Evaluation of soil pH and moisture content on in-situ ozonation of pyrene in soils.

In this study, pyrene spiked soil (300 ppm) was ozonated at pH levels of 2, 6, and 8 and three moisture contents. It was found that soil pH and moisture content impacted the effectiveness of PAH oxidation in unsaturated soils. In air-dried soils, as pH increased, removal increased, such that pyrene removal efficiencies at pH 6 and pH 8 reached 95-97% at a dose of 2.22 mg O(3)/mg pyrene. Ozonation at 16.2+/-0.45 mg O(3)/ppm pyrene in soil resulted in 81-98% removal of pyrene at all pH levels tested. Saturated soils were tested at dry, 5% or 10% moisture conditions. The removal of pyrene was slower in moisturized soils, with the efficiency decreasing as the moisture content increased. Increasing the pH of the soil having a moisture content of 5% resulted in improved pyrene removals. On the contrary, in the soil having a moisture content of 10%, as the pH increased, pyrene removal decreased. Contaminated PAH soils were stored for 6 months to compare the efficiency of PAH removal in freshly contaminated soil and aged soils. PAH adsorption to soil was found to increase with longer exposure times; thus requiring much higher doses of ozone to effectively oxidize pyrene.

Ozonation of chrysene: evaluation of byproduct mixtures and identification of toxic constituent.

The effects of chrysene and the ozonated byproducts on in vitro gap junctional intercellular communication (GJIC) were evaluated using the scrape loading/dye transfer (SL/DT) technique. A 1 mM solution of chrysene was ozonated at dosages of 1.75, 3, 4.25, and 5 mol O3/mol chrysene (Chr). The early ozonation mixture, 1.75 mol O3/mol Chr, exhibited greater inhibition to GJIC than chrysene and irreversible damage to cells leading to cell death. To determine the compounds potentially responsible for the increase in toxicity, the byproducts formed upon treatment with 1.44 mol O3/mol Chr were separated into 14 fractions using RP-HPLC. The major compounds identified in the fractions were 2-(2'-formyl) phenyl-1-naphthaldehyde, 2-(2'formyl) phenyl-1-naphthoic acid, and 2-2-carboxyphenyl-1-naphthoic acid. 2-(2'-Formyl) phenyl-1-naphthaldehyde was determined to be the compound causing GJIC inhibition in sample fractions and byproduct mixtures.