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Organochlorine concentrations.All statistically significant correlations between OC concentrations and lymphocyte proliferation had positive slopes, indicating that turtles with higher contaminant levels exhibited elevated lymphocyte proliferation responses (Figures 2 and 3).Lymphocyte proliferation stimulated by 4 days of exposure to 10 ug/mL LPS was significantly correlated with blood concentrations of ?PCBs, 4,4?-DDE, and ?chlordanes.In vitro exposure to 5 ng/mL Aroclor 1254 significantly increased PDB-induced proliferation, whereas 498 ng/mL Aroclor 1254 significantly decreased this response (Figure 4B).The mean lymphocyte proliferation responses, reported elsewhere (Keller et al. 2005), are tabulated along with the correlative results between lymphocyte proliferation and OC concentrations in Table 1.OC concentrations in samples from turtles captured in 2000 and 2001 have been reported elsewhere on both a wet-mass and a lipid-normalized basis (Keller et al. 2004a).The Spearman correlation coefficients, rS (p-values) for lysozyme versus ?PCBs, 4,4?-DDE, and ?chlordanes were -0.269 (0.074), -0.310 (0.038), and -0.368 (0.013), respectively.All of the tested concentrations of Aroclor 1254 generally increased PHA-induced proliferation, albeit not significantly, compared with the response in the DMSO control (Figure 4A).Increasing concentrations of 4,4?-DDE administered to the culture wells produced an increasing trend in PHA-induced proliferation (Figure 5A).For the purpose of comparing immune function and OC concentrations, only samples from turtles assessed for lymphocyte proliferation in July 2001 are described here (n = 27).Proliferation stimulated by 0.8 ug/mL PDB was also positively correlated with ?PCB and 4,4?-DDE concentrations.Correlations were also examined between lymphocyte proliferation and OC concentrations calculated on a lipid-normalized basis (data not shown).In vitro exposure to 4,4?-DDE significantly enhanced PHA- and PDB-induced proliferation (Figure 5).Only one concentration of 4,4?-DDE (0.5 ng/mL) caused a statistically significant effect on PDB-induced proliferation (Figure 5B).Statistically significant effects on PDB-induced proliferation were observed at lower concentrations of both contaminants compared with PHA-induced proliferation (Figures 4 and 5)Statistically significant increases from the DMSO control were observed at 48 ng/mL and 992 ng/mL 4,4?-DDE.Lymphocyte proliferation: in vitro exposure experiments.

Organochlorine concentrations.

OC concentrations in samples from turtles captured in 2000 and 2001 have been reported elsewhere on both a wet-mass and a lipid-normalized basis (Keller et al. 2004a). For the purpose of comparing immune function and OC concentrations, only samples from turtles assessed for lymphocyte proliferation in July 2001 are described here (n = 27). The mean (± SE) concentrations of ∑PCBs (the sum of PCBs), 4,4′-DDE, and ∑chlordanes (the sum of chlordanes) were 6.25 ± 1.14 ng/g wet mass, 0.721 ± 0.152 ng/g wet mass, and 0.253 ± 0.048 ng/g wet mass, respectively. The concentrations of these compounds in this group of turtles were not significantly different from turtles sampled in 2000 (Mann-Whitney t-test; all p-values > 0.05).
Plasma lysozyme activity.

We measured lysozyme activity in plasma samples from 45 animals that were assessed for OC concentrations. Lysozyme activity was 6.58 ± 0.58 μg HEL/μL (mean ± SE) with a range of 1.94–25.2 μg HEL/μL. The Spearman correlation coefficients, rS (p-values) for lysozyme versus ∑PCBs, 4,4′-DDE, and ∑chlordanes were −0.269 (0.074), −0.310 (0.038), and −0.368 (0.013), respectively. All slopes were negative, and correlations with 4,4′-DDE and ∑chlordanes were statistically significant at α = 0.05 (Figure 1). Lysozyme activity did not differ between gender and did not correlate to body condition or plasma testosterone levels.
Lymphocyte proliferation: correlations with blood OC concentrations.

The mean lymphocyte proliferation responses, reported elsewhere (Keller et al. 2005), are tabulated along with the correlative results between lymphocyte proliferation and OC concentrations in Table 1. Proliferation in this data set did not differ between sexes and did not correlate with testosterone concentrations (data not shown). Body condition correlated with lymphocyte proliferation only in media type 1 when stimulated with 0.2 μg/mL PDB for 5 days (rS = 0.528; p = 0.012).
Some proliferative responses were significantly correlated with blood OC concentrations. Lymphocyte proliferation stimulated by 4 days of exposure to 10 μg/mL LPS was significantly correlated with blood concentrations of ∑PCBs, 4,4′-DDE, and ∑chlordanes. PHA-induced proliferation (5 μg/mL PHA) correlated with blood concentrations of ∑PCBs. Proliferation stimulated by 0.8 μg/mL PDB was also positively correlated with ∑PCB and 4,4′-DDE concentrations. ConA stimulation, however, did not correlate with any contaminant. All statistically significant correlations between OC concentrations and lymphocyte proliferation had positive slopes, indicating that turtles with higher contaminant levels exhibited elevated lymphocyte proliferation responses (Figures 2 and 3). Correlations were also examined between lymphocyte proliferation and OC concentrations calculated on a lipid-normalized basis (data not shown). These correlations were very similar to those shown in Table 1.
Lymphocyte proliferation: in vitro exposure experiments.

PBLs from 16 turtles were exposed to increasing concentrations of Aroclor 1254 (0–13.5 μg/mL) or 4,4′-DDE (0–13.4 μg/mL). Cell viability was measured for 8 of these turtles after 5 days of contaminant exposure, examining only cells not stimulated with the mitogen (data not shown). Viability was unaffected by concentrations of ≤ 1,000 ng/mL of either contaminant. Both contaminants significantly decreased cell viability at concentrations of ≥ 7,500 ng/mL. Therefore, lymphocyte proliferation responses at these higher concentrations are not reported.
The effects of in vitro exposure to Aroclor 1254 on lymphocyte proliferation responses are shown in Figure 4. All of the tested concentrations of Aroclor 1254 generally increased PHA-induced proliferation, albeit not significantly, compared with the response in the DMSO control (Figure 4A). In vitro exposure to 5 ng/mL Aroclor 1254 significantly increased PDB-induced proliferation, whereas 498 ng/mL Aroclor 1254 significantly decreased this response (Figure 4B).
In vitro exposure to 4,4′-DDE significantly enhanced PHA- and PDB-induced proliferation (Figure 5). Increasing concentrations of 4,4′-DDE administered to the culture wells produced an increasing trend in PHA-induced proliferation (Figure 5A). Statistically significant increases from the DMSO control were observed at 48 ng/mL and 992 ng/mL 4,4′-DDE. Only one concentration of 4,4′-DDE (0.5 ng/mL) caused a statistically significant effect on PDB-induced proliferation (Figure 5B). Additionally, it should be noted that B-lymphocyte proliferation appeared to be more sensitive than did T-lymphocyte proliferation. Statistically significant effects on PDB-induced proliferation were observed at lower concentrations of both contaminants compared with PHA-induced proliferation (Figures 4 and 5)