Bronchiolitis Caused by Occupational and Ambient Atmospheric Particles

ABSTRACT

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.

KEYWORDS

COPD - mineral particles - air pollution - small airway remodeling - asbestos - silica - silicates

REFERENCES

• 1 Churg A. Small airways disease associated with mineral dust exposure.  Sem Respir Med . 1992;  13 140-148
• 2 Churg A, Brauer M, Carmen Avila-Casado M, Fortoul T I, Wright J. Chronic exposure to high levels of particulate air pollution and small airways remodeling.  Environ Hlth Perspect . 2003;  111 714-718
• 3 Souza M B, Saldiva P H, Pope III A C, Capelozzi V L. Respiratory changes due to long-term exposure to urban levels of air pollution: a histopathologic study in humans.  Chest . 1998;  113 1312-1318
• 4 Pinkerton K E, Green F H, Saiki C. et al . Distribution of particulate matter and tissue remodeling in the human lung.  Environ Hlth Perspect . 2000;  108 1063-1069
• 5 Green F HY. Coal workers' pneumoconiosis and pneumoconioses due to other carbonaceous dusts. In: Churg A, Green FHY, eds. Pathology of Occupational Lung Disease Baltimore: Williams and Wilkins; 1998
• 6 Churg A, Wright J L. Small-airway lesions in patients exposed to nonasbestos mineral dusts.  Hum Pathol . 1983;  14 688-693
• 7 Wright J L, Churg A. Morphology of small-airway lesions in patients with asbestos exposure.  Hum Pathol . 1984;  15 68-74
• 8 Churg A, Wright J L, Wiggs B, Pare P D, Lazar N. Small airways disease and mineral dust exposure.  Am Rev Respir Dis . 1985;  131 139-143
• 9 Churg A. Pathological findings in the lungs of long-term Quebec chrysotile miners and millers: an analysis of 247 cases. In: Nolan RP, Langer AM, Ross M, Wicks FJ, Martin RF, eds. The Health Effects of Chrysotile Asbestos Ottawa: Mineralogical Society of Canada; 2001;207-211. Special Publication No 5
• 10 Perez-Padilla R, Regalado J, Vedal S. et al . Exposure to biomass smoke and chronic airway disease in Mexican women.  Am J Respir Crit Care Med . 1996;  154 701-706
• 11 Dennis R, Maldonado D, Norman S, Baena E. Woodsmoke exposure and risk for obstructive airways disease among women.  Chest . 1996;  109 115-119
• 12 Gerrity T R, Lee P S, Hass F J, Marinelli A, Wenrer P, Lourenco R V. Calculated deposition of inhaled particles in the airway generations of normal subjects.  J Appl Physiol . 1979;  47 867-873
• 13 Churg A, Brauer M, Vedal S, Stevens B. Ambient mineral particles in the small airways of the normal human lung.  J Environ Med . 1999;  1 39-46
• 14 Churg A, Wright J L. Mineral particles in airway walls in the lungs of long-term chrysotile miners.  Ann Occup Hyg . 1988;  32 (suppl 1) S173-S180
• 15 Dai J, Gilks B, Price K, Churg A. Mineral dusts directly induce epithelial and interstitial fibrogenic mediators and matrix components in the airway wall.  Am J Respir Crit Care Med . 1998;  158 1907-1913
• 16 Dai J, Churg A. Relationship of fiber surface iron and active oxygen species to expression of procollagen, PDGF-A, and TGFβ1 in tracheal explants exposed to amosite asbestos.  Am J Respir Cell Mol Biol . 2001;  24 427-435
• 17 Dai J, Xie C, Churg A. Iron loading makes a nonfibrogenic model air pollutant particle fibrogenic in rat tracheal explants.  Am J Respir Cell Mol Biol . 2002;  26 685-693
• 18 Dai J, Xie C, Vincent R, Churg A. Air pollution particles produce airway wall remodeling in rat tracheal explants.  Amer J Respir Cell Molec Biol . 2003;  29 352-358
• 19 Black P N, Young P G, Skinner S J. Response of airway smooth muscle cells to TGFβ₁: effects on growth and synthesis of glycosaminoglycans.  Am J Physiol . 1996;  271 L910-L917
• 20 Becklake M R. Chronic airflow limitation: its relationship to work in dusty occupations.  Chest . 1985;  88 608-617
• 21 Becklake M R. Occupational exposures: evidence for a causal association with chronic obstructive pulmonary disease.  Am Rev Respir Dis . 1989;  140(suppl) S85-S91
• 22 Oxman A D, Muir D CF, Shannon H S. et al . Occupational dust exposure and chronic obstructive pulmonary disease: a systematic overview of the evidence.  Am Rev Respir Dis . 1993;  148 38-48
• 23 Dimich-Ward H, Kennedy S, Chan-Yeung M. Occupational exposures and chronic airflow obstruction.  Can Respir J . 1996;  3 133-140
• 24 Begin R, Ostiguy G, Cantin A, Bergeron D. Lung function in silica-exposed workers.  Chest . 1988;  94 539-545
• 25 Abbey D E, Mills P K, Petersen F F, Beeson W L. Long-term ambient concentrations of total suspended particulates and oxidants as related to incidence of chronic disease in California Seventh-Day Adventists.  Environ Health Perspect . 1991;  94 43-50
• 26 Abbey D E, Ostro B E, Petersen F, Burchette R J. Chronic respiratory symptoms associated with estimated long-term ambient concentrations of fine particulates less than 2.5 microns in aerodynamic diameter (PM2.5) and other air pollutants.  J Expo Anal Environ Epidemiol . 1995;  5 137-159
• 27 Sunyer J. Urban air pollution and chronic obstructive pulmonary disease: a review.  Eur Respir J . 2001;  17 1024-1033
• 28 Leigh J, Outhred K G, McKenzie H I, Glick M, Wiles A N. Quantified pathology of emphysema, pneumoconiosis, and chronic bronchitis in coal workers.  Br J Ind Med . 1983;  40 258-263
• 29 Cockcroft A, Wagner J C, Ryder R, Seal R ME, Lyons J P, Anderson N. Post-mortem study of emphysema in coal workers and non-coal workers.  Lancet . 1982;  2 600-603
• 30 Begin R, Filion R, Ostiguy G. Emphysema in silica and asbestos exposed workers seeking compensation: a CT scan study.  Chest . 1995;  108 647-655
• 31 Becklake M R, Irwig L, Kielkowski D, Webster I, de Beer M, Landau S. The predictors of emphysema in South African gold miners.  Am Rev Respir Dis . 1987;  135 1234-1241
• 32 Hnizdo E, Sluis-Cremer K, Abramowitz J. Emphysema type in relation to silica dust exposure in South African gold miners.  Am Rev Respir Dis . 1991;  143 1241-1247
• 33 Begin R, Masse S. Bureau MA.  Morphologic features and function of the airways in early asbestosis in the sheep model. Am Rev Respir Dis . 1982;  126 870-876
• 34 Bosken C H, Wiggs B R, Pare P D, Hogg J C. Small airway dimensions in smokers with obstruction to airflow.  Am Rev Respir Dis . 1990;  142 563-570
• 35 Pare P D, Wiggs B R, James A, Hogg J C, Bosken C H. The comparative mechanics and morphology of airways in asthma and in chronic obstructive pulmonary disease.  Am Rev Respir Dis . 1991;  143 1189-1193
• 36 Wiggs B R, Bosken C H, Pare P D, Hogg J C. A model of airway narrowing in asthma and in chronic obstructive pulmonary disease.  Am Rev Respir Dis . 1992;  145 1251-1258