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Linking Second-Hand Smoke And Lung Cancer

Medical News Today – July 4, 2008

It is a widely accepted notion that second-hand smoke (SHS) is linked to lung cancer. However, medical professionals and researchers have not reached consensus on the extent of the increase in cancer risk due to SHS. In an article published in The Lancet Oncology, Dr Ahmad Besaratinia and Dr Gerd Pfeifer, Beckman (Research Institute of the City of Hope National Medical Center, Duarte, CA, USA) suggest that a better approach to establishing risk level may be to screen for biological markers that are targeted to SHS and associated with lung cancer.

SHS is a mixture of two types of smoke that result from tobacco consumption: mainstream and sidestream smoke. Mainstream smoke is created when a person puffs a cigarette (or other tobacco product) and draws smoke from the burning cone and hot zone of the product. Mainstream smoke can either move through the filter or out of the mouthpiece (depending on the apparatus used). The second type of smoke, called sidestream smoke, comes from the smoldering coal of a tobacco and is generated between puffs. Researchers have found that mainstream and sidestream smoke have similar chemical compositions and carcinogenic compound, but sidestream smoke has different quantities of these chemicals due to a lower burning temperature. Mainstream smoke is often partially filtered and scrubbed by the lungs and comprises less than 15% of SHS (sidestream smoke comprises 85% of SHS). Smokers intake more carcinogens than individuals exposed to SHS because smokers are actively inhaling high doses of mainstream-smoke carcinogens.

“However,” note the authors, “the finding that sidestream smoke-condensate is more potent than mainstream smoke-condensate in inducing mouse skin tumours suggests that SHS imposed on non-smokers might be even more carcinogenic than mainstream smoke inhaled by active smokers.”

Many of the carcinogenic compounds found in smoke are able to create additional substances that lead to DNA lesions called DNA adducts. In fact, these genotoxic carcinogens often create mutations at certain locations, which are like unique signatures genes that are related to cancer. Two laboratory techniques – DNA-lesion footprinting (locates the site of DNA damage) and mutagenicity analysis (finds changes in DNA sequences) – are used together to find these carcinogen signatures. Though these techniques have already been used to find DNA lesions that are linked to smoke-derived carcinogens such as polycyclic aromatic hydrocarbons, the researchers suggest that they be implemented in cancer-relevant genes that are frequently mutated in smoke-related lung cancer.

Besaratinia and Pfeifer also note that more research is needed that can determine how the type, frequency, and distribution of DNA adducts in cancer-related genes are different for non-smokers exposed to SHS and smokers exposed to mainstream smoke. This type of comparative analysis would provide analysts with information to determine if the different risks of lung cancer development are just due to the different doses of smoke exposure seen by smokers and those affected SHS.

Further, the authors place importance on discovering if SHS can lead to lung cancer through an epigenetic pathway. That is, without changing the order of DNA molecules (the primary DNA sequence), environmental factors may cause the gene to express itself differently. They write that, “Future investigations using in-vitro systems, animal models, and biospecimens from chronically exposed individuals will be needed to determine whether SHS induces lung cancer through an epigenetic pathway.”

To conclude, Besaratinia and Pfeifer mention that environmental carcinogens contained in food, drink, and air, make it extremely difficult for models to specifically focus on the association between SHS and lung cancer in humans. In addition, SHS is not consistent in its composition and concentration, providing further barriers to research. They write: “Although the causal link between SHS exposure and lung-cancer development is well established, the estimated risk for lung cancer development consequent to SHS exposure remains somewhat debatable. Elucidation of the mechanisms of SHS action that are relevant to carcinogenesis can help identify unique biological markers that can be used for assessing lung cancer risk in relation to SHS exposure.”

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