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* From the Department of Community Medicine (Drs. Chen and Bina), School of Medicine, Mercer University, Macon, GA; and School of Public Health (Dr. Cole), University of Alabama at Birmingham, Birmingham, AL.
Correspondence to: Fan Chen, DrPH, Department of Community Medicine, School of Medicine, Mercer University, 1550 College St, Macon, GA 31207-0001; e-mail: fchen{at}gain.mercer.edu
Abstract
Background: Adenocarcinoma of the lung (ADL) increased worldwide during the last half century. We now report that a continuous decline of ADL began in the United States in 1999.
Method: Incidence rates of ADL and squamous cell carcinoma of the lung (SQL) from The Surveillance Epidemiology and End Results Program were reviewed for the 31-year period beginning in 1973. The low-tar cigarette (tar 
15 mg) consumption/per capita by year was estimated based on cigarette consumption/capita data and the market share of low-tar cigarette of the same year in the United States.
Results: From 1973 to 1998, the age-adjusted incidence rate of ADL increased 83% in men, and > 200% in women. From 1999 through 2003, the rate declined 14% in men and 8% in women. An analysis of age-specific incidence rates of ADL according to birth cohort demonstrates that rates declined progressively among persons born after 1934 for both genders. The increase in low-tar cigarette consumption did not precede the increase in ADL incidence rates, and the decline of ADL incidence after 1998 occurred without a preceding decline of low-tar cigarette consumption.
Conclusion: Since 1999, the ADL incidence has declined. The temporal trend of ADL incidence may suggest that air pollution could be the possible determining cause for the trend. Increasing use of low-tar cigarettes in the United States and the decline in environmental tobacco smoke may be contributors but are less likely to be the driving force.
Key Words: adenocarcinoma • air pollution • incidence rate • low-tar cigarette • lung cancer
Incidence rates of squamous cell carcinoma of the lung (SQL) have declined over the past 24 years. The decline in SQL is attributable to the decline in smoking that started during the 1960s. In contrast, numerous studies1234567 report that adenocarcinoma of the lung (ADL) has been increasing over the past several decades. The age-adjusted incidence of ADL in Connecticut increased nearly 17-fold in women (from 0.9 to 15.2 cases per 100 000 person-years) and nearly tenfold in men (from 2.4 to 23.2 cases per 100 000 person-years) from 1950 through 1991.8 Devesa et al9 reported that, through 1997, ADL incidence rose in virtually all areas of the world, with the increases among men exceeding 50% in many parts of Europe. It has been hypothesized that the trend of increase in ADL is mainly due to the dissemination of low-tar filter cigarettes.101112 It has been pointed out that low-yield, filter-tipped cigarettes, introduced since the 1950s, are inhaled more deeply than smoke from earlier unfiltered cigarettes. Inhalation transports tobacco-specific carcinogens more distally toward the bronchoalveolar junction where adenocarcinomas often arise. Second, blended reconstituted tobacco, introduced in the 1950s, releases higher concentrations of nitrosamines from tobacco stems. Nitrosamines from tobacco are known to induce lung adenocarcinomas in rodents when injected systemically.8 Air pollution is another concern when trying to understand the trend of lung cancer. Vineis and colleagues13 reported a significantly higher odds ratio (1.30) of lung cancer for those exposed to nitrogen dioxide (NO2) at levels 
30 µg/m3 compared to those who were exposed to NO2 at levels < 30 µg/m3. In this article, we report that the 50 years increasing trend has stopped, and a declining incidence rates of ADL after 1998 appears in the United States.
Materials and Methods
Lung cancer incidence rates from the Surveillance Epidemiology and End Results (SEER) Program were reviewed for the available 31-year period from 1973 to 2003. The SEER database provides information on persons with cancer in diverse geographic areas, which constitute approximately 10% of the US population. The nine standard SEER regions include the states of Connecticut, Hawaii, Iowa, New Mexico, and Utah, as well as the metropolitan areas of Atlanta, GA, Detroit, MI, San Francisco/Oakland, CA, and Seattle/Puget Sound, WA. We describe time trends in the age-adjusted incidence rates of ADL (International Classification of Diseases for Oncology codes 8140, 8211, 8230–8231, 8250–8260, 8323, 8480–8490, 8550–8560, 8570–8572) and SQL (International Classification of Diseases for Oncology codes 8050–8076). Birth cohort-specific rates for both genders are also presented.
To assess whether the patterns of ADL incidence are associated with the use of low-tar cigarettes (tar 15 mg per cigarette) in the United States, we describe per capita total cigarette consumption as well as per capita low-tar cigarette consumption by years. This consumption was based on the market share of low-tar cigarettes and total cigarette sales in each year. These data were obtained from the Federal Trade Commission.14
Results
Figure 1 shows that the incidence rates of ADL for men and women are parallel to one another. Since 1973, the rates of ADL increased and then leveled off from 1993 to 1998, followed by a declining trend since 1999 for both genders. This fact of similarity may suggest the major cause has similar impact on both men and women despite the different smoking behavior between the two genders. In contrast, the age-adjusted incidence rate of SQL peaked in 1982 for men but peaked in 1991 for women. The SQL incidence in 2003 compared to their peak declined 52% for men and 18% for women. These facts may reflect the difference in smoking behavior for men and women. The incidence rate of ADL in men surpassed that of SQL in 1992. The age-adjusted incidence rate of ADL in women is approximately twofold higher than that of SQL for all years. For the period 1998 to 2003, the incidence rate of ADL declined 14% for men and 8% for women.
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The increase of ADL incidence rates, especially in women, was first observed in 1950 and confirmed in 1956.15 The incidence rate of ADL among men surpassed that of SQL in 1992. These increases may be due in part to diagnostic advances that make it easier to perform biopsies on tumors in small, distal airways where these tumors often arise. However, the increase in ADL started in the 1950s, > 2 decades prior to the major diagnostic advances that occurred in 1980s. Moreover, the male to female ratio was 2.5 in 1973, and decreased to 1.3 by 2002. There is no reason to believe that diagnostic advances were greater for women than for men; therefore, the rapid increase is likely to be a real increase rather than artifact. Of course, diagnostic advances cannot explain the considerable decrease after 1998.
The similarity of the ADL incidence curves of men and women, over time, is much greater than the similarity of SQL incidence curves of men and women. The turning points of ADL incidence, ending increase and beginning decline, occurred in 1999 for both genders. This suggests that the major cause of ADL is a more general phenomenon and has impacts on men and women in the same way, such as air pollution. Different behaviors between genders, such as smoking, are less likely to be the major cause, because it cannot explain why the peaks of ADL in both genders are on the same year. In contrast, smoking is the major cause of SQL. The incidence rates of SQL peaked in 1982 for men but peaked in 1991 for women, which could be explained by different smoking behaviors between men and women. The substantial decline in SQL started in 1982 for men, approximately 18 years later than the substantial decline of cigarette consumption. This indicates that the induction period for SQL is approximately 18 years. If the induction period for ADL is similar to that for SQL, we can assume that the possible determining factor for ADL started to increase around 1940 or even earlier, and then it started to decrease in 1980. It is not clear what is the possible determining factor, ie, the major cause of ADL, that can fully explain the temporal trend of 50 years increase and the recent 5 years declining. The possible speculated factors include air pollution caused by industrialization and urbanization. The remarkable increase in automobile density as an indicator of industrialization and air pollution started in 1945 in the United States.16 The substantial decline of national air pollutant emissions started in 1980.17 This coincidence with a reasonable induction period for both increase and decline suggests the necessity for further studies in the air pollution hypothesis. Vineis et al13 conducted a nested case-control study in 10 European countries and found a 30% statistically significant increase in the risk of lung cancer developing for those who were exposed to NO2 levels 30 µg/m3 compared to those who were exposed to NO2 levels < 30 µg/m3. Nyberg et al18 reported a result of a population-based case-control study covering the lung cancer cases in Stockholm County, from 1950 to 1990. They found that those with the highest exposure to NO2 had an estimated 44% statistically significant increase in risk for lung cancer compared to those who had the lowest levels, adjusting for age, year, smoking habits, radon exposure, and occupational exposures known to be associated with lung cancer. These studies suggest a need for further studies to test whether air pollution is the major cause of ADL.
Another possible cause that is the effect of increased consumption of low-tar cigarettes since 1970s. Although the low-tar cigarette (tar 15 mg) was developed in 1955, Figure 4 demonstrated that its sales did not rise sharply until 1972. This result is similar to the results reported by Giovino et al.19 However, the increase in ADL predated this by approximately 20 years. The rapid increase of ADL incidence rate was evident by the 1950s or 1960s.20 Between 1981 and 1998, both low-tar cigarette sales and ADL incidence fluctuated at high levels, but a remarkable decline in ADL started in 1999 and continued thereafter. This decline is not preceded by a decline in consumption of low-tar cigarette. The lack of temporal association between ADL and the low-tar cigarette consumption in either rise or decline argues against the hypothesis that the use of low-tar cigarettes is the major cause of the increase in ADL incidence rate, although it is one of the causes of the ADL.
Another possible explanation for the ADL trend may be environmental tobacco smoke (ETS). In recent years, more strict regulations have been enacted that reduced ETS exposure. These changes may partially explain the recent down trend of ADL incidence. However, based on the nationwide Current Population Survey,21 only 4 states reported smoke-free public areas in 1992, but 32 states in 1995. If the policies restricting ETS were enacted in most states during 1990s, it is then less likely to be the cause of down trend of ADL that started in 1999, because the years between the policies and the down trends are too short for the expected induction period. Moreover, the total lung cancer cases attributed to ETS is approximately 3,000/yr in the United States, which accounts for < 2% of the 172,570 new lung cancer cases a year.22 If the decline in the number of people who were exposed to ETS is 10%/yr, we would expect < 0.2% changes in number of lung cancer cases. This number is therefore too small to explain the remarkable change in ADL incidence. In fact, for the period 1998 to 2003, the incidence rate of ADL declined 14% for men and 8% for women. Such large reductions could not be explained by a decline in the number of people who were exposed to ETS.
The recent 5-year decline in the age-adjusted incidence rate of ADL, especially in men, is further explained by birth cohort patterns. Both genders show the same pattern, with persons born after 1930 having progressive declines in age-specific incidence rate of ADL. This suggests that incidence rates in both genders will continue to decrease in coming years. It is not clear why the highest age-specific incidence rate for all ages occurred in 1930 to 1934 birth cohorts, and after that the age-specific incidence rates start to decline.
Limitation
This study is a descriptive study. The estimation of consumption of low-tar cigarettes is based on the average level in the whole United States. In fact, the consumption of low-tar cigarettes may vary by areas (rural vs metropolitan), race/ethnicity, gender, age, and education. The increase of consumption of low-tar cigarettes after 1973 may play some role in the increase of ADL incidence in some areas or some populations, but is not sensitive enough to be detected by this study, in which the average level of the United States was used.
In summary, this study described the fact that ADL incidence has declined since 1999. The driving force for its long period increase, and subsequent decline in recent years is not clear. The possible causes may include air pollution, low-tar cigarette consumption, and ETS.
Footnotes
Abbreviations: ADL = adenocarcinoma of the lung; ETS = environmental tobacco smoke; NO2 = nitrogen dioxide; SEER = Surveillance, Epidemiology, and End Results; SQL = squamous cell carcinoma of the lung
The authors have no conflicts of interest to disclose.
Received for publication July 6, 2006. Accepted for publication November 22, 2006.
References
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