The purpose of this study was to determine the effects of supplemental fatty acids on oxidant injury in cultured endothelial cells. Porcine pulmonary artery endothelial cells (PAEC) in monolayer culture were incubated in culture medium supplemented with 0.1 mM fatty acid or with fatty acid vehicle alone for 3 h. Monolayers were then exposed to oxidant stress (100 microM H2O2 in buffer) or to control conditions (buffer alone) for 30 min. Supplementation with stearic acid (18:0) or oleic acid [18:1(n-9)] reduced H2O2-induced PAEC injury measured as release of intracellular lactate dehydrogenase (LDH). In contrast, supplementation with linolenic acid [18:3(n-6)] or eicosatrienoic acid [20:3(n-3)] enhanced H2O2-induced injury to PAEC. Both supplemental cis-vaccenic acid [18:1(n-7)] and 18:1(n-9) reduced the production of lipid peroxidation products in oxidant-stressed PAEC, whereas supplementation with 18:3(n-6) enhanced lipid peroxidation. Supplementation with 18:1(n-9) protected PAEC from H2O2 as long as 72 h after supplementation despite the intracellular redistribution of [18:1(n-9)] from triglycerides to phospholipids. Saturated and monounsaturated supplemental fatty acids protected PAEC from oxidant injury, but polyunsaturated fatty acids enhanced oxidant injury. These results support the hypothesis that supplemental fatty acids replace resident fatty acids, alter the oxidant reactivity of the cellular lipids, and thereby modify the oxidant susceptibility of PAEC.

Precise age-specific average body weight estimates are necessary for deterministic risk assessments, and an accurate body weight distribution is equally important in probabilistic risk assessments. Age-specific body weight distributions for U.S. residents are estimated using NHANES (National Health and Nutrition Examination Survey) data collected in four surveys over the last 24 years. The weighted mean and standard deviation of natural log-transformed body weights are computed for single-year age groups and population age-specific weight patterns further described using piece-wise polynomial spline functions and nonparametric age-smoothed trend lines. These functions are used to compare distributional changes in age-specific body weight in the United States from the first NHANES survey in 1976-1980 to the most recent in 1999-2002. Analysis demonstrates that age- and sex-specific average body weight changes over this time period are not uniform. Use of these functions to compute body weight distributions for selected child-age categories is demonstrated.

A microbial risk assessment was conducted to estimate the human health risks from incidental contact recreational activities such as canoeing, boating and fishing in the Chicago Area Waterway System (CAWS) receiving secondary treated, but non-disinfected, effluent from three municipal water reclamation plants. Actual concentrations of the pathogens (pathogenic E. coli [estimated], Giardia, Cryptosporidium, adenovirus, norovirus, enteric virus) detected from the waterway field data collection at locations upstream and downstream of the effluent outfall during dry and wet weather conditions within the recreation season were included in the risk assessment. The results under the current treatment scheme with no disinfection indicated that the total expected

Although supplemental fatty acids have been shown to alter the susceptibility of experimental animals to oxidant gases, the relationship between the degree of tissue fatty acyl unsaturation and resistance to oxidant exposure remains undefined. Because vascular endothelial cells have been demonstrated to be sensitive cellular targets in oxidant-induced lung injury, we evaluated the effects of a supplemental fatty acid on the lipid composition and oxidant susceptibility of pulmonary artery endothelial cells (PAEC) in monolayer culture. PAEC were incubated in culture medium supplemented with an ethanolic solution of 0.1 mM cis-vaccenic acid (CVA), an 18-carbon monounsaturated fatty acid, or with the ethanol vehicle alone for 3 h. Cells were then exposed to either control or oxidant (hyperoxia: 95% O2; or hydrogen peroxide: 100 microM) conditions. Oxidant-induced cell injury was assessed by phase-contrast microscopy and by measuring the release of intracellular lactate dehydrogenase. Incubation with CVA increased the CVA content of PAEC lipids and protected cells from oxidant-induced injury for up to 72 h after supplementation. CVA had no effect on nonoxidant-induced cell injury. Although the mechanism by which CVA protects cells against oxidant injury remains undefined, evidence is presented that indicates the mechanism does not involve induction of antioxidant enzyme activity, alterations in the physical state of PAEC membranes, or enhancement of PAEC nucleic acid repair mechanisms. These results define a useful model for exploring the relationship between lipid composition and oxidant susceptibility and suggest that fatty acid modifications may constitute an important strategy for protecting cells against oxidant injury.