This is the first large population study to evaluate the exposure of ambient PM2.5 and the occurrence of cSLE over a long period of time. This longitudinal study showed that higher PM2.5 exposure concentrations increased the incidence rate of cSLE in Taiwanese children and suggests that ambient PM2.5 exposures may be a trigger for the development of cSLE.
Seventy years ago, the historic smog disaster, the 1948 Donora smog, killed 20 people and caused respiratory problems for 6,000 out of the 14,000 people living in Donora. [9] Since then, interest has increased regarding the harmful effects of air pollution. In 1963, the Clean Air Act was established and was last amended in 1990; it requires the Environmental Protection Agency (EPA) to set National Ambient Air Quality Standards (NAAQS) for pollutants considered harmful to public health and the environment. [10] The World Health Organization (WHO) also challenged governments around the world to improve air quality in their cities to protect peoples’ health. [11] However, from the report of WHO, there are still approximately 4.2 million deaths resulting from exposure to ambient air pollution and an additional 3.8 million deaths resulting from exposure to household air pollution, every year. Moreover, several model projections indicate that the contribution of outdoor air pollution to premature mortality could double by 2050. [4]
Air pollutants can be found anywhere in the air, both outdoors and indoors. Typically, the environment contains a mixture of gaseous and particulate pollutants. [12] Most air pollutants originate from human activities and emissions of ambient air pollution from regional sources may travel long distances across national borders. [13] To protect air quality in the US, the EPA has mandated air quality standards called NAAQS for the following six air pollutants: ozone (O3), lead (Pb), total suspended particulates (TSP) including PM2.5 and PM10, carbon monoxide (CO), sulfur dioxide (SO2), and nitrogen oxides. These six air pollutants are called “criteria pollutants”. [14] An increasing number of epidemiological studies have demonstrated that exposure to air pollutants has harmful effects on cardiovascular and respiratory morbidity and mortality, particularly in children. [15–18] Children are known to have more adverse health effects to air pollution because of their higher minute ventilation, immature immune system, tendency to spend more time outdoors, and the continuing development of their lungs.[17–20]
PM 2.5 causes more of a burden than other air pollutants because these particles are composed of sulfates, metals, and other toxic substances that are adsorbed into their molecules. [19] The physical and chemical composition and size of airborne particulate matter vary widely with time and space. [20, 21] The airborne particulate matter originates from sources such as transportation-related emissions, road/soil dust, biomass burning, and agricultural activities which enter the atmosphere by anthropogenic and natural pathways. [22] PM 2.5 are more toxic because they can reach deeper areas of the respiratory tract and can be absorbed into the bloodstream, resulting in local and systemic inflammation. Exposed to excessive PM 2.5 results in numerous diseases such as asthma, chronic bronchitis, cancer, cardiovascular disease, diabetes, and premature death.[4, 23–26] For every 10 µg per cubic meter in PM 2.5, all-cause mortality increases by 7.3%.[27]
The associations between air pollution and immune-inflammatory responses have been noticed. Exposure to air pollution may cause major autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), and type 1 diabetes mellitus (T1DM). [28] Exposure to particulate matter (PM10), sulfur dioxide, nitrogen dioxide (NO2), ozone, and carbon monoxide was found to be associated with high disease activity in juvenile-onset SLE. [6] A recent Taiwanese study discovered a positive association of NO2 exposure with the development of SLE in adults. [29] A recent Brazilian study revealed that exposure to inhalable fine particles increases airway inflammation and systemic inflammation in cSLE patients. Although the exact mode of onset and disease progression of SLE remains elusive, the urban-rural difference in prevalence, clustering of disease prevalence around polluted regions, and low concordance rates among monozygotic twins with SLE (around 24%) indicate that environment has a strong impact on SLE. [30] Experimental data strongly suggest that a complex interaction between the exposome (or environmental influences) and genome (genetic material) produce epigenetic changes (epigenome) that can alter the expression of genetic material and lead to the development of SLE in susceptible individuals. [30] Our study has some limitations. First, since air pollution is a dynamic mixture of different toxicants from natural and anthropogenic sources, including PM, O3, CO, SO2, nitrogen oxides (NOx), and so on, [17] monitoring the concentration of PM2.5 exposure does not fully eliminate the co-effects of mixed air pollutants. Second, since the monitoring stations are fixed outdoors, they may not reflect the true exposure level to air pollutants in patients. Third, since this is a retrospective study, we cannot control important confounders such as genetic factors, family history of autoimmune disease, eating habits, leisure activity, sun protection habits, attitudes, body surface area, and cigarette smoking.