Acute hemolytic anemia is associated with a deficiency in glucose 6-phosphate dehydrogenase (G6PD), an X-linked inheritable characteristic. Hemolytic anemia is thought to be caused by a depletion of glutathione and other reducing compounds in red blood cells. Dr. Amoruso and colleagues sought to experimentally test the Calabrese hypothesis, which suggests that G6PD-deficient individuals may be at an increased risk of hemolysis during exposure to low levels of oxidants such as ozone. The study used an in vitro model that would expose human G6PD-deficient erythrocytes to primaquine, ozone, and nitrogen dioxide. This experiment linked data from two sets of in vivo studies preformed by Alving and Miller that examined the dose-response of primaquine in G6PD-deficient human volunteers and the rate of ozone delivery to the lower respiratory tract respectively.