<p>Human-driven environmental change continues to reshape global patterns of disease, as seen in past pollution-related respiratory crises. Microplastics, persistent synthetic polymer particles, have now emerged as a widespread airborne contaminant with growing relevance for lung health. Continuous inhalation exposure, particularly in indoor environments rich in synthetic fibers, raises concern about their contribution to respiratory disease. Epidemiological and experimental studies increasingly link microplastic exposure to lung cancer, asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis, yet the underlying mechanisms remain poorly defined. This review integrates current evidence on how particle properties influence biological outcomes and outlines how different polymer types, sizes, and aging states affect lung cells through inflammation, oxidative stress, ferroptosis, epithelial–mesenchymal transition, and epigenetic change. Together, these findings suggest that microplastics may act as environmental modifiers that exacerbate disease progression. Recognizing their complex and persistent nature highlights the need for standardized exposure metrics, mechanistic research at realistic doses, and coordinated scientific and regulatory action.</p>