Polymorphonuclear leukocytes (PMNs) comprise the majority of early nonspecific inflammatory responses to infection or trauma and, as such, must be of sufficient number and qualitative function to properly limit and combat inflammation. Peripheral PMNs isolated from rats that received 10% or 30% body surface area full-thickness thermal injuries were quantitated and examined for functional alterations in membrane potential and cytosolic hydrogen peroxide production for 35 days after thermal injury. With 10% thermal injury, leukocytes increased quantitatively to experimental maximums that were 70% above normal on day 7 before a return to normal by day 28. Platelet levels showed a nonsignificant decrease for 2 days after thermal injury before increasing to levels 20% to 40% above normal through day 28. Phorbol myristate acetate-induced PMN membrane depolarization was inhibited as much as 30% for 21 days after 10% thermal injury. No changes in oxidative activity were apparent except for day 14, when hydrogen peroxide production was 40% above normal. With 30% thermal injury, leukocyte quantities were three to five times normal, with increased relative numbers of PMNs and decreased lymphocytes through day 28. Platelet levels decreased for 4 days before increasing to levels 30% to 47% above normal through day 21. Compared with 10% thermal injury, 30% thermal injury further reduced the ability of PMN membranes to depolarize through day 35. In addition, PMN hydrogen peroxide production was 30% lower on day 1 and increased thereafter to levels that were 40% above normal on day 21.