Researchers believe that repeated exposure to carcinogens, particularly cigarette smoke, leads to dysplasia of lung epithelium. If the exposure persists, it can cause genetic mutations and affect protein synthesis. As a result, there is a disruption in the cell cycle, which promotes carcinogenesis. The most common genetic mutations responsible for small cell lung cancer development are MYC, BCL2, and p53. 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 a risk of developing lung cancer. In the United States, active smoking is the principal cause of lung cancer, accounting for an estimated 90% of lung cancer cases, whereas occupational exposures to carcinogens account for approximately 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. The risk of cancer declines after smoking cessation, 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. Other forms of tobacco smoke, including secondhand smoke, are also associated with significant increases in the 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. Exposure to metals such as chromium, nickel, and arsenic and exposure to polycyclic aromatic hydrocarbons are also correlated with an augmented risk of lung-cancer development.
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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