By Jay Fox

New research suggests that long-term exposure to air pollution is associated with an increased risk of depression among older adults. Published in the Journal of American the American Medical Association Network Open, the study focused on the effects of fine particulate matter (PM2.5) and its major constituents: sulfate (SO4^2-), nitrate (NO3^-), ammonium (NH4⁺), elemental carbon, organic carbon, and soil dust. Increases in four of the six constituents—sulfate, elemental carbon, soil dust, and ammonium—as well as PM2.5 mass, were positively associated with depression. Simultaneous exposure to multiple constituents appears to have an even greater association with increased depression risk.

The study’s authors, Yanling Deng, Hua Hao, Qiao Zhu, Yang Liu, and Kyle Steenland—all currently based at the Gangarosa Department of Environmental Health at Emory University’s Rollins School of Public Health—relied on Medicare data from 23.7 million beneficiaries (average age: 76 years) between 2000 and 2018. When divided into quartiles based on ZIP code of residence and exposure to the noted pollutants over 5 years, each increase in quartile correlated with a 7% higher risk of depression. Risk was most pronounced following exposure to sulfate, elemental carbon, soil dust, PM2.5, and ammonium (in that order).

The study builds on previous research—also published by a team from the Rollins School of Public Health—showing an association between late-life depression and long-term exposure to PM2.5, nitrogen dioxide, and ozone.

Air Pollution and Chronic Inflammation

It’s no surprise that high concentrations of particular matter are associated with acute health effects and long-term respiratory diseases. Hospital systems have long reported a clear correlation between major smoke events and increases in emergency room visits, particularly for individuals with asthma and chronic respiratory illnesses. More anecdotally, anyone who has endured serious smoke exposure because of wildfires, or even sat too close to an overly smoky campfire, has felt this causal relationship. They can typically feel that their lungs are inflamed the day after.

The damage done by chronic inflammation can extend to all organ systems—including the brain and the membrane protecting it, the blood-brain barrier (BBB). When healthy, the BBB is highly selective and semi-permeable. It allows for signaling between the central nervous system (CNS) and the peripheral nervous system. More importantly, it also keeps pathogens and unwanted substances from crossing into the CNS. When damaged due to chronic inflammation, however, the BBB becomes more permeable and a less effective barrier. Eventually, the systemic inflammation crosses into the CNS and leads to neuroinflammation.

As scary as neuroinflammation may sound, it is also a normal process. The brain is equipped with its own specialized immune system to regulate inflammation and to communicate with the immune system outside of the CNS. It can even recruit immune cells from outside of the CNS.

Neuroinflammation may be natural, but it’s not always benign. Neuroinflammation can be a sign of serious illness, especially when it becomes chronic. As is the case in the rest of the body, chronic inflammation in the brain can damage healthy neural tissue and networks, contributing to neurological deficits. For example, many of the symptoms that emerge follow traumatic brain injury are due to chronic neuroinflammation. Neuroinflammation also plays a role in neurodegenerative diseases like dementia (including Alzheimer’s disease), Parkinson’s disease, and amyotrophic lateral sclerosis (ALS), just to name a few.

Neuroinflammation can also affect our ability to regulate stress, emotion, and mood. When neuroinflammation affects these latter networks, individuals tend to behave in a manner that mimics clinical depression, suggesting that some instances of major depressive disorder may be the downstream results of neuroinflammation.

This is not to say that neuroinflammation is the sole cause of major depressive disorder. It is not. However, the framework outlined here does provide a mechanism to explain how chronic inflammation caused by environmental factors (e.g., air pollution) is associated with depression. It also provides some context for the following two sentences taken from the study that inspired this article:

How Does Passive House Fit into This Conversation?

Resiliency is a common theme within the Passive House community. Elements of passive building techniques and high-performance materials choices go hand-in-hand with Fire-Smart practices. Meanwhile, the principles of Passive House design—high-performance windows and doors, airtight envelopes, thermal-bridge free design, continuous insulation, and mechanical ventilation—offer those who are sheltering in place during power outages and major smoke events a far better chance of survival.

Within this context, resiliency is framed as a means of persevering through a temporary crisis.

However, issues like air pollution are not temporary. The study that inspired this article wasn’t focused on a localized population that had been exposed to extreme wildfire smoke. They were people from across the United States who were regularly exposed to high enough levels of PM2.5 between 2000 and 2018 to have it affect their mental health. What this suggests is that true resiliency must be capable of continuously guarding against persistent and harmful environmental conditions.

This is the job for which passive buildings are designed. By virtue of their superior airtightness and use of mechanical ventilation to provide a constant supply of fresh, filtered air, Passive House buildings can limit chronic exposure to PM2.5 and allergens. In addition, passive buildings reduce noise pollution for occupants and ensure consistent thermal comfort.

Will passive buildings alone eliminate inflammation or cure depression? Probably not. However, better building science guided by the principles of Passive House construction can create healthier indoor environments and reduce exposure to the sources of chronic inflammation and stress. These principles offer a proven path to creating truly restorative spaces.

The top photo was taken at Jordan Pond in Acadia National Park.

References and Suggested Reading (no paywalls)

Deng Y, Hao H, Zhu Q, Liu Y, Steenland K. Exposure to Multiple Fine Particulate Matter Components and Incident Depression in the US Medicare Population. JAMA Netw Open. 2025;8(12):e2551042. doi:10.1001/jamanetworkopen.2025.51042

Gou Y, Cheng S, Kang M, et al. Association of Allostatic Load With Depression, Anxiety, and Suicide: A Prospective Cohort Study. Biol Psychiatry. 2025 Apr 15;97(8):786-793. doi: 10.1016/j.biopsych.2024.09.026. Epub 2024 Oct 10. PMID: 39395472.

Jones CG, Rappold AG, Vargo J, Cascio WE, Kharrazi M, McNally B, Hoshiko S; with the CARES Surveillance Group. Out-of-Hospital Cardiac Arrests and Wildfire-Related Particulate Matter During 2015-2017 California Wildfires. J Am Heart Assoc. 2020 Apr 21;9(8):e014125. doi: 10.1161/JAHA.119.014125. Epub 2020 Apr 15.

Qiu X, Shi L, Kubzansky LD, et al. Association of Long-term Exposure to Air Pollution With Late-Life Depression in Older Adults in the US. JAMA Netw Open. 2023;6(2):e2253668. doi:10.1001/jamanetworkopen.2022.53668

Plautz J. Ammonia, a Poorly Understood Smog Ingredient, Could Be Key to Limiting Deadly Pollution. Science. 2018 Sep 13. Accessed 2026 Jan 8. Available from: https://www.science.org/content/article/ammonia-poorly-understood-smog-ingredient-could-be-key-limiting-deadly-pollution. doi: 10.1126/science.aav3862

Seeman TE, McEwen BS, Rowe JW, Singer BH. Allostatic Load as a Marker of Cumulative Biological Risk: MacArthur Studies of Successful Aging. Proc Natl Acad Sci USA. 2001;98(8)4770-4775. doi: 10.1073/pnas.081072698.

Wettstein ZS, Hoshiko S, Fahimi J, Harrison RJ, Cascio WE, Rappold AG. Cardiovascular and Cerebrovascular Emergency Department Visits Associated With Wildfire Smoke Exposure in California in 2015. J Am Heart Assoc. 2018 Apr 11;7(8):e007492. doi: 10.1161/JAHA.117.007492. PMID: 29643111; PMCID: PMC6015400.

Yin Y, Ju T, Zeng D, et al. "Inflamed" Depression: A Review of the Interactions Between Depression and Inflammation and Current Anti-Inflammatory Strategies for Depression. Pharmacol Res. 2024 Sep;207:107322. doi: 10.1016/j.phrs.2024.107322. Epub 2024 Jul 20. PMID: 39038630.

Zhen S, Luo M, Shao Y, et al. Study on the Source of Nitrate in Atmospheric Particulate Matter in Beijing Using Nitrogen and Oxygen Dual Isotopes. Sci Rep. 2025 May 25;15(1):18174. doi: 10.1038/s41598-025-01179-9.