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Lung Cancer Prevention (PDQ®)

Health Professional Version

Overview

Note: Separate PDQ summaries on Lung Cancer Screening; Small Cell Lung Cancer Treatment; Non-Small Cell Lung Cancer Treatment; and Cigarette Smoking: Health Risks and How to Quit are also available.

Who is at Risk?

Lung cancer risk is largely a function of older age combined with extensive cigarette smoking history. Lung cancer is more common in men than women and in those of lower socioeconomic status. Patterns of lung cancer according to demographic characteristics tend to be strongly correlated with historical patterns of cigarette smoking prevalence. An exception to this is the very high rate of lung cancer in African American men, a group whose very high lung cancer death rate is not explainable simply by historical smoking patterns.[1]

In nonsmokers, important lung cancer risk factors are exposure to secondhand smoke, radon exposure, and occupational exposure to lung carcinogens, such as asbestos. Cigarette smoking often interacts with these other factors. There are several examples, including radon exposure and asbestos exposure, in which the combined exposure to cigarette smoke plus another risk factor results in an increase in risk that is much greater than the sum of the risks associated with each factor alone.

Factors associated with increased risk of lung cancer

Cigarette smoking

Starting with the 1964 Surgeon General’s Report and followed by each subsequent Surgeon General’s Report that has included a review of the evidence on smoking and lung cancer, an enormous body of scientific evidence clearly documents that cigarette smoking causes lung cancer, and that cigarette smoking is the major cause of lung cancer.

Based on solid evidence, cigarette smoking causes lung cancer. The risks of lung cancer associated with cigarette smoking are dose-dependent and increase markedly according to the number of cigarettes smoked per day and the number of years smoked. On average, current smokers have approximately 20 times the risk of lung cancer compared with nonsmokers.

Magnitude of Effect: Increased risk, very large.

  • Study Design: Numerous prospective cohort and case-control studies, combined with quasi-experimental evidence showing population-level smoking prevalence predicts the population-level burden of lung cancer.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.
Exposure to secondhand smoke

Based on solid evidence, exposure to secondhand smoke is an established cause of lung cancer.

Magnitude of Effect: Increased risk, small magnitude. Compared with nonsmokers not exposed to secondhand smoke, nonsmokers exposed to secondhand smoke have approximately a 20% increased risk of lung cancer.

  • Study Design: Prospective cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.
Radon exposure

Based on solid evidence, exposure to radon increases lung cancer incidence and mortality.

Magnitude of Effect: Increased risk that follows a dose-response gradient, with small increases in risk for levels experienced in most at-risk homes to greater increases in risk for high-level exposures.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Fair.
  • Consistency: Good.
  • External Validity: Fair.
Occupational exposure to lung carcinogens

Based on solid evidence, workplace exposure to asbestos, arsenic, beryllium, cadmium, chromium, and nickel increases lung cancer incidence and mortality.

Magnitude of Effect: Increased risk, large magnitude (more than fivefold). Risks follow a dose-response gradient, with high-level exposures associated with large increases in risk. Cigarette smoking also potentiates the effect of many of these lung carcinogens so that the risks are even greater in smokers.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.
Air pollution

Based on solid evidence, exposure to outdoor air pollution, specifically small particles, increases lung cancer incidence and mortality.

Magnitude of Effect: Increased risk; compared with the lowest exposure categories, those in the highest exposure categories have approximately a 40% increased risk of lung cancer.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Factors of uncertain association with risk

Dietary factors

Based on equivocal evidence, the observed inverse associations between lung cancer and dietary factors, such as fruit and vegetable consumption, are difficult to disentangle from cigarette smoking.

Magnitude of Effect: Inverse association, moderate magnitude, but difficult to determine if true cause-effect association or due to confounding by cigarette smoking.

  • Study Design: Numerous cohort and case-control studies, and meta-analyses.
  • Internal Validity: Fair.
  • Consistency: Fair.
  • External Validity: Good.
Physical activity

Based on equivocal evidence, the observed inverse associations between lung cancer and higher levels of physical activity are difficult to disentangle from cigarette smoking.

Magnitude of Effect: Inverse association, moderate magnitude, but difficult to determine if true cause-effect association or due to confounding by cigarette smoking.

  • Study Design: Numerous cohort and case-control studies, and meta-analyses.
  • Internal Validity: Fair.
  • Consistency: Fair.
  • External Validity: Good.

Interventions Associated With Decreased Risk of Lung Cancer

Smoking avoidance

Based on solid evidence, cigarette smoking causes lung cancer and therefore, smoking avoidance results in decreased mortality from primary lung cancers.

Magnitude of Effect: Decreased risk, substantial magnitude.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Smoking cessation

Based on solid evidence, long-term sustained smoking cessation results in decreased incidence of lung cancer and of second primary lung tumors.

Magnitude of Effect: Decreased risk, moderate magnitude.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Eliminating secondhand smoke

Based on solid evidence, exposure to secondhand smoke causes lung cancer and therefore, preventing exposure to secondhand smoke results in decreased incidence and mortality from primary lung cancers.

Magnitude of Effect: Decreased risk, small magnitude.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Reducing or eliminating occupational exposure to lung carcinogens

Based on solid evidence, occupational exposures such as asbestos, arsenic, nickel, and chromium are causally associated with lung cancer. Reducing or eliminating workplace exposures to known lung carcinogens would be expected to result in a corresponding decrease in the risk of lung cancer.

Magnitude of Effect: Decreased risk, with a larger effect, the greater the reduction in exposure.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Reducing or eliminating exposure to radon

Based on solid evidence, indoor exposure to radon increases lung cancer incidence and mortality, particularly among cigarette smokers. In homes with high radon concentrations, taking steps to prevent radon from entering homes by sealing the basement would be expected to result in a corresponding decrease in the risk of lung cancer.

Magnitude of Effect: Increased risk that follows a dose-response gradient, with small increases in risk for levels experienced in most at-risk homes to greater increases in risk for high-level exposures.

  • Study Design: Cohort and case-control studies.
  • Internal Validity: Fair.
  • Consistency: Good.
  • External Validity: Fair.

Interventions Associated With an Increased Risk of Lung Cancer

Beta-carotene supplementation in current smokers

Based on solid evidence, high-intensity smokers who take pharmacologic doses of beta-carotene have an increased lung cancer incidence and mortality that is associated with taking the supplement.

Magnitude of Effect: Increased risk, small magnitude.

  • Study Design: Two randomized controlled trials with consistent results.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Interventions That Do Not Decrease Risk of Lung Cancer

Beta-carotene in nonsmokers

Based on solid evidence, nonsmokers who take pharmacological doses of beta-carotene do not experience significantly different lung cancer incidence or mortality compared with taking a placebo.

Magnitude of Effect: No substantive effect.

  • Study Design: Randomized controlled trial.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Fair.

Vitamin E (Tocopherol)

Based on solid evidence, taking vitamin E supplements does not affect the risk of lung cancer.

Magnitude of Effect: Strong evidence of no association.

  • Study Design: Randomized controlled trials.
  • Internal Validity: Good.
  • Consistency: Fair.
  • External Validity: Good.

References

  1. Pinsky PF: Racial and ethnic differences in lung cancer incidence: how much is explained by differences in smoking patterns? (United States). Cancer Causes Control 17 (8): 1017-24, 2006. [PUBMED Abstract]
  • Updated: February 27, 2014