# Cigarette Smoking: A Modifiable Environmental Factor in the Pathogenesis of Rheumatoid Arthritis

## TL;DR

Cigarette smoking increases the risk of rheumatoid arthritis, especially in genetically susceptible individuals, by triggering autoimmune responses and altering microbiota.

## Contribution

This paper reviews how smoking acts as a modifiable environmental factor in rheumatoid arthritis pathogenesis through various biological mechanisms.

## Key findings

- Smoking increases RA risk, particularly in individuals with specific HLA subtypes.
- Smoking may induce neoantigens and disrupt microbiota, promoting autoimmunity.
- Avoiding smoking early can reduce autoimmunity risk and aid in RA prevention.

## Abstract

Cigarette smoking is increasingly recognized as a significant modifiable environmental factor in the pathogenesis of rheumatoid arthritis (RA). This review discusses the potential mechanisms through which smoking contributes to the development of RA, particularly in genetically susceptible individuals. Research has indicated that the onset of autoimmune diseases, including RA, is often preceded by a prolonged prodromal phase characterized by autoantibodies such as anti-citrullinated peptide antibodies and rheumatoid factor. Smoking has been demonstrated to increase the risk of RA, especially in individuals with specific human leucocyte antigen subtypes, and modulate the disease activity. The pathological impact of tobacco smoke may involve the induction of cellular damage and death, leading to the production of neoantigens that trigger autoimmune responses. In addition, smoking may disrupt the microbiota in the respiratory tract and intestines, which may further influence disease progression. Thus, avoiding smoking from an early age is strongly suggested in decreasing the risk of developing autoimmunity and also as a means to establish of developing preventive strategies against autoimmune diseases such as RA.