The ocular surface must maintain homeostasis to withstand continuous environmental stimuli, while increased tear evaporation represents a critical initiating event in the progression of evaporative dry eye disease. The composition, distribution, and function of the tear film lipid layer determine its anti-evaporative capacity. Multiple factors, including meibomian gland dysfunction, abnormalities of the lipid layer, blinking disorders, mucin deficiency, and epithelial barrier impairment, collectively weaken the evaporative barrier, subsequently inducing hyperosmotic stress and ocular surface inflammation, activating neuro-immune pathways, and thereby establishing a self-perpetuating cycle and contributing to disease chronicity. The environmental characteristics of northwestern regions, including low humidity, limited rainfall,strong winds, frequent windblown dust, and high evaporation rates, may further exacerbate these processes. This review integrates modern ocular surface pathological mechanisms with the theory of “Northwest dryness syndrome” to summarize the pathogenesis of evaporative dry eye disease and the effects of dry environmental exposure, aiming to provide a reference for risk assessment and intervention strategies for dry eye in Northwest China.