Toxicological appraisal of the chemical fractions of ambient fine (PM2.5-0.3) and quasi-ultrafine (PM0.3) particles in human bronchial epithelial BEAS-2B cells

Badran, Ghidaa; Verdin, Anthony; Grare, C.; Abbas, Imane; Achour, D.; Ledoux, Frédéric; Roumié, M.; Cazier, Fabrice; Courcot, Dominique; Guidice, Jean‐Marc Lo; Garçon, Guillaume

doi:10.1016/j.envpol.2020.114620

Cited by 27 publications

(14 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To a lesser extent, organic extracts gave the same effect, whereas exposure to water-soluble extracts showed no effect. Several studies have already reported the greater ability of particulate samples to induce an inflammatory response compared to their water-soluble (Shang et al, 2020) or organic extracts (Badran et al, 2020b;. As observed in this work, the literature also reported no inflammatory response following exposure of BEAS-2B cells to water-soluble and/or organic extracts (Chowdhury et al, 2018;Honda et al, 2017).…”

Section: Discussionsupporting

confidence: 79%

“…The PM induced oxidative stress has been linked to metals (Jan et al, 2020) and organic compounds (Badran et al, 2020a, Win et al, 2018. In addition, the ability of the particles themselves (Dergham et al, 2015(Dergham et al, , 2012Leclercq et al, 2018;Moufarrej, 2021), their organic extract (OE) (Abbas et al, 2019;Badran et al, 2020b;Billet et al, 2018) or their water soluble extract (WSE) (X. Shuster-Meiseles et al, 2016;Xu et al, 2018;Yan et al, 2017) to induce oxidative stress has been shown.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Oxidative stress response in pulmonary cells exposed to different fractions of PM2.5-0.3 from urban, traffic and industrial sites

Moufarrej

Verdin

Cazier

et al. 2023

Environmental Research

Self Cite

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Oxidative stress response in pulmonary cells exposed to different fractions of PM2.5-0.3 from urban, traffic and industrial sites

Moufarrej

Verdin

Cazier

et al. 2023

Environmental Research

Self Cite

View full text Add to dashboard Cite

“…PM 2.5 could induce oxidative stress by increasing the number of reactive oxygen species, leading to DNA damage, lipid peroxidation, and protein carbonylation; these factors further resulted in endoplasmic reticulum stress, mitochondrial dysfunction, and autophagy, thus causing apoptotic HaCaT cell death and mouse skin injury [ 5 ]. Similarly, inflammatory responses and oxidative stress caused by PM 0.3–2.5 in an in vitro model negatively affected the integrity and functions of skin [ 6 ]. PM 2.5 can penetrate both disrupted and intact skin; it disrupts the skin barrier by reducing the numbers of cytokeratin, filaggrin, E-cadherin, and tight junction molecules [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Farnesol-Loaded Liposomes Protect the Epidermis and Dermis from PM2.5-Induced Cutaneous Injury

Chen

et al. 2021

IJMS

View full text Add to dashboard Cite

Particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) increases oxidative stress through free radical generation and incomplete volatilization. In addition to affecting the respiratory system, PM2.5 causes aging- and inflammation-related damage to skin. Farnesol (Farn), a natural benzyl semiterpene, possesses anti-inflammatory, antioxidative, and antibacterial properties. However, because of its poor water solubility and cytotoxicity at high concentrations, the biomedical applications of Farn have been limited. This study examined the deleterious effects of PM2.5 on the epidermis and dermis. In addition, Farn-encapsulated liposomes (Lipo-Farn) and gelatin/HA/xanthan gel containing Lipo-Farn were prepared and applied in vivo to repair and alleviate PM2.5-induced damage and inflammation in skin. The prepared Lipo-Farn was 342 ± 90 nm in diameter with an encapsulation rate of 69%; the encapsulation significantly reduced the cytotoxicity of Farn. Lipo-Farn exhibited a slow-release rate of 35% after 192 h of incubation. The half-maximal inhibitory concentration of PM2.5 was approximately 850 μg/mL, and ≥400 μg/mL PM2.5 significantly increased IL-6 production in skin fibroblasts. Severe impairment in the epidermis and hair follicles and moderate impairment in the dermis were found in the groups treated with post-PM2.5 and continuous subcutaneous injection of PM2.5. Acute and chronic inflammation was observed in the skin in both experimental categories in vivo. Treatment with 4 mM Lipo-Farn largely repaired PM2.5-induced injury in the epidermis and dermis, restored injured hair follicles, and alleviated acute and chronic inflammation induced by PM2.5 in rat skin. In addition, treatment with 4 mM pure Farn and 2 mM Lipo-Farn exerted moderate reparative and anti-inflammatory effects on impaired skin. The findings of the current study indicate the therapeutic and protective effects of Lipo-Farn against various injuries caused by PM2.5 in the pilosebaceous units, epidermis, and dermis of skin.

show abstract

“…In addition, the secondary product of the photochemical reaction, SO 4 2− , also played a major role in the pro-inflammatory response and oxidative stress [ 45 ]. Organic extractable OEM 2.5−0.3 significantly induced ROS overproduction and oxidative damage [ 56 ]. PAHs, due to their relatively small contribution to PM, may have their effects masked by other components.…”

Section: Resultsmentioning

confidence: 99%

Chemical Composition and Transgenerational Effects on Caenorhabditis elegans of Seasonal Fine Particulate Matter

Yang

Liu

et al. 2023

Toxics

View full text Add to dashboard Cite

While numerous studies have demonstrated the adverse effects of fine particulate matter (PM) on human health, little attention has been paid to its impact on offspring health. The multigenerational toxic effects on Caenorhabditis elegans (C. elegans) were investigated by acute exposure. PM2.5 and PM1 samples were collected and analysed for their chemical composition (inorganic ions, metals, OM, PAHs) in different seasons from April 2019 to January 2020 in Lin’an, China. A higher proportion of organic carbon components (34.3%, 35.9%) and PAHs (0.0144%, 0.0200%) occupied the PM2.5 and PM1 samples in winter, respectively. PM1 in summer was enriched with some metal elements (2.7%). Exposure to fine PM caused developmental slowing and increased germ cell apoptosis, as well as inducing intestinal autofluorescence and reactive oxygen species (ROS) production. PM1 caused stronger toxic effects than PM2.5. The correlation between PM component and F0 generation toxicity index was analysed. Body length, germ cell apoptosis and intestinal autofluorescence were all highly correlated with Cu, As, Pb, OC and PAHs, most strongly with PAHs. The highest correlation coefficients between ROS and each component are SO42- (R = 0.743), Cd (R = 0.816) and OC (R = 0.716). The results imply that OC, PAHs and some transition metals play an important role in the toxicity of fine PM to C. elegans, where the organic fraction may be the key toxicogenic component. The multigenerational studies show that PM toxicity can be passed from parent to offspring, and gradually returns to control levels in the F3–F4 generation with germ cell apoptosis being restored in the F4 generation. Therefore, the adverse effects of PM on reproductive damage are more profound.

show abstract

Toxicological appraisal of the chemical fractions of ambient fine (PM2.5-0.3) and quasi-ultrafine (PM0.3) particles in human bronchial epithelial BEAS-2B cells

Cited by 27 publications

References 55 publications

Oxidative stress response in pulmonary cells exposed to different fractions of PM2.5-0.3 from urban, traffic and industrial sites

Oxidative stress response in pulmonary cells exposed to different fractions of PM2.5-0.3 from urban, traffic and industrial sites

Farnesol-Loaded Liposomes Protect the Epidermis and Dermis from PM2.5-Induced Cutaneous Injury

Chemical Composition and Transgenerational Effects on Caenorhabditis elegans of Seasonal Fine Particulate Matter

Contact Info

Product

Resources

About