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Earth's core has produced a global magnetic field for the last 4 Gyrs, presently sustained by inner core growth.Models of the core with high thermal conductivity suggest potentially insufficient power available for the geodynamo prior to inner core formation ~1 Ga.Precipitation of SiO2 from the liquid core might offer an alternative power source for the magnetic field before inner core growth, however, no estimates of partition coefficient exist for conditions of the early core.We present the first determination of the silicon partition coefficient at core-mantle boundary conditions and use these results to build a thermodynamic model that is integrated into a model of coupled core-mantle thermal evolution.We show that models including precipitation of silicon can satisfy constraints of inner core size, mantle convective heat flux, mantle temperature and a persistent ancient geodynamo whilst those excluding fail.Successful power from precipitation favours an oxygen poor initial core composition.

Classical nucleation theory describes the formation of the first solids from supercooled liquids and predicts an average waiting time for a system to freeze as it is cooled below the melting temperature. For systems at low to moderate undercooling, waiting times are too long for freezing to be observed via simulation. Here a system can be described by estimated thermodynamic properties, or by extrapolation from practical conditions where thermodynamic properties can be fit directly to simulations. In the case of crystallizing Earth's solid iron inner core, these thermodynamic parameters are not well known and waiting times from simulations must be extrapolated over approximately 60 orders of magnitude. In this work, we develop a new approach negating the need for freezing to be observed. We collect statistics on solidlike particles in molecular dynamic simulations of supercooled liquids at 320 GPa. This allows estimation of waiting times at temperatures closer to the melting point than is accessible to other techniques and without prior thermodynamic insight or assumption. Our method describes the behavior of nucleation at otherwise inaccessible conditions such that the nucleation of any system at small undercooling can be characterized alongside the thermodynamic quantities which define the first formed solids.

This study documents the successful use of a mysid, Mysidopsis bahia, for life-cycle toxicity tests. These tests were conducted to determine acute and chronic toxicities of metal (cadmium) and pesticide (Kepone). Delay inthe formation of mysid brood pouches and release of young were noted in low concentrations ≤6.4 μg cadmium/litre. Fewer young produced per female and decreased growth were other indicators of effects of Kepone.

Acute (96-h) flow-through toxicity tests with endosulfan (Thiodan) were conducted with several estuarine animals. The test species and their 96-h lethal concentration for 50 percent of the organisms (LC 5 0 ) values were: pink shrimp (Penaeus duorarum), 0.04 μg/litre; grass shrimp (Palaemonetes pugio), 1.3 μg/litre; pinfish (Lagodon rhomboides), 0.3 μg/litre; spot (Leiostomus xanthurus), 0.09 μg/litre; and striped mullet (Mugil cephalus), 0.38 μg/litre. In a 56-day bioconcentration study (28-day uptake, 28-day depuration), striped mullet were exposed to 0.008 and 0.08 μg endosulfan/litre seawater. The two endosulfan isomers (endosulfan I and II) were rapidly metabolized to endosulfan sulfate; only trace amounts of each isomer were detected in edible tissue or offal of mullet exposed to 0.08 μg/litre (0.035 μg/litre measured) for 28 days. Maximum bioconcentration factors of endosulfan were 2249 in edible tissue and 2755 in whole-body analyses. After 48 h in pesticide-free seawater, endosulfan was not detected in the previously exposed mullet. Our studies suggest that endosulfan in the estuarine environment would be a hazard because of its acute toxicity and bioconcentration potential, but animals surviving exposure and moving to areas free of endosulfan would lose the chemical rapidly.

A tidal marsh ditch near Pensacola, Florida was treated with 0.2 pound of DDT per acre in March 1963, and observed for 4 months. Ninety-eight per cent of the animal mortality occurred within 3 weeks after treatment. A population of cyprinodont fish was restored by reproduction of surviving and introduced fish. DDT was detected in surface water samples 8 days after treatment but not after 14 days, while DDT was not detected in bottom water samples later than 1 day after treatment. Seven weeks after treatment, vegetation samples averaged 9.1 ppm of DDT, after reaching a maximum of 75 ppm of DDT 3 to 4 weeks after treatment. Sediment samples yielded more variable residues, averaging 0.76 ppm of DDT at 7 weeks after reaching a maximum of 3.35 ppm of DDT 6 weeks after treatment. Fish accumulated up to 90 ppm of DDT within 5 weeks after treatment. Highest DDT residues detected in fiddler crabs and snails ranged from 15 to 25 per cent of the average residues detected in fish. The net water movement as i...

The polychlorinated biphenyl Aroclor® 1254 was released in an accidental leakage of heat-exchange fluid from an industrial plant, into the Escambia River, near Pensacola, Florida, USA. This material was carried downstream, and is now found in the fauna of Escambia Bay and its contiguous waters, prime nursery areas for fishes and invertebrates such as penaeid shrimp. The significance of pollution by this chemical was assessed by establishing toxicity levels, determining routes of entry, and investigating its movement and distribution in various tissues of shrimp under controlled conditions in the laboratory. Aroclor 1254 added to the water was toxic to the juvenile pink shrimp Penaeus duorarum at a concentration of 1.0 part per billion within 15 days, but was less

Our results suggest that chronic exposure to Aroclor 1254 increased susceptibility of test pinfish and spot to disease, and also appeared to be toxic to these fish. This PCB is rapidly stored by pinfish and spot, and persists in tissues for approximately three months. Our findings emphasize the need for further study on the effect of chronic exposure of aquatic organisms to polychlorinated biphenyls.

We investigated the toxicity of Kepone to, and uptake by embryo, fry, juvenile, and adult sheepshead minnows (Cyprinodon variegatus) using intermittent-flow toxicity tests. Concentration of Kepone and percentage of adult fish surviving in a 28-day exposure were: Control, 95%; 0.05 μg/liter, 95%; 0.16 μg/liter, 100%; 0.80 μ/liter, 78%; 1.9 μg/liter, 20%; and 7.8 μg/liter and 24 μg/liter, 0%. Concentration factors (concentrations in fish divided by concentrations measured in water) for adult fish averaged 5,200 (range 3,100 to 7,000). Symptoms of poisoning included scoliosis, darkening of the posterior one-third of the body, hemorrhaging near the brain and on the body, edema, fin-rot, uncoordinated swimming, and cessation of feeding. Adults surviving the first exposure were spawned, and the embryonic development, hatching, and survival and growth of fry and juveniles were monitored in a 36-day exposure to Kepone concentrations of 0.08, 0.18, 0.72, 2.0, 6.6, and 33 μg/liter. A significant number of embryos from adult fish exposed to 1.9 μg of Kepone/liter of water developed abnormally and died even when incubated in Kepone-free water. Kepone in water was not as lethal to progeny as to adults: 36-day LC50 for juveniles was 6.7μg/liter; 28-day LC50 for adults, 1.3 μg/liter. However, the average standard length of juvenile fish was significantly reduced by exposure to 0.08 μg of Kepone/liter of water; some fish developed scoliosis. Concentration factors in juvenile sheepshead minnows averaged 7,200 and increased from 3,600 to 20,000 as exposure concentrations decreased.

Recent contamination of the James River estuary, Virginia, with Kepone prompted acute flow-through bioassays to determine the 96-hour toxicity of the insectivide to four estuarine species native to that ecosystem. The species and their 96-hour LC50 values were: grass shrimp (Palaemonetes pugio), 121 μg/liter; blue crab (Callinectes sapidus), >210 μg/liter; sheepshead minnow (Cyprinodon variegatus), 69.5μg/liter; and spot (Leiostomus xanthurus) 6.6μg/liter. Surviving animals were analyzed for Kepone. Average bioconcentration factors (the concentration of Kepone in tissues divided by the concentration of Kepone measured in seawater) were: grass shrimp, 698; blue crab 8.1; sheepshead minnow, 1,548; and spot, 1,221.

Four species of marine unicellular algae were exposed to Kepone in laboratory bioassays. EC50 values after seven days’ growth, in mg/liter (ppm), were:Chlorococcum sp., 0.35;Dunaliella tertiolecta, 0.58;Nitzschia sp., 0.60;Thalassiosira pseudonana, 0.60. When exposed to 100 μg/liter (ppb) Kepone for 24 hr, residues associated with the algae, in mg/kg (ppm) wet weight, were:Chlorococcum sp., 80;D. tertiolecta, 23;Nitzschia sp., 41;T. pseudonana, 52.

Two long-term studies were conducted to determine toxicity, uptake and depuration of Kepone in blue crabs (Callinectes sapidus). In the first, Kepone was administered to crabs in seawater (0.03 or 0.3 μg Kepone/I) or food (eastern oyster,Crassostrea virginica, containing 0.25 μg/g Kepone). Uptake of Kepone in 28 days was primarily through the contaminated oysters. When these crabs were held in Kepone-free seawater and fed Kepone-free oysters for 28 days, no loss of the insecticide was evident. There were adverse effects on molting and survival in crabs fed oysters that contained 0.25 μg/g Kepone.

Accumulation, transfer, and loss of Kepone in estuarine organisms were studied in laboratory bioassays. Kepone was bioconcentrated by oysters (Crassostrea virginica), mysids (Mysidopsis bahia), grass shrimp (Palaemonetes pugio), sheepshead minnows (Cyprinodon variegatus), and spot (Leiostomus xanthurus), from concentrations as low as 0.023 μg/l seawater. Bioconcentration factors ranged from 10 to 340 in static exposures and 900 to 13,500 in flow-through bioassays, and were dependent on species and exposure duration. Depuration of Kepone from oysters in Kepone-free water was rapid (35% loss in 24 hours); however, depuration of Kepone was slow in crustaceans and fish, with tissue concentrations decreasing 30–50% in 24–28 days. Oysters, fedChlorococcum containing approximately 34 μg Kepone/g wet weight, attained 0.21 μg Kepone/g (wet tissue) in 14 days, but when fed Kepone-free plankton, depurated Kepone to below detectable concentrations ( 85%) quantities of Kepone transferred from prey to predatory fish.