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Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, with chronic inflammation playing a central role in its pathogenesis. While established risk factors such as Helicobacter pylori (Hp), diet, and lifestyle are well recognized, growing epidemiological evidence links airborne particulate matter (PM) exposure with increased GC incidence and mortality. However, the biological mechanisms underlying this association remain poorly understood. This review integrates epidemiological evidence associating elevated PM exposure with GC risk and summarizes current mechanistic knowledge regarding PM gastric translocation and retention. The influence of PM size, chemical composition, and surface reactivity on biological activity is also discussed, highlighting the stomach as a plausible yet understudied target organ. Additionally, we compiled evidence from studies published between 2010 and 2026 demonstrating the ability of PM to induce inflammatory responses through activation of NF-κB, MAPK, JAK/STAT, and COX-2 signaling pathways across diverse biological systems. Although PM-induced inflammation has been extensively characterized in respiratory and other tissues, its contribution to gastric carcinogenesis remains largely unexplored. We propose that PM exposure may exacerbate Hp-driven inflammation, promoting a persistent pro-inflammatory microenvironment conducive to tumor initiation and progression. Collectively, these findings position PM as a biologically plausible and potentially modifiable risk factor for GC.
Sánchez-Pérez et al. (Tue,) studied this question.