As I enter my physician’s office for my annual checkup, I hear the familiar string of questions about my health. “Do you smoke?” she asks. The answer should be a simple no; I know the basic detrimental effects of smoking and, therefore, I do not smoke. However, the truthful and more complex answer is that I do smoke. I “involuntarily smoke” or “passively smoke.” Living in midtown, I would venture to say that almost all of the Stern students and staff also “involuntarily smoke.” Daily, I am subjected to secondhand smoke (SHS) and inhale the smoke exhaled by smokers around me. Another term for SHS is environmental tobacco smoke (ETS). SHS is most often found near restaurants and casinos and can even stick to your clothing. In most areas of health, your choices about what you do to your body only affect you; however, when it comes to smoking, bystanders are also subjected to the toxic effects.
SHS includes both mainstream smoke, the smoke exhaled by the smoker, as well as sidestream smoke, the smoke given off by the burning tobacco product. Of the 4,800 identified compounds in cigarette smoke, sixty-nine are known carcinogens, and several of these compounds are tumor promoters. Some of these major toxins include nicotine, carbon monoxide, benzene, formaldehyde, nitric oxide, polycyclic aromatic hydrocarbons and volatile aldehydes. Through analyzing the effect of each of these chemicals on our genetic system, it is not surprising that the International Agency for Research on Cancer confirmed that SHS itself is a carcinogen.
The simplest and most direct way that SHS affects DNA is through the formation of a DNA adduct, when one of the carcinogenic chemicals within SHS covalently or ionically bonds to the DNA. The DNA becomes damaged and can no longer replicate. This could be the start of a mutation. Carcinogens can also damage DNA by causing double-stranded breaks. One experiment exposed mice embryonic stem cells to SHS and to cadmium, one of the main components of SHS. Acute, short exposure led to high levels of apoptosis in the cells. Staining followed by immunofluorescence microscopy showed DNA damage as well. Chronic, lower dosage exposure to SHS and cadmium was found to cause shortening of cell telomeres. When telomeres get too short, chromosomes become inactive and may die. Another experiment studied people who were exposed to polycyclic aromatic hydrocarbons, which are often found in SHS. It found that the peripheral blood cells of these workers displayed telomere shortening as well.
A further health risk associated with SHS is hypoxia, a medical condition in which the body is deprived of an adequate supply of oxygen. Carbon monoxide, one of the toxins found in SHS, competes with oxygen for binding sites on hemoglobin. This causes cells and tissues to die from insufficient oxygen, which can lead to many problems, including the inability of muscles to contract which can, in turn, lead to cardiac arrest.
The genetic toxicity of SHS is manifested through numerous diseases. According to the International Agency for Research on Cancer, “involuntary smoking” causes an increased risk of twenty percent for female non-smokers and thirty percent for male non-smokers for developing lung cancer. Furthermore, the U.S Surgeon General reported that between 1964 and 2014, 2.5 million people died from exposure to SHS. The report also concluded that SHS is a definitive cause of stroke. A recent study also demonstrated a positive correlation between children exposed to SHS at home and lower cognitive performances.
So for those seniors who claim that senioritis affected their performance on their midterms, exposure to SHS over the past four years may be another thing to consider.
And next time the doctor asks you if you smoke, think twice before you answer.