Bt maize was developed in the United States primarily to control the European corn borer (ECB, Ostrinia nubilalis). This moth lays its eggs on maize leaves, damaging the plant. The larvae then tunnel into the leaves and the stalk. Into the autumn they migrate down the stalk and then spend the winter in the lowest part of the stalk or the top part of the roots. The stalks of the infected plants often break off.
The European corn borer was introduced to North America between 1910 and 1920 and then spread rapidly as a pest. In Europe it is found naturally on a number of different plants. Only one of the two corn borer strains in Europe actually attacks maize. This strain is native only to some parts of Europe; for example it is not found in northern Germany or Great Britain. However, the ECB strain that attacks maize is slowly spreading northward and in Germany has been found as far as Brandenburg. In conventional agriculture ECB is usually controlled simply by ploughing the fields.
In autumn 2006, the approval to grow the GM maize MON810 in the EU will expire, which means the authorities will need to re-appraise this maize. Therefore Greenpeace has compiled the latest research from Germany and other countries, drawn up a list of open questions and clarified possible risks.
1 For Germany, the authors mostly used an analysis of research findings from a project of the German Ministry of Education and Research (BMBF 2006), "Safety research and monitoring for Bt maize cultivation 2001-2004", the results of which have only been published in part. The studies investigated MON810 and another type of GM maize (Bt 176) that is no longer being cultivated.
A report published in April 2006 by the European Commission shows that safety problems with GM crops have become more and more obvious over the last years (European Communities 2005).
The new data confirm this alarming finding. The wealth of indications that are available now show that the problems with GM maize are even more complex than originally assumed. The risks apply to the smallest soil organisms, to protected species such as butterflies and to beneficial insects such as bees and even extend to health risks for humans and animals.
The latest findings and the list of open questions clearly show that approval for commercial cultivation of the GM maize was granted prematurely and contradicts the precautionary principle that is part of EU legislation. The EU’s approval of the GM maize therefore must be withdrawn.
1. The cycle of the toxin in the environment Normally the Bacillus thuringiensis toxin only exists in soil bacteria. This toxin has been used for many years to control agricultural pests. It is considered so harmless that it is even allowed in organic agriculture. But by genetically engineering the toxin into maize plants its characteristics have been changed fundamentally.
1. In nature, the toxin only exists in very low concentrations. If it is sprayed for pest infestations, then it is used selectively and for a very short period of time.
2. The toxin in its natural form only kills certain insects. It comes in a non-active form (protoxin) and it is not turned into the active form until it is in the insect’s gut. Genetic engineering however changes the characteristics of the toxin:
1. It is produced in high concentration during the whole vegetation period of the plant and it is released through the roots, parts of the plant and pollen into the environment.
2. The toxin binds to soil particles and can survive in the soil for months. It can be passed on in the food chain and can even be passed through the gut of farm animals.
3. The toxin is not present in the inactive form, but in an active version. This changes the range of possibly sensitive organisms.
4. Although the different toxic proteins are all called Cry1Ab, they are fundamentally different from the natural protein, and they are different from each other. Cultivating Bt maize creates a completely new cycle of distribution and concentration of Bt toxin in the environment and in the food chain. This has been confirmed by the latest research. Effects of Bt plants on the soil have only been investigated since the mid/late 1990s, i.e. only after Bt maize had already been cultivated in the USA, and only after Bt176 and MON810 had been approved for cultivation in the EU. Many of the studies that have been published since the end of the 1990s on the topic of "Bt crops and soil" reveal unexpected effects, particularly negative environmental effects. These results also show that most areas have not been studied at all – and that nearly everywhere where research is done, indications of negative effects can be found.
How does the toxin get into the environment? Bt toxins can get into the soil via different routes: as a living plant material (roots, Jehle 2005), as dead fine roots and root exudates during the growth period (Saxena et al. 1999, Saxena & Stotzky 2000), pollen (Losey 1999) that is washed into the soil, harvest residues (roots, stalks, leaves) after harvest (Tapp & Stotzky 1998, Stotzky 2000, Zwahlen et al. 2003b, Baumgarte & Tebbe 2005), and in animal excrement (Einspanier et al. 2004).
In recent years a series of studies with varying approaches was conducted to study the persistence of Bt toxins in the soil, but there are only very few studies that investigate the amount and form of Bt toxin during and after the growth period. In 2005 it was still unknown how much toxin is actually exudated by the roots. “To our knowledge, it is not known how much Cry1Ab protein is produced in the rhizosphere of Btmaize under agricultural practice and how much of that protein remains in the soil after harvesting” (Baumgarte & Tebbe 2005). Apparently rather high toxin levels can be found in the soil close to the roots. Some of the toxin is found in the soil even months after the harvest, even though higher levels are found in the remaining plant residues: “The amount of Cry1Ab protein in bulk soil of MON810 field plots was always lower than in the rhizosphere, the latter ranging from 0.1 to 10 ng/g soil. Immunoreactive Cry1Ab protein was also detected at 0.21 ng/g bulk soil 7 months after harvesting, i.e. in April of the following year. At this time, however, higher values were found in residues of leaves (21 ng/g) and of roots (183 ng/g), the latter corresponding to 12% of the Cry1Ab protein present in intact roots” (Baumgarte & Tebbe 2005).
Even though it is known that roots contain Bt toxin and can exudate it into the soil, this issue is not considered a factor at all in some risk assessments of Bt maize. For example, in the approval application for Bt maize 1507 that is currently pending at the EU, the Bt concentrations for different parts of the plant are given – but not that of the roots. Nevertheless, the EU authority EFSA gave a positive opinion for the commercial cultivation of this Bt maize.
The path of the toxin through roots, pollen and plant material is not the only path through which Bt toxin is released into the environment. Initial research into the degradation of Bt protein in the gut of cows shows that “remarkable” amounts of Bt toxin are found in the gastrointestinal tract, and that the animals’ faeces contains the toxin (Einspanier et al. 2004).
Currently, the available information on human health effects associated with fumonisins is not conclusive. However, based on the wealth of available information on the adverse animal health effects associated with fumonisins (discussed in this document and in the document entitled "Background Paper in Support of Fumonisin Levels in Animal Feed" prepared by FDA's CVM), FDA believes that human health risks associated with fumonisins are possible.
Based on the current available occurrence data, levels of fumonisins in human foods derived from corn are normally quite low. At the present time, FDA believes that these levels present a negligible public health risk. Nevertheless, FDA considers the fumonisin guidance levels to be a prudent public health measure during the development of a better understanding of the human health risk associated with fumonisins and the development of a long-term risk management policy and program by the agency for the control of fumonisins in human foods and animal feeds.
The recommended maximum levels for fumonisins in corn and corn products intended for human consumption (Table 1) are based on concerns associated with hazards shown primarily by animal studies. However, based on available information on the occurrence of fumonisins, FDA believes that typical fumonisin levels found in corn and corn products intended for human consumption are much lower than the recommended levels.
Total Fumonisins(FB1 + FB2 + FB3) parts per million (ppm)
Genetic modification can transfer allergies from foods that people know they are allergic to foods they think are safe. About 2% of adults and 8% of children have true food allergies and about one quarter have reacted adversely to some type of food.
Failure to label GM foods," says the CI campaign kit, "would mean that people with allergies have no way of knowing whether they are eating potentially risky foods or, in the event of problems, what ingredient provoked the reaction
Activists also highlight the uncertain long-term effects on nutrition and health posed by GM foods. They point to the use of antibiotic-resistant genes as "markers" (to track the gene carrying the trait being transferred) in GM crops. This, they say, could add to the problem of antibiotic resistance. Genetic manipulation could also increase levels of natural plant toxins in foods or create entirely new toxins in unexpected ways.
GM organisms also threaten to diminish biological diversity, say the activists. The cultivation of GM organisms, they add, could lead to the wiping out of weeds and insects. If that happens, the species that depend on them will also suffer.
Bacillus Cereus: B. cereus food poisoning is the general description, although two recognized types of illness are caused by two distinct metabolites. The diarrheal type of illness is caused by a large molecular weight protein, while the vomiting (emetic) type of illness is believed to be caused by a low molecular weight, heat-stable peptide.
Confirmation of B. cereus as the etiologic agent in a foodborne outbreak requires either (1) isolation of strains of the same serotype from the suspect food and feces or vomitus of the patient, (2) isolation of large numbers of a B. cereus serotype known to cause foodborne illness from the suspect food or from the feces or vomitus of the patient, or (3) isolation of B. cereus from suspect foods and determining their enterotoxigenicity by serological (diarrheal toxin) or biological (diarrheal and emetic) tests. The rapid onset time to symptoms in the emetic form of disease, coupled with some food evidence, is often sufficient to diagnose this type of food poisoning.
Although no specific complications have been associated with the diarrheal and vomiting toxins produced by B. cereus, other clinical manifestations of B. cereus invasion or contamination have been observed. They include bovine mastitis, severe systemic and pyogenic infections, gangrene, septic meningitis, cellulitis, panophthalmitis, lung abscesses, infant death, and endocarditis.
Salmonella: Acute symptoms -- Nausea, vomiting, abdominal cramps, minal diarrhea, fever, and headache. Chronic consequences -- arthritic symptoms may follow 3-4 weeks after onset of acute symptoms. Onset time -- 6-48 hours. Infective dose -- As few as 15-20 cells; depends upon age and health of host, and strain differences among the members of the genus. Duration of symptoms -- Acute symptoms may last for 1 to 2 days or may be prolonged, again depending on host factors, ingested dose, and strain characteristics. Cause of disease -- Penetration and passage of Salmonella organisms from gut lumen into epithelium of small intestine where inflammation occurs; there is evidence that an enterotoxin may be produced, perhaps within the enterocyte.
S. aureus: The onset of symptoms in staphylococcal food poisoning is usually rapid and in many cases acute, depending on individual susceptibility to the toxin, the amount of contaminated food eaten, the amount of toxin in the food ingested, and the general health of the victim. The most common symptoms are nausea, vomiting, retching, abdominal cramping, and prostration. Some individuals may not always demonstrate all the symptoms associated with the illness. In more severe cases, headache, muscle cramping, and transient changes in blood pressure and pulse rate may occur. Recovery generally takes two days, However, it us not unusual for complete recovery to take three days and sometimes longer in severe cases. Infective dose--a toxin dose of less than 1.0 microgram in contaminated food will produce symptoms of staphylococcal intoxication. This toxin level is reached when S. aureus populations exceed 100,000 per gram.
Clostridium botulinum: Infective dose -- a very small amount (a few nanograms) of toxin can cause illness. Onset of symptoms in foodborne botulism is usually 18 to 36 hours after ingestion of the food containing the toxin, although cases have varied from 4 hours to 8 days. Early signs of intoxication consist of marked lassitude, weakness and vertigo, usually followed by double vision and progressive difficulty in speaking and swallowing. Difficulty in breathing, weakness of other muscles, abdominal distention, and constipation may also be common symptoms. Clinical symptoms of infant botulism consist of constipation that occurs after a period of normal development. This is followed by poor feeding, lethargy, weakness, pooled oral secretions, and wail or altered cry. Loss of head control is striking. Recommended treatment is primarily supportive care. Antimicrobial therapy is not recommended. Infant botulism is diagnosed by demonstrating botulinal toxins and the organism in the infants' stools.
Although botulism can be diagnosed by clinical symptoms alone, differentiation from other diseases may be difficult. The most direct and effective way to confirm the clinical diagnosis of botulism in the laboratory is to demonstrate the presence of toxin in the serum or feces of the patient or in the food which the patient consumed. Currently, the most sensitive and widely used method for detecting toxin is the mouse neutralization test. This test takes 48 hours. Culturing of specimens takes 5-7 days.
6:59 AM i love spongebob and patrick!
Monday, April 30, 2007
You cannot get avian influenza from properly handled and cooked poultry and eggs. There currently is no scientific evidence that people have been infected with bird flu by eating safely handled and properly cooked poultry or eggs.
Hens infected with HPAI usually stop laying eggs as one of the first signs of illness, and the few eggs that are laid by infected hens generally would not get through egg washing and grading because the shells are weak and misshapen. In addition, the flow of eggs from a facility is stopped at the first suspicion of an outbreak of HPAI without waiting for a confirmed diagnosis. Therefore, eggs in the marketplace are unlikely to be contaminated with HPAI.
Most cases of avian influenza infection in humans have resulted from direct or close contact with infected poultry or surfaces contaminated with secretions and excretions from infected birds. Even if poultry and eggs were to be contaminated with the virus, proper cooking would kill it. In fact, recent studies have shown that the cooking methods that are already recommended by the U.S. Department of Agriculture (USDA) and the Food and Drug Administration (FDA) for poultry and eggs to prevent other infections will destroy influenza viruses as well.
8:18 AM i love spongebob and patrick!
A product recall is a request to return to the maker a batch or an entire production run of a product, usually due to the discovery of safety issues. The recall is an effort to limit liability for corporate negligence (which can cause costly legal penalties) and to improve or avoid damage to publicity. Recalls are costly to a company because they often entail replacing the recalled product or paying for damages caused in use, albeit possibly less costly than indirect cost following damages to brand name and reduced trust in the manufacturer.
A good example is the recent recall of over 500,000 Toyota Tundra pickup trucks. The Tundra had a steering problem, which resulted in several accidents, forcing the manufacturer to attempt to right the problem.
A country's consumer protection laws will have specific requirements in regard to product recalls. Such regulations may include how much of the cost the maker will have to bear, situations in which a recall is compulsory (usually because the risk is big enough), or penalties for failure to recall. The firm may also initiate a recall voluntarily, perhaps subject to the same regulations as if the recall were compulsory. In the case of a compulsory recall, consumers who fail to dispose of it or return it to the manufacturer for replacement or refund could be fined for as much as $5000.
General Steps to a Product Recall
A product recall usually involves the following steps, which may differ according to local laws:
1) Maker or dealer notifies the authorities responsible of their intention to recall a product. Consumer hotlines or other communication channels are established. The scope of the recall, that is, which serial numbers or batch numbers etc. are recalled, is often specified.
2) Product recall announcements are released on the respective government agency's website (if applicable), as well as in paid notices in the metropolitan daily newspapers. In some circumstances, heightened publicity will also result in news television reports advising of the recall.
3) When a consumer group learns of a recall it will also notify the public by various means.
4) Typically, the consumer is advised to return the goods, regardless of condition, to the seller for a full refund or modification.
5) Avenues for possible consumer compensation will vary depending on the specific laws governing consumer trade protection and the cause of recall.