It’s the first study that associates neurological disorders and fine particulate matter, says Xiao Wu, co-lead author and doctoral student in biostatistics at Harvard Chan School.

Wu and colleagues carried out the epidemiological study with more than 63 million older US adults, drawing from an unparalleled amount of data. The results, however, don’t look too pretty.

In any given day, in any given place, the air contains small aerosols — liquid or solid particles suspended in the atmosphere. The amount of these microscopic particles (called particulate matter, or PM for short) can vary substantially. Normally, the concentration of particulate matter should be very low — but in polluted areas, the amount of particulates can reach high, unhealthy levels.

Particulate matter can affect human health adversely in a number of ways. Small particulates, smaller than 10 micrometers tend to be the worst for your health (the average hair is about 70 micrometers, for comparison). They can cause irregular heartbeat, aggravated asthma, decreased lung function, and many, many more problems. Now, according to a new study, PM2.5 (particulate matter with a size of 2.5 micrometers and lower) can also cause neurological disorders.

The researchers looked at 17 years of hospitalizations of US Medicare recipients. They found that for each microgram per cubic meter of air of PM2.5, there was a 13% increase in the risk of first-time hospital admission both for Parkinson’s and Alzheimer’s — even after controlling for socioeconomic factors. The risk remained elevated even below supposedly safe levels of PM2.5 exposure (which according to EPA standards, is 12 micrograms per cubic meter or less).

The study builds on a small, but growing amount of evidence suggesting a link between particulate matter and neurological diseases. In an email to ZME Science, Wu explained that air pollution might play a key role in neuroinflammation, exacerbating or initiating dysfunctional protein handling — one of the main mechanisms responsible for neurological dysfunctions.

“Toxicological studies suggest various potential mechanisms via which air pollution might contribute to neurodegenerative progression,” Wu explains.

“Systemic and brain inflammation, for example, enhance the pathogenic alteration of α-synuclein, accelerating the progression of Parkinson’s disease and Alzheimer’s disease. Oxidative stress, in addition, is also involved both in initiation and progression, and plays an important role in accelerating Parkinson’s disease progression. “

Not everyone was equally susceptible to the effects of air pollution. According to the study, women, white people, and urban populations were particularly vulnerable. But the fact that even levels that are “officially safe” are risky is particularly concerning.

“Our U.S.-wide study shows that the current standards are not protecting the aging American population enough, highlighting the need for stricter standards and policies that help further reduce PM2.5 concentrations and improve air quality overall,” said Antonella Zanobetti, principal research scientist in Harvard Chan School’s Department of Environmental Health and co-senior author of the study.

But there’s a good side to all this: cleaning the air could make a big difference, and it’s something well in our power.

“Given this effect of a 13% increased risk, reducing the air pollution by 5 microgram per cubic meter would be least associated with a reduction of 394,038 Alzheimer’s and Alzheimer’s related dementias hospitalizations, and 118,918 Parkinson’s hospitalization across 2000-2016, that is more than half million hospitalizations in total,” Wu tells ZME Science.

It’s important to note that while the study suggests a strong connection, no causal link has been demonstrated. In other words, researchers have a pretty good hunch that the pollution is causing (or accelerating) neurological problems, however, it’s still too early to draw any definite conclusions.

“I would not explain any causal link just via one single study, yet the collection of both toxicological and epidemiological evidence speak out the potential pathway. Also, We are planning on future epidemiological studies using newly developed causal inference methods which may provide more robust evidence on the causal link.”

The study has been published in The Lancet.