ArticleEnvironmental science and pollution research international2019
The toxicological analysis of secondary organic aerosol in human lung epithelial cells and macrophages.
Article in Environmental science and pollution research international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 31 citations in OpenAlex.
- [Mechanism of 2,6-DMBQ attenuates airway inflammatory responses in asthmatic mice via the mTOR signaling pathway].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Article
- Secondary Organic Aerosol Generated from Biomass Burning Emitted Phenolic Compounds: Oxidative Potential, Reactive Oxygen Species, and Cytotoxicity.Environmental science & technology · 2024Article
- In Vitro Systems for Toxicity Evaluation of Microbial Volatile Organic Compounds on Humans: Current Status and Trends.Journal of fungi (Basel, Switzerland) · 2022Review
- Air quality changes in cities during the COVID-19 lockdown: A critical review.Atmospheric research · 2021Review
- Toxicological Responses of α-Pinene-Derived Secondary Organic Aerosol and Its Molecular Tracers in Human Lung Cell Lines.Chemical research in toxicology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Secondary organic aerosol (SOA) is a component of airborne particulate matter in urban areas. However, their toxicities remain incompletely understood. In this study, we investigated the oxidative and inflammatory potency of SOA derived from three different volatile organic compounds (α-pinene, m-xylene, and trimethylbenzene) using human bronchial epithelial cells (BEAS-2B) and macrophages (U937). In BEAS-2B cells, all types of SOA extracts increased the expression of the heme oxygenase 1 (HMOX1) and interleukin-8 (IL8) genes, a typical marker for oxidative stress and inflammatory responses, respectively. Among the three types of SOA, m-xylene-derived SOA showed the strongest induction of the HMOX1 and IL8 genes, and transcriptional activity via the antioxidant response element (ARE). A causal candidate for SOA induction of oxidative stress is 2,6-dimethyl-1,4-benzoquinone (DMBQ) because only this quinone compound increased the transcriptional activity via ARE among components tested in this study. Similar to the case of BEAS-2B cells, SOA extracts increased the expression of HMOX1 and IL8 genes in U937 cells, mainly through oxidative stress, but these responses in U937 cells were prolonged when compared with BEAS-2B cells. Together, these results show that SOA affects lung epithelial cells and macrophages mainly through oxidative stress and inflammation, suggesting their contribution to the development of respiratory diseases.
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