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Home Exclusive Developmental Psychology

Common air pollutants associated with structural changes in the teenage brain

by Eric W. Dolan
January 26, 2026
Reading Time: 6 mins read
[Adobe Stock]

[Adobe Stock]

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A recent study published in Environmental Research suggests that breathing polluted air may alter the physical development of the brain during adolescence. The findings indicate that exposure to fine particulate matter and nitrogen dioxide is associated with an accelerated thinning of the cortex, particularly in regions responsible for emotional regulation and complex thinking. This research suggests that the environment in which a young person lives plays a role in their neurological maturation.

Air pollution is a global health issue that affects people in both industrial and developing nations. Most of the global population breathes air that exceeds safety guidelines established by the World Health Organization. This pollution is a complex mixture of gases and particles derived from vehicle emissions, industrial activities, and wildfires.

“This study grew out of a broader effort to understand how common environmental exposures shape health, particularly for some of our most vulnerable populations. With increasing wildfires, industrialization, and urbanization, many children are now exposed to air pollution more frequently and for longer periods of time. We wanted to better understand how typical, everyday levels of air pollution, levels many people consider ‘normal,’ may relate to brain development during adolescence,” said study author Calvin Jara, a resident physician at Oregon Health & Science University.

Previous research has firmly established links between poor air quality and respiratory or cardiovascular diseases. There is also growing concern regarding the impact of these airborne contaminants on the central nervous system. Pollutants like fine particulate matter are small enough to penetrate deep into the lungs. From there, they can enter the bloodstream and potentially cross the protective barrier that shields the brain.

Once in the brain, these particles may trigger inflammation and oxidative stress. This biological damage can disrupt the function of neurons. Adolescents may be particularly susceptible to these effects. Their bodies are still growing, and they often breathe in more air relative to their body weight than adults do.

The teenage years are a time of profound change for the brain. The brain undergoes a process known as synaptic pruning during this period. It eliminates weak or unnecessary connections between neurons to become more efficient. This natural maturation process results in a thinning of the outer layer of the brain, known as the cortex.

Because the brain is remodeling itself so actively during these years, it may be more vulnerable to environmental insults. Most prior research on pollution and brain structure focused on adults or looked at children at a single point in time. The authors of the current study sought to understand how exposure to pollution relates to changes in the brain as adolescents grow over several years.

To investigate this, the researchers utilized data from the Adolescent Brain Cognitive Development (ABCD) Study. This is the largest long-term study of brain development and child health in the United States. The dataset is designed to reflect the diverse demographics of the U.S. population.

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The analytic sample included 10,947 participants. These children were between the ages of 9 and 10 when the study began. The researchers tracked them for up to four years. The team used the residential addresses of the participants to estimate their exposure to specific air pollutants.

They focused on three common pollutants: fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3). The researchers linked geocoded home addresses to validated air monitoring data. This allowed them to calculate annual average exposure levels for each child.

The participants underwent magnetic resonance imaging (MRI) scans to measure the structure of their brains. These scans occurred at the beginning of the study, at a two-year follow-up, and at a four-year follow-up. The researchers specifically measured cortical thickness across sixty-eight different regions of the brain.

Statistical models were then used to examine the relationship between pollutant exposure and brain structure. The researchers employed linear mixed-effects models. This statistical approach allowed them to account for the fact that data was collected at multiple time points. It also handled missing data effectively.

The analysis included adjustments for various factors that could influence brain development. These variables included parental income, parental education levels, and the population density of the area where the child lived. Adjusting for these factors helped ensure that the results were not simply reflecting socioeconomic differences.

The data showed that higher exposure to PM2.5 and NO2 was associated with a faster rate of cortical thinning. This accelerated thinning was not uniform across the entire brain. The effects were most pronounced in the frontal and temporal lobes. The frontal lobe is heavily involved in executive functions. These functions include planning, attention, and impulse control. The temporal lobe plays a key role in processing emotions, language, and social cues.

The researchers observed these structural changes even though the participants were generally exposed to pollution levels that are considered common. This implies that routine exposure to standard levels of air pollution could have developmental consequences. The pattern of accelerated thinning suggests that pollution might alter the natural trajectory of brain maturation.

“We were struck by the fact that the associations appeared in brain regions involved in higher-order cognitive and emotional processing,” Jara told PsyPost. “It was also notable that these patterns emerged at pollution levels considered common or acceptable. This suggests that even relatively low-level exposures may be relevant during sensitive periods of brain development.”

In contrast to the findings for particulate matter and nitrogen dioxide, the study found minimal associations between ozone and cortical thickness. Ozone did not appear to have the same impact on the structural development of the cortex. This finding highlights that different pollutants may have distinct biological mechanisms of action.

Nitrogen dioxide is often related to traffic emissions. It may be more toxic to the nervous system due to its ability to induce specific types of oxidative stress. Ozone operates differently and may not cross the blood-brain barrier as easily as other pollutants.

The researchers noted that these findings align with previous cross-sectional studies. Earlier work has linked early-life air pollution to thinner cortices in school-age children. The current longitudinal study extends that knowledge by showing how these patterns evolve over time during the critical adolescent window.

“One important takeaway is that health is shaped not only by genetics, but also by the environments in which we live,” Jara explained. “Factors like nutrition, sleep, and physical activity matter, and things like air quality also contribute to our broader health. Our findings suggest that routine exposure to common levels of air pollution is associated with differences in how the adolescent brain matures over time—exposures that many people experience daily.”

“At the level of an individual child, these findings do not indicate damage or a medical diagnosis. However, when modest shifts in brain development, or any type of development for that matter, occur across millions of children exposed to low levels of pollution, the implications become meaningful at the population level. This is how many environmental health effects operate, being that they may be subtle for individuals, but important for public health.”

But the study, like all research, includes some caveats. The exposure estimates were based solely on residential addresses. This method does not account for the air quality at schools or other locations where the adolescents spent their time. It implies that the exposure measurement might not be perfectly precise for every individual.

Additionally, the study is observational in nature. This means it can identify associations but cannot definitively prove that pollution caused the brain changes. It is possible that other unmeasured factors contributed to the results.

“These findings should not be interpreted as evidence of direct harm or as a reason for alarm,” Jara noted. “The research also does not imply inevitability or irreversible effects. Rather, it highlights potential vulnerability during development and underscores the importance of prevention. Air pollution is one part of the equation, and there are many factors that go into one’s overall health and development.”

“My broader interest is in health-policy–relevant research that can inform decisions at a population level. Ultimately, the goal is to integrate scientific evidence into policies that protect vulnerable communities and promote healthier development across the lifespan. Environmental research in my opinion has the potential to not only extend life, but improve quality of life across generations.”

“One encouraging aspect of this work is that many environmental exposures are modifiable,” Jara added. “For example, improvements in air quality, access to green spaces, and awareness of environmental conditions can make a difference. And the broader point is that health unfolds over time and is shaped by the combined influence of many environmental exposures—air quality, water, food, psychosocial stressors, and the places we live. If we want people to live longer and healthier lives, I believe it’s important to think about how all these factors work together when thinking about health.”

The study, “Longitudinal associations between air pollution and adolescent gray matter development: Insights from the ABCD study,” was authored by Calvin A. Jara, Scott A. Jones, and Bonnie J. Nagel.

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