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Sediments from the Mississippi River estuary were suspended in solutions with a range of salinities and various initial concentrations of phosphate. After 42 days the suspensions had nearly uniform values for the ion activity product of calcium times biphosphate, [Ca2+] [HP0,2-] x 10e9 M2. Similar values were observed for this ion product in the Mississippi River and in the upper estuary, suggesting that the concentration of soluble phosphorus nlay be controlled by an equilibrium with sedimentary material. The data are consistent with a Inechanism where soluble phosphorus is controlled by hydrolysis on the surface of hydroxyapatize particles:Ca,,(PO,),(OH), + 6H2O Z 4[Ca,HPO,(OH),],,,,, + 2Ca2+ + 2HPOd2-.Phosphorus levels in the lower estuary are controlled primarily by tlilution with low-nutrient waters from-the Gulf of Mexico.

1,4-Dioxane (CAS No. 123-91-1) is used primarily as a solvent or as a solvent stabilizer. It can cause lung, liver, and kidney damage at sufficiently high exposure levels. Two physiologically based pharmacokinetic (PBPK) models of 1,4-dioxane and its major metabolite, hydroxyethoxyacetic acid (HEAA), were published in 1990. These models have uncertainties and deficiencies that could be addressed and the model strengthened for use in a contemporary cancer risk assessment for 1,4-dioxane. Studies were performed to fill data gaps and reduce uncertainties pertaining to the pharmacokinetics of 1,4-dioxane and HEAA in rats, mice, and humans. Three types of studies were performed: partition coefficient measurements, blood time course in mice, and in vitro pharmacokinetics using rat, mouse, and human hepatocytes. Updated PBPK models were developed based on these new data and previously available data. The optimized rate of metabolism for the mouse was significantly higher than the value previously estimated. The optimized rat kinetic parameters were similar to those in the 1990 models. Only two human studies were identified. Model predictions were consistent with one study, but did not fit the second as well. In addition, a rat nasal exposure was completed. The results confirmed water directly contacts rat nasal tissues during drinking water under bioassay conditions. Consistent with previous PBPK models, nasal tissues were not specifically included in the model. Use of these models will reduce the uncertainty in future 1,4-dioxane risk assessments.