Risk for systemic autoimmune rheumatic diseases higher in areas with air pollution
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Exposure to fine particulate matter — specifically particles 2.5 µm or less in diameter, or PM2.5 — in the air signals a higher risk for systemic autoimmune rheumatic diseases, according to data published in Arthritis Research & Therapy.
“Air pollution may stimulate the immune system directly or indirectly, and increasing evidence suggests that this could be a trigger for systemic autoimmune rheumatic disease — that is, it could possibly one of the ‘missing links’ explaining why some people develop these serious, disabling autoimmune conditions,” Sasha Bernatsky, MD, PhD, of the division of clinical epidemiology at McGill University, in Montreal, told Healio. “To date, no studies of air pollution and the incidence of SARDs have been published. We aimed to fill that knowledge gap.”
To investigate the link between air pollution and systemic autoimmune rheumatic diseases (SARDs), Bernatsky and colleagues created a population-based cohort using provincial administrative health data from Quebec, Canada. The cohort included 6 million adults who were aged 18 years or older as of April 1, 2000. To be included in the cohort, participants were required to have lived in Quebec for 4 years prior to enrollment and been without SARDs during that time. Participants meeting the requirement were added to the cohort each year following 2000.
Incident SARD cases were defined based on two or more physician billing claims with relevant codes within 2 years, including a code from a rheumatologist. Included SARDs were systematic lupus erythematosus, Sjögren’s syndrome, scleroderma, polymyositis, dermatomyositis, polyarteritis nodosa and related conditions, polymyalgia rheumatic, other necrotizing vasculopathies and undifferentiated connective tissue disease.
Bernatsky and colleagues used PM2.5 estimates from 2000 through 2012 from the Goddard Earth Observation System. Additionally, ozone concentrations were averaged for calendar years between 2002 and 2012. The researchers assigned annual average daily particulate concentrations and ozone to participants based on their residential addresses.
According to the researchers, the adjusted HR for SARDs relating to one interquartile range increase in PM2.5 was 1.12 (95% CI, 1.08-1.15). There did not appear to be any association between ozone and SARD incidence, the authors wrote.
“As rheumatologists, we need to remain aware of increasing current evidence linking air pollution and adverse rheumatic disease outcomes,” Bernatsky said. “We need to be prepared for questions from patients about what they can do to limit their exposure to harmful air pollution. I encourage all people to take actions toward reducing their ecological footprints, for example, by biking, carpooling, walking whenever possible. We can also learn how to advocate for policy changes that could lead to better air quality.”
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J. Nicholas Manwaring, MSN, APRN, FNP-C
The factors that contribute to the onset of systemic autoimmune rheumatic diseases (SARDs) are not fully understood. Genetics definitely plays a role, but it has long been speculated that there are environmental factors that also contribute to SARDs onset. However, there have been limited studies to show environmental associations to date. Part of the reason for the lack of available research is the difficulty in compiling data on such a large population.
This study was uniquely successful because it was able to analyze the health data of all the residents of the province of Quebec (with a population of approximately 8.2 million people in 2013). A sample of this size was only made possible because of the provincial universal health care of Canada, which provides electronic health records of every one of its citizens who have ever sought health care.
This study helps to shed some light on a potential etiology of SARDs by showing a definite association between SARDs incidence and prolonged exposure to ambient air pollutants, namely fine particulate matter of diameter 2.5 µm or less. Perhaps with the wide use of electronic health records worldwide, larger population-based samples, such as this one, will become more readily available for analysis. This could hopefully lead to finding more modifiable causes of autoimmune diseases like SARDs, which could guide the implementation of preventative measures.
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David A. McLain, MD, MACR, FACP, FRCP
Air pollution and autoimmunity. Before you dismiss this as yet another nonsensical association, realize that there are a number of scientific studies on this topic. I previously commented on a paper regarding the association of Sept. 11 dust in New York to autoimmunity in Healio Rheumatology. There is an excellent review article published by K. Michael Pollard from the Scripps Institute that details what is known and hypothesized regarding the lung, particles, fibers, nanoparticles and autoimmunity.
We know that cigarette smoking, which shares some toxins with fossil fuel emissions, has been associated with rheumatoid arthritis and with the development of anti-citrullinated protein antibodies (ACPA). Epidemiological studies have found associations between occupational silica exposure and SLE, scleroderma, and ANCA-associated vasculitis. More recently, exposure to silica-containing dust from artificial stone fabrication of countertops has been linked to both silicosis and autoimmune disease.
Researchers at the University of Verona have found that long-term exposure to high levels of air pollution was associated with an approximately 40% higher risk for rheumatoid arthritis, a 20% higher risk for inflammatory bowel disease such as Crohn’s and ulcerative colitis, and a 15% higher risk for connective tissue diseases such as lupus.
Fibrous — from asbestos — and non-fibrous — from cigarette smoke and crystalline silica — fine particulates (PM2.5) have been linked to pre-clinical autoimmunity and autoimmune diseases.
The hypothesis is that inhalation of particulate material known to be associated with human autoimmune diseases results in pathological processes including toxicity and, hence, tissue damage with the release of nucleic acids and other damage associated molecular patterns (DAMPS), oxidative stress, chronic inflammation, post-translational modification of self-antigens and the formation of lymphoid follicles, which provide an environment for the accumulation of autoreactive B and T cells necessary for the development and persistence of autoimmune responses, leading to disease.
A part of this process includes Toll-like receptors (TLRs), production of cytokines, expansion of autoreactive T and B cells and production of autoantibodies.
Particulate exposures are among the initiating events most closely linked to human autoimmune diseases, with the lungs as a major site of pathological and immunological events leading to clinical disease. An unresolved issue is how expression of particulate-induced autoreactivity in the lung results in disease specific pathogenesis in distant organs (eg, kidney in SLE or joints in RA). Continued research in this area is of importance in our search for the origin of our diseases.
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