4 resultados para Co-exposure

em Aquatic Commons


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The proportion of torpedograss tissue exposed to glyphosate at application rates of 0.28, 0.56, 1.12, 2.24, and 4.48 kg/ha affected control as measured by regrowth. The effect of tissue exposure was more pronounced as application rate decreased. This study suggests that higher rates of glyphosate need to be used during higher water levels, when less torpedograss tissue is exposed to herbicide spray and lower rates may be used during periods of low water levels. Addition of the water conditioning agent Quest (R) (0.25% v/v) to glyphosate spray mixtures diminished the influence of simulated rain events following glyphosate application. Twelve other adjuvants did not influence the effect of simulated rain events.

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This report describes the working of National Centers for Coastal Ocean Service (NCCOS) Wave Exposure Model (WEMo) capable of predicting the exposure of a site in estuarine and closed water to local wind generated waves. WEMo works in two different modes: the Representative Wave Energy (RWE) mode calculates the exposure using physical parameters like wave energy and wave height, while the Relative Exposure Index (REI) empirically calculates exposure as a unitless index. Detailed working of the model in both modes and their procedures are described along with a few sample runs. WEMo model output in RWE mode (wave height and wave energy) is compared against data collected from wave sensors near Harkers Island, North Carolina for validation purposes. Computed results agreed well with the wave sensors data indicating that WEMo can be an effective tool in predicting local wave energy in closed estuarine environments. (PDF contains 31 pages)

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Analyses of blood and liver samples from live captured sea otters and liver samples from beachcast sea otter carcasses off the remote Washington coast indicate relatively low exposure to contaminants, but suggest that even at the low levels measured, exposure may be indicated by biomarker response. Evidence of pathogen exposure is noteworthy - infectious disease presents a potential risk to Washington sea otters, particularly due to their small population size and limited distribution. During 2001 and 2002, 32 sea otters were captured, of which 28 were implanted with transmitters to track their movements and liver and blood samples were collected to evaluate contaminant and pathogen exposure. In addition, liver samples from fifteen beachcast animals that washed ashore between 1991 and 2002 were analyzed to provide historical information and a basis of reference for values obtained from live otters. The results indicate low levels of metals, butyltins, and organochlorine compounds in the blood samples, with many of the organochlorines not detected except polychlorinated biphenyls (PCBs), and a few aromatic hydrocarbons detected in the liver of the live captured animals. Aliphatic hydrocarbons were measurable in the liver from the live captured animals; however, some of these are likely from biogenic sources. A significant reduction of vitamin A storage in the liver was observed in relation to PCB, dibutyltin and octacosane concentration. A significant and strong positive correlation in vitamin A storage in the liver was observed for cadmium and several of the aliphatic hydrocarbons. Peripheral blood mononuclear cell (PBMC) cytochrome P450 induction was elevated in two of 16 animals and may be potentially related to aliphatic and aromatic hydrocarbon exposure. Mean concentration of total butyltin in the liver of the Washington beach-cast otters was more than 15 times lower than the mean concentration reported by Kannan et al. (1998) for Southern sea otters in California. Organochlorine compounds were evident in the liver of beach-cast animals, despite the lack of large human population centers and development along the Washington coast. Concentrations of PCBs and chlordanes (e.g., transchlordane, cis-chlordane, trans-nonachlor, cis-nonachlor and oxychlordane) in liver of Washington beach-cast sea otters were similar to those measured in Aleutian and California sea otters, excluding those from Monterey Bay, which were higher. Mean concentrations of 1,1,1,- trichloro-2,2-bis(p-chlorophyenyl)ethanes (DDTs) were lower, and mean concentrations of cyclohexanes (HCH, e.g., alpha BHC, beta BHC, delta BHC and gamma BHC) were slightly higher in Washington beach-cast otters versus those from California and the Aleutians. Epidemiologically, blood tests revealed that 80 percent of the otters tested positive for morbillivirus and 60 percent for Toxoplasma, the latter of which has been a significant cause of mortality in Southern sea otters in California. This is the first finding of positive morbillivirus titers in sea otters from the Northeast Pacific. Individual deaths may occur from these diseases, perhaps more so when animals are otherwise immuno-compromised or infected with multiple diseases, but a population-threatening die-off from these diseases singly is unlikely while population immunity remains high. The high frequency of detection of morbillivirus and Toxoplasma in the live otters corresponds well with the cause of death of stranded Washington sea otters reported herein, which has generally been attributable to infectious disease. Washington’s sea otter population continues to grow, with over 1100 animals currently inhabiting Washington waters; however, the rate of growth has slowed over recent years. The population has a limited distribution and has not yet reached its carrying capacity and as such, is still considered at high risk to catastrophic events. (PDF contains 189 pages)

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An investigation was conducted into the deaths of more than 220 bottlenose dolphins (Tursiops truncatus) that occurred within the coastal bay ecosystem of mid-Texas between January and May 1992. The high mortality rate was unusual in that it was limited to a relatively small geographical area, occurred primarily within an inshore bay system separated from the Gulf of Mexico by barrier islands, and coincided with deaths of other taxa including birds and fish. Factors examined to determine the potential causes of the dolphin mortalities included microbial pathogens, natural biotoxins, industrial pollutants, other environmental contaminants, and direct human interactions. Emphasis was placed on nonpoint source pesticide runoff from agricultural areas, which had resulted from record rainfall that occurred during the period of increased mortality. Analytical results from sediment, water, and biota indicated that biotoxins, trace metals, and industrial chemical contamination were not likely causative factors in this mortality event. Elevated concentrations of pesticides (atrazine and aldicarb) were detected in surface water samples from bays within the region, and bay salinities were reduced to <10 ppt from December 1991 through April 1992 due to record rainfall and freshwater runoff exceeding any levels since 1939. Prolonged exposure to low salinity could have played a significant role in the unusual mortalities because low salinity exposure may cause disruption of the permeability barrier in dolphin skin. The lack of established toxicity data for marine mammals, particularly dermal absorption and bioaccumulation, precludes accurate toxicological interpretation of results beyond a simple comparison to terrestrial mammalian models. Results clearly indicated that significant periods of agricultural runoff and accompanying low salinities co-occurred with the unusual mortality event in Texas, but no definitive cause of the mortalities was determined. (PDF file contains 25 pages.)