RE: "DIFFERENTIAL ASSOCIATION OF BODY MASS INDEX AND FAT DISTRIBUTION WITH THREE MAJOR HISTOLOGIC TYPES OF LUNG CANCER: EVIDENCE FROM A COHORT OF OLDER WOMEN"

Zubair Kabir

Department of Respiratory Medicine, CResT Directorate, St. James’s Hospital, University of Dublin (Trinity College), Dublin 8, Ireland

I read with interest the study by Olson et al. (1). The findings have inched forward our understanding of the causal pathway of lung cancer development by histologic subtypes. However, I have concerns about the external validity (generalizability) of their new findings. Residual confounding due to active smoking effects alone does not explain the overall results, but environmental tobacco smoke exposure, a potential confounder that was not ascertained, may be an alternative explanation. Second, females of younger age groups may not have a similar outcome, and we have very little knowledge about such an outcome in males. Finally, females in less-developed nations may share a different experience. In addition, there are distinct trends observed across the globe in obesity, smoking patterns, and lung adenocarcinoma, which may highlight the apparent inconsistency at the population level in the study by Olsen et al.

An increased prevalence of obesity (as defined by body mass index) is a global phenomenon (2), and overall lung cancer incidence, especially development of squamous cell carcinoma of the lung, is declining worldwide. However, there is compelling evidence of a steady rise in lung adenocarcinoma incidence across the globe with distinct gender and temporal variations over the past 30 years (e.g., a sharper rise in females in the European region (3), a rise slower in males and relatively faster in females in the North American region (4), and an equal rise across both genders in the Asian region (5)). These regional variations across genders support the possibility that a mechanism underlying the multistage carcinogenesis of lung adenocarcinoma may be linked in part to the changing patterns in diagnostic technology and histopathologic criteria over time.

There is evidence of an increased smoking prevalence in young females, who tend to double their daily cigarette consumption and to have a greater depth of inhalation to compensate for the so-called "lower yield" cigarettes (6). These particular smoking habits in females were apparent during the phase when filter cigarettes were introduced into the global market in the early 1980s. The introduction of filter cigarettes may contribute to an increased "peripheral" predisposition of lung adenocarcinoma by anatomic subsite (6), although the authors’ suggestion of an increased chemical activation of cigarette smoke in persons with increased waist circumference is not improbable (1).

The evidence of a significant increase of lung adenocarcinoma on an annual basis in the relatively young female smokers in an urban area suggests the possible role of an "urban" risk factor (7), in addition to changing smoking patterns across the populations over a period of time. Environmental tobacco smoke may be an important contributor to such observed patterns.

An ecologic fallacy is a limitation inherent in such explanations, but these time-trend observations across populations may provide an insight into the causal pathway of the development of lung adenocarcinoma. If the association of findings in the study by Olson et al. (1) is causal, would a possible lung adenocarcinoma epidemic in young female birth cohorts across the globe be worth considering in the future, despite the likelihood of an ever increasing prevalence of obesity modified by a rising smoking prevalence in young females? Is this a paradox in the association observed, or there is a missing link? Are never smokers ever free from environmental tobacco smoke exposure? I wonder if the strong hypothesis that lung adenocarinoma etiology is most likely to include factors not related to smoking is always true, particularly in the present context!

REFERENCES

  1. Olson JE, Yang P, Schmitz K, et al. Differential association of body mass index and fat distribution with three major histologic types of lung cancer: evidence from a cohort of older women. Am J Epidemiol 2002;156:606–15.[Abstract/Free Full Text]
  2. Wang Y, Monteiro C, Popkin BM. Trends of obesity and underweight in older children and adolescents in the United States, Brazil, China, and Russia. Am J Clin Nutr 2002;75:971–7.[Abstract/Free Full Text]
  3. Levi F, Franceschi S, La Vecchia C, et al. Lung carcinoma trends by histologic type in Vaud and Neuchatel, Switzerland, 1974–1994. Cancer 1997;79:906–14.[CrossRef][ISI][Medline]
  4. Travis WD, Lubin J, Ries L, et al. United States lung carcinoma incidence trends: declining for most histologic types among males, increasing among females. Cancer 1996;77:2464–70.[CrossRef][ISI][Medline]
  5. Morita T. A statistical study of lung cancer in the annual of pathological autopsy cases in Japan from 1958 to 1997, with reference to time trends of lung cancer in the world. Jpn J Cancer Res 2002;93:15–23.[ISI][Medline]
  6. Yang CP, Gallagher RP, Weiss NS, et al. Differences in incidence rates of cancers of the respiratory tract by anatomic subsite and histologic type: an etiologic implication. J Natl Cancer Inst 1989;81:1828–31.[Abstract]
  7. Kabir Z, Manning PJ, Clancy L. Epidemiologic patterns of lung cancer incident cases in the Republic of Ireland by major histologic types: 1994–1997. (Abstract). Am J Epidemiol 2002;155(suppl):S19.




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