Blood samples of 85 immature, apparently healthy, captive-reared loggerhead sea turtles (Caretta caretta) were analyzed for 13 hematologic variables and total solids of 5 age groups (8, 20, 32, 44, and 56 mo old) and for 20 plasma biochemical analytes of 4 age groups (20 to 56 mo old). Each individual turtle was sampled under similar conditions during a blood collection period of 3 days. Hematologic analytes included packed cell volume, white blood cell (WBC) counts, WBC estimates, and leukocyte differentials. Biochemical analysis included albumin, alanine aminotransferase, alkaline phosphatase, amylase, aspartate aminotransferase, blood urea nitrogen, calcium, chloride, cholesterol, creatine kinase, creatinine, gamma glutamyltransferase, globulins, glucose, phosphorous, potassium, sodium, total bilirubin, total protein, total solids, and uric acid. In due consideration of small sample size in all five age groups, the results of hematologic and biochemical analysis were used to determine ranges for these analytes and to compare values among consecutive age groups. Several significant differences in some hematologic and biochemical variables were identified and need to be considered in the interpretation of blood work of immature, growing sea turtles in human care.

Threatened loggerhead sea turtles (Caretta caretta) face numerous environmental challenges, including exposure to anthropogenic chemicals such as polychlorinated biphenyls (PCBs). Despite being banned by the USA in the 1970s, PCBs persist in the environment and produce immunotoxic effects in a wide range of marine vertebrate species. This is of particular concern, as the modulation of the immune system may enhance the susceptibility to a variety of pathogens. Blood samples were collected from 19 immature, captive-reared loggerhead sea turtles. Functional immune assays phagocytosis and natural killer (NK) cell activity were used to quantify the direct effects of PCB congeners 105, 138, and 169 on innate immune functions upon in vitro exposure of sea turtle cells to increasing concentrations (control (0), 0.5, 1, 2.5, 5, 10, 15, or 20 ppm) of each PCB. PCB 105 significantly elevated eosinophil phagocytosis at 10 and 15 ppm and PCB 138 at 15 ppm compared to unexposed (0 ppm). The effects of PCB 169 on phagocytosis were not evaluated. PCB 138 and 105 significantly decreased NK cell activity at 15 and 20 ppm, compared to unexposed (0 ppm) controls. PCB 169 did not markedly modulate NK activity. This constitutes the first study to investigate the in vitro effects of these three PCBs on sea turtle innate immune functions. These results add to our understanding of PCB-induced immunotoxicity in sea turtles and may provide a framework for establishing the relationships between chemical levels and turtle immunity.