A recent study led by researchers from Johns Hopkins University and other institutions highlights the growing risk that dry air poses to human health, particularly in the context of global warming. According to the study, which was published in Communications Earth & Environment on March 17, human airways are more susceptible to dehydration and inflammation when exposed to dry conditions—a trend likely to worsen due to rising global temperatures.
The research underscores that as the Earth’s atmosphere warms, the vapor pressure deficit (VPD)—a measure of how “thirsty” air is for water—rises rapidly, even as relative humidity remains stable. A higher VPD accelerates water evaporation, not only threatening ecosystems but also leading to dehydration in the human upper airways. Researchers indicate that this dehydration can trigger inflammatory and immune responses, increasing the risk of conditions such as asthma, allergic rhinitis, and chronic cough.
An adjunct professor of medicine at Johns Hopkins University, emphasizes that managing airway hydration is just as crucial as managing air quality. “Air dryness is as critical to air quality as air dirtiness,” he said. “Our findings suggest that all mucosa exposed to the atmosphere, including ocular mucosa, are at risk in dehydrating atmospheres.”
The team’s investigation began with an inquiry into whether a process known as transpiration—where water is lost in plants—could occur in the mucus of upper airways when exposed to dry air. Previous studies have shown that high transpiration rates in plants can cause cellular compression, endangering plant survival. The researchers wanted to know if a similar process might occur in the human upper airway cells.
To explore this, researchers exposed cultures of human bronchial epithelium cells to dry air. They observed that the cells became dehydrated, resulting in thinner mucus and increased levels of cytokines, which are proteins that signal inflammation. These findings corroborated predictions that dry air environments thin mucus, causing cellular compression and triggering inflammatory responses.
In further experiments, the team used a mouse model to examine how dry air exposure affects airway cells. Mice with preexisting dehydration—common in individuals with chronic respiratory diseases—showed signs of inflammation after being exposed to dry air for a week. In contrast, mice exposed only to moist air showed no inflammatory response.
The study also involved climate modeling, which predicts that much of the United States will face an increased risk of airway inflammation by the end of the century as temperatures rise and air dries out. This would put millions of people at greater risk of respiratory conditions.
Study co-author Justin Hanes, Ph.D., of the Wilmer Eye Institute at Johns Hopkins University, called the findings a “game changer” for medicine. “Human mucosa dehydration is currently a critical threat to human health, which will only increase as global warming continues,” he said. “Without a solution, human mucosa will become drier over the years, leading to increased chronic inflammation and associated afflictions.”
Edwards concluded that understanding how dry air leads to airway dehydration could open doors to preventive or therapeutic measures. “By identifying the causes of airway dehydration, we can develop strategies to avoid or reverse its inflammatory effects,” he said, underscoring the potential for behavioral changes and medical interventions to mitigate these risks.
The study was a collaborative effort, involving researchers from Johns Hopkins University, Boston University, Imperial College London, Sensory Cloud Inc., Illinois Institute of Technology, and the University of North Carolina.
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