Although asthma is characterized by airway inflammation, a critical component of which is oxidative stress, few data exist on genes involved in protecting against this insult. Glutathione S-transferase P1, plays an important role in cellular protection against oxidative stress and toxic foreign chemicals. It has been suggested that polymorphisms in the GSTP1 gene are associated with asthma and related phenotypes. Because full identification of GSTP1 alleles may identify stronger links with asthma phenotypes, In this study we described an amplification refractory mutation system (ARMS) assay that allows identification of all genotypes and explore whether the GSTP1 substitutions influence susceptibility to asthma, atopy and BHR. This study included 50 patients with bronchial asthma (aged 4-14 years), 35 of them were atopic and the remaining 15 cases were nonatopic. Forty normal age and sex matched children were enrolled in our work as controls. All our cases and controls were subjected to a full medical history, complete clinical examination, CBCs, pulmonary function tests , total serum IgE level, genotyping of GSTP1 genetic polymorphisms by ARMS PCR, 39 cases had GSTP1 genotype AA, 6 cases had genotype GSTP1 AB, 2 cases had GSTP1 genotype AD and 43 cases had GSTP1 genotype BB. Total IgE levels obtained from our subjects did not differentiate between atopic and nonatopic asthmatics, but the control cases had significantly lower levels of IgE. The PEFR was significantly higher among the control group compared to both atopic asthmatics and nonatopic asthmatics, but the latter two groups did not differ significantly. No significant difference between the GSTP1 genotypes were observed regarding IgE levels, eosinophilic count, and the number of allergens. While as regards the PEFR there was a high significant difference, the PEFR of the BB genotype was significantly higher compared with that of both AA and AB genotypes. The incidence of AA genotype was significantly higher among asthmatic cases compared with controls, while the incidence of genotype BB was significantly lower among asthmatic cases (atopic and nonatopic) as compared with controls, and by comparing both asthmatic groups, the incidence of genotype BB was significantly higher in atopic asthmatics compared with nonatopic asthmatics. These results proved an association between polymorphism in GSTP1 and asthma and that the frequency of GSTP1 AA was increased in patients with established asthma, while the frequencies of GSTP1 BB were reduced in asthmatic patients, thus indicating a protective effect.