Air pollution and the eyes: what polluted air does to the ocular surface and to the retina

The eye is the only mucous membrane you expose directly to the surrounding air, with no filter at all: between two blinks, its surface stays bare for several seconds at a time. On days when particle levels peak, consultations for a red eye, burning and the feeling of grit rise in the cities that have measured it. Deeper down, large cohorts have for ten years been reporting associations between the air we breathe, the retina and the optic nerve. These two levels of evidence have neither the same solidity nor the same practical consequences, and confusing them would be the surest way of worrying people without helping them. Here is what is established, what is not, and what a patient can actually do.

UNDERSTANDING

Why pollution reaches the eye before the rest of the body

Because nothing stands in the way. The cornea and the conjunctiva are in permanent contact with the surrounding air, and the tear film that covers them is the only barrier available — a few micrometres of water, mucins and lipids, renewed with every blink. Everything the air contains is deposited on it: fine particles below 2.5 micrometres (PM2.5) and below 10 micrometres (PM10), nitrogen dioxide, sulphur dioxide, carbon monoxide, ozone.

A systematic review of 102 studies, published in 2025, describes what happens next. On corneal and conjunctival cells, exposure to particles triggers apoptosis mediated by inflammation and oxidative stress; in animals, it reproduces a picture of dry eye, with a fall in tear volume and lesions of the surface; in humans, it corresponds to symptoms of itching, burning and irritation, and to clinical signs of dry eye, conjunctivitis or ocular allergy.

The overall order of magnitude comes from a meta-analysis of 55 studies published in 2026. The odds ratio for all eye diseases taken together is 1.26 there (95% confidence interval: 1.20 to 1.32) in the most exposed people, with 1.29 for damage to the surface, 1.22 for the anterior segment and 1.35 for the fundus. These are odds of occurrence around 22 to 35% higher, not multiplications. Holding on to that calibration avoids reading what follows the wrong way.

SURFACE

What pollution does to the tear film

It destabilises it, and that is measurable in days. A Chinese multicentre prospective cohort followed 387 patients with dry eye in five provinces, cross-checking their examination against their exposure to pollutants over the previous day, week and month. The ocular discomfort score rose with PM2.5, ozone and sulphur dioxide; tear film break-up time fell; corneal staining worsened; the functioning of the meibomian glands deteriorated, and the inflammatory cytokines in the tears — interleukins 6 and 8 — went up.

The most useful detail of this work is a matter of timing. The cytokines reacted within a day, the symptoms peaked within a week, the damage to the meibomian glands within a month. In other words, the ocular surface takes the hit quickly and recovers slowly: an episode of pollution is not read on the day itself alone. A study carried out in Beijing finds the same signature, with altered ocular signs and cytokine profile in exposed subjects.

This assault adds to the causes already known rather than replacing them: pollution only makes more fragile a tear film that is often already undermined by screens and the dry air of offices. A word of caution, finally, about the designated culprit. The TFOS Lifestyle report, the international reference on environmental factors, carried out its own systematic review and finds an association between dry eye and nitrogen dioxide, but not with carbon monoxide nor with PM10. The pollutant that counts is not always the one that comes to mind.

EMERGENCIES

On peak days, practices and emergency departments fill up

This is the most reproducible result in the whole file. In Hangzhou, six years of consultations for dry eye set against air quality readings give fractions attributable to pollutants of 18.7% for nitrogen dioxide, 12.3% for carbon monoxide, 10.8% for sulphur dioxide, 8.0% for PM10 and 6.4% for PM2.5. These results and those of the TFOS report quoted earlier do not bear on the same kind of study: the TFOS report pools diagnostic work, while the Hangzhou study follows a single city year after year — and the two do not agree on carbon monoxide or on PM10, which the Hangzhou study implicates and for which the TFOS report finds no association. Finally, these fractions are not additive: each one is estimated for a single pollutant taken on its own, and these exposures are correlated with one another. The effect was more marked in cold weather, in winter, and in 21- to 40-year-olds.

In Beijing, across 24,389 eye emergency attendances between 2014 and 2019, each rise of 10 µg/m³ in PM2.5 went with an increase of 0.73% in attendances for an eye complaint and of 1.34% in attendances for conjunctivitis. In Ontario, 77,439 emergency attendances for conjunctivitis show associations lagged by five to eight days with nitrogen dioxide. And in five Chinese cities, 109,985 consultations for allergic conjunctivitis give an odds ratio of 1.045 per standard deviation of sulphur dioxide, which holds up after adjustment for the other pollutants.

Not every city tells the same story. In Beer-Sheva, in Israel, 601 emergency attendances for conjunctivitis were clearly associated with temperature, and not at all with particles. These divergences are not a flaw in the literature: they are a reminder that the composition of the air, the climate and the way people live change the result. What these studies establish is that a share of consultations for a red eye follows air quality. They do not say that a given individual will fall ill on a peak day.

EXPOSURES

Traffic, wildfire smoke, wood fires: three exposures not to be confused

Urban traffic first, with the most concrete study of the lot. Fifteen cyclists in Bologna wore personal particle sensors for six months of journeys between home and work. The highest exposures were associated with conjunctival redness and with lesions of the corneal epithelium, with no effect of temperature or humidity. Above all, analysis of the tears collected after the journeys identified the particles themselves: carbonaceous matter, aluminosilicates, iron, sulphur compounds. Street air does not merely irritate the eye, it settles on it.

Wildfire smoke next, whose effect has been reproduced in the laboratory. Eighteen volunteers fitted with respirators sat for fifteen minutes 1.5 m from a vegetation fire, under a mean exposure of 1,903 µg/m³ of PM2.5. After that quarter of an hour: increased symptoms, staining of the ocular surface, redness of the limbus and of the palpebral conjunctiva, tear film break-up time shortened by 1.4 seconds, interleukin 1β raised in the tears. In the field, 338 Australian wildland firefighters report eye irritation during work in 90% of cases, and 70% afterwards.

Biomass burning last, outdoors as well as indoors. During the 2008 smoke episode in Buenos Aires, when particle levels reached four times the usual averages, 86 subjects examined during and after the crisis showed more symptoms, more conjunctival redness and a less stable tear film — the patients whose ocular surface was already fragile being the worst affected. Indoors, a review devoted to domestic air links particles, volatile organic compounds, heavy metals, tobacco smoke and the burning of solid fuels to dry eye, conjunctivitis and keratitis, through chronic inflammation, oxidative damage and the breakdown of the tight junctions of the epithelium.

RETINA

What the large cohorts see in the retina

Here we change the nature of the evidence, and this must be said before the figures: we leave behind an effect measured over a few days for associations built over decades, in which place of residence, income, smoking and noise all travel alongside pollution. The French Alienor cohort, in Bordeaux, followed 683 people aged 75 and over, with an OCT measurement of retinal nerve fibre thickness every two years from 2009 to 2020. Higher exposure to PM2.5 and to black carbon over the previous ten years was associated with faster thinning — 0.28 µm a year for PM2.5 and 0.26 µm for black carbon, per interquartile range of exposure — roughly what one year of age adds in the same model (0.36 µm a year). This association was observed at pollution levels below the European limits in force.

On AMD, the data point the same way, with small effect sizes. In the UK Biobank, among 115,954 participants, higher exposure to PM2.5 went with an odds ratio of 1.08 for self-reported AMD, and with differences in the thickness of the retinal layers on OCT: the photoreceptor synaptic region and the pigment epithelium were thinner. A meta-analysis of eight studies gives 1.16 for PM2.5, 1.17 for nitrogen dioxide and 1.06 for ozone. Its authors themselves conclude that the relationship is “positive but not causal”. That is their wording, and it deserves to be taken up as it stands.

The most telling contradiction concerns ozone precisely. A Korean survey of 15,115 adults finds an odds ratio of 0.80 for early AMD where ozone is high — that is a protective association — while a Chinese cohort of 27,923 people reports on the contrary a risk raised by 28% and by 101% in the medium and high exposure groups. Same pollutant, opposite directions. That is enough to rule out any causal reading: pollution does not “give” you AMD, and a patient under follow-up for dry AMD should not conclude that the air of his city explains his disease. Age, genetics and smoking remain the documented determinants, smoking being the only inhaled factor whose modifiable role is solidly established.

GLAUCOMA

Glaucoma: an association that keeps coming back, and a mechanism that is not pressure

The signal exists, it is weak, and it is interesting for what it rules out. In the UK Biobank, 481,113 participants followed for a median of 12.8 years produced 9,224 incident cases of glaucoma: each interquartile range of PM2.5 went with a risk higher by 3% (hazard ratio 1.03; 1.00 to 1.06), and the most exposed quartile exceeded the least exposed by 10%. That is little, on the scale of one individual.

An earlier analysis of the same cohort is more instructive than that figure. Among 111,370 participants, exposure to PM2.5 was associated both with self-reported glaucoma (odds ratio 1.06) and with a thinning of the macular ganglion cell layer, with a dose-effect relationship. But it was not linked to any clinically relevant variation in intraocular pressure. If an effect exists, it therefore does not work through pressure — the authors suggest a vascular or neurotoxic route.

The rest of the literature swings about a good deal. A meta-analysis of age-related eye diseases reports, for each rise of 10 µg/m³ in PM2.5, an odds ratio of 1.18 for glaucoma, but with a confidence interval from 0.95 to 1.47: the threshold of significance is not reached, even though the four studies included all pointed the same way. A Taiwanese cohort of 590,338 people finds on the contrary rises of 40 to 108% per standard deviation over ten years, in a setting of exposure that bears no comparison with France. The practical conclusion: air quality changes neither the monitoring nor the treatment of glaucoma. Intraocular pressure and regular follow-up remain the only levers.

DIABETES

Diabetic retinopathy: it is diabetes that governs

The question arises legitimately, since diabetic retinopathy is a disease of the small vessels and pollution impairs the microcirculation. The clearest demonstration comes from rural China: among 3,111 people with diabetes, each rise of 10 µg/m³ in PM2.5 went with an adjusted odds ratio of 1.41 (1.27 to 1.57) for retinopathy. But the median exposure there was 59.9 µg/m³, that is to say several times what a resident of the Paris region (Île-de-France) breathes. Transposing that figure to France would make no sense.

At exposure levels closer to our own, the signal weakens and blurs. The Fujian Eye study, on 8,211 people including 2,405 with diabetes, finds an association of particles and nitrogen dioxide with retinopathy, but at the limit of significance in the people with diabetes themselves, and nothing for sulphur dioxide or for ozone. Above all, a British cohort of 17,995 people with type 2 diabetes finds an association between pollutants and microvascular complications overall — but, when the organs are taken separately, with nephropathy and neuropathy, not with retinopathy.

Another analysis of the UK Biobank illustrates the same haziness: the association between PM10 and diabetic retinopathy appeared only in the myopic participants. That is a subgroup result which needs to be reproduced before being discussed with a patient. The clinical message, for its part, has not shifted an inch: what protects a diabetic retina is blood sugar control, blood pressure control and an annual screening examination. No data justify adding a worry about the air we breathe.

IN PRACTICE

What really helps, and what is of no use

Three actions have a foundation in the data above. The first is distance from the source: among Belgian schoolchildren, those who lived 100 metres closer to a major road had retinal arterioles 0.30 µm narrower. Choosing a side street rather than the main road to walk, run or cycle at rush hour really does change the dose received. The second concerns indoor air, where we control the source: not adding combustion at home — a poorly ventilated stove, incense, candles, tobacco — and ventilating rather than sealing everything up.

The third is mechanical protection when exposure is intense and predictable: building sites, prescribed burning, fires, a daily cycle commute. Wildland firefighters report that goggles reduce symptoms, but 55% of them have to take them off because of sweat or fogging, and full-face masks are removed far more often than plain sunglasses or safety glasses. The lesson is down to earth: the best eye protection is the one you keep on your face. A pair of wraparound glasses worn all the time is worth more than a perfect mask sitting on your forehead.

Then comes what I do in consultation, which has more to do with caring for the surface than with avoidance: treating dry eye when it is there — preservative-free artificial tears, eyelid hygiene — and easing the load on difficult days, for example by resting contact lenses in favour of glasses during a smoke episode. These measures are not validated as countermeasures to pollution; they treat the damage that has been found, which is not the same thing, and I prefer to put it that way rather than credit them with a virtue they do not have.

Now for what is of no use. No food supplement, no eye drop presented as “anti-pollution”, no detox cure has demonstrated a protective effect on the ocular surface or the retina against polluted air. The reviews that take up the question of protective strategies indeed conclude that this work remains to be done: putting forward possibilities is not the same as having validated them. One piece of data, on the other hand, deserves to be known by anyone choosing where to live: in a cohort of more than 4,500 incident cases of AMD, a greener residential environment was associated with a lower incidence, this relationship being partly mediated by lower pollution. It is not a prescription, it is one more argument in favour of trees in cities.

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This article is intended for information and does not replace a medical consultation. Indications, expected benefits and risks depend on each individual situation. For any question about your vision, consult an ophthalmologist.