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
