Objectives: To test the utility of zinc protoporphyrin to heme ratio (ZnPPH) as an indicator of iron status in premature infants and to evaluate the effect of oral iron supplements on oxidative injury. We hypothesized that iron sulfate supp-lementation would decrease the ZnPPH in preterm infants. Study design: Infants eligible for this prospective study were: hospitalized, 24 to 32 weeks of gestation, 7 to 60 days old, feeding≥70mLkgd, with a ZnPPH ≥the mean for age. Iron dose was determined by the ZnPPH. Iron status and oxidative injury were evaluated at study entry and completion. Concurrent control subjects met entry criteria but were not enrolled and were not treated with iron during the study interval. Statistical evaluation included repeated measures analysis of variance and Z-score conversions. Results: Entry ZnPPH of iron-treated subjects (n = 16) and control subjects (n = 16) were not different. The ZnPPH of iron-treated infants was lower at study end (P < .05) but did not change in control infants. Iron treatment (3 to 12 mgkgday)-was not associated with changes in conventional measures of iron status nor in measures of oxidative injury. Conclusions: Iron sulfate supplementation (3-12 mgkgd) decreases ZnPPH, is tolerated, and is not associated with increased oxidative injury. Objectives: To test the utility of zinc protoporphyrin to heme ratio (ZnPPH) as an indicator of iron status in premature infants and to evaluate the effect of oral iron supplements on oxidative injury. We hypothesized that iron sulfate supp-lementation would decrease the ZnPPH in Preterm infants. Study design: Infants eligible for this prospective study were: hospitalized, 24 to 32 weeks of gestation, 7 to 60 days old, feeding ≥ 70 mL kgd, with a ZnPPH ≥ the mean for age. Iron dose was determined by the ZnPPH. Iron status and oxidative injury were evaluated at study entry and completion. Concurrent control subjects met entry criteria but were not enrolled and were not treated with iron during the study interval. Statistical evaluation included repeated measures analysis of variance and Z-score conversions. Entry ZnPPH of iron-treated subjects (n = 16) and control subjects (n = 16) were not different. The ZnPPH of iron-treated infants was lower at study end (p <.05) but did not change in control infants. Iron treatment (3 to 12 mg kgday) -was not associated with changes in conventional measures of iron status nor in measures of oxidative injury. Conclusions: Iron sulfate supplementation (3-12 mgkgd) decreases ZnPPH, is tolerated, and is not associated with increased oxidative injury.