Faculty Opinions recommendation of Cigarette smoke drives small airway remodeling by induction of growth factors in the airway wall.

Author(s):  
Caroline Owen
2006 ◽  
Vol 174 (12) ◽  
pp. 1327-1334 ◽  
Author(s):  
Andrew Churg ◽  
Hsin Tai ◽  
Tonya Coulthard ◽  
Rona Wang ◽  
Joanne L. Wright

2009 ◽  
Vol 40 (4) ◽  
pp. 482-490 ◽  
Author(s):  
Andrew Churg ◽  
Steven Zhou ◽  
Xiaoshan Wang ◽  
Rona Wang ◽  
Joanne L. Wright

Author(s):  
Maria E. Laucho-Contreras ◽  
Katherine L. Taylor ◽  
Ravi Mahadeva ◽  
Steve S. Boukedes ◽  
Caroline A. Owen

2020 ◽  
Vol 178 (1) ◽  
pp. 26-35
Author(s):  
Xue Cao ◽  
Li Lin ◽  
Akshay Sood ◽  
Qianli Ma ◽  
Xiangyun Zhang ◽  
...  

Abstract Nanoscale carbon black as virtually pure elemental carbon can deposit deep in the lungs and cause pulmonary injury. Airway remodeling assessed using computed tomography (CT) correlates well with spirometry in patients with obstructive lung diseases. Structural airway changes caused by carbon black exposure remain unknown. Wall and lumen areas of sixth and ninth generations of airways in 4 lobes were quantified using end-inhalation CT scans in 58 current carbon black packers (CBPs) and 95 non-CBPs. Carbon content in airway macrophage (CCAM) in sputum was quantified to assess the dose-response. Environmental monitoring and CCAM showed a much higher level of elemental carbon exposure in CBPs, which was associated with higher wall area and lower lumen area with no change in total airway area for either airway generation. This suggested small airway wall thickening is a major feature of airway remodeling in CBPs. When compared with wall or lumen areas, wall area percent (WA%) was not affected by subject characteristics or lobar location and had greater measurement reproducibility. The effect of carbon black exposure status on WA% did not differ by lobes. CCAM was associated with WA% in a dose-dependent manner. CBPs had lower FEV1 (forced expiratory volume in 1 s) than non-CBPs and mediation analysis identified that a large portion (41–72%) of the FEV1 reduction associated with carbon black exposure could be explained by WA%. Small airway wall thickening as a major imaging change detected by CT may underlie the pathology of lung function impairment caused by carbon black exposure.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Hong Liu ◽  
Jianyu Li ◽  
Qianli Ma ◽  
Jinglong Tang ◽  
Menghui Jiang ◽  
...  

Abstract Background Diesel exhaust (DE) is a major source of ultrafine particulate matters (PM) in ambient air and contaminates many occupational settings. Airway remodeling assessed using computerized tomography (CT) correlates well with spirometry in patients with obstructive lung diseases. Structural changes of small airways caused by chronic DE exposure is unknown. Wall and lumen areas of 6th and 9th generations of four candidate airways were quantified using end-inhalation CT scans in 78 diesel engine testers (DET) and 76 non-DETs. Carbon content in airway macrophage (CCAM) in sputum was quantified to assess the dose-response relationship. Results Environmental monitoring and CCAM showed a much higher PM exposure in DETs, which was associated with higher wall area and wall area percent for 6th generation of airways. However, no reduction in lumen area was identified. No study subjects met spirometry diagnosis of airway obstruction. This suggested that small airway wall thickening without lumen narrowing may be an early feature of airway remodeling in DETs. The effect of DE exposure status on wall area percent did not differ by lobes or smoking status. Although the trend test was of borderline significance between categorized CCAM and wall area percent, subjects in the highest CCAM category has a 14% increase in wall area percent for the 6th generation of airways compared to subjects in the lowest category. The impact of DE exposure on FEV1 can be partially explained by the wall area percent with mediation effect size equal to 20%, Pperm = 0.028). Conclusions Small airway wall thickening without lumen narrowing may be an early image feature detected by CT and underlie the pathology of lung injury in DETs. The pattern of changes in small airway dimensions, i.e., thicker airway wall without lumen narrowing caused by occupational DE exposure was different to that (i.e., thicker airway wall with lumen narrowing) seen in our previous study of workers exposed to nano-scale carbon black aerosol, suggesting constituents other than carbon cores may contribute to such differences. Our study provides some imaging indications of the understanding of the pulmonary toxicity of combustion derived airborne particulate matters in humans.


Sign in / Sign up

Export Citation Format

Share Document