Pollution exposure may increase depression risk in healthy people

pollution on depression
pollution on depression
A new research looks at pollution and depression risk in persons with a genetic predisposition.
  • Pollution exposure is linked to cognitive impairments and increased risk of depression.
    Researchers recently studied how pollutants affect brain networks, altering cognitive performance and raising the risk of depression.
  • The findings imply that genetic vulnerability to depression and high pollution exposure have a disproportional effect on cognitive and stress networks in the brain.
  • The activation of brain networks encoding depression-associated genes was linked to air pollution exposure, suggesting that air pollution may harm mental health by affecting brain networks linked to genetic causes of depression.
  • Those with a hereditary predisposition to depression may be more susceptible to the negative effects of air pollution on mental health.

Prolonged exposure to air pollution is linked to negative mental health consequences in addition to having a negative impact on physical health.

Air pollution, particularly fine particulate matter, has been linked to poor cognitive performance and depression.

PM2.5, or fine particulate matter, is made up of microscopic inhalable particles smaller than 2.5 microns. Particles from industrial sources and cars are common sources of these particles.

It’s unclear how exposure to PM2.5 may enhance the chance of depression.

Furthermore, experts are unsure if air pollution might combine with a genetic predisposition to sadness to raise the risk of depression.

In the presence of specific environmental conditions or owing to activities such as smoking, people who have a genetic predisposition for a disease may have a higher risk of getting the disease.

A new study looked at the impact of PM2.5 exposure on brain networks involved in cognition and social stress when combined with a hereditary susceptibility to depression.

Dr. Hao Yang Tan, the study’s principal author and a scientist at the Lieber Institute in Baltimore, Md said;

”The study exposes for the first time how air pollution and genes combine to affect critical cognitive and emotional brain circuits. Air pollution alters the expression of genes associated with depression.”

“Previous research have found a correlation between air pollution and sadness,” he added, “but our findings are the first to indicate a direct, neurological causation.”

“What’s even more remarkable is that the two elements are related in such a manner that they have a multiplier effect on depression risk.” That is, when risk genes and poor air are combined, the risk of depression is substantially higher than when either component is considered alone.”

The research was published in the Proceedings of the National Academy of Sciences.

Anxiety and cognition

The study enlisted the help of 352 healthy people from Beijing, China. Beijing’s air pollution levels are relatively high, with high PM2.5 concentrations.

The researchers looked at numerous distinct genetic variations linked to depression in each person. They calculated their genetic predisposition to depression based on this knowledge.

The researchers utilized air monitoring data from the municipal air quality monitoring station nearest to each person’s house for 6 months before to the study to estimate PM2.5 exposure levels for each participant.

Depression is linked to cognitive impairments and elevated anxiety-depression levels. In other words, these people are more likely to react to a scenario with anxiety or depression symptoms. A questionnaire was used to assess each participant’s anxiety and depression levels.

The researchers initially looked at the impact of PM2.5 exposure on cognition and depression-related features.

PM2.5 exposure was linked to worse performance on reasoning and problem-solving tasks, according to the researchers. PM2.5 exposure was also linked to increased anxiety and sadness.

Connectivity in the brain

The researchers next looked at brain networks involved in cognition and processing stress-related information, as well as their links to PM2.5 exposure and depression genetic risk.

Using functional magnetic resonance imaging, the researchers evaluated the individuals’ brain activity while they performed a simple cognitive test.

Researchers presented participants a picture of a rival and compared their performance to that of the competition to see how social stress affected brain activity during the cognitive task.

With the cognitive activity, higher levels of PM2.5 exposure were linked to shorter reaction times, and this impact was enhanced during social stress.

Individuals with a genetic propensity for depression and higher PM2.5 exposure had a more dramatic effect on brain networks as a result of social stress.

The combined effect of genetic risk and air pollution on brain networks was higher than the sum of the effects induced by each component individually. These findings imply that air pollution may impact brain networks by interacting with genetic predisposition for depression.

The dorsolateral prefrontal cortex is a part of the brain that plays a role in a variety of functions, including cognition. In people with increased PM2.5 exposure and a genetic susceptibility to depression, it was one of the major areas whose connection altered throughout the cognitive activity.

Scientists have seen differences in the activity of the dorsolateral prefrontal cortex in healthy people with a hereditary susceptibility to depression and people who experience depression.

Depression-related brain networks

To learn more about the relationship between genetic risk for depression and air pollution, the researchers looked into whether the two variables had distinct effects on depression-related brain networks.

By identifying brain areas with high amounts of depression-associated genes, the researchers were able to map the brain networks implicated in depression.

The researchers utilized the Allen Brain Atlas database, which contains extensive gene expression data for different brain regions. They next looked for brain areas with corresponding expression of genes linked to depression.

The researchers wanted to see if the atlas-derived pattern of coexpression of depression-associated genes in brain areas matched the subjects’ brain connection patterns throughout the cognitive tests.

The atlas-derived pattern of coexpression of depression-associated genes predicted brain connectivity patterns during the cognitive task. This was true only for individuals who were exposed to higher levels of PM2.5 and had a higher genetic propensity to depression.

Individuals with a reduced genetic risk of depression or lower PM2.5 exposure had a lesser connection.

This shows that PM2.5 air pollution has an effect on brain network activities linked to depression’s genetic processes.

Similar studies were carried out on the relationship between the dorsolateral prefrontal cortex’s connection patterns with other brain regions and the coexpression of depression-related genes in these areas.

Individuals with a genetic predisposition for depression, greater PM2.5 exposure levels, or both had co-expression of depression-associated genes that followed connection patterns to and from the dorsolateral prefrontal cortex.

Interestingly, some of the co-expressed genes that linked with prefrontal cortex brain connection patterns were implicated in neuroinflammation.

PM2.5 exposure may interact with depression-associated genes to raise the risk of depression, as depression is linked to persistent, low-grade inflammation.

Dr. Tan said, “This is possibly the first study to directly implicate how genes for brain disorders work in concert with each other and affect important cognitive and emotional functions in the live functioning brain, as well as the impact of air pollution and genes in multiplying the effects of each on these brain functions.”

“It is now [in] much less doubt that there are direct impacts of air pollution on how genes operate in the brain to affect risk for these neuropsychiatric disorders,” he added.


Dr. Tan noted: “Individuals can limit their outdoor activities when pollution is high and be mindful of their risk. Our study would strongly suggest that individuals with genetic risk, e.g., [a] family history of brain disorders, may need to be more careful, and minimize [as much as] possible their exposures to any air pollution.”

“Armed with this knowledge, leaders and public health officials around the globe have ample evidence that additional air pollution controls will lead to lower rates of depression — particularly in densely populated urban areas where air pollution is highest, and stress from socioeconomic and other inequities are greater.”

– Dr. Tan

Dr. Perry Sheffield, an environmental health researcher at Icahn School of Medicine at Mount Sinai, New York, noted that this study “helps drive home the point that when we talk about vulnerable groups — and here I mean groups of people who are more likely to experience negative health effects from a certain environmental exposure — we are ultimately talking about all of us. Each of us is vulnerable probably in multiple ways, and our specific vulnerabilities change during our lives.”

“Vulnerability can certainly be socially and unjustly determined — as we see driving racial and ethnic health disparities — but it can [also be] influenced by underlying genetics, as we see here in relation to air pollution and depression, and certainly by life stage or age,” she continued.

“The value of illustrating these associations in a study like this is that it helps tell the story of why clean air, water, and the overall environment matter for the health of people and communities.”

– Dr. Sheffield

Strengths and limitations

“An key strength is that we have researched the brain repercussions of air pollution utilizing MRI technologies, which are perhaps the most direct assessments of real human brain activity,” Dr. Tan stated.

“We looked at a significant number of people.” We’ve also ruled out a slew of additional variables that may have thrown the research off.” Their sample was “socioeconomically homogenous,” for example.

“We also looked at how risk genes for depression worked together in postmortem human brains and found that these patterns matched very well with how the live human brain worked, especially in those who were genetically predisposed to depression and were exposed to high levels of pollution.”

Dr. Tan admitted that their technique had some flaws, adding that the researchers “examined only a restricted number of genes for depression, and that’s likely merely the tip of the iceberg.”

“Many more genes [for] neuropsychiatric illnesses are likely linked in the effects of air pollution on the brain.” “Knowing more about these would allow us to better identify those who are at danger and, maybe, develop various pharmaceutical or other approaches to safeguard the susceptible,” he concluded.