Mice trials suggest that city air may be even worse for your health than previously thought.
Prolonged exposure to fine particulate matter sourced air in the Los Angeles bay area does not do the brains of mice a lot of good. According to a new study published by researchers from the Cedars-Sinai Medical Center, a non-profit hospital in Los Angeles, it triggered inflammation and the appearance of cancer-associated genes in the animal’s neurons.
Brain trouble
The fact that air pollution is linked to a wide range of diseases isn’t exactly news by now — quite on the contrary. The adverse effects air pollution has on health have been widely documented and reported on. However, one new (and not exactly encouraging) discovery the team made is that certain materials in coarse air pollution — particularly nickel — may have a role promoting genetic changes that underpin the development of diseases such as cancer.
“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,” said lead author Julia Ljubimova, director of the Nanomedicine Research Center at Cedars-Sinai.
The team worked with one hundred mice — separated in groups of 6 to 10 animals. Each group was exposed to coarse (PM2.5–10: 2.5–10 µm in diameter), fine (PM<2.5: <2.5 µm), or ultrafine particles (UFPM: <0.15 µm) sourced from ambiental air in Riverside, California. Each type of particulate matter was analyzed using atomic emission spectroscopy, so the team had an idea of how much nickel, cobalt, and zinc they contained.
PM exposure lasted for 5 hours daily, 4 days per week for either two weeks (short exposure), one to three months (intermediate), or 12 months (long). One cohort of rats served as control and was kept in the same exposure chambers, for the same duration as the rats in the other groups, but was exposed to filtered air.
Afterward, the team analyzed the brains of each group to see how much of each metal had accumulated and whether this build-up had any effect on the organs’ health.
Metal build-up
They report that all three metals accumulated following intermediate-or-longer exposure. RNA sequencing revealed that intermediate exposure to PM2.5–10, which also correlated to nickel accumulation in the brain, triggered the expression of EGR2 — the early growth response gene 2 which regulates inflammatory processes — and of RAC1 — a gene that has the potential to cause cancer. The team believes the observed effects are a cumulative effect of exposure to the metals and certain toxins present in the air recovered from the Los Angeles Basin.
Furthermore, they report that coarse particulate matter from air pollution entered the body via two mechanisms. Trace metals and other pollutants could pass into the bloodstream from air inhaled through the lungs, later making their way to the brain. Alternatively, some of them could pass directly through mucosa in the nose, from where they had a much more direct pathway to the brain.
The study’s main limitations are that it only involved animal models — so the observed effects may carry over identically to humans — and that it only used a local ‘blend’ of pollutants — so the results may not be universally valid. Ljubimova notes that while the results may be unique to the Los Angeles Basin area, they do reinforce previous findings regarding the health consequences of exposure to air pollution in major cities.
Considering that most of humanity today lives with “unsafe” levels of air pollution, the findings are even more troubling.
“Our modern society is becoming increasingly urbanized and exposed to air pollution,” she says. “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.”
The paper “Coarse particulate matter (PM2.5–10) in Los Angeles Basin air induces expression of inflammation and cancer biomarkers in rat brains” has been published in the journal Scientific Reports.
