"Published Occasionally at Irregular Intervals"

Vol. 16 No. 2, April 1996

In This Issue

Diet and Environment in Cancer Risk

Trained as an epidemiologist, Clark W. Heath, Jr., M.D., is vice president for epidemiologic and surveillance research for the American Cancer Society in Atlanta, a position he has held since 1988. He also is clinical professor of community health at Emory University’s School of Public Health. Dr. Heath spent 20 years at the Centers for Disease Control and Prevention, where he directed programs related to the epidemiology of cancer, birth defects, chronic disease and environmental exposure. In this interview with Food Insight, he discusses cancer trends and environmental cancer risks, including diet.

Is the United States undergoing a cancer epidemic?

No, we're not, although on the whole cancer rates have been rising a bit. However, its quite clear that the numbers have increased at least in part because (1) our population has increased, and (2) we live a bit longer and cancer is principally a disease of older people. The real answer to the question lies with specific cancers. Overall, the cancer death rate has been going up in the United States since the 1950s, but the major cause of this increase has been lung cancer. If you exclude lung cancer deaths, cancer mortality would have declined 14 percent between 1950 and 1990.

How does the environment influence cancer risk?

Environmental causes of cancer include exposures in the community or workplace settings, as well as exposures determined by individual lifestyle choices such as smoking, sun exposure and diet. The specific degree of cancer hazard posed by such risks depends on (1) the concentration or intensity of the carcinogen in the environment and (2) the exposure dose a person receives. Together these factors create a range of risk. For example, in situations where high levels of carcinogens are present and where exposure is extensive, the hazards may be significant. But where concentrations of a carcinogen are low and exposures are limited, hazards are often negligible.

How does diet contribute to cancer risk?

Diet has been estimated to contribute to at least one-third of all cancer-related deaths. Evidence is fairly strong for the role of dietary fat and calories in some types of cancers, which may be linked to obesity. Obesity probably has a fairly pervasive influence for cancers of the breast, colon, prostate, gallbladder, ovaries, and uterus. We are talking about individuals whose weight is 40 percent or more above the recommended weight for their age and height. However, not all obesity is the same. Different body types or different forms of obesity may bear differently on cancer risk.

Can exercise or physical activity help reduce cancer risk?

The American Cancer Society (ACS) does not specifically recommend exercise as a means of reducing cancer risk. However, the exercise message is embedded in our recommendation that people maintain a desirable weight. It's a safe assumption that exercise would help reduce cancer risk in so far as physical activity, coupled with proper diet, is a key element in weight management. However, obtaining scientific evidence that supports this hypothesis is harder than one might expect. It's difficult to measure how much exercise someone gets at work or at play.

To what do scientists attribute the recent increase in breast cancers?

There has been a significant increase in the number of breast cancer cases recently, which can be accounted for by the fact that baby boomers are entering the cancer years. It's a matter of the size of the overall population. In age-adjusted terms, breast cancer incidence has been increasing just one percent a year since the 1940s.

Since the 1980s, the rate of breast cancer increase has most certainly been due to the success of mammography programs, because most of the new cases represent early-stage cancers. That increase has now leveled off, which is what we might expect with a successful program that finds cases earlier. At the same time, the mortality rate from breast cancer has been dropping slightly, which we again think means that mammography programs are detecting cases earlier so that they can be treated more effectively.

Although we’ve been able to lower breast cancer mortality rates and to improve detection, we’re still not in a position to recommend specific actions to prevent breast cancer. The major risk factors revolve around the role of estrogen in the body as it relates to early onset of menses, late menopause and never having children; these are not variables a woman can control.

Are environmental estrogens a major contributor to breast cancer?

There certainly are chemicals in the environment with weak estrogenic effects, such as polychlorinated biphenyls (PCBs) and other chlorinated compounds, many which were banned long ago. That is, like estrogen, they encourage the proliferation of breast cells, which increases the risk of carcinogenesis. However, these are weak estrogenic compounds compared to naturally occurring estrogen, maybe on the order of 1,000 times weaker. Thus, this area needs much more study before any firm conclusions can be drawn.

How do environmental exposures relate to cancer incidence in young people?

Cancer is not a common disease in people under 40. However, the incidence of one specific type of cancer, non-Hodgkin's lymphoma, has risen 65 percent in young people over the last 25 years. Risk factors for this type of cancer are largely unknown and may include some occupational or environmental exposures. However, we also know that reduced immune function, such as that experienced by AIDS patients, is associated with increased risk of non-Hodgkin's lymphoma. The significant rise since the 1970s in the incidence of the human immunodeficiency virus and human T-cell leukemia lymphoma virus-I would account for at least part of the increase in this cancer.

What about epidemiological studies that found increased risk of leukemia in children from eating nitrite-containing foods?

There are many studies that look at different risk factors and publish their results. It's part of the research process. There were two or three studies that dealt with the leukemia issue, but in some of those studies, the data on hot dogs and other nitrite-containing foods were not the principal purpose of the study. The risks related to hot dogs were teased out of a lot of other risk estimations.

Epidemiological studies are entirely legitimate ways of exploring cancer risks in humans, but they are observational, not experimental. They can be very persuasive if they discover a risk that is very high, that has also been shown in animal and laboratory experiments, and that increases with the dose response rate. Exploring a link between hot dog consumption and leukemia will require dozens of studies starting from different points but leading in the same direction, plus a good bit of data from the laboratory and animal experiments.

Parents might be concerned if hot dogs are the only food their kids eat. But not eating hot dogs at all because of a possible risk of cancer is simply not justified based on these limited data.

What is ACS's position on the Delaney clause?

The Delaney clause, part of the Food Additives Amendment to the 1958 Federal Food, Drug and Cosmetic Act, prohibits adding to food any substance found to cause cancer in laboratory animals or humans. ACS believes that the Delaney clause is a rather outdated approach to the issue of carcinogenesis and the whole issue of risk-benefit analysis. Banning any man-made chemicals with carcinogenic potential is unrealistic, given the very low concentrations involved and the value of pesticides and food additives in sustaining our food supply.

Changing the Delaney clause is very unlikely to affect U.S. cancer rates in any way, because whatever carcinogenic substances get into the food supply now in terms of added chemicals account for negligible risk. If you reduce the risk further, you just make it even more negligible. Overall, the benefits of eating fruits and vegetables far outweigh any potential carcinogenic risks from pesticide residues in foods.

Does adding chlorine to drinking water pose a significant cancer risk?

Not to any important degree. First, we add chlorine to water for good reason -- to prevent infectious diseases. In this country, we've forgotten how terrible typhoid epidemics can be. Second, there is no strong evidence that chlorine causes cancer as it is presently being added for water disinfection. Some chlorinated compounds can cause cancer, but at high dose levels that are not normally found in water.

What about adding fluoride to water to protect oral health?

Fluoride has had a very positive effect on preventing dental caries, probably the most common disease in the world. Nowadays, fluorides are added to many products like toothpaste, and so the role of fluoridation of the water supply may not be as important as it was when it was first introduced. There is no sound, scientific evidence suggesting that fluoride causes cancer.

What are some new developments in cancer research?

Much of the current research has to do with cancer mechanisms or the enzyme systems that switch on and off and how they relate to promotion and progression of carcinogenesis. These investigations may lead to discoveries that can be used to interfere with or stop the proliferation of cancer cells.

The role of diet also continues to be studied. In 1982, ACS began an epidemiological study, the Cancer Prevention Study II, that includes 1.2 million Americans. We know already from this study that a diet rich in fruits and vegetables helps reduce the incidence of colorectal cancer, confirming the findings of previous research. In 1992, 25 percent of the people in the original sample completed a six-page questionnaire on their dietary behaviors. We will be tracking this cohort with cancer registry data in the states and with the National Death Index to help develop a better understanding of diet, cancer incidence and cancer mortality.

An Ounce of Prevention....

Researchers estimate that if we apply
everything currently known about cancer prevention,
as much as "two-thirds" of all cancers would not occur.

Smoking: Cigarette smoking is responsible for some 87% of lung cancers and 30% of all cancer deaths.

Weight maintenance: Overweight individuals have an increased risk of colon, breast, prostate, and other cancers.

Diet and Nutrition: As many as one-third of all cancers are believed to be diet-related.

Sunlight: Almost all cases of basal and squamous cell skin cancers are caused by overexposure to the sun.

Alcohol: Oral cancer and cancers of the larynx, throat, esophagus and liver occur more frequently among heavy drinkers of alcohol.

Smokeless Tobacco: Use of chewing tobacco or snuff increases the risk of cancer of the mouth, larynx, throat, and esophagus.

Sexual Behavior: Early age at first intercourse, multiple sex partners, and infection with certain types of human papillomavirus (a sexually transmitted disease) are risk factors in the development of cervical cancer.

Adapted from Cancer Facts & Figures 1995, American Cancer Society

REF: Food Insight, Sept/Oct 1995.

Multiple Chemical Sensitivities (MCS)

A workshop was recently held by the World Health Organization to discuss multiple chemical sensitivities. Their recommendations for a name change and specific conclusions are listed below.

1. The name MCS (multiple chemical sensitivities) should be discontinued because it makes an unsupported judgement about causation. The recommended new name is Idiopathic Environmental Intolerances (IEI). This also recognizes the fact that many environmental intolerances other than chemicals are claimed in various countries. These are characterized by similar symptoms and include -- dental amalgams, electric and magnetic fields, and others.

2. IEI (formerly MCS) cannot be recognized as a clinically-defined disease. There are neither accepted underlying mechanisms nor validated clinical criteria for diagnosis.

3. IEI is defined as:

An acquired disorder with multiple recurrent symptoms.

Associated with diverse environmental factors tolerated by the majority of people.

Not explained by any known medical or psychiatric disorder.

4. Clinical assessment should be designed to rule out any medical or psychiatric conditions requiring therapy.

5. There are no specific tests to establish the IEI condition. Certain tests such as immunological testing, porphyria testing, neuroimaging, biological monitoring and alternate medicine tests are of no confirmatory value.

6. Effective treatment has not been validated in controlled clinical trials. There is no justification for chelation therapy or other detoxification procedures including "sauna detoxification."

7. Approaches to care based on understanding and supportive care are appropriate.

Avoidance and psychological/psychiatric care are the common approaches. Avoidance to minimize exposures may, in some instances be appropriate, but isolation of patients from the general environment may have adverse consequences.

Psychological/psychiatric approaches currently include self-regulation (relaxation, biofeedback), behavioral therapy, psycho-pharmacological treatment, cognitive therapy, and insight-oriented therapy which are tailored to the individual's condition.

8. Human research is urgently needed to determine the nature (e.g., psychogenic, toxicogenic) of IEI. The key question is whether subjects with IEI are able to distinguish in a double-blind placebo-controlled challenge study between reported environmental (e.g., chemical) triggers and placebos.

Miniblind Lead Warning Issued

The Arizona Department of Health Services (ADHS) warns parents that some types of plastic miniblinds contain dangerous levels of lead and should be kept out of the reach of young children and away from food-preparation areas.

The warning follows the identification of miniblinds as the apparent cause of a child lead poisoning incident in Yuma, Arizona and as a possible contributing factor in at least 20 other cases investigated by ADHS. Laboratory testing conducted this week confirmed the presence of lead in plastic miniblinds and in dust samples collected from the blinds, indicating that lead is transferable by hand-to-mouth activity.

The affected blinds have 1-inch-wide curved slats, have been found in a range of colors from off-white to black, and have been purchased from various outlets, including national-chain department and discount stores. Thus far, all of the problem blinds either have been labeled as imported or have contained no identification as to manufacturer or country of production.

Miniblinds pose the greatest risk to infants and small children, who frequently put objects in their mouth and are most sensitive to the health effects of lead. Lead, when eaten, can cause a variety of health problems that range from behavior and learning difficulties to convulsions and even death in the most severe cases. For older children and adults, miniblinds may pose little or no health risk.

The poisoning case with the apparent link to miniblinds involved a one-year-old boy with a blood-lead level of 37 micrograms per deciliter (mg/dL), nearly quadruple the federal and state level of concern of 10 mg/dL. The family lived in a trailer and there was no observed exposure to interior paint or any other source of lead. A set of miniblinds hung within arm’s reach of the child’s bed. The mother said the child would touch the blinds and transfer his hands to his mouth and would even mouth the blinds directly. The blinds were laboratory-tested and found to contain lead dust at 1,021 micrograms per square foot, twice the federal Housing & Urban Development child-safe limit of 500 mg/sq ft for lead dust from paint in window sills. The blinds were cream-colored and carried the label "Made in Taiwan." The mother said the blinds were less than two years old.

During at least 20 other child lead-poisoning investigations by ADHS, plastic miniblinds -- although not found to be the primary source of exposure -- have tested positive for lead in field tests. Typically parents said these blinds were purchased at discount department stores.

Field tests simply indicate whether a product contains lead. To confirm that lead from miniblinds can be transferred to the hands and mouth, dust samples from eight different sets of blinds were laboratory tested this week. All of the samples were found to contain lead and five exceeded the federal limit for lead dust in window sills. The over-the-limit readings ranged from 722 mg/sq ft to 2,874 mg/sq ft. The blinds with the three highest readings were labeled as manufactured in China. The other two exceeding the limit did not carry a manufacturer's label. The ages of the over-the-limit blinds were two months for one, two years for another and unknown for the rest. Six of the dust-tested blinds also were analyzed to determine whether the blinds themselves contained lead. All six did.

ADHS has notified the appropriate regulatory agency, the U.S. Consumer Product Safety Commission, of its findings.

ADHS recommends that parents move suspect miniblinds out of the reach of young children and away from food and kitchen utensils. Lead dust left by miniblinds in window sills and on walls and floors can be wiped away with a solution of automatic dishwasher detergent or any other type of phosphate detergent.

Parents can test their miniblinds for lead by using a field testing kit. Such kits are available for $5 or less at some hardware and discount department stores.

Parents concerned about their child’s exposure to lead should contact their doctor for a blood test. Because symptoms of lead poisoning may be subtle and difficult to recognize, blood testing is the only means of identifying a problem at an early and most treatable stage.

ADHS has identified a number of other potential sources of lead poisoning over the past two years. These have included certain types of imported crayons, bulk water tanks, wrappers of some types of Mexican candy, and two brands of pool cue chalk. The imported crayon warning led to the federal recall of at least a dozen brands of Chinese crayons.

"This series of ADHS findings underscores the need for public health agencies to remain ever vigilant about uncovering dangerous health hazards to our children," said ADHS Director Jack Dillenberg.

The most common source of lead poisoning remains lead-based paint. Soil contaminated with leaded gasoline emissions or industrial emissions also can cause poisoning if ingested. Other sources include leaded solder and plumbing fixtures, lead-glazed pottery and leaded crystal and folk-remedy powders known as "azarcon" and "greta."

REF: News Release, Arizona Department of Health Services, December 7, 1995.

The Ethics of Chemical Technology

Imagine a world full of chemical plants, synthesizing toxic compounds practically nonstop. The chemicals produced are so toxic that if released into the water and air, surely adverse biological effects would result.

Imagine that these chemicals are part of the food chain. Consider a chemical in apples that is known to cause vomiting, diarrhea, ulceration, bleeding from intestines and circulatory collapse.

Would you be appalled if no government regulation could control this incessant manufacturing process? What if no law existed that was strict enough to keep these chemicals out of the food supply?

You then might ask, what are the ethics of a society that would allow such unmitigated irresponsibility? But our culprits here are not bound by codes of conduct and responsibility. Our imaginary world is not fantasy but part of natural processes in the biosphere. Our subjects are the earth’s flora and fauna, producing through their metabolism chemicals that function to enhance their probability of survival and, ultimately, reproduction.

It has long been known that many organisms, especially plants, produce chemicals incidental to their normal energy producing biochemistry that function to ward off predators, protect seeds, or attract insects for pollination. Sometimes, these chemicals are just by-products of metabolism that may serve other purposes, or they are perhaps excretory products that would be toxic if allowed to accumulate in the cells. The chemical in the aforementioned apples is nothing but acetic acid. Although a natural component of apples, the acid is nevertheless listed as a hazardous substance. Even oxygen is incredibly toxic, but aerobic organisms have developed an incredible biochemical pathway that detoxifies the gas while simultaneously producing energy for their cells.

Many of the incidental chemicals produced by plants are incredibly toxic in high doses. Certain fungi of the genus Aspergillus grow on cereals and produce chemicals called aflatoxins that are hundreds of times more potent than any synthetic pesticide our brains have discovered. Yet, our ethics do not apply to Aspergillus, unless one considers the timely application of a fungicide on stored grains the right thing to do in protecting food safety.

If we agree that the chemicals produced by plants are functional, has evolution not resulted in a form of chemical technology? As defined by the dictionary, technology is the totality of the means employed to provide objects necessary for human sustenance and comfort. Through our chemical technology, aren’t we just "imitating" our botanical counterparts?

Members of indigenous cultures have long used plants as their medicines. The knowledge of which plants to use, how to prepare them, and the amounts to administer have been passed from generation to generation. Isn’t the use of flora for our benefit, our survival, a form of chemical technology? Perhaps we should consider generations of trial and error in discovering which plants are beneficial and which are not as analogous to a risk assessment process.

Humans have always used chemical technology. Whether the chemicals are made by plants or by our own hands is irrelevant. Some have maintained there is a difference between chemicals from the tropical rain forests and chemicals from the giant chemical industries. But principles of environmental chemistry would dictate that behavior of a chemical is governed primarily by thermo-dynamics, not how it was made.

Some would say that our coevolution with plants over many generations has allowed us to detoxify many of the natural dietary chemicals. Consider, however, that many of our foods are recent inventions of selective breeding that still possess the same potentially toxic chemicals as their wild ancestors.

Why are we not harmed? The answer is in the dose; one would have to eat an unreasonably large quantity of potatoes to overdose on solanine, a toxic but natural alkaloid. Yet, we are exposed to this known toxin and to teratogen (by EPA testing criteria) with every french fry. So, dose must make the poison, as the toxicological clich goes.

One perspective we overlook in our myth about the quality of natural chemicals versus synthetic chemicals is our own biochemistry. Our detoxification systems are quite general in their function. Perhaps as a result of exposure to a bewildering array of plant chemistry, animals have evolved a flexible oxidative enzyme system that makes no distinction as to chemical source. Why one chemical is more rapidly degraded and excreted from the body than another chemical is a matter of kinetics. The question the biochemical toxicologist asks is what is the affinity of the enzyme for the chemical and how fast does the reaction occur. Thus, even DDT, which is stored in our fat tissue (as DDE), is degraded into an acid and eventually eliminated from our body. The process just occurs more slowly than with other so-called biodegradable chemicals.

So, what are the ethics of chemical technology? A case can be made that chemicals are just tools we use to survive, no different than what we find in the botanical world. It takes time to learn what works and what doesn’t, but because we can produce new kinds of chemicals so quickly, we have conflicts about functionality and safety. We have passed legislation over the years that allows us to compress the "trial and error" approach into a comparatively fast assessment of risk.

While many would agree that the regulatory process certainly needs some adjustments, under current practices there should be no ethical dilemma in using our chemical tools.

REF: Article written by Dr. Allan Felsot, Extension Toxicologist, Washington State University for Agrichemical and Environmental News, 118, Dec 1995.

Latest Fluoride Study Finds No Support for Osteosarcoma Link

Fluoride exposure does not increase the risk of osteosarcoma and may even be protective in males, a study by New York State and Yale University researchers found.

The latest study "contributes to the body of evidence that indicates that the public can continue to enjoy the dental health benefits of fluoride with no associated major risks," said the study appearing in the December American Journal of Public Health.

For the study, researchers embarked on a population-based case-control study among New York residents, in response to a call for such research by federal health officials. The case subjects were 24-year-olds and younger who were diagnosed with osteosarcoma from 1978 to 1988. Control subjects were matched by age and sex, and exposure information was obtained from parents. The study closely examined gender variations because an earlier National Toxicology Program study found deleterious effects in male rats.

All sources of fluoride except dietary sources were examined separately and then combined to estimate lifetime exposure levels.

The researchers found that total lifetime fluoride exposure was not significantly associated with osteosarcoma among all subjects combined or among females. But a significant protective trend was spotted for males in the study, "Fluoride Exposure and Childhood Osteosarcoma: A Case-Control Study."

Decreased risk was most associated with fluoride tablets, while toothpaste and dental treatments were borderline significant and also protective.

REF: Food Chemical News, 37(44), Dec 25, 1995.

Moderate Alcohol Consumption During Pregnancy Puts Children at Risk: Study

More studies are needed on the health effects of lower levels of maternal drinking, since research has focused mainly on the most exposed or the alcoholic pregnancy, said an editorial in the December American Journal of Public Health.

University of Pittsburgh School of Medicine’s Nancy Day noted that public health officials have little information on the outcomes of the pregnancies of women who drink at lower levels, even though they represent the majority of the drinking population during pregnancy.

"Thus, the time has come to explore the effects of alcohol exposure during different stages of pregnancy, the effects of differing patterns of alcohol use during pregnancy, and the shape of the relationships between exposure and outcomes," Day said. "With this knowledge, we can begin to clarify the mechanisms of alcohol’s effects during pregnancy," she added.

Day pointed to a new study (appearing in the same issue) that detected effects on the development of the fetus’s central nervous system at maternal intake levels of three or more drinks per day. While the effects may be small, Day said it would be a mistake to ignore them.

"Although small, they serve as a marker of the effects of a teratogen and as a sign that the growth and achievement of these exposed individuals might be less than they could have been," Day said.

The study by French researchers found that moderate to heavy alcohol consumption during pregnancy, at levels well below those associated with fetal alcohol syndrome, has effects on preschool-age psychomotor development. The study is the first to confirm the effect on preschool-age children of moderate to heavy maternal drinking in a population with low socioeconomic status and no illegal drug use.

Pregnant women were interviewed during the first trimester visit to a maternity hospital in Roubaix, France; then the psychomotor development of 155 children was assessed at age 4 years. The study found that consumption of 1.5 ounces of absolute alcohol or more per day during pregnancy was significantly related to a drop of 7 points in the mean score of the general cognitive index of the McCarthy scales.

The researchers concluded in the study, "Moderate Prenatal Alcohol Exposure and Psychomotor Development at Preschool Age," that efforts to reduce alcohol drinking during pregnancy should not focus only on alcoholic mothers, because even lower levels of alcohol can put a child at risk.

REF: Food Chemical News, 37(44), Dec 25, 1995.

Tea May Have Protective Effect Against Lung Cancer, Study Finds

A case-controlled study of Japanese tea drinkers found that tea consumption seemed to exert a protective effect against lung cancer, especially in women.

Epidemiological studies of the effects of tea drinking and lung cancer have been mixed, noted the article by Yoshiyuki Ohno and colleagues in the November 1995 Japanese Journal of Cancer Research. This study of nearly 1,000 Okinawans (333 cancer cases and 666 age-, sex- and residence-matched controls) found a protective effect, especially for women and against squamous cell carcinoma.

For men, the odds ratios for lung cancer according to tea intake were: not daily -- 1; any daily -- 0.73; 1-4 cups per day -- 0.85; 5-9 cups per day -- 0.85; 10 or more cups per day -- 0.57. A cup was defined as 150 ml.

For women, the effect was greater: not daily --1; any daily -- 0.66; 1-4 cups per day -- 0.77; 5-9 cups per day -- 0.77; more than 10 cups per day -- 0.38.

Even greater protection was seen in squamous cell type cancer, which found that daily drinking of tea reduced the risk of this type of cancer by 50% for males and 92% for females.

The effects of tea drinking may even offer some protection against the effects of smoking, with daily tea drinkers who "ever smoked" having a 30% apparent protective effect for males and a 57% effect for females. The study noted, however, that these findings were not statistically significant, with a wide-ranging 95% confidence interval.

"To our knowledge, this is the first case-control study which suggests a protective effect of tea consumption against lung cancer," the scientists wrote. "Tea catechins have been demonstrated to possess inhibitory effects against various types of tumors. The features of the catechins that may affect tumorigenesis are their antioxidant activities, inhibition of nitrosation reactions, modulation of carcinogen-metabolizing enzymes, trapping of activated carcinogens, metabolizing enzymes, trapping of activated carcinogens and inhibition of activities related to cell proliferation."

The scientists said they did not know why their study results differed from others, but suggested that the high rate of consumption of Okinawan tea (which is partially fermented, but not as fermented as black or oolong tea) by the subjects could be the answer, since green (unfermented) tea contains catechins at a level of 30%-42% in solid tea extracts, as opposed to 3%-10% in black tea. In addition, the green tea contains about a 4 mg dose of the antioxidant vitamin C, while black tea contains almost none.

REF: Food Chemical News, 37(41), Dec 4, 1995.

Wastewater and Sludge on Food Crops Deemed Safe if Properly Treated: NRC

Properly treated wastewater and sludge are safe for agricultural use, but management strategies must continue to focus on reducing the concentrations of pathogens to acceptable levels, said the National Research Council (NRC) in a Feb. 28 report.

There have been no reported U.S. outbreaks of infectious diseases linked to adequately treated and properly distributed reclaimed water or sludge on agricultural land. While the report found the practice safe and effective for fertilizing and irrigating food crops, it also said that management strategies must monitor treatment efficacy and the reliability of the process to reduce pathogens.

NRC recommended some changes to testing for pathogens in sludge. Citing a recent study in Denmark that found the beef tapeworm (Taenia sp.) may survive in sludge-treated fields for up to one year, NRC urged the Environmental Protection Agency to reconsider its 30-day waiting period following the application of Class B sludge to pastures used for grazing animals. Class B restrictions are aimed at allowing a suitable time for the elimination of helminth ova, which can be transmitted to humans from improperly cooked, contaminated meat.

Until a more sensitive method for the detection of Salmonella in sludge is developed, the present test should be used for support documentation, but should not be substituted for the fecal coliform test in evaluating sludge as Class A (safe for public contact). The Salmonella test is less precise, said the report, because of the relatively low numbers of Salmonella present compared to fecal coliform. NRC also urged the Environmental Protection Agency to continue developing and evaluating effective ways to monitor for specific pathogens in sewage sludge.

Midwest farmers have been using treated sludge on crops, particularly corn and small grains for cattle feed, while reclaimed wastewater comprises less than 1% of water used for crop irrigation. NRC found the immediate or long-term threat from organic chemicals to humans consuming foods irrigated with reclaimed water was negligible.

NRC urged changes to how EPA handles treated municipal sludge. "A more comprehensive and consistent survey of municipal wastewater treatment plants is needed to show whether or not toxic organic compounds are present in sludges at concentrations too low to pose a risk to human and animal health and to the environment," said NRC. EPA should not exclude chemicals from regulatory consideration based solely on whether or not the chemicals, such as PCBs, have been barred from manufacture in the United States.

The group of experts on the NRC panel also focused on the public perception of using land application of sludge. NRC recommended that states and municipalities implement a beneficial-use program to provide assurances on the safety of the practice. Municipal wastewater treatment plant operators and those using sludge and wastewater should "implement visible, stringent management and self-regulation measures, including monitoring and reliable reporting by farmers, and should support vigilant enforcement of appropriate regulations by local or state agencies," NRC recommended.

Concerns over liability, property values and nuisance factors, "rather than scientific information on the health and safety risks from food consumption, may be the critical factors in determining whether reclaimed wastewater and sludge are beneficially used on cropland," said the report, "Use of Reclaimed Water and Sludge in Food Crop Production." NRC urged treatment plant operators and applicators to not only comply with state and federal regulations but to "take extra steps to demonstrate to various stakeholders (i.e., neighbors, farmers, food processors and consumers) that such compliance is occurring."

REF: Food Chemical News, 38(3), March 11, 1996.

Issues Surrounding Methyl Bromide*

Catherine Jacobson
Maya Komanovsky
Susan McCarthy
Phillip Nguyen
William Phillips

Methyl bromide is an extremely effective gaseous pesticide with such a broad range of toxicity that it may properly be referred to as a biocide: it kills insects, nematodes, weed seeds, fungi, and other pests. It is also an important--and controversial--compound that has received significant attention in the media and the California State Legislature in the last several months. This article examines the economic, environmental, and legislative issues surrounding methyl bromide use and the recent threat of its registration in California.

California uses approximately 15 million pounds of methyl bromide per year, making the state one of the largest users of methyl bromide in the world. Methyl bromide is used as a preplant soil sterilant, a postharvest fumigant, a fumigant for import and export commodities, and as a termiticide in structural pest control.

Canceling methyl bromide’s registration would have had a significant effect on the state’s agricultural industry, as it is used on more than 100 California-grown commodities. Strawberries are particularly dependent on methyl bromide for soil fumigation. The crop would have suffered annual losses of $106 million, while nurseries would have lost $68 million. Part of these losses would have been passed down to the consumer who would, in turn, have had to pay higher prices.

A ban on methyl bromide would have had a tremendous impact on the ability of California growers to sell their products outside of the state. Japan, Korea, Canada, Mexico, Egypt, and other countries (and some states) require the fumigation of products with methyl bromide prior to shipment in order to prevent entry of foreign pests. For example, walnuts, cherries, peaches, nectarines, cotton, strawberries, and any goods shipped in wooden crates or on pallets (e.g., electronics) must be fumigated. Loss of methyl bromide in California would have put the state at a competitive disadvantage with the rest of the world until alternative treatments could be approved by the receiving country. Heavy trade losses would have occurred until then.

The walnut industry would have suffered large losses had methyl bromide been banned in California. This state produces 45% of the world’s walnuts, and approximately one-third of the California crop is exported; the winter market in Europe receives much of the exports. Walnuts sold in Europe must be treated with methyl bromide as a condition of acceptance. Additionally, growers have little time between the walnut harvest and shipment for the winter market; methyl bromide is the only currently available pesticide that has a sufficiently short fumigation period. Inability to ship walnuts to the European winter market would have been devastating to growers.

Structural fumigation accounts for only 5% of the methyl bromide used, but it can be important under many circumstances and on a wide variety of pests. Food processing plants, bakeries, flour mills, and food storage facilities use methyl bromide because food does not have to be removed before fumigating. In addition, it has a short fumigation time, is noncorrosive to electrical equipment, and is extremely effective.

According to a Department of Food and Agriculture report, a ban on methyl bromide would have caused California to lose as much as $346 million in agricultural and other revenues. An estimated 8,000-10,000 jobs in soil, nursery, and commodity fumigation would have been lost. Adding the losses due to export and trade impacts would have increased the number of lost jobs dramatically.

Currently there are very few pest management alternatives to methyl bromide. There is an active search for economically feasible chemical and non-chemical alternatives; 220 research projects are ongoing in the U.S. However, time is the critical factor since appropriate replacements that are effective and not as toxic have yet to be found, field-tested, and integrated into large scale commercial farming practices.

Despite methyl bromide’s economic importance, it is not without its flaws, and increased production and use in recent years have drawn attention to its potential adverse effects. Among these adverse effects is stratospheric ozone depletion, (though some uncertainties remain concerning the magnitude of the role of agricultural vs. oceanic methyl bromide in the depletion problem). The 1994 Science Assessment of Ozone Depletion, a consensus document that involved over 200 of the world’s leading atmospheric scientists, uses ozone depletion potential as a regulatory benchmark to rate the level of damage expected from a particular substance. It reports the ozone depletion potential of methyl bromide to be 0.6.

Title VI of the Clean Air Act requires that all substances with an ozone depletion potential of 0.2 or greater be phased out in the United States within 7 years. Under the Act, the EPA has prohibited the production and importation of methyl bromide starting January 1, 2001. In addition, in 1994 the EPA ordered U.S. production and importation be reduced to 1991 levels. It is important to note that the phaseout under the Clean Air Act does not restrict the use of methyl bromide; pesticide use is governed by the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA).

Deleterious effects of methyl bromide on environmental health have been recognized at the international level as well. The Montreal Protocol is an international treaty designed to protect the earth from the detrimental effects of ozone depletion. It sets a number of stipulations including a ban on methyl bromide in industrialized countries by the year 2010.

Of more immediate concern to most people are adverse effects on human health. Methyl bromide was linked to more than 450 illnesses in California from 1982-1993. Eighteen deaths from exposure also occurred in that time span, all among trespassers entering fumigated structures before it was safe to do so. No deaths have been reported from the agricultural use of methyl bromide. Significant exposures to methyl bromide result in throat and eye irritation, skin lesions, weakness, despondency, headache, nausea, and vomiting. Later, numbness, defective muscular coordination, tremor, muscle spasms, lack of balance, extreme agitation, coma, and convulsions may occur. Higher concentrations can result in central nervous system failure, respiratory failure, and death.

In 1984, concerns about more chronic health effects of pesticide exposure led to an addition to the Food and Agriculture Code (Division 7, Chapter 2, Article 14) entitled the Birth Defects Prevention Act (BDPA). The bill was intended to prevent pesticide-related illnesses and reproductive dysfunction by forcing the Department of Pesticide Regulation (DPR) to identify and deny registration to agents shown to produce adverse effects in standardized animal testing protocols. The act requires that studies monitor the relationship between exposure and abortion, infertility, neoplasia, neurotoxicity, teratogenicity, mutagenicity, and overall chronic toxicity.

Much of the BDPA text outlines the hazard identification process. The act initially required the DPR to present the legislature with an assessment of all pesticide active ingredients registered for use in California at that time. Reports for each pesticide ingredient included a list of the health effect studies completed, an appraisal of the methodology, results obtained from the studies, and a timetable for filling the data gaps identified for every pesticide agent. In addition, a priority list was established to expedite testing for 200 agents determined to have both widespread use and large toxicity data gaps. These priority chemicals, one of which was methyl bromide, were initially supposed to have their toxicological profiles completed by December 31, 1991.

By 1990 it was evident that the 1991 deadline could not be met for all chemicals. Legislators and industry representatives reached an agreement that the relevant data on methyl bromide (and others) would be available by March 30, 1996, or registration would be discontinued. However, there was some disagreement between the California DPR and the U.S. EPA as to just what tests would be required. The BDPA states that, when possible, health effect assays are to be conducted with protocols established under FIFRA. EPA mandates feeding studies for all chronic exposure studies on all pesticides. But the DPR wanted to conduct inhalation studies, as that is the actual route of exposure. The DPR was also asking for additional studies that EPA did not require such as analysis of dosing studies. Naturally, registrants did not want to start exposure studies until it was decided just what studies would be required. Meanwhile, the manufacturer did some range finding studies to determine what doses could be used for the long-term studies. After looking at the results of the range finding studies, toxicologists at the U.S. EPA and the DPR agreed to encapsulate the gas and administer low doses orally. These studies are now underway but were not scheduled to be completed and analyzed by the March 30th deadline.

Because of the impact methyl bromide cancellation would have on the state’s agricultural industry, a bill was introduced last year to extend its registration and allow manufacturers more time to submit results of toxicology tests. However, the measure became stalled in the legislature. The legislature reconvened in January, and several bills to extend the deadline were proposed. But because of the time required to get legislation through the policy committees and the floors of both houses, it was unlikely that any bill would be signed into law before the March 30th deadline. So on December 29, 1995, Governor Wilson called a special session of the legislature. A special session speeds up the process of a bill becoming a law without requiring the two-thirds vote necessary for urgency legislation. SBxxx1 to extend registration of methyl bromide was proposed and eventually passed both houses.

SBxxx 1 was signed by the Governor on March 12, but technically it does not take effect for 90 days. However, with the knowledge that the legislature has expressed its desire for a registration extension for methyl bromide, the DPR will not suspend its license in the interim.

*The authors were students in Environmental Toxicology 138: Legal Aspects of Environmental Toxicology.

M.W. Stimmann


Nature Suspect in 'Sick' Buildings

According to research at the Georgia Institute of Technology, fungi and molds, not paints, carpets, and building materials or cleaning supplies, may be causing the "obnoxious emissions" in buildings that congest lungs and irritate eyes and skin. In a report titled "The Fungus Among Us," researchers concluded that many indoor problems found in "sick" buildings in the Southeast are caused by volatile organic compounds, given off by molds and fungi. The researchers collected fungi samples from "sick" buildings and allowed them to grow in a lab, and found they were "identical to those originating from solvent-based building materials and cleaning supplies." The VOCs (Volatile Organic Compounds) released by the fungi included hexane, methylene chloride, benzene, and acetone.

REF: Washington Times, March 3, 1996.

Fifty Visitors to Denver Zoo Ill With Salmonella From Lizards

Fifty people contracted a rare, virulent type of salmonella bacteria, causing bloody diarrhea in 78% of the victims, after visiting the Denver Zoo exhibit of the Komodo dragons. The Centers for Disease Control and Prevention (CDC) said the dragons had been removed from their glass enclosures and placed into a wooden structure for the zoo's "Dragon Days" exhibit. Some visitors had touched the lizards, while others who contracted salmonella had only touched the top and sides of the wooden structures. The Komodos had defecated in the enclosure, and then walked around, spreading bacteria to the barriers.

REF: Washington Times, March 4, 1996.

Food Additives With Salicylates May Help Prevent Deaths From Heart Disease

A new study finds certain food additives containing salicylates may help reduce blood clots. The clots can trigger heart attacks and strokes. Foods naturally rich in salicylates include fresh oranges and raspberries, fresh or canned tomatoes and other fruits, certain teas and commonly used spices. Heavy concentration of processed foods could be a key source of protective chemicals that reduce thrombosis (clotting), said National Center for Health Statistics' Lillian Ingster at a recent American Heart Association meeting.

REF: Food Chemical News, 38(4), March 18, 1996.

Lead and Cadmium Contamination Guidelines for Ceramics

The lead and cadmium contamination guidelines for ceramics in FDA's Compliance Policy Guides were misprinted by the agency. For cadmium the correct guidelines, in micrograms per milliliter, are as follows: flatware (average of six units) 0.5; small hollowware (any one of six units), 0.5; large hollowware (any one of six units), 0.25. For lead, the following are the correct guidelines (also in mg/mL): flatware (average of six units) 3.0; small hollowware other than cups and mugs (any one of six units) 2.0; cups/mugs (any one of six units) 0.5; large hollowware other than pitchers (any one of six units) 1.0; pitchers (any one of six units) 0.5.

REF: Food Chemical News, 37(49), Jan 29, 1996.

Treating and Preventing Snake Bites

People who frequent wilderness spots, as well as those who camp, hike, picnic, or live in snake-inhabited areas, should be aware of potential dangers posed by venomous snakes. Every state but Maine, Alaska, and Hawaii is home to at least one of 20 domestic poisonous snake species. A bite from one of these, in which the snake may inject varying degrees of toxic venom, should always be considered a medical emergency, says the American Red Cross.

Medical Treatment

Medical professionals sometimes disagree about the best way to manage poisonous snakebites. Some physicians hold off on immediate treatment, opting for observation of the patient to gauge a bite's seriousness. Procedures such as fasciotomy, a surgical treatment of tissue around the bite, have some supporters. But most often, doctors turn to the antidote to snake venom -- antivenin -- as a reliable treatment for serious snakebites.

Antivenin is derived from antibodies created in a horse's blood serum when the animal is injected with snake venom. In humans, antivenin is administered either through the veins or injected into muscle and works by neutralizing snake venom that has entered the body. Because antivenin is obtained from horses, snakebite victims sensitive to horse products must be carefully managed. The danger is that they could develop an adverse reaction or even a potentially fatal allergic condition called anaphylactic shock.

First Aid for Snakebites

According to the American Red Cross, these steps should be taken:

• Wash the bite with soap and water.

• Immobilize the bitten area and keep it lower than the heart.

• Get medical help. The main thing is to get to a hospital and don't delay.

Some medical professionals, along with the American Red Cross, cautiously recommend two other measures:

• If a victim is unable to reach medical care within 30 minutes, a bandage, wrapped two to four inches above the bite, may help slow venom. The bandage should not cut off blood flow from a vein or artery. A good rule of thumb is to make the band loose enough that a finger can slip under it.

• A suction device may be placed over the bite to help draw venom out of the wound without making cuts. Suction instruments often are included in commercial snakebite kits.

How NOT to Treat a Snakebite

Though U.S. medical professionals may not agree on every aspect of what to do for snakebite first aid, they are nearly unanimous in their views of what not to do. Among their recommendations:

No ice or any type of cooling on the bite. Research has shown this to be potentially harmful.

No tourniquets. This cuts blood flow completely and may result in loss of the affected limb.

No electric shock. This method is under study and has yet to be proven effective. It could harm the victim.

No incisions in the wound. Such measures have not been proven useful and may cause further injury.

Avoiding Snakebites

• Leave snakes alone. Many people are bitten because they try to kill a snake or get a closer look at it.

• Stay out of tall grass unless you wear thick leather boots, and remain on hiking paths as much as possible.

• Keep hands and feet out of areas you can't see. Don't pick up rocks or firewood unless you are out of a snake's striking distance. (A snake can strike half its length.)

• Be cautious and alert when climbing rocks.

What do you do if you encounter a snake when hiking or picnicking? Just walk around the snake, giving it a little berth -- six feet is plenty. But leave it alone and don't try to catch it!

REF: FDA Consumer, Nov 1995.


Invaders of the Night

The 1993 outbreak of Hantavirus infection in the Southwest serves as a reminder of ever present, unwelcome guests on farms. Hantavirus causes a flu-like illness which progresses to severe lung edema. Sixty percent of people affected by Hantavirus die. The primary reservoir for Hantavirus appears to be the deer mouse, although there is evidence of infection in pinon mice, brush mice and the western chipmunk.

Other rodents live and breed in confinement dairy facilities, most notably the Norway rat and the Roof rat. Each one of these ubiquitous pests can consume up to 40 pounds of feed per year, and contaminate much more with feces and urine. Rodents spread leptospirosis and salmonellosis. The Roof rat, which is present in western Washington, Oregon, and California, also is a carrier of "Yersinia pestis," the bacteria which causes bubonic plague.

In addition to causing substantial feed losses and spreading disease, rodents damage buildings and equipment. The rat has a biological urge to gnaw, not only for the purpose of gaining access to buildings and food. The front teeth, or incisors, of an adult rat grow about 5 inches per year, and must be continuously worn down. Rats can gnaw through wood, cinder block, fiberglass and even metal siding. Many fires in barns and feed storage buildings can be attributed to rodents gnawing on electrical wiring. Burrowing activity by rodents results in settling of building foundations and disruption of concrete slabs and feed bunks.

Rats and mice have phenomenal reproductive ability. The gestation period of the Norway rat, for instance, is 21 to 23 days, after which the female bears a litter of 6 to 12 pups. The female can rebreed within 3 or 4 days after her pups are born; her offspring reach sexual maturity at 3 months of age. A single breeding pair of rats can thus have several hundred offspring in one year.

The deer mouse can gain access to a building through a pencil-size hole. Even a large rat can squeeze through a hole with a 1 inch diameter. Rats can climb horizontal or vertical cables, chains, and conduits. An adult rat can jump 36 inches vertically and 48 inches horizontally, and rats are excellent swimmers.

How can rodent pests be controlled on a dairy? A comprehensive control program includes:

• Removal of trash and other materials which rodents use for living quarters.

• Stacking materials, such as lumber, fencing, and feeds, off the floor.

• Wherever possible, close off rodent access routes into buildings and feed supplies.

• Minimize food sources by covering garbage cans and protecting grain, and by cleaning up feed spills.

• Eliminate water sources by preventing leaks and standing water puddles.

Once these steps are taken, a baiting program may be instituted. Successful baiting relies on both the selection of a bait and bait placement. A bait should be selected for its toxicity to the target species and its palatability (bait won’t kill rats if they don’t eat it!). Safety to pets, children and livestock should also be considered. A rodenticide should be handled with the same care that is given any potentially-toxic chemical. Cost of the bait is also a consideration, taking into account the cost to kill a particular number of rodents rather than the cost per weight unit of the rodenticide.

Bait should be placed in areas of greatest rodent activity, which can be identified by burrows, gnawed boards and feedsacks, and rodent fecal material. Bait will not lure rodents away from their usual habitat; it must be placed such that they encounter the rodenticide in their normal travels. Wear gloves to protect the bait from human scent, and to protect yourself from exposure to the chemical. Protect children and non-target animals by using "bait stations." Metal stations can be purchased commercially. Other effective bait stations include a covered plastic pail with a small hole cut in the side, a piece of corrugated drainage tubing nailed to a board and placed along a wall, or simply a board nailed at an angle along the edge of a floor. Check bait stations daily and replenish as needed.

No cases of Hantavirus infection have been identified in Washington, but Oregon and Idaho have had fatalities due to the virus. Western cases have been identified in people who lived in rodent-infested housing, who trapped and handled rodents, or who entered buildings which were heavily infested. In Oregon, a young man appears to have contracted the disease while working in an orchard.

An effective rodent control program pays off in reduced feed losses as well as providing a safer environment for cattle, employees, and family members.

(Blauwiekel, R., Society for Theriogenology Newsletter, May/June 1995)

REF: Communications in Continuing Education, 12(1), January 1996.


Charm II Tetracycline Drug Test

The Charm II tetracycline drug test for chlortetracycline, oxytetracycline, and tetracycline (Competitive Assay) will bear an additional statement on its label to inform users of the "low probability of false violative results arising from the sensitivity of the test to the low levels of chlortetracycline expected in milk from approved herd-wide use of this drug in the feed of lactating cattle," according to a Dec. 21 memo from the Center for Veterinary Medicine's Stephen Sundlof.

REF: Food Chemical News, 38(1), Feb 26, 1996.

Warning: Seldane + Popular Antibiotic = Trouble

Even after two mass mailings and package labels warning of the potentially fatal interaction between the antihistamine Seldane and the antibiotic Erythromycin or the antifungal drug Ketoconazole (brand name Nizoral), two reports last week suggest that the danger is often overlooked. The drugs interfere with the metabolism of Seldane, raising its level in the blood. That can cause potentially fatal cardiac arrhythmias, or abnormal heart rhythms. The Food and Drug Administration is working with Hoechst Marion Roussel, Seldane's manufacturer, to design another follow-up alert for pharmacists and doctors.

REF: Washington Post Health, April 16, 1996.

Arthur L. Craigmill, PhD

Michael W. Stimmann, PhD