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Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada V6T 2B5
Respirable ambient particles [particulate
matter <10 µm (PM10)]
are associated with both acute and chronic adverse health effects
including chronic airflow obstruction.
PM10 can induce expression of
inflammatory and fibrogenic mediators, but there is controversy about
the types and/or sizes of particles involved and, in particular,
whether ultrafine particles are the major toxic agents. To examine
whether particle size affects mediator generation, we exposed rat
tracheal explants, an inflammatory cell-free model of the airway wall,
to various concentrations up to 500 µg/cm2 of fine (0.12 µm) or
ultrafine (0.021 µm) titanium dioxide (anatase), maintained the
explants in an organ culture in air for 1-7 days, and used RT-PCR
to examine the expression of fibrogenic mediators and procollagen. No
increase in gene expression was seen at 1 or 3 days, but at 5 days,
ultrafine dust induced a small increase in procollagen. At 7 days, fine
titanium dioxide produced significantly greater increases for
platelet-derived growth factor (PDGF)-B, transforming growth
factor-
, and transforming growth factor-
compared
with those by ultrafine dust; both dusts produced similar increases for
PDGF-A; and ultrafine dust produced increases in procollagen
expression, whereas fine dust had no effect. Expression levels were
dose related. Both dusts produced a similar decrease in expression of
PDGF receptor- and a similar increase in PDGF receptor-. These
observations suggest that ultrafine particles are intrinsically able to
induce procollagen expression even in the absence of inflammatory
cells; that chronic exposure to
PM10 may result in chronic airflow
obstruction, in part because of ultrafine particle-mediated increases
in airway wall fibrosis; and that chemically identical dusts of
differing size can produce quite different patterns of gene expression
in the airway wall. Differential upregulation of PDGF receptors does
not appear to explain dust-induced fibrosis in this model.
particulate matter less than 10 micrometers; air pollution; transforming growth factor-; transforming growth factor-; platelet-derived growth factor; platelet-derived growth factor receptor
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