Rheumatoid arthritis (RA) is an autoimmune disorder where the body’s immune system mistakenly attacks its own tissues, primarily the lining of the joints. This attack causes chronic inflammation that leads to pain, swelling, and eventual joint deformity. Scientific evidence shows a strong connection between cigarette smoking and RA. This relationship is multifaceted, influencing who develops the disease, how severely they experience it, and how well they respond to medical care.
Increased Risk of Developing Rheumatoid Arthritis
For some individuals, smoking is an environmental trigger that can initiate rheumatoid arthritis. The process begins in the lungs, where inhaling toxic substances from cigarette smoke causes localized inflammation. This inflammation can start a biochemical process called citrullination, where the amino acid arginine is converted into citrulline, changing the shape of the body’s proteins.
In people with a specific genetic makeup, like those carrying the HLA-DRB1 shared epitope gene, the immune system identifies these citrullinated proteins as foreign invaders. The body then mounts an immune response and produces antibodies to attack them. These are called anti-citrullinated protein antibodies (anti-CCP), and their presence is a marker for RA.
The production of anti-CCP antibodies can precede joint symptoms by several years, indicating the autoimmune process has begun. Smokers are significantly more likely to test positive for these antibodies, a condition known as being seropositive. Studies show that smoking can account for approximately one-third of seropositive RA cases, highlighting its role in initiating the disease.
Worsening of Disease Symptoms and Progression
For individuals with rheumatoid arthritis, continuing to smoke is associated with a more aggressive disease course. Smokers with RA report higher levels of joint pain and swelling and show higher disease activity scores. These scores, such as the DAS28, are a standard tool rheumatologists use to assess inflammation and symptom severity.
This increased disease activity leads to more significant and rapid joint damage. X-rays show that smokers with RA exhibit more severe bone erosion and a faster rate of cartilage loss than non-smokers. This deterioration of the joint’s structural integrity leads to greater long-term disability. A history of smoking is associated with a more than three-fold increased risk of rapid radiographic progression over five years.
Smoking also increases the likelihood of developing extra-articular manifestations, which are symptoms that occur outside the joints. The most common are rheumatoid nodules, which are firm lumps that form under the skin near pressure points like the elbows. Smokers are also at a higher risk for more severe complications like vasculitis (inflammation of the blood vessels) and RA-associated lung disease.
Interference with Rheumatoid Arthritis Treatments
Smoking also reduces the effectiveness of medications used to manage rheumatoid arthritis. Smokers find their treatments are less successful at controlling symptoms and slowing disease progression. This diminished response is seen across different classes of RA drugs, including traditional and modern therapies.
Smokers have a poorer response to Disease-Modifying Antirheumatic Drugs (DMARDs), like the first-line treatment methotrexate. This means they may not achieve the same symptom relief as non-smokers on the same medication. This can require higher doses or the addition of other drugs to their treatment plan.
This interference also applies to biologic therapies, which are newer drugs that target specific parts of the immune system. Smokers show a reduced response to TNF inhibitors, a common type of biologic agent. Because their medications are less effective, smokers struggle to reach low disease activity or remission, the primary goals of RA management.
The Role of Smoking Cessation in RA Management
Quitting smoking is a step individuals with RA can take to improve their health and the management of their condition. The benefits can be seen in both symptom control and long-term outcomes. Evidence shows that former smokers have lower disease activity compared to current smokers, as quitting can lead to a reduction in joint inflammation and pain.
This improvement in disease activity is complemented by an enhanced response to medication. Patients who stop smoking find their existing treatments become more effective, allowing them to achieve better control over their RA. By improving the efficacy of DMARDs and biologic therapies, smoking cessation helps slow joint damage and preserve physical function.
Beyond its direct effects on RA, quitting smoking also lowers the risk of cardiovascular disease, which is already elevated in people with RA due to chronic inflammation. Avoiding secondhand smoke is also beneficial, as exposure can contribute to inflammatory processes. Quitting is a component of a comprehensive management plan that works with medication to improve overall health.