Ultrafine particulate matter combined with ozone exacerbates lung injury in mature adult rats with cardiovascular disease

Emily M. Wong, William F. Walby, Dennis W Wilson, Fern Tablin, Edward S Schelegle

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (~ 250 lg/m3); O3 (1.0 ppm); or UFPM+O3 (~ 250 lg/m3 +1.0 ppm) combined for 6 h, followed by an 8h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3 exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3 increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.

Original languageEnglish (US)
Pages (from-to)140-151
Number of pages12
JournalToxicological Sciences
Volume163
Issue number1
DOIs
StatePublished - May 1 2018

Fingerprint

Particulate Matter
Ozone
Lung Injury
Rats
Cardiovascular Diseases
Inbred SHR Rats
Air Pollution
Air pollution
Lung
Air
Bronchioles
Air Pollutants
Inbred WKY Rats
Wounds and Injuries
Ultrafine
Atmosphere
Ducts
Morbidity
Recovery
Degradation

Keywords

  • Agents
  • Cardiovascular disease
  • Histopathology
  • Inhalation toxicology
  • Lung
  • Methods
  • Particulates
  • Polycyclic aromatic hydrocarbons
  • Pulmonary or respiratory system
  • Respiratory toxicology
  • Respiratory toxicology
  • Respiratory toxicology

ASJC Scopus subject areas

  • Toxicology

Cite this

Ultrafine particulate matter combined with ozone exacerbates lung injury in mature adult rats with cardiovascular disease. / Wong, Emily M.; Walby, William F.; Wilson, Dennis W; Tablin, Fern; Schelegle, Edward S.

In: Toxicological Sciences, Vol. 163, No. 1, 01.05.2018, p. 140-151.

Research output: Contribution to journalArticle

@article{b6bf3705d3cf480da170e2e996ba80be,
title = "Ultrafine particulate matter combined with ozone exacerbates lung injury in mature adult rats with cardiovascular disease",
abstract = "Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (~ 250 lg/m3); O3 (1.0 ppm); or UFPM+O3 (~ 250 lg/m3 +1.0 ppm) combined for 6 h, followed by an 8h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3 exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3 increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.",
keywords = "Agents, Cardiovascular disease, Histopathology, Inhalation toxicology, Lung, Methods, Particulates, Polycyclic aromatic hydrocarbons, Pulmonary or respiratory system, Respiratory toxicology, Respiratory toxicology, Respiratory toxicology",
author = "Wong, {Emily M.} and Walby, {William F.} and Wilson, {Dennis W} and Fern Tablin and Schelegle, {Edward S}",
year = "2018",
month = "5",
day = "1",
doi = "10.1093/toxsci/kfy018",
language = "English (US)",
volume = "163",
pages = "140--151",
journal = "Toxicological Sciences",
issn = "1096-6080",
publisher = "Oxford University Press",
number = "1",

}

TY - JOUR

T1 - Ultrafine particulate matter combined with ozone exacerbates lung injury in mature adult rats with cardiovascular disease

AU - Wong, Emily M.

AU - Walby, William F.

AU - Wilson, Dennis W

AU - Tablin, Fern

AU - Schelegle, Edward S

PY - 2018/5/1

Y1 - 2018/5/1

N2 - Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (~ 250 lg/m3); O3 (1.0 ppm); or UFPM+O3 (~ 250 lg/m3 +1.0 ppm) combined for 6 h, followed by an 8h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3 exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3 increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.

AB - Particulate matter (PM) and ozone (O3) are dominant air pollutants that contribute to development and exacerbation of multiple cardiopulmonary diseases. Mature adults with cardiovascular disease (CVD) are particularly susceptible to air pollution-related cardiopulmonary morbidities and mortalities. The aim was to investigate the biologic potency of ultrafine particulate matter (UFPM) combined with O3 in the lungs of mature adult normotensive and spontaneously hypertensive (SH) Wistar-Kyoto rats. Conscious, mature adult male normal Wistar-Kyoto (NW) and SH rats were exposed to one of the following atmospheres: filtered air (FA); UFPM (~ 250 lg/m3); O3 (1.0 ppm); or UFPM+O3 (~ 250 lg/m3 +1.0 ppm) combined for 6 h, followed by an 8h FA recovery period. Lung sections were evaluated for lesions in the large airways, terminal bronchiolar/alveolar duct regions, alveolar parenchyma, and vasculature. NW and SH rats were similarly affected by the combined-pollutant exposure, displaying severe injury in both large and small airways. SH rats were particularly susceptible to O3 exposure, exhibiting increased injury scores in terminal bronchioles and epithelial degeneration in large airways. UFPM-exposure groups had minimal histologic changes. The chemical composition of UFPM was altered by the addition of O3, indicating that ozonolysis promoted compound degradation. O3 increased the biologic potency of UFPM, resulting in greater lung injury following exposure. Pathologic manifestations of CVD may confer susceptibility to air pollution by impairing normal lung defenses and responses to exposure.

KW - Agents

KW - Cardiovascular disease

KW - Histopathology

KW - Inhalation toxicology

KW - Lung

KW - Methods

KW - Particulates

KW - Polycyclic aromatic hydrocarbons

KW - Pulmonary or respiratory system

KW - Respiratory toxicology

KW - Respiratory toxicology

KW - Respiratory toxicology

UR - http://www.scopus.com/inward/record.url?scp=85046997465&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85046997465&partnerID=8YFLogxK

U2 - 10.1093/toxsci/kfy018

DO - 10.1093/toxsci/kfy018

M3 - Article

C2 - 29394414

AN - SCOPUS:85046997465

VL - 163

SP - 140

EP - 151

JO - Toxicological Sciences

JF - Toxicological Sciences

SN - 1096-6080

IS - 1

ER -