Environmental Toxicology
Newsletter
"Published Occasionally at Irregular Intervals"
Arthur L. Craigmill
Extension Toxicologist
Vol. 23 No. 1 -- January 2003
"IN THIS ISSUE"
TOXICOLOGY TIDBITS
VETERINARY NOTES
Study Affirms Water Effective
for Reducing
Trace Pesticide Residues on Produce,
Finds Produce Washes Not Effective as They Claimed
A new study by Dr. Robert Krieger at the University
of California, Riverside has found that produce washes are not as effective
as they claim. The study looked to see if produce washes were more
effective in removing pesticide residues than water. “Since we knew
that water is effective in removing pesticide residues, it seemed very
unlikely that produce washes would be as effective as they advertise,”
said Dr. Krieger. The study will be published in the February 2003 edition
of Bulletin Environ Contam Toxicol.
In the first part of the study, crops that had
been normally treated with captan were separated into three groups.
The first group was rinsed with water, the second with water and produce
wash, and the third was not rinsed. The unrinsed produce had a residue
level of 6.7 parts per million. The group that was rinsed with water
had a residue level of 4.1 parts per million, 39% less than the unrinsed
group. The group that was rinsed with water and produce wash had
a residue level of 3.7 parts per million, 45% less than the unrinsed group.
In the second part of the study, fruit that
had been treated in the field with a tank mix of captan on methomyl were
separated and treated as in the first part of the study. The fruit
that was unrinsed had a residue level of 0.52 for captan and 0.87 for
methomyl. The fruit that was rinsed with water had a residue level
of 0.10 for captan and 0.71 for methomyl, 81% and 18% less than the unrinsed
fruit respectively. The fruit that was rinsed with water and produce
wash has a residue level of 0.053 for captan and 0.53 for methomyl,
90% and 39% less than the unrinsed fruit respectively.
The claims that produce washes are much more
effective than water is not supported by this study. “Our concern
about these claims is that they are misleading a public that is already
concerned about pesticide residues,” said Dr. Krieger. “Clearly,
this study shows that there is no reason to spend extra money on these washes
when water is just as effective.”
Dr. Krieger also stressed that all of these
residue levels are well below federal standards. “All levels of
residues were well within the EPA levels and far below levels that could
cause adverse health effects in rats or humans,” said Dr. Krieger.
“These studies simply reaffirm the effectiveness of water for trace pesticide
residue reduction. In no case were residues of health significance.”
REF: Alliance for Food & Farming, December 18,
2002.
Outbreaks
of Salmonella Serotype Enteritidis Infection Associated
with Eating Shell Eggs - United States, 1999-2001
A Salmonella serotype Enteritidis (SE) epidemic
emerged in the 1980s, when increasing numbers of infections were detected
in the Northeastern and Mid-Atlantic regions of the United States. In the
early 1990s, while SE rates in the Northeast began to decline, the SE
epidemic expanded to the Pacific region. Nationwide, the number of SE
isolates reported to CDC peaked at 3.8 per 100,000 population in 1995.
Although rates of culture-confirmed SE infection reported to CDC declined
to 1.9 by 1999, rates did not decline further through 2001, and outbreaks
continue to occur. Investigations of outbreaks and sporadic cases have indicated
repeatedly that, when a food vehicle is identified, the most common sources
of SE infection are undercooked and raw shell eggs. This report describes
two SE outbreaks associated with eating shell eggs and underscores the need
to strengthen SE-control measures.
South Carolina, 2001
During February-March 2001, outbreaks of gastroenteritis
occurred among inmates in four prison facilities of the South Carolina
Department of Corrections (SCDC). The first outbreak occurred in a men's
facility (M1) on February 6. The three other outbreaks, all occurring on
March 2, affected a second men's facility (M2) and two women's facilities
(F1 and F2). Among 2,317 inmates in the four prisons, 688 reported to prison
infirmaries with gastrointestinal symptoms (e.g., abdominal cramps, diarrhea,
and nausea). Stool specimens from ill inmates yielded SE phage types 2,
13a, and 23. No illness was reported among SCDC staff members.
A tuna salad served for lunch on March 2 was eaten
by 88% of the male case-patients and by 89% of the female case-patients.
The tuna salad was prepared with eggs that were reportedly hard-boiled
by kitchen staff, who also were inmates. At the time of the outbreaks,
all eggs used by the four involved SCDC facilities were supplied from a
single vendor and eggs submitted from the farm tested positive for SE phage
types 2,13a, 22, 23, and 28. Phage type 2 was the predominant SE strain
isolated from both ill patients and eggs from the farm. To protect the inmates,
SCDC switched to pasteurized egg products in April 2001.
North Carolina, 2001
In June 2001, the Statistical Outbreak Detection
Algorithm at CDC signaled an increase in SE cases reported from North
Carolina. The Division of Public Health in North Carolina was alerted
and began to review SE cases throughout the state. The North Carolina
State Laboratory of Public Health reported 51 cases in July and 31 in
August, compared with 11 cases in each of those months during 2000. Cases
occurred throughout the state. Analysis of 53 patients and 78 controls
indicated that illness was associated with eating eggs. A traceback of
implicated eggs purchased from retail outlets in North Carolina was inconclusive
for implicating a farm.
Editorial Note: During 1990-2001, state and territorial
health departments reported 677 SE outbreaks, which accounted for 23,366
illnesses, 1,988 hospitalizations, and 33 deaths. Among the 309 outbreaks
reported with a confirmed vehicle of transmission, 241 (78.0%) were associated
with shell eggs, accounting for 14,319 illnesses. Of these, 10,406 illnesses
occurred during 1990-1995, and 3,913 occurred during 1996-2001. The overall
decrease in SE incidence and the decrease in the number of illnesses related
to egg-associated SE outbreaks during the last decade might be attributed
in part to the implementation of prevention measures, including on-farm control
programs, egg refrigeration, and consumer and food worker education. However,
reported cases did not decline during 1999-2001, and outbreaks associated
with shell eggs continue to occur.
Eggs that reportedly were hard-boiled and used in a tuna salad were the
implicated vehicle in the South Carolina outbreak. A recent study
demonstrated that unless SE-containing eggs are exposed to boiling water
until the yolk is completely solidified, SE can survive the cooking process.
Cross contamination of the tuna salad by inmate food handlers also was
possible.
The outbreak in South Carolina prisons was the largest SE outbreak in
2001. Because persons residing in institutions depend entirely on their
institutions for meals, the supply of contaminated foods to these settings
can place large populations at risk for developing foodborne diseases. Persons
residing in institutions, especially elderly persons in nursing homes or
assisted living facilities, are at higher risk for dying from outbreak-associated
SE infections. During 1990-2001, a total of 83 SE outbreaks occurred
in institutional settings, representing 12% of reported SE outbreaks. Of
the 33 outbreak-associated deaths, 22 (67%) occurred in institutional facilities,
underscoring the importance of using pasteurized egg products or in-shell
pasteurized eggs for all recipes requiring pooled, raw, or undercooked
shell eggs for institutionalized persons.
Additional information about preventing SE infections associated with
eating raw or undercooked shell eggs is available at: http://www.cdc.gov/ncidod/dbmd/diseaseinfo/salment_g.htm
http://www.cfsan.fda.gov/~dms/fs-eggs.html
http://www.cfsan.fda.gov/~dms/fs-eggs2.html
http://www.cfsan.fda.gov/~dms/fs-eggs4.html
Information for retail and food service establishments and institutional
facilities about handling and cooking shell eggs is available in the Food
Code at http://www.cfsan.fda.gov/~dms/foodcode.html
To read this entire article link to: http://www.cdc.gov/mmwr
REF: Morbidity and Mortality Weekly Report,
51(51);1149-1152, January 3, 2003
Outbreak of Botulism Type
E Associated with
Eating a Beached Whale - Western Alaska, July 2002
Botulism is a neuroparalytic illness caused by toxins
produced by the bacterium Clostridium botulinum, an obligate anaerobe
found commonly in the environment. Intoxication with toxin type E is associated
exclusively with eating animal foods of marine (salt or fresh water) origin.
Persons who eat raw or fermented marine fish and mammals are at high risk
for botulism from type E toxin. On July 17, 2002, the Alaska Division of
Public Health investigated a cluster of suspected botulism cases among
residents of a fishing village in Alaska. This report summarizes the findings
of the outbreak investigation, which linked disease to eating raw muktuk
(skin and a pink blubber layer) from a beached whale. To avoid delays in
treatment, health-care providers evaluating patients suspected of having
botulism should base treatment decisions on clinical findings. Public health
authorities should be notified immediately about any suspected botulism
case.
During July 13-15, residents of a western Alaska village
on the Bering Sea shore shared a meal consisting of muktuk harvested from
a beached adult beluga whale found near their village. The villagers estimated
that the whale had been dead for at least several weeks. They cut the whale
fluke (tail) into pieces and stored them in zipper-sealed plastic bags
in a refrigerator until they were eaten 1 or 2 days later. On July 17,
after a physician from western Alaska reported three suspected cases of
botulism among patients who had eaten the muktuk, the Alaska Section of
Epidemiology began an investigation.
A case of foodborne botulism was defined as illness
in a person who had eaten the muktuk and subsequently had symmetric descending
flaccid paralysis of motor and autonomic nerves. Persons who ate muktuk
were interviewed and examined, and their hospital records were reviewed.
Serum, stool, and gastric contents from patients and leftover blubber were
tested for botulinum toxin.
Of 14 persons identified who ate the muktuk, eight
(57%) had an illness that met the case definition. Five of the eight patients
were female; the median age was 73 years (range: 13-83 years). Symptom
onset after ingestion of muktuk occurred within 36 hours in all patients.
Five patients were hospitalized, four received antitoxin, and two required
mechanical ventilation. Three stool, three gastric fluid, and seven serum
samples from the eight patients and seven samples of muktuk were tested
for botulinum toxin at CDC's National Botulism Surveillance and Reference
Laboratory. The diagnostic laboratory received all laboratory specimens
on July 26, and results were reported on August 1. Type E toxin was detected
in stool from one patient. All seven samples of muktuk were positive for
type E botulinum toxin.
Editorial Note: During 1973-1998, a total of 814 cases and
an annual median of 24 cases (range: 14-94 cases) of foodborne botulism
were reported to CDC; 236 (29%) of these cases occurred in Alaska. Although
botulism is a rare disease, its presentation is distinctive (Because of
the epidemic potential of foodborne botulism, every case should be reported
and investigated immediately.)
The probable mode of contamination of the whale in this outbreak was
either growth and toxin secretion by C. botulinum present in the
intestinal tract of the whale or traumatic introduction of C. botulinum
spores into the beached whale tissue from contact with sand, rocks, and
driftwood, and subsequent germination and toxin production. C. botulinum
type E has been found in Alaska coastline soil, and outbreaks of botulism
associated with eating beached marine mammals are documented. A previous
report on the accumulation of C. botulinum toxins in the North Sea
coastal food chain associated with beached whales suggested the disposal
of the carcasses as a preventive measure. However, because of the impracticality
of frequent scanning of the vast Alaska shoreline and high costs associated
with disposal, the U.S. Fish and Wildlife Service does not remove beached
mammal carcasses regularly.
Persons should avoid eating beached marine mammal carcasses and boil
raw or fermented Alaska Native dishes >10 minutes before eating to inactivate
botulinum toxin. Additional information on botulism prevention is available
at http://www.phppo.cdc.gov/phtn/botulism/alaska/alaska.asp
and http://www.epi.hss.state.ak.us/pubs/botulism/bot_01.htm.
For the entire report link to: http://www.cdc.gov/mmwr/
REF: Morbidity and Mortality Weekly Report,
January 17, 2003, 52(02);24-26.
Infant Botulism - New York City, 2001--2002
Infant botulism results from germination of swallowed
spores of botulinum toxin-producing clostridia that colonize the large
intestine temporarily. The annual incidence of infant botulism in the United
States is two cases per 100,000 live births. Staten Island recorded 5,899
live births in 2000; incidence of infant botulism during this 12-month period
was 68 cases per 100,000 live births. This report summarizes the investigation
of these four cases; as expected with infant botulism, a common source of
exposure was not identified. All four patients recovered after treatment
and were discharged from local hospitals. State and local health departments
should be notified promptly when infant botulism is suspected to arrange
diagnostic testing.
Infant botulism is a reportable disease in NYC, and
the NYC Department of Health and Mental Hygiene (DOHMH) investigates all
suspected cases. Botulism should be suspected in an infant aged <12
months with symptoms including constipation, lethargy, poor feeding, weak
cry, bulbar palsies, and failure to thrive. These symptoms might be followed
by progressive weakness, impaired respiration, and sometimes death.
Summary of Cases: All four patients received antibiotics during
hospitalization. None had ingested honey or had parents employed in occupations
that might increase exposure to C. botulinum spores in soil and
dust (e.g., construction, plumbing, and farming). All patients had uncomplicated
gestational histories and vaginal deliveries. All resided within a 6-mile
radius of each other. All parents reported recent construction in their
neighborhoods during the period (range: 1-31 days) before illness onset.
In the fourth case, the infant's home had been remodeled since the infant
was born.
Editorial Note: Intestinal botulism is the most common form
of human botulism in the United States, and approximately 100 cases are
reported among infants in the United States annually (Intestinal botulism
occurs rarely in older children and adults). Intestinal botulism results
from colonization and bacterial production of botulinum toxin in the colon.
Swallowing ambient C. botulinum spores, which exist worldwide in
soil and dust, has been proposed as the principal route of exposure; honey
is an avoidable source of some causative spores. A common source of exposure
generally is not identified; apparent clusters such as the four Staten Island
cases are rare and often remain unexplained after investigations are complete.
In a cluster of infant botulism cases identified previously in the mid-Atlantic
region of the United States, no common source of exposure was identified.
Botulism should be suspected in previously healthy infants aged <12
months who are constipated and who exhibit weakness in sucking, swallowing,
or crying; hypotonia; and progressive bulbar and extremity muscle weakness.
Approximately half of patients require mechanical ventilation during hospitalization.
For the entire report link to: http://www.cdc.gov/mmwr/
REF: Morbidity and Mortality Weekly Report January
17, 2003 / 52(02);21-24
Turning Up the Heat on Acrylamide
A potentially cancer-causing agent used to manufacture
certain chemicals, plastics, and dyes has recently been found to be a natural
by-product of cooking certain foods. The Food
and Drug Administration is taking a closer look at this white, odorless
chemical, acrylamide,
to determine how much of it occurs in foods and whether it could pose a
health risk. In April 2002, researchers in Sweden discovered that cooking
at high temperatures could create acrylamide in many types of foods, particularly
starchy foods such as french fries, potato chips, bread, rice, and processed
cereals.
Scientists know that acrylamide causes cancer in
laboratory rats. They also know that contact with large quantities of acrylamide
can cause nerve damage in humans. But no one knows whether the tiny amounts
of acrylamide in cooked foods can cause cancer or have any other harmful
effects when ingested by people. "As soon as we heard about this problem,
we took action and laid out a solid plan to learn more about acrylamide
and to reduce exposure to it," says Terry Troxell, Ph.D., director of the
FDA's Office of Plant and Dairy Foods and Beverages.
The FDA's draft action plan for acrylamide in food
was presented in September 2002 at the first of a series of public meetings
held to get feedback and to provide updates on FDA activities related
to acrylamide. With the goal to prevent or reduce the potential risk of
acrylamide in foods to the greatest extent feasible, the FDA's plan calls
for developing laboratory methods to measure acrylamide and surveying
the levels of acrylamide in foods. In addition, FDA scientists will study
how acrylamide is formed so that the agency can identify ways to reduce
it. "We really want to help industry understand what they might be able
to do to reduce the formation of acrylamide," says Richard Canady, Ph.D.,
a toxicologist in the FDA's Center for Food Safety and Applied Nutrition.
What We Know So Far
Following the Swedish researchers' identification of
acrylamide in foods, researchers in other countries, including Norway,
the United Kingdom, Switzerland, Canada, and the United States, analyzed
samples of foods and came up with similar findings. The FDA developed its
own method to measure levels of acrylamide in foods and has tested more
than 300 food items. Studies by the FDA and others found a wide variation
in the levels of acrylamide among different types of foods and even different
brands. "Much more testing is needed to understand the scope of occurrence
of acrylamide in food," says Troxell. The FDA's plan calls for testing
about 1,500 more samples over the next year, and more testing may be added
based on the findings.
Acrylamide was not found in uncooked or boiled food
-- studies indicate that it appears to form during certain high-temperature
(greater than 250 F) cooking processes, such as frying and baking, and that
levels of acrylamide increase with heating time. Home-cooked foods, as
well as pre-cooked, packaged and processed foods, have been found to contain
acrylamide.
Acrylamide levels in 39 samples of potato chips
ranged from less than 1.4 micrograms to 100 micrograms per ounce, according
to a group of international food safety experts who met in June 2002 in
Geneva to discuss the public health impact of acrylamide in foods.
This meeting of experts, including FDA scientists,
was hosted by the United Nations Food and Agriculture Organization (FAO)
and the World Health Organization (WHO). The FAO and WHO reported that the
short-term dietary intake of acrylamide was found to be about 50 micrograms
per day for the average adult -- an amount significantly below that known
to cause nerve damage in laboratory animals.
The FAO and WHO experts concluded that more information
was needed on acrylamide in food, but added that the substance was a "major
concern." Based on high-dose experiments in animals, acrylamide is classified
as a potential human carcinogen, as well as a genotoxicant, a substance
that can mutate and damage genetic material.
Advice for Consumers
Based on the current knowledge about acrylamide, the
FDA has re-emphasized its traditional advice to eat a balanced diet, choosing
a variety of foods that are low in fat and rich in high-fiber grains,
fruits, and vegetables. "As more information becomes available, we will
consider additional messages, for example, recommendations related to
cooking," says Troxell.
The FAO and WHO advise consumers that food should
not be cooked excessively -- for too long or at too high a temperature.
They also recommend cooking all food thoroughly, particularly meat and meat
products, to destroy foodborne pathogens, such as bacteria and viruses.
The FDA reinforces that consumers should not overreact.
"It's a bigger risk if you don't cook your food thoroughly and consume
pathogens," says Troxell. It's also a nutritional risk to avoid foods rich
in fiber such as cereals and whole-grain products.
Educating consumers will be an important part of
the FDA's acrylamide action plan. "Once we have enough information, we want
to help consumers understand the potential risks for acrylamide, how it
gets into food, and what they can do to avoid it," says Canady.
Cooperative Research
There is a high level of cooperation and information-sharing
among the FDA, other U.S. and international government agencies, research
institutions, academia, and industry, says Canady. And it's starting to
pay off. Five different labs throughout the world have announced that they
discovered what may be a primary mechanism of how acrylamide can be formed
in food. They identified a high-temperature reaction of two compounds found
in potatoes and other carbohydrates: glucose (a sugar) and asparagine (an
amino acid).
In October 2002, the Joint Institute for Food Safety
and Applied Nutrition and the National Center for Food Safety and Technology
held a workshop titled "Acrylamide in Food: Scientific Issues, Uncertainties,
and Research Strategies." Intended to determine acrylamide research needs
and facilitate coordination and collaboration among scientists worldwide,
the workshop looked at all the components of acrylamide and the current
research being done.
"People are working very hard in the agency and
around the world to understand acrylamide levels and see why it's formed,"
adds Troxell. "Once we understand what causes it, we can better address
how to reduce it."
REF: U.S. Food and Drug Administration, FDA Consumer
magazine, January-February 2003.
MSG: A Common Flavor Enhancer
Although it has no distinct taste itself, monosodium
glutamate (MSG) stimulates our taste buds and makes a variety of foods taste
better. The flavor enhancer is commonly added to Asian cuisine, canned vegetables,
soups, and processed meats. Made by a fermentation process using starch,
beet sugar, cane sugar, or molasses, MSG is sold as a white crystal substance
that resembles salt and sugar.
Many consumers often equate all "free glutamate"
products with MSG, but it is only one of several forms of glutamate -- a
major building block of proteins. Free glutamate, which results when glutamate
is released during the breakdown of a protein molecule, occurs naturally
in many foods, such as meat, milk, mushrooms, Parmesan cheese, and tomatoes.
In 1959, the Food and Drug Administration classified
MSG as a "generally recognized as safe" food ingredient under the Federal
Food, Drug, and Cosmetic Act. But the use of MSG in food has remained
controversial. In the 1980s, research showed that glutamate plays an important
role in the normal functioning of the nervous system, raising questions
about whether glutamate in food could affect the nervous system.
The FDA also received numerous reports of MSG-related
adverse events, including headaches, palpitations, vomiting, and nausea.
While these voluntary reports were useful for drawing attention to potential
problems, they were unconfirmed by controlled testing.
Because of concerns about the adverse event reports,
the FDA sponsored several safety assessments which all concluded that
MSG is safe when consumed at levels typically used in cooking and food
manufacturing. In 1986, FDA's Advisory Committee on Hypersensitivity to
Food Constituents found that MSG was generally safe, but that short-term
reactions may occur in some people. Other reports from the American Medical
Association's Council on Scientific Affairs and the European Community's
Scientific Committee for Foods reported similar findings.
Then in 1992, the FDA contracted with the Federation
of American Societies for Experimental Biology (FASEB), an independent
group of scientists, to complete the most comprehensive review of available
scientific data on glutamate safety to date. The 1995 FASEB report
reaffirmed the safety of MSG when it is consumed at usual levels by the
general population, and found no evidence of any connection between MSG
and any serious long-term reactions. The report indicated that no evidence
exists to suggest that dietary MSG or glutamate contributes to Alzheimer's
disease, Huntington's disease, or any other long-term or chronic diseases.
There was also no evidence suggesting that dietary MSG or glutamate causes
brain lesions or damage to nerve cells in humans.
But the report did identify short-term reactions known
as MSG Symptom Complex in two groups of people. The first group includes
people who may have a reaction after eating large doses of MSG, particularly
on an empty stomach. A large dose would be three grams or more per meal.
A typical serving of glutamate-treated food contains less than 0.5 grams
of MSG. The second group includes people with severe and poorly controlled
asthma. MSG Symptom Complex can involve symptoms such as numbness, burning
sensation, tingling, facial pressure or tightness, chest pain, headache,
nausea, rapid heartbeat, drowsiness, and weakness. Asthmatics may experience
these symptoms as well as difficulty in breathing. Additional studies in
asthmatics under controlled conditions have not produced consistent results.
Glutamate is commonly found in food, primarily from
protein sources. Foods and ingredients that contain glutamate as an inherent
component are not required to list glutamate on the label. Examples include
tomatoes, cheeses, meats, hydrolyzed protein products such as soy sauce,
and autolyzed yeast extracts. These ingredients are declared on the label
by their common or usual names.
It's when MSG is added to food that the FDA requires
"monosodium glutamate" to be listed on the label. Other salts of glutamic
acid -- such as monopotassium glutamate and monoammonium glutamate --
also have to be declared on labels and can't be lumped together under "spices,"
"natural flavoring" or other general terms.
For the entire article link to: http://www.fda.gov/fdac/
REF: U.S. Food and Drug Administration, FDA Consumer
magazine, January-February 2003.
Toxicology Tidbits
~~ Household Contamination
with Salmonella enterica
Household contamination with Salmonella enterica
increases when occupational exposure exists (cattle farms with known salmonellosis
in cattle, a salmonella research laboratory, or a veterinary clinic experiencing
an outbreak of salmonellosis). Fifteen of 55 (27.2%) vacuum cleaner bags
from households with occupational exposure to S. enterica were
positive versus 1 of 24 (4.2%) without known exposure. Use of a carpet
cleaner and several cleaners/disinfectants reduced, but failed to eliminate,
S. enterica from artificially contaminated carpet.
Read the entire article at: www.cdc.gov
REF: Emerging Infectious Diseases, Vol. 9, No. 1,
January 2003.
~~ New Website
Compiles FDA's Spanish Publications
Dozens of FDA's
Spanish-language publications are within easy reach on a new website
that includes materials related to all products the agency regulates. Many
of the publications are written for consumers; others provide guidance
for FDA-regulated companies. Subjects found on the site include rare diseases,
using medicine wisely, eating for a healthy heart, mammograms, and foodborne
illness.
The site also links to general information about health
conditions such as diabetes, the flu, and hearing loss.
REF: FSnet Dec. 20/02
~~ More on "Toxic Mold"
Neuropsychologist debunks "toxic mold" claims. Paul
R. Lees-Haley, Ph.D., has written a lengthy article criticizing the diagnosis
of "mold
neurotoxicity" and the many lawsuits filed by alleged victims. He states
that (a) there is no consistent pattern of symptoms or test results through
which that diagnosis of "mold neurotoxicity" can be defined, and (b) there
is no scientific evidence that breathing mold spores in household and commercial
office settings causes neuropsychological impairment. The article concludes:
"Toxic tort attorneys and a handful of experts they favor would like
you to believe that "toxic mold" is disabling people in epidemic proportions
by damaging their brains. In order for this to be correct, the overwhelming
majority of physicians, toxicologists, and mental health professionals
who have studied this issue would have to be completely wrong, and doctors
in day-to-day practice would have to be overlooking the diagnosis. . . .
"The mold neurotoxicity debate is not simply about health care and science
-- a focus on money and litigation is pervasive in the communications of
the toxic mold promoters. . . . The campaign being waged to convince people
of the dangers of "toxic mold" is not merely an amusing example of folly
in modern society. The people who are bypassing scientific evidence and
engaging in wholesale dissemination of "toxic mold" rhetoric are not neutral
forces. If it turns out that these exposures are neuropsychologically harmless,
the hysterical claims and unfounded alarms sounded by lawyers, doctors,
and others will nonetheless have harmed many victims. . . . Further exploration
of the effects of inhaling mycotoxins and mold spores should be through
high-quality, well controlled, scientific studies, not speculation in adversarial
settings."
REF: Consumer Health Digest #02-53, December 31,
2002.
~~ World Health
Organization's Website
The World Health Organization's Department of Food Safety
website has a couple of topics that may be of interest to our readers. http://www.who.int/fsf/
Answers to the 20 Most Common Questions on Genetically
Modified (GM) Foods (available in Arabic, Russion, Chinese in addition
to English, French and Spanish) and
Acrylamide
in Food -- Frequently Asked Questions.
VETERINARY NOTES......
Safety Guidance Issued for
Using Raw Meat
in Diets of Pets and Zoo Animals
Prompted by an increased use of raw meat for
pets and zoo animals, FDA has issued a draft guidance for industry on the
manufacture and labeling of diets containing
raw meat, or other raw animal tissue, for consumption by these animals.
The guidance includes warnings about bacterial contamination and dental
or gastrointestinal trauma, and it recommends measures to minimize contamination
and disease transmission.
REF: FDA News Digest, December 23, 2002.
Revision of the Definition
of the Term "No Residue" in the New Animal Drug Regulations
SUMMARY: The Food and Drug Administration (FDA) is amending
its regulations regarding carcinogenic compounds used in food-producing
animals. Specifically, FDA is deleting the operational definition of the
term "no residue" and is making conforming amendments to other parts of these
regulations. FDA is making these amendments in response to a legal opinion
issued by the Department of Justice (DOJ), Office of Legal Counsel, which
concluded that the operational definition of "no residue" is not legally
supportable. This rule is effective January 22, 2003.
REF: Federal Register, Volume 67, Number 246,
December 23, 2002
!! Click on the Pig !!
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