
Authors: Du, H., Bing, J., Hu, T., Ennis, C. L., Nobile, C. J., & Huang, G.
M

Name of study: Candida albicans pathogenicity and epithelial immunity
Date: 2014
Abstract Naglik, J. R., Richardson, J. P., & Moyes, D. L.
URL:

Name of study: Candida albicans interactions with the host: crossing the intestinal epithelial barrier
Date: 2019
Abstract: [Unavailable in given data]
Authors: Basmaciyan, L., Bon, F., Paradis, T., Lapaquette, P., & Dalle, F.
URL: https://doi.org/10.1080/21688370.2019.1612661

Name of study: ACG Clinical Guideline: Treatment of Helicobacter pylori Infection
Date: 2017
Abstract: Authors: Chey WD, Leontiadis GI, Howden CW, Moss SF.
URL: https://doi.org/10.1038/ajg.2016.563

Name of study: Asthma is inversely associated with Helicobacter pylori status in an urban population
Date: 2008
Abstract: [Unavailable in given data]
Authors: Reibman J, Marmor M, Filner J, et al.
URL: https://doi.org/10.1371/journal.pone.0004060

Name of resource: H pylori Probiotics: A Comprehensive Overview for Health Practitioners
Date: 2020
Abstract: Authors: Ruscio M.
URL: https://drruscio.com/h-pylori-probiotics/

Name of resource: Treatment regimens for Helicobacter pylori in adults
Date: 2022
Abstract:
Authors: Lamont JT.

Name of study: Effects of probiotics on the recurrence of bacterial vaginosis: a review
Date: 2014
Abstract:
Authors: Homayouni A, Bastani P, Ziyadi S, et al.

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World Asthma Day Summary

On the day after World Asthma Day, May 3, 2022, we scanned the globe to find a statement that best sums up the current state of affairs regarding Asthma.

Kudos to tbe U.S National Institute of Environmental Health NIH Statement on World Asthma Day 2022: Toward Improved Asthma Care

Good enough of summary that we want to publish this in its entirety.

Asthma is a serious lung disease; causes chest tightness, wheezing, and coughing; can often be controlled with proper treatment.

Today (May 3, 2022) on World Asthma Day, the National Institutes of Health reaffirms its commitment to biomedical research aimed at preventing the onset of asthma, understanding its underlying causes, and improving the treatment of it. This chronic airway disease, which is characterized by periodic worsening of inflammation that can make it hard to breathe, affects more than 25 million people in the United States, including more than 5 million children. Left untreated, it can be life-threatening.

While scientists have made substantial progress in understanding asthma diagnosis, management, and treatment, therapies to permanently improve breathing for those who suffer from asthma remain elusive. Researchers around the globe are working steadily toward this goal while they seek to better understand and find new ways to manage the disease. They also are continuing research on the underlying causes of disparities in the incidence, care, and prevention of the disease. On the heels of recently updated management and treatment guidelines, researchers anticipate a brighter future for people living with asthma.

Three NIH institutes primarily support and conduct studies on asthma — the National Heart, Lung, and Blood Institute (NHLBI); the National Institute of Allergy and Infectious Diseases (NIAID); and the National Institute of Environmental Health Sciences (NIEHS). Other NIH Institutes and Centers also support and conduct asthma research. NIH scientists and grantees made important advances in understanding, treating, and managing asthma in 2021, which are briefly highlighted as follows:

Asthma and COVID-19

An NHLBI-funded study showed that during the pandemic, asthma attacks, also known as asthma exacerbations, significantly decreased in a large group of children and adolescents, compared to the year before the pandemic. The study also found that telehealth visits among these patients increased dramatically during this time. The study included nearly 4,000 participants aged 5-17 years with a prior diagnosis of asthma. Researchers believe a better understanding of the factors that contributed to these improved outcomes could lead to better asthma control in all children and adolescents, as researchers noted no racial or ethnic differences in health outcomes in this population.

A NIAID-funded study found that asthma does not increase the risk of becoming infected with SARS-CoV-2, the virus that causes COVID-19. This finding came from a six-month household survey of more than 4,000 children and adults conducted between May 2020 and February 2021.

Asthma Disparities

Researchers have known for decades that social determinants of health – conditions like housing, neighborhood, education, income, and healthcare access – can affect the quality of life and asthma-related health outcomes of people living with the disease. NIH scientists are now reporting new advances in understanding the relationship between social determinants of health and asthma.

Black and Hispanic children who live in low-income urban environments in the United States are at particularly high risk for asthma attacks. These children tend to be underrepresented in large trials of new biologic therapies for asthma.

In a recent NIAID-supported clinical trial, the monoclonal antibody mepolizumab decreased asthma attacks by 27% in Black and Hispanic children and adolescents who have a form of severe asthma, are prone to asthma attacks, and live in low-income urban neighborhoods.

In one study, NHLBI-funded investigators demonstrated the importance of housing interventions in improving the health of children with asthma. Poor quality housing is associated with a high level of asthma triggers – including mold, cockroach, mouse, and dust mite allergens – that can pose a health threat to children with asthma. The study showed the feasibility of using targeted interventions – including better pest management, improved ventilation, and moisture reduction – to achieve healthy housing. It showed that such interventions can result in reduced symptoms and hospitalizations due to asthma.

Environmental Exposures and Asthma

Researchers have known for years that asthma can be triggered by substances in the indoor and outdoor environment. New research shows that exposure to some asthma triggers might even occur before birth.

In an NIH-supported study that included grant support from NIEHS and the NHLBI, researchers reported that prenatal exposure to tiny air pollution particles significantly increased the risk for developing asthma in children. The study, which analyzed data from two different study cohorts, focused on a group of mothers and their children, mostly Black or Hispanic, in the Boston area who lived near major roadways with heavy traffic. It found that more than 18% of the children who were exposed to high levels of these so-called ultrafine particles in the womb developed asthma in their preschool years, compared to 7% of children overall in the United States.

An NIEHS clinical study will assess how environmental factors affect disease progression in non-smoking adults who have moderate or severe asthma. The study will focus on the microbiological and genetic factors associated with atopic asthma, also known as allergic asthma, which is triggered by pollen, dust mites, and other allergens. A better understanding of this data might lead to improved treatments for people with this type of asthma, researchers say.

Climate Change and Asthma

Studies have shown that climate change can increase air pollutants such as ground-level ozone, fine particulates, wildfire smoke, and dust, and that these pollutants can exacerbate asthma. Climate change can also affect the production, distribution, and severity of airborne allergens.

NIEHS, NHLBI, and other NIH institutes and centers are leading the NIH Climate Change and Health Initiative. This is a cross-cutting NIH effort to reduce health threats such as asthma that can develop or worsen because of climate change. The initiative will look at these threats across the lifespan and find ways to build health resilience in individuals, communities, and nations around the world. A strategic framework for the Initiative will help guide NIH investments in this area.

An NIEHS-funded study provides examples of how extreme weather events can affect asthma outcomes. For example, as heat waves and droughts become more frequent and prolonged, the risk of large wildfires will likely increase, resulting in poor air quality that makes it more difficult to control asthma. Other climate-change events can lead to longer and more intense pollen seasons, while mold and dampness in homes may cause asthma to develop or worsen preexisting cases.

About the National Institute of Allergy and Infectious Diseases (NIAID): NIAID conducts and supports research—at NIH, throughout the United States, and worldwide—to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website.

About the National Heart, Lung, and Blood Institute (NHLBI): NHLBI is the global leader in conducting and supporting research in heart, lung, and blood diseases and sleep disorders that advances scientific knowledge, improves public health, and saves lives. For more information, visit www.nhlbi.nih.gov. For additional information about NHLBI’s asthma resources, visit https://www.nhlbi.nih.gov/BreatheBetter.

About the National Institute of Environmental Health Sciences (NIEHS): NIEHS supports research to understand the effects of the environment on human health and is part of the National Institutes of Health. For more information on NIEHS or environmental health topics, visit

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

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Bisphenol A or BPA in Pregnancy and Asthma Study

The Barcelona Institute for Global Health supported study concludes suggests that in utero BPA exposure may be associated with higher odds of asthma and wheeze among school-age girls.

Study Background

In utero, (before birth) exposure to bisphenols, widely used in consumer products, may alter lung development and increase the risk of respiratory morbidity in the offspring. However, evidence is scarce and mostly focused on bisphenol A (BPA) only.

Study Objectives

There is growing concern over the role of chemical pollutants on early life origins of respiratory diseases (Gascon et al., 2013, Vrijheid et al., 2016, Casas and Gascon, 2020, Abellan and Casas, 2021), specifically on bisphenols due to their large production worldwide (CHEMTrust, 2018) and its widespread exposure to human populations (Calafat et al., 2008, Haug et al., 2018). Bisphenol A (BPA) is the most commonly used bisphenol. It is present in polycarbonate plastics and epoxy resins, used in many consumer products, and diet is the main source of exposure (Liao and Kannan, 2013). In 2017, the European Chemical Agency considered BPA as a “substance of very high concern” (Calafat et al., 2008, Agency and Bisfenol, 2017). Consequently, BPA production is restricted in some countries, which has resulted in the emergence of substitutes such as bisphenol F (BPF) and bisphenol S (BPS), with suspected similar toxicity (Lehmler et al., 2018, Rochester and Bolden, 2015). Bisphenols can cross the placenta and are also found in breastmilk, which results in exposure to foetuses and newborns (Lee et al., 2018). To examine the associations of in utero exposure to BPA, bisphenol F (BPF), and bisphenol S (BPS) with asthma, wheeze, and lung function in school-age children, and whether these associations differ by sex.

Methods

We included 3,007 mother–child pairs from eight European birth cohorts. Bisphenol concentrations were determined in maternal urine samples collected during pregnancy (1999–2010). Between 7 and 11 years of age, current asthma and wheeze were assessed from questionnaires and lung function by spirometry. Wheezing patterns were constructed from questionnaires from early to mid-childhood. We performed adjusted random-effects meta-analysis on individual participant data.

In utero exposure to bisphenols, widely used in consumer products, may alter lung development and increase the risk of respiratory morbidity in the offspring. However, evidence is scarce and mostly focused on bisphenol A (BPA) only.

Study Objective

To examine the associations of in utero exposure to BPA, bisphenol F (BPF), and bisphenol S (BPS) with asthma, wheeze, and lung function in school-age children, and whether these associations differ by sex.

Results

Exposure to BPA was prevalent with 90% of maternal samples containing concentrations above detection limits. BPF and BPS were found in 27% and 49% of samples. In utero exposure to BPA was associated with higher odds of current asthma (OR = 1.13, 95% CI = 1.01, 1.27) and wheeze (OR = 1.14, 95% CI = 1.01, 1.30) (p-interaction sex = 0.01) among girls, but not with wheezing patterns nor lung function neither in overall nor among boys. We observed inconsistent associations of BPF and BPS with the respiratory outcomes assessed in overall and sex-stratified analyses.

Conclusion

This study suggests that in utero BPA exposure may be associated with higher odds of asthma and wheeze among school-age girl

According the U.S. National Institute of Health, Bisphenol A (BPA) is a chemical produced in large quantities for use primarily in the production of polycarbonate plastics. It is found in various products including shatterproof windows, eyewear, water bottles, and epoxy resins that coat some metal food cans, bottle tops, and water supply pipes.

How does BPA get into the body?

The primary source of exposure to BPA for most people is through the diet. While air, dust, and water are other possible sources of exposure, BPA in food and beverages accounts for the majority of daily human exposure.

Bisphenol A can leach into food from the protective internal epoxy resin coatings of canned foods and from consumer products such as polycarbonate tableware, food storage containers, water bottles, and baby bottles. The degree to which BPA leaches from polycarbonate bottles into liquid may depend more on the temperature of the liquid or bottle, than the age of the container. BPA can also be found in breast milk.

Why are people concerned about BPA?
One reason people may be concerned about BPA is because human exposure to BPA is widespread. The 2003-2004 National Health and Nutrition Examination Survey (NHANES III) conducted by the Centers for Disease Control and Prevention (CDC) found detectable levels of BPA in 93% of 2517 urine samples from people six years and older. The CDC NHANES data are considered representative of exposures in the United States. Another reason for concern, especially for parents, may be because some animal studies report effects in fetuses and newborns exposed to BPA.

If I am concerned, what can I do to prevent exposure to BPA?

Some animal studies suggest that infants and children may be the most vulnerable to the effects of BPA. Parents and caregivers can make the personal choice to reduce exposures of their infants and children to BPA:

  • Don’t microwave polycarbonate plastic food containers. Polycarbonate is strong and durable, but over time it may break down from over use at high temperatures.
    Plastic containers have recycle codes on the bottom. Some, but not all, plastics that are marked with recycle codes 3 or 7 may be made with BPA.
  • Reduce your use of canned foods.
    When possible, opt for glass, porcelain or stainless steel containers, particularly for hot food or liquids.
  • Use baby bottles that are BPA free.

There is growing concern over the role of chemical pollutants on early life origins of respiratory diseases (Gascon et al., 2013, Vrijheid et al., 2016, Casas and Gascon, 2020, Abellan and Casas, 2021), specifically on bisphenols due to their large production worldwide (CHEMTrust, 2018) and its widespread exposure to human populations (Calafat et al., 2008, Haug et al., 2018). Bisphenol A (BPA) is the most commonly used bisphenol. It is present in polycarbonate plastics and epoxy resins, used in many consumer products, and diet is the main source of exposure (Liao and Kannan, 2013). In 2017, the European Chemical Agency considered BPA as a “substance of very high concern” (Calafat et al., 2008, Agency and Bisfenol, 2017). Consequently, BPA production is restricted in some countries, which has resulted in the emergence of substitutes such as bisphenol F (BPF) and bisphenol S (BPS), with suspected similar toxicity (Lehmler et al., 2018, Rochester and Bolden, 2015). Bisphenols can cross the placenta and are also found in breastmilk, which results in exposure to foetuses and newborns (Lee et al., 2018).

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Asthma and Indoor Air Pollution:

Key insights for Asthmatics:

  • Makes Asthma Worse
  • Significant Association with Exacerbations
  • Among this panel of relatively moderate to severe asthmatics, the respiratory irritants produced by several domestic combustion sources were associated with increased morbidity.
  • Although there is abundant clinical evidence of asthmatic responses to indoor aeroallergens, the symptomatic impacts of other common indoor air pollutants from gas stoves, fireplaces, and environmental tobacco smoke have been less well characterized. These combustion sources produce a complex mixture of pollutants, many of which are respiratory irritants.
  • Results of an analysis of associations between indoor pollution and several outcomes of respiratory morbidity in a population of adult asthmatics residing in the U.S. Denver, Colorado, metropolitan area. A panel of 164 asthmatics recorded in a daily diary the occurrence of several respiratory symptoms, nocturnal asthma, medication use, and restrictions in activity, as well as the use of gas stoves, wood stoves, or fireplaces, and exposure to environmental tobacco smoke.
  • Multiple logistic regression analysis suggests that the indoor sources of combustion have a statistically significant association with exacerbations of asthma. For example, after correcting for repeated measures and autocorrelation, the reported use of a gas stove was associated with moderate or worse shortness of breath (OR, 1.60; 95% CI, 1.11-2.32), moderate or worse cough (OR, 1.71; 95% CI, 0.97-3.01), nocturnal asthma (OR, 1.01; 95% CI, 0.91-1.13), and restrictions in activity (OR, 1.47; 95% CI, 1.0-2.16
  • The WAF Editorial Board wishes to thank and acknowledge B D Ostro 1 , M J Lipsett, J K Mann, M B Wiener, J Selner
    California Environmental Protection Agency, Berkeley for their contribution to Asthma education and research.
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Declaring War on Severe Asthma-COPD Overlap Syndrome

Highly Prevalent But Terribly Underappreciated

Folsom, CA. War has been declared on Severe Asthma-COPD Overlap Syndrome (ACOS).
It’s tied in with recognition of World Asthma Day May 7, 2013.

The World Asthma Foundation (WAF) is leading the charge to raise awareness and to elevate the discussion about this highly prevalent but terribly underappreciated ACOS syndrome.

ACOS, which was formerly called “asthmatic bronchitis,” is a commonly experienced, yet loosely defined clinical entity. It accounts for approximately 15 to 25 percent of the general population with obstructive airway diseases who experience more severe outcomes compared to asthma or COPD alone.

The prevalence of frequent exacerbations in ACOS is nearly two-and-a-half times higher than COPD and risk of severe exacerbations in ACOS is twice as high as COPD. However, standard treatment options are not as aggressive as needed to treat the asthma-COPD syndrome.

“ACOS is concerning because it’s much worse in terms of exacerbations, or acute attacks of breathlessness, as compared to COPD.” said Amir Zeki, MD, assistant professor of medicine pulmonary, critical, and sleep medicine at the Center for Comparative Respiratory Biology and Medicine at the University of California Davis School Of Medicine and World Asthma Foundation Board Member.

“We are entering a new era of public awareness of people living with chronic lung disease such as asthma and COPD,” said Sam Louie, MD and professor of medicine, director of the UC Davis Asthma Network (UCAN), director of the UC Davis Reversible Obstructive Airway Disease (ROAD) Center, which serves adults and adolescents in Northern California who have difficult to control asthma, bronchiectasis and COPD.

“Our mission at UC Davis is to transform health care by integrating and provide quality patient care services these conditions, which promote patient education and safety, social networking, and to align our goals with national efforts to transform people’s lives,” Louie said. “But we can achieve success without recognizing the clear and present danger from not being aware of the Asthma-COPD Overlap syndrome.”

“It really all begins with empathy.” Louie said. “Empathy of healthcare providers for how asthma, COPD and ACOS patients suffer when they are given prescription drugs without education on an individual level. We have to ignite that empathy by increasing awareness and providing education.”
The two physicians are board members of the World Asthma Foundation, which provides educational resources that inform patients, medical professionals and the general public about the latest clinical advances, management and treatment options for asthma disorders, including ACOS.

“People with asthma, COPD and ACOS deserve better,” Louie said. “It requires that we all take responsibility, patients too, but physicians must take their empathy one step further and realize how reversible asthma, COPD and ACOS can be.”

William Cullifer, executive director of the World Asthma Foundation, said, “This is a fascinating new development in the understanding of asthma and COPD and it’s fantastic to be on the forefront of educating the public and the healthcare community about this issue.”

Louie added, “When you get done taking care of the disease, you’re taking care of people. We must fight indifference and the only way to do that is to get the word out that we all have much more to achieve together to empower patients with reversible obstructive airway diseases.”

For more information visit: http://asthmacopdoverlapsyndrome.org

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Asthma and Bacteria: Exposure May Help Body Beef Up Immunity, Study Says

Asthma and Bacteria: Exposure May Help Body Beef Up Immunity, Study Says

The research was done in mice, but it supports the “hygiene hypothesis”: the idea that bacteria are needed to shape a healthy immune system, and that our bacteria-fearing lifestyles are increasing levels of asthma, allergy and other autoimmune diseases.

In the study, which was published in the journal Science, the researchers compared normal mice with mice that were raised in special germ-free environments. They found high levels of special white blood cells called invariant natural killer T cells (iNKT) in the lungs and intestines of the germ-free mice.

These iNKT cells release proteins that cause inflammation and attract more inflammatory white blood cells. Inflammation plays an important role in many autoimmune diseases, and iNKT cells are known to be an active ingredient in asthma, which is in the lungs, and ulcerative colitis, an inflammatory disease of the bowel.

Even when exposed to normal bacteria later in life, the germ-free mice still had abnormally high levels of iNKT cells and diseased lungs and intestines. This indicated that an “immune priming event” happens very early in life and is essential for the proper formation of the immune system, the researchers said.

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Asthma and Asthma Medication – Take Your Meds!

Improved Medication Use Could Reduce Severe Asthma Attacks

Researchers at Henry Ford Hospital have found that one-quarter of severe asthma attacks could be prevented if only patients consistently took their medication as prescribed.

Moreover, an asthma attack was only significantly reduced when patients used at least 75 percent of their prescribed dose, according to the study.

Patients often poorly take their medication based on the onset and degree of symptoms.

Henry Ford researchers say this is the first time that asthma medication use has been tracked closely over time and related to the likelihood of severe asthma attacks. The findings are published online in the December issue of The Journal of Allergy and Clinical Immunology http://www.jacionline.org/article/S0091-6749%2811%2901481-3/abstract

“Our findings demonstrated a relationship between medication adherence and asthma events in a manner that accounts for the changing patterns of inhaler use over time,” says lead author Keoki Williams, M.D., MPH, an Internal Medicine physician and associate director of Henry Ford’s Center for Health Policy and Health Service Research.

Inhaled corticosteroid (ICS) medication is the most effective treatment for controlling symptoms and preventing attacks, which can lead to a visit to the emergency department or hospitalization or death if left untreated.

Working from their theory that ICS use changes with the episodic nature of asthma, Dr. Williams and his team of researchers set out to measure changes in medication use over time and to estimate the effect of ICS use on asthma attacks among 298 patients. Patients were followed on average for two years and had 435 asthma attacks during that time.

“We found that every 25 percent increase in ICS adherence was associated with an 11 percent decrease in asthma attacks,” Dr. Williams says. “But most importantly, we found that causal use of these medications is not enough, especially among patients whose asthma is not controlled. Patients must use their asthma controller medication as prescribed if they want to have the best chance of preventing serious asthma attacks.”

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Asthma Study: Getting Patients to Take Their Asthma Meds

Asthma Patients More Likely To Take Meds Under Physician Supervision

Armed with the right information, physicians can play a stronger role in ensuring asthma patients don’t waver in taking drugs proven to prevent asthma attacks, according to researchers at Henry Ford Hospital in Detroit.

The study finds patients are more likely to routinely take inhaled corticosteroids (ICS) for asthma control when physicians kept close watch over their medication use and reviewed detailed electronic prescription information, including how often patients fill their prescriptions and the estimated number of days each prescription would last.

“Better inhaled corticosteroid adherence means better overall asthma control, and less hospitalization,” says lead study author L. Keoki Williams, M.D., MPH, Center for Health Services Research and Department of Internal Medicine at Henry Ford Hospital.

“Unfortunately, overall patient adherence to ICS medication is poor, accounting for an estimated 60 percent of asthma hospitalizations. So it’s important, as we move forward with health care reform, to look for more effective ways to make sure patients stay with their prescription regimens.”

The study – the first large-scale, controlled study to test the effectiveness of routinely providing patient medication adherence information to physicians – appears online in the Journal of Allergy and Clinical Immunology (www.jacionline.org).

ICS, taken using an inhaler, help prevent and reduce airway swelling, and are considered the cornerstone therapy for controlling persistent asthma in patients, says Dr. Williams.

The Henry Ford scientific team set out to design an intervention that would provide physicians information on the most recent national asthma guidelines and methods for discussing medication non-adherence with their patients.

The intervention also offered physicians electronic access to patients’ medication prescription fill/refill information via Henry Ford’s ePrescribing application, part of its electronic medical record system that allows physicians to prescribe and review patient medications electronically.

The study enrolled 193 Henry Ford primary care physicians (family medicine, internal medicine, pediatrics). Eighty-eight were randomly assigned to the intervention group, while 105 were assigned to the control group (no intervention).

Physicians in the intervention group used ePrescribing to track medication fills and refills. The application also offered physicians the option to take it one step further: To review detailed adherence data, including estimates of the proportion of time that the patients took their medication.

Medication adherence for both groups was measured by using both electronic prescriptions and pharmacy claims for medication fills and refills.

Researchers found ICS adherence to be very similar among patients in the intervention group and those in the control group (21.3 percent vs. 23.3 percent).

But adherence was significantly higher in the intervention group (35 percent) when the patient’s physician elected to view detailed adherence information via the ePrescribing application.

Few physicians, however, in the intervention group accessed the detailed adherence information. “Going forward, one of the obstacles will be finding time for physicians to review and discuss this information with patients in their typically busy practices,” says Dr. Williams.