Fine particulate matter (PM2.5) is a Group 1 carcinogen that can penetrate into peripheral blood and critically affect all organs and tissues of the human body. It is estimated to cause 5 to 8 million deaths worldwide each year. Major causes of death linked to PM2.5 exposure include lung cancer, cardiovascular disease, and chronic pulmonary disease, with particularly high mortality among the elderly and people with chronic conditions. Therefore, in rapidly aging societies, research to elucidate how PM2.5 affects vital life‑sustaining mechanisms is an urgent and important task.

In this context, a research team at Jeonbuk National University (JBNU) has used animal models to newly elucidate the pathological mechanisms linking PM2.5 exposure to the high incidence of lung cancer in old age, drawing attention from the international academic community.

JBNU Professor Seong-Ho Guk (Graduate School, Department of Bioactive Material Sciences) and Professor Jeong-Chae Lee (Department of Dentistry) jointly announced on the 27th that their co-research team demonstrated specific mechanisms by which PM2.5 exposure induces shortened lifespan and lung cancer development using aged mice and prion protein (PrPC)-deficient animal models.

According to the research team, compared with young mice, aged mice showed decreased expression levels of PrPC and Sirt1 proteins in the lung, whereas expression of HIF-1α was increased. The team confirmed that this pattern is closely associated with the observed sharp rise in mortality and increased susceptibility to lung cancer after PM2.5 exposure.

In particular, they clearly demonstrated that PM2.5 exposure in PrPC-deficient mice causes dysregulation of the Sirt1–p53–HIF-1α signaling pathway, which in turn sequentially promotes emphysema, hypoxia, angiogenesis, and tumor formation.

They also found that PM2.5 rich in heavy metals and polycyclic aromatic hydrocarbons (PAHs) triggers lung cancer far more aggressively than PM2.5 composed mainly of ions and organic acids. This suggests that specific chemical components of particulate matter are key determinants of lung cancer incidence and progression.

This study is highly valued for demonstrating the causal relationships among PM2.5 exposure in old age, prion protein levels, and lung cancer development through an extensive four-year longitudinal observation. The findings were published in the latest issue of the leading environmental science journal Environmental Science & Technology (IF=11.3). (Paper title: PrPC glycoprotein modulates atmospherically relevant artificial particulate matter-induced development of lung cancer in mice)

Professors Seong-Ho Guk and Jeong-Chae Lee emphasized, "Considering that Korea ranks first among OECD member countries in PM2.5 pollution levels, the implications of this study are considerable," and added, "The occurrence and progression of lung cancer caused by PM2.5 are strongly influenced by age and the particulate matter's chemical composition; therefore, special care for the elderly is essential."

They added, "We expect that reduced PrPC expression due to aging and genetic variation will serve as a biomarker for susceptibility to air pollution–related lung disease and lung cancer, and will play a central role in disease prevention and therapeutic development."

The study involved JBNU's Dr. QT Jang (Department of Bioactive Material Sciences) and Dr. Hyun-Jeong Shim (Bioactive Material Sciences Research Institute) as co-first authors, and was conducted through the Mid‑Career Researcher Support Program of the Ministry of Science and ICT.