Abstract
Risk assessments for toxicants in environmental media via oral exposure often rely on measurements of total concentration in a collected sample. However, the human digestive system cannot dissolute all of a toxicant present in the binding matrix, and cannot absorb it with nearly 100% efficiency. In vitro bioaccessibility has been developed as a method to estimate oral bioavailability of a toxicant using a physiologically-based extraction procedure. Bioaccessibility measurements are more physiologically relevant than strong acid leaching measurements of concentration. A method for measuring bioaccessible lead in house dust was derived from the bioaccessibility method currently used for heavy metals in contaminated soils. House dust was collected from carpets in typical urban residences. Bioaccessible lead was measured in house dust (<75 microm) from the homes of 15 participants. The bioaccessibility ranged from 52.4% to 77.2% in gastric fluid, and 4.9% to 32.1% in intestinal fluid. House dust samples from five homes were analyzed to assess the relationship among lead bioaccessibility of three particle size fractions (<75, 75-150, and 150-250 microm). Changes in lead bioaccessibility as a function of particle size fraction were not significant for gastric fluid (p= 0.7019); however they were significant for intestinal fluid (p= 0.0067). This decrease of bioaccessibility may result from the readsorption of dissolved lead onto the dust particles or precipitation of lead with phosphates in a high-pH environment. The bioaccessibility data obtained for two biofluids were applied to the IEUBK model, and results for intestinal bioaccessibility of lead provide support for the model default value of 30% lead bioavailability of dust as a reasonable population indicator for dose, but the higher values for gastric bioaccessibility of lead appeared to provide an upper bound that approached actual blood lead levels in the children living in the studied homes. This upper bound seemed to overcome some of the limitations of the model when it lacks child-specific activity data and characterization of all exposure routes.
Published Version
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