Wildfire smoke inhalation
LLNL researchers are studying the long-term health impacts of wildfire smoke inhalation, with a focus on potential adverse outcomes when toxic particles enter the brain. Their aim is to better understand how exposure to wildfire smoke can affect the blood–brain barrier, which protects the brain from harmful substances. This type of exposure can cause molecular and cellular changes in the brain that are associated with cognitive and neurological dysfunctions.
Researchers use LLNL’s bioAMS capabilities to trace the pathways the particles follow on their journey to the brain and quantify the components of inhaled wildfire smoke that reach the brain. Their initial research focused on the effects of eucalyptus wood smoke extract on the brain’s endothelial cells, which line the blood–brain barrier. They found evidence of neuroinflammation in the brain and a decrease in protective components in the blood–brain barrier.
What’s next: Researchers are expanding their studies of health hazards caused by combustion sources to include inhaled particles, as well as volatile compounds produced by the combustion of mixed fuels. The aim of these studies is to better understand which combustion products, when inhaled, are more toxic to the brain.
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The toxicology of environmental carcinogens
Researchers from LLNL, and their collaborators, are studying how exposure to toxins, such as polycyclic aromatic hydrocarbons (PAHs), can be the catalyst for a range of medical conditions, including lung cancer, cardiovascular disease, and neurological damage. These toxic substances are produced during incomplete combustion of carbon-based materials, such as wood, petroleum, coal, and tobacco. Human exposure occurs through environmental contamination (e.g., oil spills), ingestion, smoking, or occupational exposures (e.g., asphalt paving).
For example, researchers are using the Lab’s AMS capabilities to study the uptake, metabolism, and elimination of one type of PAH, known as benzo[a]pyrene (BaP), in human plasma, from exposure to smoked meats. Up to 70% of PAH exposure for non-smoking humans is associated with diet and an oral route of exposure in non-occupational settings. Their experimental approach incorporates CAMS instruments, offering a technique that is sensitive enough to produce relevant data using oral micro-dosing. This data is crucial to validate exposure models, as internal dose metrics used for risk assessment do not necessarily scale allometrically.
In addition, scientists are studying the carcinogenic potential of naphthalene, the smallest PAH. Naphthalene is an ubiquitous combustion product used in industrial processes, and a significant component of jet fuel. Chronic exposure to this toxin can cause damage to the respiratory track when particles are inhaled, including tumor formation. Researchers explored health risks associated with chronic oral ingestion of low doses of naphthalene. They used the Lab’s AMS instrument to measure how the toxin is metabolized after being orally ingested, including its presence in lungs and livers. They also investigated the formation of DNA adducts, which play a key role in carcinogenic mechanisms.
Key collaborators: Oregon State University; University of California, Davis; and University of Arizona
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