Molecular mechanisms of passive smoking-induced respiratory diseases

Abstract

Cigarette smoke, including second hand and third hand smokes, is a well-established risk factor for respiratory diseases, and accounts for one in five deaths in the United States annually. Passive smoking involves second hand smoke (SHS) and third hand smoke (THS) that contain the similar carcinogenic compounds, oxidants and toxicants that are present in mainstream smoke (MS) such as formaldehyde, acrolein, aromatic amines, polycyclic aromatic hydrocarbons (PAHs), and various inorganic substances. SHS particles are smaller than those in MS, enabling them to reach the distal regions of the lungs. These toxic chemicals are considerably deleterious to lungs’ health and cause serious respiratory diseases. The inhaled toxicants in SHS and THS directly damage airway epithelial cells of the lungs, leading to oxidative stress, inflammation and tissue damage, and interfere with cellular repair mechanisms leading to mucociliary dysfunction, thereby exacerbating chronic inflammatory responses. The molecular mechanisms associated with SHS exposure include DNA adduct formation, epigenetic modifications of the genes and altered signaling mechanisms leading to lung dysfunction. These changes are irrespective of age or gender, and raise significant concerns regarding long-term pathological consequences of exposure to passive smoke. Here we have reviewed the major molecular pathways that play crucial roles in manifesting the lung pathogenesis related to passive smoking.