Ambient mineral particles in the small airways of the normal human lung

Churg, Andrew; Brauer, Michael; Vedal, Sverre; Stevens, Bonnie

doi:10.1002/(sici)1099-1301(199901/03)1:1<39::aid-jem6>3.3.co;2-x

Cited by 5 publications

(5 citation statements)

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“…Analytical electron microscopic studies by Churg and colleagues (23) have revealed that the concentration of particles in respiratory bronchioles can be 25-100 times greater than the concentration of particles in the mainstem bronchus (23). This finding is in keeping with our own observations.…”

Section: Discussionsupporting

confidence: 86%

Distribution of particulate matter and tissue remodeling in the human lung.

Pinkerton

Green

Saiki

et al. 2000

Environ Health Perspect

184

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We examined the relationship between intrapulmonary particle distribution of carbonaceous and mineral dusts and remodeling of the airways along anatomically distinct airway paths in the lungs of Hispanic males from the central valley of California. Lung autopsy specimens from the Fresno County Coroner's Office were prepared by intratracheal instillation of 2% glutaraldehyde at 30 cm H(2)O pressure. Two distinct airway paths into the apico-posterior and apico-anterior portions of the left upper lung lobe were followed. Tissue samples for histologic analysis were generally taken from the intrapulmonary second, fourth, sixth, and ninth airway generations. Parenchymal tissues beyond the 12th airway generation of each airway path were also analyzed. There was little evidence of visible particle accumulation in the larger conducting airways (generations 2-6), except in bronchial-associated lymphoid tissues and within peribronchial connective tissue. In contrast, terminal and respiratory bronchioles arising from each pathway revealed varying degrees of wall thickening and remodeling. Walls with marked thickening contained moderate to heavy amounts of carbonaceous and mineral dusts. Wall thickening was associated with increases in collagen and interstitial inflammatory cells, including dust-laden macrophages. These changes were significantly greater in first-generation respiratory bronchioles compared to second- and third-generation respiratory bronchioles. These findings suggest that accumulation of carbonaceous and mineral dust in the lungs is significantly affected by lung anatomy with the greatest retention in centers of lung acini. Furthermore, there is significant remodeling of this transitional zone in humans exposed to ambient particulate matter.

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Section: Discussionsupporting

confidence: 86%

Distribution of particulate matter and tissue remodeling in the human lung.

Pinkerton

Green

Saiki

et al. 2000

Environ Health Perspect

184

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“…Within the human lung, it was observed that PM2.5 ambient air pollutant particles can accumulate in the SA, particularly in the distal bronchioles at up to 25 times greater doses than bronchial regions [31]. Similar findings have been observed for other fine-sized particles including those from tobacco smoke [32, 33] and inorganic dusts such as silica and asbestos, where concomitant SA disease is also observed [34-40]. Due to airflow and structural differences within the respiratory tract, smaller ultrafine (<0.1 μm) and larger coarse (2.5–10 μm) particles preferentially deposit in nasal regions more than fine-sized particles [41, 42].…”

Section: Structural Considerations and Regional Airway Susceptibilitymentioning

confidence: 74%

Small Airway Susceptibility to Chemical and Particle Injury

Fransen

Leonard²

2021

Respiration

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Small airways (SA) in humans are commonly defined as those conducting airways <2 mm in diameter. They are susceptible to particle- and chemical-induced injury and play a major role in the development of airway disease such as COPD and asthma. Susceptibility to injury can be attributed in part to structural features including airflow dynamics and tissue architecture, but recent evidence may indicate a more prominent role for cellular composition in directing toxicological responses. Animal studies support the hypothesis that inherent cellular differences across the tracheobronchial tree, including metabolic CYP450 expression in the distal conducting airways, can influence SA susceptibility to injury. Currently, there is insufficient information in humans to make similar conclusions, prompting further necessary work in this area. An understanding of why the SA are more susceptible to certain chemical and particle exposures than other airway regions is fundamental to our ability to identify hazardous materials, their properties, and accompanying exposure scenarios that compromise lung function. It is also important for the ability to develop appropriate models for toxicity testing. Moreover, it is central to our understanding of SA disease aetiology and how interventional strategies for treatment may be developed. In this review, we will document the structural and cellular airway regional differences that are likely to influence airway susceptibility to injury, including the role of secretory club cells. We will also describe recent advances in single-cell sequencing of human airways, which have provided unprecedented details of cell phenotype, likely to impact airway chemical and particle injury.

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“…12 We investigated this process using electron microscopic analysis of microdissected airway mucosa (i.e., all tissues from the lumen to the cartilage or adventitia) of airways of varying generations in human autopsy lungs. 13 Particle concentrations in the airway tissues were remarkably high, ranging from 10 ϫ 10 6 to almost 10 ϫ 10 9 particles/gm dry tissue. The lowest mean particle concentrations were seen in the mainstem bronchi, higher concentrations in the segmental bronchi, and the highest concentrations in the MB and especially the RB (Fig.…”

Section: Pathogenesis Of Particle-induced Small Airways Diseasementioning

confidence: 99%

Bronchiolitis Caused by Occupational and Ambient Atmospheric Particles

Churg

Wright²

2003

Seminars in Respiratory and Critical Care Medicine

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Occupationally encountered mineral dusts such as asbestos, silica, silicates (talc, mica), and metals can produce a distinctive pattern of fibrosis and distortion of the small airways, particularly the distal membranous bronchioles (MB) and the respiratory bronchioles (RB). Recent reports show that the same types of changes, accompanied by considerable muscle hyperplasia, are found in individuals living in regions with high levels of particulate air pollutants (PM). Models and actual measurements suggest that these changes occur because the small airways are sites of high particle deposition, and inhaled and deposited particulates, including PM, enter the airway walls. Studies from our laboratory using a tracheal explant model have shown that, for many types of particles, entry into the airway wall causes expression of mediators that lead to airway wall fibrosis and airway wall smooth muscle hyperplasia, probably through oxidant mechanisms. These reactions are intrinsic properties of the particles and do not require exogenous inflammatory cells. There is considerable evidence that individuals with occupational exposure to a wide variety of mineral dusts, as well as individuals with chronic exposure to high levels of PM, develop chronic airflow obstruction. The type of small airway remodeling seen in particle-induced bronchiolitis appears to be one cause of chronic airflow obstruction in this setting.

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Ambient mineral particles in the small airways of the normal human lung

Cited by 5 publications

References 0 publications

Distribution of particulate matter and tissue remodeling in the human lung.

Distribution of particulate matter and tissue remodeling in the human lung.

Small Airway Susceptibility to Chemical and Particle Injury

Bronchiolitis Caused by Occupational and Ambient Atmospheric Particles

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