Table 2.

Take-home messages of this review article.

Non-smoking related risk factor	Lung cancer	COPD
Air pollution	Airborne PM and ozone lead to chronic respiratory inflammation and create ROS, paving the way for lung cancer PM persist in the airways as particle deposits Particles from diesel exhaust lead to radical-induced oxidative lesions Day-to-day mortality from lung cancer is associated with airborne PM readings	An increase in emergency department visits of COPD and asthma patients is observed as a consequence of increased particulate matter readings Diesel exhaust is particularly related to COPD development, reducing phagocytosis of alveolar macrophages
Oxidative stress	Ozone, via redox effects, causes chronic oxidative stress in the lungs The exposure to a combination of air pollutants (ozone and PM) leads to a synergistic increase of lung cancer risk Pulmonary antioxidant capacity, as a crucial tumor-suppressive event, is significantly impaired by ROS	ROS from ambient air pollution cause immunological changes leading to lung tissue damage Activated macrophages and neutrophils from the bloodsteam of COPD patients release ROS as well, further promoting COPD development Oxidative stress from air pollution increases the expression of proinflammatory genes, damaging the alveoli
Asbestos	Asbestos exposure is associated with an increased lung cancer, and especially, pleural mesothelioma risk Alveolar macrophages harbor inhaled asbestos fibers, and an increased amount of collagenic fibroblasts and tissue remodeling surrounding these fibers is observed Immune cell functions, and the associated anti-tumor defense mechanisms, are impaired due to chronic asbestos exposure	Chronic asbestos exposure leads to lung tissue remodeling, ultimately resulting in COPD Asbestos and other occupational lung irritants cause an increased secretion of cytokines and chemokines from immune cells, as well as growth factors responsible for lung tissue damage
Silica	The anti-tumor activity of alveolar macrophages is largely impeded by silica exposure The loss of normal pulmonary macrophage function is one of the key events leading to lung cancer upon silica dust exposure In mouse models, silica also led to a reduction in B- and T-lymphocytes, and a reduction in antigen-presentation and priming of antigen-specific T- and B-lymphocytes
Pulmonary fibrosis	Fibrotic lung conditions predispose patients to lung cancer Fibrosis leads to a chronic low-level inflammatory state Excessive connective tissue remodeling and alveolar microinjuries render the lung tissue more susceptible for malignant transformation Smoking, in addition to lung fibrosis, synergistically augments lung cancer risk
Pulmonary infectons	Pulmonary infections caused my Mycobacterium tuberculosis increase the risk for lung cancer later in life Colonization with Chlamydia pneumoniae may also increase the risk for malignant transformation
Lung microbiome	Alterations of the lung microbiome by recurrent bacterial and viral infections (e.g. in immunosuppressed patients) may facilitate malignant transformation in the lung tissue Periodontal disease and opportunistic microorganisms have been found to alter the lung microbiome, posing a possible risk factor for lung cancer as well Haemophilus influenzae, Enterobacter spp., Pneumococcus, Legionella and Moraxella genera count among the microbes that have been linked to lung carcinogenesis