Research reveals the possible effects of changes in air quality associated with global warming on human airways

From hot summer days to cold winter nights, many people can experience worsening respiratory symptoms of asthma, allergic rhinitis, or viral infections. The incidence of extreme temperature conditions has increased over decades, exposing the upper airways of humans to high steam pressure (VPD), also known as “air drying.” Researchers are currently reporting how these dehydrated airway breathing can promote inflammation in the airways and have disease-causing effects on the lungs.

The study, published in Communications Earth & Environment, reveals that reductions in humidity associated with global warming can exacerbate respiratory diseases by dehydrating and inflamming the human airways.

The cross-system research led by John Hopkins’s David A. Edwards, MD, includes members of the Marsico Lung Research Institute at the UNC School of Medicine. It also includes research conducted by Dr. Justin Haynes of Johns Hopkins. Kian Hwangcheong, Maryland, Imperial College London. Dr. Britt Burton Freeman and Dr. Indica Endilishet of Illinois Institute of Technology.

This study aims to understand that our airways are designed to breathe dry air and the effects of long-term dehydration associated with global warming. It also explores how dehydration and inflammation can worsen with increased incidence of mouth breathing and increased exposure to air-conditioned and heated indoor air.

As global temperatures rise due to climate change, the air’s ability to retain water vapor increases, facilitating the rise in VPD. This is a measure of air drying that quantifies the difference between saturation and actual water vapor pressure. This change, already revealed over the past century, amplifies water evaporation from ecosystems around the world, and has had a major impact on both plant and human life.

According to climate models, high VPD, exacerbated by extreme weather events, is becoming more frequent, especially in urban and rural areas of the United States.

This study introduces a novel mechanism to explain how increased VPD affects airway epithelial cells. The researchers observed how airway mucus, a diluted hydrogel made up of salts, globular proteins, and mucin polymers secreted by the airway epithelium, undergoes evaporation. This is a way to undergo a water loss process similar to the water loss process that occurs when water evaporates on the surface of the leaf. In plants, high VPD drives evaporation through hydrogel-like leaf membranes, which ultimately leads to cell compression when water is drawn from the roots, causing leaves to wilt.

Similarly, under conditions such as rapid mouth breathing in low-humidity air, high VPD evaporates water from the mucus layers lined with the airways, concentrating mucin near the surface to form a dense gel. This process is modeled using continuum mathematics with DRS. Edwards and Chong inhibit mucus and compress epithelial cells – sufficient stimulation to cause inflammation –

Experimental evidence from donor human bronchial epithelium (HBE) cell cultures and mouse models suggest that low-humidity environments that prevent the increase in climate-driven vapor pressure injury (VPD) are responsible for thinning airway mucus and causing inflammation. Dr. Button’s experiments show that HBE cells (higher VPD) exposed to dry air are thinner and more concentrated mucus, making it difficult to clear the airways.

Furthermore, joint research with the doctor. Freeman and Endirisinghe showed that these cells secrete high levels of cytokines, a marker of airway inflammation. These results are consistent with the theoretical prediction that mucus thinning can occur in dry air environments and produce sufficient cellular compaction to cause inflammation.

“This is not just a lab experiment. Breathing hotter, dryer air gives us a glimpse of how more asthma burns, worse allergies, and more difficult breaths for millions of individuals,” Button said. “It’s a red flag of public health that we cannot ignore.”

The mucus evaporation hypothesis increases the likelihood of representing a global threat to human respiratory health, along with global warming, along with increased human chronic mouth respiration due to obesity, allergic rhinitis, and aging. Excessive mucus evaporation can exacerbate conditions on other mucosal surfaces, including the eyes. This is because the lack of humidification can also destroy the lining of the eye mucus.

“This study highlights the urgent need to address airway hydration as a public health priority, suggesting that without intervention, millions of people could be at increased risk of chronic respiratory disease by the end of the century, but open the door to new protective measures such as humidity control and strengthening targeted therapies.”

The team also confirmed that inflammatory mucus evaporation occurs during normal, relaxed breathing (also known as tidal breathing) in an animal model of mucus inflammatory lung disease. Livraghi-Butrico found that airway mucus clearance showed increased lung inflammation when defective mice were exposed to intermittent dry air compared to the same type of mice exposed to standard chamber air. These in vivo findings identify airway dehydration as an important mechanism that links climate change to worsening lung health in susceptible individuals.

“This is the tip of the iceberg,” said Livragi Boutriko. “Our research line cannot change the trajectory of climate change, but we can work on effective measures to prevent the worsening these changes are causing. So, our work can lead a healthier life, and in this case, when breathing is better, our work is the most rewarding.”