Smoking and Lung Cancer

According to the Centers for Disease Control and Prevention (CDC), smoking is linked to between 80% and 90% of lung cancer deaths in the United States. This makes smoking the number one risk factor for the disease. Although quitting dramatically reduces the risk, the effects of smoking can stay with you and increase the likelihood of lung cancer even after 25 years of abstinence.

Even so, quitting offers benefits no matter how long you have smoked, reducing your risk of lung cancer by around 39% after five years—even if you are a heavy smoker.

Statistics

Lung cancer is the leading cause of cancer-related deaths in both males and females in the United States, according to the CDC. Overall, around 6.3% percent of people in the United States will be diagnosed with lung cancer at some point during their lifetime.

Cigarette smoking can also cause other types of cancers, including throat, laryngeal, esophageal, stomach, kidney, pancreatic, liver, bladder, cervical, colorectal cancer, and acute myeloid leukemia (AML). In fact, 40% of all cancers are linked to tobacco smoke in some way.

The lifetime risk of lung cancer is as high as 15% for a lifelong smoker. Overall, it is thought that chronic smokers have 10 fewer years of life and that roughly half of them will die from tobacco-related diseases, including chronic obstructive pulmonary disease (COPD).

It is important to note that never-smokers can may also develop lung cancer, though cigarette smoking remains the leading cause of the disease.

How Smoking Causes Lung Cancer

Lung cancer is a complex, multifactorial disease in which genetics, environment, and lifestyle all play a role. Cigarette smoking contributes by directly damaging the DNA (the genetic coding) of lung cells and altering the way the lungs and immune system work.

Cigarette smoke contains a toxic mix of over 7,000 chemicals, around 70 of which are classified as carcinogenic (cancer-causing). These include arsenic, benzene, cadmium, chromium, formaldehyde, N-nitrosamines, nickel, and vinyl chloride.

When exposed to these and other chemicals in cigarette smoke, the cells of the lungs can begin to mutate and form cancerous tumors. There are a number of intersecting mechanisms that contribute to this:

• Direct DNA damage: When exposed to carcinogens, the strands of DNA can begin to break apart. This causes cells to multiply excessively and prevents apoptosis, the normally programmed cell degeneration that provides space for replacement with healthy new cells. Due to these changes, cancer cells can replicate out of control and become almost "immortal."
• Impaired cell repair: Damaged DNA can usually be repaired, and mutated cells can often be destroyed—mechanisms that help the body fight cancer. Tumor suppressor genes code for enzymes that trigger degeneration of damaged cells and instruct the body to make new, healthy ones. Chromium from cigarette smoke can bind to DNA and effectively silence tumor suppressor genes. Arsenic and nickel can do the same by promoting mutations in tumor suppressor genes.
• Inflammation: When exposed to cigarette smoke, the body will respond by releasing pro-inflammatory compounds (such as interleukin-1β, prostaglandin E2, and transforming growth factor-β) in an attempt to minimize cell damage. Over time, persistent inflammation can damage cellular DNA and alter the way that cells adhere to each other, allowing cancer cells to migrate freely and become invasive.
• Damage to cilia: Cilia are tiny, hair-like structures lining the airways that brush debris out of the lungs. Certain toxins in tobacco smoke, like formaldehyde, can paralyze cilia and, over time, damage them irreparably. This causes harmful particles in cigarette smoke to remain in the lungs longer.
• Impaired immune function: Although carcinogens in tobacco smoke are implicated in the formation of cancerous tumors, other chemicals can contribute by suppressing the immune system as a whole. Both nicotine and tar impair the body's innate (inborn) immune response, hindering some of the mechanisms that might otherwise prevent cancer (such as apoptosis).

Effect of Pack-Years on Lung Cancer Risk

The risk of developing lung cancer is ultimately related to the number of pack-years a person has smoked. Pack-years are calculated by multiplying the number of packs of cigarettes smoked daily by the number of years of smoking. The greater the number of pack-years, the higher the risk of disease.

According to a 2018 study in BMC Cancer, the number of pack-years was directly associated with a person's risk of lung cancer compared to the risk seen in never-smokers:

Lung Cancer in Former Smokers

Around 40% of lung cancer diagnoses occur in former smokers. Even after smoking is stopped, the risk of lung cancer can persist and remains above that of a non-smoker for a lifetime.

The age in which a person quits can roughly estimate the life-years lost to smoking. A 2013 study published in the New England Journal of Medicine broadly outlined the losses based on the age in which smoking was stopped:

Cancer Risk by Cigarette Type

In addition to pack-years, the type of cigarette smoked can affect cancer risk. Different types of tobacco leaves, the presence or absence of filters, chemical additives, and the ambient conditions can all play a role in a cigarette's ability to induce cancer.

Japanese cigarettes, for instance, are manufactured so that fewer carcinogens are created during combustion. This, in addition to the use of activated charcoal filters, appears to reduce the overall risk of lung cancer among people in Japan, according to research from Pennsylvania State University.

This is evidenced by data released by the World Health Organization in which Japanese men have a lower lung cancer mortality rate compared to American men (however, American men are more likely to smoke at an early age, which can also be a factor). Moreover, lung cancer deaths in Japanese men tend to occur about 10 years later than what is seen in American men.

A 2013 study in the journal Chest further reported that lifelong smokers who use filtered cigarettes are between 20% and 40% less likely to develop lung cancer compared to lifelong smokers who use non-filtered cigarettes.

It is for this reason the Food and Drug Administration (FDA) banned the use of the terms "light" or "ultralight" from cigarette labels and marketing under the Family Smoking Prevention and Tobacco Control Act (FSPTCA) of 2009.

Other Forms of Smoking

Cigarettes are not the only form of tobacco that raises cancer risk. Bidis and kreteks (clove cigarettes) imported from Asia can also increase the risk too. Bidis and kreteks have higher concentrations of nicotine, tar, and carbon monoxide than conventional cigarettes sold in the United States.

Pipe and cigar smoking are almost as likely to cause lung cancer as cigarette smoking. In fact, the additional fermentation process used to cure these tobacco products can increase the concentration of carcinogenic N-nitrosamines compared to regular cigarettes.

It remains unclear what risks hookah smoking pose with regard to lung cancer, although a 2014 review in the International Archives of Medicine listed no less than 27 carcinogens identified in the vaporized fumes. Among these is the carcinogen benzene, which is found in higher concentrations in hookah smoke than conventional cigarettes.

By contrast, studies have been mixed as to whether marijuana smoking increases the risk of lung cancer. The same applies to e-cigarettes, which the American Cancer Society suggests may pose a risk of lung cancer.

A Word From Verywell

The facts are simple: Smoking causes lung cancer, and even former smokers are at risk of the disease. With that said, it is never too late to quit. Many people who have kicked the habit feel better and are motivated to improve their health in other ways as well. 

If you have smoked heavily for years, don't assume that the "damage is done" and that there is no point in quitting. Even if your risk of lung cancer remains elevated, there are safe and effective ways for you to be monitored for cancer.