No abstract

The effects of operational parameters and coal type on N2O emissions in a pilot-scale circulating fluidized-bed combustor (CFBC) were examined. Operational parameters included combustor temperature, excess combustion air, limestone feed rate, and primary:secondary combustion air split. Seven coals ranging in rank from lignite to high-volatile A bituminous were used to study coal-related effects. At typical operating conditions (20% excess air, 1120 K), N20 emissions ranged from 30 to 170 ppmv at 3% excess 0 2 or 16 to 100 mg N20/MJ heat input due to variations in coal type. The relative impact of operational parameters on N2O emissions is given for Salt Creek coal by the relation: temperature > excess air, primary/secondary air split > sorbent feed. Increasing combustion temperature was shown to decrease N2O emissions, while increasing excess air was shown to increase N2O emissions. The effect of limestone addition waa shown to be coal-dependent, with both increasing and decreasing trends in N2O emissions observed. The primary air-to-total-air ratio has a minimal impact on N20 emissions but tends to decrease emissions at higher temperatures, while the opposite trend occurs at lower temperatures.

The interaction between nickel and iron was confirmed in rat metabolism. In a fully-crossed, two-way, three by four, factorially designed experiment, female weanling rats were fed a basal diet supplemented with iron at 0, 25, 50, and 100 μg/g and with nickel at 0, 5, and 50 μg/g. The basal diet contained about 10 ng of nickel and 2.3 μg of iron/g. After nine weeks, dietary iron affected growth, hematocrit, hemoglobin, plasma cholesterol, and in liver affected total lipids, phospholipids, and the contents of copper, iron, manganese, and zinc. By manipulating the iron content of the diet, effects of dietary nickel were shown in rats that were not from dams fed a nickel-deprived diet. Nickel affected growth, hematocrit, hemoglobin, plasma alkaline phosphatase activity, plasma total lipids, and in liver affected total lipids, and the contents of copper, manganese, and nickel. The interaction between nickel and iron affected hematocrit, hemoglobin, plasma alkaline phosphatase activity, and plasma phospholipids, and in liver affected size, content of copper, and perhaps of manganese and nickel. In severely iron-deficient rats, the high level of dietary nickel partially alleviated the drastic depression of hematocrit and hemoglobin, and the elevation of copper in liver. Simultaneously, high dietary nickel did not increase the iron level in liver and was detrimental to growth and appearance of severely iron-deficient rats. In nickel-deprived rats fed the borderline iron-deficient diet (25 μg/g) hematocrit and hemoglobin also were depressed. However, 5 μg Ni/g of diet were just as effective as 50 μg Ni/g of diet in preventing those signs of nickel deprivation. The findings in the present study suggested that nickel and iron interact with each other at more than one locus.

No abstract