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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Based on solid evidence, taking vitamin E supplements does not affect the risk of lung cancer.
Magnitude of Effect: Strong evidence of no association.
Lung cancer has a tremendous impact on the health of the American public, with an estimated 221,200 new cases and 158,040 deaths predicted in 2015 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 78.6 cases per 100,000 men in 2011. 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 2015. Lung cancer is the leading cause of cancer deaths in both men and women. In 2015, it is estimated that 71,660 deaths will occur among U.S. women due to lung cancer, compared with 40,290 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. Between 2007 and 2011, the incidence rate in black men was higher than in white men (93 vs. 72.4 cases per 100,000 men, respectively), whereas among women no racial difference in incidence rates was present (51.1 vs. 51.2 cases per 100,000 women, respectively). Similarly, the mortality rates among black men were higher than among white men during the same time frame (87.5 vs. 68.3 deaths per 100,000 men, respectively), whereas the mortality rates among black women were lower than among white women (36.5 vs. 39.8 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. 
The most important risk factor for lung cancer (and for many other cancers) is cigarette smoking.    Epidemiologic data have established that cigarette smoking is the predominant cause of lung cancer. This causative link has been widely recognized since the 1960s, when national reports in Great Britain and the United States brought the cancer risk of smoking prominently to the public’s attention.  The percentages of lung cancers estimated to be caused by tobacco smoking in males and females are 90% and 78%, respectively. The manufactured cigarette has changed over time, but there is no evidence to suggest that changes such as “low tar” or “low nicotine” cigarettes have resulted in reduced lung cancer risks.  Cigarette smoking is the most important contributor to the lung cancer burden because of its high prevalence of use and because cigarette smokers tend to smoke frequently, but cigar and pipe smoking have also been associated independently in case-control and cohort studies with increased lung cancer risk.   The cigar risks are of particular concern because of the increased prevalence of cigar use in the United States. 
The development of lung cancer is the culmination of multistep carcinogenesis. Genetic damage caused by chronic exposure to carcinogens, such as those in cigarette smoke, is the driving force behind the multistep process. Evidence of genetic damage is the association of cigarette smoking with the formation of the DNA adducts in human lung tissue. A strong link between tobacco smoke and lung carcinogenesis has been established by molecular data.  
Secondhand tobacco smoke is also an established cause of lung cancer.  Secondhand smoke has the same components as inhaled mainstream smoke, though in lower absolute concentrations, between 1% and 10% depending on the constituent. Elevated biomarkers of tobacco exposure, including urinary cotinine, urinary NNK metabolites, and carcinogen-protein adducts, are seen in those who are exposed to secondhand cigarette smoke.   
A positive family history of lung cancer is a risk factor for lung cancer. The results of a meta-analysis of epidemiologic studies indicated that those with a positive family history of lung cancer were at approximately twice the risk of lung cancer compared with those with no affected relatives.   Cigarette smoking behavior tends to run in families and family members are exposed to secondhand smoke, so the extent to which measured family history represents a genetic predisposition to lung cancer independent of the shared risk factor of cigarette smoking is uncertain.
HIV infection has been observed to be statistically associated with an increased lung cancer risk; for example, the results of a meta-analysis of 13 studies indicated HIV-infected individuals had a 2.6-fold higher risk of lung cancer than non-HIV-infected individuals (standard incidence ratio = 2.6; 95% confidence interval [CI] 2.1–3.1).  The clinical significance of this association remains to be elucidated, as it raises the possibility that HIV infection increases susceptibility to lung cancer, but may merely reflect the high smoking prevalence (study estimates ranged from 59% to 96%) among those infected with HIV compared with the general population (smoking prevalence approximately 20%).
Several environmental exposures other than tobacco smoke are causally associated with lung cancer, but the proportion of the lung cancer burden due to these exposures is small compared with cigarette smoking. Many lung carcinogens have been identified in studies of high occupational exposures. Considered in total, occupational exposures have been estimated to account for approximately 10% of lung cancers.  These carcinogens include asbestos, radon, tar and soot (sources of polycyclic aromatic hydrocarbons), arsenic, chromium, nickel, beryllium, and cadmium.  For many of these workplace carcinogens, cigarette smoking interacts synergistically to increase the risk.  In developed countries, workplace exposures to these agents have largely been controlled.
Approximately 10% of all lung cancer deaths and 30% of lung cancer deaths in lifetime nonsmokers are estimated to be attributable to indoor exposure to radon, estimations that are supported by a meta-analysis and pooled-analyses of case-control studies of lung cancer and indoor radon exposure.   Due to a synergistic interaction between cigarette smoking and radon exposure, the radon-associated risk of lung cancer among smokers is considerably greater than for nonsmokers.  The prevention strategy for residents of homes with high radon concentrations is to have the basement sealed to prevent radon gas from leaking into the home. 
Although early evidence from case-control and cohort studies did not support an association between air pollution and lung cancer, the evidence now points to a genuine association.  In particular, two prospective cohort studies provide evidence to suggest that air pollution is weakly associated with the risk of lung cancer. In an extended follow-up of a study of six U.S. cities, the adjusted relative risk (RR) of lung cancer mortality for each 10 µg/m3 increase in concentration of fine-particulate was 1.27 (95% CI, 0.96–1.69).  Using data from the American Cancer Society's Cancer Prevention Study II, it was observed that compared with the least polluted areas, residence in areas with high sulfate concentrations was associated with an increased risk of lung cancer (adjusted RR = 1.4; 95% CI, 1.1–1.7) after adjustment for occupational exposures and the factors mentioned above.  In a subsequent update to this report, the risk of lung cancer was observed to increase 14% for each 10 μg/m3 increase in concentration of fine particles.  The evidence indicating an association between constituents of ambient air pollution and increased lung cancer mortality continues to strengthen, with reports from Asia,   New Zealand,  and Europe,  documenting increased risks with exposure to certain components of particulate matter.
The results of many case-control and prospective cohort studies show that individuals with high dietary intake of fruits or vegetables have a lower risk of lung cancer than those with low fruit or vegetable intake.  In a systematic review of the evidence, the World Cancer Research Fund (WCRF) rates the evidence as “limited suggestive” that nonstarchy vegetable consumption decreases lung cancer risk and “probable” that fruit consumption and foods containing carotenoids decrease lung cancer risk. However, a subsequent systematic review and meta-analysis limited to prospective studies that adjusted for cigarette smoking found the evidence for carotenoids to be equivocal. 
While the focus has been on fruit and vegetable consumption and micronutrients, a wide range of dietary and anthropometric factors have been investigated. Anthropometric measures have been studied, indicating a tendency for leaner persons to have increased lung cancer risk relative to those with greater body mass index.   The results of a meta-analysis showed that alcohol drinking in the highest consumption categories only (in excess of about a drink a day) was associated with an increased risk of lung cancer.
Studies of dietary factors have yielded intriguing findings, but because the diets of smokers tend to be less healthy than those of nonsmokers, it is challenging to separate the influence of dietary factors from the effects of smoking. When considering the relationships between lung cancer and dietary factors, confounding factors related to cigarette smoking cannot be dismissed as a possible explanation.
A meta-analysis of leisure-time physical activity and lung cancer risk revealed that higher levels of physical activity protect against lung cancer.  The overall evidence for physical activity has been mixed, but several studies have reported that individuals who are more physically active have a lower risk of lung cancer than those who are more sedentary,    even after adjustment for cigarette smoking. The WCRF evidence review rated the inverse association between physical activity and lung cancer as “limited suggestive” evidence. 
Studies of physical activity yield findings consistent with an inverse association, but because physical activity behaviors differ between smokers and nonsmokers, it is difficult to infer that there is a direct relationship between physical activity and lung cancer risk.
In countries where cigarette smoking is common, about 10% to 20% of lung cancer cases occur in never smokers.  Radon and second-hand smoke exposure are established causes of lung cancer in never smokers. An increase in lung cancer risk among never smokers also has been observed with exposure to asbestos, ionizing radiation from sources other than radon, and indoor air pollution caused by combustion of coal or other solid fuel.  Limited data are available about the association of lung cancer in never smokers with physical activity, diet, alcohol, and anthropometry, yet they typically suggest that the relationships do not differ markedly from those in ever smokers.       Nevertheless, the inability to fully control for confounding by smoking in epidemiologic analyses of ever smokers and the possibility of different lung cancer causal pathways from never and ever smokers warrants care when extrapolating results for ever smokers to never smokers.
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.
Nicotine dependence exposes smokers in a dose-dependent fashion to carcinogenic and genotoxic elements that cause lung cancer.  Overcoming nicotine dependence is often extremely difficult. The Agency for Healthcare Research and Quality (formerly the Agency for Health Care Policy and Research [AHCPR]) developed a set of clinical smoking-cessation guidelines for helping nicotine-dependent patients and health care providers.  The six major elements of the guidelines include the following:
Many pharmacotherapies for smoking cessation, including nicotine replacement therapies (e.g., gum, patch, spray, lozenge, and inhaler) and other smoking cessation pharmacotherapies (e.g., varenicline and bupropion), result in statistically significant increases in smoking cessation rates compared with placebo. Based on a synthesis of the results of 110 randomized trials, nicotine replacement therapy treatments, alone or in combination, improve cessation rates over placebos after 6 months (RR, 1.58; 95% CI, 1.50–1.66).  Since the AHCPR guidelines were published, additional evidence of the effectiveness of such pharmacotherapies for smoking cessation has been published.    The choice of therapy should be individualized based on a number of factors, including past experience, preference, and potential agent side effects. (Refer to the PDQ summary on Cigarette Smoking: Health Risks and How to Quit for more information on pharmacotherapy for smoking cessation.)
In addition to individually focused cessation efforts, a number of tobacco control strategies at the community, state, and national level have been credited with reducing the prevalence of smoking. Strategies include the following:  
A review of more than 50 studies found that smoke-free workplace legislation was consistently associated with reduced secondhand smoke exposure, whether measured in reduced time of exposure (71%–100% reduction) or prevalence of persons exposed to secondhand smoke (22%–85% reduction), with particularly marked reductions among hospitality workers.  Smoke-free workplace legislation was associated with consistent and statistically significant reductions in levels of nicotine, dust, benzene, and particulate matter. Health indicators including respiratory systems, sensory symptoms, and hospital admissions were reported as outcomes in 25 studies. With respect to health outcomes, a consistent finding was reduced hospital admissions for cardiac events. Evidence suggested that smoke-free workplace legislation may also result in reduced prevalence of active cigarette smoking; for example, one study observed a 32% decreased smoking prevalence in a county that enacted smoke-free workplace legislation compared with a 2.8% decrease in nearby counties with no smoke-free workplace legislation.
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.
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.
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.
Two other randomized controlled trials of beta-carotene were carried out in populations that were not at excess risk of lung cancer. The PHS was designed to study the effects of beta-carotene and aspirin in cancer and cardiovascular disease. The study is a randomized, double-blind, placebo-controlled trial begun in 1982 involving 22,071 male physicians aged 40 to 84 years. After 12 years of follow-up, beta-carotene was not associated with overall risk of cancer (RR = 0.98) or lung cancer among current (11% of study population) or former (39% of study population) smokers. 
In the Women’s Health Study (WHS) approximately 40,000 female health professionals were randomly assigned to 50 mg beta carotene on alternate days or placebo. After a median of 2.1 years of beta-carotene treatment and 2 additional years of follow-up, there was no evidence that beta-carotene protected against lung cancer, as there were more lung cancer cases observed in the beta-carotene (n = 30) than placebo (n = 21) group.  The strong evidence from rigorous randomized, placebo-controlled trials clearly indicate that beta-carotene supplementation does not lower the risk of lung cancer in populations that are not high-risk for lung cancer.
The Heart Outcomes Prevention Evaluation (HOPE) trial began in 1993 and continued follow-up as the HOPE-The Ongoing Outcomes (HOPE-TOO) through 2003. In this randomized, placebo-controlled trial, patients aged 55 years or older with vascular disease or diabetes were assigned to 400 IU vitamin E or placebo. With a median follow-up of 7 years, the group randomly assigned to vitamin E had a significantly lower lung cancer incidence rate (1.4%) than the placebo group (2.0%) (RR = 0.72; 95% CI, 0.53–0.98).  However, the protective association between vitamin E supplements and lung cancer in the HOPE-TOO study needs to be interpreted in the context of evidence from other randomized trials. In the ATBC study, supplementation with alpha-tocopherol produced no overall effect on lung cancer (RR = 0.99; 95% CI, 0.87–1.13). In the WHS of 40,000 female health professionals, using 600 IU of vitamin E every other day showed no evidence of protection against lung cancer in women (RR = 1.09; 95% CI, 0.83–1.44).  The Medical Research Council/British Heart Foundation Heart Protection Study (HPS) is a randomized placebo-controlled trial to test antioxidant vitamin supplementation with vitamin E, vitamin C, and beta-carotene among 20,536 United Kingdom adults with coronary disease, other occlusive arterial disease, or diabetes. The trial began recruitment in 1994, and as of the 2001 follow-up the results showed a slightly higher rate of lung cancer in the vitamin group compared with the placebo group (1.6% vs. 1.4%, respectively). 
Looking at the vitamin E results for the ATBC, HPS, and HOPE-TOO studies combined, the summary odds ratio was 0.97 (95% CI, 0.87–1.08),  and adding the results from the WHS to this would bring the association even closer to the null. The combined evidence for vitamin E supplementation thus continues to be consistent with no effect on lung cancer risk.
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 2015 (cited American Cancer Society as reference 1).
Revised text to state that between 2007 and 2011, the incidence rate in black men was higher than in white men, whereas among women no racial difference in incidence rates was present. Also revised text to state that similarly, the mortality rates among black men were higher than among white men during the same time frame, whereas the mortality rates among black women were lower than among white women.
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