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A model to evaluate past exposure to 2,3,7,8-TCDD
1National Center for Environmental Assessment, U.S. Environmental Protection Agency, Washington, DC 20460, USA. pinsky-paul@epamail.epa.gov
Summary
Dioxin exposure peaked in the late 1960s, with levels declining significantly since then. This study reconstructs historical dioxin exposure patterns using a pharmacokinetic model and body burden data.
Area of Science:
- Environmental Science
- Toxicology
- Biostatistics
Background:
- Dioxin concentrations in the environment rose from the 1930s to the 1960s/70s, followed by a decline.
- Human exposure to dioxins primarily occurs through the food supply, but the link between environmental deposition and food concentrations is complex.
- Understanding historical human exposure trends to dioxins, particularly 2,3,7,8-TCDD (TCDD), is crucial for public health.
Purpose of the Study:
- To statistically reconstruct past human exposure patterns to 2,3,7,8-TCDD (TCDD).
- To assess the temporal trends of TCDD exposure using a pharmacokinetic model fitted to body burden data.
Main Methods:
- A simple pharmacokinetic (PK) model incorporating a time-varying TCDD exposure dose was developed.
- The PK model was fitted to TCDD body burden data from five U.S. studies (1972-1987) using a Bayesian statistical approach.
- Model parameters, excluding exposure, were based on existing knowledge or estimations.
Main Results:
- A time-varying exposure dose provided a significantly better fit to body burden data than a constant dose, indicating historical fluctuations in TCDD exposure.
- Peak TCDD exposure was estimated in the late 1960s, aligning with sediment core data.
- Average peak exposure doses were estimated at 1.4-1.9 pg TCDD/kg-day, decreasing to <0.10 pg TCDD/kg-day by the late 1980s.
Conclusions:
- Human exposure to TCDD has varied significantly throughout the 20th century, peaking in the late 1960s.
- The modeled decline in TCDD exposure aligns with environmental trends and recent exposure estimates.
- The study highlights the utility of pharmacokinetic modeling for reconstructing historical toxicant exposure.