# Contaminant Metal Content in Wildfire Smoke and Neuroinflammation

> **NIH NIH R01** · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · 2024 · $592,021

## Abstract

SUMMARY
Wildland fire disasters raged throughout the western US in recent years, continuing a trend for increasing
frequency and severity of such events driven by climate change. Smoke arising from these events covered
much of the continent, exposing over 100 million people. Wildland fires in the New Mexico region can cross
over regions of legacy mining contamination or nuclear development. Evidence from past fires in Los Alamos,
for instance, revealed significant elevations of arsenic, nickel, and cadmium in the urine from first responders.
We have further identified that wood obtained near abandoned uranium mine sites that have elevated uranium,
chromium, nickel and vanadium. Our recent studies with naturally-occurring wildland fire smoke (WFS)
exposures from the California October 2020 wildfires demonstrate clear neuroinflammatory outcomes in
otherwise healthy mice. Interestingly, however, after 20 days of exposure, cerebrovascular endothelial cells
exhibited an evolving phenotype, with signs of reduced inflammation, signifying an adaptation to the relatively
acute circulating inflammatory stimulus. There is a significant gap in knowledge regarding how environmental
stressors like WFS promote cerebrovascular inflammation, and even less appreciation for mechanisms
governing neuroinflammatory resolution. In the present renewal proposal, we will take what we have learned
from extensive field work on uranium mine sites in Laguna Pueblo and Navajo Nation, and return to more
precise, laboratory-based exposure systems to address pulmonary and neuroinflammatory risks of wood
smoke from metals-contaminated biomass obtained from these regions. Thus, in Aim 1, we will determine the
toxic influence of metals in biomass combustion inhalation. We hypothesize that wood obtained near
abandoned uranium mine sites, enriched with several metal contaminants, has a greater potency than similar
biomass fuels from non-impacted sites. In the 2nd Aim we will elucidate the role of endothelial adhesion
molecules in driving neuroinflammatory consequences of wood smoke inhalation. We hypothesize that
neuroinflammatory outcomes of woodsmoke are dependent on cerebrovascular expression of adhesion
molecules (e.g., ICAM-1, VCAM-1), induced by circulating factors following inhalation exposure. Lastly in Aim 3
we propose to delineate and accelerate the resolution of neuroinflammation after WFS exposures. We
hypothesize that neuroinflammatory resolution following woodsmoke exposure, from the standpoint of
activated microglia, is actually dependent on the effective recruitment of peripheral immune cells through the
neurovascular unit. We will thus ascertain mechanisms underlying the progression of neurovascular tolerance
to wood smoke inhalation, thereby identifying potential molecular foundations of vulnerability to long-term
consequences of repeated exposure. Furthermore, we will assess the value of pro-resolving lipid mediators in
accelerating the resolution, as a potential di...

## Key facts

- **NIH application ID:** 10825586
- **Project number:** 5R01ES026673-07
- **Recipient organization:** UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR
- **Principal Investigator:** Matthew J Campen
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $592,021
- **Award type:** 5
- **Project period:** 2016-08-01 → 2028-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10825586

## Citation

> US National Institutes of Health, RePORTER application 10825586, Contaminant Metal Content in Wildfire Smoke and Neuroinflammation (5R01ES026673-07). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10825586. Licensed CC0.

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