Lung cancer represents a significant public health concern, with a considerable disease burden. Among the numerous environmental factors linked to the onset of lung cancer, the impact of PM2.5 is well documented. In 2013, the IARC classified air pollution as a Group 1 carcinogen, indicating a definitive relationship between the two with regard to the incidence of lung cancer. The mechanisms by which the response induced by PM2.5 exposure mediates the development of lung cancer have been described in detail in the existing literature.
While environmental factors contribute to the development of lung cancer, personal susceptibility also plays a role. The risk of developing lung cancer is increased in individuals who have previously been infected with a disease that can cause permanent damage to the lungs, such as tuberculosis. In the case of COPD, the mechanisms leading to its development are known to be shared with those that give rise to lung cancer. The mutual risk between lung cancer and COPD may be influenced by the fact that they share a major environmental risk factor, such as smoking. However, a notable elevation in lung cancer risk was also observed in a cohort comprising solely non-smokers with COPD, indicating that COPD may serve as an independent risk factor for lung cancer even after accounting for shared risk factors.
Although air pollution is a known cause of lung cancer, as previously stated, individual susceptibility may be related to the risk of developing lung cancer. A recent study utilising the UK Biobank dataset has reported that genetic factors interact with air pollution exposure in relation to lung cancer incidence. However, this study did not focus on pulmonary function. It is reasonable to hypothesise that the effects of exposure to air pollution may vary depending on individual susceptibility. Therefore, the objective of this study is to evaluate the risk of lung cancer according to the degree of lung function in a large population.
