Prolonged exposure to particulate matter in air pollution in the Los Angeles Basin triggered inflammation and the appearance of cancer-related genes in the brains of rats, a study has found.
Authors sourced ambient particulate matter (PM) from Riverside, California, and selectively exposed rats to coarse (PM2.5–10: 2.5–10 µm), fine (PM<2.5: <2.5 µm), or ultrafine particles (UFPM: <0.15 µm). They characterized each PM type via atomic emission spectroscopy and detected nickel, cobalt and zinc within them.
Then the authors exposed rats separately to each PM type for short (2 weeks), intermediate (1–3 months) and long durations (1 year). All three metals accumulated in rat brains during intermediate-length PM exposures. Via RNAseq analysis authors then determined that intermediate-length PM2.5–10 exposures triggered the expression of the early growth response gene 2 (EGR2), genes encoding inflammatory cytokine pathways (IL13-Rα1 and IL-16) and the oncogene RAC1. Gene upregulation occurred only in brains of rats exposed to PM2.5–10 and correlated with cerebral nickel accumulation.
Corase particulate matter may play a role in genetic changes related to disease development, said the lead author of the paper, published in Scientific Reports.
"This study, which looked at novel data gathered in the Los Angeles area, has significant implications for the assessment of air quality in the region, particularly as people are exposed to air pollution here for decades," author said.
The study found that coarse particulate matter in the region's air pollution found its way into bodily systems in two ways: inhaled through the lungs, where trace metals and other materials enter the bloodstream and then the brain; and through the nose, where the materials are absorbed more directly into the brain.
Air pollution causes gene expression changes in brain
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