UNIVERSITY OF CALIFORNIA
ENVIRONMENTAL TOXICOLOGY NEWSLETTER
Vol. 8 No. 2 November 1988
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Table of Contents
I. Grape Pesticides Targeted by United Farm Workers
as Threats to Worker and Consumer Safety
II. Household Hazardous Waste
III. Hazards of New Rodenticides to Pets
IV. Indoor Air Pollution
V. An Unusual Case of Widespread Chemical Toxicity
VI. Something to Think About
I. Grape Pesticides Targeted by United Farm Workers as Threats to Worker and Consumer Safety
The United Farm Workers (UFW) has recently demanded that five pesticides used on grapes be banned due to their potential to poison field workers. The UFW has also asked consumers to boycott table grapes until the pesticide ban is enforced and has implied that residues of the pesticides also pose serious threats to consumer health.
The five pesticides cited by the UFW are dinoseb, methyl bromide, phosdrin (mevinphos), parathion, and captan. Collectively, the chemicals have been termed "the most lethal substances used in the growing of table grapes" by UFW President Cesar Chavez.
The toxicology, use patterns, and residue findings for the five chemicals are summarized in the following paragraphs:
Dinoseb: The use of the herbicide dinoseb on California grapes was cancelled in October 1986 when research findings indicated that the pesticide had the potential to cause birth defects, cancer, and male sterility. Limited use of the chemical is still allowed in the states of Washington, Oregon, and Idaho, but no attempts have been made to reintroduce the use of dinoseb in California. Threats to farm workers and to consumers from dinoseb are therefore considered to be negligible.
Methyl bromide: Methyl bromide is used as a soil-injected, pre-plant fumigant. It does not produce residues on the grape vines or in the fruit. Methyl bromide is a highly toxic material and produces symptoms which range from nausea and vomiting to convulsions. Most occupational injuries from exposure to methyl bromide have involved structural fumigations; actual farm worker injuries have been low due to the low potential for exposure to the chemical.
Phosdrin (mevinphos): Phosdrin is a highly toxic organophosphate insecticide which causes toxicity in mammals by inhibiting cholinesterase enzymes which play an important role in the normal functioning of the central nervous system. Its oral LD50 in mammals has been reported in the range of 3.7 to 12 mg/kg, while its dermal LD50 has been reported to be 4.2-4.7 mg/kg, which suggests that the chemical is rapidly absorbed through the skin. Field studies have indicated that phosdrin breaks down rapidly in the environment and its worker re-entry interval on grapes is 4 days. Phosdrin is not suspected to cause cancer.
The most recent use data for phosdrin indicates that 169 applications of the material were made to 12,043 acres of California grapes in 1986. Total grape acreage in California in 1986 has been reported to be 671,000 acres; figures indicate that less than two percent of California grapes were treated with phosdrin in 1986.
During 1986 and 1987, 344 grape samples were analyzed for phosdrin in the California Department of Food and Agriculture's (CDFA) Market Surveillance Program. No samples contained any detectable residues of the pesticide.
Parathion: Parathion, like phosdrin, is a highly toxic organophosphate insecticide which also acts on the central nervous system by interfering with cholinesterase enzymes. Oral LD50's for parathion in rodents range from 3 to 13 mg/kg, while dermal LD50's have been reported between 6.8 and 21 mg/kg. Some studies have indicated that parathion may be a potential carcinogen. Parathion breaks down more slowly than phosdrin, and a 21-day worker re-entry interval has been established on grapes.
In 1986, 163 applications of parathion were made to 7,873 acres of grapes in California. This acreage constitutes slightly greater than one percent of all harvested grapes in 1986. During 1986 and 1987, only one grape sample out of 344 tested contained a detectable residue of parathion. The residue level was 0.2 parts per million, which was below the established tolerance level for parathion on grapes of 1.0 part per million.
Captan: Unlike methyl bromide, phosdrin, and parathion, the fungicide captan does not possess the potential to cause acute toxicity. LD50 values for captan in rodents range from 9,000 to 15,000 mg/kg. Since 1980, captan has been under special investigation by the EPA due to its potential to cause cancer in laboratory experiments. The EPA review should be completed within the next year, at which time the agency will decide whether to restrict or withdraw the use of the chemical. Captan breaks down fairly rapidly in the environment and degrades in the presence of water to tetrahydrophthalidimide, thiophosgene, and hydrochloric acid. No worker re-entry interval for captan has been established.
In 1986, 1,016 applications of captan to 85,703 acres of grapes were reported in California. This undoubtedly is an underestimation, since captan is not a restricted material and its use is therefore not required to be reported. Multiple applications of captan may be applied to the same grape acreage, however, which may serve to overestimate the total acreage to which the material was applied. Over 700 grape and raisin samples were analyzed by CDFA for captan residues during 1986 and 1987; less than ten percent of these samples contained detectable residues. All residues detected were at levels below ten percent of the established tolerances. Residues of captan on grapes can be removed by washing.
Summary: Use pattern data and residue levels do not indicate that the five pesticides targeted by the UFW pose significant threats to the health of field workers or consumers. For dinoseb and methyl bromide, the potential for any human exposure is negligible. In the cases of phosdrin and parathion, consumer exposure appears negligible while the potential for field worker exposure is extremely low since the materials are applied to such low percentages of California grapes (1.7 and 1.1 percent, respectively). The presence of worker re-entry intervals for these two pesticides further stands to reduce the potential for field worker exposures. The potential for adverse effects from human exposure to captan is currently being reviewed by the EPA and regulatory decisions regarding this pesticide are expected in the next several months.
II. Household Hazardous Waste
The Kansas Pesticide Newsletter April 12, 1988 issue (I am getting caught up) contained a description of an article originally published in Chemical and Engineering News in October, 1987. The article reported on the results of an EPA study of trash in Marin County and in New Orleans. The EPA looked at the disposal of hazardous wastes from households and grouped the waste into 8 categories such as pesticide and yard maintenance, prescription drugs, selected cosmetics, batteries and electrical, household cleaning, etc. Their findings indicated that the average household discarded 55 to 60 grams (about 2 ounces) of hazardous waste per week. This amounted to about 0.35 to 0.4% of the total trash discarded. While this does not seem like much, when multiplied out over a year, it amounts to 259 metric tons (a metric ton is 100 kilograms, or 2,200 lbs) per year for the Marin County area. For New Orleans, it amounted to over 600 metric tons per year.
The types of hazardous materials that were the most numerous were batteries and electrical items and cosmetics. The chemicals that are hazardous in these two categories include sulfuric acid, mercuric oxide, alcohols, acetone, toluene, phthalates, and ethyl acetate. The waste group which contributed the most by weight was household maintenance products (paints, glues, caulk, strippers, stains, thinners, etc.). This information is quite startling, and points to a real need to develop educational programs to help diminish the amounts of these chemicals released unwittingly into the environment.
We have been working on the production of a slide-tape show which will cover the topic of household hazardous waste, and hope that it will be finished within the next six months. We welcome ideas and contributions to the program, so if you have any, please send them to us.
III. Veterinary Toxicology Notes: Hazards of New
Rodenticides to Pets
A few recent additions have been made to the rodenticide armamentarium available to homeowners for control of rats and mice. Some of the newer products contain an active ingredient called cholecalciferol, also known as vitamin D3. Two of these products which are registered for use in California are CEVA True Grit RampageR and Ortho Rat-B-Gone Rat and Mouse KillerR. The concentration of the active ingredient is 0.075% in each of these products. Cholecalciferol is not an anticoagulant rodenticide, and has a unique mechanism of action. Cholecalciferol is activated by metabolism in the body, to a form which increases the absorption of calcium and phosphorus from the gut, and also has other effects which result in very high serum levels of calcium. The prolonged hypercalcemia produced by cholecalciferol ingestion is delayed in onset, and insidious in progression and ultimately leads to death.
The vitamin D3 rodenticides have not been considered to be a great hazard to pets since the published LD50 is very high. A report in the AVMA Journal in July 1988 indicates that these rodenticides may indeed pose a hazard to dogs, and that appropriate measures to prevent pet access to baits should be employed. A 30 gram packet of bait would contain about 21 mg of cholecalciferol, and the authors of the study cited above found that a dose of 10 mg/kg killed each of two dogs tested. It is likely that the LD50 is less than 10 mg/kg. Prompt action by a veterinarian must be taken to save pets which accidentally ingest these baits.
Gunther, R., Felice, L., Nelson, R. and Franson, A. Toxicity of a vitamin D3 rodenticide to dogs. JAVMA 193:211-214, 1988.
Animal Health Beat Newsletter, University of Nevada-Reno.
IV. Indoor Air Pollution
The May 1988 issue of Scientific American contained an article by Dr. Anthony Nero, Jr. from the Lawrence Berkeley Laboratory titled "Controlling Indoor Air Pollution." I highly recommend this article to anyone interested in the comparative risks of environmental chemical exposure (homes are indeed a part of the environment). Perhaps the most recently publicized indoor air pollutant is radon, which is the product of radioactive decay of radium. Radon is a gas which undergoes further radioactive decay to "daughters" (other radioactive elements) which may actually be more damaging to tissues than radon itself. Fortunately for most of us in California, surveys of indoor air from homes in buildings in California are "average" and not nearly as high as those levels found in some areas of the east and mid-west.
Other important sources of indoor air pollution are smoking, cooking, heaters (gas, oil, wood, kerosene, coal), fibers from insulation, organic chemicals that "off-gas" from building materials and furniture (e.g. formaldehyde), paints, cleaners, and even pesticides. In addition there are spores of fungi that grow indoors, bacteria, and even mites. These are just a few examples of the possible pollutants that can be found indoors.
Dr. Nero uses radon as an example of the variability of pollutant levels throughout the nation, and presents the fact that radon levels in indoor air vary by four orders of magnitude (10,000 fold) across the U.S.A. The average home in the U.S. has radon levels that result in 50 becquerels (abbreviated bq and meaning one radioactive breakdown per second) per cubic meter of air and that this exposure to natural radiation taken over a lifetime, is about three times more radioactivity exposure than people will get during their lifetimes from medical X-rays. For those people that live in highly contaminated homes, they may receive exposures every year that are greater than the people living in the vicinity of Chernobyl did, when the reactor exploded!
Dr. Nero then goes on in his article to compare the hazards of exposure to certain indoor air pollutants, and relate that to the exposure levels set for other environmental chemicals. He starts by mentioning that the risk of developing lung cancer from exposure to average levels of radon, is about 1 in 250. The uncertainty of this figure is much less than the uncertainty associated with risk assessments for most environmental chemical exposures, because there is a wealth of epidemiological data on miners who have been exposed to high levels of radon. For people exposed to the highest indoor concentrations of radon, the doses are equivalent to those to which the miners were exposed, so there is virtually no uncertainty. People who have lived in houses with levels of 1000 bq/m3 for 20 years (the author states that there are tens of thousands of homes with levels this high) have a 2-3% additional chance of developing lung cancer.
Dr. Nero then compares this to other chemical associated risks, and other risks in general, with the perspective that chemical exposure risks are generally regulated to reduce premature death to less than 1 in 100,000. He also mentions that the risk of lung cancer from "passive smoking" is estimated at about 1 in 1000. A few other figures that I found interesting were that the risk of dying in an auto accident, taken for a whole lifetime, is about 2 in 100 in the U.S. Likewise, about 1 person in 200 will die as a result of a fall or fire. Taking all this into consideration, indoor air pollution ranks as a very significant hazard.
Dr. Nero then concentrates on mitigating indoor air pollution, and addressing the topic of regulating it, which of course would present enormous problems. The last paragraph of the paper again addresses the subject of risks of indoor air pollution in comparison with other types of pollution, and he ends his paper with a very important concept, which I will quote. He writes in reference to rethinking the basis of regulatory structures for risk management;
"The resulting science and policy of indoor air quality might even change how we think about other pollutant exposures, leading to a more realistic perspective on environmental risks in general."
V. An Unusual Case of Widespread Chemical Toxicity
Shortly after returning from sabbatical I encountered an unusually well written article in a magazine I found on an airplane (the name of which has gone from my memory). It was unusual in that it was written by a physician who had discovered a cluster of thyroid related illnesses in several small towns in rural Minnesota. The physician is an endocrinologist, and had several patients referred to him who were suffering from symptoms of hyperactive thyroid, but who showed no signs of thyroid enlargement or thyroid tumor. I found his story quite remarkable, and will relate what I recall of it, because it demonstrates just how people react to finding unexplained clusters of illness, and how the physician reacted in his search for the cause of the disease.
The endocrinologist (who we will refer to as Dr. Sherlock) who wrote the story was presented with several patients from the same town, who were suffering from thyrotoxicosis. The cause of thyrotoxicosis is excess thyroid hormone in the circulation, and is usually related to overproduction by the thyroid. The symptoms of thyrotoxicosis are nervousness, weakness, sweating, weight loss, headache, hypertension (high blood pressure) and others. The patients that were presented were clearly ill, but not in immediate danger of dying, and none of them did. The physician did complete work-ups on each patient and could find none of the usual causes of thyrotoxicosis. He referred to the literature and found an obscure report of something similar in a small community several years before, the cause of which was never established. He contacted the author of the report, and did not discover any additional information that would be helpful.
After a few weeks, more cases from the locale were referred to him, and he began to believe that there was a public health problem that needed further investigation. Because of the pattern of cases seen, often people from the same family, an infectious agent was suspected. He and other public health professionals then started looking around the community, and uncovered several more cases, but still no clues about the potential cause. Word leaked out in the community about this strange disease epidemic, and toxic chemical contamination was highly suspect.
The physician thought that indeed he had good reason to suspect an infectious agent or environmental exposure, and was preparing to delve deeper when he was presented with two patients from a community more than 30 miles away, who also had the disease, but no contact with anyone else who was affected. This stumped him for awhile, and of course made the chemical contamination a more attractive prospect, but the question was, what chemical could do this? The only answer known at that time, was thyroid hormone itself, and there was no identified likely source. He started over, and did a fairly thorough epidemiologic investigation of the cases and controls, looking at all aspects he could think of, and of course diet. There did not seem to be any links that could be established, except that a couple of the cases reported that they only bought their meat from a small processing plant several miles from the town first affected. They drove the extra distance to buy there because the processor sold this fantastic, extra-lean hamburger. The physician asked the other cases about it, and they too, bought meat from the plant, and most of them mentioned one particular kind, extra-lean ground beef.
Dr. Sherlock then took it upon himself to visit the plant, and was persistent enough to even observe a few animals taken through the whole process from start to finish. As it turned out, when the skinned heads were sent for further cleaning, much of the meat from the head and upper neck was pared off and processed into the extra-lean ground beef. He finally had his source of the toxic chemical. He took some samples and analyzed them and they were indeed contaminated with a chemical that could cause the disease. The chemical was natural thyroid hormone which came from the thyroid gland, portions of which was inadvertently being cut off and ground up with the other meat. Changes were made in the processing of the head to prevent inclusion of any part of the thyroid into the human food chain, and the thyrotoxicosis outbreak disappeared.
I found this story especially interesting because of the physicians persistence, and his desire to completely understand what was happening. Thus he was not content to just pin the disease on an unknown virus, or environmental chemical contaminant. He thoroughly investigated the problem, and finally found the underlying cause. He was lucky in many ways, primarily because he had a cluster of cases of a relatively unusual disease. Epidemiological investigations of the causes of more common diseases, like cancer, are much more difficult because there are so many potential causes, and it is so common. Exposure to chemicals in the environment must always be considered as a possible source of illness, however they should always be kept in perspective with relation to other causes of disease. This is especially true for non-specific symptoms. I hope that this story has been as interesting to you as it was to me.
VI. Something to Think About Playground-Related Injuries in Preschool-Aged Children United States, 1983-1987
From 1983 to 1987, nearly 6.72 million emergency room visits in the United States were for product-related injuries among preschool children 1-4 years old. Approximately 305,000 (4.5%) of these injuries involved playground equipment. These playground equipment-related injuries occurred most frequently at home (38.3%), in sports or recreation settings (29.4%), or at school (8.9%).
Editorial Note: By 1984, more than 11 million children attended day-care facilities. The potential injury hazards of organized day-care and day-care playgrounds have been documented.
A CPSC-sponsored hazard analysis showed that falls to the ground surface account for 60% of playground equipment-related injuries. A 1-foot fall directly on the head onto concrete or asphalt or a 4-foot fall onto packed earth can be fatal. In contrast, surfaces made of energy-absorbing mats or loose materials such as wood chips or sand may reduce the likelihood of head injury even from falls of 8 feet. Yet over 48% of day-care playground equipment is not installed over impact-absorbing surfaces. Although in some cases the Occupational Safety and Health Administration requires that guard rails be installed to protect workers as low as 4 feet above ground level, no such protective legislation exists for children on playground equipment, some of which is more than 10 feet above the ground.
Injury control programs should address the safety aspects of public and other playgrounds for all ages. Recommendations to improve playground safety include installing playground equipment over energy-absorbing surfaces, locating the equipment away from obstructions, properly anchoring the equipment, checking the integrity of the equipment frequently, covering protrusions, removing broken equipment promptly, and instructing and supervising children in proper playground use. If wood chips or sand are used as surfacing, they should be well maintained and not allowed to compact or fall below an adequate depth. Limiting the height of playground equipment may also be helpful. Parents should consider the safety aspects of playgrounds in day-care centers, schools, and public areas before allowing their children to use them.
MMWR, Vol. 37, No. 41, October 21, 1988.
Statewide Pesticide Coordinator