Elsevier

Lung Cancer

Volume 61, Issue 1, July 2008, Pages 13-20
Lung Cancer

Second hand smoke, age of exposure and lung cancer risk

https://doi.org/10.1016/j.lungcan.2007.11.013Get rights and content

Summary

Background

Exposure to second hand smoke (SHS) has been identified as a risk factor for lung cancer for three decades. It is also known that the lung continues to grow from birth to adulthood, when lung growth stops. We hypothesize that after adjusting for active cigarette smoking, if SHS exposure took place during the period of growth, i.e. in the earlier part of life (0–25 years of age) the risk of lung cancer is greater compared to an exposure occurring after age 25.

Method

Second hand smoke exposure was self-reported for three different activities (leisure, work and at home) for this study population of 1669 cases and 1263 controls. We created variables that captured location of exposure and timing of first exposure with respect to a study participant's age (0–25, >25 years of age). Multiple logistic regressions were used to study the association between SHS exposure and lung cancer, adjusting for age, gender and active smoking variables.

Result

For study participants that were exposed to SHS at both activities (work and leisure) and compared to one or no activity, the adjusted odds ratio (AOR) for lung cancer was 1.30 (1.08–1.57) when exposure occurred between birth and age 25 and 0.66 (0.21–1.57) if exposure occurred after age 25 years. Respective results for non-smokers were 1.29 (0.82–2.02) and 0.87 (0.22–3.38), and current and ex-smokers combined 1.28 (1.04–1.58) and 0.66 (0.15–2.85).

Conclusion

All individuals exposed to SHS have a higher risk of lung cancer. Furthermore, this study suggests that subjects first exposed before age 25 have a higher lung cancer risk compared to those for whom first exposure occurred after age 25 years.

Introduction

Lung cancer is the leading cause of cancer death for both men and women in the United States. Past studies have demonstrated the association between active cigarette smoking (mainstream smoke, MSS) or second hand smoke (SHS) exposure and the risk of adult non-small cell lung cancer (NSCLC). However, less is known about the effect of the age of exposure, particularly to SHS, on the risk of NSCLC [1], [2], [3]. Most studies [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18] have focused on paternal and maternal smoking during pregnancy and the effect on childhood illnesses and cancers in general or more recently the risk of lung cancer for non-smoking women exposed to tobacco smoke during childhood [19], [20], [21], [22], [23], [24], [25], [26], [27], [28]. Very few studies [19], [22], [29], [30] have focused on the effect of the period of exposure relevant for lung cancer development while also assessing the significance of lifetime exposure by location.

The lung continues to grow from birth to adulthood [31] and most lung growth is over by age 18 [32], [33], [34], but lung volume continues to expand to 25, suggesting additional growth may occur [35], [36], [37], [38], [39]. Exposure of target organs to carcinogens during periods of rapid cell division or childhood is known to increase the risk of cancer and elevated exposure to carcinogens has been associated with higher levels of both DNA-adducts and somatic aberrations in cancer cells and may lead to genetic abnormalities that result in the development into cancer [40], [41].

SHS consists of emissions from cigarettes, pipes and cigars, as well as exhaled materials from MSS, which contains several chemicals including over 50 known carcinogens [40], [42], [43]. The concentrations of benzol(a)pyrene, toluene, dimethylnitrosamines in SHS is much higher than in MSS, and the smaller particles in SHS are more likely to be deposited in the lung. SHS may induce DNA-adducts, sister chromosome exchange [44], oxidative DNA damage [45], [46], and increased number of p53 mutations in lung cancer [47], [48], suggesting a similar etiologic mechanism for cases exposed to SHS and to MSS.

SHS exposure may occur at home (including childhood exposure from parents/other family members and exposure from spouse/family members in adulthood), at work (occupational exposure), and at leisure (exposure at public places other than work). Due to public health education and as a result of legislation in several developed countries, exposure to second hand smoke is declining at work and public places but direct marketing to younger populations by tobacco companies has contributed to continued high exposure among youths [49], [50], [51], [52]. The intensity or frequency of exposure in work places has been noted to be generally higher than that of at home or leisure places [53], and results from a previous study has suggested that SHS exposure at work places may have a stronger effect on NSCLC risk than exposure at home or at leisure places [54].

We hypothesize that after adjusting for active cigarette smoking, if the SHS exposure took place during the critical period of growth, i.e. in the earlier part of life (0–25 years of age) the risk of lung cancer is greater compared to an exposure occurring after age 25.

Section snippets

Study population

This study was reviewed and approved by the Institutional Review Boards of the Massachusetts General Hospital and the Harvard School of Public Health. The study population of 1669 cases and 1263 controls is derived from a large case–control study evaluating the molecular epidemiology of lung cancer, which began in 1992 at the Massachusetts General Hospital (MGH). Eligible cases included any person over the age of 18 years, with a diagnosis of primary lung cancer. An MGH lung pathologist

Patient characteristics

There were a total of 1669 cases and 1263 controls. The distribution of demographic and clinical characteristics by smoking status is summarized in Table 1. Overall median age (standard deviation) was 62 years [12], males were 49%; 604 (21%) non-smokers, 1464 (50%) ex-smokers, 864 (29%) current smokers; median pack–years (standard deviation) for ex- and current smokers 39 [37]. Patients with early stage (stages I and II) numbered 803 (50%), with adenocarcinoma 698 (42%), squamous 339 (21%) and

Discussion

Previous studies of biochemical markers of exposure and toxicological studies, confirm that there is a causal association between the risk of NSCLC and exposure to SHS (2). Similar conclusions have been reached by past summary scientific reports [43], [55]. We suggest further that subjects first exposed before age 25 have a higher lung cancer risk compared to those for whom first exposure occurred after age 25 years. Consistent results are seen in our study for different smoking categories,

Conflict of interest statement

None.

Acknowledgements

The authors gratefully acknowledge the assistance of Linda Lineback, Barbara Bean, Andrea Shafer, Jessica Shin, Jeanne Jackson and Andrea Solomon for patient recruitment and data collection; Lucy Ann Principe, Salvatore V. Mucci, and Richard Rivera-Massa for data entry.

References (58)

  • D.P. Sandler et al.

    Cancer risk in adulthood from early life exposure to parents’ smoking

    Am J Public Health

    (1985)
  • H.E. Johnston et al.

    The Inter-Regional, Epidemiological Study of Childhood Cancer (IRESCC): case–control study in children with germ cell tumours

    Carcinogenesis

    (1986)
  • E.M. John et al.

    Prenatal exposure to parents’ smoking and childhood cancer

    Am J Epidemiol

    (1991)
  • M.A. Norman et al.

    Prenatal exposure to tobacco smoke and childhood brain tumors: results from the United States West Coast childhood brain tumor study

    Cancer Epidemiol Biomark Prev

    (1996)
  • B.T. Ji et al.

    Paternal cigarette smoking and the risk of childhood cancer among offspring of nonsmoking mothers

    J Natl Cancer Inst

    (1997)
  • T. Sorahan et al.

    Childhood cancer and parental use of tobacco: deaths from 1971 to 1976

    Br J Cancer

    (1997)
  • A.J. Sasco et al.

    From in utero and childhood exposure to parental smoking to childhood cancer: a possible link and the need for action

    Hum Exp Toxicol

    (1999)
  • J. Brondum et al.

    Parental cigarette smoking and the risk of acute leukemia in children

    Cancer

    (1999)
  • J. Hu et al.

    Parental cigarette smoking, hard liquor consumption and the risk of childhood brain tumors—a case–control study in northeast China

    Acta Oncol

    (2000)
  • T. Sorahan et al.

    Childhood cancer and parental use of tobacco: findings from the inter-regional epidemiological study of childhood cancer (IRESCC)

    Br J Cancer

    (2001)
  • D. Pang et al.

    Parental smoking and childhood cancer: results from the United Kingdom Childhood Cancer Study

    Br J Cancer

    (2003)
  • T. Sorahan et al.

    Parental cigarette smoking and childhood risks of hepatoblastoma: OSCC data

    Br J Cancer

    (2004)
  • Z. Chen et al.

    Risk of childhood germ cell tumors in association with parental smoking and drinking

    Cancer

    (2005)
  • J.S. Chang et al.

    Parental smoking and the risk of childhood leukemia

    Am J Epidemiol

    (2006)
  • K.C. Johnson et al.

    Lifetime residential and workplace exposure to environmental tobacco smoke and lung cancer in never-smoking women, Canada 1994–1997

    Int J Cancer

    (2001)
  • K.E. Anderson et al.

    Metabolites of a tobacco-specific lung carcinogen in nonsmoking women exposed to environmental tobacco smoke

    J Natl Cancer Inst

    (2001)
  • L. Wang et al.

    Lung cancer and environmental tobacco smoke in a non-industrial area of China

    Int J Cancer

    (2000)
  • C.H. Lee et al.

    Lifetime environmental exposure to tobacco smoke and primary lung cancer of non-smoking Taiwanese women

    Int J Epidemiol

    (2000)
  • L. Zhong et al.

    A case–control study of lung cancer and environmental tobacco smoke among nonsmoking women living in Shanghai, China

    Cancer Causes Control

    (1999)
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    1

    These authors contributed equally to this work.

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