UNIVERSITY OF CALIFORNIA
ENVIRONMENTAL TOXICOLOGY NEWSLETTER
Vol. 5 No. 4 December 1985
Table of Contents
I. Smoking Revisited
II. Health Hazards Associated with Elevated Levels of Indoor
Radon -- Pennsylvania
III. Acute Hepatic Failure After Occupational Exposure to 2-
IV. Sulfates and Nitrates in Water
V. Peanut Butter Riskier Than Ever
The November issue of Scientific_American contains an article titled "The Treatment of Diseases and the War Against Cancer" by John Cairns, Professor of Microbiology, Harvard University. In this article Dr. Cairns examines various cancer therapy and prevention programs and compares costs and effectiveness of these programs. In particular, Dr. Cairns examines the benefits and risks of chemotherapy (drug therapy) of certain cancers and concludes that indeed, chemotherapy saves 5,000-10,000 lives per year. At the same time, more than 5% of patients treated with chemotherapy will die as a direct result of the drugs (often due to drug induced leukemia).
Some of the strongest points made by Dr. Cairns relate to cigarette smoking. He states that each year in the U.S., 100,000 people die of lung cancer as a result of cigarette smoking. Little has been done to regulate this known human carcinogen, and this may be due in part to the fact that tobacco taxes generate approximately $6 billion a year for state and federal governments. In addition, Dr. Cairns states, smoking actually saves the government money by decreasing old age benefits. In general, smokers cost slightly more than nonsmokers with respect to health care, but because they generally die sooner from smoking related illnesses (heart and lung disease), each smoker saves the government about $35,000 in post-retirement social security.
Dr. Cairns closes his article with a comparison of the amounts of money spent by the government to provide chemotherapy to cancer patients (hundreds of millions/year), and the amount spent to protect the public from cigarettes (practically nothing). I think he brings his point home very clearly.
II. Health_Hazards_Associated_with Elevated_Levels_of_Indoor_Radon__--__Pennsylvania
As part of the safety program at the Limerick Nuclear Power Plant in Pennsylvania, personnel entering the plant must pass through a radiation monitoring area. In December 1984, the monitoring device detected an abnormally high level of radiation in one construction worker. When an investigation was made to determine how and where this worker was being exposed to radiation, investigators found that the air in the man's home contained extremely high levels of "radon daughters", the short- lived decay products of radon-222. Radon is an inert, radioactive gas formed in the decay chain of uranium-238. For each year the worker and his family lived in this house, they were exposed to over 50 times the annual occupational limit of exposure for uranium miners. The family relocated until remedial actions to lower the indoor radon levels could be completed.
As a result of this incident, in January 1985 state officials in Pennsylvania began a sampling program in which over 2,000 homes around the construction worker's house were examined. The homes are in an area of natural uranium deposits. Approximately 40% of the homes had radon levels exceeding the U.S. Environmental Protection Agency (EPA) guideline for indoor radon of 0.02 "working levels".
Editorial Note: The elevated radon levels near the eastern border of Pennsylvania are associated with natural uranium deposits that extend into northern New Jersey and southern New York. Since similar geologic deposits are found throughout the country, the elevated radon levels in Pennsylvania may indicate a much broader national problem. Radon enters a building through cracks, such as those in a basement floor, and through openings around pipes and wiring. Once inside, the radon builds up in the air, particularly in poorly ventilated houses. As radon daughters are formed, they attach to airborne particulates. When inhaled, these particulates can deliver a substantial dose of radiation to the bronchial epithelium.
Exposure to radon daughters increases a person's lifetime risk of lung cancer. The risk rises in direct relationship with the length of exposure and with radon daughter levels.
The two risk estimates are derived from studies of uranium miners and have been extrapolated from relatively high occupational exposures to environmental levels. The highest lifetime risk calculated from studies of uranium miners is 7.3 x 10-4 deaths per working level month, and the lowest generally accepted risk is 3.0 x 10-4 deaths per working level month. These estimates are for the general population, including smokers. Each year, approximately 5,000-30,000 deaths may be attributed to background levels of indoor radon. The health threat from radon can be addressed by identifying geographic areas that could produce elevated levels of indoor radon, developing strategies to reduce exposure, conducting research on effective remedial measures to be taken in buildings, and providing educational programs for health officials and the public. The educational programs can be used to inform health officials and the public about the health threat from radon and about associated risk factors, such as smoking.
MMWR, November 1, 1985/Vol. 34/No. 43
III. Acute_Hepatic_Failure After_Occupational_Exposure_to_2-Nitropropane
On June 28, July 1, and July 2, 1985, two construction workers applied an epoxy resin coating to a water main in an underground concrete vault in San Jose, California. Over the 3 work days, the men applied 10 gallons of the resin coating. The vault was unventilated, and the workers used no respiratory or skin protection.
In the evening of July 2, both men went to a local hospital because of persistent nausea, vomiting, weakness, and dizziness. Initial laboratory tests showed slightly elevated serum glutamic-oxaloacetic transaminase (SGOT)--60 units per liter (U/L) for worker 1 and 79 U/L for worker 2 (normal SGOT is less than 40 U/L). The men were admitted for observation and discharged the following day, after their symptoms had subsided.
Three days later, worker 1 returned to the hospital with persistent nausea, vomiting, anorexia, and onset of scleral icterus. He died 9 days after his initial presentation. Autopsy findings were consistent with fulminant hepatic necrosis.
Worker 2 has remained clinically well, although for at least 6 weeks he continued to have elevation of liver enzymes (SGOT and SGPT) in a range of 1.5 to 2 times the normal maximum. Both men had histories of moderate alcohol use (12 cans of beer/week); neither had significant past medical histories, including previous hepatic disease.
According to the manufacturer's labelling information, the coating material contained a mixture of cyclohexanone, toluene, tri(dimethylaminomethyl)phenol, and 2-nitropropane (2-NP), combined with coal tar pitch and epoxy resin. The analysis of leftover compound by the California Department of Health Services confirmed the presence of 2-NP.
Editorial Note: 2-Nitropropane (2-NP), a notroparaffin, CH3CH(NO2)CH3, is used industrially as a solvent in coatings, printing inks, and adhesives. In 1977, 15 million pounds of nitroparaffins were used in paint and coatings in the United States, and 2-NP accounted for about 80%. Estimates by the National Institute for Occupational Safety and Health (NIOSH) indicate that 185,000 U.S. workers are potentially exposed to 2- NP during its production and use.
At least five occupationally related deaths have resulted from exposure to 2-NP. Typically, workers coated the surface of an enclosed structure (tank, vault, or shiphold), using sealant containing 2-NP. No forced ventilation or personal protection was used. After many hours of exposure, they complained of headache, nausea, vomiting, dyspepsia, and chest pain. A few days later, acute jaundice, hematemesis, enlarged liver, edema, and oliguria/anuria developed, followed by coma and death. The following control measures should be considered for preventing acute toxicity and potential long-term health consequences of 2-NP exposure: paint, sealant, or other coating materials must not be applied in confined spaces without sufficient forced ventilation and respiratory and cutaneous protection, products containing 2-NP should be labelled to reflect its toxicity; workers should be warned that odor does not serve as a warning sign, since toxic levels are below the odor threshold of 83 ppm, and 2-NP should be replaced whenever possible by other less toxic solvents in paint and coating formulations.
MMWR, November 1, 1985/Vol. 34/No. 43
The following articles, by Dr. Melville Palmer, O.S.U.
Extension Agricultural Engineer, appeared in the Agr-Eng Water
Digest #27 (Summer 1985).
"We recently received reports of suspected health problems in livestock due to high levels of sulfates in their drinking water. Sulfates occur naturally in ground water, since they are leached from soil and rock formations such as those that occur in sections of northwest Ohio. Calcium and magnesium sulfates cause water to be hard, and may be associated with sulfate-reducing bacteria that produce hydrogen sulfide with the odor of rotten eggs. Magnesium sulfate (Epsom salts) can have a laxative effect on people and animals, and sodium sulfate (Glauber's salt) gives water a bitter taste. The maximum level of sulfates in drinking water for humans should not exceed 250 mg/liter according to USEPA Secondary Regulations (for contaminants that primarily affect the aesthetic qualities of water). For livestock, the recommended maximum level of sulfates in water is more uncertain due to insufficient research. Young animals are more sensitive to sulfates than mature animals. The 1983 University of Minnesota bulletin "Water Quality for Livestock and Poultry" points out that in young animals, sulfate concentrations in excess of 350 to 600 mg/liter may be associated with severe chronic diarrhea, electrolyte imbalance and, in a few instances, death.
Home water softeners commonly used to remove carbonates from hard water do not remove sulfates, since calcium or magnesium sulfate are simply converted to sodium sulfate. For removing sulfates from drinking water in a home, distillation or reverse osmosis water treatment systems are generally the most satisfactory. These are available from several manufacturers or dealers in home water treatment equipment. Removing sulfates from livestock water is often impractical due to the cost of treating large amounts of water. Alternatives would be to use a farm pond for livestock water or consult a ground water geologist about drilling a well in a different formation.
Nitrates are common compounds in our environment. However, they seldom occur naturally in ground water. When found there, they usually indicate contamination. Nitrates are soluble in water and widely dispersed in soils, human and animal wastes, fertilizers, crop residues, certain industrial wastes, and the atmosphere. Rainfall brings down large amounts of nitrogen, about 17 pounds falling on an acre each year in Ohio. Health hazards for humans and certain animals drinking water high in nitrates are due mainly to bacterial conversion of nitrates to nitrites in the digestive tract. Nitrites restrict the oxygen- carrying ability of blood in infants, ruminant animals, young monogastric animals such as pigs and chickens, and horses of all ages. This can cause a disease called methemoglobinemia, where suffocation occurs. USEPA drinking water standards limit nitrate-nitrogen (NO3-N) in water to 10 mg/liter, so there are "nitrate alerts" when public water supplies (usually from rivers) exceed this level. The nitrate-nitrogen standard of 10 mg/liter was established to protect infants less than six months of age and other sensitive persons. Many adults can tolerate higher nitrate levels. There are no regulatory standards for livestock water at this time. However, the National Academy of Sciences and several State universities recommend a limit of 100 mg/liter for nitrate-nitrogen in livestock water to provide a reasonable margin of safety. When water is tested for nitrates, it is important to know whether the numbers reported are for nitrate- nitrogen (NO3-N) or total nitrates (NO3). To change total nitrates to nitrate-nitrogen, multiply by 0.23. To change nitrate-nitrogen to nitrates, multiply by 4.5 (10 mgl/liter NO3-N is equivalent to 45 mg/liter total nitrates).
To avoid high nitrate levels in ground water, it is important to maintain good sanitary practices for well location, construction, and maintenance as outlined in Ohio's Private Water System Rules administered by Boards of Health. Special care should be taken where there are shallow wells drilled or driven in sandy soils with high permeability. This means that nitrate sources such as fertilizers and manures should be used with greater discretion than where soils (such as clays) are slowly permeable. Nitrates are tasteless and odorless, so chemical tests are needed to determine the nitrate content of water. Removal of nitrates from human drinking water is possible with distillation or reverse osmosis units available from water treatment equipment suppliers. Treatment processes that do_not remove nitrates include chlorination, softening, activated carbon filtration, and boiling (nitrates are actually concentrated). It is usually impractical to remove nitrates from livestock water due to cost. An alternative source of water, such as a farm pond, may be needed. Farm pond water usually has low nitrate content where the watershed is properly maintained.
Ohio Veterinary Newsletter - 11/1/85
Two recent scientific studies have concluded that drinking water laced with toxic chemicals may not be as hazardous as previously reported. A $1 million study financed by several industry groups including the Chemical Manufacturers Association and the US Chamber of Commerce has found little scientific evidence of serious health problems associated with living near hazardous waste sites. The report by the Universities Associated for Research and Education in Pathology, Inc. does not conclude that no health risks are linked to the sites. At the same time an expert on diet and cancer from the University of California at Berkeley, Bruce Ames, has concluded that one liter of the most contaminated well water may be less likely to cause cancer than a peanut butter sandwich. He has devised a "Carcinogenicity Potency Data Base" to compare cancer-causing elements in food and medicine. Using a liter of chlorinated tap water (containing "carcinogenic" chloroform) as a base unit, he has found that contaminated well water in the Silicon Valley is twice as likely to be cancer-causing; while an average peanut butter sandwich (due to a tasteless, invisible mold by-product) carries nineteen times the risk.
US Water News, May 1985 via Pesticide Pipeline, CSU reprinted in Vet. Hum. Toxicol. 27(6), December, 1985.
For the past 2 1/2 years I have been involved in a USDA Extension Service Residue Avoidance Program project called the Food Animal Residue Avoidance Databank (FARAD). FARAD is available for service at UCD at (916)752-7507. If you have any questions that relate to the FARAD data files listed below, please call.
Arthur L. Craigmill