Abstract
The current major issue affecting global populations in terms of health, economy, and society is the problem of pollution from airborne particulate matter (PM). This has led to a notable increase in deaths due to exposure to fine PM, especially PM2.5, over the past decade. Moreover, there are reports indicating the economic impact of hazardous PM, accounting for 1.4-2.3% of the overalls in China. PM can be categorized into three sizes based on their diameters: coarse PM, fine PM, and ultrafine PM. Previous studies have shown that fine PM, specifically PM2.5, greatly affects health and is linked to the development and exacerbation of respiratory diseases, including asthma. However, there is still a lack of standardized studies on the impact of PM2.5 from various locations in Thailand on the development of respiratory disease in both normal individuals and allergic rhinitis (AR) patients. Additionally, there's also a need for distinct studies on the physical properties associated with causing diseases. This study aims to find the impact of PM2.5 on AR, using primary nasal epithelia from AR patients as representatives in the study to establish prevention, alleviation, and treatment of AR caused by PM2.5 from various sources in Thailand. The study revealed that respiratory epithelial cell lines, which are RPMI-2650 representing upper airway epithelium from nasal passages, and A549, H1975, and H2228 representing lower airway epithelium from the lung epithelium, responded differently to PM10 and PM2.5. PM10 was found to be less toxic to RPMI-2650 and H2228 cells compared to H1975 cells. However, PM2.5, obtained from car exhaust, was more toxic to H1975 cells than to H2228 cells. In the study of cytokine production, it was found that the H1975 and H2228 cells, when exposed to PM10 dust, produced different levels of cytokines. Specifically, the H2228 cells generated more TGF-β cytokines compared to the H1975 cells. This disparity might be related to the cellular responses of each type to particulate matter. Analysis of PM10 and PM2.5 components collected from urban areas in Bangkok revealed elements with short to medium half-lives, such as Aluminum (Al-28), Chlorine (Cl-38), Manganese (Mn-56), Sodium (Na-24), Vanadium (V-52), and Calcium (Ca-49). Furthermore, this study observed the impact on primary nasal epithelia isolated from AR patients. It revealed that PM2.5 posed toxicity to primary nasal epithelial cells, leading to reduced cell survival rates. This toxicity induced apoptotic cell death and escalated the production of Reactive Oxygen Species (ROS) within the cells. Consequently, it affected the functionality of both innate and adaptive immunity systems, triggering the secretion of varying cytokines like IL-1β, IL-6, and TNF-α, notably influencing the inflammatory processes of the cells. Higher levels of IL-6 secretion and increased expression of the IL-1β gene were noted in the group with AR compared to the control group (non-AR). Additionally, there was an increase in the secretion of various other cytokines in peripheral blood mononuclear cells (PBMC) from AR patients, including IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-17, G-CSF, GM-CSF, MIP-1β, and TNF-α. In addition, there was an observed trend towards increased activity of the SOD and CAT enzymes in primary nasal epithelial cells. Thus, further studies are necessary to thoroughly investigate these mechanisms. Furthermore, this ex-vivo model using nasal epithelium cells from AR patients in a primary cell culture may be used to help predict the levels or quantities of PM2.5 in the atmosphere (by computing from the amount of particles in the ex-vivo model back to atmospheric levels), at what thresholds could cause health impacts or disrupt daily life for vulnerable groups, such as AR patients. This could be pivotal in establishing a national guideline and novel therapeutic intervention to alleviate symptoms of AR during the high season of PM2.5.
