7000 carcinogens in tobacco smoke can directly damage the DNA in lung cells. These adducts can cause mutations if not repaired correctly. Smoking causes chronic inflammation in the lungs, leading to the release of reactive oxygen species (ROS) and other inflammatory mediators. These can further damage DNA and contribute to carcinogenesis. Smoking can lead to mutations in key tumor suppressor genes which normally prevent cells with damaged DNA from proliferating.
The tissues in the mouth, throat, and larynx are directly exposed to the carcinogens in tobacco smoke. These carcinogens can cause mutations in the epithelial cells lining these areas.Smoking can inhibit DNA repair mechanisms, making it harder for cells to repair the damage caused by carcinogens. In individuals who smoke and consume alcohol, the risk is even higher due to the synergistic effect, where alcohol increases the permeability of mucosal linings to tobacco carcinogens.
The tissues in the mouth, throat, and larynx are directly exposed to the carcinogens in tobacco smoke. These carcinogens can cause mutations in the epithelial cells lining these areas.Smoking can inhibit DNA repair mechanisms, making it harder for cells to repair the damage caused by carcinogens. In individuals who smoke and consume alcohol, the risk is even higher due to the synergistic effect, where alcohol increases the permeability of mucosal linings to tobacco carcinogens.
The esophagus is exposed to carcinogens in swallowed tobacco smoke or saliva containing dissolved carcinogens. It can increase the risk of gastroesophageal reflux disease (GERD), which can lead to Barrett’s esophagus—a condition that increases the risk of esophageal adenocarcinoma.
Carcinogens from tobacco smoke are absorbed into the bloodstream and eventually excreted in the urine. The bladder’s lining cells are exposed to these carcinogens, leading to DNA damage. These chemicals can form DNA adducts and induce mutations in bladder epithelial cells.
These carcinogens from smoking can be transported to the pancreas through the bloodstream, where they can cause mutations. It can induce chronic inflammation in the pancreas, which is a known risk factor for pancreatic cancer.
Nitrosamines Formation: Smoking promotes the formation of N-nitroso compounds. These compounds can form in the stomach and damage the DNA of stomach lining cells. Smoking can alter the gastric mucosa and promote chronic gastritis, which is a precursor to stomach cancer.
Smoking can exacerbate the risk of HPV and it is the primary cause of cervical cancer. It can damage the immune system, making it harder to clear HPV infections. Carcinogens from smoking can accumulate in cervical mucus, leading to direct exposure of the cervix to these harmful substances.
The kidneys filter the blood and concentrate carcinogens from tobacco smoke, leading to direct exposure of renal cells to these harmful substances. Smoking increases oxidative stress, which can damage kidney cells and contribute to the development of cancer.
Smoking can contribute to liver cancer indirectly by promoting liver damage and cirrhosis, both of which are risk factors for liver cancer.
Cigarette smoke is known to damage bone marrow and is a risk factor for acute myeloid leukemia (AML). It can cause chromosomal abnormalities in hematopoietic cells.