MTBE ambient water quality criteria development: a public/private partnership.

A public/private partnership was established in 1997, under the administrative oversight of the American Petroleum Institute (API), to develop aquatic toxicity data sufficient to calculate ambient water quality criteria for methyl tertiary-butyl ether (MTBE), a gasoline oxygenate. The MTBE Water Quality Criteria Work Group consisted of representatives from private companies, trade associations, and USEPA. Funding was provided by the private entities, while aquatic biological/toxicological expertise was provided by industry and USEPA scientists. This public/private partnership constituted a nonadversarial, cost-effective, and efficient process for generating the toxicity data necessary for deriving freshwater and marine ambient water quality criteria. Existing aquatic toxicity data were evaluated for acceptability, consistent with USEPA guidance, and nineteen freshwater and marine tests were conducted by commercial laboratories as part of this effort to satisfy the federal criteria database requirements. Definitive test data were developed and reported under the oversight of industry study monitors and Good Laboratory Practice standards auditors, and with USEPA scientists participating in advisory and critical review roles. Calculated, preliminary freshwater criteria for acute (Criterion Maximum Concentration) and chronic (Criterion Continuous Concentration) exposure effect protection are 151 and 51 mg MTBE/L, respectively. Calculated, preliminary marine criteria for acute and chronic exposure effect protection are 53 and 18 mg MTBE/L, respectively. These criteria values may be used for surface water quality management purposes, and they indicate that ambient MTBE concentrations documented in U. S. surface waters to date do not constitute a risk to aquatic organisms.

Focal localization of the NHE-1 isoform of the Na+/H+ antiport: assessment of effects on intracellular pH.

Na+/H+ exchange (antiport) is a major pathway for the regulation of intracellular pH. Antiport activity is stimulated when suspended cells adhere to the substratum. In this report, immunofluorescence was used to study the subcellular localization of the ubiquitous NHE-1 isoform of the antiport. NHE-1 was not distributed homogeneously on the surface of the cells. Instead, antiports were found to accumulate along the border of lamellipodia and near the edge of finer processes. Dual immunofluorescence experiments demonstrated that vinculin, talin and F-actin are concentrated at sites of NHE-1 accumulation. A mutated construct of NHE-1 lacking residues 566-635 of the cytosolic domain also accumulated near marginal lamellae. In contrast, the focal distribution observed in adherent cells was not detectable in cells grown in suspension. Fluorescence ratio imaging was used to define the functional consequences of focal accumulation of NHE-1. In the steady state, the pH was virtually identical throughout the cytosol. Moreover, no pH gradients were found to develop when cells recovered from an acid load by activation of Na+/H+ exchange. This is probably because of the presence of high concentrations of mobile buffers in the cytosol. The focal accumulation of antiporters near the cell margins may be involved in stimulation by adherence and/or generation of local osmotic gradients.

Distribution of antibody to hepatitis a antigen in urban adult populations.

To investigate the prevalence and distribution of antibody to hepatitis A antigen we tested 947 randomly selected people in the Greater New York City area; 45 per cent were antigen positive, as determined by the immune adherence method. Antibody was detected two to three times more frequently in lower social classes (72 to 80 per cent) than in middle and upper-middle classes (18 to 30 per cent). The rate of antibody detection was strongly correlated with age; the prevalence gradually increased throughout adulthood and reached its peak level in people 50 years of age and older. Those with serologic evidence of past exposure to hepatitis B virus were significantly more often antibody positive than those without such evidence (61 vs. 40 per cent; P less than 0.001). Very few of the positive subjects had had hepatitis. The prevalence of this antibody varies among different population groups, increases with age, decreases with rise in socioeconomic status, is independent on sex and race, and correlates with serologic evidence of hepatitis B virus infections.