Alkyl organophosphate flame retardants (OPFRs) induce lung inflammation and aggravate OVA-simulated asthmatic response via the NF-кB signaling pathway

Yuan, Meng; Xu, Xin; Xie, Guangming; Zhang, Yunwei; Chen, Shiyan; Qiu, Yanling; Zhu, Zhiliang; Zhang, Hua; Yin, Daqiang

doi:10.1016/j.envint.2022.107209

Cited by 24 publications

(9 citation statements)

References 68 publications

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“…In vivo and in vitro studies have shown that exposure to OPFRs can induce adverse effects on the respiratory system. For example, Meng et al have confirmed that inhalation of alkyl-OPFRs will induce lung inflammation and aggravate asthmatic responses in mice (Meng et al, 2022). In another study, it was found that TDCIPP and exposure induced an adverse effect on the immunological health of the respiratory tract (Canbaz et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Tris(1,3-dichloro-2-propyl) phosphate-induced cytotoxicity and its associated mechanisms in human A549 cells

Feng,

Li,

Yin

et al. 2024

Toxicol Ind Health

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Tris(1,3-dichloro-2-propyl) phosphate (TDCIPP) is a widely used organophosphorus flame retardant and has been detected in various environmental matrices including indoor dust. Inhalation of indoor dust is one of the most important pathways for human exposure to TDCIPP. However, its adverse effects on human lung cells and potential impacts on respiratory toxicity are largely unknown. In the current study, human non-small cell carcinoma (A549) cells were selected as a cell model, and the effects of TDCIPP on cell viability, cell cycle, cell apoptosis, and underlying molecular mechanisms were investigated. Our data indicated a concentration-dependent decrease in the cell viability of A549 cells after exposure to TDCIPP for 48 h, with half lethal concentration (LC50) being 82.6 µM. In addition, TDCIPP caused cell cycle arrest mainly in the G0/G1 phase by down-regulating the mRNA expression of cyclin D1, CDK4, and CDK6, while up-regulating the mRNA expression of p21 and p27. In addition, cell apoptosis was induced via altering the expression levels of Bcl-2, BAX, and BAK. Our study implies that TDCIPP may pose potential health risks to the human respiratory system and its toxicity should not be neglected.

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Section: Introductionmentioning

confidence: 99%

Tris(1,3-dichloro-2-propyl) phosphate-induced cytotoxicity and its associated mechanisms in human A549 cells

Feng,

Li,

Yin

et al. 2024

Toxicol Ind Health

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“…An occupational cohort exposed to diesel engine exhaust (DEE) revealed that workers have a significantly thicker airway wall indicative of airway remodeling and lower spirometry measurements indicative of airway obstruction (H Liu H. et al, 2021). Meng et al (2022) reported that tri-n-butyl phosphate (TnBP), as a typical flame retardant ubiquitously detected in indoor and outdoor environments, induces airway hyperresponsiveness and the secretion of inflammatory mediators that exacerbate asthma. Thus, adverse effects on the airway induced by air pollutants can lead to a variety of lung diseases, and identifying potential hazard factors that are harmful to the airway and evaluating their toxic effects are of critical significance for the prevention of associated pulmonary disease.…”

Section: Introductionmentioning

confidence: 99%

Human airway organoids as 3D in vitro models for a toxicity assessment of emerging inhaled pollutants: Tire wear particles

Jiang

et al. 2023

Front. Bioeng. Biotechnol.

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Three-dimensional (3D) structured organoids have become increasingly promising and effective in vitro models, and there is an urgent need for reliable models to assess health effects of inhaled pollutants on the human airway. In our study, we conducted a toxicity assessment of human airway organoids (hAOs) for tire wear particles (TWPs) as an emerging inhaled pollutant. We induced primary human bronchial epithelial cells (HBECs) to generated human airway organoids, which recapitulated the key features of human airway epithelial cells including basal cells, ciliated cells, goblet cells, and club cells. TWPs generated from the wearing of tire treads were considered a major source of emerging inhaled road traffic-derived non-exhaust particles, but their health effect on the lungs is poorly understood. We used human airway organoids to assess the toxicology of tire wear particles on the human airway. In an exposure study, the inhibitory effect of TWPs on the growth of human airway organoids was observed. TWPs induced significant cell apoptosis and oxidative stress in a dose-dependent manner. From the qPCR analysis, TWPs significantly up-regulated the expression pf genes involved in the inflammation response. Additionally, the exposure of TWPs reduced SCGB1A1 gene expression associated with the function of the club cell and KRT5 gene expression related to the function of basal cells. In conclusion, this was first study using human airway organoids for a toxicological assessment of TWPs, and our findings revealed that human airway organoids provide an evaluation model of inhaled pollutants potentially affecting the lungs.

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“…The inflammation caused by organophosphates in the brain increases cytokines (interleukin 1 beta, IL-1β; tumor necrosis factor-alpha, TNFα; interleukin 6, IL-6), and chemokines and remains high for several days [16] . Exposure to organophosphates causes pulmonary damage through oxidative stress and inflammatory responses mediated by the Fkbp5/Nos3/MAPK/NF-κB signal pathway [17] . Recently, numerous studies have been focused on the role of miRs in OPCs toxicity.…”

Section: Introductionmentioning

confidence: 99%

Role of miRNAs in mediating organophosphate compounds induced toxicity

et al. 2023

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Alkyl organophosphate flame retardants (OPFRs) induce lung inflammation and aggravate OVA-simulated asthmatic response via the NF-кB signaling pathway

Cited by 24 publications

References 68 publications

Tris(1,3-dichloro-2-propyl) phosphate-induced cytotoxicity and its associated mechanisms in human A549 cells

Tris(1,3-dichloro-2-propyl) phosphate-induced cytotoxicity and its associated mechanisms in human A549 cells

Human airway organoids as 3D in vitro models for a toxicity assessment of emerging inhaled pollutants: Tire wear particles

Role of miRNAs in mediating organophosphate compounds induced toxicity

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