June T Spector1, Anneclaire J De Roos2, Cornelia M Ulrich3, Lianne Sheppard4, Andreas Sjödin5, Mark H Wener6, Brent Wood7, Anne McTiernan8. 1. Department of Environmental & Occupational Health Sciences, School of Public Health, University of Washington, 4225 Roosevelt Way NE, Seattle, WA 98105, USA; Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA. Electronic address: spectj@uw.edu. 2. Epidemiology Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, P.O. Box 19024, Seattle, WA 98109, USA; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA. Electronic address: ajd335@drexel.edu. 3. Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA; Cancer Prevention Program, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, P.O. Box 19024, Seattle, WA 98109, USA; National Center for Tumor Diseases and German Cancer Research Center, Heidelberg, Germany. Electronic address: neli.ulrich@nct-heidelberg.de. 4. Department of Environmental & Occupational Health Sciences, School of Public Health, University of Washington, 4225 Roosevelt Way NE, Seattle, WA 98105, USA; Department of Biostatistics, School of Public Health, University of Washington, Seattle, WA, USA. Electronic address: sheppard@uw.edu. 5. National Center for Environmental Health, CDC, 4770 Buford Highway NE, Atlanta, GA 30341, USA. Electronic address: asjodin@cdc.gov. 6. Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA. Electronic address: wener@u.washington.edu. 7. Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA. Electronic address: woodbl@u.washington.edu. 8. Department of Medicine, School of Medicine, University of Washington, Seattle, WA, USA; Epidemiology Program, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, P.O. Box 19024, Seattle, WA 98109, USA; Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA. Electronic address: amctiern@fhcrc.org.
Abstract
BACKGROUND: Polychlorinated biphenyl (PCB) exposure has been associated with non-Hodgkin lymphoma in several studies, and the immune system is a potential mediator. OBJECTIVES: We analyzed associations of plasma PCBs with immune function measures. We hypothesized that higher plasma PCB concentrations are associated with lower immune function cross-sectionally, and that increases in PCB concentrations over a one year period are associated with decreases in immune function. METHODS: Plasma PCB concentrations and immune function [natural killer (NK) cell cytotoxicity and PHA-induced T-lymphocyte proliferation (PHA-TLP)] were measured at baseline and one year in 109 postmenopausal overweight women participating in an exercise intervention study in the Seattle, Washington (USA) area. Mixed models, with adjustment for body mass index and other potential confounders, were used to estimate associations of PCBs with immune function cross-sectionally and longitudinally. RESULTS: Associations of PCBs with immune function measures differed across groups of PCBs (e.g., medium- and high-chlorinated and dioxin-like [mono-ortho-substituted]) and by the time frame for the comparison (cross-sectional vs. longitudinal). Higher concentrations of medium- and high-chlorinated PCBs were associated with higher PHA-TLP cross-sectionally but not longitudinally. The mean decrease in 0.5 µg/mL PHA-TLP/50.0 pmol/g-lipid increase in dioxin-like PCBs over one year was 51.6 (95% confidence interval 2.7, 100.5; P=0.039). There was no association between plasma PCBs and NK cytotoxicity. CONCLUSIONS: These results do not provide strong evidence of impaired cellular immunity from PCB exposure. Larger longitudinal studies with greater variability in PCB exposures are needed to further examine temporal associations of PCBs with immune function.
BACKGROUND:Polychlorinated biphenyl (PCB) exposure has been associated with non-Hodgkin lymphoma in several studies, and the immune system is a potential mediator. OBJECTIVES: We analyzed associations of plasma PCBs with immune function measures. We hypothesized that higher plasma PCB concentrations are associated with lower immune function cross-sectionally, and that increases in PCB concentrations over a one year period are associated with decreases in immune function. METHODS: Plasma PCB concentrations and immune function [natural killer (NK) cell cytotoxicity and PHA-induced T-lymphocyte proliferation (PHA-TLP)] were measured at baseline and one year in 109 postmenopausal overweight women participating in an exercise intervention study in the Seattle, Washington (USA) area. Mixed models, with adjustment for body mass index and other potential confounders, were used to estimate associations of PCBs with immune function cross-sectionally and longitudinally. RESULTS: Associations of PCBs with immune function measures differed across groups of PCBs (e.g., medium- and high-chlorinated and dioxin-like [mono-ortho-substituted]) and by the time frame for the comparison (cross-sectional vs. longitudinal). Higher concentrations of medium- and high-chlorinated PCBs were associated with higher PHA-TLP cross-sectionally but not longitudinally. The mean decrease in 0.5 µg/mL PHA-TLP/50.0 pmol/g-lipid increase in dioxin-like PCBs over one year was 51.6 (95% confidence interval 2.7, 100.5; P=0.039). There was no association between plasma PCBs and NK cytotoxicity. CONCLUSIONS: These results do not provide strong evidence of impaired cellular immunity from PCB exposure. Larger longitudinal studies with greater variability in PCB exposures are needed to further examine temporal associations of PCBs with immune function.
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