The pathophysiology of lung cancer is complex and not fully understood. Due to advances in research, medical experts continue to gain deeper insights about the pathogenesis and risk factors associated with an increased risk of lung cancer.

Researchers hypothesize that repeated exposure to carcinogens, particularly cigarette smoke, leads to dysplasia of lung epithelium. Prolonged exposure can cause genetic mutations and affect protein synthesis. As a result, there is a disruption in the cell cycle, which promotes carcinogenesis. The genetic mutations MYC, BCL2, and p53 are the most common mutations responsible for the development of small cell lung cancer. Mutations in epidermal growth factor receptor, KRAS, and anaplastic lymphoma kinase are mutually exclusive in patients with non–small cell lung cancer.

Both exposure (environmental or occupational) to particular agents and an individual’s susceptibility to these agents are believed to contribute to the risk of developing lung cancer. In the United States, an estimated 90% of lung cancer cases are the result of active smoking, whereas occupational exposures to carcinogens account for an estimated 9% to 15% of lung cancer cases.

The development of lung cancer is directly correlated to the number of cigarettes smoked, the extent of smoking history, and the tar and nicotine content of cigarettes. Risk is greatest among current smokers and lowest among nonsmokers. After cessation of smoking, the risk of cancer declines, but the level of risk is never restored to baseline in never-smokers, and an estimated 15% to 20% of individuals who develop lung cancer have never smoked or have smoked minimally. According to the U.S. National Cancer Institute, lung cancer in never-smokers occurs more frequently in women, with projections rising in this patient population and at an earlier age compared with lung cancer in smokers. Other forms of tobacco smoke, including secondhand smoke exposure, are also associated with a considerably higher risk of lung cancer. Secondhand tobacco smoke exposure at a younger age is linked to an elevated risk of lung cancer.

Exposure to asbestos is the most common occupational risk factor for lung cancer. Studies have shown that radon exposure is associated with 10% of lung cancer cases, whereas outdoor air pollution accounts for perhaps 1% to 2% of cases. In addition, preexisting nonmalignant lung diseases, such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and tuberculosis, have all been shown to be associated with an expanded risk of lung cancer independent of smoking. Examples of other risk factors include radiation for non–lung cancer treatment, especially non-Hodgkin lymphoma and breast cancer. An increased risk of lung cancer development is also linked to exposure to other carcinogens found in some work environments, such as chromium, nickel, silica, vinyl chloride, coal products, diesel exhaust, arsenic, and polycyclic aromatic hydrocarbons.

The content contained in this article is for informational purposes only. The content is not intended to be a substitute for professional advice. Reliance on any information provided in this article is solely at your own risk.

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