Aging is one of the biggest risk factors for developing glaucoma or cataracts — but as scientists look more closely at what happens to the eyes over a lifetime, they are finding that people's exposure to air pollution also plays a role in whether they develop these eye conditions.

Glaucoma, which affects about 80 million people worldwide, is a group of diseases that damage the optic nerve, which carries visual information from the eye to the brain. It can lead to permanent vision loss, usually affecting peripheral vision at first and later central vision. Cataracts are even more common, affecting more than 94 million people globally; the condition occurs when the eye's lens becomes cloudy, causing blurred vision and, eventually, blindness.

Aging raises the risk of both diseases, as do certain medical conditions, such as diabetes. But now, a review of 41 studies suggests that people who are exposed to higher levels of air pollution may also face a greater risk of these diseases. The research, presented in September at the 44th Congress of the European Society of Cataract and Refractive Surgeons in London, brought together evidence from dozens of studies collectively involving millions of people across East Asia and the U.K.

The studies were observational, meaning they can only draw a link between air pollution and the eye conditions, rather than prove that air pollution causes the diseases. But still, "this reframes glaucoma and cataract as conditions shaped by where you live and breathe, not just how long you've lived," said study co-author Dr. Ahmed Alnabihi, an ophthalmologist at King Khaled Eye Specialist Hospital and Research Center in Saudi Arabia, who presented the findings. These environmental exposures may compound age-related decline in the eye as they do in cardiovascular disease, he said.

PM2.5 shows the clearest links

The researchers examined exposure to several pollutants, including different sizes of particulate matter (PM), such as fine PM2.5 and larger PM10. They also looked at nitrogen dioxide, sulfur dioxide, ozone and carbon monoxide.

Most studies included in the review estimated people's long-term exposure based on the pollution levels around their homes and in their communities. They used a range of methods, including government monitoring systems, satellite data and computer models designed to estimate pollution levels. A few studies examined short-term exposure and its relation to more sudden eye issues, such as acute angle-closure glaucoma, a medical emergency that can quickly cause vision loss.

Using this wealth of data, the team compared pollution exposure with rates of glaucoma, cataracts and age-related macular degeneration (AMD), another common eye condition that impairs vision. PM2.5 — tiny particles that measure 2.5 micrometers or smaller — showed the clearest associations with glaucoma and cataract risk.

People with the highest exposure to PM2.5 had 70% higher odds of glaucoma, compared to those with the least exposure. Plus, an increase in PM2.5 exposure equivalent to the difference between the 25th and 75th percentiles of exposure within each study was associated with 8% higher odds of glaucoma and a 4% higher hazard of cataracts.

The evidence was less consistent for air pollution and age-related macular degeneration, which damages the central part of the retina that's responsible for sharp, detailed vision. And unlike the clear connection seen with PM2.5, other pollutants showed less consistent links to eye disease. For instance, nitrogen dioxide was not significantly tied to AMD, ozone was not tied to cataracts, and neither pollutant was linked to glaucoma. Sulfur dioxide and PM10 showed no significant associations with any of the three conditions.

The association between PM2.5 and glaucoma was relatively consistent across the reviewed studies, said Nidhi Singh, an environmental epidemiologist at the IUF-Leibniz Research Institute for Environmental Medicine in Germany, who was not involved in the study. The findings for PM2.5 and cataracts were moderately consistent, albeit more variable than the glaucoma data; still, she said that the analysis seems to support a link.

Singh did caution that the underlying evidence is observational. "Therefore, the results demonstrate an association, not by themselves a causal effect of PM2.5 on glaucoma or cataract," she told Live Science.

What explains the increased risk?

The exact biological mechanisms behind these links remain unclear, but Alnabihi noted that fine particulate matter is small enough to be absorbed into the body. This can trigger oxidative stress, in which harmful molecules overwhelm natural defenses and cause damage. It also drives chronic, low-grade inflammation, in which the immune system stays mildly activated for long periods, he explained.

In the eye's lens, these processes can "damage the crystallin proteins that keep it transparent, causing them to misfold and cloud, which is what a cataract is," Alnabihi said.

In the optic nerve, the same processes are thought to damage retinal ganglion cells, a special type of neuron that relays information from the retina to the brain. This can contribute to glaucoma independent of internal eye pressure, he said, which is another big risk factor.

"Unlike the lungs or gut, its [the eye's] surface is in direct, continuous contact with outdoor air, giving pollutants a uniquely direct route that might cause damage," he added.

Other studies have found clues that support the link between PM2.5 and eye damage. Mice that were exposed to ambient PM2.5 for nine months developed elevated pressure inside their eyes, a glaucoma risk factor. The researchers observed both oxidative stress and nitrative stress — a similar phenomenon — in the tissues that drain fluid from the eye, which may help to explain the rise in pressure.

Studies of humans and human cells have uncovered similar patterns. In data from more than 480,000 people in the UK Biobank, a large repository of health information, those exposed to higher PM2.5 were more likely to develop glaucoma over time. In another study, scientists exposed lab-grown human retinal tissue made from stem cells to PM2.5. The particles disrupted retinal cell development, including that of retinal ganglion cells, while increasing cell death.

These studies offer pieces of a possible mechanism, but for now, how those pieces fit together in people remains unclear.