Soil cleanup guidelines were developed for diesel fuel No. 2 that are protective of human health. Guidelines were conservatively based on a residential land use scenario. This scenario estimates human health risks associated with long-term exposure to site soil via the inhalation, dermal, and ingestion routes of exposure. Lifetime dermal cancer studies were selected as the basis for deriving a safe level of diesel fuel in soil. Soil cleanup guidelines for diesel fuel No. 2 ranged from 1166 to 11,287 mg/kg for adult or child residents and represent contaminant levels that pose acceptable health risks for both present and proposed future uses of a site.

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Hurricane Katrina's storm surge displaced and damaged a 250,000 barrel storage tank causing a Nigerian crude oil blend (API 36.4 degrees) to be released and dispersed into the adjacent evacuated residential area by the retreating floodwaters. The subsequent environmental assessment involved sampling and chemical fingerprinting of nearly 15,000 wipe and soil samples collected both inside and outside of buildings to determine which properties were impacted by the spilled crude oil. Tier 1 qualitative analysis of gas chromatograms and Tier 2 quantitative (revised Nordtest-type) and qualitative (ASTM D5739-type) analysis of petroleum biomarkers revealed the extent of crude oil contamination-as well as the widespread occurrence of hydrocarbons derived from (i) lubricating, hydraulic, and transmission oils, most likely from vehicles in the flooded area, and (ii) allochthonous natural organic matter (NOM) from the surrounding bayous. Conventional oil spill fingerprinting protocols and two-component mixing models (crude oil/lube oil and crude oil/NOM) were used to confirm the presence of the spilled crude oil-even when mixed at low concentrations with other hydrocarbon sources-as a means to develop and govern a settlement and remedial program with the affected property owners.

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Previous studies have suggested a significant role for reproductive tract glutathione in protecting against chemical-induced germ-cell mutations. Therefore, a number of compounds were tested for their ability to perturb glutathione levels in the testes and epididymides as well as liver following single acute dosages to rats. Phorone (250 mg/kg), isophorone (500 mg/kg), and diethyl maleate (500 mg/kg) significantly reduced glutathione in the liver and in both reproductive organs examined. Methyl iodide (100 mg/kg), trimethyl phosphate (600 mg/kg), naphthalene (500 mg/kg), acetaminophen (1500 mg/kg), and pentachlorophenol (25 mg/kg) affected hepatic and epididymal glutathione, but had little or no effect on testicular levels. The ability of isophorone to enhance the covalent binding of tritiated ethyl methanesulfonate (3H-EMS) to spermatocytes was assessed. Perturbation of reproductive tract glutathione by isophorone treatment significantly enhanced the extent of 3H-EMS-induced binding to sperm heads. The temporal pattern of ethylations in sperm heads was consistent with the stage of sperm development known to be susceptible to ethylations by EMS. Therefore, chemical-induced lowering of glutathione in the male reproductive tract may be a mechanism for potentiation of chemical-induced germ-cell mutations.