Chronic exposure to diesel exhaust may cause small airway wall thickening without lumen narrowing: a quantitative computerized tomography study in Chinese diesel engine testers

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.

2-IPMA Ameliorates PM2.5-Induced Inflammation by Promoting Primary Ciliogenesis in RPE Cells

“…Numerous studies have demonstrated the significant induction of proinflammatory cytokines in diabetes patients; moreover, diabetic retinopathy is the most common microvascular complication of diabetes and the leading cause of retinopathy [ 47 ]. In addition, PM2.5 induces inflammation and cell death in human trabecular meshwork cells to trigger ocular hypertension and glaucoma [ 48 ]. Given these previous findings, we chose to assess proinflammatory cytokine levels and found that RPE cells exposed to PM2.5 showed a large increase in the secretion of IL-6 and TNF-α, which are both associated with retinopathy [ 27 , 47 ].…”

Fine particulate matter contributes to COPD-like pathophysiology: experimental evidence from rats exposed to diesel exhaust particles

“…Wang et al showed that long-term exposure to ambient PM 2.5 or black carbon correlated significantly with computed tomographic defining emphysema in adults [ 32 ]. Liu et al suggested that chronic exposure to diesel exhaust may be related to small airway wall thickening in diesel engine testers [ 33 ]. In the present study, we confirmed the causal effects of DEP exposure on small airway remodeling as well as lung emphysema and associated lung function impairments.…”

CXCL17 Attenuates Diesel Exhaust Emissions Exposure-Induced Lung Damage by Regulating Macrophage Function

“…Several epidemiological studies have reported a higher incidence of asthma among children in high DEE exposure areas, as well as a higher frequency of hospitalization for asthma and COPD exacerbation among long-term DEE-exposed populations [ 27 , 28 , 29 ]. Our prior study revealed that small airway walls were significantly thickened in the workers under chronic exposure to diesel exhaust [ 30 ]. In this study, we found that mice exposed to DEE developed airway epithelial damage, airway smooth muscle hyperplasia, and excessive peribronchial collagen deposition, which was accompanied by worse respiratory parameters (reduced respiratory flow rate, tidal volume, airway relaxation time, etc.).…”