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Review
. 2024 Oct 17;13(10):1256.
doi: 10.3390/antiox13101256.

Particulate Matter-Induced Emerging Health Effects Associated with Oxidative Stress and Inflammation

Affiliations
Review

Particulate Matter-Induced Emerging Health Effects Associated with Oxidative Stress and Inflammation

Eun Yeong Lim et al. Antioxidants (Basel). .

Abstract

Environmental pollution continues to increase with industrial development and has become a threat to human health. Atmospheric particulate matter (PM) was designated as a Group 1 carcinogen by the International Agency for Research on Cancer in 2013 and is an emerging global environmental risk factor that is a major cause of death related to cardiovascular and respiratory diseases. PM is a complex composed of highly reactive organic matter, chemicals, and metal components, which mainly cause excessive production of reactive oxygen species (ROS) that can lead to DNA and cell damage, endoplasmic reticulum stress, inflammatory responses, atherosclerosis, and airway remodeling, contributing to an increased susceptibility to and the exacerbation of various diseases and infections. PM has various effects on human health depending on the particle size, physical and chemical characteristics, source, and exposure period. PM smaller than 5 μm can penetrate and accumulate in the alveoli and circulatory system, causing harmful effects on the respiratory system, cardiovascular system, skin, and brain. In this review, we describe the relationship and mechanism of ROS-mediated cell damage, oxidative stress, and inflammatory responses caused by PM and the health effects on major organs, as well as comprehensively discuss the harmfulness of PM.

Keywords: inflammation; oxidative stress; particulate matter; reactive oxygen species.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
PM classification by aerodynamic particle size and possible routes of penetration and accumulation by particle size in the lungs. Particulate matter: PM; red blood cell: RBC. Created with BioRender.com. accessed on 20 September 2024.
Figure 2
Figure 2
Major organs affected by PM exposure and related diseases and symptoms. Chronic obstructive pulmonary disease: COPD; nonalcoholic fatty liver disease: NAFLD. Created with BioRender.com. accessed on 20 September 2024.
Figure 3
Figure 3
Onset and exacerbation pathogenesis of chronic inflammatory respiratory disease by PM exposure and associated ROS signaling pathway. C-C motif chemokine ligand 2: CCL2; cadherin 1: CDH1; chronic obstructive pulmonary disease: COPD; cyclooxygenase 2: COX2; intercellular adhesion molecule 1: ICAM1; interferon gamma: IFNγ; interleukin: IL; inducible nitric oxide synthase: iNOS; matrix metalloproteinase: MMP; myeloperoxidase: MPO; mucin 5AC: MUC5AC; mucin 5B: MUC5B; nicotinamide adenine dinucleotide phosphate: NADPH; occludin: OLCN; particulate matter: PM; reactive oxygen species: ROS; transforming growth factor beta: TGFβ; tight junction protein 1: TJP1; tumor necrosis factor alpha: TNFα. Created with BioRender.com. accessed on 20 September 2024.
Figure 4
Figure 4
Effects and major pathways of ROS-mediated pathophysiology on cardiovascular diseases following PM exposure. Myeloperoxidase: MPO; neutrophil elastase: NE; particulate matter: PM; reactive oxygen species: ROS. Created with BioRender.com. accessed on 20 September 2024.
Figure 5
Figure 5
Pathogenesis of inflammatory skin disease and aging by PM exposure and associated ROS signaling pathway. Atopic dermatitis: AD; aryl hydrocarbon receptor: AhR; BCL2-associated agonist of cell death: BAD; BCL2-associated X protein: BAX; cyclooxygenase 2: COX2; cytochrome P450: CYP; exogenous ROS: exROS; intercellular adhesion molecule 1: ICAM1; interleukin: IL; inducible nitric oxide synthase: iNOS; mitogen-activated protein kinase: MAPK; matrix metalloproteinase: MMP; NADPH oxidase: NOX; nuclear factor kappa B: NFκB; occludin: OLCN; particulate matter: PM; phorbol-12-myristate-13-acetate-induced protein 1: PMAIP1; reactive oxygen species: ROS; transepidermal water loss: TEWL; Toll-like receptor: TLR; tumor necrosis factor: TNFα. Created with BioRender.com. accessed on 20 September 2024.
Figure 6
Figure 6
Effects and major pathways of ROS-mediated pathophysiology on neurodegenerative diseases, mental disorders, and impairment of brain development following PM exposure. Blood–brain barrier: BBB; particulate matter: PM; reactive oxygen species: ROS. Created with BioRender.com. accessed on 20 September 2024.

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