Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction

Mazuryk, Olga; Stochel, Grażyna; Brindell, Małgorzata

doi:10.3389/fchem.2020.581752

Cited by 11 publications

(6 citation statements)

References 72 publications

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“…Various mechanisms of the cytotoxicity have been discussed in other studies, including membrane damages, accumulation of reactive oxygen species, and induction of apoptosis. Polluting particles have been shown to induce expression of proinflammatory cytokines and other signaling molecules 29 – 31 . Most probably particles tested in our study does not have direct effect on cell viability, but impact on cellular metabolism, expression and secretion of cytokines, growth factors and other signaling molecules would be beneficial to evaluate in further studies.…”

Section: Resultsmentioning

confidence: 99%

In vitro impact preliminary assessment of airborne particulate from metalworking and woodworking industries

Pavlovska

Ramata-Stunda

Martinsone

et al. 2021

Sci Rep

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Inhalation is the main route of exposure to airborne pollutants. To evaluate the safety and assess the risks of occupational hazards different testing approaches are used. 3D airway epithelial tissues allow to mimic exposure conditions in vitro, generates human-relevant toxicology data, allows to elucidate the mode of action of pollutants. Gillian3500 pumps were used to collect the airborne particulate from woodworking and metalworking environments. EpiAirway tissues were used to model half working day (4 h), full working day (8 h), and 3 working day exposures to occupational pollutants. Tissue viability was assessed using an MTT assay. For preliminary assessment, RT-qPCR analyses were performed to analyze the expression of gelsolin, caspase-3, and IL-6. Tissue morphology was assessed by hematoxylin/eosin staining. An effect on the proliferation of lung epithelial cell line A549 was assessed. Acute exposure to workspace pollutants slightly affected tissue viability and did not change the morphology. No inhibiting effect was observed on the proliferation of A549 cells. Preliminary analysis showed that both types of particles suppressed the expression of gelsolin, with the effect of metalworking samples being more pronounced. A slight reduction in caspase-3 expression was observed. Particles from metalworking suppressed IL-6 expression.

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Section: Resultsmentioning

confidence: 99%

In vitro impact preliminary assessment of airborne particulate from metalworking and woodworking industries

Pavlovska

Ramata-Stunda

Martinsone

et al. 2021

Sci Rep

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“…This decreased viability likely reflects the abundance of metals in these UFPs, including Fe, Zn, Mn, Pb, Cu, Cr, and Ni [ 12 , 13 ]. Transition metals can catalyse ROS production in situ via the Fenton reaction, leading to oxidative damage to lipids, DNA, and proteins, and eventually cell death [ 81 ]. The majority of the analysed metals occur in greatest concentrations in the Mexico City UF-RDPs ( Figure 2 ; Supplementary Table S2 ).…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress, Cytotoxic and Inflammatory Effects of Urban Ultrafine Road-Deposited Dust from the UK and Mexico in Human Epithelial Lung (Calu-3) Cells

et al. 2022

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Road-deposited dust (RD) is a pervasive form of particulate pollution identified (typically via epidemiological or mathematical modelling) as hazardous to human health. Finer RD particle sizes, the most abundant (by number, not mass), may pose greater risk as they can access all major organs. Here, the first in vitro exposure of human lung epithelial (Calu-3) cells to 0–300 µg/mL of the ultrafine (<220 nm) fraction of road dust (UF-RDPs) from three contrasting cities (Lancaster and Birmingham, UK, and Mexico City, Mexico) resulted in differential oxidative, cytotoxic, and inflammatory responses. Except for Cd, Na, and Pb, analysed metals were most abundant in Mexico City UF-RDPs, which were most cytotoxic. Birmingham UF-RDPs provoked greatest ROS release (only at 300 µg/mL) and greatest increase in pro-inflammatory cytokine release. Lancaster UF-RDPs increased cell viability. All three UF-RDP samples stimulated ROS production and pro-inflammatory cytokine release. Mass-based PM limits seem inappropriate given the location-specific PM compositions and health impacts evidenced here. A combination of new, biologically relevant metrics and localised regulations appears critical to mitigating the global pandemic of health impacts of particulate air pollution and road-deposited dust.

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“…Most air pollution proportion is predominantly linked with particulate matter (PM) pollutants, ranging from 0.1 to 2.5 μm in diameter (PM 0.1 and PM 2.5 ). These pollutants can penetrate the pulmonary tract, accumulate within host cells, and induce cellular oxidative stress by increasing Reactive Oxygen Species (ROS) production in alveolar cells ( Mazuryk et al., 2020 ). In addition, particulate pollutants can induce complex immune inflammatory response directly but molecular pathway of airway inflammation related lung damage has not been clearly understood so far ( Esposito et al., 2014 ).…”

Section: Pm 25 Induced Airway Inflammationmentioning

confidence: 99%

Possible modulating functions of probiotic Lactiplantibacillus plantarum in particulate matter-associated pulmonary inflammation

Gupta,

Abd EL-Gawaad,

Osman Abdallah

et al. 2024

Front. Cell. Infect. Microbiol.

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Pulmonary disease represents a substantial global health burden. Increased air pollution, especially fine particulate matter (PM2.5) is the most concerned proportion of air pollutants to respiratory health. PM2.5 may carry or combine with other toxic allergens and heavy metals, resulting in serious respiratory allergies and anaphylactic reactions in the host. Available treatment options such as antihistamines, steroids, and avoiding allergens/dust/pollutants could be limited due to certain side effects and immense exposure to air pollutants, especially in most polluted countries. In this mini-review, we summarized how PM2.5 triggers respiratory hyperresponsiveness and inflammation, and the probiotic Lactiplantibacillus plantarum supplementation could minimize the risk of the same. L. plantarum may confer beneficial effects in PM2.5-associated pulmonary inflammation due to significant antioxidant potential. We discussed L. plantarum’s effect on PM2.5-induced reactive oxygen species (ROS), inflammatory cytokines, lipid peroxidation, and DNA damage. Available preclinical evidence shows L. plantarum induces gut-lung axis, SCFA, GABA, and other neurotransmitter signaling via gut microbiota modulation. SCFA signals are important in maintaining lung homeostasis and regulating intracellular defense mechanisms in alveolar cells. However, significant research is needed in this direction to contemplate L. plantarum’s therapeutic potential in pulmonary allergies.

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Variations in Reactive Oxygen Species Generation by Urban Airborne Particulate Matter in Lung Epithelial Cells—Impact of Inorganic Fraction

Cited by 11 publications

References 72 publications

In vitro impact preliminary assessment of airborne particulate from metalworking and woodworking industries

In vitro impact preliminary assessment of airborne particulate from metalworking and woodworking industries

Oxidative Stress, Cytotoxic and Inflammatory Effects of Urban Ultrafine Road-Deposited Dust from the UK and Mexico in Human Epithelial Lung (Calu-3) Cells

Possible modulating functions of probiotic Lactiplantibacillus plantarum in particulate matter-associated pulmonary inflammation

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