Numerous studies have identified mechanisms and specific risk factors that modulate adverse response to air pollutants.These studies have guided development of personal mitigation strategies to decrease adverse effects of exposure to air pollutants.Our studies have shown that ozone,bioaerosols and PM augment airway and systemic inflammatory responses.We have also shown that genetic or nutritional deficiencies in antioxidant defenses increase risk for inflammatory response to pollutants.Based on these observations,our group has examined three specific interventions which have antioxidant,anti-inflammatory or combined actions as potential methods for mitigating adverse response to pollutants.The first of these are high dose inhaled corticosteroids.We have shown that pretreatment with inhaled corticosteroids blunts or prevents airway inflammation associated with experimental challenge to ozone and the PM component endotoxin.We have also shown that IL-1β is increased in airways of persons exposed to ozone,endotoxin and woodsmoke.This observation let to our conducting a proof-of concept study of the ability of pre-challenge systemic dosing of IL-1 receptor antagonist(IL-1RA)to inhibit endotoxin-induced airway inflammation.We also observed that oxidative stress is a risk factor for increased response to ozone and endotoxin.This led to proof of concept studies of the impact of gamma tocopherol(gT),a variant of vitamin E with both antioxidant and anti-inflammatory properties.In rodent models gT inhibits allergen,endotoxin and ozone induced inflammation.In human volunteers,gT inhibits endotoxin-induced airway inflammation and ex vivo IgE mediated responses to basophils.Other treatments being explored include sulforaphane(which induced multiple cytoprotective enzyme expression)and hypertonic saline(which can clear the airway of particles).We hypothesize that mechanism driven development of chemoprophylactic interventions is an important addition to decreasing health impacts associated with environmental pollution.