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Review
. 2020 Mar;52(3):329-337.
doi: 10.1038/s12276-020-0394-0. Epub 2020 Mar 17.

Mechanisms of ultrafine particle-induced respiratory health effects

George D Leikauf  1 , Sang-Heon Kim  2 , An-Soo Jang  3
Affiliations
Review

Mechanisms of ultrafine particle-induced respiratory health effects

George D Leikauf et al. Exp Mol Med. 2020 Mar.

Abstract

Particulate matter (PM) is the principal component of air pollution. PM includes a range of particle sizes, such as coarse, fine, and ultrafine particles. Particles that are <100 nm in diameter are defined as ultrafine particles (UFPs). UFPs are found to a large extent in urban air as both singlet and aggregated particles. UFPs are classified into two major categories based on their source. Typically, UFPs are incidentally generated in the environment, often as byproducts of fossil fuel combustion, condensation of semivolatile substances or industrial emissions, whereas nanoparticles are manufactured through controlled engineering processes. The primary exposure mechanism of PM is inhalation. Inhalation of PM exacerbates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain unclear. This review offers insights into the mechanisms by which particles, including UFPs, influence airway inflammation and discusses several mechanisms that may explain the relationship between particulate air pollutants and human health, particularly respiratory health. Understanding the mechanisms of PM-mediated lung injury will enhance efforts to protect at-risk individuals from the harmful health effects of air pollutants.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1. The proposed mechanism of ultrafine particle (UFP)-induced lung diseases.
PM causes the activation of oxidative stress and reactive oxygen species, innate immunity, adaptive immunity, and other mechanisms, leading to the development and exacerbation of respiratory diseases such as bronchial asthma, COPD, lung fibrosis, and lung cancer.
Fig. 2
Fig. 2
Schematic of the inflammasome cascade in the lungs of the TiO2 particle-exposed model.
Fig. 3
Fig. 3
PM exposure initiates innate immunity through macrophage migration inhibitory factors, leading to exacerbation of respiratory symptoms.
Fig. 4
Fig. 4
Th2 cytokine changes in macrophages exposed to TiO2 particles.
Fig. 5
Fig. 5
PM exposure triggers neuroinflammation causing cough and airway inflammation.
See this image and copyright information in PMC

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