A study carried out in Los Angeles has linked prolonged exposure to particulate matter air pollution to brain inflammation and the appearance of cancer-related genes in rats.
Carried out by researchers at Cedars-Sinai Hospital in the Los Angeles Basin, the study found markers indicating certain materials in coarse air pollutionnickel, in particularmay play a role in genetic changes related to disease development.
During the study, researchers exposed rats separately to air containing either PM2.5, PM10, Ultra-fine Particulate Matter or filtered air.
Using inductively coupled plasma atomic emission spectroscopy (ICP-AES), the researchers analysed the metal content of the PM samples and sought to establish if these metals accumulated in the brains of rats that were exposed to PM.
Six metals: cadmium, cobalt, lead, nickel, vanadium and zinc were detected in the samples.
According to the researchers, rats in all experimental groups, including those exposed to filtered air, had detectable levels of Nickel, Cobalt and Zinc in their brains.
The Nickel content remained approximately constant over 12 months. However, the cobalt content increased significantly after 12 months of exposure to filtered air, the researchers claimed.
The study went on to suggest that the prolonged exposure to Particulates triggered the expression of genes related to inflammation and oncogenesis [the growth of cancerous cells] in rat brains.
Researchers noted that the findings may be unique to the Los Angeles Basin region, due to the composition of air in the region.
Julia Ljubimova, the MD who led the research, said: 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.
There are many examples of potentially damaging effects of air pollution exposures in major cities. Our modern society is becoming increasingly urbanized and exposed to air pollution. This trend underscores the need for additional research on the biology of air-pollution-induced organ damage, along with a concerted effort aimed at reducing ambient air pollution levels.