Rationale: Although oxidative stress is a cardinal feature of asthma, the roles of oxidant air pollutants and antioxidant genes Heme oxygenase1 (HMOX1), catalase (CAT) and manganese superoxide dismutase (MNSOD) in asthma pathogenesis have yet to be determined. Objective: We hypothesized that the functional polymorphisms of HMOX1 ((GT)_n repeat), CAT (-262C>T -844C>T) and MNSOD-(Ala-9Val) are associated with new onset asthma, and the effects of these variants vary by exposure to ozone, a potent oxidant air pollutant. Method: We assessed this hypothesis in a population-based cohort of non-Hispanic (N=1,125) and Hispanic-White (N=586) children who resided in 12 California communities and who were followed annually for 8 years to ascertain new onset asthma. Measurements: Air pollutants were continuously measured in each of the study communities during the 8 years of study follow-up. Main Result: HMOX1 'short' alleles (< 23 repeats) were associated with a reduced risk for new onset asthma among non-Hispanic Whites (Hazard ratio(HR) 0.64, 95% CI 0.41-0.99). This protective effect was largest in children residing in low-ozone communities (HR 0.48, 95% CI 0.25-0.91) (interaction p-value=0.003). Little evidence for an association with HMOX1 was observed among Hispanic children. In contrast, Hispanic children with a variant of the CAT-262 'T' allele (CT or TT) had an increased risk for asthma (HR 1.78, p-value=0.01). The effects of these polymorphisms were not modified by personal smoking or secondhand-smoke exposure. Conclusions: Functional promoter variants in CAT and HMOX1 showed ethnic-specific associations with new onset asthma. Oxidant gene protection was restricted to children living in low-ozone communities.