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

Abstract

Several epidemiologic and toxicological studies have commonly viewed ambient fine particulate matter (PM2.5), defined as particles having an aerodynamic diameter of less than 2.5 µm, as a significant potential danger to human health. PM2.5 is mostly absorbed through the respiratory system, where it can infiltrate the lung alveoli and reach the bloodstream. In the respiratory system, reactive oxygen or nitrogen species (ROS, RNS) and oxidative stress stimulate the generation of mediators of pulmonary inflammation and begin or promote numerous illnesses. According to the most recent data, fine particulate matter, or PM2.5, is responsible for nearly 4 million deaths globally from cardiopulmonary illnesses such as heart disease, respiratory infections, chronic lung disease, cancers, preterm births, and other illnesses. There has been increased worry in recent years about the negative impacts of this worldwide danger. The causal associations between PM2.5 and human health, the toxic effects and potential mechanisms of PM2.5, and molecular pathways have been described in this review.

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

“…With increasing levels of smog in cities worldwide, the impact of air pollution on human health is attracting global attention. 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 μ m in the atmosphere [ 1 ]. 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.…”

Remarkable contribution of particulate matter-induced macrophage ferroptosis to the pathology of pulmonary fibrosis

“…Particulate matter (PM) is a type of environmental air pollutants. Once inhaled into the human airway, it will trigger a series of disorders of the respiratory system, including pulmonary fibrosis through inflammation [1][2][3] . After crossing the air-blood barrier, PMs can even elicit harmful effects on distant organs through blood circulation, including joint injury and nervous system impairment [4][5][6] .…”

Untitled

“…After crossing the air-blood barrier, PMs can even elicit harmful effects on distant organs through blood circulation, including joint injury and nervous system impairment [4][5][6] . Recently, it has been recognized that macrophage damage caused by inhalation exposure of PMs is closely associated with fibrogenesis via multiple fibrogenic cytokines, such as transforming growth factor β (TGF-β), tumor necrosis factor α (TNF-α), interleukin (IL) 1β, IL-4, IL-6, IL-10 and IL-13 3,[7][8][9][10][11] . Remarkably, inhalation exposure to PMs could induce alveolar macrophage damage as well as different programmed cell death such as apoptosis, necroptosis, autophagy, pyroptosis and ferroptosis [11][12][13][14] .…”