The Correlation of PM2.5 Exposure with Acute Attack and Steroid Sensitivity in Asthma

Abstract

Bronchial asthma is a common chronic inflammatory disease of the respiratory system. Asthma primarily manifests in reversible airflow limitation and airway inflammation, airway remodeling, and persistent airway hyperresponsiveness. PM2.5, also known as fine particulate matter, is the main component of air pollution and refers to particulate matter with an aerodynamic diameter of ≤2.5 μm. PM2.5 can be suspended in the air for an extensive time and, in addition, can contain or adsorb heavy metals, toxic gases, polycyclic aromatic hydrocarbons, bacterial viruses, and other harmful substances. Epidemiological studies have demonstrated that, in addition to increasing the incidence of asthma, PM2.5 exposure results in a significant increase in the incidence of hospital visits and deaths due to acute asthma attacks. Furthermore, PM2.5 was reported to induce glucocorticoid resistance in asthmatic individuals. Although various countries have implemented strict control measures, due to the wide range of PM2.5 sources, complex components, and unknown pathogenic mechanisms involving the atmosphere, environment, chemistry, and toxicology, PM2.5 damage to human health still cannot be effectively controlled. In this present review, we summarized the current knowledge base regarding the relationship between PM2.5 toxicity and the onset, acute attack prevalence, and steroid sensitivity in asthma.

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

“…When the concentration of PM2.5 is high, severe asthma exacerbation are more likely to occur, and hospital stays may be longer. The findings above may be due to PM2.5‐induced airway inflammation and hyperresponsiveness, mediated by various inflammatory cells and their released cytokines 14 . PM2.5 can encourage the creation of reactive oxygen, resulting in mitochondrial structural disturbance and bronchial epithelial cell death, which can cause severe asthma 15 .…”

How does particulate air pollution affect barrier functions and inflammatory activity of lung vascular endothelium?

“…By utilizing μFTIR spectroscopy, the team found polymer particles, mostly in the form of fragments and fibers, to consist mostly of polypropylene, polyethylene, polystyrene, and resins with a detection threshold of 3 μm in size. Apart from increasing the risk of asthma, PM2.5 is likely to reduce steroid sensitivity in asthma patients 39 . Inhaled PM not only deposits in lung tissues, but may also penetrate to the bloodstream and urine 40 .…”

“…Apart from increasing the risk of asthma, PM2.5 is likely to reduce steroid sensitivity in asthma patients. 39 Inhaled PM not only deposits in lung tissues, but may also penetrate to the bloodstream and urine. 40 This indicates that PM may cross the epithelial barrier and affect the vascular endothelium (cf.…”

Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis

“…263 PM2.5 exposure exasperates asthma and augments the risk of asthma exacerbations. 264,265 Yunxia Zhao et al discovered that PM 2.5 exposure elevated the expression of RIPK3 and MLKL in mouse lung tissue, and blocking necroptosis lowered PM2.5-induced airway inflammation and airway hyperresponsiveness. 266 TNF-α is a proinflammatory cytokine closely linked to neutrophilic asthma and could be beneficial in refractory asthma.…”