Abstract and Introduction
Abstract
Background: Systemic lupus erythematosus (SLE) is a chronic disease of unclear etiology, characterized by an overactive immune system and the production of antibodies that may target normal tissues of many organ systems, including the kidneys. It can arise at any age and occurs mainly in women.
Objective: Our aim was to evaluate the potential influence of particulate matter (PM) air pollution on clinical aspects of SLE.
Methods: We studied a clinic cohort of SLE patients living on the island of Montreal, followed annually with a structured clinical assessment. We assessed the association between ambient levels of fine PM [median aerodynamic diameter ≤ 2.5 μm (PM2.5)] measured at fixed-site monitoring stations and SLE disease activity measured with the SLE Disease Activity Index, version 2000 (SLEDAI-2K), which includes anti–double-stranded DNA (anti-dsDNA) serum-specific autoantibodies and renal tubule cellular casts in urine, which reflects serious renal inflammation. We used mixed effects regression models that we adjusted for daily ambient temperatures and ozone levels.
Results: We assessed 237 patients (223 women) who together had 1,083 clinic visits from 2000 through 2007 (mean age at time of first visit, 41.2 years). PM2.5 levels were associated with anti-dsDNA and cellular casts. The crude and adjusted odds ratios (reflecting a 10-μg/m increase in PM2.5 averaged over the 48 hr prior to clinical assessment) were 1.26 [95% confidence interval (CI), 0.96–1.65] and 1.34 (95% CI, 1.02–1.77) for anti-dsDNA antibodies and 1.43 (95% CI, 1.05–1.95) and 1.28 (0.92–1.80) for cellular casts. The total SLEDAI-2K scores were not associated with PM2.5 levels.
Conclusions: We provide novel data that suggest that short-term variations in air pollution may influence disease activity in established autoimmune rheumatic disease in humans. Our results add weight to concerns that pollution may be an important trigger of inflammation and autoimmunity.
Introduction
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unclear etiology, with a prevalence as high as 1 in 2,500 women (Bernatsky et al. 2007). It is characterized by an overactive immune system that targets normal tissue in nearly any body organ. The resulting inflammation causes dysfunction and damage; involvement of major organs such as the kidneys can be particularly devastating and even life-threatening (Bernatsky et al. 2007).
The factors driving SLE are complex, but it is clear that there are definite, albeit ill-defined, exogenous triggers. Different possible environmental triggers have been considered, but at present there are relatively few relevant studies (Parks and Cooper 2006) and essentially no work has examined the effect of air pollution on SLE manifestations. This is an important knowledge gap, because there is a growing interest in pollution emissions and particulate matter (PM) exposures and their effects on health. This interest stems from recent data that have suggested that these exposures may be important triggers of systemic inflammation that could have important effects in terms of autoimmunity. Recent data have suggested that these exposures may be important triggers of systemic inflammation [for a review, see U.S. Environmental Protection Agency (EPA) 2004] that could have important effects in terms of autoimmunity.
Our aim in this study was to evaluate the potential influence of PM air pollution on the clinical course of SLE. We have focused on the effects of variations in levels of fine ambient PM with median aerodynamic diameter ≤ 2.5 μm (PM2.5). The main sources of PM2.5 in the region of the study include road-vehicle emissions and industrial emissions. Such small particles enter the body through airways and can affect immune system pathways (U.S. EPA 2004).