Air Pollution and Dry Eye Disease: Exploring Their Relationship

Air pollution is widely recognized for its adverse effects on cardiovascular health, respiratory diseases, and even neurological disorders. In recent years, increasing attention has been paid to how polluted air may also affect the ocular surface. Dry eye disease (DED), a condition characterized by tear film instability, inflammation, and discomfort such as redness, grittiness, and visual fatigue, continues to rise in prevalence around the world. Although many risk factors—such as age, gender, and lifestyle habits—have been associated with DED, the potential influence of air pollutants remains an area of growing interest and concern.

Dry eye disease not only causes discomfort and visual impairment in millions of individuals but also imposes a significant socioeconomic burden due to reduced productivity and increased healthcare visits. While epidemiological research has traditionally focused on the cardiopulmonary effects of air pollution, the ocular surface, which is in continuous direct contact with the ambient environment, may be uniquely vulnerable to these pollutants. In this article, we summarize the current evidence linking air pollution to dry eye disease, highlight research findings from various regions—including the rapidly growing city of Urumqi in northwest China—and discuss potential mechanisms and mitigation strategies.

Numerous studies have indicated that pollutants such as particulate matter (PM), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), carbon monoxide (CO), and even ozone (O₃) are implicated in various ocular conditions. Despite the protective barrier provided by the tear film, some pollutants can penetrate or disrupt the delicate balance of the ocular surface, leading to subclinical inflammation and tear film instability that may predispose individuals to DED.

Understanding Dry Eye Disease and Its Prevalence

Dry eye disease is defined as a multifactorial disorder of the ocular surface that arises from an imbalance in tear film homeostasis. Clinical manifestations include ocular discomfort, increased tear osmolarity, tear film instability, inflammation of the conjunctiva and cornea, and, over time, direct ocular surface damage. The condition is especially prevalent among postmenopausal women, and studies have noted that in North America, nearly 7.8% of women and 4.7% of men over the age of 50 suffer from severe symptoms.

In Asia, and more specifically in China, the prevalence of DED has been reported to range between 17% and 21% in the general population, with outpatient clinics reporting figures as high as 61.57%. Recent national surveys have highlighted regional differences within China, with higher prevalence reported in the western and northern regions compared with the southeastern areas. These regional variations underscore the importance of environmental and climatic factors, including ambient air quality.

Aside from demographic factors such as age and gender, lifestyle elements like chronic sleep deficiency, prolonged use of digital screens, and even smoking have been implicated in exacerbating dry eye symptoms. However, relatively fewer studies have focused on the role of environmental pollutants. The ocular surface’s direct exposure to ambient air and its inherent vulnerability render it an important, yet often overlooked, target for studying pollution-related health effects.

How Air Pollution Affects the Ocular Surface

The ocular surface is composed primarily of the corneal and conjunctival epithelia, which are protected by a thin, multi-layered tear film. This film functions to lubricate the eye, remove debris, and serve as a barrier against pathogens and environmental irritants. However, in polluted environments, particulate matter and reactive gaseous compounds can disrupt this delicate balance.

The following mechanisms have been proposed to explain how air pollution may lead to dry eye disease:

Evidence from Epidemiological Studies

Epidemiological studies have investigated the association between air pollution and dry eye disease by analyzing outpatient visits, self-reported symptoms, and clinical signs. Time-series analyses conducted in various regions—including eastern cities in China, Taiwan, and South Korea—have generally found a positive correlation between increased levels of pollutants and the incidence of dry eye disease outpatient visits.

In one study conducted in Urumqi, the capital of Xinjiang in northwest China, researchers aimed to investigate the relationship between six major air pollutants and dry eye disease outpatient visits. Urumqi, known for its harsh climatic conditions—characterized by large temperature variations, dryness, and frequent sand-dust storms—is an ideal location to study air pollution effects on ocular health. Despite its rapid economic growth and increased vehicular emissions, few studies had examined the direct impact of local air pollution on eye health in this region.

Using a retrospective time-series design with a large sample of outpatient data collected between 2013 and 2020, researchers analyzed various pollutants, including particulate matter (PM₂.₅ and PM₁₀), NO₂, SO₂, CO, and ozone. They applied statistical models that adjusted for confounding variables such as meteorological factors (temperature, humidity, wind speed) and even considered lag effects—investigating how exposure on a given day might influence DED visits several days later. Evidence from these models suggested that short-term exposure to key pollutants, particularly PM₂.₅, NO₂, and SO₂, was significantly associated with an increased risk of dry eye disease outpatient visits.

Similar findings have emerged from other regions. For instance, in urban centers of South Korea and eastern China, higher concentrations of traffic-related pollutants have been linked with both increased symptoms and more frequent hospital visits for DED. In addition, several studies have noted that these effects may be more pronounced in certain subgroups—for example, younger patients or women may be more sensitive to specific pollutants.