Summary: Researchers have found that wildfire smoke can trigger prolonged inflammation in the brain. Their study shows this inflammation is especially pronounced in the hippocampus, the region essential for learning and memory.
In experiments with rodents exposed to wood smoke, scientists observed lasting changes in neurotransmitters and signaling molecules that persisted for more than a month after exposure. These results raise urgent concerns for people regularly exposed to wildfire smoke, particularly older adults, firefighters, and those with chronic respiratory conditions.
Key Facts:
- Wildfire smoke can cause brain inflammation that lasts longer than a month.
- The hippocampus appears especially vulnerable, which could threaten learning and memory functions.
- Intermittent, rather than continuous, smoke exposure may be more harmful because it produces spikes in inflammatory activity.
Source: University of New Mexico
Smoke from the massive wildfires that have been burning in northern Canada has spread across much of North America this summer, prompting widespread health concerns for older adults and people with chronic lung disease.
A new paper in the Journal of Neuroinflammation by researchers at the University of New Mexico Health Sciences adds a new layer of concern. The team reports that inhalation of biomass-derived smoke can produce a persistent neuroinflammatory response that may extend for a month or longer after exposure.
The study’s senior author, Matthew Campen, PhD, Regents’ Professor in the College of Pharmacy and co-director of the UNM Clinical & Translational Science Center, explained that the inflammatory effects were concentrated in the hippocampus, a brain area crucial for memory formation and learning. In addition to immune activation, the investigators detected significant shifts in neurotransmitters and signaling molecules in that region.
Lead researcher David Scieszka, PhD, a postdoctoral fellow in Campen’s lab, exposed mice to wood smoke every other day for two weeks to mimic intermittent real-world exposures. “We wanted to reproduce the patterns of smoke exposure people experience during wildfire events and see how those exposures affect the brain over time,” he said.
The team documented both pro-inflammatory and anti-inflammatory responses as fine particulate matter from the smoke crossed from the lungs into the bloodstream and passed the blood-brain barrier—a protective layer of tightly packed cells that lines the brain’s blood vessels.
“We measured the size and timing of the inflammatory response,” Scieszka said. “We expected it would resolve more quickly, but some effects persisted up to 28 days with no complete resolution observed during that period.”
By day 14, cells of the blood-brain barrier had largely adjusted to the smoke exposure, but immune cells within the brain remained abnormally activated. That sustained microglial activation suggests a lingering inflammatory state even after the initial exposure ended.
Campen emphasized the public health implications given the growing incidence of large-scale wildfires. “Neuroinflammation can be the starting point for many adverse brain outcomes, including risks related to dementia and Alzheimer’s disease, disruptions in brain development, and mood disorders,” he said.
“People who experience intense smoke events—firefighters and residents of affected communities—may suffer neurocognitive or emotional effects for weeks or months after the exposure has ended,” Campen added.
As practical protection measures, the researchers recommend that when smoke levels are high, people stay indoors if possible. Homes vary in how well they block outdoor particles—houses with evaporative coolers, for example, may allow more outdoor air inside—so residents should consider how well their homes seal against particulates. For those who must be outdoors, properly fitted N95 masks can reduce inhalation of fine particles.
The investigators noted that while the human body can adapt to steady, chronic particulate exposure to some degree, repeated intermittent exposures appear particularly problematic. Those repeated spikes in exposure trigger surges of inflammation, and the harmful effects seem more closely tied to these fluctuations than to the background level of air pollution.
“What makes intermittent wildfire smoke exposure especially concerning is that it hits communities that normally enjoy clean air with sudden, intense pollution,” Campen said. “A naïve system experiences a powerful inflammatory shock that can have lasting consequences.”
About this neuroinflammation and environmental neuroscience research news
Author: Chris Ramirez
Source: University of New Mexico
Contact: Chris Ramirez – University of New Mexico
Image: The image is credited to Neuroscience News
Original Research: Open access. “Biomass smoke inhalation promotes neuroinflammatory and metabolomic temporal changes in the hippocampus of female mice” by Matthew Campen et al. Journal of Neuroinflammation
Abstract
Biomass smoke inhalation promotes neuroinflammatory and metabolomic temporal changes in the hippocampus of female mice
Previous preclinical work has shown that smoke from wildland fires can induce neuroinflammation, marked by infiltration of immune cells such as neutrophils and monocytes and changes in the behavior of neurovascular endothelial cells. This study investigated how long those effects persist and how they evolve over time following biomass smoke inhalation.
Two-month-old female C57BL/6J mice were exposed to wood smoke every other day for two weeks at an average concentration of 0.5 mg/m3. Groups of animals were euthanized at 1, 3, 7, 14, and 28 days after the final exposure to assess temporal changes.
Flow cytometry of the right hemispheres identified two endothelial populations distinguished by CD31 expression levels: CD31Hi and CD31Med. Wood smoke exposure increased the relative proportion of the CD31Hi population. The CD31Hi and CD31Med profiles were associated with anti-inflammatory and pro-inflammatory responses, respectively, and these endothelial inflammatory signatures largely trended toward resolution by day 28.
Despite that endothelial adaptation, activated microglial populations (CD11b+/CD45low) remained elevated in smoke-exposed mice at day 28, indicating persistent brain immune activation. Infiltrating neutrophil counts declined below control levels by day 28, but peripheral immune cells retained high expression of activation markers such as MHC-II, and neutrophils continued to show increased CD45 and Ly6C expression.
An unbiased metabolomic analysis revealed significant alterations in hippocampal neurotransmitters and signaling molecules, including glutamate, quinolinic acid, and 5-α-dihydroprogesterone. Targeted assessment of the NAD+ metabolic pathway—associated with aging—showed fluctuations across the 28-day timeline and culminated in reduced hippocampal NAD+ levels at day 28.
In summary, the study demonstrates a dynamic and sustained neuroinflammatory response to biomass smoke inhalation, with potential resolution extending beyond 28 days. These findings suggest possible long-term behavioral and neurological consequences directly linked to wildfire smoke exposure and underscore the need for public health measures to reduce exposures during wildfire events.