Children’s Environmental Health in Michigan
Childhood Cancer: Second Hand Smoke
From Michigan Network for Children's Environmental Health
“Secondhand smoke (SHS) contains at least 250 toxic chemicals, including more than 50 that can cause cancer (Harris et al. 2009).” The U.S. Environmental Protection Agency and the International Agency for Research on cancer have both classified SHS as a known human carcinogen. Second hand smoke exposure has been associated with an increased risk of lung cancer development for nearly three decades (Asomaning et al. 2007). Nearly 60% (22 million) of children in American, aged 3-11 years, are exposed to second hand smoke (Harris et al. 2009). Paternal smoking during preconception, pregnancy, after birth, and ever smoking is associated with increased risk of offspring developing cancer (Liu, 2011). The developing fetus is vulnerable to the impacts of SHS, and that vulnerability continues through infancy, childhood, adolescence, and into adulthood. However, most lung growth occurs before the age of 18 - as a result, exposure to carcinogens (such as SHS) during these adolescence years have been shown to have increased adverse health effects.
This section provides background information on the presence and potential health effects of second hand smoke and reviews existing Michigan policies related to environmental tobacco regulation. Best policy practices from other states are highlighted and recommendations are provided to further protect Michigan’s children from exposure to second hand smoke.
In addition to cancer, second hand smoke (SHS) has been linked to other health impacts including neurotoxicity and asthma. Information regarding these indicators and children’s health can be found in other sections of this wiki. In this section, relevant data on the relationship between SHS and cancer is discussed in detail.
Sources of SHS
Please refer to Chapter I, Section VII (link to subsection)
Childhood Exposure to SHS
Please refer to Chapter I, Section VII (link to subsection)
Cancer and Second Hand Smoke
Second hand smoke (SHS) is classified as known to be carcinogenic to humans by both the International Agency for Research on Cancer and the U.S. Environmental Protection Agency (IARC 2002; EPA). In particular, there is a well-established scientific link between SHS and cancer; however, studies have tended to focus on the links between adult SHS exposure and cancer. Based on the studies to date that have assessed childhood exposure to SHS, it has been difficult provide strong evidence supporting an increased risk of cancer in adulthood from this exposure, in part due to difficulties of assessing childhood exposure (Boffetta et al. 2000). Below, we will discuss the associations between SHS and certain types of cancers, and the evidence associating exposure to SHS during childhood and the development of those cancers.
SHS exposure has a well-established dose-response relationship to the development of lung cancer in non-smokers. In simple terms, this means that the risk of a non-smoker developing lung cancer increases the more time they spend around smokers and the more smoke they are exposed to (Hackshaw et al. 1997). However, studies assessing childhood exposure to SHS have showed conflicting evidence for an association between childhood exposure to SHS and the development of lung cancer. A small case-control study by Wang and others found that women in China who reported that their mothers smoked during childhood (from 0-22 years old) had a significantly increased odds of developing lung cancer than those whose mothers did not smoke during their childhood (Wang et al. 1994). This association, however, was not present for the father’s smoking status. A meta-analysis of 18 case-control studies that assessed exposure to SHS during childhood found that there was no consistent association suggesting that childhood exposure to SHS alone was a risk factor for lung cancer, although the authors did report a consistent finding among studies that exposure to SHS in adults, spouses, and in one’s occupation, was associated with lung cancer. The authors acknowledged, however, that these studies were potentially weakened by the difficult of adult study subjects estimating their exposure to SHS during childhood (Zhong et al. 2000).
More recently, a large case-control study in Massachusetts found that while all individuals exposed to SHS have an increased risk for developing lung cancer, those first exposed at ages younger than 25 have an increased risk compared to those first exposed after 25 (Asomaning et al. 2008). This is consistent with a Taiwanese study that found that having early life exposure to SHS was associated with an increased effectrisk of later in life SHS exposure on lung cancer risk (Lee et al. 2000). In effect, the study suggests that exposure to SHS in childhood increases the carcinogenic effects of adult SHS on the lungs.
Although there is a strong association between first hand smoke and bladder cancer, the association between SHS exposure and bladder cancer is less strong. A study in China found that non-smokers exposed to high levels of SHS had roughly three times the odds of developing bladder cancer than non-smokers who were not exposed to SHS (Tao et al. 2010). The authors of this study also noted that the risk was higher among individuals possessing certain types of the cytochrome p450 and NAT2 liver enzymes, indicating that some individuals may be more susceptible to the carcinogenic effects of SHS on the bladder than others (Tao et al. 2010). The association between SHS and bladder cancer has been further supported by a retrospective study of epigenetic effects in which people who never smoked were profiled for their exposure to SHS in adulthood, childhood, and their occupations. The authors found that exposure to SHS in all three of these settings, including childhood, was associated with epigenetic effects on genes that have associations with bladder cancer. The findings of this study lend additional biological plausibility to the epidemiologic associations between SHS exposure and bladder cancer (Wilhelm-Benartzi et al. 2011).
Smoking is a well-established risk factor for pancreatic cancer. Based on this, Vrieling and others assessed the effects of SHS exposure on pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study. The authors found that, in people who had never smoked, childhood exposure to SHS was associated with a significantly increased risk for pancreatic cancer (Vrieling et al. 2010).
Childhood Cancers and Second Hand Smoke
In addition to the evidence that links SHS exposure to lung cancer and bladder cancer, there have been studies which have assessed the link between SHS exposure as well as maternal smoking during pregnancy and childhood brain tumors, leukemia, and lymphoma. While more research is needed to better understand the relationship between SHS exposure and these cancers (Buka et al. 2007), the evidence suggests there is a link. A few studies have linked parental smoking with childhood leukemia and lymphoma (Zahm and Devesa 1995), and results from a meta-analysis suggest associations between prenatal exposure to paternal tobacco smoke and brain tumors and lymphomas (Boffetta et al. 2000). Findings from another meta-analysis of over 30 studies suggest that maternal smoking during pregnancy may be associated with a small increased risk of overall neoplasms; however, no cancer-specific increased risk was observed (Boffetta et al. 2000).
Tobacco smoke contains benzene, which has a well-established association with the development of leukemia (Anderson 2006). To assess the link between maternal smoking during pregnancy and the development of acute lymphocytic leukemia (ALL) and acute myeloid leukemia (AML), Klimentopoulou and others conducted a case-control study/multiple study meta analysis, with a total of over 10,000 leukemia cases and over 25,000 controls. In this large study, the authors found no evidence to suggest a significant association between maternal smoking during pregnancy and the development of leukemia. However, the authors noted that further studies may be needed to assess what sort of risk may exist for individuals with specific genetic susceptibility towards tobacco smoke exposure (Klimentopoulou et al. 2012).
However, a 2011 meta-analysis found that paternal smoking at every time period tested -- during preconception, pregnancy, after birth, and ever smoking -- was associated with increased risk of childhood acute lymphoblastic leukemia (ALL) (Liu, 2011).
While data directly correlating SHS with increased childhood cancer risk is not definitive, the links between childhood exposure to SHS and cancer development later in life are better substantiated. Furthermore, exposure to carcinogens during critical periods of developmental (such as childhood) has been clearly linked with an increased risk of developing genetic abnormalities that can lead to the development of cancer (Sorahan et al. 2001). Because of this and the stronger associations between SHS exposure and adverse respiratory and neurological outcomes in children (please refer to Chapter I, Section VII, and Chapter II, Section I), as well as cancer and respiratory outcomes in adults, Michigan and other states should continue to pursue policies that will reduce the burden of SHS on the public. There is sufficient evidence for serious adverse health effects from SHS exposure that policies to minimize the harmful collateral effects of tobacco smoking are warranted.
Policy Summary and Analysis
Please refer to Chapter I, Section VII (link to subsection)
Summary of Policy Recommendations for SHS in Michigan
Please refer to Chapter I, Section VII, (link to subsection)
Anderson LM. 2006. Environmental genotoxicants/carcinogens and childhood cancer: Bridgeable gaps in scientific knowledge. Environmental Genotoxins in Children and Adults 608(2): 136-156.
Asomaning K, Miller D, Liu G, Wain J, Lynch W, Su L, Christiani D. 2008. Second hand smoke, age of exposure and lung cancer risk. Lung Cancer 61: 13-20.
Boffetta P, Tredaniel J, Greco A. 2000. Risk of childhood cancer and adult lung cancer after childhood exposure to passive smoke: a meta-analysis. Environmental Health Perspectives 108:73-82.
Buka I, MB, Koranteng S, Osornio, Vargas AR. 2007. Trends in Childhood Cancer Incidence: Review of Environmental Linkages. Pediatric Clinics of North America 54:177–203.
Hackshaw AK, Law MR, Wald NJ. 1997. The accumulated evidence on lung cancer and environmental tobacco smoke. British Medical Journal 315: 980-988.
Harris J, Luke D, Zuckerman R, Shelton S. 2009. Forty Years of Secondhand Smoke Research: The gap between discovery and delivery. American Journal of Preventative Medicine. 36(6): 538-548.
Klimentopoulou A, Anotonopoulos CN, Papadopoulou C, Kanavidis P, Tourvas AD, Polychronopoulou S, Baka M, Athanasiadou-Piperopoulou F, Kalmanti M, Sidi V, Moschovi M, Petridou ET. Maternal smoking during pregnancy and risk for childhood leukemia: A nationwide case-control study in Greece and meta-analysis. Pediatric Blood and Cancer 58(3): 344-351.
International Agency for Research on Cancer (IARC). 2002. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 83: Tobacco Smoke and Involuntary Smoking. http://monographs.iarc.fr/ENG/Monographs/vol83/volume83.pdf
Lee CS, Ko YC, Goggins W, Huang JJ, Huang MS, Kao EL, Wang HZ. 2000. Lifetime environmental exposure to tobacco smoke and primary lung cancer in non-smoking Taiwanese women. International Journal of Epidemiology 29: 224-231.
Ruiling Liu, Luoping Zhang, Cliona M. McHale, and S. Katharine Hammond, “Paternal Smoking and Risk of Childhood Acute Lymphoblastic Leukemia: Systematic Review and Meta-Analysis,” Journal of Oncology, vol. 2011, Article ID 854584, 16 pages, 2011. doi:10.1155/2011/854584
Sorahan T, Lancashire RJ, Hulten MA, Peack I, Stewart AM. 1997. Childhood cancer and parental use of tobacco:deaths from 1953 to 1955. British Journal of Cancer 75(1): 134-138.
Lexis Nexis. Legislative Database.
Tao L, Xiang YB, Wang R, Nelson HH, Gao YT, Chan KK, Yu MC, Yuan JM. 2010. Environmental tobacco smoke in relation to bladder cancer risk – the Shanghai bladder cancer study. Cancer Epidemiology, Biomarkers &Prevention. doi: 10.1158/1055-9965.EPI-10-0823.
Vrieling A, Bueno-de-Mesquita HB, Boshuizen HC, Michaud DS, Severinsen MT, Overvad K, Olsen A, Tjønneland A, Clavel-Chapelon F, Boutron-Ruault MC, Kaaks R, Rohrmann S, Boeing H, Nöthlings U, Trichopoulou A, Moutsiou E, Dilis V, Palli D, Krogh V, Panico S, Tumino R, Vineis P, van Gils CH, Peeters PH, Lund E, Gram IT, Rodríguez L, Agudo A, Larrañaga N, Sánchez MJ, Navarro C, Barricarte A, Manjer J, Lindkvist B, Sund M, Ye W, Bingham S, Khaw KT, Roddam A, Key T, Boffetta P, Duell EJ, Jenab M, Gallo V, Riboli E. Cigarette smoking, environmental tobacco smoke exposure and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition. International Journal of Cancer 126(10):2394-403.
Wang FL, Love EJ, Liu N, Dai XD. 1994. Childhood and adolescent passive smoking and the risk of female lung cancer. International Journal of Epidemiology 23(2): 223-230.
William-Benartzi CS, Christensen BC, Koestler DC, Housman EA, Schned AR, Karagas MR, Kelsey KT, Marsit CJ. Association of SHS exposures with DNA methylation in bladder carcinomas. Cancer Causes & Control. 22(8): 1205.
Zahm SH, Devesa SS. 1995.Environmental Health Issues. Environmental Health Perspectives 103(S6):177-184.
Zhong L, Goldberg MS, Parent ME, Hanley JA. 2000. Exposure to environmental tobacco smoke and the risk of lung cancer: a meta-analysis. Lung Cancer 27(1): 3-18.