Review: Evolution of evidence on PFOA and health following the assessments of the C8 Science Panel
Por:
Steenland K, Fletcher T, Stein CR, Bartell SM, Darrow L, Lopez-Espinosa MJ, Barry Ryan P and Savitz DA
Publicada:
1 dic 2020
Ahead of Print:
18 sep 2020
Categoría:
Environmental science (miscellaneous)
Resumen:
Background: The C8 Science Panel was composed of three epidemiologists charged with studying the possible health effects of PFOA in a highly exposed population in the mid-Ohio Valley. The Panel determined in 2012 there was a 'probable link' (i.e., more probable than not based on the weight of the available scientific evidence) between PFOA and high cholesterol, thyroid disease, kidney and testicular cancer, pregnancy-induced hypertension, and ulcerative colitis.
Objective: Here, former C8 Science Panel members and collaborators comment on the PFOA literature regarding thyroid disorders, cancer, immune and auto-immune disorders, liver disease, hypercholesterolemia, reproductive outcomes, neurotoxicity, and kidney disease. We also discuss developments regarding fate and transport, and pharmacokinetic models, and discuss causality assessment in cross-sectional associations among low-exposed populations.
Discussion: For cancer, the epidemiologic evidence remains supportive but not definitive for kidney and testicular cancers. There is consistent evidence of a positive association between PFOA and cholesterol, but no evidence of an association with heart disease. There is evidence for an association with ulcerative colitis, but not for other auto-immune diseases. There is good evidence that PFOA is associated with immune response, but uneven evidence for an association with infectious disease. The evidence for an association between PFOA and thyroid and kidney disease is suggestive but uneven. There is evidence of an association with liver enzymes, but not with liver disease. There is little evidence of an association with neurotoxicity. Suggested reductions in birthweight may be due to reverse causality and/or confounding. Fate and transport models and pharmacokinetic models remain central to estimating past exposure for new cohorts, but are difficult to develop without good historical data on emissions of PFOA into the environment.
Conclusion: Overall, the epidemiologic evidence remains limited. For a few outcomes there has been some replication of our earlier findings. More longitudinal research is needed in large populations with large exposure contrasts. Additional cross-sectional studies of low exposed populations may be less informative.
Filiaciones:
Steenland K:
1518 Clifton Rd, Rollins School of Public Health, Emory U., Atlanta, GA 30324, United States
Fletcher T:
London School of Hygiene and Tropical Medicine, London, United Kingdom
Stein CR:
Hassenfeld Children's Hospital at NYU Langone, NY, NY, United States
Bartell SM:
Program in Public Health, University of California Irvine, Irvine, Cal, United States
Darrow L:
University of Nevada, Reno, Nev, United States
:
Epidemiology and Environmental Health Joint Research Unit, FISABIO, Universitat Jaume I-Universitat de València, Valencia, Spain
Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Madrid, Spain
Barry Ryan P:
1518 Clifton Rd, Rollins School of Public Health, Emory U., Atlanta, GA 30324, United States
Savitz DA:
Brown University School of Public Health, Providence, Rhode Island, United States
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