Real-world exposure of airborne particulate matter triggers oxidative stress in an animal model
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Updated: Jun 3, 2026
Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Abstract:
Epidemiological studies have shown a strong link between air pollution and the increase of cardio-pulmonary mortality and morbidity. In particular, inhaled airborne particulate matter (PM) exposure is closely associated with the pathogenesis of air pollution-induced systemic diseases. In this study, we exposed C57BIV6 mice to environmentally relevant PM in fine and ultra fine ranges (diameter < 2.5 μm, PM(2.5)) using a "real-world" airborne PM exposure system. We investigated the pathophysiologic impact of PM(2.5) exposure in the animal model and in cultured primary pulmonary macrophages. We demonstrated that PM(2.5) exposure increased the production of reactive oxygen species (ROS) in blood vessels in vivo. Furthermore, in vitro PM(2.5) exposure experiment suggested that PM(2.5) could trigger oxidative stress response, reflected by an increased expression of the anti-oxidative stress enzymes superoxide dismutase-1 (SOD-1) and heme oxygenase-1(HO-1), in mouse primary macrophages. Together, the results obtained through our "real-world" PM exposure approach demonstrated the pathophysiologic effect of ambient PM(2.5) exposure on triggering oxidative stress in the specialized organ and cell type of an animal model. Our results and approach will be informative for the research in air pollution-associated physiology and pathology.
Insights
Exposure to fine particulate matter (PM2.5) from air pollution triggers oxidative stress in blood vessels and macrophages. This study reveals PM2.5
Area of Science:
- Environmental Health
- Toxicology
- Cardiovascular Research
Background:
- Air pollution, particularly fine particulate matter (PM2.5), is linked to increased cardio-pulmonary disease.
- PM2.5 exposure is associated with the development of systemic diseases.
Purpose of the Study:
- To investigate the pathophysiologic effects of PM2.5 exposure.
- To examine PM2.5's impact on an animal model and primary pulmonary macrophages.
Main Methods:
- Mice (C57BIV6) were exposed to real-world PM2.5 using an advanced exposure system.
- In vivo and in vitro experiments were conducted on mice and cultured macrophages.
- Oxidative stress markers, including reactive oxygen species (ROS) and antioxidant enzymes (SOD-1, HO-1), were measured.
Main Results:
- PM2.5 exposure increased reactive oxygen species (ROS) production in mouse blood vessels.
- In cultured macrophages, PM2.5 exposure induced an oxidative stress response.
- Increased expression of superoxide dismutase-1 (SOD-1) and heme oxygenase-1 (HO-1) was observed in macrophages.
Conclusions:
- Real-world PM2.5 exposure triggers oxidative stress in animal models.
- PM2.5 affects both specialized organs and cell types, contributing to air pollution-related pathology.
- The findings provide insights into air pollution's impact on physiology and pathology.
