PM 2.5 Health Complications

The GBD study estimated the attributable levels of PM2.5 in 195 countries and territories worldwide. 

Ambient PM2.5 and household PM2.5 ranked among the top ten leading global risk factors for disease [48]

. Exposure to environmental PM2.5 has been associated with an increase in the incidence and mortality of many diseases.

 High risk of PM2.5-related death from stroke, ischemic heart disease, chronic obstructive pulmonary disease (COPD), lung cancer, and other diseases around the world has been demonstrated in several studies [49,50,51,52,53,54].

 The lungs, the initial sites of PM2.5 deposition in the airway, are among the primary targets of PM2.5-induced toxicity, which leads to airway inflammation, impairing normal immune responses of the lungs and making them susceptible to various respiratory infections [55]

. It’s been hypothesized that PM2.5 impairs the normal immune responses by various mechanisms.

 Firstly, PM2.5 can damage the bronchial mucociliary system, reducing bacterial clearance [56]. 

Secondly, PM2.5 and PM2.5-induced inflammatory cytokine net disruption may cause the death of lung epithelial cells and fibroblasts, as well as the inhibition of gap junctional intercellular communication between these cells, increasing epithelial barrier permeability and impairing their function as physical barriers for pulmonary innate immunity [57].

 Thirdly, alveolar macrophages are essential inflammation regulators and are required for antibacterial activity in the lower airway [58].

 Recently, increasing evidence has shown that PM2.5 not only inhibits alveolar macrophage phagocytosis by disrupting the normal physical and immunological function of lung surfactants, such as di-palmitoyl-phosphatidylcholine and amino acids related to opsonin proteins [59]

, but they also impair the response of natural killer (NK) cells [60] and inhibit antibacterial capabilities through transferrin-mediated Fe3+ transport [61],

 disrupting the expression of toll-like receptors (TLRs) and microtubule architecture [62,63]. 

Recently, increasing evidence has shown that PM2.5 not only inhibits alveolar macrophages phagocytosis by disrupting the normal physical and immunological function of lung surfactants, such as di-palmitoyl-phosphatidylcholine and amino acids related to opsonin proteins [59], which generally act as opsonins and enhance alveolar macrophages phagocytosis to bacteria, and impairing the response of natural killer (NK) cells [60], 

which also enhance alveolar macrophages phagocytosis, but also directly inhibiting alveolar macrophages antibacterial capabilities through a variety of methods. These methods include influencing transferrin-mediated Fe3+ transport to alveolar macrophages [61], affecting the expression of toll-like receptors (TLRs); disrupting microtubule architecture; and decreasing their phagocytic activities [62,63]. All of these would lead to reduced pulmonary immunity and facilitate infectious illnesses. Recently, chronic exposure to PM2.5 was found to be linked with the development of diabetes mellitus (DM), inducing multiple abnormalities associated with the development of type 2 diabetes mellitus (T2DM), insulin resistance (IR), adipose inflammation, and hepatic endoplasmic reticulum (ER) stress. Alterations in ER stress and inflammatory pathways have been proposed to be the mechanisms by which PM2.5 induces IR and T2DM [64]. Furthermore, PM2.5 exposure not only leads to subclinical changes in cardiovascular function, but also impairs the function of the cardiac autonomic nervous system (ANS), leading to a decline in heart rate variability, which is inevitably related to cardiovascular morbidity and mortality [65]. Epidemiological evidence suggests that PM2.5 is a risk factor for chronic kidney disease (CKD). Moreover, PM2.5 leads to a decrease in glomerular filtration rate (GFR) and is related to the prevalence and incidence of CKD [66]. Protecting the environment and the environmental health of mothers and infants remains a top global priority. Epidemiological evidence suggests that maternal PM2.5 exposure during pregnancy is associated with negative birth outcomes, including preterm birth, low birth weight, and post neonatal infant mortality [67,68,69,70,71]. The health impacts of PM2.5 are summarized (Table 2). In addition, PM2.5 influences several other adverse health effects such as bone damage, liver fibrosis, lung cancer, macrosomia, Alzheimer’s disease, ovarian dysfunction, hormone dysregulation, and compromised antiviral immunity [72,73,74,75,76,77,78].

Ref

Int J Environ Res Public Health. 2022 Jun 19;19(12):7511. doi: 10.3390/ijerph19127511

Recent Insights into Particulate Matter (PM2.5)-Mediated Toxicity in Humans: An Overview

Prakash Thangavel 1, Duckshin Park 2,*, Young-Chul Lee 1,3,*

Editor: Paul B Tchounwou