Bovine spongiform encephalopathy (BSE) is believed to be transmitted by the ingestion of proteinaceous agents called prions which accumulate in the brain and spinal cord of infected bovines. Concern has been expressed about the risks of transmission of BSE to humans through BSE prions discharged to the aquatic environment from rendering plants, abattoirs and landfills. The disease‐related form of the prion protein is relatively resistant to degradation, and infectivity decays rather slowly in the environment. Levels of disinfection used for drinking water treatment would have little effect. This paper presents the assumptions which were used to model the risks from a rendering plant disposing of cull cattle carcasses in the catchment of a chalk aquifer which is used for a drinking water abstraction. The risk assessment approach focused on identifying the hydrogeological and physical barriers which would contribute to preventing BSE infectivity gaining entry to the aquifer. These barriers included inactivation of BSE agent by the rendering process, removal from the effluent by treatment at the plant, filtration and adsorption in the clay and chalk, and dilution in the ground water. The importance in environmental risk assessment of the cow‐to‐man species barrier is considered. Two key conclusions about the environmental behaviour of the BSE agent are that prion proteins are ‘sticky’ and bind to particulates, and that the millions of BSE prion molecules comprising a human oral ID50 are subject to some degree of dispersion and hence dilution in the environment. Assuming the rendering plant processes 2000 cull cattle carcasses per week, the risks to drinking water consumers were estimated to be remote. Indeed, even using worst case assumptions an individual would have to consume 2 l d−1 of tap water for 45 million years to have a 50% chance of infection through drinking water drawn from the aquifer.
Over the last few years rises in the nitrate content of ground water from wells and springs in the principal aquifers of the United Kingdom have been observed. In a number of cases the concentrations have exceeded the WHO lower recommended limit. In order to determine the reason for the rise, to assess whether it will continue and the eventual nitrate levels, the Water Research Centre has undertaken an extensive programme of drilling and sampling on the Chalk and Bunter Sandstone, and by August 1976, twenty‐two sites had been examined. This work has established that high nitrate concentrations (peaks up to 60 mg/l NO3‐N have been observed) are present in the unsaturated aquifers at fertilized arable/ley sites. At unfertilized grassland sites nitrate concentrations are low (less than 4 mg/l NO3‐N) and below fertilized established grassland values are in the intermediate range. At one farm site near Winchester, models to predict the rate of movement of nitrate through the unsaturated and saturated Chalk have been developed. These suggest that the nitrate levels at this site will remain at an essentially constant value of about 4 mg/l NO3‐N until the late 1970's when they will rise progressively to about 4 mg/l NO3‐N. The models have been checked against tritium data and the approach is now being extended to other sites.
A study of methemoglobin levels in infants from birth through six months showed that even healthy babies not exposed to excessive nitrate levels in diets have higher levels when young. Babies with diarrhea or respiratory illness had the highest levels in this population. Ingestion of water or formula high in nitrates appears to increase the frequency of elevated methemoglobin. More than 60% of formulae showed bacterial contamination. Long-term consequences should be investigated.
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