COOPERATIVE EXTENSION UNIVERSITY OF CALIFORNIA
EXTENSION TOXICOLOGY NEWSLETTER

Vol. 9 No. 4 November 1989

" MORE OF THE SAME "

Table of Contents Page No.

I. Introduction
II. Cadmium and Lead Exposure Associated with Pharmaceuticals Imported from Asia -- Texas .
III. Seizures Temporally Associated with Use of DEET Insect Repellent -- New York and Connecticut .
IV. Pesticide Residues and Dietary Risks
V. Consumers Need to Realize Their Responsibility in Food Safety
VI. Fatalities Attributed to Methane Asphyxia in Manure Waste Pits -- Ohio, Michigan, 1989
VII. Multivitamins Can Cause Toxic Vitamin A Build-Up in Older People
VIII.Aldicarb on Watermelons
IX. Pesticide Poisoning Handbook
X. Staggers in Sheep and Cattle: Humboldt County
XI. Is Hay Treated with Preservatives O.K. for Horses?
XII. New Field Tests for Veterinarians
XIII.Pamphlet from the UC Santa Cruz Agroecology Program: "Pesticides in Food: Are You Adequately Informed"

I.Introduction

I always know when it is past time to get out another issue of the Environmental Toxicology Newsletter; the "newsletter" file will hold no more articles. This issue is one of our longer ones, and I have split it into two major sections, one dealing with mostly human problems, and another with veterinary ones. There are some short announcements included in each section, however the most substantial announcement is the recent appointment of Allison Beale as Environmental Toxicology and Water Advisor for Sacramento, Yolo, Calaveras, El Dorado and Amador Counties. Allison received a Masters degree in Pharmacology and Toxicology from UC Davis, and previously worked with the Food Animal Residue Avoidance Databank, one of our Veterinary Extension projects. She also participated in the writing of the Pesticide Information Profiles from EXTOXNET, a copy of which was sent to every County Office. In the future she will also be contributing to this newsletter as well as to other county-based newsletters. Those of you who have the good fortune to work with her will find her to be very energetic, competent and reliable. Welcome to Cooperative Extension.

II.Cadmium and Lead Exposure Associated with Pharmaceuticals Imported from Asia -- Texas

In August 1988, the Texas Department of Health (TDH) investigated illegal sales in rural west Texas of pharmaceutical drugs manufactured in Asia. These drugs, identified by TDH and Food and Drug Administration (FDA) agents as "chuifong tokuwan" (a pharmaceutical compound manufactured by the Nan Ling Pharmaceutical Company of Hong Kong), are sold in pill form. Chuifong tokuwan contains a drug combination (diazepam (a tranquilizer found in Valium,, indomethacin (an anti-inflammatory drug), hydrochlorothiazide (a diuretic), mefenamic acid (another anti-inflammatory drug), dexamethasone (a steroid with good anti-inflammatory properties), lead, and cadmium) that is not approved by FDA and not legal for sale in or importation into the United States. The drugs usually were repackaged and relabeled as "The Miracle Herb - Mother Nature's Finest."

TDH tested 93 self-referred persons who had ingested the pills for exposure to lead and cadmium. Of these, 57 (61%) were female; >90% were white non-Hispanics; the mean age was 55 years. Sixty-six (71%) reported taking the pills to relieve symptoms of medical conditions such as arthralgias (joint pain) (51%) and other pain (headache, stiff neck, back pain [26%]). Twenty-two (24%) persons had elevated urine levels of cadmium; none had elevated levels of lead (blood lead >25 mg/dL). However, 39 (42%) persons had elevated urine values for retinol-binding protein (RBP), a low-molecular-weight protein indicative of renal tubular dysfunction. The mean urine cadmium level for exposed persons was 1.8 mg/mL, compared with 0.5 mg/mL for a nonrandom sampling of 14 unexposed persons. In exposed persons, 22 (24%) urine samples tested for cadmium were >2.5 mg/mL, the upper limit of normal. None of the samples from unexposed persons had elevated values.

The chuifong tokuwan seized in this investigation was destroyed. The investigation in continuing.

Editorial Note: Chuifong tokuwan first appeared in the United States in 1974. Although it was banned by FDA in 1978, the drug is distributed illegally in certain parts of the United States and is sometimes sold by mail. The primary users of chuifong tokuwan in this study were long-time residents of Texas; however, use of unapproved imported drug combinations is common among recent immigrants to the United States, particularly those from Asia and Latin America. Although these products are frequently perceived as relatively harmless herbal "folk remedies," they often contain cortico- or anabolic steroids; nonsteroidal anti-inflammatory drugs (NSAIDs); prescription antibiotics, such as tetracycline and chloramphenicol; and controlled substances, such as diazepam or narcotics, and have potentially serious or fatal health effects.

Use of chuifong tokuwan may increase the body burden of cadmium and may have contributed to renal tubular dysfunction in persons using this compound. Through chronic exposure, cadmium can accumulate in certain organs, particularly the kidneys. Both cadmium and several of the prescription analgesics in chuifong tokuwan can cause renal tubular cell damage. Cadmium can adversely affect function of the proximal renal tubules; increased urinary protein excretion of low-molecular-weight proteins (e.g., RBP) is an early consequence of proximal renal tubular damage by cadmium.

Cadmium is a cumulative toxicant, with a biological half-life of >10 years in humans. Medical evaluation, including urine cadmium and urinary RBP values, is recommended for persons who have used chuifong tokuwan. Additional renal-function evaluation should be included in the medical follow-up of persons whose urinary RBP or urine cadmium values are abnormal.

Complex cultural and linguistic barriers necessitate cooperation with traditional healers (e.g., acupuncturists, herbalists) and local leaders of immigrant communities to inform these groups about the hazards associated with use of specific products.

Reference: MMWR, Vol. 38/No. 35, September 8, 1989.

III.Seizures Temporally Associated with Use of DEET Insect Repellent -- New York and Connecticut

In August 1989, epidemiologists from the New York State Department of Health (NYSDH) investigated five reports of generalized seizures temporally associated with topical use of N,N-diethyl-m-toluamide (DEET). Three of the case-patients, one from New York and two from Connecticut, were reported by a pediatric neurologist who practices in both states. One case was reported initially to an entomologist in New York, and one was reported directly to the NYSDH. The cases occurred in June through August 1989.

The patients, four boys aged 3-7 years and one 29-year-old man, had few prodromal symptoms (symptoms which occur before the onset of the seizure) and recovered quickly. All five had unremarkable medical histories, and none had had a previous seizure or neurologic event. Each had had topical cutaneous exposure to varying concentrations of DEET; four had had fewer than three applications. The interval between last use of DEET and onset of seizures ranged from 8 to 48 hours. One patient developed urticaria (hives) before his seizure; he was one of two patients who developed an urticarial reaction to phenytoin (an anticonvulsant drug) administered to control seizures.

While reinforcing the importance of DEET in preventing Lyme disease (LD [Lyme borreliosis]), health officials in New York, Connecticut, and New Jersey issued a health alert on August 22 advising caution in the use of DEET-containing repellents.

Editorial Note: DEET has been marketed in the United States since 1956 and is used by an estimated 50-100 million persons each year. Since 1961, at least six cases of toxic systemic reactions from repeated cutaneous exposure to DEET have been reported. Six girls, ranging in age from 17 months to 8 years, developed behavioral changes, ataxia (loss of balance), encephalopathy (brain disorder), seizures, and/or coma after repeated cutaneous exposure to DEET; three died. Another six systemic toxic reactions have been reported following ingestion of DEET. Additionally, episodes of confusion, irritability, and insomnia have been reported by Everglades National Park employees following repeated and prolonged use of DEET.

DEET is partially absorbed through the skin and has been used to enhance dermal delivery of other drugs. Adverse reactions include allergic responses, direct neurotoxicity, and dermatitis (skin rash). One of the girls who died after dermal exposure was partially deficient in the enzyme ornithine carbamoyltransferase; DEET may interfere with the urea cycle metabolic pathway.

Anecdotal reports of seizures are difficult to interpret. None of the recent cases in New York and Connecticut have been clearly established as DEET toxicity. In contrast to cases described in the medical literature, the New York and Connecticut patients were all male, DEET exposure was less intense, few prodromal symptoms or encephalopathy were seen, and recovery was more rapid and complete. With the dramatic increase in the prevalence of DEET use in areas with endemic LD, the reported cases of seizures temporally related to DEET use may be coincidental. However, these cases may represent a different, previously unreported spectrum of toxic reactions. Careful toxicologic and epidemiologic studies must be conducted, including adequate documentation of DEET levels in affected and unaffected persons.

Clinicians evaluating patients with unexplained seizures should consider the possibility of exposure to DEET. However, since the exact circumstances under which DEET-related neurotoxicity may occur are unclear, DEET should not be accepted as the cause of a seizure until appropriate evaluation has reliably excluded other possible etiologies.

The optimal concentration of DEET for prevention of tick bites is unknown. However, repellents containing 20%-30% DEET applied to clothing are approximately 90% effective in preventing tick attachment. To minimize the possibility of adverse reactions to DEET, the following precautions are suggested:

Apply repellent sparingly only to exposed skin or clothing. Avoid applying high-concentration products to the skin, particularly of children. Do not inhale or ingest repellents or get them into the eyes. Wear long sleeves and long pants, when possible, and apply repellent to clothing to reduce exposure to DEET. Avoid applying repellents to portions of children's hands that are likely to have contact with eyes or mouth. Never use repellents on wounds or irritated skin.Use repellent sparingly; one application will last 4-8 hours. Saturation does not increase efficacy. Wash repellent-treated skin after coming indoors. If a suspected reaction to insect repellents occurs, wash treated skin, and call a physician. Take the repellent can to the physician.

Specific medical information about the active ingredients in insect repellents is available from the National Pesticide Telecommunications Network, telephone (800) 858-7378.

Reference: MMWR, Vol. 38/No. 39, October 6, 1989.

IV.Pesticide Residues and Dietary Risks
Carl K. Winter, Ph.D.

A recent report issued by the National Resources Defense Council (NRDC) made the claim that as many as 6,200 American preschoolers may develop cancer in their lifetimes from eating apple products containing the plant growth regulator Alar (daminozide) and its breakdown product UDMH. The NRDC has also concluded from a 1987 report of the National Academy of Sciences that approximately 1.5 million Americans may get cancer from pesticide residues in their diets.

Such numbers are frightening when presented to the general population. To understand the true meaning of the numbers, however, it is important to ask several questions, such as: How are these numbers calculated? How accurate are they? How likely is it that more people will develop cancer from pesticide residues? How likely is it that anyone will actually get cancer from pesticide residues?

When the process of calculating human cancer risk estimates is evaluated from a toxicological perspective, one major conclusion can be drawn: The risk estimates do not provide accurate estimations of actual human cancer risks from exposure to chemicals.

The basic challenge of cancer risk assessment is to calculate risks to humans exposed to tiny amounts of suspected cancer-causing chemicals (carcinogens, or more accurately, oncogens) based upon the results of cancer studies performed in laboratory animals (usually mice and rats) given large doses of the chemicals. Such a task involves much scientific uncertainty. To compensate for this uncertainty, several critical assumptions that cannot be scientifically validated are factored into mathematical models used to predict risk estimates. It is generally accepted that these assumptions are highly conservative and produce exaggerated estimates of risk. Reported cancer risk estimates usually represent the highest, or "upper-bound" estimates predicted from theoretical risk assessment models; the lower bound may be several orders of magnitude lower or even zero. As such, cancer risk estimates may be useful for regulatory purposes and for comparing risks associated with various pesticides and other manufactured or natural chemicals, but do not predict actual human cancer incidence. It is a misrepresentation of the risk assessment process to convert risk estimates (usually represented as excess cancers per million) into actual human "body-counts", as has been done by the NRDC.

The two major steps in the cancer risk assessment process are 1) to determine if a particular chemical is a possible carcinogen, and 2) if so, what is the relationship between the dose of that chemical and the potential for cancer.

While determining whether a chemical is a potential carcinogen might appear to be a rather simple task, it turns out to be a very difficult one. Cancer studies are performed by exposing laboratory animals to various doses of a chemical (usually a control [zero] dose, a medium dose, and a high dose) continuously throughout their lifetimes (up to two years) and determining if the treated animals developed more tumors than those in the control groups. In a theoretical effort to maximize the chance of detecting cancer in the animal studies, special strains of animals that are more susceptible to cancer are commonly used. Evaluations of tumors are conducted by pathologists and may be rather subjective; one pathologist may classify a particular condition as a tumor while another may not. Although the condition of cancer requires tumors to be malignant (invading other tissues), benign tumors (non-invasive) are also counted in determining if a chemical is a suspected carcinogen.

Cancer studies for an individual chemical often produce conflicting results. In some cases, cancer may be produced only in a particular animal species or strain of animal. In other cases, one study using a particular strain of animal may show evidence of cancer while another study with the same strain may produce negative results. Since we rarely have enough evidence to show if a particular chemical is carcinogenic in humans, our regulatory agencies typically consider positive results in at least one scientifically-acceptable cancer study as evidence for potential human carcinogenicity. Using such guidelines, the Environmental Protection Agency (EPA) considers about 66 pesticides (of over 300 total) to be potential carcinogens.

The basic principle of toxicology that "the dose makes the poison" holds for all chemicals, including suspected carcinogens. In the process of carcinogenic risk assessment, however, the risks for suspected carcinogens are calculated differently than for non-carcinogens due to our lack of understanding of the mechanisms by which chemicals may cause cancer. For virtually all toxicological effects, a toxicity "threshold" dose is assumed to exist; exposure to a chemical at a level below this threshold is not expected to cause any adverse effects. In the case of suspected carcinogens, however, a theory that thresholds do not exist has been proposed. This theory suggests that any exposure to a carcinogen may have some possibility of leading to cancer, although higher doses would pose greater risks for developing cancer than lower doses. While there is considerable scientific debate regarding the validity of this theory, the lack of a threshold has been incorporated into the mathematical models used by our regulatory agencies to estimate cancer risks. Such an assumption is considered to be highly conservative by much of the scientific community and may overestimate cancer risks by several orders of magnitude.

What are the cancer risks posed by pesticide residues in the diet? This question has been recently addressed by the National Research Council (NRC) of the National Academy of Sciences (Regulating Pesticides in Food: The Delaney Paradox, National Academy Press, Washington, D.C., 1987). The NRC developed estimates of dietary cancer risks from pesticides currently in use and explored alternative approaches for the regulation of potentially carcinogenic pesticides.

Results of the NRC study, using the conservative risk assessment procedures described previously, indicated that the total risk (the additional risk of cancer from 70 years of exposure to 28 potentially carcinogenic pesticides) was slightly less than 0.006, or six per thousand. This is in addition to the current general cancer risk for the U.S. population of 0.25, or one in four. Fungicides were found to comprise the largest proportion (nearly 60 percent) of estimated risk; risks posed by herbicides and insecticides were 27 and 14 percent, respectively. Twelve pesticides were identified by the NRC as contributing 96 percent of estimated dietary risk, while fifteen foods accounted for nearly 80 percent of total dietary risk with the greatest risks calculated from exposure to tomatoes, followed by beef, potatoes, oranges, lettuce, apples, peaches, pork, wheat, soybeans, beans, carrots, chicken, corn, and grapes. From this analysis, the NRC concluded that exposure to potentially carcinogenic pesticides was likely to be concentrated in a few foods and from a relatively small number of pesticides.

The NRC study has been critical in reforming existing pesticide policy. Upon closer inspection of the NRC study, however, it appears that the NRC's risk estimates are likely biased due to additional conservative assumptions that were made concerning pesticide residue levels on foods. In the absence of actual pesticide use patterns and residue levels, the NRC assumed that all pesticides registered for use on a specific crop were always used at maximum levels allowed and were always present on the crop at levels equal to the legal allowable level. Using this approach, the NRC estimated "legally allowable risk" which is quite different than actual risk.

Pesticide use patterns indicate that many pesticides registered for use on particular commodities may not actually be used, and if they are used, they may be applied to only a small percentage of the acreage of the commodity.

Setting residues at legally allowable (tolerance) levels leads to additional upward bias. Despite a lack of consensus on estimates of actual food residues, historical data from the Food and Drug Administration (FDA) and the California Department of Food and Agriculture (CDFA) over the past two decades consistently shows that residues in excess of established tolerances are encountered infrequently (generally in less than one percent of the samples). In California in 1987, for example, 1,839 lettuce samples and 259 tomato samples were analyzed by CDFA for residues of over 100 pesticides. No residues were detected in 78 percent of the lettuce samples and 81 percent of the tomato samples. In the majority of lettuce and tomato samples in which residues were detected, residue levels were within 10 percent of the established tolerances.

Another factor not taken into account in the NRC study was that pesticide residue levels may be dramatically altered through the effects of transportation, handling, preparation, and processing, all of which have the potential to significantly decrease residues before the food may be eaten. More accurate data to estimate human exposure to pesticides comes from the results of FDA's 1987 Total Diet Study, in which inspectors purchased "market baskets" of selected food items, including meat and poultry, and had the food prepared in "ready-to-eat" fashion in institutional kitchens before analyzing for residues.

A comparison of the NRC's cancer risk estimates with those obtained using results of the FDA's 1987 Total Diet Study has recently been made by Archibald and Winter (Pesticide Residues and Cancer Risks, California Agriculture, Nov./Dec. 1989; Pesticides in Food: Assessing the Risks, in Winter, Seiber, and Nuckton, eds., Chemicals in the Human Food Chain, Van Nostrand Reinhold, New York, 1990*). Results suggest that the NRC's risk estimates may be several orders of magnitude greater than those calculated using more realistic exposure data. For example, the risks for exposure to captan were reported to be 474 excess cancers per million by the NRC but only 0.06 cancers per million using FDA data. Similar differences were seen for acephate (37 per million vs. 0.032 per million), linuron (1520 vs. 0.33), permethrin (421 vs. 2.13), chlorothalonil (237 vs. 0.0024), parathion (15 vs. 0.011) and folpet (324 vs. 0.034).

Such differences are important when one considers that the risk numbers are often used to guide regulatory decisions. The EPA, for example, has recently adopted a "negligible risk" standard of one additional cancer per million as a guideline to determine if regulatory action concerning individual pesticides should be considered. In the case of captan, for example, several of its registrations were removed by the EPA due to food safety concerns resulting from NRC's cancer risk estimates. With the exception of permethrin, however, risks posed by all of the pesticides discussed previously, including captan, were well below the negligible risk standard when using FDA Total Diet Study exposure.

Concerns about the cancer risks posed by pesticides in the food chain have triggered calls for regulatory action and legislative reform. The choice of methods used to evaluate cancer risks and the criteria for establishing which risks are excessive should be made on the basis of the best scientific data available. In its present state, the process of cancer risk assessment is plagued by much scientific uncertainty but promises to improve through scientific advancement. In this era of public concern about cancer-causing chemicals in the food chain, it is important that the limitations of cancer risk assessment are noted and that cancer risk estimates are properly interpreted and kept in perspective.

* Report is currently available for $5.00 from Publications, UC Division of Agricultural and Natural Resources, 6701 San Pablo Ave., Oakland, CA 94608. Please ask for "CHEM-5 Pesticides in Food: Assessing the Risks", and make checks payable to UC Regents.

V.Consumers Need to Realize Their Responsibility in Food Safety

Research has shown that sixty percent of Listeria illness happens in the home. One way to avoid falling into a problem with home convenience is to specify the different cooking times needed for variable microwave oven wattages, according to Dr. William Brown, president, ABC Research Corporation. Brown was one of several speakers at a Listeria workshop sponsored by the American Meat Institute.

"There is a problem in getting consumers to realize their responsibility in food safety. A Missouri study showed consumers believe ninety percent of food contamination occurs in the processing plant, ten percent in restaurants, and zero percent in their kitchen. The actual numbers are about thirty-five percent in restaurants, five percent in processing plants, and sixty percent in the consumers kitchen," said Brown.

Reference: News from Livestock Conservation Institute, August, 1989.

VI.Fatalities Attributed to Methane Asphyxia in Manure Waste Pits -- Ohio, Michigan, 1989

In June and July 1989, a total of seven farm workers in two separate incidents died after they were asphyxiated by methane gas in manure pits. Brief reports follow.

Ohio. On June 26, 1989, a 31-year-old male dairy farmer and his 33-year-old brother died after entering a 25-foot-square by 41-foot-deep manure pit inside a building on their farm. A pump intake pipe in the pit had clogged, and the farmer descended into the pit to clear the obstruction. While in the pit, he was overcome by lack of oxygen and collapsed. His brother apparently saw him collapse and entered the pit in an attempt to rescue him. The brother, too, was overcome and collapsed inside the pit. Four hours later, another family member discovered the two men, and the local fire department was called to rescue them. The coroner's report attributed the cause of death in both cases to drowning, secondary to loss of consciousness from methane asphyxia.

Michigan. On July 26, 1989, five farm workers in one family died after consecutively entering an outdoor manure pit on a farm. The pit measured 20 feet by 24 feet by 10 feet deep. The victims were a 65-year-old male dairy farmer, his two sons (aged 37 and 28 years), a 15-year-old grandson, and a 63-year-old nephew. The index victim, the 37-year-old son, initially entered the pit by ladder to replace a shear pin on an agitator shaft. While attempting to climb out of the pit, he was overcome and fell to the bottom of the pit. The grandson then entered the pit to attempt rescue. He, too, was overcome and collapsed. One by one, the nephew, the younger son, and the dairy farmer entered the pit in attempts to rescue the others, were overcome by lack of oxygen, and collapsed. A carpet installer working at the farm then entered the pit as a rescuer and was overcome; however, he was rescued by his assistant and subsequently recovered.

Finally, the owner of a nearby business arrived with two additional workers and, using a rope, extricated the five victims from the pit. When paramedics arrived, they began cardiopulmonary resuscitation. The nephew was pronounced dead at the scene, and the other four victims were transported to the emergency room of a nearby hospital. The dairy farmer and his younger son were pronounced dead on arrival at the hospital; the 37-year-old son died 1 hour after reaching the emergency room. The grandson was transferred by helicopter to a major trauma center but died within 6 hours of his removal from the pit. For the four older victims, the medical examiner attributed the cause of death to methane asphyxia. Assignment of the official cause of death for the grandson awaits completion of the autopsy report.

Editorial Note: Acute traumatic occupational deaths in the United States are monitored by the Division of Safety Research, National Institute for Occupational Safety and Health (NIOSH), CDC, through the National Traumatic Occupational Fatalities (NTOF) file. For 1980 through 1985, the NTOF data file includes 16 work-related deaths that involved asphyxiation of workers in manure pits (or similar waste tanks) on farms. These deaths resulted from nine separate incidents in nine different states. Five of these episodes resulted in multiple fatalities. Because NTOF only includes deaths of workers >16 years of age that are clearly identified as work-related, these 16 deaths represent the minimum number of asphyxiation fatalities that occurred during this period among U.S. farmers, farm family members, farm workers, and others working in manure pits.

A farm manure waste pit is a confined space, defined by NIOSH as a space that "by design has limited openings for entry and exit; unfavorable natural ventilation which could contain or produce dangerous air contaminants; and which is not intended for continuous worker occupancy." Manure pits are fermentation tanks where raw animal wastes undergo anaerobic bacterial decay. This bacterial action generates methane, hydrogen sulfide, and other gases. Methane is a colorless, odorless, and flammable gaseous hydrocarbon. It can displace oxygen in confined areas, resulting in an oxygen-deficient atmosphere. Hydrogen sulfide is a highly toxic, colorless gas that at concentrations of >300 ppm can cause unconsciousness, respiratory failure, and sudden death. If these gases are not properly vented from a tank or other confined space, an oxygen-deficient or toxic atmosphere may be created. In industrial settings, the Occupational Safety and Health Administration (OSHA) limits permissible peak exposures to hydrogen sulfide to a ceiling of 50 ppm (for <10 minutes); NIOSH recommends a ceiling of 10 ppm (for <10 minutes). There is no OSHA permissible exposure limit for methane. OSHA exposure standards are not enforceable on farms with <10 employees.

Approximately 43% of confined-space-related deaths involved co- workers or other persons who were attempting to rescue the initial victim(s) (NIOSH, unpublished data).

NIOSH is preparing information for farm operators on the hazards of manure pits and recommendations for safely evaluating, ventilating, and entering (when absolutely necessary) manure pits. Recommendations will also be provided for the safe conduct of rescue operations in circumstances such as those described in this report. NIOSH will disseminate this information during the fall.

Reference: MMWR, Vol. 38/No. 33, August 25, 1989.

VII.Multivitamins Can Cause Toxic Vitamin A Build-Up in Older People

A multivitamin-a-day may seem like a good insurance policy for obtaining the Recommended Dietary Allowance (RDA) of essential vitamins. If you're over 60, however, you may want to consult your physician about this daily health ritual. New scientific evidence shows that prolonged daily use of supplements containing vitamin A can lead to a low-level toxicity in older people.

Researchers at the Human Nutrition Research Center on Aging at Tufts University surveyed hundreds of men and women over age 60 and found that half reported taking supplements, primarily multivitamin-multiminerals. Of those who had taken the supplements daily for more than five years, a small number had signs of liver damage associated with too much vitamin A. Those showing toxic symptoms reported daily vitamin A intake ranging from the RDA level (5,000 I.U.) to four times the RDA. Researchers did not find the toxic build-up among younger people. While the liver has a great capacity to store vitamin A, the researchers hypothesize that older people may have used much of this capacity and their "margin of safety" is reduced for vitamin A intake, as compared to younger people.

The problem of toxic build-up may be compounded by the vitamin manufacturers' practice of "overage" -- including in supplements as much as 40 percent more than the labeled amount of vitamin A to insure the vitamin's stated potency throughout its shelf life.

The results of the Tufts study support the recommendation of most nutritionists that - for people of all ages - it is better to obtain the nutrients you need from good foods, rather than from supplements. The best insurance that you're getting enough vitamin A is to eat a balanced diet that includes foods rich in beta-carotene, a form of vitamin A that is not toxic. Deep orange fruits and vegetables - such as carrots, sweet potatoes, squash, peaches, apricots, cantaloupe, and watermelon - as well as dark green leafy vegetables - such as spinach, broccoli, kale, collards, and beet greens - are all excellent, healthful beta- carotene sources.

Reference: American Institute for Cancer Research Newsletter, Issue 22, Winter 1989.

VIII.Aldicarb on Watermelons
M. W. Stimmann

Two Kern County growers have paid $65,000 in civil penalties arising out of charges they misused the pesticide aldicarb on
watermelons in 1985.

This settlement concludes a civil case filed in connection with an investigation of several illnesses suffered in July, 1985 by persons who ate watermelons. Some watermelons were later found to be contaminated with the pesticide aldicarb. Aldicarb, sold under the trade name Temik, is not registered for use on watermelons.

The illnesses prompted field-by-field sampling and testing of California watermelons. This resulted in three growers being charged with violations of pesticide regulations and the state's business and professions code.

IX.Pesticide Poisoning Handbook

"Recognition and Management of Pesticide Poisoning" is the title of a pesticide poisoning handbook published by EPA. It is available free from the National Pesticide Telecommunications Network at the toll-free 24-hour phone 1-800-858-7378. (From: P&TCN, Vol. 17, No. 33). Note: I called the above number and found that anyone ordering over 20 copies of the book must make their request in writing to: Jerry Bondel, 8556 Tyrolean Way, Springfield, VA 22143. (Don Cress).

Reference: Kansas Pesticide Newsletter, Vol. 12, No. 7, July 13, 1989.

X.Staggers in Sheep and Cattle: Humboldt County

Livestock Farm Advisor Gary Markegard in Humboldt County reported the appearance of staggers in some animals last year. The staggers appeared again this year and Gary obtained videotapes of the affected animals and samples of forage that might be responsible for the intoxication. In cooperation with Dr. Frank Gayley in the California Veterinary Diagnostic Laboratory, further investigations are being performed to discover the actual cause of the problem. Gary collected several grasses that were severely infected with ergot fungus (identified by Extension Plant Pathologist Dr. Mike Davis). This fungus has been responsible for various livestock poisonings in the past, including the staggers syndrome. If you have encountered similar episodes with stock, please let us know about it. Thank you.

XI.Is Hay Treated with Preservatives O.K. for Horses?

Most hay dealers that sell hay to horse operations will tell you that horse managers and owners do not want to buy hay that has been treated with preservatives. This negativism is due to: 1) bad experiences in using "preserved" hay; or 2) fear and lack of understanding of the chemical nature of hay preservatives.

The most reliable hay preservative is one containing high concentrations of propionic acid. In order for this to be effective, it must be applied at the proper rate. Therefore, when purchasing hay treated with "preservatives," it is important to look, feel, and smell the quality of the hay checking for mold or dustiness.

Do Preservatives Harm Horses?

Recently, three independent studies performed at Cornell University, University of Illinois, and the University of Kentucky compared hay baled at high moisture and treated with a preservative containing a mixture of propionic acid and acetic acid to low moisture hay that was untreated. The following are some points made from these studies:

1. There was no difference in crude protein or digestibility of the treated hay versus the untreated hay.

2. The appearance of treated hay varied from green to brown bales; however, forage analysis showed no difference in available crude protein. The result of the brown color was not due to heating.

3. When horses were given a choice between treated and untreated hay, horses preferred the untreated hay; however, when fed only one type of hay at a time, horses consumed both treated and untreated hays equally (Cornell study). At Illinois, intake of the treated and untreated hays were identical.

4. Generally, the untreated hay was dustier than the treated hay; therefore, treated hay may be better for horses with respiratory problems.

Drying Agents Used on Hay

A newer type of product being used by some hay producers is the chemical drying agent, also referred to as chemical conditioning. These products are different from preservatives. Drying agents are applied at mowing and aid in rapidly drying the forage. They do not preserve wet hay. The chemicals used as drying agents usually include potassium carbonate and sodium carbonate. These are rather simple salts that have not been shown to cause harm to livestock. The amounts of potassium and sodium applied from drying agents are far less than typical amounts that are taken out of the soil by the forage plants; therefore, there should be no potential problem of salt toxicity.

Reference: Forage and Seed Facts, Vol. 14/No. 3, September 1989.

XII.New Field Tests for Veterinarians

The following list includes a number of new field tests that may be suitable for use by a veterinarian in checking milk or urine samples for presence of inhibitory agents:

Penzyme - specific for betalactams. SmithKline Animal Health, 800/877-7303 ext. 7506.

CITE - specific for sulfamethazine. Agritech Systems, Inc., 800/548-6733.

Charm Cowside-betalactam and Charm Cowside-sulfonamide - Penicillin Assays, Inc., 617/322-1523.

SOS (Sulfa on Site) - suitable for use on urine, feed; - SMZ and other sulfonamides. Environmental Diagnostics, 800/335-1116.

Signal Quik-Card (also sold as EZ Screen) - SmithKline Animal Health, 800/877-7303 ext. 7506.

Reference: Herd Health Memo, December 1988.

XIII.Pamphlet from the UC Santa Cruz Agroecology Program: "Pesticides in Food: Are You Adequately Informed"

Many readers may have already seen this pamphlet but those who have not should be aware of its existence. It was produced by the Agroecology Program, which is part of the Division of Social Sciences at UC Santa Cruz. This pamphlet contains a considerable amount of misinformation about the potential hazards of pesticide residues in foods, and an irresponsible recommendation to consumers to wash produce using soap and water. It has been distributed widely. We have received many calls and letters from people and organizations who are very concerned about the effect this publication will have on programs that are trying to bring rationality to this emotionally charged topic. The California Department of Food and Agriculture is preparing an analysis of the pamphlet which should be available soon. When it has been released, we will forward a copy to each county office, along with a copy of the UCSC pamphlet.

Art Craigmill
Extension Toxicologist
U.C. Davis

Carl Winter
Extension Toxicologist
U.C. Riverside

Mike Stimmann
Statewide Pesticide Coordinator
UC Davis