We investigated whether patients with immunoglobulin E-mediated food allergy differed from healthy individuals with regard to genotype of the polymorphic enzyme N -acetyltransferase 2 (NAT2). The genetic polymorphism of acetylation can alter the toxic and therapeutic response to certain xenobiotics and may be also a factor that influences the susceptibility toward certain partly chemically induced diseases. We compared 136 children with immunoglobulin E-mediated food allergy with 123 healthy children. The NAT2 alleles (*4, *5, *6, and *7 ) were determined by polymerase chain reaction-restriction fragment length polymorphism methods with DNA extracted from peripheral blood. A statistically significant increase in the proportion of homozygous slow acetylators (76.5%) was found among patients with food allergy compared with healthy subjects (53.7%; P < .001). There were no homozygous fast acetylators within this group of individuals with severe forms of food allergy. The risk of development of immunoglobulin E-mediated food allergy was almost 3-fold greater in slow acetylators than that in the healthy subjects (odds ratio, 2.8; 95% confidence interval, 1.6 to 4.9). We therefore concluded that the slow acetylation genotype may be an important factor of individual susceptibility to immunoglobulin E-mediated food allergy.