There are a number of reasons why smoking does cause cancer: among these, DNA damage is a primary factor. We do also know that most lung cancers are caused by smoking, and smoking is also responsible for most lung cancer-related deaths. But not all smokers develop lung cancer — and scientists have now found that a lucky genetic dice roll may be a factor.
Published in Naturelast month, researchers found that some smokers who have never developed lung cancer have a lining of surface cells in their lungs that are less likely to mutate over time — moreover, they also may have stronger DNA repairing genes. Surface cells are the ones most likely to turn cancerous; “[t]hese lung cells survive for years, even decades, and thus can accumulate mutations with both age and smoking,” said Simon Spivack from the Albert Einstein College of Medicine, who co-authored the paper.
The researchers charted how the cells mutate over time using a measure called “pack years” — or the equivalent of smoking a pack of cigarettes a day for a year. They found that the mutation risk steadily rises over time as the frequency of smoking increases. However, after 23 pack–years, the risk of cell mutation plateaus in some people.
“Our data suggest that these individuals may have survived for so long in spite of their heavy smoking because they managed to suppress further mutation accumulation. This leveling off of mutations could stem from these people having very proficient systems for repairing DNA damage or detoxifying cigarette smoke,” the researchers explain in their paper.
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To be clear: smoking is proven to cause 90% of all lung cancers in the world. The research is meant to highlight genetic factors that could play a role in mitigating that risk for some, and perhaps pave the way for potentially assessing risk factors for developing cancers in advance.
But the key is in the DNA’s ability to repair and resist environmental toxins such as cigarette smoke. Previous research has also found that B-vitamins — particularly B6 — are important in maintaining DNA health. “Basically, these B vitamins and nutrients are all involved in the pathway which is responsible for the creation and maintenance of DNA,” said Paul Brennan, who led the study published in JAMA. Other studies have also shown that some DNA mutations enhance lung function.
The other side of the coin is that there are also genetic flaws that make some people more susceptible to becoming addicted to and developing lung cancer from smoking than others. This research was published in Nature way back in 2008, and showed how a particular gene makes some people more likely to develop lung cancer than others.
“There’s not a public health message here that you can find out what version of the gene you have and decide whether to keep on smoking or not… You have to bear in mind that there are so many other disease[s] that are caused by smoking,” Brennan had said at the time. But this could be about to change, with new research painting a clearer picture about what makes some smokers more vulnerable than others to the deadly disease.
“This may prove to be an important step toward the prevention and early detection of lung cancer risk and away from the current herculean efforts needed to battle late-stage disease, where the majority of health expenditures and misery occur,” Spivack said, regarding the current research.
The scientific consensus remains clear on the fact that smoking is deadly on several fronts, and accounts for a majority of lung cancers. But determining who shoulders much of that burden, and why, is the next frontier for assessing and preventing risks.
