Vision · 6 authors, 3 centres
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This review examines how environmental toxins, including air pollutants, pesticides, and cleaning products, damage the ocular surface through oxidative stress, inflammation, and cell death. It covers traditional animal testing (Draize test) and modern alternatives like in vitro and in silico models. The clinical significance is that recognizing and minimizing these exposures is crucial to prevent conditions ranging from dry eye to blindness.
**Background:** The ocular surface, comprising the cornea, conjunctiva, limbus, and tear film, is directly exposed to the external environment and vulnerable to damage from ambient pollutants, chemicals, and physical agents. This narrative review synthesizes current knowledge on how toxic external exposures—including air pollutants, pesticides, cleaning products, and climate-related factors—cause ocular surface injury. It also discusses historical and modern methods for assessing ocular toxicity, from the Draize rabbit eye test to in vitro reconstructed human cornea-like epithelium (RhCE) models and in silico quantitative structure–activity relationship (QSAR) models.
**Methods:** The authors conducted a narrative review of the literature, covering topics such as the Draize eye test, in vitro models (EpiOcular™ and SkinEthic™), in silico QSAR models, pollution effects (ozone, particulate matter, nitrogen oxides), air bag deployment injuries, pesticide exposure (herbicides, insecticides, fungicides), workplace ocular injuries (foreign objects, chemical burns), and climate change impacts (temperature, air quality, UV radiation). The review draws on epidemiological, laboratory, and clinical studies.
**Key Results:** The Draize test uses 3–6 rabbits per substance, scoring corneal opacity (80 points), conjunctival irritation (20 points), and iris inflammation (10 points). In vitro RhCE models like EpiOcular™ and SkinEthic™ use MTT or LDH assays to measure viability; a viability ≤60% indicates an irritant. QSAR models predict toxicity from chemical structure without animal testing. Air pollutants: Ozone causes conjunctival chemosis and injection; PM2.5 exposure in mice reduced tear volume and increased corneal inflammation and apoptosis; PM10 exposure correlated with increased conjunctivitis and keratitis (0.10 and 0.05 per 1,000 ER patients, respectively). Nitrogen dioxide (NO₂) exposure was linked to dry eye symptoms and meibomitis. Combined pollutants (PM10, NO₂, CO) were associated with blepharitis and age-related macular degeneration. Pesticides: Paraquat causes conjunctivalization and pannus; glyphosate leads to conjunctival irritation and corneal injury; organophosphates inhibit acetylcholinesterase and increase oxidative stress. Workplace injuries: ~2,000 U.S. workers daily require medical treatment for eye injuries; 65% from object contact, 26% from harmful substances. Chemical burns: bleaches account for >25% of ocular exposures reported to poison control centers (2000–2016). Climate change: Rising temperatures increase corneal damage, cataracts, glaucoma, and infections; UV radiation causes photokeratitis, pterygium, cataracts, and may accelerate age-related macular degeneration.
**Clinical Implications:** The ocular surface is highly susceptible to a wide range of environmental toxins. Prevention through protective eyewear (goggles, face shields) and immediate irrigation after exposure is critical. Understanding the mechanisms of toxicity—oxidative stress, inflammation, apoptosis—can guide development of protective strategies and treatments. Modern in vitro and in silico testing methods reduce reliance on animal models while providing reproducible toxicity assessments. Clinicians should be aware of occupational and environmental risk factors for ocular surface disease and counsel patients on protective measures.