Ph. Michelson et al., Ozone effects on the immediate-phase response to allergen in the nasal airways of allergic asthmatic subjects, OTO H N SUR, 120(2), 1999, pp. 225-232
Epidemiologic and clinical trials have suggested that exposure to ozone inc
reases airway hyperresponsiveness and inflammatory response to inhaled nasa
l allergen challenge in allergic asthmatic subjects. Previous studies have
demonstrated an increased late-phase response to nasal allergen challenge;
however, the early-phase response is unknown,We sought to characterize the
early-phase response by measuring mast-cell inflammatory mediators and cell
ular influx at time points immediately following ozone exposure and subsequ
ent allergen challenge, A cohort of mild, asymptomatic dust mite-sensitive
asthmatic subjects was identified. Each subject underwent two separate expo
sures to both 0.4 ppm ozone and clean air in a randomized manner, Nasal rav
age was performed before and after each exposure, Nasal allergen was then a
dministered to a defined clinical end point, followed by nasal lavage, Diff
erential cell counts and mast-cell products were identified in each lavage
specimen, The mast-cell mediators tryptase and prostaglandin D-2 were analy
zed, as was a marker of epithelial cell permeability, albumin, Although all
ergen produced an increase in early-onset mediator release (mast cell-deriv
ed), no enhancement was noted after exposure to ozone, Neutrophil and eosin
ophil inflammatory mediators were not increased after ozone exposure or enh
anced after allergen exposure, although ozone did enhance eosinophilic infl
ux after exposure to allergen, Ozone exposure does not promote early-phase-
response mediator release or enhance the response to allergen challenge in
the nasal airways of extrinsic asthmatic subjects, Ozone, however, may prom
ote an inflammatory cell influx, which helps induce a more significant late
-phase response in this population.