Risk Factors for Lung Cancer
The strongest determinant of lung cancer in smokers is duration of smoking. Risk also increases with the number of cigarettes smoked. Cessation of smoking for 10 years reduces risk but never to control levels. However, the risk of ex-smokers for lung cancer remains elevated for years after cessation, compared to the risk of never smokers.
Smoking increases the risk of all histologic types of lung cancer: squamous , small cell, adeno (including bronchiolar-alveolar), and large cell carcinoma. It causes lung cancer in both men and women. Adenocarcinoma has replaced squamous cell carcinoma as the most common type of lung cancer caused by smoking in the United States and elsewhere.
Occupational/ Environmental exposure
Exposure to Radon (a radioactive gas produced from the decay of Radium or Uranium) has been reported to increase the risk of developing lung cancer.
Occupational exposure to Asbestos has been reported to increase the incidence of lung cancer in workers in mines, textile and other mills, and shipyards.
Similarly, higher incidence of lung cancer has been observed in people with occupational/environmental exposure to chemicals like arsenic, beryllium, cadmium, silica, chloromethyl ethers, hexavalent chromium, mustard gas, nickel, coal products, and polycyclic aromatic hydrocarbons.
People living in an area with a high level of air pollution are considered to be at an increased risk of developing lung cancer.
Gender and Ethnicity
Women smokers are more likely than men to develop adenocarcinoma of the lung, and women who have never smoked are more likely to develop lung cancer than men who have never smoked. Furthermore, the 5-year survival rate for women who have lung cancer is 15.6%, while it is 12.4% for men. Women survive longer after surgical resection of early-stage lung cancer as well as after treatment of metastatic disease; female sex has been associated with longer survival in SCLC as well.
Hormonal, genetic, and metabolic differences between the sexes are believed to account for these clinical differences. Indeed, estrogens were found to be involved in lung carcinogenesis, either by acting as estrogen receptor ligands and activating cellular proliferation pathways, or by metabolic activation to reactive intermediates that can produce DNA adducts and cause oxidative damage.
The lung cancer incidence rates vary by nearly five fold in men and over 10-fold in women across the WHO regions, reflecting differences in historical patterns of smoking. The highest rates are among men in Eastern Europe, Southern Europe, and North America, whereas the lowest rates are observed in Central America and South Central Asia.
Lung cancer incidence and death rates among men have begun to fall in North America, Northern Europe, Australia, and New Zealand but continue to rise in many other countries.
Lung cancer patterns in women differ from those in men because the uptake of widespread cigarette smoking among women lagged behind that in men by approximately 25 years, even in industrialized countries.
The prevalence of cigarette smoking is still low among women in much of Asia and Africa, but in Europe and parts of South America, teenage girls are now smoking more than teenage boys.
The highest lung cancer rates among women are currently in North America, Northern Europe (especially Scandinavia), and Australia and New Zealand.
Factors other than cigarette smoking contribute to the relatively high background rate of lung cancer among women in parts of China.
The lung cancer incidence rate per 100,000 for 2008 among Chinese women (21.3/100,000) is higher than that among women in Germany (16.4) and France (14.7), despite their lower prevalence of smoking.
Factors thought to contribute to the high lung cancer rate among Chinese women in certain regions of China include
- indoor exposure to coal smoke
- indoor emissions from burning other fuels
- exposure to fumes from frying foods at high temperatures
- secondhand smoke.
Personal or Family history
Risk of developing lung cancer increases in individuals with a personal or family history of lung cancer, especially in first-degree relatives (parents, brother, sister, or child) diagnosed with the disease at a younger age.
Some inherited genetic alterations have been reported to be associated with a high incidence of lung cancer. Individuals with inherited mutations in following genes have been reported to be at higher risk of developing lung cancer: retinoblastoma, p53 (Li-Fraumeni syndrome), gene for epidermal growth factor receptor (EGFR), etc.
Individuals with germ line mutations affecting expression of genes regulating cell cycle progression or response to DNA damage appear to have increased lung cancer risk. A threefold increase in lung cancer risk has been observed in patients with Li-Fraumeni syndrome who smoke relative to smokers without p53 germ line mutations.
Interestingly lung cancer susceptibility is influenced by genetic variation in a gene encoding for a nicotine receptor. The association of this genetic variant with lung cancer may actually be mediated through its effect on smoking behavior. Individuals with this variant generally smoked more cigarettes per day and showed more nicotine dependence than people without the variant.
This finding suggests that the gene variant actually influences an individual’s exposure to an environmental agent (tobacco smoke), and it is this higher exposure that is then responsible for the individual’s increased risk of cancer.
Exposure to radiation
Individuals with a history of radiation treatment (for other cancer) or exposure to ionizing radiation to the chest (for example, during an x-ray or computed tomography scan) are considered to be at increased risk of developing lung cancer, especially if they smoke.
The presence of underlying pulmonary conditions like chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis may also increase the risk of lung cancer.