Vol. 11 / No. 4 - September 1991

Table of Contents



The time has come once again to renew subscriptions, and this year, more than ever, we really need the help. A cartoon first posted in our department about 3 years ago comes to mind: Picture two dinosaurs walking through a field covered with other dinosaurs "belly up". One says to the other; "Frankly, I don't like the way things are going." In these times of tight money and fewer positions, inexpensive forms of extension education (like newsletters) become more important.

I promise at least one more issue before the end of this calendar year, and the next one will focus on the current status of the food safety issue, as perceived from different viewpoints. As a closing thought (parting shot?) I would like to copy a recent innovation seen in the last two DANR Newsletters. That is the inclusion of inspirational "quotes" from business managers, motivators or whatever they are called these days. This quote was recently sent to me by another specialist, and seems particularly poignant as history repeats itself again: "We trained hard, but it seemed that every time we were beginning to form into teams, we would be reorganized. I was to learn later in life that we tend to meet any new situation by reorganizing, and a wonderful method it can be for creating the illusion of progress while producing confusion, inefficiency, and demoralization," by Petronius Arbiter, Roman General, 66 A.D.


Dr. Roger Garrett, Acting Director of the Aquaculture and Fisheries Program, UC Davis, noticed an error in our Newsletter of June 1991. In the article on Chlorination of Animal Drinking Water the contact time should be:

Contact Time = Volume of Container (Gal) / Flow Rate of Water (Gal/Min)

This calculation of contact time assumes uniform flow through any lines or in an enclosed holding tank. Any opportunity for water from the inlet to short circuit quickly to an exit where chlorine can dissipate will invalidate the calculation. In particular, one should NOT use a "mixing" tank; a well mixed tank would allow some of the input water to reach the exit of the tank almost instantaneously.

Eosinophilia-Myalgia Syndrome:
Follow-up Survey of Patients - New York, 1990-1991

As of December 1, 1990, 151 cases of eosinophilia-myalgia syndrome (EMS) had been reported to the New York State Department of Health (NYSDOH); 10 of these patients died. Of the 151 case-patients, 149 were known to have used supplemental L- tryptophan (LT) before onset of illness. Because anecdotal reports indicated that some patients in New York had changes in mental status and other symptoms not previously described in association with EMS, the NYSDOH conducted a survey from December 1990 through March 1991 to determine the prevalence of self- reported symptoms in patients with EMS.

Patients reported symptoms involving multiple organ systems during their illness. At least 75% of patients reported musculoskeletal, neurologic, and dermatologic symptoms. Specific cognitive problems at any time during illness included difficulty concentrating (63%), difficulty remembering words or names of persons (52%), difficulty thinking logically (52%), difficulty conversing (43%), and impairment of short-term memory (42%). Of the 74 patients who reported depression and/or anxiety as an EMS symptom, pre-EMS medical and psychiatric history was available for 54. Of these patients, 32 (59%) denied psychiatric problems before developing EMS.

At follow-up, 64% of patients reported having moderately or extremely severe EMS symptoms. The most commonly reported persistent symptoms included fatigue (64%), muscle weakness (60%), muscle cramping (57%), myalgia (55%), arthralgia (48%), anxiety (46%), depression (41%), tight skin (40%), and difficulty concentrating (40%). Seventy-five (82%) patients reported that symptoms had become less severe since peak illness; nine (10%) patients reported that they were symptom-free.

Editorial Note: There are at least three potential explanations for the high prevalence of cognitive and psychiatric symptoms reported by patients with EMS in New York. First, these symptoms may reflect the adjustment made by EMS patients to living with a chronic disease with an unknown course and no proven treatments. Second, these symptoms may be a primary manifestation of inflammatory central nervous system effects, similar to those observed in peripheral nerves and other organ systems. Third, because many of these manifestations are subtle, they may be obscured by the severe pain and disability that characterize EMS, thereby resulting in delayed clinical recognition.

Reference: MMWR, Vol. 40/No. 24 - June 21, 1991.

Acute and Chronic Poisoning from Residential Exposures to Elemental Mercury - Michigan, 1989-1990

From May 1989 through November 1990, eight episodes of elemental mercury exposure in private residences or schools in the United States were reported to the Agency for Toxic Substances and Disease Registry (ATSDR). The case studies in this report document two of these episodes (both in Michigan) of residential mercury poisoning---one involving acute mercury exposure, and the other, chronic exposure to elemental mercury.

Episode 1. On August 7, 1989, four adult occupants (two men and two women ranging in age from 40 to 88 years) of a private home were hospitalized for evaluation of nausea, diarrhea, shortness of breath, and nonspecific chest pain. During hospitalization, the patients experienced progressive dyspnea (difficulty breathing) and pulmonary insufficiency. On August 11,investigators learned that one of the patients had been smelting dental amalgam in a casting furnace in the basement of the home in an attempt to recover silver from the amalgam. Mercury fumes released during the operation apparently had entered air ducts in the basement and had circulated throughout the house.

Despite chelation therapy and vigorous ventilatory support treatment, the condition of the patients continued to deteriorate. All of the patients died within 11-24 days after exposure to the mercury vapor. The cause of death was considered to be mercury poisoning, which resulted in adult respiratory distress syndrome and subsequent respiratory failure. Postmortem mercury concentrations in organs from the four patients were 300- 2100 ug/g (kidney), 3-2400 ug/g (liver), <1-100 ug/g (brain), and 1-150 ug/g (lung); concentrations in blood ranged from 58 ug/L to 369 ug/L.

Measurements of ambient indoor air concentrations of mercury taken 11-18 days after the exposure were as high as 786 ug/m3 in the basement and 912 ug/m3 on the first floor. The house was extensively cleaned to reduce the mercury contamination; however, decontamination efforts did not reduce indoor air mercury concentrations to an acceptable level, and the house was subsequently demolished.

Episode 2. On August 21, 1989, a young girl was admitted to the hospital because of impaired gait. She was diagnosed as having a postinfectious viral syndrome and was discharged on August 23. On September 11, she was readmitted to the hospital when she could no longer walk. On September 19, an older sister of the patient was admitted to the hospital with similar symptoms. Clinical evaluation of both girls revealed numbness in the fingers and toes, absence of deep tendon reflexes, elevated blood pressure, and an elevated level of protein in the cerebrospinal fluid. Mercury poisoning was diagnosed, and chelation therapy was started in the two children. Subsequently, on October 3, their asymptomatic brother was hospitalized for a chelation challenge, which detected a substantial mercury load.

After chelation therapy, the brother remained asymptomatic, and the older sister improved and was discharged from rehabilitation therapy. The index patient had numerous residual neurologic abnormalities, including visual field defects, mild upper and lower extremity weakness, and some emotional lability.

Subsequent investigations revealed that earlier that summer about 20 cm3 (about a tablespoon) of liquid mercury had been spilled in the boy's bedroom. Examination of the house using a mercury vapor analyzer detected indoor air mercury concentrations of 10- 40 ug/m3. Clean-up efforts included removing carpet from several areas in the house, replacing the carpet and wooden subfloor in the bedroom where the spill occurred, and commercially cleaning all other carpet and furniture.

Editorial Note: Although the toxic properties of elemental mercury have been recognized since at least the 1500s, occupational and residential exposures to mercury remain a source of poisoning.

Although death is an infrequent outcome of acute exposure to mercury, the first episode described in this report illustrates the clinical progression following exposure. Patients are usually asymptomatic during the first 1-4 hours following acute exposure to high air concentrations of mercury vapor. Symptoms start abruptly and may include fever, chills, nausea, general malaise, and respiratory difficulties (shortness of breath, pain and tightness in the chest and paroxysmal coughing). In severe cases, pulmonary edema may cause death within a few days.

After inhalation, elemental mercury is readily absorbed through the alveolar membranes and transported by blood to the brain and other tissues of the nervous system. Mercury is rapidly converted by the blood to mercuric ions, which are then excreted in the urine and feces. Diagnosis of mercury toxicity is aided by the detection of elevated concentrations of mercury in blood or urine samples.

Residential and occupational cases of mercury poisoning more commonly result from chronic exposures, as illustrated by the second episode described in this report. Spilled mercury gravitates to cracks in the floor and into the pile of carpets. Even though it may not be visible, the mercury can slowly volatilize indoors and may lead to chronic mercury poisoning through inhalation exposure. Vacuuming a contaminated area may facilitate the spread of mercury vapor throughout the house.

The potential for indoor mercury exposure is increased when indoor air exchange is reduced (e.g., when doors and windows are kept closed). Warm air from heating ducts and vents may enhance volatilization when circulated over spilled mercury. Mercury vapor concentration is likely to be higher near the floor, and children may be exposed to higher concentrations of mercury than adults. Potential sources of elemental mercury in the home include mercury switches and mercury-containing devices such as thermostats, thermometers, and barometers. Family members may also bring into the home elemental mercury obtained from laboratories, dental offices, or other industrial sources.

Reference: MMWR, Vol. 40/No.23, June 14, 1991.

Multistate Outbreak of Salmonella poona Infections -- United States and Canada, 1991

During June and July 1991, more than 400 laboratory-confirmed infections with Salmonella poona occurred in 23 states and in Canada.

Editorial Note: Salmonella is the most frequently reported cause of foodborne outbreaks of gastroenteritis in the United States. Foods containing poultry or other meat, eggs, or dairy products are most often the vehicles for foodborne salmonellosis. Food preparation practices contributing to past outbreaks include improper food storage or holding temperature and poor hygiene by foodhandlers. Fruits and vegetables are not often identified as vehicles for Salmonella infection; however, in 1990, two multistate outbreaks of salmonellosis associated with fruits and vegetables occurred. In this report, the association of illness with consumption of cantaloupe in fruit salads or from salad bars suggests that contaminated fruit may have incubated for several hours at room temperature after preparation.

It is difficult to trace melons once they are unpacked from crates. Although industry sources identified the lower Rio Grande Valley in Texas as the probable source of the implicated cantaloupes, some may have come from Mexico. Grown on the ground, melons may be contaminated on their surface with dirt, chemicals, animal excreta, or bacteria, including Salmonella. Although large produce companies wash and dip melons in a chlorine solution, field-packed melons do not receive such treatment. Cutting an unwashed melon through a contaminated rind may lead to contamination of the edible part via the cutting knife or subsequent contact of dirty rinds with cut pieces of melons. Excessive time at room temperature may then permit bacterial growth.

To reduce the risk for S. poona infection from melons, the FDA recommends that both produce retailers and consumers thoroughly clean melons with potable water before cutting them, prepare cut melons using clean and sanitized utensils and surfaces, hold cut melons at <45 F (< 7 C) until served or sold, and limit display of cut cantaloupes to less than 4 hours if not kept refrigerated. To decrease the risk for Salmonella food poisoning, it is prudent to wash all fruits and vegetables before they are handled and consumed.

Reference: MMWR, Vol. 40/No. 32, August 16, 1991.

"Roundup" Herbicide Found Relatively Benign

In a 13-week toxicity study, glyphosate, a widely-used herbicide marketed under the tradename "Roundup", was given a relatively clean bill of health. A draft NTP technical report found no evidence of genetic or reproductive toxicity.

At doses of 25,000 and 50,000 ppm in the feed, glyphosate reduced body weight gain, caused cytoplasmic alteration and hypertrophy of the salivary gland acinar cells, elevated serum bile acids, alkaline phosphatase, and alanine aminotransferase activities. There was no histopathologic evidence of liver injury. The no-observed-adverse-effect-level (NOAEL) for the salivary gland lesion was 3125 ppm in the feed for mice, but the lesion was observed at all dose levels studied in rats.

Reference: Food Chemical News, July 15, 1991.

FDA's Computer Food Safety Network Goes "On-Line"

The Food and Drug Administration's "Prime Connection" network that allows free access to agency information on retail food protection, milk, and seafood safety has gone on-line.

The food safety information package has been dubbed FDA Prime Connection. The available information includes technical text references, the interstate certified shellfish shippers list, the interstate milk shippers list, the fish list, and the 40-chapter foodborne pathogenic micro book.

The information will be available 24 hours a day 7 days a week through 2,000 local phone numbers and an 800 number. Application forms are available by writing to: FDA Prime Connection, 200 C St. SW, HFF-342, Washington, DC 20204-001.

Reference: Food Chemical News, July 29, 1991.


Chopped Newspaper Bedding

(Editor: Found in an old stack of papers)

Recycled, chopped newspaper can be used as an acceptable alternative bedding for lactating dairy cows. However, there appears to be little advantage of the use of recycled newspaper in reducing exposure of teat ends to mastitis pathogens compared to use of other organic materials.

An experiment was conducted at the Ohio Agricultural Research and Development Center dairy to investigate the use of recycled chopped newspaper as tie-stall bedding for lactating dairy cows. Bacterial counts associated with recycled, chopped newspaper, hard wood shavings, and pelleted corn cob bedding materials were compared in a nine-week trial. Newspaper was chopped into 2 x 4 inch sections using a straw chopper.

Bacterial counts in pelleted corn cob and chopped newspaper bedding were similar. On the other hand, Klebsiella species and staphylococcal counts in chopped newspaper were greater than in wood shavings. Coliform and streptococcal counts did not differ between chopped newspaper and wood shavings bedding.

The number of bacteria on teat skin did increase as bacterial counts in bedding increased. Transfer of bacteria from bedding to teat skin may have been associated with bedding particle size and adherence. Corn cob pellets tended to crumble into a fine granular material and adhere to teats more readily than the arger particle sizes of chopped newspaper and wood shavings. This difference in adherence of bedding to teats was evident by the fact that bacterial counts in chopped newspaper and pelleted corn cob bedding did not differ, but the number of mastitis pathogens on teat skin were less for cows bedded on chopped newspaper than those bedded on pelleted corn cobs. Teats of cows bedded on chopped newspaper and wood shavings had similar coliform counts. Streptococcal and staphylococcal populations on teats of cows bedded on chopped newspaper were greater than those for cows bedded on wood shavings.

Reference: J. S. Hogan, Ohio Vet Newsletter, Winter 1989.

Drought-related Poisoning Hazards in Livestock
Dr. Frank Galey, CVDLS, UCD

The current drought in California has contributed to a number of poisoning cases diagnosed recently at the California Veterinary Diagnostic Laboratory System.

Animals have been exposed to less than optimum feedstuffs that may also be toxic because of the limitations of feed supplies imposed by the drought. Recent cases have included interstitial pneumonia in cattle caused by feeding moldy sweet potatoes. In other cases, moldy pomegranates have been blamed for killing cattle, horses, and sheep. The lack of available feeds also may contribute to nutritional diseases such as deficiencies of the essential elements selenium and copper or a basic lack of energy and protein. The laboratory also recorded an increased incidence of abomasal impactions that were believed to have resulted from feeding feeds high in fiber and low in digestibility to cattle in the drought-related absence of higher quality forages.

Forage that is available may be drought-stressed or loaded with drought-resistant weeds. The stress of drought can cause some forages, such as sudan grass and oat hay, to accumulate toxic levels of nitrate (> 1%). In addition, hay contaminated with weeds known to accumulate nitrate such as pigweed (Amaranthus sp) or smartweed (Polygonum sp) can cause nitrate toxicosis in cattle.

As a general rule, drought conditions increase the incidence of plant toxicoses. For example, hungry cattle with a lack of adequate pasture grasses may begin to feed on potentially toxic plants that they would normally avoid. Recently, sheep on one farm in the Central Valley were presented with hepatic damage and secondary photosensitization. The animals had ingested excessive quantities of puncture vine (Tribulus terrestris) which is thought to contain a hepatotoxic mycotoxin. In another case, cattle in the coastal foothill region died after developing stupor and gastroenteritis. The animals had been on dry pasture and had ingested toxic, Durango root (Datisca glomerata). Durango root toxicosis had been reported from the area only during drought years, leading to speculation that either drought increased its toxicity or, more likely, the sparse pastures led hungry animals to ingest the toxic plant.

A third example of probable drought-related plant toxicosis involved outbreaks of stringhalt in horses in the north-central coastal region of California. Horses in those cases were found to have ingested flatweed (Hypochoeris radicata), a dandelion like plant in the overgrazed pastures. Horses in nearby pastures that were not overgrazed had not ingested the flatweed. Once animals started to eat the flatweed, however, they apparently began to crave the plant. Flatweed has been associated with outbreaks of stringhalt in Australia and New Zealand.

There have been other plant poisonings diagnosed in the last couple of years that may have been drought-related. Poison hemlock (Conium maculatum) in weedy alfalfa hay caused toxicosis in two cattle herds. Several cases of fiddleneck (Amsinckia intermedia) toxicosis in cattle and horses have also been recorded.

In addition to exposures to suboptimal feed on account of the drought, animals have also been exposed to limited and/or lower quality water supplies. Toxic constituents of water include excessive nitrate, sulfate, or salts such as sodium and magnesium. Additionally, some poor-quality water supplies may contain large amounts of sulfur-containing compounds that may adversely affect palatability and hence, production.

During periods of drought, producers and veterinarians are encouraged to be especially careful about the quality of feed and water available for their animals. Hay should be carefully scrutinized for weed content. Animals on overgrazed pastures should be provided with supplemental feed. If water is of poor quality and potentially affecting production, it can be tested for minerals and salts. Although it is best to avoid using poor quality water, it is possible to treat some problems. For example, cattle exposed to water that is high in molybdenum and/or moderately high in sulfates can be supplemented with copper. Water that is high in sulfur/sulfides can be run over a splashboard (any system of boards or devices to aerate the water) to remove some sulfur and improve palatability. If questions arise regarding the potential hazards of some feedstuffs or water, please contact the CVDLS - Toxicology Laboratory.

Reference: Lab Notes, Vol. 4, No.2, Spring 1991.

Illegal Use of Clenbuterol In Food Animals

FDA is investigating the illegal use of the drug, clenbuterol, in animals used for food, particularly animals being prepared for livestock show competition. The following description of an outbreak of clenbuterol residue toxicity demonstrates the potential public health consequences of illegal use of drugs in animals used for food.

Numerous cases of illness, which appeared to be due to food poisoning, were reported in Spain between March and July in 1990. No deaths or serious complications are believed to have occurred. The two most commonly reported symptoms were muscle tremors and heart palpitations with increased heart rate. Nervousness, headache, and muscle pain were also reported. An epidemiologic investigation revealed that two main outbreaks of this illness had occurred: The first from March 22 to April 4, in Asturias, Leon y Palencia, and the second from May 22 to June 17 in Madrid- Toledo. Other isolated cases were also recorded. In all, forty- three families including a total of 135 people were involved. The epidemiologic investigation also revealed that a food item consumed by all families was beef liver, and of the family members consuming beef liver, 97% reported symptoms. This information indicated the agent that produced the illness was contained in beef liver consumed by the affected individuals.

Based on analysis of available information, the investigators predicted that an agent responsible for the observed illness should have the following characteristics: sympathomimetic activity (produces muscle tremors and cardiac effects), highly concentrated in the liver, administered by either injection or in feed to animals, and of apparent therapeutic or production value in animal husbandry. Based on these criteria, it was suspected that illegal use of a b agonist in cattle was responsible for the poisoning outbreak. Prompt follow-up on a number of patients had allowed the investigators to collect samples of the suspected food, as well as urine samples from the individuals. Analysis of these samples revealed that a b agonist, clenbuterol, was present at levels of 2-4 ppb in patients' urine and 160-291 ppb in beef liver samples. This confirmed the investigators' suspicions that an illegal animal drug residue present in liver had produced the outbreak of food-borne poisoning.

An investigation of the epidemiologic chain, from the families involved to the meat markets, slaughter houses, farms, and finally the drug suppliers was made in order to determine the source of the outbreak. As a result of this investigation, ten people were detained by Spanish authorities in November 1990 for their alleged involvement in the illicit sale and use of clenbuterol as an anabolic growth promoter in cattle. Spanish authorities have initially suggested that the animals involved may have been mistakenly overdosed with clenbuterol, and then slaughtered for use as human food when they began showing signs of toxicity. A similar outbreak of food poisoning has been recently reported from France involving 22 people from 8 families who consumed beef liver. Clenbuterol was identified at levels of 375-500 ppb in the liver implicated in the outbreak in France. Based on the liver concentrations in these two incidents, the dose-response relationship is consistent with other information available for clenbuterol.

While residue-produced clenbuterol toxic effects have been described as mild, the FDA Center for Veterinary Medicine considers all unintended effects to be unacceptable. Additionally, it is possible that individuals being treated with adrenergic agents, or otherwise similarly compromised, may be far more severely effected by toxic levels of clenbuterol than are normal healthy individuals. Further, at very high doses b2 agonists have produced cardiac necrosis.

Synthetic adrenergic agents and their potentially active metabolites may be sequestered in the liver reaching levels much higher than those found in muscle. Thus liver may contain toxic levels of drug while muscle consumption may not produce toxicity. During the FDA food animal drug approval process this and other appropriate phenomena are thoroughly examined, safety factors are applied, and withdrawal times established to ensure all tissues are safe for human consumption. This protection is not available to consumers of products containing illegal drugs.

Finally CVM is concerned about the illicit use of clenbuterol leading to occupationally-related illness or death. Clenbuterol effects on the cardiovascular system may be more hazardous via occupational inhalation exposure than via ingestion in food. The Agency is aware of a report of the deaths of two farmers in Ireland while preparing clenbuterol for feeding to livestock.

Reference: FDA Veterinarian, Vol. VI, No. IV, July/August 1991.

Food Animals -- Bovine

Let's All Work At This One

A number of years ago, when beef carcasses were hung and shipped to butchers to cut up the carcasses, a few lesions were found that indicated some type of carelessness or misuse of parenteral injections into the animal. In some cases, hard knots of fibrous tissue indicated an old abscess that had turned into scar tissue by body processes. Whatever the cause, the carcass had to be trimmed and the primal cuts made into hamburger.

With the advent of "breaking" beef and deboning carcasses, an increase in the number of these lesions has been noted. Recent surveys reveal that carcasses have a 10 to 20 percent incidence with the greatest percentage found deep in the muscle. This is very disconcerting because of the problem of trimming and causing the primal cuts to be reduced to hamburger or tanked. The majority of these lesions are found on the back of the hip or on the top of the round.

Extensive studies of this condition have been executed by major packing companies, feedyards, and cattlemen associations. Therefore, there is ample documentation of this serious situation. Losses are estimated to run into millions of dollars but, more serious, is consumer reaction if lesions are encountered or if general knowledge of this condition is made public. To date, the situation has been well-handled so that no public health problem has been encountered.

Further research has revealed some of the major causes of the condition and, in review, the majority can be prevented. Thus, any person associated with the beef industry, whether producer, educator, veterinarian or with an affiliated industry, has a responsibility of understanding this condition and to aid in its prevention because prevention is the key.

Here are the main causes of this problem:

1. Injections of any kind -- vaccine, antibiotics or others, should not be given in the hip region to any animal of any age. The neck region is preferred.

2. Many injections are recommended to be given subcutaneously. Yet, the operator, whether owner or employee, will "punch" the injection needle through the skin and underlying tissue into a muscle. This occurs even if they use a half-inch needle. If the skin is lifted or pinched and the injection is administered, the injected material is in the subcutaneous tissue and not in the muscle. Remember, to do it right takes a little more time.

3. Frequently too large or too long a needle is used and intramuscular injections can't be avoided.

4. If an intramuscular injection is recommended, use only in the neck muscle.

5. Dirty needles are a frequent cause of these lesions. Care should be exercised in using clean needles and precautions should be exercised so as not to inject through mud or manure on the animal's coat.

6. It has been a common practice to use repeated injections of vaccines. For example, the producer may inject his calves with a clostridial product, repeating it again at weaning. Once the animals arrive in the feedyard, clostridial injections are given again. Apparently an allergic manifestation can occur by repeated clostridial injections, adding to the tissue damage. In checking health records in some feedlots, 8 to 10 injections may be given to one group of cattle during their feeding period. This is particularly true with a set of cattle with health problems.

7. Combination products which have been approved or licensed for safe and effective use in cattle can reduce the number of injection sites in an animal.

8. Herd owners should be advised of this problem and their injection procedures reviewed. Likewise, the vaccinating crews in feedlots should be trained to administer injections in the proper manner and should be closely supervised. This is an industry problem. It can be solved in a very short time. Your interest and assistance is needed.

Reference: J.B. Herrick, Personal Communication, Animal Health Spectrum, Mississippi Extension Veterinary Medicine, Vol. 2, No. 1, June 1991.


On April 18 and 19, 1991, the Center to Study Human-Animal Relationships and Environments (CENSHARE) presented a two-day conference entitled The Ethics of Humans Using Animals for Food and Fiber. Videotapes from the teleconference (first day only) and audiocassettes (from both days) are available for purchase. This series of programs provides a structured yet balanced discussion among experts of various disciplines such as philosophy, anthropology, law, ecology, veterinary and agricultural science, public health, nutrition, and economics. If you have any questions or are interested in purchasing these videotapes or audiocassettes, please contact Annette Mike, CENSHARE, Box 197 Mayo Memorial Building, 420 Delaware Street SE, Minneapolis, Minnesota, 55455, (612) 626-1051 or (612) 624-7906.

The Morbidity and Mortality Weekly Report (MMWR) has recently published a report entitled "Public Health Service Report on Fluoride Benefits and Risks", June 14, 1991. If you are interested in receiving a copy of this report, please send a stamped, self-addressed envelope to our office.

A reprint of the article "Food and Drug Administration Pesticide Program - Residues in Foods - 1990," is now available. This is the fourth in a series of annual reports from the FDA that describe the FDA's pesticide monitoring program and present findings from the monitoring. The 1990 report explains the 3 approaches FDA uses to carry out its pesticide program, regulatory monitoring, incidence/level monitoring, and the Total Diet Study; gives results for Fiscal Year 1990; and compares findings with those for the 3 previous years. If you would like to receive a copy, please send a stamped, self-addressed envelope to our office.

Recently Published:

The Dose Makes the Poison: A Plain Language Guide to Toxicology, Second Edition by Dr. M. Alice Ottoboni.

Dr. Alice Ottoboni recently completed the publication of the second edition of her toxicology book. I highly recommend this book to people who wish to learn more about how chemicals interact with humans (and vice versa). The book costs $24.95 and is available from Von Nostrand Press, P.O. Box 668, Florence KY 41022-0668. Alice has a wonderful, interesting writing style, and the gift to explain complex subjects in very understandable terms. This book should be in every public library.

Recently Completed:

Household Hazardous Waste, a slide/tape program of 73 slides lasting about 20 minutes. This slide set (number 91/108) is available for loan or purchase from Visual Media, University of California, Davis CA 95616. (916) 757-8980. This is a product of our office with the help of Jack Chambers and the rest of the Visual Media crew, and various Environmental Toxicology students during the last couple years. Naturally, I recommend it.


Recently "hit the fan":

The National Cancer Institute Office of Cancer Communications recently released an announcement related to a paper published in the Journal of the National Cancer Institute, Vol. 83, No.17, p. 1226-1231, 1991, titled "Case-control study of canine malignant lymphoma: Positive association with dog owners use of 2,4- dichlorophenoxyacetic acid herbicides." The announcement, along with a question and answer section, details the conclusions of the authors of the paper that dogs whose owners who used 2,4-D herbicides on their lawns had an increased rate of malignant lymphomas. I have a copy of the paper but have not had the opportunity to review it yet. Stay tuned for further information.

Arthur L. Craigmill
Extension Toxicologist