Background Air pollution is caused by substances that consists of solid particles, liquid droplets, or gases including carbon monoxide (CO), nitrate (NO), sulfur dioxide (SO2), ozone (O3), lead, toxic product from tobacco smoke and particulate matter (PM). Inhaled air pollutants can induce oxidative stress and this can contribute to trigger or exacerbate systemic inflammation and autoimmunity. The relations of air pollution with rheumatic diseases have been reported, especially in rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis and juvenile idiopathic arthritis. Gout is an inflammatory disease caused by deposition of monosodium urate (MSU) crystals. Acute gout flares is initiated with activation of the NLRP3 inflammasome and release of IL-1β by MSU crystals. PM <10μm in diameter (PM10) exposure has been reported to activate NLRP3 inflammasome in airway epithelial cells. The influence of air pollutants including PM10 to acute gout flares has not yet been known.
Objectives To investigate the association between air pollution and acute gout flares
Methods We obtained data from the National Health Insurance Database between 2007 and 2015 in Incheon, Republic of Korea by Health Insurance Review and Assessment (HIRA) service. The HIRA data included age, gender, national health insurance type, diagnosis code based on the International Classification of Diseases version 10 (ICD–10), visit date, procedure code, and prescription code. We studied the subjects of age ≥19 years who visited emergency department (ED) due to acute gout flare between 2008 and 2015. Acute gout flare was defined as an ED visit due to gout (ICD-10, M10) with any prescription of non-steroidal anti-inflammatory drugs (NSAIDs), acetaminophen, steroids, or colchicine. Comorbidities and prescription history were collected. The data of ambient PM10, O3, NO2, CO, and SO2 levels were obtained from the Ministry of Environment data sources. We performed time-series study. The generalized additive models with Poisson distribution were used to investigate the association between single air pollutant level and acute gout flares. To examine the delayed effect of air pollutant exposure before the ED visit day on acute gout flare, we established cumulative lag models (averaging levels of consecutive days).
Results The total number of ED visits for acute gout flare from 2008 to 2015 in Incheon was 139,665, including 48.8% of 40–59 year-old men. The ED visits for acute gout attack were most likely to occur in summer (29.1%). Among the ED cases of acute gout flares, 11.0% had a prescription history of allopurinol or febuxostat for the six months before the visit. The relative risks (RRs) of PM10 and O3 at lag0–7 were 1.02 (1.01–1.03) and 1.07 (1.06–1.08), respectively. NO2, CO, and SO2 did not show significant association with acute gout flares. Acute gout flares showed more significant association with O3 in the cases with hypertension and use of NSAIDs, colchicine, or statins. PM10 was more significantly associated with acute gout flares in the cases with congestive heart failure.
Conclusions Ambient air pollution can induce acute gout flares and its influence on acute gout flares may increase according to the comorbidities or medications.
Disclosure of Interest None declared