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'Safe' Air Pollution Levels May Harm Children's Brain

Air pollution levels considered safe by the Environmental Protection Agency (EPA) may affect the function of developing brain, a study finds.

Air pollution is linked to a wide range of diseases, including cancer, cardiovascular disease, and asthma, and is especially dangerous for children.

Although regulators such as the EPA set limits on emissions to prevent harmful effects, a new study published in the journal Environment International finds that even "safe" levels of pollution are associated with changes in children's brain function over time.

The researchers at the University of Southern California investigated the effects of three common pollutants: fine particulate matter (PM2.5) and nitrogen dioxide (NO2), which primarily come from the burning of fuel, and ozone (03), which is formed through chemical reactions between pollutants.

They analyzed functional MRI brain scan data from 9,497 children in the Adolescent Brain Cognitive Development (ABCD) study, none of whom had major medical or neurological conditions and a history of premature birth or low birth weight.

The first brain scans were collected from children when they were nine to 10 years old, and roughly half underwent follow-up scans two years later. This data allowed the researchers to analyze changes in brain connectivity, particularly the salience, frontoparietal, and default-mode brain networks. They also looked at the amygdala and hippocampus — key brain regions involved in emotion, learning, memory, and other complex functions.

Then the researchers mapped annual averages of pollutant concentrations to the child's primary residential address. They also controlled for sex, race/ethnicity, parental education level, household income, and other factors that could explain differences in brain development.

The study found that greater exposure to PM2.5 was linked to relative increases in functional connectivity between regions, while more exposure to NO2 predicted relative decreases in connectedness. Exposure to higher levels of O3 was associated with greater connections within the brain's cortex but fewer connections between the cortex and other regions, such as the amygdala and hippocampus.

The authors say that while the opposing effects of individual particles may seem counterintuitive, the differences may be the result of a compensatory restructuring of crosstalk between brain regions resulting from exposure.

"On average, air pollution levels are fairly low in the U.S., but we're still seeing significant effects on the brain. That's something policymakers should take into account when they're thinking about whether to tighten the current standards," says Megan M. Herting, PhD, associate professor of population and public health sciences at the Keck School of Medicine and the study's senior author.

The research, however, has limitations. The ABCD study lacks air pollution exposure during the prenatal period, early life, and beyond the nine to 10-year age period for participants.

Additionally, although the study observed only small effects of pollution, it cannot be ruled out that cumulative exposure to these low levels may have more significant effects on a population level.

The findings of the study may provide further support for new guidelines with more stringent limits on emissions, such as those recommended by the World Health Organization (WHO) in September: 5 micrograms of PM2.5 per cubic meter (µg/m3), 100 µg/m3 of O3, and 10 µg/m3 of NO2.

Earlier this year, the EPA proposed strengthening standards for PM2.5 that have not changed since they were first set in 1971. The agency estimates that a new PM2.5 standard at a level of 9 µg/m3 would help to prevent up to 4,200 premature deaths per year.

The new study's authors say that further research is necessary to determine whether pollution exposure-related changes in brain function during the transition to early adolescence may contribute to various mental health disorders that typically emerge later in the teenage years.

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