Environmental Drivers of Dry Eye Disease: A Narrative Review of Pollutants, Climate, and Indoor Exposures with Practice Recommendations

Abstract

Dry eye disease (DED) is a multifactorial and prevalent condition of the ocular surface that is associated with a wide range of risk factors. In the modern world, environmental conditions and pollution have become increasingly relevant contributors. Recent findings from the Tear Film & Ocular Surface Society Dry Eye Workshop III (TFOS DEWS III) highlight the contribution of oxidative stress, inflammatory cytokines, and neurosensory alterations to environmentally associated DED. This narrative, non-systematic review aims to synthesize current evidence on the impact of climate change and exposure to pollutants on the epidemiology, pathophysiology, and management of DED, with a particular emphasis on clinical practice. A targeted search of peer-reviewed literature was conducted in PubMed and Scopus, focusing on previous reviews and original human studies evaluating environmental exposures and DED, and findings were synthesized qualitatively due to heterogeneity in study design and diagnostic criteria. Environmental influences on the ocular surface encompass a wide range of factors, including climate conditions such as temperature, humidity, wind speed, altitude, dew point, ultraviolet radiation, and allergens, as well as exposure to air pollution from gases, particulate matter, volatile organic compounds, and other airborne contaminants. Individuals living in densely populated cities, industrial zones, and dry climates are at increased risk, and emerging challenges such as wildfires and desertification warrant increasing attention due to their rising global impact. Exposure to these agents may induce or exacerbate tear film instability, epithelial damage, immune dysregulation, and ocular surface inflammation. Although most available studies are cross-sectional or observational, and therefore limited in establishing causality, environmental exposures remain a key contributor to DED and can impair occupational performance, exacerbate pre-existing health conditions, and diminish overall quality of life. Comprehensive screening, environmental risk assessment, patient counseling, and personalized management strategies are essential to the prevention and management of DED in the face of accelerating environmental change.

Key Summary Points

Why carry out this study?

Environmental exposures are increasingly recognized as relevant contributors to dry eye disease (DED); however, current evidence derives from studies with significant variability in populations, diagnostic criteria, and exposure measurements.

While several reviews have examined the role of environmental exposures in DED, there is limited work that comprehensively integrates climate-related, outdoor and indoor exposures into a single clinically oriented framework translating current evidence into practical management recommendations for eye care professionals.

What was learned from the study?

Climatic variables such as temperature, humidity, wind, altitude, and ultraviolet radiation can destabilize the tear film, promote evaporation, and trigger ocular surface inflammation.

Outdoor pollutants, including particulate matter, ozone, and nitrogen dioxide, are associated with increased DED symptoms and reduced tear stability, particularly in urban and industrialized areas.

Indoor factors such as poor ventilation, low humidity, chronic air-conditioning, and prolonged digital screen use contribute to sick building-related ocular symptoms and increased DED prevalence in occupational and residential settings.

Most available evidence is observational, emphasizing the need for longitudinal studies, and highlighting the importance of individualized environmental risk assessment, patient counseling, and targeted therapeutic strategies.

Introduction

Dry eye disease (DED) is a multifactorial and prevalent ocular surface disease. In recent years, environmental exposures have become increasingly recognized as important contributors to its onset and exacerbation, particularly in the context of global climate change and rapid urbanization [1, 2]. The condition is characterized by tear film instability, ocular discomfort, visual fluctuation, and inflammation of the ocular surface [3]. Additionally, recent findings highlight the contribution of oxidative stress, inflammatory cytokines, and neurosensory dysfunction to environmentally associated DED [3–6]. In 2023, the Tear Film & Ocular Surface Society (TFOS) published the first extensive and multidisciplinary effort to compile robust evidence on the role that environmental and behavioral exposures have in the development and progression of various ocular surface conditions [2, 7]. This narrative, non-systematic review aims to synthesize current knowledge on how climate-related factors, outdoor pollutants, indoor exposures, and lifestyle stressors influence the epidemiology, mechanisms, and management of DED, with a particular emphasis on clinical practice.

Epidemiology

The prevalence of DED varies globally, affecting between 5% and 50% of adults depending on geography, study design, and diagnostic criteria [1, 8]. When applying the standardized Tear Film & Ocular Surface Society Dry Eye Workshop II (TFOS DEWS II) criteria, a Bayesian model-based analysis estimated a global prevalence of approximately 29.5% [9]. Studies show a higher prevalence in Asia, around 20.1% [10], 13.7–21.6% in Europe [11–15], and 3.9–14.5% in North America [16–18]. In Latin America, prevalence ranges from approximately 12.8% in Brazil to 41% in Mexico [19–21]. Moreover, population-based studies in São Paulo found an overall prevalence of 24.4%, with severe symptoms in 16.07% of women and 8.48% of men [22]. Published data from Africa report a prevalence of 32.5%, although available studies remain scarce, indicating publication bias and the need for future regional studies [23].

Higher prevalence is consistently reported in women and older adults, with increased rates after the age of 40 in both sexes, and above 50 years of age in women [1, 8, 24]. Other significant risk factors include exposure to air pollution, prolonged digital screen use, contact lens wear, meibomian gland dysfunction (MGD), autoimmune disease, poor sleep and nutritional habits, frequent use of cosmetics, and the use of systemic medications [1, 7, 8]. Despite limited data on individuals under 40 years of age, the available evidence highlights the impact of DED and the importance of early diagnosis and targeted management, particularly in high-risk populations [25]. In order to illustrate how prevalence estimates vary according to population characteristics and diagnostic methodology, Table 1 summarizes epidemiological data from representative studies, adapted from the Tear Film & Ocular Surface Society Dry Eye Workshop III (TFOS DEWS III) Digest and other key sources.

Table 1.

Reported prevalence of dry eye disease (DED) according to diagnostic definitions, arranged in decreasing order of estimated prevalence

Diagnostic criteria	Brief description	Estimated prevalence	Key references
MGD (any severity)	Any degree of meibomian gland obstruction or dysfunction, regardless of symptom severity	0.0–66.3%	[1, 20, 26–30]
Signs and symptoms of DED	Requires both subjective symptoms and at least one clinical sign	4.7–62.9%	[1, 23, 27, 28, 31–35]
TFOS DEWS II criteria	Standardized diagnosis combining symptoms and objective measures	5.4–44.2%	[1, 8, 26, 31, 36, 37]
Symptomatic DED	Diagnosis based solely on patient-reported symptoms	7.3–31.6%	[1, 15, 24, 31–35, 37–44]
Women’s Health Study criteria	Prevalence based on self-reported symptoms using validated questionnaires and/or a diagnosis of DED by a practitioner	2.7–30.1%	[1, 13, 16–18, 24, 26, 31, 38–40, 45]
Clinically significant MGD	Symptomatic MGD with clinical evidence of ocular surface disease	1.8–23.3%	[1, 8, 28, 29]
Prior clinical diagnosis of DED	Clinician-confirmed diagnosis documented in the medical record	1.0–15.3%	[1, 24, 37, 39, 42, 46, 47]
Claims data	Diagnosis inferred from insurance or healthcare database coding (International Classification of Diseases)	2.8–8.5%	[1, 48]

MGD meibomian gland dysfunction, DED dry eye disease, TFOS DEWS II Tear Film & Ocular Surface Society Dry Eye Workshop II

Environmental Conditions

Climate change and increasing urbanization have substantially altered atmospheric dynamics, influencing the distribution and concentration of airborne particles, allergens, and pollutants. Given the ocular surface’s direct and continuous exposure to external conditions, it is particularly vulnerable to various stressors. Environmental conditions, such as temperature (°C), humidity (%), ultraviolet (UV) radiation, wind speed (m/s), and altitude (m), as well as exposure to airborne pollutants, can disrupt protective ocular surface mechanisms and destabilize the tear film [2, 49]. In addition to classical pollutants such as particulate matter (PM_2.5 and PM₁₀), nitrogen dioxide (NO₂), sulfur dioxide (SO₂), ozone (O₃), and carbon monoxide (CO), chronic exposure to solvents and cleaning agents can exacerbate tear film instability and ocular inflammation. Resulting changes include altered lipid layer thickness, increased osmolarity, oxidative stress, epithelial barrier dysfunction, and inflammatory pathway activation involving interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and matrix metalloproteinase 9 (MMP-9) [4–6]. Recent findings also implicate neurosensory alterations and MGD at the molecular level [50]. Occupational exposures, especially among healthcare workers, laboratory staff, and industrial employees, represent emerging high-risk scenarios requiring proactive counseling [1, 5, 51].

Although multidisciplinary efforts have advanced our understanding of environmental influences on ocular surface health, significant knowledge gaps remain, particularly regarding the long-term effects of chronic low-level exposures and the cumulative impact of multiple stressors acting simultaneously [2, 52].

Methods

The present review focuses on the impact of climate change and pollution on DED. For didactic purposes, the environmental exposures were grouped into three primary categories: (1) climate-related factors; (2) outdoor factors and pollutants; and (3) indoor factors and pollutants. A targeted search of peer-reviewed literature was conducted using PubMed and Scopus for English-language studies published from May 2000 to November 2025, using exemplar terms such as “dry eye” AND “air pollution,” “climate,” “indoor air quality,” and “environmental exposures.” We prioritized large epidemiologic studies, meta-analyses, recent clinical guidelines, previous reviews, and original studies evaluating human exposure to environmental conditions and pollutants in relation to DED. The selected studies were analyzed with attention to diagnostic criteria, study design heterogeneity, and methods of environmental exposure assessment. No formal risk-of-bias assessment or PRISMA [Preferred Reporting Items for Systematic reviews and Meta-Analyses] flow diagram was performed. Additionally, due to methodological diversity and regional variability across studies, definitive causal relationships could not be established. Findings were synthesized qualitatively, emphasizing mechanistic plausibility, epidemiological trends, gaps in knowledge, and clinically meaningful associations. This approach reflects the narrative, non-systematic nature of the review and the current lack of standardized methodology for evaluating environmentally associated DED. The present article is based on previously conducted studies and does not contain any new research involving human participants or animals performed by any of the authors.

Climate-Related Factors

Climate-related factors have received increasing attention for their influence on ocular health, particularly concerning DED. As climate dynamics evolve globally and meteorological data become more accessible, the relationship between the ocular surface homeostasis and environmental conditions is becoming clearer. Local variations in temperature, humidity, wind speed, dew point, altitude, and UV radiation may alter ocular surface mechanisms and contribute to the pathogenesis or aggravation of DED, along with other ocular surface conditions [1, 2]. These variables often interact with one another and are influenced by geographic, seasonal, and urban factors, which makes it difficult to isolate their individual effects. However, studies have attempted to measure the cumulative impact of these conditions and document them over time in both population-based and experimental settings [2, 53, 54]. Nevertheless, quantitative estimates remain limited, restricting direct comparisons across regions. Figure 1 displays climate factors, possible mechanisms, clinical signs/symptoms, and management for related DED.

Fig. 1.

Climate factors and dry eye disease. DED dry eye disease, MGD meibomian gland dysfunction, UV radiation ultraviolet radiation. Created in BioRender. Alves (2025) https://BioRender.com/ef5f7i5

Temperature fluctuations have been shown to affect multiple aspects of tear film and ocular surface stability [2, 5, 55]. Low ambient temperatures (< 10–15 °C) can increase tear evaporation rates, decrease lipid layer thickness, reduce overall ocular surface temperature, and solidify the meibum, transiently narrowing meibomian gland orifices, which can impair lipid secretion and further promote tear film instability and evaporation, contributing to dryness symptoms [56–60]. Conversely, elevated ocular surface temperatures (> 35–40 °C), potentially associated with increased inflammatory blood flow, and high ambient temperatures, particularly those exceeding 40 °C, may disrupt lipid properties and destabilize the tear film [37, 55, 60–62]. Studies from South Korea and other populations have demonstrated positive correlations between higher ambient temperatures and DED prevalence [37, 60]. To further explore these associations, controlled environment chamber studies have also shown that even slight adjustments in indoor temperature can influence tear breakup time and symptom severity [1, 10, 63]. These findings suggest that both indoor and outdoor thermal environments may significantly influence patient-reported experiences and objective signs of DED.

Relative humidity (RH) is another key determinant of ocular surface homeostasis and health. Low RH (< 30–40%) has been consistently associated with increased tear evaporation, ocular surface irritation, and aggravation of clinical signs in individuals with DED [1, 2, 63]. When exposed to desiccating environments, patients presented measurable reductions in tear breakup time, lipid layer stability, and overall tear production [61, 64]. On the other hand, excessively high RH conditions (> 60–70%) may induce microbial growth, contributing to meibomian gland dysfunction and infectious ocular disease, highlighting the importance of optimal levels of ambient humidity in DED management [50, 63, 65].

A wide range of other environmental factors can also contribute to the pathophysiology of DED, with varying degrees of supporting evidence, including wind speed, dew point, altitude, and UV radiation [37, 56, 57, 66]. Increased wind velocities (> 3–5 m/s) have been associated with higher tear evaporation rates, with outdoor workers exposed to high-wind conditions presenting with greater incidence of corneal injury and dry eye symptoms [66]. Although less studied, dew point—the measure of water vapor content in the air—has been positively linked to enhanced tear breakup time, which suggests a potential protective role [54]. Moreover, high-altitude environments tend to combine multiple stressors, including cold temperatures, UV radiation, and reduced atmospheric oxygen, which may exacerbate symptoms, especially when pre-existing ocular surface vulnerabilities are present [67–70]. UV exposure from natural or artificial sources can induce oxidative stress and corneal epithelium damage [4, 71], and population-based studies suggest that prolonged unprotected sun exposure may increase the risk of DED [36, 72]. These findings reinforce the importance of protective eyewear and environmental exposure awareness, particularly in susceptible individuals.

Outdoor Factors and Urban Pollution

Airborne pollutants represent a major environmental factor influencing the ocular surface, particularly in highly urbanized and industrialized areas [2]. These substances originate from various sources, both natural and human-made, including vehicle emissions, industrial activities, fossil fuel combustion, agriculture, and natural phenomena like wildfires and dust storms [49]. Common air pollutants include PM_2.5 and PM₁₀, NO₂, O₃, SO₂, and CO [2, 49, 73, 74]. A wide range of negative health effects has been associated with exposure to these substances, such as cardiovascular, respiratory, and ocular surface impairments [75]. Due to their direct exposure to the atmosphere, ocular external structures are constantly interacting with airborne pollutants, which can disturb tear film stability, trigger inflammation and oxidative stress, and disrupt ocular surface homeostasis [74, 76–78]. Despite these known associations, it is important to note that most studies are observational, so causality cannot be firmly established. Figure 2 displays outdoor factors and pollutants, proposed mechanisms, clinical signs/symptoms, and management strategies for DED associated with outdoor exposure.

Fig. 2.

Outdoor exposure and dry eye disease. DED dry eye disease, MGD meibomian gland dysfunction. Created in BioRender. Alves (2025) https://BioRender.com/ef5f7i5

Epidemiological studies from different geographic regions have shown robust evidence linking airborne pollutants to increased prevalence of DED. A study conducted in South Korea identified a positive correlation between elevated levels of O₃ and NO₂ and dry eye symptoms and diagnosis, regardless of possible demographic and health-related confounders [79, 80]. Similar findings were observed in population-based studies from the Netherlands and Argentina, especially in urban and industrial areas where pollutant rates exceeded World Health Organization (WHO) guidelines, such as PM_2.5 > 12 µg/m³ or NO₂ > µg/m³ [11, 78, 81]. Among the most common pollutants, exposure to NO₂ appears to have a more consistent relationship with ocular surface pathologies than PM_2.5 and PM₁₀, which can be explained by its enhanced capability to penetrate and interact with mucosal tissues [77, 82]. Reported manifestations include elevated tear film instability, diminished tear production, alterations in mucin expression, and a higher prevalence of MGD [11, 77–79, 81–85].

Volcanic ash represents another natural source of environmental airborne exposure with overall health and ocular consequences, especially since approximately 9% of the global population lives within proximity to potentially active volcanoes [86–90]. Volcanic ash is mostly formed by fine particulate matter and toxic gases, such as SO₂, which together have the ability to trigger acute inflammatory responses, especially in vulnerable individuals [86]. While serious and long-term complications tend to be rare, some of the most common short-term symptoms include foreign body sensation, irritation, tearing, and conjunctival hyperemia [86, 90]. Series of population-based observational studies conducted in different eruption sites have described a wide variety of symptoms, particularly in individuals with pre-existing dry eye or history of contact lens use [86–90].

Coal and dust exposure represent additional environmental stressors that can affect the ocular surface. Studies conducted in China and Nigeria showed evidence that coal miners and workers who are regularly exposed to airborne dust exhibit reduced levels of tear secretion and shorter tear breakup times relative to control populations [91, 92]. Asian dust particles, characterized by aluminosilicates and surface-bound nitrates that originate primarily from regions near the Gobi and Taklamakan deserts, have also been linked to increased conjunctival inflammation and ocular discomfort [93]. Other studies reported similar symptoms among people exposed to coal smoke and urban pollutants, further reinforcing the relationship between particulate exposure and DED [91–93].

Tobacco smoke is another airborne contaminant with established effects on the ocular surface. It contains a complex mixture of over 6000 chemical constituents, including particulate matter, volatile organic compounds, NO₂, CO, and other toxic gases. Exposure to cigarette smoke, whether active or passive, has been linked to lipid layer disruption, tear film instability, shortened tear breakup time, increased oxidative stress, and disruption of autophagy processes [94–97]. Furthermore, alterations in mucin production and a reduction in goblet cell density help explain the shortened tear breakup time commonly observed in smokers [98]. These mechanisms contribute to ocular surface inflammation and epithelial damage, particularly with chronic exposure [99]. Interestingly, although clinical studies consistently document adverse ocular surface effects, large epidemiological cohorts and a systematic review found no clear association between current smoking and the presence of DED [11, 100]. This suggests that tobacco smoke may exacerbate symptoms and ocular surface signs rather than serve as a primary causal factor, which remains relevant in clinical practice given the prevalence of passive exposure in urban environments.

Additionally, certain chemical contaminants and heavy metals may contribute to DED. A population-based study conducted in South Korea showed evidence that elevated blood mercury levels could be associated with dry eye symptoms [101]. An increased prevalence of Sjögren’s syndrome was also described in regional studies conducted in Taiwan, especially in areas with high soil chromium concentrations, although no similar and significant associations could be observed for lead, copper, or arsenic [102, 103]. These findings suggest a potential role of environmental toxicants in immune-mediated ocular surface disorders. However, precise biological pathways remain to be fully elucidated, and further research is needed. Table 2 displays the most common air pollutants and their effects on the ocular surface.

Table 2.

Correlation among pollutants and effects on the ocular surface

Air pollutants	Emission source	Effects on ocular surface	Key references
Particulate matter (PM2.5/PM10)	Vehicle emissions, industrial processes, wildfires	Increased tear film instability, oxidative stress, inflammation, dry eye symptoms	[2, 56, 73, 74, 76, 78, 104, 105]
Ozone (O3)	Vehicle emissions, industrial processes	Oxidative stress, inflammation, exacerbation of dry eye symptoms	[2, 73, 74, 79, 80]
Nitrogen dioxide (NO2)	Vehicle emissions, industrial processes	Inflammation, oxidative stress, reduced tear production	[2, 73, 74, 79, 80]
Sulfur dioxide (SO2)	Fossil fuel combustion, industrial processes	Conjunctival irritation, dry eye symptoms, increased inflammation	[2, 56, 106, 107]
Carbon monoxide (CO)	Vehicle emissions, industrial processes	Increased oxidative stress, irritation of ocular surface	[2, 73]
Volatile organic compounds (VOCs)	Industrial processes, paints, cleaning agents	Tear film instability, irritation, exacerbation of inflammation	[2, 56, 73]
Tobacco smoke	Active and passive exposure	Tear film instability, increased evaporation, oxidative stress, mucin alteration, goblet cell loss, inflammation	[2, 94, 95, 97–100, 108]
Other toxic gases	Vehicle emissions, industrial processes	Corneal damage, inflammation, irritation of the ocular surface	[2, 56]

Note: Because duration of exposure (acute vs. chronic) is not uniformly reported in all studies, pollutants were not further categorized by exposure type in order to avoid overinterpretation

Indoor Factors and Pollutants

Indoor air quality is another important determinant of DED, particularly in the context of sick building syndrome (SBS) [109]. The condition describes various nonspecific symptoms, including ocular irritation, dry throat, headache, and fatigue sensation, that usually resolve upon leaving a particular indoor environment. A number of factors can contribute to SBS, such as poor ventilation, chemical emissions from construction materials, microbial contamination, mold, dampness, and airborne particulate matter [2, 109–113]. Clinical and cross-sectional studies have shown that inadequate humidity contributes to ocular symptoms, with higher colony-forming unit (CFU) counts reported in older, poorly maintained buildings [114, 115]. Epidemiological surveys from North America, Europe, and Asia have reported high rates of ocular surface-related symptoms among office workers, particularly in buildings with air conditioning and restricted airflow [74, 111, 113]. Figure 3 illustrates indoor environmental factors, proposed mechanisms, clinical signs and symptoms, and management approaches for DED associated with indoor exposure.

Fig. 3.

Indoor exposure and dry eye disease. DED dry eye disease, MGD meibomian gland dysfunction. Created in BioRender. Alves (2025) https://BioRender.com/ef5f7i5

Among the most common complaints are dry eye sensation and eye irritation, with around 20–40% of individuals reporting symptoms consistent with SBS, as shown in cross-sectional studies [112, 116–119]. Objective tests and measurements in affected populations have shown reduced tear film stability, altered lipid layer thickness, and increased conjunctival staining [2, 111]. The shared pathophysiological features between SBS and DED suggest that individuals in environments with poor ventilation may be at increased risk for ocular surface disturbances, particularly when other environmental or behavioral risk factors are also present [2, 109, 113].

Sick house syndrome (SHS), a related condition occurring in residential environments, shares many similar characteristics with SBS. Studies have shown that residents of poorly ventilated or contaminated homes tend to report high rates of mucosal and ocular symptoms [110]. These findings also highlight the importance of monitoring and improving indoor environments as a means to prevent or reduce DED symptoms in susceptible populations.

Although prolonged digital screen use is traditionally addressed mainly as a lifestyle-related factor, it often overlaps with indoor environmental exposures and has become a key contributor to DED in modern society [2, 120]. Extended screen time often leads to reduced blink rate and incomplete blinking, accelerating tear evaporation and destabilizing the tear film, both mechanisms strongly associated with the onset of DED and symptom exacerbation [120–125]. These effects are amplified in climate-controlled or polluted indoor environments, where low humidity levels, particulate matter, and chemical irritants further compromise ocular surface homeostasis [2, 7, 120]. Patients frequently report worsened dryness, foreign body sensation, and fluctuating vision after long hours of digital device use, while objective findings demonstrate reduced tear breakup time and increased ocular surface staining [120, 123]. Given the central role of digital screens and technology in contemporary society, preventive measures are necessary to reduce symptom severity and protect the ocular surface. Recommended initial strategies include conscious blinking, regular breaks from screen activity, adequate hydration, optimization of indoor humidity between 40% and 50%, ergonomic workstation adjustments, and the use of lubricating eye drops to support tear film stability [50].

Practical Recommendations to Manage DED Associated with Environmental Factors

Managing patients at higher risk of DED requires a proactive and individualized approach that considers environmental, systemic, and lifestyle factors. Overall, several environmental conditions, including low humidity, high temperatures, ultraviolet radiation, outdoor pollutants, and poor indoor air quality, have been identified over the years as relevant mediators in the development and exacerbation of DED [2, 7]. These stressors can often contribute to the ongoing ocular surface inflammation and damage by inducing oxidative stress and tear film instability, disrupting the local microbiome, and causing neurosensory dysfunction [1, 2]. Because these alterations are often underdiagnosed in routine clinical practice, identifying environmental triggers is essential for effective patient management. Table 3 provides practical recommendations for eye care professionals to manage patients at higher risk of environmentally related DED.

Table 3.

Practical recommendations for managing patients at risk of dry eye disease (DED) related to environmental factors and pollution

Recommendation	Management	Clinical purpose
Assess environmental risk factors	Evaluate occupational exposure	Identify external triggers and guide environmental control
	Assess outdoor pollution levels
	Identify air-conditioning or low-humidity environments
	Screen for prolonged digital device use
	Assess exposure to tobacco smoke
Assess intrinsic factors	Autoimmune diseases (e.g., Sjögren syndrome)	Enable individualized treatment based on patient susceptibility
	Systemic medications (e.g., antihistamines, antidepressants)
	Hormonal status (e.g., menopause, HRT, thyroid disease, diabetes)
Patient education	Educate on environmental influences	Empower patients for behavior change and proactive self-care
	Train symptom recognition and self-monitoring
	Reinforce treatment adherence
Lifestyle modifications	Increase indoor humidity and improve ventilation	Minimize modifiable risk factors and enhance protective habits
	Use air purifiers and humidifiers
	Take regular screen breaks
	Maintain hydration
	Adopt omega-3-rich diet
	Avoid smoke exposure
	Use protective eyewear or moisture chamber goggles
	Practice safe cosmetic use and hygiene
Artificial tears and lubricating agents	Preservative-free lubricants and gels	Alleviate symptoms and improve tear film stability
MGD-targeted management	Lid hygiene	Restore meibomian gland function and lipid layer integrity
	Warm compresses
	Lid massage
	Lipid-containing eye drops
	Topical and systemic treatment options
	Consider treatment of demodex when indicated
In-office device-based interventions	Thermal pulsation	Improve meibomian gland function, enhance lipid layer stability, and reduce inflammatory burden in refractory DED
	Pulsed light-based therapies
	QMR electrotherapy
Anti-inflammatory therapy (for persistent or severe cases)	Topical corticosteroids (short-term)	Control ocular surface inflammation and prevent progression
	Immunomodulators (e.g., cyclosporine A, lifitegrast)

DED dry eye disease, MGD meibomian gland dysfunction, HRT hormone replacement therapy, QMR quantum molecular resonance

Ophthalmologists must be vigilant and start by assessing environmental risk factors during the initial evaluation. This includes assessing occupational, geographic, and behavioral exposures, particularly in outdoor workers, residents of highly urbanized areas, and individuals spending extended hours in air-conditioned or polluted spaces [2]. Based on this assessment, a series of practical measures can be advised, such as increasing indoor humidity, improving ventilation, using air purifiers, and taking regular breaks from screen activity [50]. For patients with coexisting ocular conditions, such as DED and MGD, protective eyewear or moisture-chamber goggles and thermally induced humidifying devices may be considered as adjunctive options to help reduce the impact of external irritants and prevent symptom exacerbation [50, 126]. These devices create a localized warm and humid microenvironment that can enhance tear film retention and promote meibum liquefaction, which may benefit patients with evaporative DED or obstructive MGD [50, 127–130]. However, clinicians should also be aware of potential limitations, as insufficient cleaning or prolonged device use may increase microbial load, particularly on the internal surfaces of these devices, underscoring the importance of appropriate hygiene protocols and patient education [131]. Additionally, while these devices may improve ocular surface hydration, eye care professionals should also consider cost, patient adherence, and the environmental impact of disposable plastic components when recommending them in clinical practice.

Early identification of environmental mediators, even in asymptomatic individuals, allows for the implementation of preventive strategies that may delay disease onset or reduce symptom severity. Patient education plays a central role and may include scheduled screen breaks, regular blinking, adequate hydration, and dietary modifications, in addition to avoiding known environmental triggers when possible [50]. Regarding nutritional supplements, omega-3 fatty acids may be considered as an adjunctive option, although robust evidence supporting clinical benefit remains limited [132, 133]. Recommending cessation of smoking or vaping may contribute as part of a holistic strategy to support ocular and systemic health, even though a definitive link between all forms of tobacco exposure and DED has not yet been firmly established [95–99, 108]. Moreover, physical protective measures and air purification systems can complement these interventions by minimizing ocular surface exposure to irritants [50, 126]. In parallel, clinicians should also monitor systemic comorbidities, particularly autoimmune diseases such as Sjögren’s syndrome, in order to ensure individualized and comprehensive patient care [50].

Given the multifactorial nature of DED, targeted therapies are crucial for effective management. Lubricating eye drops remain the first line of treatment for symptom relief, particularly in patients exposed to environmental factors, such as pollution and low-humidity conditions [50]. For more severe or persistent cases, anti-inflammatory and immunomodulatory treatments, including corticosteroids and cyclosporine A, can be prescribed to reduce ocular surface inflammation [3, 50]. When MGD is a significant contributor, eye care professionals should also prioritize lid hygiene and warm compresses, and consider the use of lipid-containing artificial tears [50, 126]. In recent years, many other therapies, such as thermopulsation, intense pulsed light procedures, and quantum molecular resonance (QMR) electrotherapy have also been studied as an adjunctive treatment for aqueous-deficient, evaporative, and mixed-type DED. Published clinical trials and a systematic review have reported improvements in symptoms, tear film stability, and meibomian gland function, with a favorable safety profile [50, 134, 135]. While promising, long-term data on QMR are still limited, and additional studies are needed to clarify durability of outcomes and ideal patient selection. Incorporating environmental awareness into routine care not only improves patient outcomes and long-term DED control, but also contributes to public health initiatives and understanding regarding the impact of climate change and pollution on ocular health.

Conclusion

Dry eye disease (DED) represents one of the most prevalent and multifactorial ocular surface disorders worldwide, and its relationship with environmental exposures has become increasingly relevant in recent years. In this non-systematic narrative review, we sought to synthesize current knowledge on how climatic variables, air pollution, and indoor environmental factors influence the onset and progression of DED, with particular emphasis on practical approaches for prevention and management. Despite considerable progress in understanding the impact of these exposures, important gaps remain regarding their cumulative and long-term effects, as well as the most effective strategies to mitigate them in clinical practice.

It is also important to acknowledge that the current body of evidence linking environmental factors to DED is largely based on cross-sectional and observational studies. Such designs limit the ability to establish causality, while heterogeneity in diagnostic criteria, exposure assessment methods, and different study populations limit direct comparisons across regions. High-quality longitudinal and interventional studies remain scarce, highlighting the need for further research to clarify the strength and direction of the proposed associations.

Studying environmentally associated DED remains methodologically challenging. Exposure estimates frequently rely on air-quality monitoring situations, remote-sensing data, or statistical models rather than individual-level measurements. Moreover, environmental factors rarely act in isolation, and significant knowledge gaps remain, particularly regarding the long-term effects of chronic low-level exposures and the cumulative impact of multiple stressors. In addition, many published studies do not clearly distinguish between acute and chronic exposure effects, underscoring the need for standardized reporting and longitudinal designs capable of determining dose–response relationships and temporal causality.

Following the publication of the TFOS Lifestyle Report, there has been a growing interest in understanding the complex and multifactorial relationship between air pollution and ocular surface impairment [52, 105, 136–138]. Recent studies have expanded on earlier epidemiological findings by incorporating more detailed exposure assessments [105, 137, 138]. Moreover, emerging evidence also suggests that the ocular surface may serve as a sensitive biomarker for broader environmental health risks, prompting efforts to integrate ocular data into public health surveillance systems [138].

Despite these limitations, and with promising directions for future research, environmental exposure clearly represents an important contributor to the global burden of DED. The ocular surface is uniquely vulnerable to external stressors, and identifying these risk factors provides an opportunity for earlier diagnosis, preventive measures, and personalized management. By combining targeted therapies with preventive strategies and patient education, eye care professionals can offer comprehensive care that addresses the complexities of DED in high-risk populations.

Author Contributions

Bruna Duarte contributed to study conception and design, literature review, data interpretation, table preparation, and drafting of the manuscript. Eduardo Xavier contributed to data interpretation, table preparation, critical revision of the manuscript, and approval of the final version. Helga Caputo Nunes contributed to data interpretation, figure preparation, critical revision of the manuscript, and approval of the final version. Caroline Nascimento Barquilha contributed to data interpretation, figure preparation, critical revision of the manuscript, and approval of the final version. Mariane Aparecida Risso contributed to data interpretation, figure preparation, critical revision of the manuscript, and approval of the final version. Mônica Alves contributed to study conception and design, table and figure preparation, critical revision of the manuscript, and approval of the final version. All authors reviewed and approved the final manuscript and agree to be accountable for its contents.

Funding

No funding or sponsorship was received for this study or publication of this article.

Data Availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Declarations

Conflict of Interest

Bruna Duarte has nothing to disclose. Eduardo Xavier has nothing to disclose. Helga Caputo Nunes has nothing to disclose. Caroline Nascimento Barquilha has nothing to disclose. Mariane Aparecida Risso has nothing to disclose. Mônica Alves has nothing to disclose.

Ethical Approval

This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors.