Particulate matter (PM) is the principal component of air pollution. PM includes a range of particle sizes, such as coarse, fine, and ultrafine particles. Particles that are <100 nm in diameter are defined as ultrafine particles (UFPs). UFPs are found to a large extent in urban air as both singlet and aggregated particles. UFPs are classified into two major categories based on their source. Typically, UFPs are incidentally generated in the environment, often as byproducts of fossil fuel combustion, condensation of semivolatile substances or industrial emissions, whereas nanoparticles are manufactured through controlled engineering processes. The primary exposure mechanism of PM is inhalation. Inhalation of PM exacerbates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain unclear. This review offers insights into the mechanisms by which particles, including UFPs, influence airway inflammation and discusses several mechanisms that may explain the relationship between particulate air pollutants and human health, particularly respiratory health. Understanding the mechanisms of PM-mediated lung injury will enhance efforts to protect at-risk individuals from the harmful health effects of air pollutants.

Recent investigations suggest genetic susceptibility of allopurinol-induced severe cutaneous adverse reactions (SCARs). However, the strength of association was variable according to phenotypes and ethnic backgrounds. To explore genetic markers for allopurinol-induced SCARs in Koreans, we genotyped human leukocyte antigen (HLA) class I alleles of 25 cases of allopurinol-induced SCARs (20 cases of drug-induced hypersensitivity syndrome and five cases of Stevens–Johnson syndrome/toxic epidermal necrolysis) and 57 patients tolerant to allopurinol. Frequencies of B*5801 [92.0 vs. 10.5%, P_c=2.45×10⁻¹¹, odds ratio (OR)=97.8], Cw*0302 (92.0 vs. 12.3%, P_c=9.39×10⁻¹¹, OR=82.1), and A*3303 (88.0 vs. 26.3%, P_c=3.31×10⁻⁶, OR=20.5) were significantly higher in SCARs compared with tolerant controls. In contrast, A*0201 was not found in SCARs patients despite relatively high frequency in tolerant controls (29.8%). We found strong positive association of HLA-B*5801 and negative association of HLA-A*0201 with the development of allopurinol-induced SCARs in the Korean population.

Background: There are limited data regarding the relationship between interstitial lung disease (ILD) and the natural course of COVID-19. In this study, we investigate whether patients with ILD are more susceptible to COVID-19 than those without ILD and evaluate the impact of ILD on disease severity in patients with COVID-19.Methods: A nationwide cohort of patients with COVID-19 (n=8070) and a 1:15 age-, sex- and residential area-matched cohort (n=121 050) were constructed between 1 January 2020 and 30 May 2020 in Korea. We performed a nested case–control study to compare the proportions of patients with ILD between the COVID-19 cohort and the matched cohort. Using the COVID-19 cohort, we also evaluated the risk of severe COVID-19 in patients with ILDversusthose without ILD.Results: The proportion of patients with ILD was significantly higher in the COVID-19 cohort than in the matched cohort (0.8%versus0.4%; p<0.001). The odds of having ILD was significantly higher in the COVID-19 cohort than in the matched cohort (adjusted OR 2.02, 95% CI 1.54–2.61). Among patients in the COVID-19 cohort, patients with ILD were more likely to have severe COVID-19 than patients without ILD (47.8%versus12.6%), including mortality (13.4%versus2.8%) (all p<0.001). The risk of severe COVID-19 was significantly higher in patients with ILD than in those without ILD (adjusted OR 2.23, 95% CI 1.24–4.01).Conclusion: The risks of COVID-19 and severe presentation were significantly higher in patients with ILD than in those without ILD.

Introduction: Chronic systemic corticosteroid (CS) therapy is associated with an increased risk of mortality in patients with many chronic diseases. However, it has not been elucidated whether chronic systemic CS therapy is associated with increased mortality in patients with asthma. The aim of this study was to determine the effects of chronic systemic CS therapy on long-term mortality in adult patients with asthma.Methods: A population-based matched cohort study of males and females aged ≥18 years with asthma was performed using the Korean National Health Insurance Service database from 2005 to 2015. Hazard ratio (HR) with 95% confidence interval for all-cause mortality among patients in the CS-dependent cohort (CS use ≥6 months during baseline period) relative to those in the CS-independent cohort (CS use <6 months during baseline period) was evaluated.Results: The baseline cohort included 466 941 patients with asthma, of whom 8334 were CS-dependent and 458 607 were CS-independent. After 1:1 matching, 8334 subjects with CS-independent asthma were identified. The HR of mortality associated with CS-dependent asthma relative to CS-independent asthma was 2.17 (95% CI 2.04–2.31). In patients receiving low-dose CS, the HR was 1.84 (95% CI 1.69–2.00); in patients receiving high-dose CS, the HR was 2.56 (95% CI 2.35–2.80).Conclusions: In this real-world, clinical practice, observational study, chronic use of systemic CS was associated with increased risk of mortality in patients with asthma, with a significant dose–response relationship between systemic CS use and long-term mortality.

Previous studies have suggested that respiratory virus infections may be associated with new-onset asthma. However, whether coronavirus disease 2019 (COVID-19) is associated with an increased risk of new-onset asthma remains unclear. We aimed to evaluate whether recent COVID-19 infection increases the risk of new-onset asthma and whether COVID-19 vaccination could mitigate this risk. We constructed three different study designs using the Korean National Health Insurance claim-based database: Study 1: COVID-19 diagnosed participants (COVID-19 cohort) and their matched controls; Study 2: COVID-19 vaccinated participants (vaccination cohort) and their matched controls; Study 3: vaccination cohort and their matched controls, excluding participants diagnosed with COVID-19. In Study 1, 1.6% of the COVID-19 cohort and 0.7% of the matched cohort developed new-onset asthma, with incidences of 31.28 and 14.55 per 1,000 person-years, respectively (p<0.001). COVID-19 cohort had a higher risk of new-onset asthma (adjusted hazard ratio [aHR], 2.14; 95% confidence interval [CI], 1.88-2.45) than matched controls. In Study 2, vaccination cohort had a lower risk of new-onset asthma than matched controls (aHR, 0.82; 95% CI, 0.76-0.89). However, among participants without a COVID-19 diagnosis, COVID-19 vaccination was not associated with a reduced risk of new-onset asthma in Study 3 (aHR, 0.95; 95% CI, 0.87-1.04). In subgroup analysis, the risk of new-onset asthma was significantly lower in fully vaccinated participants and higher in older individuals and in those with diabetes mellitus compared to their counterparts. COVID-19 was associated with a higher incidence of new-onset asthma, which might be preventable by COVID-19 vaccination.