Interactions between an individual’s genetic background and their exposure to environmental factors are thought to result in a cascade of immune reactions, ultimately leading to the development of autoimmune diseases such as rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), systemic lupus erythematosus (SLE) and juvenile dermatomyositis.1,2 For example, an environmental factor that conclusively affects susceptibility to the development of RA is smoking, but with risk magnified by the presence and number of copies of shared epitope.3,4
Air pollution is a recognized risk factor for respiratory and cardiovascular disease, but has also been associated with immune-mediated diseases, such as inflammatory bowel disease and multiple sclerosis.5,6 Air pollution may mediate its effect on autoimmune disease by directly stimulating an inflammatory response or indirectly through alterations in the microbiome.7-9 Thus, air pollution has been hypothesized to influence the development of rheumatic diseases. In this review, we summarize sources of air pollution, how levels can be measured and what evidence exists for associations between rheumatic disease development and exposure to air pollution.
Sources of Air Pollution
Air pollution comprises a complex mixture of particles and gases from a variety of industrial and private sources. Fossil fuel use is the main source of emission of airborne pollutants in developed countries. In general, exposure to air pollution can result in activation of the immune response; an early study demonstrated measurable differences in immunoglobulins, complement components, haptoglobin and a-1-glycoprotein between a female population exposed to higher compared to lower atmospheric pollution.10
Particulate matter (PM) <2.5µm in size (PM2.5) has been the focus of most of the published literature on air pollution and health. PM air pollution is a mixture of solid, liquid, or solid and liquid particles suspended in air that can travel long distances from remote sources or be concentrated by weather-related factors (e.g., winter inversions). It is largely composed of ammonium sulfate and ammonium nitrate derived from diesel fuel combustion and products of motor vehicle gas combustion and coal-powered power plants.11,12 PM2.5 particles can penetrate the gas-exchange region of the lung, creating oxidative stress and triggering activation of macrophages and epithelial cells in the alveolar tissues, ultimately resulting in an inflammatory response and secretion of pro-inflammatory cytokines.11,13
Other measured pollutants include particulate matter <10µm in size (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2). PM10 particles are larger and are, therefore, less likely to be carried from distant sources or penetrate the trachea-bronchial tree. SO2 is formed during petroleum refining or cement manufacturing and also from coal-fired power plants, locomotives, ships and some non-road diesel-burning equipment.14