Interaction of pulmonary surfactant with silica and polycyclic aromatic hydrocarbons: Implications for respiratory health

Zhao, Qun; Li, Yingjie; Chai, Xintao; Geng, Yingxue; Cao, Yan; Xu, Linzhen; Zhang, Linfeng; Huang, Jianhong; Ning, Ping; Tian, Senlin

doi:10.1016/j.chemosphere.2019.02.002

Cited by 21 publications

(12 citation statements)

References 48 publications

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“…Among all physical parameters, the size of silica dust determines how the particle behaves in the air and where it stays in the respiratory tract. With an average diameter of ~20 nm, SiNPs used here are physically ultra‐fine particles, most of which can enter and deposit on the terminal bronchial and alveoli, and part can even penetrate the blood‐air barrier and flow with the circulatory system 18–20 . Images taken by TEM show that SiNPs are phagocyted by macrophages, resulting in cell membrane rupture, pseudopodia reduction, and blurred cell boundaries, consistent with findings in SiNP‐exposed trophoblast, the Chinese Hamster Ovary (CHO‐K1) cells, and HepG2 cells 21–24 …”

Section: Discussionsupporting

confidence: 76%

NF‐κB mediates silica‐induced pulmonary inflammation by promoting the release of IL‐1β in macrophages

Zhang

Yang

et al. 2022

Environmental Toxicology

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Long‐term exposure to respirable silica particles causes pulmonary inflammation and fibrosis primarily promoted by cytokines released from alveolar macrophages, yet the underlying mechanism is still unclear. From the perspective of nuclear factor kappa B (NF‐κB), we studied the mechanism of IL‐1β biosynthesis and release. Utilizing BAY 11‐7082, an NF‐κB specific inhibitor, we showed the alteration of macrophage viability and examined the expression of both IL‐1β and NF‐κB in vitro. We found that silica nanoparticles (SiNPs) were internalized by macrophages and caused damage to cell integrity. The immunofluorescence assay showed that SiNPs exposure enhanced the expression of IL‐1β and NF‐κB, which could be effectively suppressed by BAY 11‐7082. Besides, we built silica exposure mouse model by intratracheally instilling 5 mg of SiNPs and checked the effect of silica exposure on pulmonary pathological changes. Consistently, we found an upregulation of IL‐1β and NF‐κB after SiNPs exposure, along with the aggravated inflammatory cell infiltration, thickened alveolar wall, and enhanced expression of collagens. In conclusion, SiNPs exposure causes pulmonary inflammation and fibrosis that is regulated by NK‐κB through upregulating IL‐1β in alveolar macrophages.

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Section: Discussionsupporting

confidence: 76%

NF‐κB mediates silica‐induced pulmonary inflammation by promoting the release of IL‐1β in macrophages

Zhang

Yang

et al. 2022

Environmental Toxicology

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“…Also, the microenvironment in lungs is an important factor that deserves attention. In particular, in an ideal in vitro model of respiratory exposure to NPs, the influence of pulmonary surfactant should be considered since it could be adsorbed on NPs (Silina et al 2016;Zhao et al 2019) and alter their characteristics as well as their toxicity (Jia et al 2019). Hence, in vitro studies on AuNP toxicity to lung cells should consider reliable models to better reflect the Fig.…”

Section: Discussionmentioning

confidence: 99%

Exposure to airborne gold nanoparticles: a review of current toxicological data on the respiratory tract

Berardis¹,

Marchetti²,

Risuglia

et al. 2020

J Nanopart Res

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In recent years, the introduction of innovative low-cost and large-scale processes for the synthesis of engineered nanoparticles with at least one dimension less than 100 nm has led to countless useful and extensive applications. In this context, gold nanoparticles stimulated a growing interest, due to their peculiar characteristics such as ease of synthesis, chemical stability and optical properties. This stirred the development of numerous applications especially in the biomedical field. Exposure of manufacturers and consumers to industrial products containing nanoparticles poses a potential risk to human health and the environment. Despite this, the precise mechanisms of nanomaterial toxicity have not yet been fully elucidated. It is well known that the three main routes of exposure to nanomaterials are by inhalation, ingestion and through the skin, with inhalation being the most common route of exposure to NPs in the workplace. To provide a complete picture of the impact of inhaled gold nanoparticles on human health, in this article, we review the current knowledge about the physico-chemical characteristics of this nanomaterial, in the size range of 1–100 nm, and its toxicity for pulmonary structures both in vitro and in vivo. Studies comparing the toxic effect of NPs larger than 100 nm (up to 250 nm) are also discussed.

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“…A similar result was observed in which DPPC showed higher adsorption capacity on the surface of silica particles compared to BSA, with lower Freundlich affinity coefficient values of Phe in DPPC solution (1.73) than BSA solution (2.32). 46 Consequently, it can be suggested that PM 2.5 -PAHs may be released into respiratory tracts mainly by micelle solubilization, and in the presence of DPPC, can also be desorbed because of competitive adsorption between PAHs and DPPC on PM 2.5 particles.…”

Section: Resultsmentioning

confidence: 99%

Inhalation Bioaccessibility of Polycyclic Aromatic Hydrocarbons in PM_2.5 under Various Lung Environments: Implications for Air Pollution Control during Coronavirus Disease-19 Outbreak

Zhou

Kong

Cui

2022

Environ. Sci. Technol.

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Global spread of coronavirus disease-19 (COVID-19) is placing an unprecedented pressure on the environment and health. In this study, a new perspective is proposed to assess the inhalation bioaccessibility of polycyclic aromatic hydrocarbons (PAHs) in PM 2.5 for people with various lung health conditions. In vitro bioaccessibility (IVBA) was measured using modified epithelial lung fluids simulating the extracellular environment of patients with severe and mild lung inflammation. The average PAH IVBA in PM 2.5 of 24.5 ± 4.52% under healthy conditions increased ( p = 0.06) to 28.6 ± 3.17% and significantly ( p < 0.05) to 32.3 ± 5.32% under mild and severe lung inflammation conditions. A mechanistic study showed that lung inflammation decreased the critical micelle concentrations of main pulmonary surfactants (i.e., from 67.8 (for dipalmitoyl phosphatidylcholine) and 53.3 mg/L (for bovine serum albumin) to 44.5 mg/L) and promoted the formation of micelles, which enhanced the solubilization and competitive desorption of PAHs from PM 2.5 in the lung fluids. In addition, risk assessment considering different IVBA values suggested that PAH contamination levels in PM 2.5 , which were safe for healthy people, may not be acceptable for patients with lung inflammation. Because of the large number of COVID-19 infections, and the fact that some survivors of COVID-19 were observed to still show symptoms of interstitial lung inflammation, the finding here can provide important implications for both the scientific community and policy makers in addressing health risk and air pollution control during the COVID-19 outbreak.

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Interaction of pulmonary surfactant with silica and polycyclic aromatic hydrocarbons: Implications for respiratory health

Cited by 21 publications

References 48 publications

NF‐κB mediates silica‐induced pulmonary inflammation by promoting the release of IL‐1β in macrophages

NF‐κB mediates silica‐induced pulmonary inflammation by promoting the release of IL‐1β in macrophages

Exposure to airborne gold nanoparticles: a review of current toxicological data on the respiratory tract

Inhalation Bioaccessibility of Polycyclic Aromatic Hydrocarbons in PM_2.5 under Various Lung Environments: Implications for Air Pollution Control during Coronavirus Disease-19 Outbreak

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Interaction of pulmonary surfactant with silica and polycyclic aromatic hydrocarbons: Implications for respiratory health

Cited by 21 publications

References 48 publications

NF‐κB mediates silica‐induced pulmonary inflammation by promoting the release of IL‐1β in macrophages

NF‐κB mediates silica‐induced pulmonary inflammation by promoting the release of IL‐1β in macrophages

Exposure to airborne gold nanoparticles: a review of current toxicological data on the respiratory tract

Inhalation Bioaccessibility of Polycyclic Aromatic Hydrocarbons in PM2.5 under Various Lung Environments: Implications for Air Pollution Control during Coronavirus Disease-19 Outbreak

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Inhalation Bioaccessibility of Polycyclic Aromatic Hydrocarbons in PM_2.5 under Various Lung Environments: Implications for Air Pollution Control during Coronavirus Disease-19 Outbreak