COOPERATIVE EXTENSION UNIVERSITY OF CALIFORNIA
ENVIRONMENTAL TOXICOLOGY NEWSLETTER

Vol. 11 No. 3 June 1991

Table of Contents

VET NOTES

Introduction

This issue of the Environmental Toxicology Newsletter is the first utilizing our newest desktop publishing program. The Environmental Toxicology Extension (ETXEXT) Administrative Assistant, Mrs. Sandy Ogletree deserves all credit for this attractive format, and has promised to make it look even nicer in the future.

Included in this issue are reports of two tragic and preventable childhood poisonings from lead and carbon monoxide. I have also included a substantial article about Paralytic Shellfish Poisoning because it is still a problem in California, particularly among recent Asian immigrants. Also included are tips about storing pool chemicals, recent findings about pesticide levels in house dust, some guidelines for chlorination of animal drinking water, and an article about fluoride written by the ETXEXT Staff Research Associate, Scott Wetzlich.

In the next issue of the Environmental Toxicology Newsletter, we will take a look at the current status of the food safety issue, and discuss another issue (identified by USDA/CES as a national initiative area); waste management.

Fatal Pediatric Poisoning from Leaded Paint - Wisconsin, 1990

Although fatal lead poisoning among children occurs rarely in the United States, it represents a medical and public health emergency. This report summarizes the investigation of a child who died from poisoning associated with ingestion of lead-based paint.

On September 12, 1990, a 28-month-old Wisconsin boy was admitted to a hospital with a 4-day history of lethargy and reduced appetite. Although the child had no known past medical problems, his parents reported that he had eaten flaking paint. On initial neurologic examination, the child had extreme lethargy with facial palsy (weakness) and gasping respirations, consistent with lead encephalopathy; laboratory results revealed severe lead toxicity and hematologic abnormalities (blood lead level [BLL] 144 ug/dL; erythrocyte protoporphyrin level 593 ug/dL; hemoglobin 8.1; and basophilic stippling). Despite chelation therapy with British antilewisite (BAL) and calcium disodium edetate (CaNa2- EDTA), the child developed seizures, became comatose, and died 26 hours after admission. On September 20, staff from the Wisconsin Division of Health and the Waukesha County Health Department inspected the child's residence. The child and his parents had lived for at least 4 months on the second floor of a two-story, nonresidential structure built in 1923. The interior paint was badly deteriorated with paint chips visibly flaking from the walls and accumulating on floors, windowsills, and stairs. Eleven paint chip samples from the apartment ranged from 0.2% to 33.1% lead by weight (average: 9.1%); the U.S. Consumer Product Safety Commission (CPSC) permits a maximum of 0.06% lead in new residential paint. House dust from the child's bedroom floor contained 3900 ug lead/ft2, and dust from a windowsill above the child's bed contained 31,128 mg lead/ft2. These levels are more than 10 times higher than those proposed in recent guidelines issued by the U.S. Department of Housing and Urban Development, which recommend the maximum dust lead levels permissible before reoccupancy of a unit following lead paint abatement.

Editorial Note: Lead encephalopathy usually is associated with a BLL >100 ug/dL, although it has been reported at BLLs as low as 70 ug/dL. As in this report, children with acute lead encephalopathy often have a recent history of prodromal symptoms, including anorexia, apathy, decreased play activity, hyperirritability, aggressiveness, poor coordination, and sporadic vomiting. Because lead encephalopathy in a child can rapidly progress to death, either a BLL >70 ug/dL in a child or the onset of encephalopathy constitutes an acute medical emergency.

At least four factors may account for the dramatic decline in the incidence of acute lead encephalopathy and childhood deaths from lead poisoning since the 1960s, including 1) increased screening of children at risk, 2) recognition of toxicity before the onset of life- threatening symptoms, 3) improvements in the treatment for lead poisoning, and 4) reduction of lead exposure from certain environmental sources. Although childhood deaths from poisoning associated with exposure to lead-based paint are now rare in the United States (the most recently reported lead-based paint-associated death occurred in the mid-1970s), subclinical toxicity is a widespread and persistent public health problem. BLLs as low as 10 ug/dL, once considered safe, are now known to adversely affect cognitive development and behavior in children, with potentially long-term sequelae. In 1984, an estimated 3-4 million U.S. children had BLLs >15 ug/dL.

The primary source of high-dose lead exposure among children in U.S. urban areas is lead-based paint. Although CPSC banned lead- based paint for residential use in 1978, an estimated 12 million children <7 years of age reside in homes containing previously applied lead-based paint. Interior paints used before 1940 contained as much as 50% lead. Although children can ingest lead directly by eating paint chips, ingestion of lead-contaminated house dust and soil during normal mouthing and exploratory behaviors contributes substantially to elevating BLLs. The child reported in Wisconsin appeared to have been ingesting paint chips and was exposed to highly contaminated house dust.

All cases of lead poisoning are preventable. A national health objective for the year 2000 is to reduce the prevalence of children aged 6 months through 5 years with BLLs >15 ug/dL to less than 500,000 and the prevalence of those with BLLs >25 ug/dL to zero. Recently, several federal agencies responsible for housing, health, and the environment have focused attention on this problem and have set goals to abate lead-based paint in privately owned housing, reduce the number of children with elevated BLLs, and promote national efforts to eliminate childhood lead poisoning.

Reference: MMWR, Vol. 40/No. 12, March 29, 1991.

Fatal Carbon Monoxide Poisoning in a Camper-Truck - Georgia

On December 27, 1990, three children, aged 6, 10, and 11 years, died as a result of carbon monoxide (CO) inhalation while riding in the back of their parents' pickup truck, which had a camper shell cover. The family was returning overnight to Georgia from Mississippi, and the children were sleeping in the back of the truck. After 50 miles of travel, they stopped at a service station; the children did not complain of headache or other problems. During a second stop 250 miles further, the children appeared to be asleep. On arrival at their destination in Georgia, following a total drive of 550 miles, the children could not be aroused; resuscitation attempts were unsuccessful. The parents and two younger children riding in the truck cab were asymptomatic.

An inspection of the 1970 truck by the Georgia Bureau of Investigation found that the muffler had been replaced, but the original tailpipe was not securely joined to the muffler. Several holes in the wall of the truck bed behind the cab allowed fumes leaking from the muffler to enter the enclosed bed. In addition, the camper shell cover was attached to the truck without a gasket, and the rear door of the cover was loose.

Editorial Note: Death from CO poisoning associated with vehicles is entirely preventable. The three deaths described in this report were caused by the combination of an aging vehicle, a defective exhaust system, and passengers being transported in an inadequately ventilated space.

Any moving vehicle with a vertical rear tailgate or door (e.g., a station wagon or pickup truck with a camper shell cover) creates negative air pressure behind it. Because of this vacuum, opening the rear window of a camper or station wagon can result in high concentrations of exhaust fumes entering the vehicle. Holes in the body of the vehicle or leaks around windows or doors may also allow fumes to enter the passenger compartment.

CO production by vehicles can be minimized by regular preventive maintenance, inspection of exhaust systems, and emissions testing. Use of leaded gasoline in cars with catalytic converters or bypassing the pollution-control systems will result in production of higher levels of CO and nitrogen oxides. Annual inspections of vehicles should include an examination for rust holes or defects in the body or floor that could permit exhaust fumes to enter the passenger compartment.

Reference: MMWR, Vol. 40/No. 9, March 8, 1991

Paralytic Shellfish Poisoning - Massachusetts and Alaska, 1990

Paralytic shellfish poisoning (PSP) is a foodborne illness caused by consumption of shellfish or broth from cooked shellfish that contain either concentrated saxitoxin, an alkaloid neurotoxin, or related compounds. This report summarizes outbreaks of PSP that occurred in Massachusetts and Alaska in June 1990.

Massachusetts

On June 6, 1990, the Massachusetts Department of Public Health (MDPH) was notified that, on June 5, foodborne illness had occurred in six fishermen aboard a fishing boat in the Georges Bank area off the Nantucket coast. Onset of illness occurred after the men had eaten blue mussels (Mytilus edulis) harvested in deep water about 115 miles from the island of Nantucket.

The six men (age range: 24-47 years) developed symptoms 1-2 1/2 hours after consuming the shellfish (Table 1). Symptoms included numbness of mouth (five men), vomiting (four), paresthesia of extremities (four), numbness and tingling of tongue (two), numbness of face (two), numbness of throat (one), and periorbital edema [swelling around the eyes] (one). In all six men, lower back pain occurred approximately 24 hours after onset. The median duration of neurologic symptoms was 14 hours, and for lower back pain, 3.3 days. Approximately 10 hours after onset, when the fishermen presented to a local hospital emergency room, four were recovering; however, two, including one who had recovered from loss of consciousness, required hospitalization for 2-3 days.

The six fishermen had boiled the mussels for approximately 90 minutes before consuming them with baked fish, boiled rice, boiled potatoes, green salad, and other food items. They did not consume alcoholic beverages with the implicated meal.

Laboratory examination of the uneaten mussels detected saxitoxin concentrations of 24,400 ug/100 g in the raw mussels and 4280 ug/100 g in the cooked mussels (maximum safe level: 80 ug/100 mg). The difference in the levels of PSP toxin between raw and cooked mussels suggested that much of the saxitoxin had dissipated into the boiling water.

Alaska

On June 26, 1990, a physician reported to the Alaska Department of Health and Social Services (ADHSS) that a Native Alaskan man had died after consuming shellfish collected from a beach on the Alaska Peninsula. On the evening of June 25, while aboard a fishing boat, the decedent had consumed 25-30 steamed butter clams and 2 teaspoons of butter clam broth. Within an hour, he complained of numbness and tingling around his mouth, face, and fingers. Two hours later, he suffered a cardiopulmonary arrest; despite cardiopulmonary resuscitation efforts by emergency personnel, the patient died. Based on the symptoms reported, PSP was diagnosed. The patient's gastric contents contained 370 ug/100 g of PSP toxin, and a sample of the butter clam broth from the meal contained 2650 ug/100 g.

Two other crewmembers had also consumed butter clams. One developed numbness and tingling of the face and hands and dizziness approximately 1 1/2 hours later and recovered uneventfully; the other had no symptoms. Four crewmembers from two other fishing boats also had shared the butter clams presumed to be the vehicle for illness; all four had symptoms consistent with PSP.

Editorial Note: The neurotoxins that cause PSP are among the most potent toxins known and can impair sensory, cerebellar, and motor functions. Saxitoxin is heat-stable and unaffected by standard cooking or steaming, is water-soluble, and can be concentrated in broth. Symptoms usually occur within 2 hours after ingestion of shellfish; high doses can lead to diaphragmatic paralysis, respiratory failure, and death.

The diagnosis of PSP is based on patient exposure history and clinical manifestations and on epidemiologic information. Predominant manifestations include paresthesia of the mouth and extremities, ataxia, dysphagia, and muscle paralysis; gastrointestinal symptoms are less common. Coma, total muscular paralysis, and respiratory arrest with death can occur. The prognosis is favorable for patients who survive beyond 12-18 hours. Because PSP has no specific treatment or antidote, treatment is supportive. Prompt evacuation of stomach contents may help by removing the remaining toxin-containing shellfish.

Most cases of PSP occur in individuals or small groups who gather shellfish for personal consumption. Although PSP has traditionally been considered a risk only in shellfish harvested from cold water, the incidence in tropical areas may be increasing: outbreaks have been reported recently from Central and South America, Asia, and the Pacific region.

Shellfish can become toxic when toxin-producing dinoflagellates create massive algal blooms known as "red tides." However, shellfish can become toxic even in the absence of such blooms; detoxification may require a month or more in clean waters.

To prevent outbreaks of PSP and other shellfish intoxications, samples of susceptible mollusks are periodically collected in the coastal states and tested for toxin by mouse bioassay. When toxin levels exceed 80 ug/100 g, affected growing areas are quarantined, and sale of shellfish is prohibited. Warnings posted in shellfish-growing areas and on beaches and placed in the news media can alert the public to the hazard.

Reference: MMWR, Vol. 40/No. 10, March 15, 1991.

Editor's Note: Dr. Bob Price, UCD, has developed an excellent fact sheet on PSP which can be obtained from his office. In California, mussels are quarantined from May 1 - October 31 each year, and the California Department of Health Services maintains a PSP message line (415-540-2605) for current information about shellfish and PSP.

Pool Chemical Safety

Many chemicals used in swimming pools may release chlorine an extremely hazardous substance (EHS). Some pools use gaseous chlorine to kill bacteria and other microorganisms. Other pools use solid or granular compounds (calcium hypochlorite or chlorinated isocyanates) or liquids (sodium hypochlorite). In contact with water, these chemicals form hypochloric acid or chlorine ions to disinfect the water.

Careless storing, wetting, mixing, or contamination of any of these chemicals or the systems used to feed them can cause fires, explosions, burns or the release of gaseous chlorine. A chlorine gas release occurred in an Erie County School during 1989, resulting in evacuation and closing of the high school.

Below are some guidelines suggested by the EPA for facilities, including schools, that use these chemicals.

1) Begin by identifying the pool chemicals currently being used in your district.

2) Minimize the likelihood of chlorine release during handling and storage by following the guidelines and procedures outlined by the manufacturer.

In addition:
Be sure the area used to store pool chemicals is dry and well vented, free from any water leakage.

Thoroughly clean all lines in your system before switching from one type of pool chlorination to another. (Even similar chlorination products can react violently with one another).

If a tank is used to store liquid pool chemicals, be sure the tank is not overfilled, and that a diking system is set up to contain leaks.

Check that chemical containers are not leaking, broken or torn.

If chlorine gas is used, cylinders of chlorine should be stored separately from all other chemicals, preferably outdoors or in well-vented detached areas.

If muriatic acid is used to clean the lines of your system, be sure it does not mix with any chlorine containing chemical.

3) Provide an adequate training program to educate all personnel on the hazards of chlorine gas and pool chlorinatic chemicals.

Make sure MSDS sheets are available for all pool chemicals used at your facility.

Provide proper protective equipment as recommended by the manufacturer for all personnel.

4) Give careful attention to pool chemicals in emergency planning.

Report the presence of pool chemicals directly to your local emergency planning committee (LEPC) and local fire department. (Even though many pool chlorination chemicals are not listed under SARA Title III, or reporting thresholds may not be met, the EPA recommends they be reported because of their widespread use and potential to release chlorine gas.)

Include swimming pools in your districts' Emergency Management Plans. You should have a safety plan in place for all school buildings with pools.

Reference: CUSSCO Newsletter (College, University & School Safety Council of Ontario), Vol. 10/Issue 1, Jan-Feb 1991.

Pesticide Levels in House Dust Higher Than in Soil, ACS Told

"Levels of many of the targeted pesticides in soil 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 April 18 to the American Chemical Society (ACS) meeting in Atlanta, GA.

"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."

Reference: Pesticide & Toxic Chemical News, April 24, 1991.

Toxic Air Pollutants and Noncancer Health Risks - United States

Previous evaluations of the health risks associated with chemical pollutants of ambient air have focused on the potential for carcinogenic effects. However, other potential health effects that may result from exposure to these pollutants include nonmalignant respiratory disease, hematopoietic abnormalities, neurotoxicity, renal toxicity, developmental toxicity, and reproductive toxicity. To address these concerns, the U.S. Environmental Protection Agency (EPA) conducted a national study to assess the noncancer risks of toxic air pollutants (EPA, unpublished data). This report summarizes the findings of this assessment.

United States

During 1987 and 1988, air monitoring data were used to examine exposure to individual and multiple pollutants. During 1987, ambient monitored data were obtained on 319 volatile organic compounds from 123,000 samples collected during 1980-1987 in 310 U.S. cities and, during 1988, on six trace metals monitored primarily during 1980-1988 across the country at more than 1500 sites. Average annual concentrations were estimated, or modeled, for 40 pollutants emitted from more than 3500 individual facility sites (e.g., factories and businesses). Information on potential health effects and estimated exposures were available for 143 (43%) of 334 pollutants.

For the 143 pollutants, the maximum and median concentrations monitored during a 24-hour period or the average modeled annual concentrations, as applicable, were compared to the lowest- observed-adverse-effect-level (LOAEL=the lowest dose or exposure level at which an adverse effect has been observed) and to the health reference level (the adjusted LOAEL divided by appropriate uncertainty factors, i.e. to account for intra- and interspecies variations and differences between no effect and LOAEL). This study concluded that combined exposures may pose risks for the respiratory, neurologic, and reproductive systems and a risk for adverse developmental effects.

Editorial Note: In 1988, the U.S. manufacturing sector emitted an estimated 2.4 billion lbs of toxic pollutants into the atmosphere. Although the data base available for assessing noncancer health risks is limited, the findings in this report underscore the need to focus attention on the noncancer health risks of toxic air pollution.

The 1970 Clean Air Act required the EPA to publish a list of hazardous air pollutants and develop a national emission standard for each. Under those provisions, only eight chemicals have been listed as hazardous air pollutants in part because of the difficulties in determining risks to the public's health and developing appropriate standards. These difficulties, coupled with regulatory procedures, have prompted major changes in the strategies for controlling hazardous air pollutant emissions, as reflected in the Clean Air Act Amendments of 1990. Under these provisions, the EPA has listed 189 substances as hazardous air pollutants. Initially, the EPA will develop and implement technology-based emission standards; the EPA will then evaluate the remaining emissions and associated residual risks. If warranted, the EPA will develop risk-based emission standards.

The 1990 provisions require that the EPA perform risk assessments throughout the 1990s. In addition, the act provides a basis for state and local agencies to perform risk assessments. For example, states are required to conduct public hearings on air-quality permit applications and emission-control decisions. At such hearings, the public may request information on the health risks posed by emissions from facilities requesting permits. Therefore, state and local health departments and air quality management agencies also have an important role in implementing the 1990 amendments.

The final report of the studies cited will be available from the Pollutant Assessment Branch, Emissions Standards Division, Office of Air Quality Planning and Standards, EPA, Research Triangle Park, NC 27711; telephone (919) 541-5346.

Reference: MMWR, Vol. 40/No. 17, May 3, 1991.

Fluoride in Drinking Water
Scott Wetzlich

In the 1940's, studies found that the prevalence of dental caries declined as natural fluoride levels in drinking water increased. This lead to the practice of adjusting the fluoride level in public drinking water to 1 ppm. The optimal range for reducing dental caries with the minimum risk of causing dental fluorosis is 0.7 to 1.2 ppm. Over half of the U.S. population uses fluoridated water today. An even greater percentage of the population is exposed to fluoride from toothpaste, other dental products, and dietary supplements, which have had fluoride incorporated into them since the 1950's.

Fluoridation is not without its health risks. Fluoride can be toxic. Too much fluoride in the diet causes dental fluorosis, which has a mottled teeth look. A few studies in the 1970's claimed a link between cancer mortality and fluoridated water systems. Many researchers have since refuted this claim. Because of these health concerns, the U.S. Public Health Service (PHS) released a report,"Review of Fluoride Risks and Benefits," in February of this year.

The report concluded that fluoride is beneficial in preventing tooth decay. It found that while fluoridated toothpaste and mouthrinses, professional fluoride treatment, and fluoride dietary supplements reduce tooth decay, water fluoridation is the most cost-effective method at providing the greatest benefit to those who can least afford it. When water fluoridation was first introduced in the 1940's, children drinking fluoridated water had a 60 percent reduction in their caries scores. Recent studies still show reductions in caries scores, but not at such high levels as observed earlier because of the other fluoridated products now on the market.

The report found no evidence linking fluoride in drinking water with birth defects, gastrointestinal, genito-urinary, reproductive, or respiratory system problems. Dental fluorosis is on the rise, though. It is more of a cosmetic problem than a serious health threat. Increased levels of dental fluorosis is a sign that certain segments of the population may be exposed to greater levels of fluoride than is necessary to prevent tooth decay.

Animal studies have failed to link fluoride to cancer. A National Toxicology Program study of the PHS found "equivocal evidence" of carcinogenicity. "Equivocal evidence" describes results where the association between a chemical and a tumor response is uncertain. A recent study sponsored by Procter & Gamble found no evidence. Epidemiological studies have found no credible evidence linking water fluoridation with increased cancer.

The report made these recommendations: 1) PHS should continue recommending fluoride to prevent dental caries, and to support optimal fluoridation of drinking water (0.7 to 1.2 ppm); 2) PHS should sponsor a scientific conference addressing both the optimal exposure from all sources of fluoride and the appropriate use of dental products containing fluoride; 3) health professionals and the public should avoid excessive and inappropriate fluoride exposure; 4) state health and drinking water programs should keep physicians, dentists, and the community informed about the fluoridation status of drinking water; 5) further research on the risks and benefits of fluoridation is needed.

Reference: Health & Environment Digest, 5(3), April 1991.

EPA Issue Update - Questions & Answers

Dr. Gene Carpenter at the University of Idaho, recently sent us a copy of the latest issue of Questions/Answers from EPA. Due to budget restrictions, we cannot provide a copy automatically to each county office. If you want a copy of particular sheets, please send a list, and a stamped, self-addressed envelope (penalty mail is all used up for this year).

The topics available are:

These sheets are EPA's response, and while a bit biased, do provide useful information.

Editor

Aldicarb (Temik) Use on Bananas Voluntarily Withdrawn
M.W. Stimmann

Rhone-Poulenc voluntarily withdrew the use of its brand of aldicarb on bananas. This withdrawal followed residue tests that showed that bananas could have residues over tolerance. It will take approximately 90 days for treated crops to clear marketing channels.

There are no health concerns associated with bananas currently on the market. Of 368 banana samples taken in California between 1986 and 1990, 98.4% had no detectable residues. Chlorpyrifos was found in 5 samples and one banana had measurable aldicarb. The aldicarb was below the federally established tolerance. In late May 1991, 39 lots of bananas were analyzed. One banana was found to have .31 ppm aldicarb. The tolerance is .3 ppm. The vast majority of the samples were negative.

FDA monitoring over the past five years has not shown any residues over allowable levels.

Reference: CDFA ENF 91-47

VET NOTES
Chlorination of Animal Drinking Water

Of late there has been increased interest in chlorination of drinking water in swine operations. Much of this interest is due to the increased incidence of Salmonella cholerasuis. While there is a lack of epidemiologic evidence that drinking water is the source of infection, many producers and veterinarians are installing chlorinators as a preventive measure. Proper installation and monitoring are necessary, if chlorinators are to be used effectively.

Free residual chlorine is needed for effective disinfection of water. Attainment of free residual chlorine levels is related to water pH, bacterial contamination, and/or water mineral levels. These relationships are illustrated as follows:

pH <7.5 -- 1 ppm of free residual chlorine is necessary
pH >7.5 -- 2 ppm of free residual chlorine is necessary

Bacteria Control

1 ppm of free residual chlorine is necessary

Giardia + Virus Control

>1 ppm of free residual chlorine is necessary

Veterinarians may monitor for free residual chlorine with test kits which can be purchased from most local swimming pool suppliers.

An important consideration of water chlorination is contact time. A minimum of 5 minutes is necessary for effective disinfection. Frequently mixing or holding tanks must be installed as water lines generally do not allow adequate contact time. Contact time is calculated as:

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

There are three available sources of chlorine. Listed below are the products available and the advantages and disadvantages of each:

1. Sodium hypochlorite (bleach)

Advantage - Readily Available
Disadvantage - Less concentrated than Calcium hypochlorite (5.25%)

2. Calcium hypochlorite (Granular Calcium hypochlorite)

Advantage - Concentrated (65%)
Disadvantage - Mineral deposits may form in water lines

3. Chlorine gas

Advantage - Inexpensive
Disadvantage - Dangerous - Corrosive

Reference: Veterinary Newsletter, University of Georgia, sometime in 1991.

No Animal Drug Residues in Milk Found by FDA

Results of the first quarter 1991 National Drug Residue Milk Monitoring Program, which ran from February 11 to March 29, found no detectable residues of animal drugs, as expected. No sulfonamides or tetracyclines were found in any of the 35 raw milk samples analyzed during the reporting period. FDA said future quarterly reports will cover 3-month periods, with an annual report issued after the end of the federal fiscal year. The methods of analysis and the limits of detection for sulfonamides were 5 ppb for sulfadiazine, sulfamethazine, sulfaquinoxaline, sulfapyridine, sulfamerazine, sulfathiazole, sulfachloropyridazine, and sulfadimethoxine. Methods for the tetracyclines and limits of detection were 30 ppb for oxytetracycline, 40 ppb for tetracycline, and 30 ppb for chlortetracycline.

Reference: Food Chemical News, April 29, 1991.

Arthur L. Craigmill
Extension Toxicologist
UC Davis

Michael W. Stimman
Statewide Pesticide Coordinator
UC Davis