Dm. Walters et al., Ambient urban Baltimore particulate-induced airway hyperresponsiveness andinflammation in mice, AM J R CRIT, 164(8), 2001, pp. 1438-1443
Airborne particulate matter (PM) is hypothesized. to play a role in increas
es in asthma prevalence, although a causal relationship has yet to be estab
lished. To investigate the effects of real-world PM exposure on airway reac
tivity (AHR) and bronchoalveolar lavage (BAL) cellularity, we exposed naive
mice to a single dose (0.5 mg/ mouse) of ambient PM, coal fly ash, or dies
el PM. We found that ambient PM exposure induced increases in AHR and BAL c
ellularity, whereas diesel PM induced significant increases in BAL cellular
ity, but not AHR. On the other hand, coal fly ash exposure did not elicit s
ignificant changes in either of these parameters. We further examined ambie
nt PM-induced temporal changes in AHR, BAL cells, and lung cytakine levels
over a 2-wk period. Ambient PM-induced AHR was sustained over 7 d. The incr
ease in AHR was preceded by dramatic increases in BAL eosinophils, whereas
a decline in AHR was associated with increases. in macrophages. A Th2 cytok
ine pattern (IL-5, IL-13, eotaxin) was observed early on with a shift towar
d a Th1 pattern (IFN-gamma). In additional studies, we found that the activ
e component(s) of ambient PM are not water-soluble and that ambient PM-indu
ced AHR and inflammation are dose-dependent. We conclude that ambient PM ca
n induce asthmalike parameters in naive mice, suggesting that PM exposure m
ay be an important factor in increases in asthma prevalence.