Posted on 12/28/2003 10:27:14 AM PST by Pubbie
One thing that seems to support Purdey and refute the conventional wisdom that prions are the infectious agent themselves, is the burning of cow corpses in the UK during their epidemic. They state that prions transmitted in the brain tissue etc can cause nvCJD in humans, and that they cannot be neutralized with standard sterilization techniques such as cooking. Thus, when they burned all those carcasses, would they not have spread the infectious agent far-and-wide in the smoke and/or leave infected agent buried in the soil to be presented eventually back into the food system?
Obviously the carcasses needed to be burned to prevent other infectious diseases, but this doesn't explain why if prions are so infectious and can be spread so easily, then why isn't there vast infection spread during the extermination of the UK herds?
This, to me, lends credibility of Purdey's theory of causation vs. coincidence, although I still think his presentation could use a bit more refinement....I mean really....."Concorde takeoffs?" Puhleazee.
CWD might have something to do with deer blocks, but it is possible that they contained MBM (rendered bone meal, etc) before the feeding ban. Also antler growth has more to do with large amounts of calcium, MAGNESIUM, and phosphorus than the traces of the mineral manganese. Deer blocks like deer feeding in general tend to concentrate the deer population and spread disease. Some people believe the spread of CWD may also be related to the use of deer urine processed from farmed deer for attracting deer. In any case CWD is highly infectious in white tail deer. On one Texas ranch over 50% of white tails were found to be infected in a very large enclosure - - including fawns under 6 mos old.
The reason there has been no intense effort to eradicate CWD in Colorado is that wildlife biologists there feel that the environment is so highly contaminated with CWD prions that it would be impossible. All they can do is try to keep the deer population low.
More than forty thousand cows born after the UK's 1988 ban on MBM inclusion in cattle feed have still developed BSE. Furthermore, a small number of cows born after the further additional 1996 ban on MBM inclusion in feed destined for all types of livestock have already developed BSE.Organophosphate insecticides.
There have been no cases of BSE in the other ruminants, such as goats and sheep, susceptible to transmissible spongiform encephalopathy, despite the customary inclusion of an MBM protein source in their feeds.
Four of the original five kudu antelope that developed BSE at the London zoo had no possible access to MBM-containing feeds.
The UK government's former experimental farm at Liscombe on Exmoor was designed to raise suckler beef cattle on a pure grass-and-silage system without any resort to feeding concentrated feeds at all. Yet BSE struck down four animals on this holding.
Carry may be able to answer that.
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Yes, organophosphates were the principal replacement for DDT and have not been superceded. Organophosphate is far more toxic than DDT.
Ditto
TOXICOLOGICAL EFFECTS of PHOSMET
ACUTE TOXICITY
Phosmet is a moderately toxic compound by ingestion but requires the signal word WARNING on the label because it is more highly toxic by other routes of exposure.
It has a moderately high toxicity through the skin and a very high toxicity through inhalation.Typical of other organophosphates, phosmet is an inhibitor of the enzyme cholinesterase.
Symptoms of acute phosmet poisoning include nausea, vomiting, abdominal cramps and diarrhea. Acute exposure at high levels may result in muscle spasms, loss of muscle coordination, mental confusion and drowsiness. The insecticide may also adversely affect breathing and salivation.The oral LD50 of phosmet ranges from 113 to 369 mg/kg in rats of both sexes and 23.1 to 50.1 mg/kg in mice. Signs of acute poisoning are rapid, generally occurring within 30 minutes after exposure. The dermal LD50 for phosmet in the rabbit ranges from 1,560 to 4,640 mg/kg. Inhalation experiments showed that 50 to 800 ml/l resulted in behavior changes but no mortality to rats.
The compound appears to be more toxic to many domestic animals such as cattle, sheep and goats than to rodents.The LD50 values for these animals range from 25 to 50 mg/kg.
CHRONIC TOXICITY
Rats fed phosmet for sixteen weeks at moderate to very high doses (22.5 mg/kg to 300 mg/kg) suffered some mortality and exhibited a number of toxic effects. Over a six month period, doses of phosmet of 1 mg/kg/day in the diets of rats produced no observable chronic effects (NOEL). In another study conducted over two years the NOEL was 2 mg/kg/day. These two studies indicate that even small amounts of phosmet can cause chronic toxic effects.Dogs also had a 1 mg/kg/day NOEL in a two-year feeding study. In a 20- week experiment, dogs exhibited changes in their blood enzyme activity (cholinesterase) at doses at or above 3.7 mg/kg/day.
Cattle also showed a blood enzyme activity decrease when fed varying amounts of phosmet (1 to 2 mg/kg) for eight weeks.
No delayed neurotoxic effects were noted in chickens fed diets with moderate levels of phosmet for six weeks.
Rabbits which had phosmet applied to their skin for five days a week for three weeks suffered high mortality rates at doses of 300 to 600 mg/kg/day. At 50 mg/kg/day there was significant brain enzyme (cholinesterase) depression.
Estimates place field worker exposure to the pesticide at levels ranging from 0.1 to 1.4 mg/kg/day one day following field application. The worst case estimate of homeowner exposure was no greater than 0.005 mg/kg/day. Despite its high toxicity, over an eight year reporting interval only sixteen cases of phosmet poisoning were reported in California. One year during this period (1986) approximately 240,000 pounds of phosmet were sold in the state indicating the relative safety with which the product was handled.
The signs and symptoms of chronic toxicity are generally consistent with those for the class of organophosphate insecticides.
Reproductive Effects
A three-generation study with rats indicated that there were no reproductive effects when the animals were fed small amounts (2.0 mg/kg) of the compound for the first generation and slightly higher amounts (4 mg/kg) for the second and third generations . Female rabbits given phosmet both dermally and orally for three weeks prior to mating and for 18 consecutive days of gestation showed no effects on reproductive parameters. The doses tested ranged from 10 to 60 mg/kg for both routes of exposure.Teratogenic Effects
No birth defects were noted in studies with pregnant rabbits fed 10 to 60 mg/kg for three weeks during pregnancy or in monkeys given 8 to 12 mg/kg on days 22 to 32 of gestation.Rats fed 10 to 30 mg/kg on days 6 through 15 of gestation suffered some maternal toxicity at the higher doses but no abnormalities appeared in the pups. In another study however, single moderate doses of 30 mg/kg administered to rats between day nine and thirteen of gestation, produced an increase in brain damage (hydrocephaly) in 33 of the 55 embryos examined. Embryo toxicity was dose-dependent. The results of these studies, viewed together, are somewhat ambiguous and make it difficult to draw firm conclusions about possible teratogenic effects in humans.
Mutagenic Effects
The tests on the mutagenicity of phosmet have produced mixed results. Several tests with bacteria did not cause any mutations though there was one positive test with one strain of bacteria (S. typhimurium). There have been no tests conducted directly on animal or human cells. However, among workers producing the compound Safidon, some changes in their chromosomes were noted.Carcinogenic Effects
A group of rats fed diets containing 1 to 20 mg/kg/day of phosmet for two years showed no differences with respect to neoplasms when compared to the controls. However, the study has been deemed inadequate because too few rats were analyzed at the end of the test.A two-year mouse study showed that phosmet is associated with a significant increase in liver tumors in male mice. The dose in this test was not noted in the report. In female mice, there was a positive dose-related trend for liver tumors and carcinomas. Phosmet has a "tentative" category C carcinogen rating (possible carcinogen). The EPA has requested that additional testing be conducted.
Organ Toxicity
Observations of occupationally exposed workers indicate that the compound may cause a reduction in enzyme activity (peripheral cholinesterase). No other observable adverse effects were noted among the workers.Phosmet is a mild irritant to the eyes, and only mildly irritating to the skin.
Fate in Humans and Animals
Phosmet is rapidly absorbed, distributed, and eliminated in mammals. Rats given single doses of 23 to 35 mg/kg phosmet excreted greater than three quarters of the dose in urine, about fifteen percent in the feces. Less than three percent was found in body tissues after two days. Other figures show nearly eighty percent eliminated in the urine and twenty percent eliminated in the feces after three days.
Phosmet applied to a steer's back was moderately absorbed and rapidly broken down in the blood to phthalamic and phthalic acids.Rat studies indicate that phosmet crosses the placenta. Phosmet also appeared in the milk of goats fed a single dose of 70 mg/kg. The level in the milk after eight hours was 0.38 mg/kg but after 24 hours and 48 hours none could be detected.
Cows fed silage with an average residue level of 19 mg/kg for nearly two months showed no residues in the milk above the detection level of 0.01 mg/kg. Cattle fed dietary levels of 20 to 100 ppm showed no residues in the tissues at levels higher than 0.005 ppm.
Metabolic breakdown is primarily by hydrolytic pathways and the breakdown products are similar to those resulting from other organophosphate pesticides. The major metabolite is phthalamic acid with phthalic acid produced in smaller quantities.
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