Vol 13 No 1 March 1993


Researchers at the Canadian Centre for Toxicology in Guelph, Ontario, have reported the results of a study designed to test human absorption of 2,4-D from sprayed turf. Total body dose of 2,4-D was determined in 10 volunteers following exposure to sprayed turf 1 hour after application and in 10 volunteers exposed 24 hours after application. The experimental design incorporated various types and amounts of clothing. Each volunteer was exposed to a 2 x 15 meter area of turf for 1 hour, during which the volunteers alternated between walking and sitting or lying on the treated turf. No detectable residues were found in 4-day urine samples supplied by the volunteers except for 3 people who were barefoot and wearing shorts who contacted the turf 1 hour after application. The highest dose was measured in a volunteer who removed his shirt for 30 minutes of the exposure session. No detectable residues were found in volunteers exposed 24 hours after application.

REF: Kansas Pesticide Newsletter, January 18, 1993, Volume 16, No. 1.


Carbon monoxide (CO) poisoning was a major health consequence of a severe storm that struck the Puget Sound region of western Washington state the morning of January 20, 1993. Wind gusts up to 94 miles per hour interrupted electrical power for an estimated 776,000 residents, and during the 4 nights following the storm, temperatures fell to near freezing. Because of the use of alternative sources of energy for indoor cooking and home heating, the risk of exposure to CO increased for many persons. This report summarizes cases of storm-related CO poisoning.

Within 9 hours of the onset of the storm, case patients began seeking care in emergency rooms. Eighteen patients were Asian, 14 were non-Hispanic white, nine were Hispanic, two were of Middle Eastern ancestry and unknown ethnicity, and one was black. Fifty percent of the patients did not speak English, including 11 who were Asian and all nine who were Hispanic.

The source of CO was burning charcoal briquettes in 11 incidents (all involving racial/ethnic minorities), gasoline-powered generators in four, a generator and a propane-powered space heater in one, and an automobile in one.

During the night of January 21, radio stations first broadcast reports of CO poisoning and the danger of using charcoal briquettes, gasoline-powered generators, and propane-powered heaters in poorly ventilated areas; newspaper and television reports appeared during January 22-23. On January 22, one fire department distributed more than 2000 written warnings door-to-door. All reports and warnings were in English only.

Editorial Note: The findings in this report differ from previous descriptions of CO poisoning following winter storms in the northern United States because of the large number of cases involved, especially among non-English-speaking persons.

In Washington, burning charcoal briquettes were a common source of CO, especially for persons who were members of racial/ethnic minorities. Nonstorm-related CO poisoning resulting from indoor cooking with charcoal briquettes has been reported as a problem in Korea and for non-English-speaking residents of the United States. A previous health advisory about the danger of CO poisoning was targeted at Asian immigrants because of their traditional use of briquettes for cooking.

The relation of culture and language to the risk of CO poisoning following this storm is under investigation. However, when such storms occur, public health and safety agencies and other organizations should attempt to provide public health warnings that are prepared in both English and the languages of groups that might be at increased risk because of cultural or linguistic factors.

REF: Morbidity and Mortality Weekly Report (MMWR), February 19, 1993, Vol. 42/No. 6.


During June 1992-January 1993, five children aged 11-18 months in the Los Angeles area died after ingesting iron supplement tablets. This report summarizes preliminary information from an investigation of these cases.

Case 1. A 16-month-old boy died in June 1992 after ingesting 30-35 prenatal iron tablets that had been in a loosely capped container on a table. Prenatal 325 mg ferrous sulfate tablets, with an elemental iron content of 60 mg per tablet, were identified as the toxic agent. Medical treatment was delayed because clinical manifestations were not present initially.

Case 2. An 18-month-old boy died in September 1992 after consuming an estimated 30-40 prenatal iron tablets. Prenatal 325 mg ferrous sulfate tablets, with an elemental iron content of 60 mg per tablet, were identified as the toxic agent. The tablets were in an uncapped bottle on a table.

Case 3. A 12-month-old boy died in November 1992 after consuming an estimated 30 iron tablets. No container was available for confirmation of the strength of the dosage.

Case 4. An 11-month-old girl died in December 1992. A 2-year- old sibling had fed the younger child 30-35 prenatal iron tablets. Prenatal 325 mg ferrous sulfate tablets, with an elemental iron content of 60 mg per tablet,were identified as the toxic agent. The iron tablets were in a box on the floor.

Case 5. A 13-month-old girl died in January 1993 after consuming an unknown number of prenatal iron tablets prescribed for an older sister. Prenatal 325 mg ferrous sulfate tablets, with an elemental iron content of 60 mg per tablet, were identified as the toxic agent. The tablets were spilled on the floor for an unspecified period of time before the child was observed to have them in her mouth.

The prenatal iron supplements ingested in these five cases were red or green disk-shaped tablets with a glossy sugar coating; they are commonly used as an iron supplement for prenatal patients. All of the recovered containers had child-resistant safety caps and a warning that specified the need to keep all medications away from children.

Editorial Note: Iron is the most common cause of pediatric poisoning deaths reported to poison control centers in the United States. During 1991, 5144 ingestions of iron supplements were reported to poison control centers in the United States; 11 were fatal. In addition, 18,457 ingestions of iron in the form of multivitamin or combination preparations were reported; 87% occurred among children aged <6 years. During 1991, consumption of multivitamin preparations in the form of prenatal vitamins with iron caused two additional deaths among children aged 17 and 18 months.

Although a toxic dose of elemental iron is 30 mg/kg, and a fatal dose is typically more than 250 mg/kg, ingestion of doses as low as 60 mg/kg have resulted in death. Although in three cases the iron supplement was a prescription item, the 60 mg per tablet dosage is also available in over-the-counter preparations. Ingestion of as few as five or six tablets of a high-potency preparation could be fatal for a 10- kg (22-lb) child.

Iron poisoning is characterized by four clinical signs. The first stage (with a duration of up to 6 hours after ingestion) is characterized by acute onset of gastrointestinal symptoms (i.e., vomiting and diarrhea) that may progress to shock, coma, seizures, and death. During stage two (from 6 to 24 hours after ingestion) patients may be asymptomatic; however, evaluation and treatment for iron poisoning should not be delayed. During stage three (from 12 to 48 hours after ingestion) there may be hepatic and renal failure and cardiovascular collapse. Stage four (from 3 to 4 weeks after ingestion) may include gastrointestinal obstruction and hepatic cirrhosis.

From 1982 through 1992, three children died from iron toxicity in Los Angeles County. Thus, the five deaths in 7 months reported here represent a substantial increase in iron-related deaths. The following measures may help prevent iron toxicity-associated deaths: 1) iron supplements should be prescribed in limited amounts and dosages and when medically indicated; 2) health-care providers and others who prescribe or dispense iron supplements should emphasize to parents the hazards of unintentional iron consumption by children; and 3) adults should be instructed in the proper use of child-resistant packages when they receive them. Other considerations include: re-evaluate the effectiveness of child-resistant packaging and warning labels (i.e., tablets packaged in child-resistant individual blister packs may limit the number of tablets a child can access); eliminate the use of sugar coating or attractive colors; and finally, educational efforts should be aimed at persons who use iron supplements and who have young children at home.

REF: MMWR, February 19, 1993, Vol. 42/No. 6.


From December 23-27, a total of 29 persons in six households had reported illness associated with the use of an aerosol leather conditioner. On December 27, the product producer issued a voluntary nationwide recall of this product. Following the public announcement of the recall, the number of preliminary reports of illness associated with use of this spray increased to 400 and involved approximately 550 persons.

Reported symptoms typically began within a few minutes to several hours after applying the conditioner to leather products. Manifestations of the illness most commonly reported included prolonged cough, shortness of breath, and pleuritic chest pain. Many persons also reported headache, malaise, chills, and fever as high as 104 F (40 C). At least three persons exhibited signs of pulmonary infiltrates based on radiographic examination; one person was admitted to a hospital with a diagnosis of adult respiratory distress syndrome. For many persons, the symptoms appeared to resolve in less than 24 hours.

Following publicity, the Centers for Disease Control and Prevention received reports from 17 other states. Following the prompt voluntary recall, by December 31, all cans of the leather conditioner were reported to have been removed from stores and distribution channels. Editorial Note: Preliminary information indicates this outbreak is associated with the u e of Wilsons Leather Protector, distributed nationally by Wilsons, the Leather Experts, headquartered in Minneapolis. Leather Protector is sold nationally at more than 550 stores owned by Wilsons; the stores are operated under several names. This investigation suggested that in most households where persons developed symptoms, the product had been used indoors or in other areas with limited ventilation. The product is packaged in 5-ounce black aerosol cans with red and white lettering. The product is a new formulation of Wilsons Leather Protector and sold exclusively by Wilsons. The product changes involved the propellant (from carbon dioxide to propane), the solvent (from 1-1-1 trichloroethane to isooctane), and an active ingredient (from 1% FC-905 to 1.2% FC-3537 [which are both fluoroalkyl polymers in different solvents]).

The most commonly reported symptoms suggest an acute chemical pneumonitis or a hypersensitivity pneumonitis. Some patients have had symptoms consistent with inhalation fevers such as polymer-fume fever (e.g., chest tightness, headache, shivering, fever, weakness, and shortness of breath). This syndrome is caused by inhalation of fumes containing pyrolytic products released when fluoropolymers are heated to high temperatures. In most cases, patients with polymer-fume fever have been cigarette smokers, however, it is also possible that an unknown contaminant in the leather spray may be causing this illness.

Consumers should be warned against using Wilsons Leather Protector. In addition, any spray containing polymers or solvents should be used only in areas where there is adequate ventilation. Further consumer information regarding this product is available from the Consumer Product Safety Commission Hotline, 800-638-2772.

REF: MMWR, January 8, 1993, Vol. 41/Nos. 52 & 53.

COCCIDIOIDOMYCOSIS -- United States, 1991-1992

During 1991, reported cases of coccidioidomycosis (i.e., valley fever) in California increased more than three-fold over the annual number of cases reported since 1986; during 1992, the number of reported cases increased 10-fold. Coccidioidomycosis, a fungal disease caused by Coccidioides immitis, is endemic in certain parts of Arizona, California, Nevada, New Mexico, Texas, and Utah. Sporadic cases occur each year in parts of the United States in which the disease is not endemic and may present diagnostic difficulties and laboratory hazards because health-care workers may be unfamiliar with coccidioidomycosis. Outbreak in California

In 1991, 1208 new cases of coccidioidomycosis were reported to the California Department of Health Services (CDHS), compared with an average of 450 cases per year during the previous 5 years. Of these cases, 80% were reported from Kern County, where coccidioidomycosis is known to be endemic and where the county health department serves as a referral laboratory for coccidioidomycosis serologic tests.

Nonendemic Coccidioidomycosis

Although no national surveillance system exists for coccidioidomycosis, each year several cases are reported to CDC that occur outside of the southwestern United States, where the disease is endemic. Three such case-reports follow.

Case 1. In September 1992, a 24-year-old black man from Virginia developed pulmonary coccidioidomycosis 2 weeks after driving through California.

Case 2. In August 1992, a 13-year-old black male from Georgia developed symptoms that included hoarseness, noisy breathing, and difficult breathing 2 months after visiting southern California, Nevada, and northern Mexico.

Case 3. In October 1992, a 30-year-old black woman, who had previously resided in Arizona, was hospitalized in Florida because of chronic disseminated coccidioidomycosis.

Editorial Note: C. immitis resides in the soil in certain parts of the southwestern United States, northern Mexico, and a few other areas in the Western Hemisphere. Infection is caused by inhalation of airborne, infective arthroconidia, one stage in the organism's life cycle. In the host, these conidia convert into endosporulating spherules, the organisms's other morphologic form. The disease is not transmitted from person to person. The current outbreak in California may be associated with weather conditions, especially a recent protracted drought followed by occasional heavy rains. The magnitude of the outbreak may be partially explained by recent migration of persons previously unexposed to C. immitis into areas of California where coccidioidomycosis is endemic. This outbreak illustrates how factors such as weather and demographic changes can affect the emergence of public health problems from infectious diseases.

Approximately 60% of persons infected with C. immitis remain asymptomatic. Symptoms range from mild influenza-like illness to serious pneumonia to widespread dissemination. Dissemination outside the lungs occurs in approximately 0.5% of infections. Coccidioidal meningitis is a particularly serious manifestation of disseminated coccidioidomycosis. Among persons who become infected, blacks, Filipinos and other Asians, Hispanics, and women who acquire the primary infection during the later stages of pregnancy are at increased risk for disseminated coccidioidomycosis. Extrapulmonary coccidioidomycosis is an acquired immunodeficiency syndrome-defining illness when it occurs in a person with evidence of infection with human immunodeficiency virus.

Infection with C. immitis in persons residing outside coccidioidomycosis-endemic areas may occur as a result of travel in these areas, laboratory exposure, or inhalation of contaminated fomites (e.g., soil, cotton, packing material, or museum artifacts) taken from areas with endemic coccidioidomycosis.

Clinicians should consider the diagnosis of coccidioidomycosis in persons with undiagnosed respiratory illnesses or syndromes that could represent disseminated coccidioidomycosis for those who reside in, or have traveled to, areas where the disease is endemic, or who have had occupational exposure to C. immitis. Laboratory personnel should be reminded of necessary safety precautions when handling C. immitis.

REF: MMWR, January 22, 1993, Vol. 42/No. 2.


The recent report of the U.S. Environmental Protection Agency on the respiratory health effects of passive smoking and the known adverse effects of active smoking emphasize the need to quantify the exposure of the U.S. population to tobacco smoke. Measurements of cotinine (a nicotine metabolite) in serum, urine, and saliva have been used effectively to quantify exposure to tobacco smoke. As part of the Third National Health and Nutrition Examination Survey (NHANES III), CDC's National Center for Environmental Health and National Center for Health Statistics is measuring serum levels of cotinine to assess exposure to tobacco smoke by persons in the United States aged **4 years. This report presents preliminary findings on the first 800 persons in this survey of tobacco-smoke exposure.

CDC developed an isotope dilution-liquid chromatography-tandem mass spectrometry method to measure serum cotinine at levels as low as 0.030 nanograms per milliliter (ng/mL). Serum samples have been analyzed for cotinine for 800 persons aged 4-91 years. All (100%) of the 800 persons tested had measurable levels of cotinine in their serum. For the 800 persons tested, serum cotinine levels ranged from 0.030 to 650 ng/mL, a span of more than four orders of magnitude.

Editorial Note: Cotinine in serum results from exposure to nicotine. The most common sources of nicotine exposure are active smoking and exposure to environmental tobacco smoke (ETS). Appropriate interpretation of serum cotinine levels must also consider other nicotine sources including nicotine gum, nicotine dermal patches, chewing tobacco, and snuff. Investigators have found that levels of serum cotinine greater than approximately 10-15 ng/mL characterize smokers, and serum cotinine levels less than this amount characterize nonsmokers.

REF: MMWR, January 22, 1993, Vol. 42/No. 2.



A substantial proportion of mortality among young persons is preventable. National vital statistics were used to establish a baseline for the surveillance of rates of years of otential life lost before age 65 (YPLL <65) in the United States. Rates of YPLL <65 were calculated for 1986 through 1988 for leading causes of preventable death, by race, Hispanic origin, and sex. U.S. racial and ethnic populations differed widely in YPLL <65. Among males, the rate (per 1,000 population <65 years) of YPLL <65 was highest for non-Hispanic blacks (140.0), followed by American Indians/Alaska Natives (100.9), Hispanics (74.3), non-Hispanic whites (68.3), and Asians/Pacific Islanders (38.2). Among females, the rate was highest for non-Hispanic blacks (73.7), followed by American Indians/Alaskan Natives (52.0), non-Hispanic whites (35.7), Hispanics (32.9), and Asians/Pacific Islanders (23.2). For non-Hispanic blacks, the high rate of YPLL <65 was due to increased rates for all causes of death considered, particularly homicide. The high rate for American Indians/Alaskan Natives was due principally to deaths from four causes: unintentional injuries, cirrhosis, suicide, and diabetes. Asians/Pacific Islanders had low rates for most causes of death. In setting health-care priorities and prevention strategies to reduce the large racial-ethnic gap in early deaths, it is essential to recognize the differences in causes of premature mortality among sex, racial, and ethnic populations. Periodic reassessment of YPLL <65 among these groups provides a simple, timely, and representative means of conducting surveillance to measure the impact of intervention strategies on a national basis.


Mortality statistics based on crude and adjusted death rates fail to assess the burden of deaths among younger persons, since these rates are dominated by deaths of the elderly. The measure of years of potential life lost before some selected age -- most often 65 (YPLL <65) -- gives a more accurate picture of premature mortality by weighting deaths occurring at younger ages more heavily than those occurring at older ages. Periodic assessment of YPLL <65 is a useful means of surveillance for setting priorities, guiding prevention program design, and planning the delivery of health-care services.

REF: MMWR, November 20, 1992, Vol. 41/No. SS-6.


In September 1992, the Centers for Disease Control's (CDC) National Institute for Occupational Safety and Health (NIOSH) began quarterly reporting of adult elevated blood lead level (BLL) data from state-based surveillance programs. To support these efforts, NIOSH has established the Adult Blood Lead Epidemiology and Surveillance (ABLES) program. In this report, 17 states are participating in the quarterly reporting (Table 1).

NIOSH surveillance research recently identified excessive lead exposures in the construction industry among bridge workers, workers conducting home paint removal, and workers performing paint removal on commercial superstructures such as water tanks. In October 1992, the U.S. Department of Labor was directed by Congress to issue an interim final regulation covering occupational exposures to lead in the construction industry; this interim standard is to be published in April 1993. In addition to setting standards for construction workers, the regulation directs the U.S. Environmental Protection Agency, the U.S. Department of Housing and Urban Development, CDC, and other federal agencies to ensure that workers engaged in lead paint removal are properly trained and that contractors engaged in such activities are certified.

TABLE 1. Number of reports of elevated blood lead levels (BLLs) in adults -- 17 states,* third quarter, 1992

Reported BLL (ug/dL) Third quarter, 1992 Cumulative, 1992
25-39 3,048 9,384
40-49 709 2,245
50-59 234 614
**60 128 319
TOTAL 4,119 12,562

*Alabama, California, Colorado, Connecticut, Illinois, Iowa, Maryland, Massachusetts, Michigan, New Hampshire, New Jersey, New York, Oregon, South Carolina, Texas, Utah, and Wisconsin.

REF: MMWR, February 5, 1993, Vol. 42/No. 4.


On July 2, 1991, during routine monitoring, the Food and Drug Administration (FDA) isolated toxigenic Vibrio cholerae 01, serotype Inaba, biotype El Tor from oysters and intestinal contents of an oyster-eating fish taken from closed oyster beds in Mobile Bay. This isolate was indistinguishable from the Latin American epidemic strain and differed from the strain of V. cholerae 01 that is endemic to the Gulf Coast.

On July 18, Gulf Coast residents were advised by the Mobile County Health Department and the Alabama Department of Public Health (ADPH) to wash their hands after handling raw seafood and to eat seafood well cooked. FDA and ADPH initiated biweekly sampling of oysters from Mobile Bay, and on July 22 and September 16, 1991, the Latin American strain was again isolated from oysters. The Mobile Bay oyster bed remained closed to harvesting until November 4, 1991. On June 15, 1992, toxigenic V. cholerae 01 was again isolated from a sample of oysters and the area was closed to harvesting. On August 19, 1992, the oyster beds were reopened after samples were repeatedly negative. No toxigenic vibrios have been isolated since June 1992.

Editorial Note: No cases of cholera have been identified in Alabama in recent decades. Introduction of toxigenic vibrios into Mobile Bay may have resulted from discharge of contaminated ballast water from freighter vessels. To control buoyancy, ships take on large volumes of ballast water in a harbor and discharge it in other locations. This process may have been responsible for the introduction of other harmful species such as the zebra mussel in the Great Lakes. In 1991, the FDA isolated toxigenic V. cholerae 01 from the ballast tanks of ships that had originated form Latin American ports and arrived at Mobile Bay. To reduce the risk of introducing harmful organisms through contaminated freighter ballast water, the International Maritime Organization has recommended that freighters empty and refill their ballast water tanks twice on each voyage while in international water. The efficacy of ballast water exchanges in reducing the level of contamination of ballast water has not been assessed. Although ballast water exchanges may decrease the risk of introduction of V. cholerae O1 from other ports into U.S. harbors, this approach would not eliminate the strain already endemic in U.S. Gulf Coast waters.

Since 1973, 91 cases of cholera have occurred in the United States that were unrelated to international travel. Most of these followed consumption of raw or undercooked seafood harvested from the U.S. Gulf Coast contaminated with the Gulf Coast strain of V. cholerae 01. The risk for transmission of cholera can be reduced by avoiding consumption of raw or undercooked seafood.

REF: MMWR, February 12, 1993, Vol. 42/No. 5.


During January 1-29, 1993, 230 persons with culture- confirmed infection with Escherichia coli O157:H7 resulting in bloody diarrhea and, in some cases, hemolytic uremic syndrome (HUS) were reported in the state of Washington. Culture results are pending for 80 others with similar illnesses. Preliminary investigations by public health agencies linked cases to consumption of hamburgers from one fast-food restaurant chain. E. coli O157:H7 has been isolated from epidemiologically implicated lots of ground beef; an interstate recall was initiated by the restaurant on January 18. Meat from the same lots of ground beef had been distributed to at least three other western states in which increased numbers of cases of bloody diarrhea have been reported. The Centers for Disease Control, the U.S. Department of Agriculture, state and county health departments, and state agriculture investigators are investigating whether cases of bloody diarrhea in the other states are linked to consumption of meat from the same lots of ground beef and are determining the possible sources of the contaminated meat.

Editorial Note: E. Coli O157:H7 is an emerging infectious agent first linked to human illness in 1982; its importance as a human pathogen appears to be increasing. Infection with E. coli O157:H7 may result in a spectrum of illnesses, including mild diarrhea, severe bloody diarrhea (hemorrhagic colitis), HUS often leading to acute renal failure requiring dialysis, and death. Infection with this organism has been associated with consumption of contaminated beef and raw milk and through person-to-person transmission by the fecal-oral route. Measures to prevent transmission include thorough cooking of beef, pasteurization of milk, and careful handwashing with soap. In particular, ground beef should be cooked until it is no longer pink.

REF: MMWR, February 5, 1993, Vol. 42/No. 4.



Recently, EPA has gone on the record that environmental tobacco smoke is considered to be carcinogenic (not surprising). At a presentation on Environmental Tobacco Smoke at the Society of Toxicology meeting in 1992, Dr. Neal Benowitz from UCSF (Univ of CA San Francisco) presented some of the following information.

For cigarettes, mainstream smoke (MS), which is what the smoker gets (whether they inhale or not..) is very different from sidestream smoke (SS) since the combustion conditions are different. This results in different pH (5.6 for MS, and 7.4 for SS) and different ratios of combustion products. The ratios of SS to MS are: ammonia - 4.6; nitrogen oxides - 3.6; benzpyrene (a known carcinogen) - 3.7; tars - 2.1; particulates - 3.3; carbon monoxide - 2.5; and nicotine - 1.8. These combustion products may build up such that a person may "smoke" the equivalent of 1/4 cigarette per hour in a smoky room. This exposure was estimated by measuring nicotine and other metabolites in the urine of nonsmokers exposed to SS.


The Centers for Disease Control recently lowered the maximum acceptable blood lead level in children from 25 ug/dl to 10 ug/dl. A recent study in Washington, D.C. showed that 21% of children tested had levels above 10 ug/dl (the new standard) but only 1.5% of them were above 25 ug/dl. Some individuals question this new, lower level for defining "lead poisoning" noting that the great increase in "lead poisoned" children will divert scarce resources from those at greatest risk. Other argue that the evidence supporting the lowered level is consistent, thus the new level is justified. This should continue to be an interesting area of controversy during the next several years since the cost of screening, treatment, and environmental lead remediation are high.

REF: Journal Watch, Vol. 10/No. 11, December 1, 1992.


A recent editorial in the Journal of the American Medical Association has endorsed irradiation of high-risk foods to reduce bacterial counts (especially Salmonella and Campylobacter) to acceptable ranges.

During a Food Safety Symposium sponsored by the School of Veterinary Medicine at the University of California, Davis, Dr. Craig Hedberg from the Minnesota Department of Health reported on several studies in which he was personally involved. In one of these studies, the epidemiologists began to suspect that low-level microbial contamination of widely distributed food products may be responsible for geographically dispersed outbreaks of food poisoning. In a 1989 outbreak of Salmonellosis from contaminated mozzarella cheese, at least 164 individuals became ill from eating cheese which contained from 0.36 to 9.1 organisms per gram.

Another investigation traced Shigellosis caused by contaminated airline food. This incident was identified because 65 members of the Minnesota Vikings football team and staff were among those affected! Dr. Hedberg noted that there have been very few incidents of foodborne illness reported from commercial airline food, but also noted that it was very difficult to identify such occurrences because of the mobility of passengers, and that no one has looked at this possibility very closely.

A ten year review of outbreaks of Campylobacter enteritis found that 75% of them occurred in children during field trips to dairy farms where the children were given raw milk to drink.

REF: Food Chemical News, December 14, 1992.


A continuing study of people affected by "Oil Disease" in Taiwan has showed that children who were affected in utero show signs of poor cognitive development. "Oil Disease" was caused by contamination of cooking oil with polychlorinated biphenyls (PCBs). The outbreak occurred in 1979 and involved 2000 people, some of whom ingested the contaminated oil for 9 months and may have consumed up to 1 gram of PCBs resulting in blood levels of 40-60 ppb (10-20 times the background level). PCBs are very fat soluble and are stored in fatty tissues from which they are excreted very slowly. The children in the study were born to exposed women for up to 6 years after exposure. The children scored lower than age matched controls using two intelligence tests when they were 4-5, and 6-7 years old.

REF: Food Chemical News, December 14, 1992.


The Food and Drug Administration recently issued a warning about chaparral herbal products stating that such products should not be consumed. Chaparral is made from Larrea tridentada (Creosote Bush) and may be used in tablets, teas, and capsules. Seven cases of severe disease have been associated with the use of this product.

REF: Food Chemical News, December 14 and 21, 1992.


A National Academy of Sciences committee report on the above has been expected for some time, and may actually be available within the next couple of months. The report is eagerly anticipated by some, and greatly feared by others. Security surrounding the report has been very tight and rumors abound. Stay tuned for more information after the report is released and we have a chance to review it.

REF: Food and Chemical News, December 14, 1992


Nitrosamines are considered to be carcinogenic to humans, and they have been found in beer and other barley malt beverages. The source of nitrosamines appears to be dimethylamine which is "biosynthesized during germination and in the early stage of kilning in the malt manufacturing process." Commercial malt was found to contain 0.4-9.4 ppm dimethylamine, and beer contained about 10% of the amount found in malt.

REF: Food Chemical News, December 21, 1992.


Yep. The Joint Expert Committee on Food Additives (JECFA) of the FAO/WHO issued a report about cyanogenic glycosides in foods and recommended that steps be taken to insure such compounds are limited as much as possible. Foods which contain these glycosides include: cassava (manioc), bamboo shoots, almonds and stone fruits, and some types of beans. During food preparation and digestion these may release hydrogen cyanide. Our bodies have the ability to metabolize small quantities of cyanide without adverse effect. Higher levels have been associated with chronic neurological damage, thus the concern of JEFCA. As noted in the report, there are many unsafe food sources, but there are safe ways of preparing them for consumption. JEFCA is also concerned that as new plant cultivars are developed, there may be increases in naturally occurring toxins which must be considered.

REF: Food Chemical News, February 22, 1993.


In the February 26, 1993 issue of Science, Vol. 259, there was an editorial on Pesticides and Food. The author discusses some of the results of the rigid enforcement of the Delaney Clause. If anyone would like to obtain a copy please call or write to our office.


The popularity of microwave ovens has introduced a new breakfast hazard. According to the New England Journal of Medicine, microwaved egg yolks have, when pierced with a fork, exploded and caused serious burns to the face and eyes. To avoid creating a fowl explosion, microwave manufacturers advise: Never use a microwave to hardcook or reheat an egg in the shell. When poaching an egg in the microwave, always cover the container according to manufacturer's instructions, and always wait at least one minute after cooking to puncture the yolk.

REF: The Health Letter (published by the UC Davis Medical Center), Fall 1992.


The USDA Weed Science Lab at Beltsville, MD, is investigating the virtues of the weed purslane as a potential new vegetable crop. Scientists there have confirmed that Portulaca oleracea contains more of one omega-3 fatty acid than any other green leafy vegetable investigated to date. A 100-gram serving has about 300 to 400 milligrams of alpha- lineolenic acid - 10 times more than spinach. Omega-3 fatty acid has been linked in some studies to reduced heart disease and other health benefits. The researchers also found that the plants contain higher levels of Vitamin E than spinach.

REF: Kansas Pesticide Newsletter, February 12, 1993, Vol. 16/No. 2.


"Levels of many of the targeted pesticides in soils outside the home were lower than those found in house dust," according to preliminary results of the EPA house dust/infant pesticides exposure study delivered to the American Chemical Society (ACS) meeting in Atlanta, GA. An EPA researcher stated that: "House dust collected from carpets showed the highest levels of contamination. In older homes, pesticides banned long ago were still present in house dust. Although the preliminary results of this limited study do not permit an accurate assessment of the quantities of house dust small children may ingest, they do suggest that ingestion of house dust may be a major route of exposure to pesticides for infants and toddlers. Residues of many pesticides are found in and around the home even when there has been no known use of them on the premises. Small children spend much of their time on the floor and are very likely to come into intimate contact with yard dirt and lawns. They also exhibit frequent hand-to-mouth contact and pica tendencies. It has been estimated that children under the age of five ingest 2.5 times more soil from around the home than adults, yet they possess only about 20% of the body weight."

Another paper presented noted development by scientists at the California Department of Food and Agriculture (CDFA) of a method to estimate indoor dermal pesticide exposure: the CDFA/Jazzercize method. They applied the method to a commonly used home fogger (containing chlorpyrifos). The paper stated: "Using air data collected concurrently with the dermal study, and allowing for a transfer of skin residues on the hand to mouth (for example, via eating) estimated absorbed dosage for an adult and a child in constant motion for six hours on a treated carpet were seven micrograms of chlorpyrifos per kilogram of body weight for the adult, and 25 ug/kg for the child. The study concludes that under labeled use conditions fogger products of this type result in lower than previously estimated levels of exposure, and should pose no significant risks to consumers."

REF: Pesticide & Toxicology Chemical News, 1992, Vol. 19/No. 25.


If you or your clients are seeking information in regard to pesticide toxicity, environmental effects, chemical characteristics, or appropriate use, the National Pesticide Telecommunications Network (NPTN) can be of assistance. NPTN can provide factual information on these and other topics involving pesticides.


We have received a set of Issues Papers produced by the Health Protection Branch of the Department of National Health and Welfare in Canada. The topics are listed below. If you would like a copy of any of these papers, please write or call.


Health Risks of "Dioxins": A Review of Environmental and Toxicological Considerations. Vet Hum Toxicol, 35(1) February 1993.

Allelochemicals in Plant Foods and Feedingstuffs: 1. Nutritional, Biochemical and Physiopathological Aspects in Animal Production. Vet Hum Toxicol, 35(1) February 1993.


E. Coli O157:H7 Food Poisoning

The recent outbreak of E. coli O157:H7 food poisoning from hamburgers at a fast-food chain in the state of Washington has created concern over the safety of meat. Over 300 people have developed enteritis or hemorrhagic enteritis, and some children have developed hemolytic uremia syndrome in this outbreak. At least two deaths have been reported. The Food Animal Concerns Trust (FACT, an animal rights activist group) released statements recently about the pressing need to control food-borne pathogens at their source on the farm and that this outbreak is just more evidence against intensive animal agriculture. The hamburger is believed to have come from California cows.

Food experts say that the outbreak points to the need for a better meat inspection system and cooking processes. The Center for Science in the Public Interest called for a new department for consumer protection because USDA is an advocate for the meat industry and not for consumers. FSIS-USDA personnel say that the department must take some drastic measures to insure that subsequent outbreaks do not occur. These may include increased monitoring of slaughterhouses, safe handling instructions on meat packaging, or changes in condemnation procedures for products contaminated with pathogens. They have also stated that no other food product is inspected as carefully as meat and poultry and that people face a greater risk of illness from hamburgers cooked on the backyard grill than they do from fast-food hamburgers. They have stated that a foolproof method to ensure safe meat is to cook the product thoroughly.

Washington had passed new standards to cook hamburger to 155o, but the fast-food chain admitted to following the old standard, the federal standard, of 140o. Federal officials are considering the new standard as a minimum for the nation. Given this new outbreak and the events that are unfolding with regard to food safety, what do we already know about this pathogen, its pathogenesis, and its epidemiology? And, why do we still have food poisoning outbreaks due to E. coli O157:H7?

The Bacterium

There are numerous strains of E. coli bacteria, many of which live as commensals in the intestinal tract of humans and other animals. Some strains have the ability to produce toxins which can cause disease. E. coli O157:H7 was first recognized as a pathogen in 1982.

Dr. Richard Wilson, Director and researcher at the E. coli Reference Center, Department of Veterinary Science, Penn State, has been studying the genetics of the various types of E. coli, in particular, O157:H7. This strain of E. coli is an emerging pathogen and appears most closely related to enteropathogenic E. coli isolated from children in the early part of the century."

E. coli O157:H7 has one or two verotoxins. The genes controlling their production are bacteriophage encoded. Adhesion of the bacteria to intestinal cells may be an important part of its pathogenesis, and the organisms are probably not invasive.

The Disease Syndromes

People infected with E. coli O157:H7 often develop severe diarrhea with abdominal cramps. Blood streaks or gross blood are often seen in the stool (hemorrhagic colitis) or the diarrhea may be nonbloody. There may be a low-grade fever and all symptoms usually resolve after a few days. Infection and shedding may occur without symptoms.

A serious complication of infection occurs in children and rarely in adults. Hemolytic Uremia Syndrome (HUS) affects the kidneys and blood-clotting system. It may be mild or severe. It is a triad of acquired hemolytic anemia, thrombocytopenia, and renal failure. In severe cases, kidney function is reduced and dialysis is often necessary. Children may have a bleeding tendency and anemia and require transfusions. Most people with HUS recover. It is not clear why some people develop HUS while most do not. Females are more likely than males to develop HUS after infection with O157:H7. HUS also may result from other infections.

Thrombotic thrombocytopenic purpura has been associated with this bacterium in two adult patients who had bloody diarrhea the week before. This disease syndrome is similar to HUS except that the central nervous system is involved. Patients often develop clots in the brain.

The diagnosis of E. coli O157:H7 hemorrhagic diarrhea can be made from stool cultures, however, routine culturing techniques will not identify this particular strain. Hemolytic uremia syndrome is diagnosed by a number of tests including kidney function tests, blood clotting tests, and blood counts.

Treatment of the hemorrhagic diarrhea is by supportive therapy. Antimicrobials and antidiarrheal agents are usually not recommended. Once a child has been infected with the bacterium, there is no known medical treatment that will prevent the development of HUS. Fortunately, the majority of children do not develop this complication.

Although rabbits, pigs, and other laboratory animals have been experimentally infected with this organism, no good animal model exists that produces the symptoms of hemorrhagic colitis and HUS.

The Epidemiology

E. coli O157:H7 have been found in samples of raw hamburger and raw milk. Cooking will kill the bacteria, and there is no risk of illness if the meat is thoroughly cooked. Bacteria may be spread from one person to another if there is inadequate hygiene.

The first reported outbreak due to this organism was from Oregon in 1982. A few months later, in Michigan, a similar set of outbreaks occurred. Illness was epidemiologically associated with hamburgers at the same fast-food chain. At this time, the USDA laboratory and the E. coli Reference Center at Penn State had no reports of O157:H7 from animals in the US. The enteric laboratory at the Centers for Disease Control had reported only one isolate out of 3,000 serotyped since 1973. An outbreak in a nursing home in 1984 was also linked to hamburger.

Additional outbreaks have been associated with ham, turkey, or cheese sandwiches and raw milk when children on a farm visit were supplied with bulk tank milk. Two cases of HUS were linked to drinking raw milk in 1986. The bacterium was isolated from healthy heifers from both implicated farms. In an intensive study by CDC and the USDA, O157:H7 was isolated from primarily heifers and calves, demonstrating that cattle may serve as reservoirs. The bacteria are apparently excreted transiently in cattle. The investigators found it curious that products of apparently healthy animals may become contaminated and that dairy herds are more likely to harbor the organism than beef herds. In a Canadian study of risk factors for the disease in an urban community, no increased risk could be detected for ground meat consumption although an association between ingestion of undercooked meat and infection was found.

Other outbreaks in 1987 and 1988 in Utah, Wisconsin, and Minnesota, were associated with roast beef and precooked hamburger patties. Frozen patties may be more of a risk factor since a study done in 1977 showed that reduction of bacterial viability by cooking was more readily accomplished in 12-day refrigerated patties than in frozen hamburger patties.

Additional outbreaks of hemorrhagic colitis have occurred in at least four nursing homes. In addition, person-to-person transmission was documented in Washington's first year of disease surveillance in 1987. Although outbreaks of the disease are possible from a common source, sporadic cases of this illness are widely distributed both in Canada and the US.

In an outbreak in Missouri, contaminated municipal water was the source of 240 cases of diarrhea, 85 of which were bloody. E. coli O157:H7 was isolated from 21 stool specimens. There were 34 hospitalizations, three deaths and two cases of HUS.

E. coli O157:H7 is not a reportable disease in Pennsylvania as it has been in the state of Washington since 1987. However, any food poisoning outbreak is reportable to the Pennsylvania Department of Health. It is possible that sporadic cases of disease can be attributed to this agent although no outbreaks of food poisoning due to this organism have been reported in Pennsylvania.

The Veterinarian's Role

The veterinarian is a source of information to his/her clients, whether they be livestock owners or pet owners. The veterinarian is knowledgeable about a wide range of disease problems, especially zoonotic ones. Since cattle may serve as a reservoir of infection of E. coli O157:H7, a veterinarian may serve as a likely source of information.

The main points to stress to clients are:

1. E. coli O157:H7 may be found in asymptomatic, carrier cattle.

2. Milk and raw or undercooked hamburger have been implicated in a number of outbreaks of human illness including bloody diarrhea and hemolytic uremia syndrome.

3. The best means to avoid infection is to drink pasteurized milk and cook all meat thoroughly.

4. Any farmer hosting school groups on his/her farm should refrain from supplying children with raw milk. In addition to E. coli O157:H7, children can pick up other pathogens from raw milk.

5. The potential for person-to-person transmission exists. Good hygiene, including frequent handwashing will help to prevent spread of disease.

6. There are still many questions to be answered about the ecology of the bacteria in cattle herds, the mechanisms by which meat and milk become contaminated, and the potential for herd-based control measures to prevent this public health problem.

References are available on request.

-- Dale A. Moore, MS DVM MPVM, Extension Veterinarian

REF: Penn State Veterinary News, February 1993


Gossypol is a polyphenolic compound that is produced by the cotton plant. It is located primarily in the pigment glands of the cottonseed, but is also found in the roots, leaves, stalk, boll valves, seed hulls, pericarp, and flowers. Species and varieties of cotton plants can differ widely in their concentrations of gossypol in the seed, but most cottonseeds contain between approximately 400 parts per million (ppm) and 20,000 ppm. The gossypol content of the seed is affected by several factors, but it has been positively correlated with rainfall and negatively correlated with temperature. Gossypol levels are believed to be directly related to the insect resistance of the cotton plant. While the mechanism of action of gossypol is not known, problems from gossypol tend to develop in summer wh en the stress of heat and humidity is greatest.

Gossypol exists in two forms: "free" and "bound." Free gossypol is that part of the total gossypol which is soluble in 70 percent acetone and is considered to be the toxic form. The bound form of gossypol is generally considered nontoxic because it is supposedly irreversibly bound to proteins.

The concentration of free gossypol in cottonseed meal is influenced by the method of cottonseed oil extraction. There are currently three methods of extraction in use -- screw pressing, prepressed solvent extraction, and expander solvent extraction. Expander solvent extraction is the mostly widely used method. A fourth method, direct solvent extraction was used in the past, but is no longer utilized. These methods use different temperatures, pressures, and cooking times. High temperatures and pressures favor the formation of stable bonds between gossypol and other molecules.

Representative values of free and total gossypol content for screw pressed, prepressed solvent, and direct solvent extracted cottonseed meal are included in the following table. Free gossypol levels in cottonseed meal following expanded solvent extraction average approximately 0.1 percent (1000 ppm).

Although the total gossypol content did not differ greatly, the physiologically active free gossypol content was approximately six times greater in the direct solvent extracted cottonseed meal compared to the screw pressed or prepressed solvent extracted cottonseed meal.

There are several published reports of gossypol toxicity in calves and swine, and non-ruminants (e.g., veal calves) are generally considered to be much more susceptible to gossypol than ruminants. There is a very limited number of published studies involving gossypol in dairy cows. An article by S.A. Smalley and E.J. Bicknell which appeared in the Compendium on Continuing Education for the Practicing Veterinarian covered a suspected gossypol toxicosis in six dairies in the Phoenix area in the late spring to summer of 1980. All herds in which deaths occurred were fed 6 to 10 pounds of ammoniated cottonseed per head per day. The one herd that developed severe reproductive problems was fed 8 pounds of cottonseed and 3 pounds of cottonseed meal per head per day.

Gossypol is also a well-established male infertility drug. Studies have shown that feeding free gossypol at approximately 5 to 6 mg/kg of body weight per day for at least two months will produce significant histologic changes in the seminiferous tubules. These changes indicate that gossypol has detrimental effects to the spermatogenic tissues and associated cells of bulls.

Gossypol levels in milk, liver, and plasma of dairy cows were obtained in a study by T.O. Lindsey et al. (Journal of Dairy Science, 1980). In this study, two groups were fed approximately 3.6 and 24.2 g of free gossypol per day for 14 weeks and the gossypol levels in milk were below the minimum detection limit of 0.5 ppm. The mean levels of total gossypol in the liver for the two groups were 139 and 230 ppm. After five weeks, the mean bound gossypol levels in plasma plateaued at approximately 1.6 to 1.9 ppm in both groups.

In a study by Morgan et al. (1990), five lambs fed 409 mg of gossypol per day all died within 30 days and had an average of 86 ppm of free gossypol in the liver. The livers of these lambs had higher levels of gossypol than the kidney. There were no significant levels of free or bound gossypol in the skeletal muscle of any of the lambs.

These levels of free gossypol in the liver, kidney, milk, muscle, and plasma from these two studies were less than the 450 ppm of free gossypol allowed in modified cottonseed products intended for human consumption (under Title 21, Part 172.894 of the Code of Federal Regulations).

Several researchers have made recommendations on levels of gossypol in feed. In an article published in 1989, S.E. Morgan recommended that calves, lambs, and possibly other ruminants under 4 months of age should not receive more than 100 ppm of free gossypol in the feed. L.M. Hudson et al. recommended that in young cattle, in which the rumen is not mature, total gossypol concentrations in feed should be less than or equal to 500 to 1000 ppm. A study by T.O. Lindsey et al. indicated that dairy cows consuming an average of 3.6 g of free gossypol per day did not develop signs of gossypol toxicity. Several researchers have recommended limiting the consumption of cottonseed products to 6 pounds (2.7 kg) per cow per day. If a dairy farmer limits the consumption of cottonseed products to 2.7 kg per cow per day and assumes that cows can safely consume 3.6 g of free gossypol per day, then cottonseed products containing less than 1333 ppm of free gossypol would not be expected to produce any adverse effects in dairy cows.

Since gossypol toxicity in dairy cows has been associated with hot weather, it may be prudent to further restrict the use of cottonseed products in the ration during periods of excessive heat.

FDA handles cases of gossypol contamination on a case-by-case basis. The Agency has not established regulatory guidance levels for gossypol in cattle feed, meat, or milk. A list of references for this presentation are available from the FDA Veterinarian.

REF: FDA Veterinarian, Jan/Feb 1993, Vol. VIII/No. 1.


Monensin, lasalocid, salinomycin, narasin, and maduramicin are carboxylic ionophores intended for use as anticoccidial drugs for poultry and as growth promotants for ruminants. Generally, ionophores have been found safe and effective in the target animals receiving recommended dosage levels. However, toxic syndromes can result from overdosage and misuse situations. More information and reports of adverse reactions are available for monensin than the other ionophores because of monensin's longstanding and widespread use in the poultry and livestock industries. Care must be exercised in the diagnosis of ionophore toxicoses since clinical signs and lesions are not pathognomonic. However, a feed-related problem characterized clinically by anorexia, diarrhea, dyspnea, ataxia, depression, recumbency and death, and pathologically by focal degenerative cardiomyopathy, skeletal muscle necrosis, and congestive heart failure may warrant a presumptive diagnosis of ionophore toxicity. Confirmatory diagnosis will require considerations of differential diagnoses and laboratory assay to determine the specific ionophore involved. Presently, there is no antidote or treatment for toxicoses induced by the ionophores. Judicious use, avoidance of overdosing, and adherence to species recommendation will help prevent the occurrence of adverse effects associated with this class of compounds.

REF: Penn State Veterinary News, February 1993