Following the devastating fires that swept through Los Angeles in January, concerns are on the rise about the long-term health impacts of smoke inhalation.
In a study published in the International Journal of Molecular Sciences, researchers from Lawrence Livermore National Laboratory (LLNL) and the Environmental Protection Agency seek to close the knowledge gap on how wildfire smoke exposure can affect the blood-brain barrier, which protects the brain from harmful substances. Such exposure can cause molecular and cellular changes in the brain that are associated with cognitive and neurological dysfunctions, such as Alzheimer's disease, Parkinson's disease and dementia.
While previous studies have mainly focused on understanding the effect of wildfire smoke in the lungs and heart, the latest research has aimed to help identify and understand the potential impacts and adverse outcomes that wildfire smoke exposure can elicit when these particles enter the brain.
The team's study, supported by LLNL's Laboratory Directed Research and Development program (23-ERD-020), evaluated the responses of two types of in vitro brain cell cultures - brain microvascular endothelial cells (HBMEC) and an immortalized human brain endothelial cell line (hCMEC/D3) - when exposed to varying doses of eucalyptus wood smoke extract over the course of 24 hours.
Eucalyptus trees are of particular interest due to their highly flammable, oil-rich leaves and bark, as well as the high levels of toxicity they release when burned. These factors, combined with their abundance across California and large size-with some reaching between 150-200 feet tall-pose significant threats to the population.
To the knowledge of the experimental team, this was the first study to investigate the immediate effects of wood smoke extract in brain endothelial cells (which line the blood-brain barrier) using HBMEC and hCMEC/D3.
The research team found that wood smoke exposure induces immune responses in the brain, leading to an increased production of interleukin-8: a cytokine protein, often linked to neuroinflammation, that is released in response to injury or trauma in the body. They also saw evidence of a significant decrease in some of the tight junction markers-a protective component of the blood-brain barrier that seals the space between brain endothelial cells.
Both brain cell types exhibited similar responses to the wood smoke extract, suggesting that either could offer a promising route to study the molecular mechanism of neuroinflammation in the brain from wildfire/wood smoke exposure. The team notes the need for future studies that test longer wood smoke exposure times and analyze other types of brain cells beyond endothelial cells. Taken together, this research may lend new insights into the potential neurotoxicity and crosstalk between the cells.
Additionally, because wildfire smoke particulate matter (fine particles less than 2.5 microns) and volatile combustion products significantly vary in composition depending on the stage of combustion, location, weather, fuel and temperature of the fire, the researchers assert that other types of biomasses beyond smoldering eucalyptus should be assessed to identify which biomass can be more toxic to the brain.
Currently, the LLNL scientists are tracing and quantifying the components of inhaled wildfire smoke in the brain, aiming to identify potential mechanisms of translocation (i.e., the pathway of smoke particles to the brain) using LLNL's Biological Accelerator Mass Spectrometry (bioAMS) capabilities. They also plan to evaluate in vivo neuroinflammatory outcomes of wildfire smoke exposure, which may contribute to neurological dysfunction.
LLNL co-authors of the study include Dorothy You, Bria Gorman, Noah Goshi, Nicholas Hum, Aimy Sebastian, Heather Enright and Bruce Buchholz.
-Shelby Conn
