Abstract
INTRODUCTION: Rheumatoid arthritis (RA) is a common autoimmune disease with a complex and poorly understood etiology that includes genetic, hormonal, and environmental factors. OBJECTIVE: Our objective was to assess current literature that investigated the association between exposure to environmental and occupational air pollutants and RA-related biomarkers rheumatoid factor (RF) and anti-citrullinated peptide antibody (ACPA). DESIGN: PubMed and Web of Science were used to identify epidemiological studies that measured or estimated air pollution and at least one RA biomarker. Information was charted for comparison of evidence, including pollutant(s) studied, exposure assessment, biomarker measurement, analysis method, study population, size, dates, adjustment variables, and findings. RESULTS: Several common air pollutants (including two mixtures) and a few dozen occupational inhalants were assessed in 13 eligible studies. Associations between industrial sulfur dioxide and particulate matter less than 2.5 µm in diameter with ACPA were observed most frequently, including associations between residential proximity to pollution sources and ACPA positivity. Consistency of associations with other pollutants was either not observed or limited to single studies. Three studies evaluated the modifying impact of SE alleles (a genetic factor associated with RA) and found that pollutant associations were stronger among participants positive for SE alleles. CONCLUSION: Based on mixed results, there was no consistent link between any single pollutant and RA-related biomarker outcomes. Comparisons across studies were limited by differences in study populations (e.g., by RA status, by sociodemographic groups) and study design (including designs focused on different sources of air pollution, methodological approaches with varying levels of potential exposure misclassification, and assessments of inconsistent biomarker cut-points). However, given that multiple studies reported associations between exposure to air pollution and RA biomarkers, continued exploration utilizing studies that can be designed with a more robust causal framework, including continued consideration of effect modification by genetic status, may be necessary.