Particulate Matter and Its Molecular Effects on Skin: Implications for Various Skin Diseases

Abstract

Particulate matter (PM) is a harmful air pollutant composed of chemicals and metals which affects human health by penetrating both the respiratory system and skin, causing oxidative stress and inflammation. This review investigates the association between PM and skin disease, focusing on the underlying molecular mechanisms and specific disease pathways involved. Studies have shown that PM exposure is positively associated with skin diseases such as atopic dermatitis, psoriasis, acne, and skin aging. PM-induced oxidative stress damages lipids, proteins, and DNA, impairing cellular functions and triggering inflammatory responses through pathways like aryl hydrocarbon receptor (AhR), NF-κB, and MAPK. This leads to increased production of inflammatory cytokines and exacerbates skin conditions. PM exposure exacerbates AD by triggering inflammation and barrier disruption. It disrupts keratinocyte differentiation and increases pro-inflammatory cytokines in psoriasis. In acne, it increases sebum production and inflammatory biomarkers. It accelerates skin aging by degrading ECM proteins and increasing MMP-1 and COX2. In conclusion, PM compromises skin health by penetrating skin barriers, inducing oxidative stress and inflammation through mechanisms like ROS generation and activation of key pathways, leading to cellular damage, apoptosis, and autophagy. This highlights the need for protective measures and targeted treatments to mitigate PM-induced skin damage.

Keywords: atopic dermatitis; particulate matter; psoriasis; skin aging; skin disease.

Figure 1

Primary molecular mechanisms of PM-induced skin damage. (A) PM can penetrate the skin, infiltrating both the barrier-disrupted interfollicular epidermis and the intact follicular epidermis. (B) PM activates cellular signaling pathways such as AhR and TLR, leading to increased ROS production, while PM itself also generates ROS. ROS from PM causes oxidative stress, damaging lipids, proteins, and DNA, impairing cellular functions, and causing apoptosis. It activates NF-κB, promoting cytokines (TNF, IL-1α, IL-1β), adhesion molecules (ICAM1), and enzymes (COX2). ROS also activate MAPK pathways (ERK, JNK, p38), leading to inflammatory responses in skin.

Figure 2

A schematic representation of the molecular effects of particulate matter on skin diseases, illustrating the disease-specific pathways involved. TEWL = transepidermal water loss, FLG = filaggrin, LOR = loricrin, IL = interleukin, TRPV = transient receptor potential vanilloid, AKT = protein kinase B, mTOR = mammalian target of rapamycin, HIF-1a = hypoxia inducible factor 1 subunit alpha, CCL, CXCL = chemokine ligand, IRE1α = Inositol-requiring transmembrane, kinase/endoribonuclease 1α, SCF = stem cell factor, ET-1 = endothelin 1, MMP = matrix metalloproteins, COX = cyclooxygenase, ECM = extracellular matrix.