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Cigarettes & Immunity

Smoking weakens the immune system by depressing antibodies and cells that are in the body to protect against foreign invaders. There is an association between smoking and the increased incidence of certain malignant diseases and respiratory infections, according to the National Center for Biotechnology Information (NCBI). There is also a significant decrease in immune cells that normally help the body. But this process can be reversed if a smoker gives up cigarettes. Smokers who stop show increased levels of natural killer cell (NK) activity that targets cancerous cells in the body.

Many cancer-causing chemicals from cigarette smoke travel throughout a smoker’s bloodstream to reach the organs of the body and damage the immune response. Carbon monoxide is carried through the body by smoke, interfering with oxygen levels. Less oxygen reaches the brain, heart, muscles and other organs. Lung function is reduced because of the narrowing of the lung airways and excess mucus in the lungs.

Lung irritation and damage result from invading substances, leading to lung infection. Blood pressure and heart rate are affected negatively by smoking chemicals carried through the blood. The immune system does not work as well and smokers become more prone to infections, such as pneumonia and influenza. It takes smokers longer than nonsmokers to get over illnesses.

Smoking can cause the body’s immune system to attack lung tissue and result in severe respiratory disorders, according to research at the University of Cincinnati, Ohio. Health scientists examined mice to study the link between cigarette exposure, the immune system and chronic obstructive pulmonary disorder (COPD), a serious lung disease characterized by emphysema and severe inflammation of the lung tissue.

After lung cells were damaged from cigarette smoke in the lab research, the cells signaled the immune system when the damaged cells needed to be destroyed. The research shows that smoking actually activates certain parts of the immune system, which works against the lungs and attacks the tissue, it was reported in the March 2009 issue of the “Journal of Clinical Investigation.” The researchers found a strong correlation between cellular stress signals, activation of the immune system and development of diseases similar to COPD.

Researchers compared the results with tissue samples from humans who included nonsmokers, smokers with COPD and smokers who did not have COPD. They found that patients who had never smoked had no trace of the lung cells that triggered the immune system to attack lung tissue. Current and former smokers who developed the disease had evidence of those lung signals.


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