Use of Indoor Dust Levels to Reconstruct Exposure to Semivolatile Organic Compounds: Evaluation with NHANES biomarkers

摘要

Background/Aims: House dust can serve as a marker of exposure. Many studies have found that polybrominated diphenyl ether (PBDE) concentrations in indoor dust are correlated with concentrations in biological samples. However, the role of indoor dust levels on predicting human body burden for other chemical classes remains mostly unexplored. Our objective is (1) to quantify exposures from indoor dust levels for a suite of semivolatile organic compounds (SVOC) with indoor sources and (2) to better understand how much indoor dust levels can inform human body burden depending on chemical properties and indoor source strength. Methods: Compounds of interest include PBDEs, phthalates, polycyclic aromatic hydrocarbons (PAHs), and bisphenol A (BPA). We couple measured levels in indoor dust with the partitioning relationships among the gas phase, airborne particles and settled dust to estimate concentrations in the gas phase and airborne particles. We model intake rates (iR) using the exposure concentrations (i.e., dust levels, gas phase and airborne particles) and recommended exposure factors (e.g., inhalation rate, dust ingestion rate). We then compare the modeled total iRs with those inferred from the measured urine or blood levels in the NHANES survey. Results: The contribution of individual exposure pathways (e.g., inhalation, dermal uptake, dust ingestion) to the total iRs is similar to the results in previous studies. For compounds with large octanol-air partition coefficients (log Koa >9), the primary exposure pathway is dust ingestion (>70%), but our methods underestimate the total iRs (only 2 to 16% of the total iRs from biomonitoring data). It is likely that exposure for these compounds is driven by non-indoor exposure pathways or that the gas-phase concentrations are not equilibrated with the settled dust levels. We also found that our results are very sensitive to the Koa, which involves in partitioning relationships between the gas phase and the particle phase as well as between the gas phase and settled dust. Conclusion: The results from this study indicate that reconstructed exposure from measured indoor dust levels and estimated gas- and particle-phase concentrations can better inform human body burden than that from the dust levels only, especially for SVOCs with small Koa. Our methods can provide reliable exposure estimates in a high-throughput manner when biomarker measurements are lacking but indoor dust levels are known.