COOPERATIVE EXTENSION UNIVERSITY OF CALIFORNIAENVIRONMENTAL TOXICOLOGY NEWSLETTER

COOPERATIVE EXTENSION UNIVERSITY OF CALIFORNIA
ENVIRONMENTAL TOXICOLOGY NEWSLETTER

NPTN is a toll free telephone service available to provide a variety of accurate, impartial information about pesticides to anyone in the United States. The service operates 24 hours a day, 365 days a year. It is funded by the U.S. EPA and operates from the Texas Tech University Health Sciences Center, School of Medicine at Lubbock, Texas.

The general public is also provided pesticide information ranging from: product information, protective equipment, safety, health and environmental effects, clean-up procedures, disposal, regulatory laws, etc. The NPTN hotline number is 1-800-858-7378.

Reprinted from Nov. 1, 1985 Pesticide newsletter of Ohio State University. As reported in Cooperative Extension Service Massachusetts Pesticide News, Volume 10(3), March, 1986.

Note: This number can serve as a source of information to you and your clientele. Try it and see if it fills your needs. I would appreciate feedback from you about it.

At 4 a.m., July 4, 1985, three adults who ate a solid green watermelon purchased in Oakland, California, had rapid onset of nausea, vomiting, diarrhea, profuse sweating, excessive tearing, muscle fasciculations, and bradycardia (slow heartbeat). The most severely ill was a 59-year-old woman who had been receiving digoxin and who, on examination, had a heart rate of 32 and 4-second periods of asystole (no heartbeat). The treating physician diagnosed cholinesterase-inhibitor poisoning, and the patient responded rapidly to atropine. The California Department of Health Services (CDHS) had been alerted the day before by Oregon State Health Division officials of similar, although milder, clusters of illness in Oregon associated with ingestion of striped watermelons, possibly of California origin. CDHS notified the San Francisco Bay Area Regional Poison Control Center to be alert for watermelon-associated illness. When the attending physician consulted the Poison Control Center, CDHS was alerted to the outbreak in California.

CDHS contacted 10 California poison-control centers, 20 selected emergency rooms, and a county health department and identified 12 additional cases in different areas of the state. Later on July 4, Oregon officials reported that aldicarb sulfoxide (ASO) had been detected in several melons associated with similar illnesses. ASO is the primary toxic metabolite of aldicarb (TemikR), a systemic pesticide not registered in the United States for use on watermelons. In the melon associated with the index cases in California, ASO was found at 2.7 parts per million.

At 1 p.m. that same day, CDHS ordered an immediate statewide embargo on watermelon sales and issued state media advisories recommending that persons refrain from eating watermelons. Because watermelons had become so intermingled in the distribution chain, melons harvested in fields thought to be contaminated could not be separated from other melons. Therefore, on July 7, it was decided to destroy all watermelons in the California distribution chain.

Between July 4 and July 8, CDHS developed a case definition. All local health departments and poison-control centers in California participated in a surveillance program for acute illnesses related to melon ingestion. In addition to establishing the extent and severity of illnesses that occurred before July 4, surveillance was continued for illnesses related to melons stickered and presumed to be in compliance with a California Department of Food and Agriculture testing program and sold after July 10. Active surveillance continued until August 31, although case reports were received through September 30. A total of 1,350 cases were reported from all regions of California and were classified as follows: before July 10, 1,005 reports were received __ 493 (49%) probable cases, 269 (27%) possible cases, and 195 (19%) unlikely cases; for 48 (5%), information was incomplete. For July 10 and after, 345 reports were received __ 197 (57%) probable cases, 101 (29%) possible cases, and 40 (12%) unlikely cases; for seven (2%), information was incomplete. There were 18 reports with date of illness missing. The majority (61%) were one-person incidents. Approximately 22% of the illnesses were two-person clusters, 10% were three-person clusters, and 3% were four-person clusters. The remainder involved clusters of five, six, nine, and 13 persons.

The most severe signs and symptoms included seizures, loss of consciousness, cardiac arrythmia, hypotension, dehydration, and anaphylaxis (rapid onset shock). Seventeen persons were hospitalized. Six deaths and two stillbirths following acute illnesses associated with watermelon ingestion were reported; however, none of the deaths were attributed by the coroners to ASO ingestion, and fetal tissues from both stillbirths tested negative for ASO. In a third pregnancy, decreased fetal movement was noted the same day as a watermelon-related illness in the mother. The mother subsequently gave birth to a normal child.

Of 250 laboratory tests on melons for ASO, 10 (4%) were positive. These 10 included one ASO-positive stickered watermelon associated with illness reported after July 10; an additional ASO-positive stickered watermelon was reported from Canada. Neither of these two positive melons could be traced back to specific fields.

In addition to the reports of watermelon-related illness, 77 illnesses associated with about 25 cantaloupes were reported. All cantaloupe specimens tested negative for ASO, and approximately half were screened for other pesticides (carbamates, organophosphates, and chlorinated pesticides) and were negative. Fewer complaints associated with other types of melons were reported.

Editorial_Note: This is the largest recorded North American outbreak of foodborne pesticide illness. In addition to the 692 probable cases reported by California, 10 other jurisdictions in the United States and Canada reported 483 probable or possible cases according to their own case definitions: Alberta (20), Alaska (47), Arizona (one), British Columbia (206), Colorado (one), Hawaii (two), Idaho (80), Nevada (four), Oregon (104), and Washington (18).

Aldicarb is a carbamate insecticide used in citrus groves and potato fields. Unlike organophosphates, which also interfere with cholinesterase activity, inhibition of cholinesterase by carbamates is rapidly reversible.

Aldicarb has the lowest LD50 of any pesticide registered in the United States (LD50 1 mg/kg body weight). Aldicarb sulfoxide has nearly the same LD50. It has been associated with at least two deaths among agricultural workers. (Note: One of these deaths occurred in California and aldicarb did not kill the victim, but incapacitated him such that he was killed by a tractor.) It is a highly effective systemic insecticide, readily taken up by the roots and carried into the stem, leaves, and fruit of the plant. Severe and potentially lethal contamination levels can result from intentional or inadvertent misapplication to certain crops, as seen in several prior episodes of foodborne aldicarb poisoning involving cucumbers and mint. It is not registered for use on melons.

Existing toxicologic data on aldicarb did not predict the severity of the acute illnesses associated with the dose levels found in this outbreak. Animal data do not predict long-term or reproductive effects from aldicarb and its metabolites, and it is not a suspected carcinogen. However, few reproductive studies have been conducted at doses that cause maternal toxicity, and, in rats, it has been shown to cause acetyl cholinesterase inhibition in fetal tissues.

In the California outbreak, coincidental onset of gastrointestinal illness within 2 hours of eating melon may explain some of the sporadic cases occurring through September. However, the source of illnesses is not clear among those who had illnesses compatible with carbamate poisoning but where laboratory testing of the melons was negative for ASO. Although some of these may have been coincidental, it is possible that the laboratory analyses are too insensitive to detect ASO at levels that can cause human illness. This issue has implications for monitoring pesticide residues in foods and needs further study.

On October 29, 1985, the Epidemiology Division, Vermont Department of Health, learned of two persons with symptoms consistent with ciguatera fish poisoning. Both had eaten barracuda at a local restaurant on October 19. One ill person, a 48-year-old woman, had vomiting, diarrhea, myalgia (muscle pains), and chills 4 hours after the meal, followed the next morning by pruritus (itching), flushing, burning of the tongue, and reversal of hot and cold temperature sensation of objects held in her hands. The second ill person, a 30-year-old male bartender at the restaurant, sought medical attention for severe myalgia and gingival (gum) and dental dysesthesia (abnormal sensation) several hours after eating barracuda. In both patients, most symptoms subsided; however, some pruritus and temperature reversal persisted 6 weeks later. A third patron reported pruritus to the restaurant after the meal but was lost to follow-up. No additional cases were identified by contacting the two local emergency rooms and requesting case reports in the Vermont Disease Control Bulletin.

Editorial_Note: Human ciguatera poisoning can occur after consumption of a wide variety of coral reef fish, such as barracuda, grouper, red snapper, amberjack, surgeonfish, and sea bass. Ciguatoxin and related toxins are derived from dinoflagellates, which herbivorous fish consume while foraging through the macro-algae. Humans ingest the toxin by consuming either herbivorous fish or carnivorous fish that have eaten the contaminated herbivores. Larger, more predacious reef fish are generally more likely to be toxic. Since the toxin is heat- stable, cooking does not make the fish safe to eat.

As the domestic and imported fish industry expands its market, the diagnosis of this "tropical" disease must be considered even in areas to which coral-reef fish are not native. Ciguatera fish poisoning can be diagnosed by the characteristic combination of gastrointestinal and neurologic symptoms in a person who ate a suspect fish. The diagnosis can be supported by detection of ciguatoxin in the implicated fish.

Hawaii now uses a "stick test" immunoassay to detect ciguatoxin in fish. The test is sensitive, specific, inexpensive, and easy to use in the field. In Hawaii, if an outbreak-related fish tests positive for ciguatoxin, the reef area of catch is posted to discourage further fishing in that area. In Miami, Florida, because barracuda have been frequently associated with ciguatera poisoning, a city ordinance bans the sale of barracuda.

Between December 31, 1985, and January 4, 1986, three restaurants in Alabama and Tennessee received complaints of illness from nine customers and one employee who ate Pacific amberjack fish (also called yellowtail or kahala). Detailed information was obtained on four of the 10 persons. Illness onset occurred 10-90 minutes after eating (median 23 minutes). Symptoms included red facial rash (4/4), body rash (2/4), severe headache (2/4), oral paresthesias (abnormal sensations) (1/4), shortness of breath (2/4), vomiting (1/4), and diarrhea (3/4). Of the three persons who sought medical evaluation, one had diastolic hypotension, and one had bronchospasm (constriction of the bronchi resulting in a severe, asthma like attack).

All three were diagnosed as having food or fish allergy and were treated with an antihistamine. Rash persisted for 2-5 hours (median 3 hours), and all other symptoms resolved in 3-36 hours (median 14 hours). One restaurant cook, who did not eat the fish, reported a transient red rash on the hands shortly after handling the fish.

In November 1985, a Florida seafood company procured 1,100 pounds of fresh amberjack from southern California. A 120-pound portion was resold December 30 to a distributor that in turn supplied the fish to nine restaurants in Alabama, Kentucky, and Tennessee. After receiving complaints from three of the restaurants, the distributor promptly notified all recipient restaurants and collected 20 pounds of amberjack. Analysis of the leftover fish by the U.S. Food and Drug Administration (FDA) showed 19 of 20 subsamples had markedly elevated levels of histamine (257-430 mg%). (Fresh fish normally contains less than 1 mg% of histamine.) The remaining fish, which had not been distributed, was destroyed under FDA supervision.

Editorial_Note: The symptoms of scombroid fish poisoning resemble those of a histamine reaction; the illness is characterized by flushing, headache, dizziness, burning of the mouth and throat, abdominal cramps, nausea, vomiting, and diarrhea. Urticaria (hives) and generalized pruritus often occur. In severe cases, bronchospasm and respiratory distress may develop. Some victims complain that the toxic food has a sharp or peppery taste. Typical incubation periods are less than 1 hour, although wide variations can occur among individuals.

Scombroid means mackeral-like; mackeral, tuna, and bonito are related species that are often implicated in outbreaks of scombroid poisoning. However, nonscombroid species, such as the amberjack reported here, have also been implicated in scombroid poisoning. Of the 73 outbreaks of scombroid poisoning reported to CDC during the 5-year period 1978-1982, 31 (42%) implicated mahi-mahi (dolphin fish), a nonscombroid fish.

Poisoning is caused by the ingestion of spoiledfish. Histamine and probably other toxic byproducts are produced by bacterial action on histidine, a normal muscle constituent of dark-meat fishes. Scombroid poisoning is a response to toxic by-products __ not an allergic reaction to fish. Once formed, the toxins are heat-stable, so the best defense against poisoning is prompt storage of freshly caught fish at 0 C (32 F) or below. Laboratory confirmation of scombroid fish poisoning is based on demonstrating elevated histamine levels in incriminated fish. Public health authorities should be notified when this or other fish-related illness is suspected so that the distribution of the implicated food can be determined.

On October 30, 1985, the Wisconsin Division of Health was informed by the state poison control center of two elementary schoolchildren who presented with severe burning of the mouth and throat, as well as nausea. The symptoms developed within 1 hour of drinking milk packaged in half-pint containers with an expiration date of 11/9 from a Wisconsin milk processor. An investigation into the source of the milk determined that, 5 days previously, the milk processor had noted an ammonia leak in one of its cooling chambers, where approximately 250,000 half-pint milk containers with an expiration date of 11/9 were stored. The liquid ammonia, used to cool the tanks and stored under pressure, had sprayed about the storage tank for an undetermined number of hours. On discovery of the leak, the milk processors destroyed those cartons with obvious external damage to the paper and polyethylene containers. After tasting and smelling approximately 75 of the remaining 250,000 cartons, they determined the milk was safe and began distributing the product throughout the state.

Thirty milk containers with expiration date 11/9 were retrieved from the index elementary school. An analysis of these 30 containers by the Wisconsin Department of Agriculture identified seven (23%) that were contaminated with ammonia at levels ranging from 530 ppm to 1,524 ppm (normal = less than 15 ppm). The pH levels of these contaminated samples ranged from 9.1 to 10.0 (normal milk pH = 6.7-6.9).

This surveillance effort identified approximately 520 cartons of milk ingested before notification. Twenty children fulfilling the case definition were identified (attack rate 3.9%). None required hospitalization, and no deaths occurred. Schools were instructed to return the unused cartons to the milk processer, where they were destroyed. This is the first reported incident of acute ammonia poisoning associated with contaminated milk.

Editorial_Note: Ammonia (NH3) is a colorless gas with a characteristic strong, pungent, penetrating odor. It is one of the more common industrial chemicals; an estimated 20-30 million tons are used per year in the United States. It is widely used in fertilizer manufacture; other uses include dye, synthetic fiber, plastic, and nitric acid production, as well as refrigeration. In its aqueous form as ammonium hydroxide (NH4OH), it is extremely alkaline and can be highly caustic. Aqueous ammonia is 28% (280,000 ppm) ammonia, whereas household ammonia is 10% ammonia (100,000 ppm). Mild to moderate ammonia exposures can produce headaches, salivation, burning of the throat, anosmia, nausea, vomiting, and substernal pain. Moderate doses may produce laryngospasm or bronchospasm.

The Occupational Safety and Health Administration standard for ammonia inhalation is 50 ppm as an 8-hour time-weighted average, but the National Institute for Occupational Safety and Health has recommended that 50 ppm be a 5-minute ceiling for exposure. The characteristic ammonia odor is readily perceptible below toxic levels. Most persons can detect an odor at 30 ppm, and eye and nose irritation become more severe as the levels increase to 50 ppm. The students involved in this incident were unable to smell the ammonia probably because the milk cartons were closed. The students first became aware of a problem when they felt burning in their throats.

Outbreaks of ammonia poisoning of milk, other beverages, or food have not been previously documented. The ammonium hydroxide apparently penetrated the milk cartons when the refrigerant tank leaked. Additional studies need to be done to determine how the ammonia contaminated the milk, and criteria need to be established to prevent contaminated milk from being distributed.

On February 15, 1985, morning and afternoon water samples from drinking fountains in the Jacob K. Javits Federal Building (JFB) in New York City were collected because of the poor taste of the water. The U.S. Environmental Protection Agency (EPA) tested samples from five of the 41 floors of the 19-year-old JFB for the presence of heavy metals. Elevated levels of lead were reported for the afternoon samples from fountains at the north end of the building; concentrations ranged from 100 ug/l to 210 ug/l; the EPA standard maximum contaminant level for lead in drinking water is 50 ug/l. Levels of copper were also elevated (up to 5,900 ug/l).

On May 20, the use of drinking water from the entire JFB was temporarily discontinued in favor of bottled water. The intake pipes, which contained lead solder and had sampling taps with lead solder joints, were subsequently replaced with stainless steel pipes; the mechanical water chillers, which had copper tubing, were repaired; and the corrosiveness (acidity) of the water was decreased.

Because of the uncertainty of employee exposure to lead and the duration of any exposure, a voluntary screening program for blood lead was offered July 9 and July 10 to all of the approximately 10,000 federal employees who worked in the JFB to determine the extent of lead absorption. Three hundred sixty- nine (4%) of the employees were tested for blood lead levels. Each employee provided demographic information and exposure- related data concerning the average daily amount of water consumed in the JFB. Blood lead determinations were made at the NYCDH Toxicology Laboratory by atomic absorption spectrophotometry (extraction method) with a lower limit of detection of 10 ug/dl.

Of the 369 employees, 188 (51%) were women. The women ranged in age from 16 years to 74 years (median 37 years); the men ranged in age from 23 years to 69 years (median 42 years). Six women reported they were pregnant, and one woman reported she was possibly pregnant. Two hundred thirty-eight (64%) of the employees resided in New York City; the others lived in New York City suburbs.

Of the employees tested, 85% had blood lead levels of 10 ug/dl or lower. The highest detected blood lead level, found in one employee, was 27 ug/dl. The percentage of employees with blood lead levels greater than 10 ug/dl increased significantly with increasing age, with a drop-off among persons aged at least 60 years (p < 0.05). Blood lead levels did not differ significantly among persons when categorized by sex, agency of employment, floor of employment, self-reported average daily consumption of water while at work, or place of residence. Of the seven pregnant or possibly pregnant women, six had blood lead levels of 10 ug/dl or less, and one had a level of 13 ug/dl.

Editorial_Note: None of the 369 adults tested had abnormal absorption of lead from the environment, as evidenced by the blood lead levels. The majority of office workers tested had blood lead levels of 10 ug/dl or less. A national survey of adults revealed a mean blood lead level of 9.2 ug/dl in 1980, a 37% decline over 4 years. Overall, for the 4 years 1977-1980, the national survey revealed age-group-specific mean levels for adults of between 13.1 ug/dl and 15.3 ug/dl, with the peak among persons aged 45-54 years. The results of the New York City survey parallel the national survey. In addition, nationally, blood lead levels were higher among urban residents.

VII. Erosion_of_Dental_Enamel_in_Swimmers_Due_to Gas-Chlorinated_Swimming_Pools

A study was recently conducted at a private club when several swimmers exhibited dental enamel erosion consistent with exposure to acid. Thirty-nine percent of the swim team members and twelve percent of the other club swimmers had erosion of enamel. An examination of the gas-chlorinated pool revealed corrosion of metal fixtures and etching of the cement exposed to pool water. The pH was tested and discovered to be 2.7, an acid concentration 100,000 times that recommended for pools (7.2-8). Acid erosion of dental enamel is a painful, costly and irreversible condition which can be caused by inadequately maintained gas-chlorinated swimming pools.

Centerwall BS et al. Am J Epidemiol 123:641-647, Apr 1986. As reported in Human and Veterinary Toxicology 28(3):266, 1986.

In surveys conducted from 1981 to 1983, 76% of the U.S. adult population reported that they did not use seat belts (i.e., used seat belts sometimes, seldom, or never). The percentages of men and women who did not use seat belts were similar, but the percentages were significantly higher for people who were younger, who were black, and who had completed fewer years of education. These differences persisted after adjusting for the other demographic characteristics. The percentage of persons who did not use seat belts also varied widely by state, ranging from 68% in California to 89% in Arkansas. Persons who exhibited another particular risk behavior, i.e., smoking, binge drinking, chronic drinking, drunk driving, overweight, or inactivity, were significantly more likely to report not using seat belts than persons who did not exhibit that particular risk behavior. For example, 80% of smokers did not use seat belts, compared with 74% of nonsmokers (p < 0.05).

Editorial_Note: Injuries from motor vehicle collisions (MVCs) are the fourth leading cause of death in the United States. In 1984, the most recent year for which complete data are available, 36,271 occupants of motor vehicles (including motorcycles) died on U.S. highways. Of these, 14,528 (28%) were under 25 years old, making MVC-associated injuries the leading cause of death among persons aged 5-24 years. In 1984, MVC-associated mortality among persons aged 15-24 years, 36.5 per 100,000, was nearly three times that associated with any other cause and accounted for more than one-third the total mortality in this age group. Because MVCs affect the young disproportionately, injuries from MVCs are the third leading cause of years of potential life lost. For 1984, MVC-associated injuries resulted in 1.3 million years of potential life lost before age 65. In addition, injuries from MVCs accounted for 27% of the occupational fatalities in 1984. Of the estimated $33 billion in direct and indirect costs for occupational injuries in 1984, $11 billion may be attributable to injuries from MVCs.

During 1982-1984, highway fatalities among occupants of passenger vehicles (excluding motorcycles, trucks, and buses) remained essentially unchanged in the United States. Throughout this period, occupant restraints were used by fewer than 6% of fatally injured persons. Nationwide data for 1985, the first year any state required seat belt use by adults, are not yet available.

Injury data are not currently available for states with MULs (mandatory-use laws). However, the experience in Great Britain strongly suggests that the incidence of severe injuries is reduced by such laws. During 1983, the first year after the British law went into effect, 15% fewer patients were brought to the hospital following MVCs, and 25% fewer required admission than during the preceding year.

Nonetheless, MULs alone will not eliminate injuries and deaths on U.S. highways. Better enforcement of existing speeding and drunk-driving laws, augmentation of seat belts with passive restraints (e.g., air bags) and other vehicle-design changes to maximize occupant protection, improved engineering of highways to minimize crash occurrence, and effective public education about all aspects of highway safety are needed to reduce highway fatalities.

Recently the question was asked, "How much is a part per trillion, anyway?" In an accompanying table the concepts of a part per million, billion and trillion were put into perspective. It was pointed out a part per million was equivalent to an ounce of salt per 31 tons of potato chips, a part per billion to a drop of vermouth in 500 barrels of gin and a part per trillion to a six-inch leap on a journey toward the sun.

Even a minute concentration can add up to a sizable total amount of material when contained in a large sample. For example, consider the amount of material that would be involved in the amount of water used in the Los Angeles area (3,000,000 acre-feet/year) if some selected contaminants were present at a part per billion level. Obviously a part per million would be 1,000 times more and a part per trillion 1,000 times less.

Substance	One ppb in 3,000,000 acre-feet/year would amount to enough to:
lead	cast 1,000,000 bullets
chromium	plate 50,000 car bumpers
mercury	fill 4,000,000 rectal thermometers
phenols	produce 250,000 bottles of Lysol
herbicide	kill all the dandelions in 100,000 lawns
insecticides	fill 5,000,000 aerosol cans of bug killer
gold	run the federal government for nearly 20 minutes or support 50 average families for eternity

Colin D. Chriswell, Ames Laboratory, Iowa State University from Chemecology, November 1977. As reported in Vet Hum Toxicol 28(1), February 1986.

Note: According to my calculations, each ppb in 3 x 106 acre ft of water is equal to 8,142_lbs of material. The point of these calculations is to remind us that while low ppb quantities are usually not significant toxicologically, they can indicate the release of significant quantities into the environment.

1 acre-foot of H20 = 43,560 ft3
1 ft3 of H20 = 62.297 lbs	1 in3 = 16.3871 cc 1 ft3 = 28316.9 cc= 28.3169 liters x 2.2 1 ft3 = 62.297 lbs
1 acre-foot = 2,713,657 lbs of H20
In each acre-foot there would be 2.714 lbs/ppm
For 3 x 106 acre-foot each ppb = 8,142 lbs of material