National Cancer Institute


Posted Date: Apr 27, 2014

Expert-reviewed information summary about factors that may influence the risk of developing lung cancer and about research aimed at the prevention of this disease.

Lung Cancer Prevention

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.

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.

Interventions Associated With Decreased Risk of Lung Cancer

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.

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.

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.

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.

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

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

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.

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.

Description of the Evidence

Background

Lung cancer has a tremendous impact on the health of the American public, with an estimated 224,210 new cases and 159,260 deaths predicted in 2014 in men and women combined. Lung cancer causes more deaths per year in the United States than the next four leading causes of cancer death combined. Lung cancer incidence and mortality rates increased markedly throughout most of the last century, first in men and then in women. The trends in lung cancer incidence and mortality rates have closely mirrored historical patterns of smoking prevalence, after accounting for an appropriate latency period. Because of historical differences in smoking prevalence between men and women, lung cancer rates in men have been consistently declining since 1990. The incidence rate in men declined from a high of 102.1 cases per 100,000 men in 1984 to 80.0 cases per 100,000 men in 2010. Consistent declines in women have not been seen. In the United States, it is estimated that lung cancer will account for about 13% of new cancer cases and about 27% of all cancer deaths in 2014. Lung cancer is the leading cause of cancer deaths in both men and women. In 2014, it is estimated that 72,330 deaths will occur among U.S. women due to lung cancer, compared with 40,000 deaths due to breast cancer.

Lung cancer incidence and mortality is highest in African Americans compared with any other racial/ethnic group in the United States, primarily due to the very high rates in African American men. In 2007, the incidence rate in black men was 33% higher than in white men (101.2 vs. 76.3 cases per 100,000 men, respectively), whereas among women no racial difference in incidence rates was present (54.8 vs. 54.7 cases per 100,000 women, respectively). Similarly, the mortality rates among black men were 28% higher than among white men for the same year (87.5 vs. 68.3 deaths per 100,000 men, respectively), whereas the mortality rates among black women were 5% lower than among white women (39.6 vs. 41.6 deaths per 100,000 women, respectively).

Surgical treatment or radiation therapy is the treatment of choice for early stages of cancer. The overall 5-year relative survival rate from lung cancer was 16% in 2006. Lung cancer survival is worse for men compared with women and for blacks compared with whites. For example, 5-year lung cancer survival was 18% lower in black men compared with white men (11.3% vs. 13.8%, respectively) and 23% lower in black women compared with white women (14.4% vs. 18.6%, respectively).

The hypothesis has been proposed that women may be more susceptible than men to smoking-caused lung cancer. However, the results of studies that have compared the association between smoking and lung cancer in men and women using appropriate comparisons do not support this hypothesis.

The results of the Multi-Ethnic Cohort Study indicated that for a given degree of cigarette smoking, African Americans had a higher risk of lung cancer compared with other racial/ethnic groups. Menthol cigarettes have been hypothesized as one potential factor contributing to the observed greater susceptibility to smoking-caused lung cancer in African Americans, but menthol cigarettes have not been observed to be associated with a higher risk of lung cancer than nonmenthol cigarettes.

The epidemic of lung cancer in the 20th century was primarily due to increases in cigarette smoking, the predominant cause of lung cancer. The threefold variation in lung cancer mortality rates across the United States more or less parallels long-standing state-specific differences in the prevalence of cigarette smoking. For example, average annual age-adjusted lung cancer death rates for 1996 to 2000 were highest in Kentucky (78 deaths per 100,000 individuals) where 31% were current smokers in 2001; whereas the lung cancer death rates were lowest in Utah (26 deaths per 100,000 individuals), which had the lowest prevalence of cigarette smoking (13%).

Understanding the biology of carcinogenesis is crucial to the development of effective prevention and treatment strategies. Two important concepts in this regard are the multistep nature of carcinogenesis and the diffuse field-wide carcinogenic process. Epithelial cancers in the lung appear to develop in a series of steps extending over years. Epithelial carcinogenesis is conceptually divided into three phases: initiation, promotion, and progression. This process has been inferred from human studies identifying clinical-histological premalignant lesions (e.g., metaplasia and dysplasia). The concept of field carcinogenesis is that multiple independent neoplastic lesions occurring within the lung can result from repeated exposure to carcinogens, primarily tobacco. Patients developing cancers of the aerodigestive tract secondary to cigarette smoke also are likely to have multiple premalignant lesions of independent origin within the carcinogen-exposed field. The concepts of multistep and field carcinogenesis provide a model for prevention studies.

Risk Factors

Interventions Associated With Decreased Risk of Lung Cancer

Substantial harm to public health accrues from addiction to cigarette smoking. Compared with nonsmokers, smokers experience a dose-dependent increase in the risk of developing lung cancer (and many other malignancies).

Approximately 85% of all lung cancer deaths are estimated to be attributed to cigarette smoking. Substantial benefits accrue to the smoker by quitting smoking. (Refer to the PDQ summary on Cigarette Smoking: Health Risks and How to Quit for more information.) Avoidance of tobacco use is the most effective measure to prevent lung cancer. The preventive effect of smoking cessation depends on the duration and intensity of prior smoking and upon time since cessation. Compared with persistent smokers, a 30% to 50% reduction in lung cancer mortality risk has been noted after 10 years of cessation.

The benefits of tobacco control at the population level provide strong quasi-experimental evidence that reducing population-level exposure to cigarettes has resulted in population-level declines in the occurrence of lung cancer. Reduced tobacco consumption, due to both decreases in smoking initiation and increases in smoking cessation, led to a decline in overall age-adjusted lung cancer mortality among men since the mid-1980s, consistent with reductions in smoking prevalence among men since the 1960s. Gender differences in time trends for lung cancer are a reflection of (1) the later adoption of cigarette smoking in women compared with men and (2) the later reduction in smoking prevalence among women compared with men.

After cigarette smoking and exposure to secondhand smoke, occupational exposure to lung carcinogens, such as asbestos, arsenic, nickel, and chromium, is the most important contributor to the lung cancer burden. When occupational exposure to lung carcinogens are all considered together, 9% to 15% of all lung cancer deaths can be attributed to occupational exposure to lung carcinogens. Reducing or eliminating workplace exposures to known lung carcinogens would be expected to result in a corresponding decrease in the risk of lung cancer. Consequently, the proportion of the lung cancer burden attributable to occupational exposures is declining over time in countries like the United States that have taken steps to protect the workforce from exposure to known lung carcinogens.

Interventions Associated With Increased Risk of Lung Cancer

Results of the National Cancer Institute (NCI) Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) trial were first published in 1994. This trial included 29,133 Finnish male chronic smokers aged 50 to 69 years in a 2 x 2 factorial design of alpha-tocopherol (50 mg/day) and beta-carotene (20 mg/day). Subjects were randomly assigned to one of the following four groups for 5 to 8 years: beta-carotene alone, alpha-tocopherol alone, beta-carotene plus alpha-tocopherol, or placebo. Subjects receiving beta-carotene (alone or with alpha-tocopherol) had a higher incidence of lung cancer (RR = 1.18; 95% CI, 1.03–1.36) and higher total mortality (RR = 1.08; 95% CI, 1.01–1.16). This effect appeared to be associated with heavier smoking (one or more packs/day) and alcohol intake (at least one drink/day). Supplementation with alpha-tocopherol produced no overall effect on lung cancer (RR = 0.99; 95% CI, 0.87–1.13).

In 1996, the results of the U.S. Beta-Carotene and Retinol Efficacy Trial (CARET) were published. This multicenter trial involved 18,314 smokers, former smokers, and asbestos-exposed workers who were randomly assigned to beta-carotene (at a higher dose than the ATBC trial, 30 mg/day) plus retinyl palmitate (25,000 IU/day) or placebo. The primary endpoint was lung cancer incidence. The trial was terminated early by the Data Monitoring Committee and NCI because its results confirmed the ATBC finding of a harmful effect of beta-carotene over that of placebo, which increased lung cancer incidence (RR = 1.28; 95% CI, 1.04–1.57) and total mortality (RR = 1.17; 95% CI, 1.03–1.33). In a follow-up study of CARET participants after the intervention discontinued, these effects attenuated for a period of time. After 6 years of postintervention follow-up, the postintervention RR for lung cancer incidence was 1.12 (95% CI, 0.97–1.31) and for total mortality was 1.08 (95% CI, 0.99–1.71). During the postintervention phase a larger RR among women, rather than men, emerged for both outcomes in subgroup analyses; the reason for this observation, if reliable, is not known.

The overall findings from the ATBC and CARET studies, which include over 47,000 subjects, demonstrated that pharmacological doses of beta-carotene increase lung cancer risk in relatively high-intensity smokers. The mechanism of this adverse effect is not known. Lung cancer risks were not increased in subsets of moderate-intensity smokers (less than a pack per day) in the ATBC study, or in former smokers in the CARET study. Evidence from other studies, such as the Physicians’ Health Study (PHS), does not indicate that beta-carotene supplementation increases lung cancer risk in nonsmokers. Subsequent analyses of participants in these trials and cohorts suggest that the beneficial outcomes associated with high beta-carotene plasma levels may be due to increased dietary intake of fruits and vegetables. These findings show the importance of randomized controlled trials to confirm epidemiologic studies.

Interventions With Adequate Evidence That They Do Not Reduce Risk

Studies have examined whether it is possible to prevent cancer development in the lung using chemopreventive agents. Chemoprevention is defined as the use of specific natural or synthetic chemical agents to reverse, suppress, or prevent carcinogenesis before the development of invasive malignancy. So far, agents tested for efficacy in lung cancer chemoprevention have been micronutrients, such as beta-carotene and vitamin E.

Changes to This Summary (02/27/2014)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

Description of the Evidence

Updated statistics with estimated new cases and deaths for 2014 (cited American Cancer Society as reference 1).

This summary is written and maintained by the PDQ Screening and Prevention Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.

Questions or Comments About This Summary

If you have questions or comments about this summary, please send them to Cancer.gov through the Web site’s Contact Form. We can respond only to email messages written in English.

About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about lung cancer prevention. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

Board members review recently published articles each month to determine whether an article should:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

Permission to Use This Summary

PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

National Cancer Institute: PDQ® Lung Cancer Prevention. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://cancer.gov/cancertopics/pdq/prevention/lung/HealthProfessional. Accessed <MM/DD/YYYY>.

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