Stomach cancer, also known as gastric cancer, remains a significant global health concern, with approximately 968,000 new cases diagnosed worldwide in 2022. It is the fifth most common cancer globally and the fifth leading cause of cancer-related deaths. Understanding the factors that contribute to this disease is important for prevention, and smoking has been identified as a significant and well-established risk factor.
The Link Between Smoking and Stomach Cancer
Research consistently demonstrates a strong association between smoking and an increased risk of stomach cancer. Globally, smoking is estimated to contribute to about 11% to 20% of all stomach cancer cases. This link is supported by numerous epidemiological studies.
The risk of stomach cancer increases with both the duration and intensity of smoking. For current smokers, the risk is approximately 1.25 times higher compared to never smokers, rising to about 1.32 times higher for those who smoke more than 20 cigarettes per day. This elevated risk also extends to individuals exposed to secondhand smoke, as it contains many of the same harmful chemicals.
Smoking has a particularly pronounced effect on cancers affecting the upper part of the stomach, near the esophagus, known as gastric cardia adenocarcinoma. The risk for this type of stomach cancer can be more than double for smokers compared to non-smokers, showing a clear dose-response relationship. While the association is stronger for gastric cardia cancer, smoking also increases the risk for other types of stomach cancer, including non-cardia gastric adenocarcinoma.
Mechanisms of Harm
Tobacco smoke contains over 7,000 chemicals, with at least 70 identified as carcinogens. These harmful chemicals include polycyclic aromatic hydrocarbons (PAHs), tobacco-specific nitrosamines (TSNAs), and heavy metals like arsenic, cadmium, and lead. When inhaled, these carcinogens enter the bloodstream and are delivered throughout the body, including to the stomach lining.
Some of these chemicals can also be swallowed with saliva, directly exposing stomach cells to their damaging effects. Once in the stomach, these carcinogens can cause direct damage to the DNA within gastric epithelial cells, leading to DNA adducts. This DNA damage can result in mutations in oncogenes and tumor suppressor genes.
Beyond direct DNA damage, smoking also contributes to chronic inflammation and oxidative stress in the stomach lining. Chronic inflammation can create an environment conducive to cancer development, while oxidative stress, caused by unstable molecules called free radicals, can further damage cells and their DNA. Nicotine, although not directly mutagenic, can also promote tumor progression by activating specific receptors on gastric cells, triggering signaling pathways that increase inflammation and blood vessel growth.
Reducing Risk Through Quitting
Quitting smoking offers significant health benefits, including a reduction in the risk of stomach cancer. Even for individuals who have smoked for many years, stopping tobacco use allows the body to begin repairing damage caused by tobacco carcinogens. This reduction in risk is observed across various types of cancer, with stomach cancer risk decreasing progressively the longer a person remains smoke-free.
Studies indicate that the risk of gastric cancer among former smokers steadily declines over time. After approximately 10 to 15 years of cessation, the risk for former smokers can approach that of never smokers. While some elevated risk may persist, especially for those with a history of heavy or long-term smoking, the overall reduction is substantial.
Quitting smoking also improves overall gastric health by lessening inflammation and oxidative stress, and by reducing the harmful effects of nicotine and other chemicals on the stomach lining. This process can help reverse precancerous changes and reduce the likelihood of malignant transformation. Stopping smoking at any age provides health advantages, including improving treatment outcomes for those already diagnosed.