The Effects of Indoor Pollutants Exposure on Allergy and Lung Inflammation: An Activation State of Neutrophils and Eosinophils in Sputum

Abstract

Background: To explore the inflammation phenotypes following indoor pollutants exposure based on marker expression on eosinophils and neutrophils with the application of chemometric analysis approaches. Methods: A cross-sectional study was undertaken among secondary school students in eight suburban and urban schools in the district of Hulu Langat, Selangor, Malaysia. The survey was completed by 96 students at the age of 14 by using the International Study of Asthma and Allergies in Children (ISAAC) and European Community Respiratory Health Survey (ECRHS) questionnaires. The fractional exhaled nitric oxide (FeNO) was measured, and an allergic skin prick test and sputum induction were performed for all students. Induced sputum samples were analysed for the expression of CD11b, CD35, CD63, and CD66b on eosinophils and neutrophils by flow cytometry. The particulate matter (PM2.5 and PM10), NO2, CO2, and formaldehyde were measured inside the classrooms. Results: Chemometric and regression results have clustered the expression of CD63 with PM2.5, CD11b with NO2, CD66b with FeNO levels, and CO2 with eosinophils, with the prediction accuracy of the models being 71.88%, 76.04%, and 76.04%, respectively. Meanwhile, for neutrophils, the CD63 and CD66b clustering with PM2.5 and CD11b with FeNO levels showed a model prediction accuracy of 72.92% and 71.88%, respectively. Conclusion: The findings indicated that the exposure to PM2.5 and NO2 was likely associated with the degranulation of eosinophils and neutrophils, following the activation mechanisms that led to the inflammatory reactions.

The association between PM2.5 concentration and the severity of acute asthmatic exacerbation in hospitalized children: A retrospective study in Chongqing, China

“…Three groups of kids with varying levels of PM2. 35 By increasing the pulmonary polymorphonuclear leukocyte (PMN)/white blood cell ratio and the PMN count in human peripheral blood, which was both mediated by VCAM-1, high PM2.5 exposure (>75 μg/m 3 ) was found to be able to cause inflammation and lung damage. This study involved 32,704 participants.…”

“…Khairul Nizam Mohd et aI. 's 35 study showed that exposure to PM2.5 can trigger inflammatory response mechanisms by causing eosinophils to granulate. 37 This finding also suggested that the primary alteration during exposure to ambient PM2.5 in the real world may be neutrophil inflammation brought on by infection and inflammation.…”

Integrated Human Exposure to Air Pollution

“…A cross-sectional study conducted in Selangor (Malaysia) focused on assessing the allergy and lung inflammation promoted by exposure to different indoor pollutants (PM 2.5 , PM 10 , NO 2 and CO 2 ) in scholar environments, based on marker expression on eosinophils and neutrophils [ 14 ]. A total of 96 students from eight suburban and urban schools answered to standardized questionnaires and their fractional exhaled nitric oxide (FeNO) was evaluated, along with allergic skin prick test and sputum induction (which was later analysed for the expression of CD11b, CD35, CD63 and CD66b on eosinophils and neutrophils).…”

Analysis of 19 urinary biomarkers of oxidative stress, nitrative stress, metabolic disorders, and inflammation using liquid chromatography–tandem mass spectrometry

“…Inflammation is a part of body’s defense in response to injury or infection, but chronic inflammation, which can result from exposure to environmental chemicals, plays a key role in many disorders, such as autoimmune diseases and asthma [ 23 – 25 ]. Eosinophils and neutrophils are two types of white blood cells that are activated to fight diseases, infections, and inflammation.…”

“…Eosinophils and neutrophils are two types of white blood cells that are activated to fight diseases, infections, and inflammation. Eosinophilia and neutrophilia are conditions in which the number of eosinophils or neutrophils, respectively, increases above the normal levels in affected tissue [ 23 , 26 ]. Under these conditions, neutrophil myeloperoxidase and eosinophil peroxidase overproduce halogenated species such as HOCl or HOBr that react with tyrosine, increasing chlorotyrosine (CY) [ 27 , 28 ] and bromotyrosine (BY) [ 28 ] levels, which are recognized as inflammatory biomarkers (IBs) [ 17 , 28 ].…”