Background: Sensitisation to is linked to worse outcomes in patients with COPD; however, its prevalence and clinical implications in domestic (residential) settings remains unknown.
Methods: Individuals with COPD (n=43) recruited in Singapore had their residences prospectively sampled and assessed by shotgun metagenomic sequencing including indoor air, outdoor air and touch surfaces (a total of 126 specimens). The abundance of environmental and the occurrence of (Asp f) allergens in the environment were determined and immunological responses to allergens determined in association with clinical outcomes including exacerbation frequency.
The evidence associating traffic-related air pollution (TRAP) with allergic asthma is growing, but the underlying mechanisms for this association remain unclear. The airway epithelium is the primary tissue exposed to TRAP, hence understanding its interactions with TRAP and allergen is important. Diesel exhaust (DE), a paradigm of TRAP, consists of particulate matter (PM) and gases.
View Article and Find Full Text PDFTraffic-related air pollution (TRAP) exposure is associated with systemic health effects, which can be studied using blood-based markers. Although we have previously shown that high TRAP concentrations alter the plasma proteome, the concentration-response relationship between blood proteins and TRAP is unexplored in controlled human exposure studies. We aimed to identify concentration-dependent plasma markers of diesel exhaust (DE), a model of TRAP.
View Article and Find Full Text PDFAir pollution exposure is harmful to human airways, and its impacts are best studied using concentration-response relationships. However, most concentration-response research on airway health has investigated chronic exposures, with less being known about acute effects, which can be robustly studied using controlled human exposures. To investigate the concentration relationship between airway health measures and diesel exhaust (DE).
View Article and Find Full Text PDFBackground: Traffic-related air pollution (TRAP) exposure causes adverse effects on wellbeing and quality of life, which can be studied non-invasively using self-reported symptoms. However, little is known about the effects of different TRAP concentrations on symptoms following controlled exposures, where acute responses can be studied with limited confounding. We investigated the concentration-response relationship between diesel exhaust (DE) exposure, as a model TRAP, and self-reported symptoms.
View Article and Find Full Text PDFBackground: Autoimmunity has been reported in patients with severe coronavirus disease 2019 (COVID-19). We investigated whether anti-nuclear/extractable-nuclear antibodies (ANAs/ENAs) were present up to a year after infection, and if they were associated with the development of clinically relevant post-acute sequalae of COVID-19 (PASC) symptoms.
Methods: A rapid-assessment line immunoassay was used to measure circulating levels of ANAs/ENAs in 106 convalescent COVID-19 patients with varying acute phase severities at 3, 6 and 12 months post-recovery.
J Allergy Clin Immunol
August 2022
Background: Exposure to traffic-related air pollution is associated with increased morbidity and mortality. Negative health impact of diesel exhaust (DE) exposure may in part be mediated via epigenetic modulation. Ten-eleven translocation (TET) enzymes catalyze the active DNA demethylation process and play important roles in epigenetic regulation.
View Article and Find Full Text PDFThere is growing evidence that chronic obstructive pulmonary disease (COPD) can be caused and exacerbated by air pollution exposure. To document the impact of short-term air pollution exposure on inflammation markers, proteases, and antiproteases in the lower airways of older adults with and without COPD. Thirty participants (10 ex-smokers with mild to moderate COPD and 20 healthy participants [9 ex-smokers and 11 never-smokers]), with an average age of 60 years, completed this double-blinded, controlled, human crossover exposure study.
View Article and Find Full Text PDFEicosanoids are potent regulators of homeostasis and inflammation. Co-exposure to allergen and diesel exhaust (DE) have been shown to lead to eosinophilic inflammation, impaired airflow, and increased airway responsiveness. It is not clear whether eicosanoids mediate the mechanism by which these exposures impair lung function.
View Article and Find Full Text PDFBackground: Thrombotic thrombocytopenic purpura (TTP) is a rare but potentially fatal disorder caused by ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) deficiency. Prompt identification/exclusion of TTP can thus be facilitated by rapid ADAMTS13 testing. The most commonly utilized (enzyme-linked immunosorbent assay [ELISA]-based) assay takes several hours to perform and so does not generally permit rapid testing.
View Article and Find Full Text PDFHeparin induced thrombocytopenia (HIT) is a rare but potentially fatal complication of heparin therapy. In some patients, HIT causes platelet activation and thrombosis (sometimes abbreviated HITT), which leads to adverse clinical sequalae ('pathological HIT'). The likelihood of HIT is initially assessed clinically, typically using a scoring system, of which the 4T score is that most utilised.
View Article and Find Full Text PDFDiesel exhaust (DE), an established model of traffic-related air pollution, contributes significantly to the global burden of asthma and may augment the effects of allergen inhalation. Newer diesel particulate-filtering technologies may increase NO emissions, raising questions regarding their effectiveness in reducing harm from associated engine output. To assess the effects of DE and allergen coexposure on lung function, airway responsiveness, and circulating leukocytes, and determine whether DE particle depletion remediates these effects.
View Article and Find Full Text PDFObjective: To assess lifestyle and pharmacological interventions aiming to delay type 2 diabetes mellitus (T2DM) in prediabetes.
Methods: We searched the Cochrane Register of Controlled Trials, MEDLINE, EMBASE, CINAHL, PsycINFO, Web of Science, BIOSIS and LILACS databases, examined reference lists and contacted authors. We included randomised controlled trials (RCTs) on both lifestyle and medication interventions in prediabetes.