PM2.5 induced/aggravated allergic diseases? Free Presentation Template by EaTemp Recommended AQG levels and interim targets Overview of allergic diseases Allergic diseases, or hypersensitivity disorders, involve the immune system’s excessive or inappropriate response to foreign antigens, leading to hypersensitivity reactions that can impact multiple systems and damage various organs.ß Common allergic conditions include allergic rhinitis (AR), atopic dermatitis (AD), and allergic asthma (AA). ß Currently, affect an estimated 30–40 % of the global population, with projections indicating that approximately 50 % of the world’s population may be affected by 2050, resulting in a substantial socioeconomic burden. € ß Zhao ZY. Expert consensus on diagnosis and treatment of allergic diseases in children. Chin J Pediat 2019;57(3). https://doi.org/10.3760/cma.j.issn.0578- 1310.2019.03.002. € Burbank AJ, Sood AK, Kesic MJ, Peden DB, Hernandez ML. Environmental determinants of allergy and asthma in early life. J Allergy Clin Immunol 2017; 140(1):1–12. https://doi.org/10.1016/j.jaci.2017.05.010. Mechanism of PM2.5 induced/aggravated allergic diseases the mechanisms which induces or worsens allergic diseases remain unclear. The latest experimental research findings indicate that PM2.5 induces senescence in airway smooth muscle cells and elicits a senescence-associated secretory phenotype (SASP) through autophagy-induced GATA4/TRAF6/NF-κB signaling, thereby promoting the synthesis of collagen-i and α-smooth muscle actin ( α-SMA) and leading to airway smooth muscle remodeling. Cheng PP, Yu F, Chen SJ, Feng X, Jia ZH, Hu SH, et al. PM2.5 exposure-induced senescence-associated secretory phenotype in airway smooth muscle cells contributes to airway remodeling. Environ Pollut 2024;347:123674. https://doi. org/10.1016/j.envpol.2024.123674. https://www.biorender.com/template/senescence-associated-secretory-phenotype-sasp disrupts barrier function the potential mechanism of PM2.5 exposure resulting in disruption of the barrier function. https://www.sciencedirect.com/science/article/pii/S2949913524000120 increases oxidative stress the potential mechanism of PM2.5 exposure resulting in increased OS Created with MedPeer (www.medpeer.cn). interferes with immune balance the potential mechanism of PM2.5 exposure causing interference with the immune balance. https://www.sciencedirect.com/science/article/pii/S2949913524000120 synergistic sensitization effect the potential mechanism of the mechanism of PM2.5 inducing/aggravating allergic diseases. https://www.sciencedirect.com/science/article/pii/S2949913524000120 The results demonstrate that exposure with PM significantly exacerbates ocular allergy, evidenced by increased eye-lid edema, mast cell degranulation, inflammatory cytokines (IL-4, IL-5 and TNF-α), cell proliferation (Ki67), and serum IgE, polymorphonuclear leukocytes (PMN), and apoptosis and reduced goblet cells. These findings elucidate the detrimental impact of PM exposure on exacerbating the severity of AED. Noticeably, diminished goblet cells highlight disruptions in ocular surface integrity, while increased PMN infiltration with an elevated production of IgE signifies a systemic allergic response with inflammation. Schematic illustration of the mouse AED model with OVA sensitized PM exposed conjunctiva and cornea. Inflammation in the conjunctiva and cornea, indicative of allergic responses, was observed following sensitization with OVA and exposure to PM. (C) Eye features of naive, OVA and OVA+PMexposedgroupswereassessedbyslit-lamp microscopy. (D) Changes in the serum IgE concentration level in naive, OVA and OVA + PM exposed groups. In D, data are presented in bar graph with mean ± SEM (n = 8, * p < 0.05, *** p < 0.001), significant difference using one-way ANOVA followed by the Tukey test). • Exposure to PM2.5 significantly raised the likelihood of ocular redness (adjusted OR: 12.39, 95% CI), watering (adjusted OR: 2.56, 95% CI), and dryness (adjusted OR: 5.06, 95% CI). • Additionally, these symptoms had an exposure-response relationship with increasing 1-OHP levels. • Ocular symptoms worsened in frequency and severity during the high PM2.5 season, showing a strong link to elevated PM2.5 levels. • Lymphocyte counts were also positively correlated with redness, watering, and dryness during high PM2.5 exposure. • In conclusion,this study shows that subjects exposed to higher PM2.5 levels presented more significant ocular surface alterations. This illustration clearly portrays the impact of PM2.5 exposure on ocular health through inhalation and direct penetration into the eye. PM2.5 induces lacrimal and Meibomian gland dysfunction, leading to neovascularization, inflammation, apoptosis, and oxidative. Daily PM2.5 concentrations found in the Subdistrict, Thung Satok during the sampling period. Mean 1-hydroxypyrene (1-OHP) levels (µmol/mol Cr) during low and high PM2.5 seasons. Bars represent mean values with standard deviation (p < 0.001). Asian Pac J Allergy Immunol 2020;38:19-28 DOI 10.12932/AP-100619-0579 “Particulate matter exposure can exacerbate pre-existing asthma and may contribute to developing asthma, allergic rhinitis, and aeroallergen sensitization. Short-term and long-term strategies are needed to reduce disease severity and prevent new-onset disease development. Additional research is needed to identify effective avoidance strategies and therapeutic approaches.” J.-Z. Wu et al. / Chronic Diseases and Translational Medicine 4 (2018) 95e102 PM2.5-10 activates neutrophils and eosin ophils PM2.5 induces oxidative stress PM2.5 induces antigen-presenting cell-mediated inflammatory responses PM2.5 leads to apoptosis and autophagy PM2.5 causes imbalance of T helper cells. The contribution of particulate matter to respiratory allergies according to recent evidence Model showing the possible interactions between genetics, particulate matter exposure, and aeroallergen exposure in asthma pathogenesis องค์การอนามัยโลกคาดว่า ครึง่ หนึง่ ของประชากรโลก จะเกิดโรคภูมแ ิ พ ้ทางเดินหายใจในอีก 28 ปี ข ้างหน ้า(พ.ศ.2593) และปั ญหามลพิษ ั เจนแสดงถึงความสม ั พันธ์ ของการเพิม ทางอากาศของโลกมีแนวโน ้มเพิม ่ ขึน ้ อย่างต่อเนือ ่ ง มีหลักฐานชด ่ ขึน ้ ของมลพิษทางอากาศและ สภาพภูมอ ิ ากาศที่ เปลีย ่ นแปลงจากการเพิม ่ ขึน ้ ของอุณหภูมโิ ลก ทาให ้กลุม ่ ผู ้ป่ วยภูมแ ิ พ ้ทางเดินหายใจเพิม ่ ขึน ้ ได ้แก่ โรคจมูกอักเสบจาก ภูมแ ิ พ ้dและโรคหืด ผู ้ป่ วยโรคภูมแ ิ พ ้โพรงจมูกอักเสบ และโรคหืด เป็ นโรคทีม ่ ก ี ารอักเสบของ ทางเดินหายใจสว่ นบน ่ ไรฝุ่ น ละอองหญ ้า ขน และทางเดินหายใจสว่ นล่างเรือ ้ รัง ซงึ่ จะถูกกระตุ ้นด ้วยสารแพ ้ต่าง ๆ เชน ั ว์ และทีส สต ่ าคัญมากคือพบว่ามลพิษทางอากาศ โดยเฉพาะ pm2.5 สง่ ผลให ้โรคเหล่านีก ้ าเริบ ได ้มากขึน ้ พบข ้อมูลการเพิม ่ อุบต ั ก ิ ารณ์การเกิดโรคหืด และ ในหญิงตัง้ ครรภ์ทอ ี่ ยูใ่ นมลพิษ pm2.5 มากกว่าเกณฑ์dมีโอกาสคลอดบุตรทีเ่ ป็ นโรคหืดสูงขึน ้ ถึง 30% • Increased hospital visits • significant link between atopic dermatitis (AD) and exposure to PM2.5. Specifically, there was a 1–3% increase in hospital visits for AD for every 10 μg m−3 increase in PM2.5 with even higher rates observed in vulnerable groups. • Worsening symptoms • particularly pediatric populations, with almost 10% increase in symptom severity. • increase in effects among specific groups • Males, children, and the elderly • Weather plays a key role • the spring (16.5% increase) and in the winter (12.6% increase), “dry, moderate” days were correlated with a higher association between PM2.5 and AD, as an OR of 1.165 , At indoor temperatures below 25.5 °C, there was a 6.7% increase in AD symptoms, and in homes without air purifiers, there was a 15.0% increase in AD symptoms • attributed to factors • epidermal dysfunction, hormonal dysregulation, and heightened immune responses, all of which are notably more pronounced in these vulnerable groups. Increased PM concen trations may contribute to disturbed barrier function, in creased facial erythema, and uneven skin tone even in healthy human skin. (Ann Dermatol 33(3) 263∼270, 2021) J ALLERGY CLIN IMMUNOL FEBRUARY 2025
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