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According to a recent study, researchers have discovered that exposure to wildfire or structural-fire smoke—even briefly—can reprogram the human immune system.

Even brief exposure to wildfire or structural-fire smoke can reprogram the human immune system, according to a single-cell exposomic analysis published in Nature Medicine.

“We’ve known that smoke exposure causes poor respiratory, cardiac, neurological, and pregnancy outcomes, but we haven’t understood how,” explained corresponding author Kari C. Nadeau, MD, PhD, of the Harvard T.H. Chan School of Public Health in a news release. “Our study fills in this knowledge gap, so that clinicians and public health leaders are better equipped to respond to the growing threat of difficult-to-contain, toxic wildfires.”

The research team profiled blood samples from 31 firefighters and civilians recently exposed to smoke and 29 matched control participants, uncovering a surge in activated memory CD8⁺ T cells and widespread shifts in chemokine-receptor expression.

Methylation Changes at Gene Loci

Using a newly adapted mass-cytometry method that quantifies metal ions bound to single cells, the authors detected elevated mercury in dying cells and cadmium in both live and dead immune cells. Mercury burden rose in tandem with cumulative years of smoke exposure, according to results. Parallel epigenetic mapping identified methylation changes at 133 gene loci linked to allergy and asthma, suggesting that toxic metals may help drive durable gene-regulatory alterations. Lead study author Mary M. Johnson, MD, PhD, of Harvard T.H. Chan School of Public Health, emphasized the clinical implications: “Our findings demonstrate that the immune system is extremely sensitive to environmental exposures like fire smoke, even in healthy individuals.”

Toward Earlier Detection & Policy Change

The authors suggested that their single-cell signatures could enable blood-based screening to detect smoke-induced immune dysregulation before overt disease emerges.

“Knowing exactly how may help us detect immune dysfunction from smoke exposure earlier and could pave the way for new therapeutics to mitigate, or prevent altogether, the health effects of smoke exposure and environmental contaminants,” Dr. Johnson noted.

Beyond clinical translation, the data strengthen the case for stricter air-quality thresholds during wildfire seasons and improved protective protocols for firefighters, according to the authors.

“Knowing more about exactly how smoke exposure is harming the body, we may increase public health campaigns about the dangers of smoke exposure and the importance of following evacuation procedures during wildfires,” Dr. Nadeau added. “We may also reconsider what levels of smoke exposure we consider toxic.”

As wildfires intensify worldwide, these cellular insights offer a crucial roadmap for both immediate risk reduction and long-term policy reform.