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Airway exposure to urban aerosolized PM2.5 particles induces neuroinflammation and endothelin-mediated contraction of coronary arteries in adult rats

Voss, Ulrikke LU ; Uller, Lena LU ; Ansar, Saema LU ; Mahmutovic Persson, Irma LU ; Akbarshahi, Hamid LU ; Cerps, Samuel LU ; Isaxon, Christina LU and Ohlsson, Lena LU (2022) In Environmental Advances 8.
Abstract

Ambient airborne particles with an aerodynamic diameter of <2.5 µm (PM2.5), which contain particles from combustion processes, are linked to increased risks for cardiovascular and respiratory diseases. In this experimental study, the short-term and long-term physiologic consequences of PM2.5 inhalation were investigated with the focus on inflammatory parameters and vascular tonus. PM2.5 collected from urban environments in southern Sweden were aerosolized with a nebulizer and delivered to male Sprague Dawley rats. The rats were divided into two treatment groups (n=8 in each): short-term exposed (8 h with an estimated lung exposure rate of 90 μg PM2.5/h); and long-term exposed (3 h/day, 5... (More)

Ambient airborne particles with an aerodynamic diameter of <2.5 µm (PM2.5), which contain particles from combustion processes, are linked to increased risks for cardiovascular and respiratory diseases. In this experimental study, the short-term and long-term physiologic consequences of PM2.5 inhalation were investigated with the focus on inflammatory parameters and vascular tonus. PM2.5 collected from urban environments in southern Sweden were aerosolized with a nebulizer and delivered to male Sprague Dawley rats. The rats were divided into two treatment groups (n=8 in each): short-term exposed (8 h with an estimated lung exposure rate of 90 μg PM2.5/h); and long-term exposed (3 h/day, 5 days/week, for 8 weeks, with an estimated lung exposure rate of 30 μg PM2.5/h). A group of non-particle-exposed control animals (n=8) was run in parallel with each test group. The results showed that short-term exposure increased the numbers of lymphocytes in the bronchoalveolar lavage fluids. Long-term exposure led to impaired substance P-induced relaxation and increased endothelin-1-induced contraction of the coronary arteries. The contractile response was found to be mediated by endothelin receptor A. Long-term exposure led to increased interleukin-6 levels in brain tissues, as compared to the controls. In summary, this explorative study reveals that exposure to aerosolized, ambient PM2.5 leads to impaired coronary artery function and neuroinflammation. Further investigations into the impacts on health effects of short-term and long-term exposures to urban air pollution are warranted.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Air pollution, Airway exposure, Ambient PM, Immune response, Physiology
in
Environmental Advances
volume
8
article number
100184
publisher
Elsevier
external identifiers
  • scopus:85124898488
ISSN
2666-7657
DOI
10.1016/j.envadv.2022.100184
language
English
LU publication?
yes
id
56169bf4-fa72-433d-9a6e-d99a808043d1
date added to LUP
2022-04-12 11:58:40
date last changed
2023-11-10 03:36:30
@article{56169bf4-fa72-433d-9a6e-d99a808043d1,
  abstract     = {{<p>Ambient airborne particles with an aerodynamic diameter of &lt;2.5 µm (PM<sub>2.5</sub>), which contain particles from combustion processes, are linked to increased risks for cardiovascular and respiratory diseases. In this experimental study, the short-term and long-term physiologic consequences of PM<sub>2.5</sub> inhalation were investigated with the focus on inflammatory parameters and vascular tonus. PM<sub>2.5</sub> collected from urban environments in southern Sweden were aerosolized with a nebulizer and delivered to male Sprague Dawley rats. The rats were divided into two treatment groups (n=8 in each): short-term exposed (8 h with an estimated lung exposure rate of 90 μg PM<sub>2.5</sub>/h); and long-term exposed (3 h/day, 5 days/week, for 8 weeks, with an estimated lung exposure rate of 30 μg PM<sub>2.5</sub>/h). A group of non-particle-exposed control animals (n=8) was run in parallel with each test group. The results showed that short-term exposure increased the numbers of lymphocytes in the bronchoalveolar lavage fluids. Long-term exposure led to impaired substance P-induced relaxation and increased endothelin-1-induced contraction of the coronary arteries. The contractile response was found to be mediated by endothelin receptor A. Long-term exposure led to increased interleukin-6 levels in brain tissues, as compared to the controls. In summary, this explorative study reveals that exposure to aerosolized, ambient PM<sub>2.5</sub> leads to impaired coronary artery function and neuroinflammation. Further investigations into the impacts on health effects of short-term and long-term exposures to urban air pollution are warranted.</p>}},
  author       = {{Voss, Ulrikke and Uller, Lena and Ansar, Saema and Mahmutovic Persson, Irma and Akbarshahi, Hamid and Cerps, Samuel and Isaxon, Christina and Ohlsson, Lena}},
  issn         = {{2666-7657}},
  keywords     = {{Air pollution; Airway exposure; Ambient PM; Immune response; Physiology}},
  language     = {{eng}},
  publisher    = {{Elsevier}},
  series       = {{Environmental Advances}},
  title        = {{Airway exposure to urban aerosolized PM<sub>2.5</sub> particles induces neuroinflammation and endothelin-mediated contraction of coronary arteries in adult rats}},
  url          = {{http://dx.doi.org/10.1016/j.envadv.2022.100184}},
  doi          = {{10.1016/j.envadv.2022.100184}},
  volume       = {{8}},
  year         = {{2022}},
}