Tags

Type your tag names separated by a space and hit enter

Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice.
Toxicol Lett. 2013 Nov 25; 223(2):146-53.TL

Abstract

BACKGROUND

Air pollution is associated with significant adverse health effects including increased cardiovascular morbidity and mortality. However research on the cardiovascular effect of "real-world" exposure to ambient particulate matter (PM) in susceptible animal model is very limited. In this study, we aimed to investigate the association between Beijing ambient particle exposure and the atherosclerosis development in the apolipoprotein E knockout mice (ApoE(-/-) mice).

METHODS

Two parallel exposure chambers were used for whole body exposure among ApoE knockout mice. One of the chambers was supplied with untreated ambient air (PM group) and the other chamber was treated with ambient air filtered by high-efficiency particulate air (HEPA) filter (FA group). Twenty mice were divided into two groups and exposed to ambient PM (n=10 for PM group) or filtered air (n=10 for FA group) for two months from January 18th to March 18th, 2010. During the exposure, the mass concentrations of PM2.5 and PM10 in the two chambers were continuously monitored. Additionally, a receptor source apportionment model of chemical mass balance using 19 organic tracers was applied to determine the contributions of sources on the PM2.5 in terms of natural gas, diesel vehicle, gasoline vehicle, coal burning, vegetable debris, biomass burning and cooking. At the end of the two-month exposure, biomarkers of oxidative stress, inflammation and lipid metabolism in bronchoalveolar lavage fluid (BAL) and blood samples were determined and the plaque area on the aortic endothelium was quantified.

RESULTS

In the experiment, the concentrations of PM10 and PM2.5 in PM chamber were 99.45μg/m(3) and 61.0μg/m(3) respectively, while PM2.5 in FA chamber was 17.6μg/m(3). Source apportionment analysis by organic tracers showed that gasoline vehicle (39.9%) and coal burning (24.3%) emission were the two major sources contributing to the mass concentration of PM2.5 in Beijing. Among the ApoE knockout mice, the PM group were significantly higher than the FA group in terms of serum total cholesterol, low-density lipoprotein, tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein as well as TNF-alpha and interleukin-6 in BAL. Also the total antioxidant capacity and oxidized low-density lipoprotein were significantly different between the two groups. In addition, pathological analysis of aortic arch reveals that the plaques area in the PM group increased significantly compared to the FA group.

CONCLUSIONS

Our results demonstrated that ambient PM exposure could induce considerable oxidative stress and systemic inflammation in ApoE knockout mice and contribute to the progression of atherosclerosis.

Authors+Show Affiliations

Department of Occupational and Environmental Health Sciences, School of Public Health, Peking University, Beijing 100191, PR China. Electronic address: chentian@bjmu.edu.cn.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24045146

Citation

Chen, Tian, et al. "Beijing Ambient Particle Exposure Accelerates Atherosclerosis in ApoE Knockout Mice." Toxicology Letters, vol. 223, no. 2, 2013, pp. 146-53.
Chen T, Jia G, Wei Y, et al. Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice. Toxicol Lett. 2013;223(2):146-53.
Chen, T., Jia, G., Wei, Y., & Li, J. (2013). Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice. Toxicology Letters, 223(2), 146-53. https://doi.org/10.1016/j.toxlet.2013.09.004
Chen T, et al. Beijing Ambient Particle Exposure Accelerates Atherosclerosis in ApoE Knockout Mice. Toxicol Lett. 2013 Nov 25;223(2):146-53. PubMed PMID: 24045146.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Beijing ambient particle exposure accelerates atherosclerosis in ApoE knockout mice. AU - Chen,Tian, AU - Jia,Guang, AU - Wei,Yongjie, AU - Li,Jiucun, Y1 - 2013/09/14/ PY - 2013/07/26/received PY - 2013/09/06/revised PY - 2013/09/08/accepted PY - 2013/9/19/entrez PY - 2013/9/21/pubmed PY - 2014/1/15/medline KW - Ambient particle KW - ApoE knockout mice KW - Atherosclerosis KW - Lipid metabolism KW - Oxidative stress KW - Systemic inflammation SP - 146 EP - 53 JF - Toxicology letters JO - Toxicol Lett VL - 223 IS - 2 N2 - BACKGROUND: Air pollution is associated with significant adverse health effects including increased cardiovascular morbidity and mortality. However research on the cardiovascular effect of "real-world" exposure to ambient particulate matter (PM) in susceptible animal model is very limited. In this study, we aimed to investigate the association between Beijing ambient particle exposure and the atherosclerosis development in the apolipoprotein E knockout mice (ApoE(-/-) mice). METHODS: Two parallel exposure chambers were used for whole body exposure among ApoE knockout mice. One of the chambers was supplied with untreated ambient air (PM group) and the other chamber was treated with ambient air filtered by high-efficiency particulate air (HEPA) filter (FA group). Twenty mice were divided into two groups and exposed to ambient PM (n=10 for PM group) or filtered air (n=10 for FA group) for two months from January 18th to March 18th, 2010. During the exposure, the mass concentrations of PM2.5 and PM10 in the two chambers were continuously monitored. Additionally, a receptor source apportionment model of chemical mass balance using 19 organic tracers was applied to determine the contributions of sources on the PM2.5 in terms of natural gas, diesel vehicle, gasoline vehicle, coal burning, vegetable debris, biomass burning and cooking. At the end of the two-month exposure, biomarkers of oxidative stress, inflammation and lipid metabolism in bronchoalveolar lavage fluid (BAL) and blood samples were determined and the plaque area on the aortic endothelium was quantified. RESULTS: In the experiment, the concentrations of PM10 and PM2.5 in PM chamber were 99.45μg/m(3) and 61.0μg/m(3) respectively, while PM2.5 in FA chamber was 17.6μg/m(3). Source apportionment analysis by organic tracers showed that gasoline vehicle (39.9%) and coal burning (24.3%) emission were the two major sources contributing to the mass concentration of PM2.5 in Beijing. Among the ApoE knockout mice, the PM group were significantly higher than the FA group in terms of serum total cholesterol, low-density lipoprotein, tumor necrosis factor-alpha (TNF-alpha) and C-reactive protein as well as TNF-alpha and interleukin-6 in BAL. Also the total antioxidant capacity and oxidized low-density lipoprotein were significantly different between the two groups. In addition, pathological analysis of aortic arch reveals that the plaques area in the PM group increased significantly compared to the FA group. CONCLUSIONS: Our results demonstrated that ambient PM exposure could induce considerable oxidative stress and systemic inflammation in ApoE knockout mice and contribute to the progression of atherosclerosis. SN - 1879-3169 UR - https://www.unboundmedicine.com/medline/citation/24045146/Beijing_ambient_particle_exposure_accelerates_atherosclerosis_in_ApoE_knockout_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-4274(13)01311-8 DB - PRIME DP - Unbound Medicine ER -