Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles

Dongyoub Lee, Chris Wallis, Laura S. Van Winkle, Anthony S. Wexler

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 pm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.

Original languageEnglish (US)
Pages (from-to)520-531
Number of pages12
JournalInhalation Toxicology
Volume23
Issue number9
DOIs
StatePublished - Aug 2011

Fingerprint

Ozone
Growth
Air
Lung
Rats
Sprague Dawley Rats
Ultrafine
Control Groups
Recovery

Keywords

  • Children
  • Development disruption
  • Lung architecture
  • Ozone
  • Particles

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

Cite this

Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles. / Lee, Dongyoub; Wallis, Chris; Van Winkle, Laura S.; Wexler, Anthony S.

In: Inhalation Toxicology, Vol. 23, No. 9, 08.2011, p. 520-531.

Research output: Contribution to journalArticle

Lee, Dongyoub ; Wallis, Chris ; Van Winkle, Laura S. ; Wexler, Anthony S. / Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles. In: Inhalation Toxicology. 2011 ; Vol. 23, No. 9. pp. 520-531.
@article{eebfc47895934eb0a51b27ed75908580,
title = "Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles",
abstract = "This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 pm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.",
keywords = "Children, Development disruption, Lung architecture, Ozone, Particles",
author = "Dongyoub Lee and Chris Wallis and {Van Winkle}, {Laura S.} and Wexler, {Anthony S.}",
year = "2011",
month = "8",
doi = "10.3109/08958378.2011.591447",
language = "English (US)",
volume = "23",
pages = "520--531",
journal = "Inhalation Toxicology",
issn = "0895-8378",
publisher = "Informa Healthcare",
number = "9",

}

TY - JOUR

T1 - Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles

AU - Lee, Dongyoub

AU - Wallis, Chris

AU - Van Winkle, Laura S.

AU - Wexler, Anthony S.

PY - 2011/8

Y1 - 2011/8

N2 - This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 pm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.

AB - This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 pm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.

KW - Children

KW - Development disruption

KW - Lung architecture

KW - Ozone

KW - Particles

UR - http://www.scopus.com/inward/record.url?scp=80051526069&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80051526069&partnerID=8YFLogxK

U2 - 10.3109/08958378.2011.591447

DO - 10.3109/08958378.2011.591447

M3 - Article

C2 - 21780864

AN - SCOPUS:80051526069

VL - 23

SP - 520

EP - 531

JO - Inhalation Toxicology

JF - Inhalation Toxicology

SN - 0895-8378

IS - 9

ER -