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Statement
to
US Food and Drug Administration
Consumer Briefing
BSE/TSE
JEAN HALLORAN
DIRECTOR, CONSUMER POLICY INSTITUTE/CONSUMERS
UNION
April 16, 2001
Washington, D.C.
Thank you for inviting me to discuss FDA's policies and programs related to mad cow disease and other transmissible spongiform encephalopathies (TSEs), on behalf of Consumers Union, publisher of Consumer Reports.
I would particularly like to focus on the FDA feed rule, which falls under the jurisdiction of the Center for Veterinary Medicine. We think that the current feed rule is not sufficiently precautionary-this "firewall" has some gaps in it . To adequately protect US citizens and our cattle industry from the possibility of a TSE epidemic in the United States, the FDA, as a priority, should eliminate all exemptions to the current mammal to ruminant feed ban. Thus FDA should no longer permit remains of swine, or the blood of any mammal, to be fed to cows and other ruminants.
I will also briefly address improvements which are needed in programs of other agencies, including USDA surveillance programs.
Feed Rule
The FDA took an important and positive step in 1997 when it issued new regulations banning the feeding of mammal remains (with certain exceptions) to ruminants. Although we still do not know definitively what caused the mad cow disease epidemic in the United Kingdom, the evidence strongly suggests that the feeding of infected animal remains to cows transmitted the infectious agent.
The United States is fortunate to have been spared this epidemic. However it is imperative that we learn from the British experience and take steps to prevent a similar problem here. Until 1997, we were engaging in the same practices which are believed to have created the epidemic in Britain. We too were feeding the remains of cows, sheep and other ruminants back to ruminants. Meanwhile, TSE diseases similar to mad cow were known to occur in American sheep and in wild and farm-raised deer and elk Colorado and Wyoming.
The 1997 FDA rule banned the feeding of mammal remains to ruminants. However it allowed several big exceptions, most notably for swine protein and blood. These exceptions must be eliminated. Indeed, we would recommend that the US adopt the same precautionary policies that are currently in place in Britain, where there is a ban on feeding any mammal remains to any food animal.
As a priority, FDA should eliminate the exemption for blood. When the FDA feed rule was promulgated in 1997, there was some doubt about whether blood could carry infection from one animal to another. Since then, however, Dr. Paul Brown of the National Institutes of Health announced at a World Health Organization meeting that his lab had injected blood from mice infected with CJD into the brains of healthy mice, and the latter subsequently developed a TSE. This work conclusively demonstrates that blood and blood products do carry the TSE-causing agent. (Brown et al, 1998)
If this is true for CJD, we must assume that it would be true for other TSEs.
In regulating the human blood supply, FDA, acknowledging this risk, has prohibited
blood donations from anyone who has lived in the UK for more than six months
during the late 1980s and early 1990s. FDA should likewise acknowledge the potential
for transmission of TSE agents through blood in feed. Allowing blood in ruminant
feed is of particular concern because some of the feed products are fed to calves,
maximizing the time any disease would have to develop, and because these products
are freeze dried, which means there is no reduction of infectivity through heating.
For example, an article in the October 1997 issue of Dairy Herd Management entitled
"Consider using spray-dried bovine plasma," touts how feeding spray-dried
bovine plasma can increase the weight gain in post-weaned calves.
FDA should also eliminate the exemption for swine protein. FDA exempted swine because no "naturally occurring" TSE has yet been positively identified in pigs under natural conditions. However, this could just mean that the government has not looked hard enough. In a British experiment, a pig injected with brain material from a BSE cow contracted a TSE, showing they are susceptible to this disease. (Dawson et al., 1990).
Most commercial pigs are slaughtered at the age of six months, long before the pigs would be expected to exhibit any signs of the disease. The government does not monitor any swine brains for evidence of TSEs.
Scientific evidence from the US suggests that swine may actually already be infected with a TSE. Hogs in a 1979-80 USDA study at a packing plant in upstate New York showed many of the same behaviors found in BSE animals. USDA recently re-reviewed this study, and Dr. William Hadlow, one of the foremost TSE pathologists in the world, examined slides from one animal's brain. Dr. Hadlow concluded that it was suggestive of a TSE. (Hadlow, 1997). However, FDA stated that salt toxicity/water deprivation can produce similar clinical symptoms and brain lesions.
In addition, two small case-control epidemiological studies of some US victims of CJD, a human TSE, have found suggestive links to pigs. A 1985 study found that consumption of six pork products (smoked pork, roast pork, pork chops, ham, scrapple and hot dogs) increased the risk of CJD compared to a control group. (Davanipour et al., 1985: 443). The other study, from 1973, found that one third of the CJD patients ate brains, much higher than the US population overall. The patients also had a greater preference for hog brains compared to controls. (Bobowick et al., 1973: 381).
It is also important to note that recent research has shown that animals that show no signs of a TSE disease can nevertheless be carriers. In a study done by scientists at the National Institute of Health published in Nature in April, 1998 (Race and Chesebro, 1998). the scientists injected the infectious agent for hamster scrapie (i.e. hamster mutant prion) into the brains of mice. Mice are highly resistant to the hamster disease, and as expected did not develop symptoms. But the NIH scientists found that a year later that brain and spleen from these mice could cause disease when put back into hamsters.
This data suggests that swine could be asymtomatic carriers of TSEs. Two top European TSE specialists, Drs. Adriano Aguzzi and Charles Weissmann, discussed the potential implications of this data in an accompanying commentary: "Pigs and chickens that have been fed with cattle-derived bone and meat meal are thought to be safe to eat with respect to BSE, because these animals do not develop disease after oral exposure to bovine prions. But, to the best of our knowledge, bovine prions from BSE-exposed pigs and poultry have never been assayed using calves as 'indicator' animals" (Aguzzi and Weissmann, 1998: 764).
Perhaps the most egregious problem with the FDA rules is that they permit known TSE-positive material to be used in feed. Thus, carcasses of scrapie-infected sheep and TSE-infected deer could legally be sent to the renderer and converted into pet and pig rations.
We do not think that the FDA should permit TSE-positive material to be used for any purpose. The FDA decision flies in the face of recommendations from World Health Organization's International Consultation on TSEs and Public Health. WHO urged that "No part or product of any animal which has shown signs of a TSE should enter any food chain (human or animal)." (WHO, 1996).
Enforcement
One further argument in favor of eliminating the swine exemption is the difficulty FDA has had enforcing its current rule. The current rule allows cow and sheep remains to be fed to swine and poultry, and swine and poultry remains to be fed to sheep, and all remains to be made into pet food. Keeping all these streams separate and properly labeled has turned out to pose enormous difficulties on the ground. According to the General Accounting Office 1700 out of 9100 renderers and mills did not know about the rules when FDA and state regulators contacted them, and depending on the category, 10% to 30 % were not complying (GAO, 2000). The stark meaning of these statistics is that today, in the year 2001, we are still feeding cattle remains to some cattle, the practice believed to have triggered the mad cow problem in the UK. We fully support the efforts FDA and state agencies have made to enforce rule, and support strengthening these efforts. But perhaps a simpler rule, one which prohibited all mammal to ruminant feeding, might lessen both the confusion and the enforcement burden.
Research and Surveillance
We have a great need to increase USDA surveillance of US animals for TSEs. USDA currently has a program which tested the brains of approximately 2000 cows last year for mad cow disease. This highly commendable program needs to be expanded. With the current program, one would expect to see any infection rate that was running one in a thousand animals or higher. However the US has approximately 100 million cattle on the hoof. If even one in ten thousand were infected with a disease, that would amount to ten thousand infected animals-a very significant number. We therefore think USDA surveillance should be increased by a factor of ten. While there would be increased cost, the existence of new cheaper screening tests in Europe could be employed to keep costs down.
We also ask that the National Institutes of Health reconsider its decision to shut down its own research laboratory looking into TSEs. This lab has a history of making scientific breakthroughs, including the important recent research on blood transmission. The government is funding, and should continue to fund research at independent academic institutions on this topic. But we also need intra-government expertise. With NIH having just received a significant increase in funding, surely it can afford to retain its own expertise in this important area. We specifically urge that new epidemiology of CJD victims be undertaken , funded by NIH, that would examine dietary habits .
Finally FDA should assess the potential risks to humans posed by TSE-infected deer and elk. As noted above, the World Health Organization recommends that no TSE-positive animal be allowed in food, animal or human. FDA should examine whether it is doing everything it should to insure the safety of both venison sold commercially and food consumed by hunters.
Summary
In sum, all indications are that the United States has been extremely lucky, and has avoided a mad cow outbreak like that in Britain. But should we count on luck to protect us in the future? We think we should not press out luck, but rather should take additional protective measures, of which the most important right now is to ban the feeding of swine protein and blood to ruminants.
References
Aguzzi, A. and C. Weissmann. 1998. The prion's perplexing persistence. Nature, 392: 763-764.
Bobowick, A.R., Brody, J.A., Matthews, M.R., Roos, R. and D.C. Gajdusek. 1973. Creutzfeldt-Jakob disease: A case-control study. American Journal of Epidemiology 98: 381-394.
Davanipour, Z., Alter, M., Sobel, E., Asher, D.M. and D.C. Gajdusek. 1989. A case-control study of Creutzfeldt-Jakob disease: Dietary risk factors. American Journal of Epidemiology 122: 433-451
Dawson, M., Wells, G.A.H., Parker, B.N.J. and A.C. Scott. 1990. Primary parental transmission of bovine spongiform encephalopathy to the pig. Veterinary Record, pg. 338.
General Accounting Office. 2000. Controls Can Be Strengthened to Reduce The Risk of Disease Linked to Unsafe Animal Feed. GAO, September, 2000.
Hadlow, W.J. 1997. Letter to Patrick
McCaskey, USDA/FSIS/Eastern Lab, dated April 10, 1997
Race, R. and B. Chesebro. 1998. Scrapie infectivity found in resistant species.
Nature, 392: 770.
World Health Organization. 1996. Report of a WHO Consultation on Public Health Issues related to Human and Animal Transmissible Spongiform Encephalopathies. Geneva, Switzerland, April 2-3, 1996.
