COOPERATIVE EXTENSION
UNIVERSITY OF CALIFORNIA
ENVIRONMENTAL TOXICOLOGY NEWSLETTER
" Published occasionally at irregular intervals "
Vol. 11 No. 2 April 1991
" GET THE LEAD OUT, 1991 ! "
Table of Contents
I. A "New" Source of Lead
II. Cancer Mortality in Workers Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin
III. Darn Government Regulations Get in the Way
IV. Multistate Outbreak of Poisonings Associated With Illicit Use of Gamma Hydroxy Butyrate
V. Animal Model Found for L-Tryptophan-Linked EMS
VI. NCI-er Says Evidence Links Vitamin C to Cancer Prevention
VII. FDA/APHIS Find Low Pesticide Residues in Processed Foods
VIII. Absorption of Sulfamethazine Residues in Meat
IX. Clenbuterol Cause of Spanish Food Poisonings
VETERINARY TOXICOLOGY NOTES:
X. Moldy Corn Poisoning in California
XI. Update on Criminal Contempt Case
XII. FDA Revises Policy on Aflatoxin from Peanuts in Feed
XIII. Of Painkillers & Pets-Forethought & Care Would Make Accidents Rare
Introduction
As promised, this second newsletter for 1991 follows closely on the heels of the first, and the lead article is on lead (I hope you all appreciate this unfortunate, but intentional pun). I would like to call your attention to a new statement printed just underneath our logo for the newsletter. This was suggested by Dr. Carl Koehler shortly before his retirement (2 days to be exact). In a very nice letter Carl mentioned that I would not have to waste any more space apologizing for late newsletters if I simply added this disclaimer. Thanks, Carl, and all the best. I promise to keep the issues occasional and irregular. There are a few items which I think deserve particular attention in this newsletter. The first is the finding that lead crystal is a potential source of dietary lead for humans. The second is the confirmation in Spain of "secondary" human toxicity from an illegally used animal drug, clenbuterol. The third is the discovery of moldy corn poisoning in horses in California, as reported by Dr. Frank Galey. To my knowledge, this is the first reported incident in California, and it is likely that more will follow.
I. A "New" Source of Lead
Routine use of lead crystal should be avoided, the Food and Drug Administration's Jerry Burke recommended last week. Burke, director of the Office of Physical Science in FDA's Center for Food Safety and Applied Nutrition, was commenting on a published report of lead leaching into wine from crystal decanters (See Food Chemical News, Jan. 28, Page 14, and Feb. 11, Page 48) and an unpublished report of lead leaching into apple juice and infant formula from crystal baby bottles. The article noted that Steuben has temporarily suspended the manufacture and sale of its lead crystal decanters and flasks, and that Waterford has ceased manufacture of crystal baby bottles. In an article appearing in the Feb. 20 edition of the Times, Burke was said to have made the following recommendations:
"Do not use lead crystal every day. Occasional use is all right, but if you have a daily glass of wine, don't drink it from a crystal goblet; don't store foods or beverages for long periods (a week or two, according to Burke, overnight according to others) in crystal. This is particularly true for acidic juices, vinegar, and alcoholic beverages. Women of childbearing age should not use crystalware. Don't feed children from crystal bottles or tumblers." Research performed at Columbia University found that storage of wine in lead crystal decanters raised the Pb concentrations to as high as 7 ppm. The EPA standard for lead in drinking water is 50 ppb.
Reference: Food Chemical News, Vol. 32, No. 52, February 25, 1991. Food Chemical News, Vol. 33, No. 3, March 18, 1991.
Editor Note: These new data show that lead crystalware is a source of lead in the human diet. Because of the ability of lead to accumulate in humans, it is prudent to decrease exposure as much as possible. Personally I think Burke's recommendations are a bit severe. Certainly alcoholic beverages should not be stored in leaded crystal decanters for long periods (not even overnight), however I would not hesitate to use crystal glasses for a daily glass of wine since the contact time would be minimal (at least for me). This is of course a matter of personal choice and I hope you can convey this information to your clientele.
II. Cancer Mortality in Workers Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin
Abstract Background. In both animal and epidemiologic studies, exposure to dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, or TCDD) has been associated with an increased risk of cancer. Conclusions. This study of mortality among workers with occupational exposure to TCDD does not confirm the high relative risks reported for many cancers in previous studies. Conclusions about an increase in the risk of soft-tissue sarcoma are limited by small numbers and misclassification on death certificates. Excess mortality from all cancers combined, cancers of the respiratory tract, and soft-tissue sarcoma may result from exposure to TCDD, although we cannot exclude the possible contribution of factors such as smoking and occupational exposure to other chemicals.
Reference: N Engl J Med, 324:212-8, 1991.
III. Darn Government Regulations Get in the Way
In a highly unusual RCRA case, six individuals who allegedly ran a clandestine methamphetamine laboratory in Atlanta were indicted by a federal grand jury recently on felony charges of illegally disposing of hazardous waste. The eight-count indictment charged the six individuals with the RCRA violation in addition to drug and firearms violations. EPA said the defendants, who operated their facility under the name Metro Fab, dumped all their wastes and substandard product batches on adjacent property. The U.S. Drug Enforcement Agency participated in the investigation with EPA. (From: P&TCN, Vol.19, No. 3)
Reference: Kansas Pesticide Newsletter, Vol. 13, No. 12, December 14, 1990.
IV. Multistate Outbreak of Poisonings Associated with Illicit Use of Gamma Hydroxy Butyrate
On August 7, 1990, the San Francisco Bay Area Regional Poison Control Center notified the regional office of the Food and Drug Administration (FDA) and the California Department of Health Services of acute poisonings attributed to ingestion of gamma hydroxy butyrate (GHB), which recently has been illicitly marketed nationwide. Manifestations included gastrointestinal symptoms, central nervous system (CNS) and respiratory depression, and uncontrolled movements. Subsequent surveillance, based on contacts among poison-control centers, led to the recognition that similar poisonings had been independently identified in several states. This report summarizes findings from the preliminary investigation of this problem. Patients have presented with histories of ingesting 1-3 teaspoons of GHB dissolved in water; ingestion is followed within 15-60 minutes by onset of one or more of the following: vomiting, drowsiness, hypnagogic state, hypotonia (low muscle tone), and/or vertigo. Loss of consciousness, irregular and depressed respiration, tremors, or myoclonus may follow. Seizure-like activity, bradycardia (slow heart rate), hypotension, and/or respiratory arrest have also been reported. Spontaneous resolution occurs in 2-96 hours. The severity and duration of symptoms appear to depend on the dose of GHB and/or the presence of other CNS depressants, most frequently ethanol. In 11 of 12 Georgia patients, four of five Florida patients, and three of four California patients for whom concurrent drug status was known, other psychoactive drugs--including ethanol, benzodiazepines, cannabis, and amphetamines--also had been used. Although no deaths have been reported, most patients have required emergency room care; at least 11 were hospitalized, and nine required ventilator support of other intensive care. Therapeutic efforts consisted of nonspecific supportive care. On November 8, FDA issued an advisory warning that GHB use outside of FDA-approved physician-supervised protocols was unsafe and illicit and should stop.
Editorial Note: In the United States, the only legal use of GHB (HOOC-CH2-CH2-CH2OH) has been under specific FDA exemptions for investigational research protocols (e.g., treatment of narcolepsy). During controlled clinical use, the same dose of GHB sometimes caused different responses in different patients and different responses in the same person at different times. GHB has been illegally marketed under a variety of names, including Gamma Hydroxybutyric Acid, Sodium Oxybate, Sodium Oxybutyrate, Gamma Hydroxybutyrate Sodium, Gamma-OH, 4-Hydroxy Butyrate, Gamma Hydrate, and Somatomax PM. It is distributed as the sodium salt in powder or tablet form and is commonly dissolved in water. GHB has been marketed illicitly to body builders since at least May 1990; it also has been promoted illicitly for weight control and as a sleep aid. In addition, GHB has been illicitly touted as a "replacement" for L-tryptophan, which had been marketed as a food supplement but was recalled in November 1989 when the epidemic of eosinophilia-myalgia syndrome was recognized. GHB allegedly produces a "high," which has led to its further use as an illicit drug. Although the concurrent use of other drugs with similar toxicities may confuse the clinical, toxicologic, and epidemiologic presentation of this problem, the reported symptoms of GHB toxicity are the same as the known pharmacologic effects of the drug. A causal association between use of GHB and these poisonings is also supported by the rapid onset of symptoms after ingestion of GHB, more severe and prolonged symptoms associated with larger doses of GHB, and occurrence of illness in persons who have not used other drugs. GHB is produced by the body as a normal metabolite and is not a nutritional requirement. GHB is present in the brain and many peripheral sites, including the kidney, heart, skeletal muscle, and brown fat. GHB is well absorbed orally, readily crosses the blood-brain barrier, and is subsequently metabolized to carbon dioxide and water without active metabolites. Effects include amnesia and hypotonia from doses as low as 10 mg/kg, a normal sequence of REM and non-REM sleep from 20-30 mg/kg doses (1-3 g per dose were used in US narcolepsy studies), and anesthesia from doses of approximately 50 mg/kg. In doses >50 mg/kg, GHB decreases cardiac output and subsequently produces increasingly severe respiratory depression, seizure-like activity, and/or coma. Other effects suggest that, during hypoxia and other energy-limiting conditions, GHB may play a role in reducing energy-substrate demand and consumption and in preventing the production of free radicals. GHB acts synergistically with ethanol to produce CNS and respiratory depression; ethanol also increases the endogenous levels of GHB. GHB may potentiate the effects of narcotic analgesics and skeletal muscle relaxants and may be potentiated by the actions of benzodiazepines and neuroleptics. The focus of public education efforts should be that products such as GHB that are promoted for physiologic effects act on the body as drugs. In this context, advertising terms such as "natural," "organic," or "supplement" do not imply safety or legality.
Reference: MMWR, Vol. 39/No. 47, November 30, 1990.
V. Animal Model Found for L-Tryptophan-Linked EMS
Scientists from five Public Health Service agencies have found an animal model to determine L-tryptophan-linked eosinophilia-myalgia syndrome. "This study, in which we identified specific inflammatory changes in the rats treated with tainted L-tryptophan, is the first evidence in a living system of a cause-and-effect relationship between this substance and the disease," the senior author said. "Animals receiving implicated L-tryptophan, but not those receiving USP grade L-tryptophan or vehicle, developed histologic signs consistent with fasciitis and perimyositis, specific pathogenic features of human L-tryptophan-EMS," an abstract said. Noting that the female Lewis rat "is known to be susceptible to a wide variety of inflammatory diseases," the authors said "identification of specific inflammatory changes in this rat following exposure to implicated L-tryptophan indicates that this animal model will be important in subsequent investigations into the etiology, pathogenesis, and treatment of human L-tryptophan-EMS." "An animal model is important to identify a cause-and-effect relationship between contaminated L-tryptophan and the development of L-tryptophan-EMS and to define the pathogenesis of this complex syndrome."
Reference: Food Chemical News, Vol. 32, No. 36, November 5, 1990.
VI. NCI-er Says Evidence Links Vitamin C to Cancer Prevention
Eighty-nine of 99 studies show a statistically significant association between fruit and vegetable consumption and cancer prevention, reported Gladys Block, a National Cancer Institute epidemiologist, at an Oct. 26 meeting of the American Nutritionists Association in Bethesda, MD. However, despite evidence linking vitamin C to cancer prevention, Block said there is a "prejudice against vitamin C" and a negative reaction to such health claims. Because researchers are looking for that "magic bullet," something in fruits and vegetables that is overwhelmingly protective has been overlooked, she said. Twenty-six of 28 studies found significantly protective effects of vegetables from lung cancer; most studies found significant protective effects of fruit intake and cancer of the oral cavity; two studies found frequent fruit intake to affect larynx cancer; 20 of 21 studies found vitamin C to protect against esophageal cancer; 14 of 15 studies found fruit and raw vegetables to be protective against stomach cancer; and most studies found vegetables to prevent bladder and pancreas cancers.
Reference: Food Chemical News, Vol. 32, No. 36, November 5, 1990.
VII. FDA/APHIS Find Low Pesticide Residues in Processed Foods
The Food and Drug Administration and the US Department of Agriculture's Animal and Plant Health Inspection Service, in the first year of a joint monitoring effort, found that the incidence and levels of pesticide residues in processed foods were low. An interagency summary released last month noted that overall, 174 residue detections were made in 3,502 analyses. No over-tolerance levels of permitted pesticides were found and no residue level exceeded 15% of existing tolerance. There were no detections of non-permitted pesticides.
FDA and APHIS looked at pesticide residues in commercially prepared baby foods, methyl bromide in nuts, as well as ETU and daminozide in processed foods. They were also instructed to analyze aldicarb in bananas and citrus, but that task has been carried over into 1991. A total of 631 samples of baby foods were analyzed for organochlorine (OC) and organophosphorus (OP) residues. The Limits of Quantitation (LOQ) and Limits of Detection (LOD) based on chlorpyrifos were 0.01 and 0.005 ppm for fruit and vegetable products, and 0.02 and 0.01 ppm for other baby foods, respectively. The foods examined included baked goods (cookies and teething biscuits), cereals, soy and milk-based infant formulas, vegetables, fruits and fruit juices, meat and poultry dinners, and desserts. Malathion was found in 34 samples, all baked goods or cereal products. The findings ranged from trace levels (<0.01 ppm) to 0.045 ppm. Chlorpyrifos was found in 9 samples: 5 cereal, 3 mixed fruit, and 1 applesauce sample at trace levels to 0.013 ppm. Dieldrin was found at a trace level in a single sample of carrots.
A total of 659 samples of baby foods, encompassing essentially the same breakout of products as for the OC and OP analyses, were analyzed for residues of ethylenethiourea (ETU), a degradation product of EBDCs. The LOQ and LOD for the method were 0.010 and 0.005 ppm, respectively. ETU was found in 50 samples: 12 mixed fruit/juice samples, 9 pear, 8 applesauce, 7 fruit dessert, 4 squash, 3 pea, 2 spinach, 2 carrot, 1 plum, 1 biscuit, and 1 cereal sample at trace levels to 0.061 ppm.
A total of 285 samples were examined for residues of N-methylcarbamates. The LOQ and LOD (based on aldicarb sulfoxide and carbaryl) were 0.025 and 0.013 ppm, respectively. Carbaryl was the only carbamate residue detected, and was found in 26 samples: 5 peach, 5 fruit dessert, 4 apricot, 3 beef dinner, 2 plum, 2 mixed fruit, 2 applesauce, 2 cereal, and 1 grape juice sample at trace levels (<0.025 ppm) to 0.132 ppm. A total of 190 samples were examined for daminozide residues. The LOQ and LOD were 0.050 and 0.025 ppm, respectively. Only one sample, mixed fruit, was found to contain a daminozide residue at a trace level (<.05 ppm). The APHIS laboratory detected methyl bromide residues in four of 1,100 processed nut samples: 2 pistachio and 2 walnut samples, at levels ranging from trace (<0.02 ppm) to 0.09 ppm.
A total of 356 samples of processed foods were analyzed for residues of ETU: grape juice, peanut butter, peanuts, tomato juice, and almonds. Residues were detected in 18 samples: 10 grape juice, 5 peanut, and 3 tomato juice samples at trace levels (<0.010 ppm) to 0.016 ppm. The LOQ and LOD were 0.010 and 0.005 ppm, respectively. Residues of daminozide were detected in 31 samples, all apple juice, of 281 samples of processed foods. The residues were found at levels ranging from trace (<0.05 ppm) to 0.175 ppm. The LOQ and LOD were 0.050 and 0.025 ppm, respectively.
Reference: Food Chemical News, Vol. 32, January 14, 1991.
VIII. Absorption of Sulfamethazine Residues in Meat
Humans ingesting cooked pork containing sulfamethazine residues may completely absorb the sulfamethazine residues. Researchers noted that previous USDA-supported studies indicated that the cooking of various cuts of pork containing sulfamethazine residues did not reduce concentrations of the drug in the meat. The objective of the current phase of the project is to determine the rate and extent of absorption in dogs of unchanged sulfamethazine when ingested as a residue in cooked pork. "These data indicate that sulfamethazine is absorbed from the gastrointestinal tract at a slower rate when ingested as a residue in meat, but the extent of absorption is equal to that obtained when the drug is given in its most bioavailable form," the researchers said. "It can be speculated from these data that humans ingesting cooked pork containing sulfamethazine residues may exhibit blood levels of sulfamethazine consistent with slow but nearly complete absorption of the drug residue," they said.
Reference: Food Chemical News, Vol. 32, No. 40, December 3, 1990.
IX. Clenbuterol Cause of Spanish Food Poisonings
Clenbuterol, administered to cattle through feed or by injection, was responsible for a total of 135 cases of food poisoning in Spain between March and July this year. In a letter to The Lancet, Dr. J.F. Martinez-Navarro reports that 135 cases of food poisoning were detected, following consumption of bovine liver, with clinical symptoms compatible with clenbuterol effects (rapid heart rate and tremors). Ten cases were rejected because they were unrelated to the outbreak in question or were not compatible with the clinical description. Cases typically occurred in families (43 families affected) which had consumed liver. Clenbuterol was found in urine specimens of two patients, at concentrations of 4 and 2 ppb, and in the remains of liver consumed by the patients. Five liver samples contained concentrations of 160-291 ppb. The substance is licensed in Spain as a bronchodilator for use in veterinary (and human) medicine, and is illicitly used in animal feed, causing muscle growth and weight gain. When intoxication occurs in cattle, animals suffer from tremors and have to be slaughtered immediately. This could explain why some outbreaks occurred in a limited time-space frame.
Editors Note: Clenbuterol is thought to be used illegally in the US in calves, pigs, and lambs intended for exhibition. USDA-FSIS has expressed an intent to randomly survey slaughtered show animals for the presence of this drug. Abstracted from: Animal Pharmacology, December 21, 1990
Reference: Veterinary Newsletter, The University of Georgia Cooperative Extension, No. 269, February 1991.
VETERINARY TOXICOLOGY NOTES
X. Moldy Corn Poisoning in California
Dr. Frank Galey
Veterinary Toxicologist, CVDLS, UC Davis
A recent case involving deaths of 5 horses and 4 foals out of a total of 91 horses on the same feed (corn-based) at 3 locations is highly suspicious of moldy corn poisoning (equine leukoencephalomalacia). Samples of corn (cracked with fines) and mixed feed with that corn all contained high levels of the mycotoxin, fumonisin B-1. Fumonisins have been associated with this disease by American and South African researchers although a direct cause-effect hasn't yet been established. The only definitive diagnostic evidence of moldy corn toxicosis is leukoencephalomalacia in brains from affected horses. Some may have liver necrosis. Brain samples were not available for this case. Horses with moldy corn poisoning can exhibit disorientation (only sign in this case), delirium, head-pressing, and other central nervous system abnormalities after about 7 days of exposure to tainted corn.
Affected horses frequently die. Diagnosis of the syndrome is supported by typical clinical signs, appropriate lesions in the brain, and identification of fumonisins in corn. Thus, if this disease is suspected, please submit samples of fixed brain and liver, and fresh corn/mixed feed with corn. Although difficult to prevent, the incidence of moldy corn poisoning can be decreased by strict avoidance of feeding damaged corn and corn screenings. Another species affected by fumonisin in corn is swine. Ruminants are thought to be less sensitive, although much of that research remains to be completed.
XI. Update on Criminal Contempt Case
On September 7, 1990, the Food and Drug Administration announced that a California animal drug dealer, was sentenced to 6 months in prison without probation for criminal contempt of an April 22, 1988, consent decree. The corporation, Solid Gold Health Products for Pets, a.k.a. the Solid Gold Holistic Animal Equine Nutrition Center, El Cajon, California, was fined $10,000 and placed on 5-years probation. The judge ordered the defendant removed from the courtroom in handcuffs. He said at no time did the defendant acknowledge any guilt and was "totally unrepentant."
In 1988 FDA's Center for Veterinary Medicine obtained a permanent injunction against the company, barring them from manufacturing, marketing, and promoting 13 specific new animal drugs and any other similar products for treatment of diseases in animals, because the therapeutic claims made for these drugs were fraudulent. FDA said that, following the April 1988 decree, the firm continued to market the products as useful in the treatment of many serious animal diseases including cancer, arthritis, and immunological diseases.
The court agreed with FDA that Solid Gold Health Products had defrauded customers out of hundreds of thousands of dollars a year since 1978 (when FDA first attempted to obtain compliance), had continued to put animal lives at risk, deterred consumers from obtaining effective veterinary drugs, and endangered animal handlers and pet owners by exposing them to certain diseases, e.g., parasitic diseases, which are transmissible to humans.
The nature of the business at Solid Gold was one of rapid growth. The firm began operations in 1974 in a residential basement with gross sales of approximately $70,000 by 1978 and expanded to gross sales of over $1 million in 1989. In 1990, the company claimed to be producing more than 35 tons of one product every other week and was considering the purchase of a $21 million facility in Indianapolis, Indiana, to produce some products. The firm promoted more than 50 different health care products in approximately 50 different national trade publications in the dog, cat, and horse fields. The Center for Veterinary Medicine has concerns about other firms that have entered the market in recent years with fraudulent products, including individual versions of some of Solid Gold's products and advertising. As a result, the Agency has begun investigations of these types of firms with a view toward appropriate regulatory action. FDA hopes this case, the current conviction and stiff sentence will deter others from engaging in similar fraudulent activities which threaten the public health. Reference: FDA Veterinarian, Vol. V, No. VI, November/December, 1990.
Editor Note: People are not the only profitable targets for health care fraud!
XII. FDA Revises Policy on Aflatoxin from Peanuts in Feed
The Food and Drug Administration on December 7 revised its policy on aflatoxin from peanut products used in animal feed, setting levels which follow the policy changes that had already been made for corn in feed. The corn levels -- which will be extended to peanut products -- were described as follows: "... (F)or finishing swine, aflatoxin levels in excess of 200 ppb can support the adulteration charge, while levels above 300 ppb aflatoxin in corn can support a #402(a)(1) charge when the corn is intended for finishing (i.e., feedlot) beef cattle. For breeding cattle, breeding swine, and mature poultry, corn containing aflatoxin in excess of 100 ppb aflatoxin can support the adulteration charge. For immature animals and dairy cows, aflatoxin levels in excess of 20 ppb can support the adulteration charge. For all other species and commodities the action level remains at 20 ppb until revisions to (the) CPG ... are warranted."
Reference: Food Chemical News, Vol. 32, No. 43, December 24, 1990.
XIII. Of Painkillers & Pets-Forethought & Care Would Make Accidents Rare
Over the past year and a half, veterinary toxicologists staffing the Georgia Animal Poison Information Center have noted an increasing number of inquiries and reports of exposure and toxicosis in small animal pets ingesting common, over-the-counter pain medications called nonsteroidal anti-inflammatory drugs (NSAIDs). Why? And how might this be prevented? An overwhelming 98% of calls to the Georgia Animal Poison Information Center involved four agents, ibuprofen, acetaminophen, aspirin, and indomethacin. "All four of these drugs are strong medications that can cause serious complications for dogs and cats," note Dr. Jones. "Ibuprofen, for example, is known to affect the kidneys, causing various types of renal dysfunction which in turn can affect the body's blood flow. It can cause gastrointestinal irritation, ulceration and hemorrhage. Because in dogs, more of the drug is absorbed and it remains in the body longer, its effects in dogs are more severe than in humans, and the margin of safety is smaller. Indomethacin is strongly ulcerogenic, and should not be used at all in dogs." Because of indiscriminatory canine feeding habits, dogs were most apt to be poisoned by ingesting large doses of medication which owners had left accessible. For ibuprofen and acetaminophen, for example, more than 3/4 of the cases of canine poisoning were the results of accidental exposure. The high percentage of accidental cases reported to the center, particularly with ibuprofen and dogs, suggests that people have not been securing these drugs adequately from their pets, and perhaps that dogs find the substances attractive in some way. Cats, being more selective, were less apt to poison themselves. They were less likely to accidentally get into these medications, and ingested smaller doses. However, cats were at a particularly high risk of complications from inappropriate dosing by well-intentioned but ill-informed owners. For example, all the feline cases of aspirin toxicosis were the result of owner administration. The researchers are concerned that the public seems to be unaware of the potential problems of dosing their pets with medicines intended for humans. "This is risky business," Dr. Baynes emphasizes, "for a dog or cat's body does not handle these drugs in quite the same way the human body does. Acetaminophen, for example, should never be given to cats at any dose, because they lack the specific enzyme needed to safely detoxify its metabolites. Aspirin, likewise, is extremely dangerous to cats and has caused vomiting, convulsions, hyperthermia and death." UPFRONT, The Veterinary Med Exp Station, UGA, Dr. John M. Bowen, Director, Janice Matthews, Editor. Reference: Veterinary Newsletter, The University of Georgia Cooperative Extension Service, No. 267, December 1990.
Art Craigmill
Extension Toxicologist
UC Davis