A Swedish study in JAMA Neurology finds that long-term exposure to air pollution is linked to a higher risk of motor neuron disease (MND), including ALS, and may accelerate disease progression.

Even at relatively low pollution levels common in Sweden—often just above WHO guidelines—the long-term exposure raises the risk of developing MND by about 20% to 30%.

The findings suggest air pollution could be a driver of MND even in countries with comparatively clean air, underscoring the importance of improving air quality for neurodegenerative disease prevention and outcomes.

The study adjusted for several socioeconomic and environmental factors but lacked data on smoking and indoor air pollution, a limitation not believed to fully explain the observed associations.

Researchers frame the findings as part of the broader puzzle toward understanding MND and advancing treatment and prevention.

Funding came from multiple organizations, including the US CDC and Karolinska Institutet, with analyses based on Swedish registry data.

The study is observational, so it cannot prove causality, though inflammation and oxidative stress from pollution are plausible mechanisms supported by prior work.

Results hint that local, near-home traffic pollution may have a stronger impact on risk and progression than distant pollution, though the exact biology remains unclear.

Motor neuron disease comprises disorders that destroy motor neurons, causing muscle weakness, paralysis, and respiratory failure, with no cure.

Exposure to four main pollutants was measured at participants’ homes, with relative risk increases of 20%–30% and stronger associations for the 10-year exposure window.

The study analyzed 1,463 MND patients in Sweden, comparing them to 1,768 siblings and over 7,000 general population controls, using home-based pollution data up to ten years before diagnosis.

By examining pollution at each participant’s home over 1, 3, 5, and 10 years before diagnosis, the association persisted even when comparing siblings, helping account for shared genetics and early-life environment.