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Lung cancer remains a leading global health challenge, with an estimated 1,572,045 new cases among men and 908,630
among women in 2022, and adenocarcinoma represents the largest proportion in both sexes. Although tobacco, occupational
exposure, and ambient particulate matter pollution are well-established drivers, airborne nanoplastics are increasingly
recognized as underappreciated inhalation hazards. Generated through the degradation of larger plastic materials, these
ultrafine particles can remain suspended in air, be inhaled into the distal airways, and potentially persist in lung tissues
beyond normal clearance. Experimental studies in human lung adenocarcinoma A549 cells link polystyrene nanoplastics
exposure to cytotoxicity, mitochondrial dysfunction, oxidative stress with elevated reactive oxygen species and
malondialdehyde, and pro-inflammatory cytokine release, including IL-6, IL-1β, and TNF-α, alongside disrupted cell cycle
progression, changes that may promote genomic instability. Chronic exposure to environmentally relevant concentrations
further supports the tumorpromoting potential of PFOS, enhancing lung cancer cell proliferation, migration, and invasion,
and accelerating tumor growth in orthotopic models through PERK-ATF3 activation and ATF3-driven PCK2 upregulation,
consistent with metabolic reprogramming that favors malignancy. These findings support urgent preventive action through
strengthened plastic source reduction, waste management, targeted filtration technologies, and sustained exposure and
mechanistic research to inform regulations. This article aims to highlight airborne nanoplastics as a credible, emerging
contributor to lung carcinogenesis and outline priority actions for public health and policy.