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#31
24-10-2006, 10:57 AM
posted to uk.business.agriculture,alt.animals.ethics.vegetarian,uk.environment.conservation,uk.rec.birdwatching,uk.rec.gardening
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Blight spray clouds organic claims *Another Soil Association CON?
On Tue, 24 Oct 2006 10:10:51 +0100, Geoff
wrote: On 24 Oct 2006 09:01:58 GMT, (Nick Maclaren) wrote: In article , Geoff writes: | | All this may leave consumers wondering if there is any evidence of | copper residues in potatoes that reach the shops. And whether it is enough to give them their RDA of copper :-) Give or take, it far, far exceeds our minimal requirements Copper Recommended Dietary Allowance (milligrams/day) Adult 0.9 Pregnant woman 1.0 Nursing mother 1.3 And we get more than enough in a good diet, without adding any! Sources of copper The table below indicates the approximate copper content in a range of foods: Food Copper (mg/100g edible portion) Potato 0.22 Baked, without salt, flesh only Potato 0.17 Boiled, no skin, no salt Mushrooms 0.24 Canned, drained Green Peas 0.14 Frozen, cooked, drained, no salt Banana 0.10 Raw Raisins 0.36 Golden, seedless Peanuts 0.67 Dry roasted, no salt Peanuts 1.14 Raw Brazil Nuts 1.77 Dried, unblanched Chick Peas 0.17 Canned Chick Peas 0.85 Raw Sunflower Seeds 1.75 Kernels, dried Chocolate (Dark) 0.80 Dark chocolate bar So. What happens if we get too much copper? HIGH COPPER Copper levels are more often too high rather than too low. High copper can be toxic. Physical Symptoms of High Copper: Headaches….Hypoglycemia….Increased heart rate….Nausea Copper deposits in the brain and liver….Damage to the kidneys….Inhibit urine production….Causes anemia….Causes hair loss in women….High copper interferes with zinc, which is needed to manufacture digestive enzymes. Many high copper people dislike protein and are drawn to high-carbohydrate diets because they have difficulty digesting protein foods….Excessive copper in children is associated with hyperactive behavior, learning disorders such as dyslexia, ADD and infections such as ear. Psychological Symptoms of High Copper: Autism type symptoms….Depression….Hallucinations Hyperactivity….Insomnia….Paranoia….Personality changes….Psychosis….Schizophrenic type symptoms Overstimulation….Disperception of the senses, time, body, self and others. Produces hypomanic states Detachment from reality. As we can see, I would suggest many here already exhibit many of these symptoms! |
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#32
24-10-2006, 11:06 AM
posted to uk.business.agriculture,alt.animals.ethics.vegetarian,uk.environment.conservation,uk.rec.birdwatching,uk.rec.gardening
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Blight spray clouds organic claims *Another Soil Association CON?
On Tue, 24 Oct 2006 10:57:58 +0100, Geoff
wrote: On Tue, 24 Oct 2006 10:10:51 +0100, Geoff wrote: On 24 Oct 2006 09:01:58 GMT, (Nick Maclaren) wrote: In article , Geoff writes: | | All this may leave consumers wondering if there is any evidence of | copper residues in potatoes that reach the shops. And whether it is enough to give them their RDA of copper :-) Give or take, it far, far exceeds our minimal requirements Copper Recommended Dietary Allowance (milligrams/day) Adult 0.9 Pregnant woman 1.0 Nursing mother 1.3 And we get more than enough in a good diet, without adding any! Sources of copper The table below indicates the approximate copper content in a range of foods: Food Copper (mg/100g edible portion) Potato 0.22 Baked, without salt, flesh only Potato 0.17 Boiled, no skin, no salt Mushrooms 0.24 Canned, drained Green Peas 0.14 Frozen, cooked, drained, no salt Banana 0.10 Raw Raisins 0.36 Golden, seedless Peanuts 0.67 Dry roasted, no salt Peanuts 1.14 Raw Brazil Nuts 1.77 Dried, unblanched Chick Peas 0.17 Canned Chick Peas 0.85 Raw Sunflower Seeds 1.75 Kernels, dried Chocolate (Dark) 0.80 Dark chocolate bar So. What happens if we get too much copper? HIGH COPPER Copper levels are more often too high rather than too low. High copper can be toxic. Physical Symptoms of High Copper: Headaches….Hypoglycemia….Increased heart rate….Nausea Copper deposits in the brain and liver….Damage to the kidneys….Inhibit urine production….Causes anemia….Causes hair loss in women….High copper interferes with zinc, which is needed to manufacture digestive enzymes. Many high copper people dislike protein and are drawn to high-carbohydrate diets because they have difficulty digesting protein foods….Excessive copper in children is associated with hyperactive behavior, learning disorders such as dyslexia, ADD and infections such as ear. Psychological Symptoms of High Copper: Autism type symptoms….Depression….Hallucinations Hyperactivity….Insomnia….Paranoia….Personality changes….Psychosis….Schizophrenic type symptoms Overstimulation….Disperception of the senses, time, body, self and others. Produces hypomanic states Detachment from reality. As we can see, I would suggest many here already exhibit many of these symptoms! Further CHEMICAL FOOD SAFETY QUARTERLY REPORT from DEFRA themselves shows whats going into the food chain, one way or another! POTENTIAL FOOD SAFETY INCIDENTS OCTOBER - DECEMBER 2005 SPECIES INCIDENT NO. DATE VLA LABORATORY TOXIN Avian 2005/76 25.11.05 Bury St Edmunds Organophosphorus Cattle 2005/66 03.10.05 Penrith Botulism Cattle 2005/67 03.10.05 Penrith Botulism Cattle 2005/71 18.11.05 Shrewsbury Botulism Cattle 2005/75 24.11.05 Preston Botulism Cattle 2005/77 08.12.05 Thirsk Botulism Cattle 2005/79 13.12.05 Newcastle Botulism Cattle 2005/80 13.12.05 Preston Botulism Cattle 2005/68 18.10.05 Starcross Copper Cattle 2005/73 28.11.05 Carmarthen Lead Cattle 2005/78 06.12.05 Newcastle Lead Cattle 2005/83 22.12.05 Langford Lead Cattle 2005/74 23.11.05 Starcross Metaldehyde Cattle 2005/81 19.12.05 Shrewsbury Mycotoxin Cattle 2005/69 21.10.05 Aberystwyth Rodenticide Sheep 2005/82 19.12.05 Preston Botulism Sheep 2005/70 12.11.05 Langford Copper Sheep 2005/72 18.11.05 Luddington Copper LEAD POISONING IN CATTLE 2005/73 Lead poisoning was diagnosed in a 6-week-old calf, the second to die in a group of 27 that were individually penned in an old cowshed. Two animals at the back of the shed were adjacent to a wooden wall that had lead paint on it. Prior to this group being housed, pallets had prevented access to this wooden wall. 2005/78 Lead poisoning was diagnosed in a group of suckler cows and calves when one calf was found dead and a second showed clinical signs consistent with lead poisoning. Both calves had been on the same pasture since birth. There was a small mound of earth in the field, which appeared to be an old rubbish tip with a significant amount of agricultural and domestic rubbish including fencing material, glass, ceramics and metallic waste. Only October – December 2005 low levels of lead were found in environmental samples collected from the site but no other possible sources of lead could be identified. 2005/83 A raised kidney lead level was found in a 1-year old Red Devon cow which died from hypomagnesaemia. The elevated lead level was thought due to geochemical exposure from Roman and other lead mining on the Mendips. COPPER IN CATTLE 2005/68 Investigations were carried out after a cow submitted for post-mortem examination was found to have a liver copper level of 536 mg/kg WM, although the cause of death of the cow was bronchopneumonia. The diet had included a high level of concentrates with copper levels of between 45-50 mg/kg. It was calculated that an average yielding cow would have had a copper intake of approximately 36.6 mg Cu/kg DM, which exceeds the legal limit without a veterinary prescription of 35 mg Cu/kg DM. The cows received no other copper supplementation. The dietary management was changed and a mixer wagon was put into use feeding a TMR. After the changes a high yielder was estimated to have a maximum copper intake of 22 mg Cu/kg DM daily. COPPER IN SHEEP 2005/70 Copper toxicity was diagnosed in a small flock of North Ronaldsay ewes. Three ewes were found dead over a period of a few days. The third animal to die was submitted for examination. Post-mortem findings were strongly suggestive of copper poisoning which was confirmed by copper analysis. The liver copper was 514 mg/kg WM. The history of the incident suggested that there was a strong possibility that pig feed had been fed to the sheep. However North Ronaldsay sheep are particularly prone to copper poisoning and can succumb to poisoning even when fed sheep concentrate at only slightly higher than recommended levels. 2005/72 Copper poisoning was diagnosed in an adult Friesland ewe that had died suddenly on a 750 dairy sheep farm with previous cases of copper poisoning. The copper level in the liver was 571 mg/kg WM. Friesland sheep are susceptible to copper toxicity and the need for intensive concentrate feeding predisposes the ewes to chronic accumulation of copper. Blood samples from 14 ewes indicated elevated GLDH levels in ten. Although other causes of liver damage could not be ruled out it was thought that the raised GLDH was a likely result of excess copper in the feed. It was recommended to assess the copper liver levels of fallen stock on a regular basis. BOTULISM IN CATTLE 2005/66 and 2005/67 Botulism, caused by poultry litter from the same chicken farm, was suspected as the cause of deaths on two farms. A total of nine animals died. They were all grazing fields adjacent to where the litter had been spread and clinical signs occurred within a week of that event. Six carcases were received for post mortem examination and no alternative diagnosis could be made, suggesting that botulism was the cause of death. A sample of intestinal contents from one case was sent for analysis and, although toxin could not be detected in gut contents, Clostridium botulinum Type D was recovered on culture. Poultry carcases were recovered from the spread litter and the local Trading Standards were informed. 2005/67 2005/71 Botulism was suspected in two 8-9-month-old dairy heifers at grass. They had been grazing in fields adjacent to a neighbouring farm on which a large broiler enterprise was sited. Disease occurred approximately 7 and 12 days after depopulation of the broiler flock at which time the litter was removed from the houses and heaped for 3-4 days before collection for incineration. The dairy farmer commented that chicken carcases had been found on his premises in the past and the moving of broiler carcase material by foxes from the litter to the dairy farm was suspected to be the cause in this case. 2005/75 A 4-year-old dry cow was submitted after being euthanased with clinical signs of recumbency which was unresponsive to standard milk fever therapy. Three out of 40 animals had been affected. Botulism was suspected as the animals were bedded on broiler litter. Post-mortem examination identified acute abomasal ulceration and haemorrhage and an acute haemorrhagic enteritis but no alternative findings were detected to account for the clinical signs. 2005/77 Botulism was suspected in a 2-year-old pregnant dairy heifer on a farm that had cases of suspected botulism in September 2005 (SFS 05/65). The heifer was one of a group of 20 pregnant and non-pregnant heifers brought back in batches after grazing away from the home farm. They were initially put onto the same field where disease had occurred in September, for only 3-4 days, before being housed. Although broiler litter was not present on the farm, there was a broiler farm sited across the road from the farm. 2005/79 Weakness, ataxia and recumbency were reported among a group of yearling bulls and botulism was considered as a possible differential diagnosis. The worst affected animal was euthanased on humane grounds and submitted for post-mortem. No evidence to refute the diagnosis of botulism could be found on gross examination, histopathology, biochemistry or haematology. The source of the toxin could not be detected. 2005/80 Botulism was suspected when an 18-month-old beef store-heifer on rented grazing was found dead and two days later two further animals of the group of 26 were found recumbent. One died, but the other made a gradual recovery. Clinical signs were consistent with botulism and a haemorrhagic enteritis was found on gross post-mortem examination. Laboratory tests failed to identify any other cause of disease. The group did not have direct access to poultry litter, although there was a large stack of the material in a neighbour’s field adjacent to where the affected cattle were grazing. BOTULISM IN SHEEP 2005/82 A large outbreak of botulism was seen in pregnant ewes due to lamb in March. A total of at least 80 were lost out of a group of 230. They had been kept for 36 hours on pasture top dressed with broiler litter five weeks previously, prior to being dosed and moved to fresh pasture. OTHER INCIDENTS Rodenticide 2005/69 A report was received that a group of 120 housed cows have been exposed to the rodenticide bromadiolone. The cows had been turned out into a collecting yard and three cows gained access to a bucket of rodenticide in an adjacent disused milking parlour. The rodenticide had been placed there without the knowledge of the stockman. The three cows consumed most of the contents of the 3 kg bucket but none showed any clinical signs. The exposed animals were suckler cows not intended for the food chain. Metaldehyde 2005/74 Metaldehyde poisoning was diagnosed when two cows and two yearling heifers broke into a shed and gained access to slug pellets. The animals developed neurological signs soon afterwards. One cow and one heifer died, the others recovered. The dead heifer was submitted for post-mortem examination. Blue-green fluid poured from the nose when the carcase was hoisted and the mucosa of the fore-stomachs was discoloured blue, although no recognisable slug pellets were found. Metaldehyde was confirmed in the rumen contents. Mycotoxin 2005/81 Two intensively reared bulls were submitted for post-mortem examination within four days of each other. A third bull had died with acute onset gasping and collapse when the animals were moved to be weighed. At that time the two other animals were noticed to be unwell, and as pneumonia was suspected, they were treated with antibiotic. One of the bulls died two days later, the second was found collapsed six days later. Post-mortem examinations revealed similar pathological features with jaundice, swollen tan-coloured livers and dark swollen kidneys. A large amount of bilirubin and haemoglobin was detected in the urine. Kidney copper concentration was significantly elevated in the first animal, consistent with copper poisoning. Although the liver and blood copper concentrations were increased in the second, the kidney copper concentration was within the reference range. The animals were fed good quality proprietary concentrate and good quality straw but were bedded on poor quality 2-year old straw on which weed and mould growth was reported. Histopathological examinations revealed severe hepatopathy and a tubulo-nephritis, lesions consistent with, although not confirmatory of, a mycotoxic cause. The copper toxicity in one of the animals was considered secondary to underlying hepatic changes. All the straw used as bedding was removed from the pens, which were rebedded using alternative clean straw. No further disease was reported. 2005/82 Organophosphorus 2005/76 Malicious poisoning of pheasants with an organophosphate pesticide was diagnosed when approximately 190 of about 500 birds released into a wooded area were found dead over a period of four days. A blue chemical was found in the area and blue crop content in one of the birds indicated exposure. Samples sent for toxicological investigation were shown to contain the organophosphate omephoate (‘Folimat’: Bayer Cropscience). FOOD SAFETY INCIDENTS 2005 Toxin No. of Incidents Species Lead 44 (47) Cattle 41, Sheep 2, Avian 1 Botulism 23 (22) Cattle 20, Sheep 3 Copper 7 (3) Cattle 1, Sheep 6 No Toxin 2 (0) Cattle 1, Avian 1 Organophosphorus 2 (0) Cattle 1, Avian 1 Metaldehyde 1 (2) Cattle Mycotoxin 1 (1) Cattle Nitrate 1 (1) Cattle Rodenticide 1 (0) Cattle Not Established 1 (2) Cattle Total 83 (81) Cattle 69, Sheep 11, Avian 3 2004 figures in brackets “Stories in the press” |
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