Food Safety
Authors
The information in this chapter was prepared by the following individuals.
Description of pesticides in the food supply:
o A. J. Battistone, La Paz County Health Department
o Tim Flood, M.D., Medical Director, Chronic Disease Epidemiology Section, Arizona Department of Health
o Glen Sipes, Ph.D., Head, Department of Pharmacology and Toxicology, College of Pharmacology; and Head, Department of Pharmacology, College of Medicine, University of Arizona
Description of dioxin in the food supply:
o Norman Peterson, S.M., Assistant Director, Arizona Department of Health
Pesticides in the Food Supply
Introduction
Most food produced in our society must pass through several stages before it is consumed, including growing, harvesting, storage, transportation, processing, cooking, and serving.
If something goes awry during any of these stages, the consumer can potentially ingest harmful food products.
To perform an assessment of consumer exposures to harmful food products, the Committee considered four aspects:
o Pesticide residues on food at the time of consumption
o Microbial contamination
o Naturally-occurring toxins
o Antibiotics used on animals
Pesticide Residues
Cancer Risk
Studies of the issue of pesticide residues on food consistently show that this is an area of high public concern. Scientists who study this issue, however, usually rank it rather low on the list of hazards. Obviously, there is a large gap between scientists' perceptions and the public's perception of this issue.
Pesticides are used to grow many foods and non-food crops. There is no doubt that pesticides reduce the damage, at least in the short term, caused by unwanted insects, mites, fungi, and weeds.
There are about 1,600 known active ingredients and tens of thousands of formulations and combinations of the active ingredients. Over 1,200 pesticides are registered in the U.S. (McConnell, 1994).
From 1964 until 1980 there was a steady increase in the use of agricultural pesticides in the U.S. Since 1980, the amount of pesticides applied agriculturally in the U.S. has remained constant at around 800 million pounds per year (EPA, 1992). However, the amount of pesticides applied per acre has actually increased over the past decade.
A disturbing occurrence relative to pesticide usage is insects' and plants' development of resistance to pesticides. Pesticide usage itself may select pesticide- resistant organisms.
This issue of resistance will present long-term challenges for pesticide users. Resistance means that larger quantities and more potent pesticides will need to be applied to achieve control, or that alternative methods of pest control will need to be found.
Alternatives do exist in many situations, and this topic is now being explored through concepts such as crop rotations, cover crops, and biological controls to control pests (Curtis, 1993). Unfortunately, federal and state funding to support alternative approaches to pesticide usage has been little and slow in coming.
Some scientists believe that pesticide residues on food have the potential to cause human illness, particularly cancer (Miller, 1991). According to the Natural Resources Defense Council, there are 71 pesticides used on food crops which have been found to cause cancer in animals and humans (Curtis, 1993).
The monitoring of pesticide levels on food in the United States is conducted by the federal agencies listed in Table 4.1.
Table 4.1 Federal Monitoring Agencies for Food Pesticide Levels
------------------------------------------------------------------------------------------------- | Agency | What They Monitor | ================================================================================================= | Food and Drug Administration | Dietary intake of selected pesticides, toxic elements, | | (FDA): Total Diet Survey | industrial chemicals, and radionuclides | ------------------------------------------------------------------------------------------------- | FDA: Pesticide Residue | Current laboratory techniques can search for only half of | | Analysis | the pesticides used on food products | ------------------------------------------------------------------------------------------------- | U.S. Department of Agriculture | Residues in meat and poultry and some egg products | ------------------------------------------------------------------------------------------------- | EPA: National Human | Total body exposure to toxic substances, including | | Monitoring Program | pesticide products sold or distributed in the U.S. | -------------------------------------------------------------------------------------------------
In 1988, the FDA analyzed approximately 18,100 samples of domestically-produced food from all 50 states, and imported food from 89 countries. The analysis was performed in search of over 300 pesticide residues as part of the FDA's regulatory monitoring program.
Imported foods made up more than 57% of the samples, reflecting the emphasis placed on the monitoring of imported foods. The food groups which were analyzed included grain products; milk and dairy products; fish, seafood, and other meats; fruits, vegetables, and other food products.
The lower limit of residue measurement in the FDA's analysis for a given pesticide was well below the tolerance level. Overall:
o No residues were found in 61% of the samples
o No violative residues were found in 96% of the samples
The FDA states that the dietary intakes of pesticide residues are well below the standards set by the World Health Organization.
In 1989, a survey for any level of pesticides on 936 food items also found:
o Residues of at least 29 pesticides in about 1-6% of the samples (Palmer, 1992)
o Malathion, DDT, which was banned 20 years ago; and chlorpyrifos in 20%, 13%, and 10% of the items
One interpretation of these findings is that pesticides are used, that they are persistent, and that the levels of detection are very low.
In the FDA survey, the levels of pesticides were well below the FDA's reference dose and the acceptable daily intake. The measured levels were one to four orders of magnitude lower than the acceptable dose for persons aged 6-11 months, 12-16 years, or 60-65 years. The intake levels of most pesticides were in the range of 0.01 microgram of pesticide per kilogram of body weight per day.
The FDA report of samples taken in 1992 shows similar findings. There were:
o 313 pesticides that were potentially detectable using current laboratory techniques; in actuality, 99 pesticides were found
o Violative residues on domestically-produced foods, including:
Grains = 0%
Milk and dairy products = 0%
Fish and seafood = 0.9%
Fruits = 0.7%
Vegetables = 1.7%
Other foods = 1.4%
o Violative residues on imported products from 94 countries:
Grains = 3.5%
Milk and diary products = 0.5%
Fish and seafood = 12.5%
Fruits = 3.3%
Vegetables = 4.6%
Other foods = 4.6%
In Arizona there are no state or local agencies that monitor foods for the presence of pesticide residues. Therefore, the Committee used the national FDA data and assumed that it applied to the population of Arizona.
A recent analysis by the EPA (1990) was conducted to provide a relative ranking of dietary cancer risk with other environmental concerns. The study analyzed pesticide residue data for 39,578 samples collected over a 2-1/2 year period.
In the analysis, the EPA estimated the level of anticipated residues for seven pesticides selected on the basis of cancer potency and data about their patterns of use and food consumption.
The EPA then estimated the number of additional cancer cases which would occur, noting that the estimates were the upper bounds on cancer risk. The true risk may be as low as zero.
Using the data and methodology presented by the EPA, the Committee estimates that the number of cancer deaths in Arizona ranges from 1.3 to 8.6 per year, as shown in Table 4.2.
Table 4.2 Estimated Additional Cancer Deaths in Arizona in 1994 for 7 Selected Pesticide Residues on Food
----------------------------------------------------------------------------------------------------------------- | | FDA Data Base | | Foodcontam Data | | | | Pesticide | (USFDA) | | Base (Mississippi | | Comments | | | | | State University) | | | ----------------------------------------------------------------------------------------------------------------- | | Low | High | Low | High | | | | | | | | | | | Anticipated | Anticipated | Anticipated | Anticipated | | | | | | | | | | | Residue | Residue | Residue | Residue | | ================================================================================================================= | Benomyl | 0.1 | 0.1 | 0.1 | 0.1 | Not Available | ----------------------------------------------------------------------------------------------------------------- | Captan | 0.9 | 0.9 | 0.2 | 0.2 | Not Available | ----------------------------------------------------------------------------------------------------------------- | Chlorothalonil | 0.1 | 0.2 | 0.4 | 1.3 | Female Rat Renal | | | | | | | Tumors | ----------------------------------------------------------------------------------------------------------------- | EBDCs | 2.1 | 4.7 | 0.6 | 4.3 | Not Available | | (carbamates) | | | | | | ----------------------------------------------------------------------------------------------------------------- | Permethrin | 0.1 | 0.3 | 0.1 | 0.4 | Mouse Lung And | | | | | | | Liver Tumors | ----------------------------------------------------------------------------------------------------------------- | Simizine | 0.0 | 2.3 | Not | Not | Female Rat | | | | | Available | Available | Mammary Tumors | ----------------------------------------------------------------------------------------------------------------- | Trifluralin | 0.0 | 0.1 | 0.0 | 0.0 | Male Rat Thyroid | | | | | | | Adenoma/carc | | | | | | | Inoma | ----------------------------------------------------------------------------------------------------------------- | Total | 3.2 | 8.6 | 1.3 | 6.3 | | -----------------------------------------------------------------------------------------------------------------
For perspective, these cases, which are assumed to be fatal, would occur among the 7,648 cancer deaths each year in Arizona.
Because of the comparatively common occurrence of cancer among the state's population, it would be difficult, if not impossible, to detect the 1.3 to 8.6 cases that were potentially due to pesticide residues. The six-fold range of the estimate reflects just one aspect of the uncertainty behind these figures.
The EPA report concentrated on seven pesticides that they considered to "represent a substantial portion of the dietary risk of cancer." Neither the EPA nor the Committee were able to carry out a similar analysis on six other pesticides of concern to the EPA (propioconazole, acifluorfen, alachlor, atrazine, diclofop-methyl, oxyfluoren), nor on the 600 other pesticides that are registered by the EPA for use on foods.
Foods contain natural carcinogens and anticarcinogens. Some scientists who study the cancer risk associated with food have produced the following estimates of the risk associated with carcinogens in food:
o Pesticides contribute 0.01%
o Additives contribute 0.2%
o Spices and flavors contribute 0.98%
o The food itself contributes 98% of the risk
Thus, pesticide residues on food contribute a very small portion of the risk associated with food. The majority of the cancer risk comes from the natural carcinogens produced by the plant or food itself.
Non-Cancer Effects
There is increasing concern that pesticide residues at low levels also may cause health problems to consumers.
The evidence for this concern, however, is weak. This is an area that only recently has received attention, so the amount of epidemiologic evidence is scanty. Additionally, it is difficult to recognize such pesticide-related illness unless it affects a large number of persons and one is looking for the problem specifically.
For example, the ADHS pesticide poisoning registry has not received any reports of anyone in Arizona getting sick from exposure to pesticide residues on food. However, it is likely that an acute episode of pesticide poisoning probably would be diagnosed as microbial food poisoning.
Even if doctors suspect pesticide poisoning was the cause, the diagnosis would be difficult to make or confirm.
The EPA assessment did not look at illnesses other than cancer. Outbreaks of illness, with mostly acute systemic effects, have been associated with pesticide residues, although such incidents are rare but highly publicized. From 1988 to 1994 the ADHS pesticide poisoning registry did not receive any reports of illness due to pesticide residue on food.
There is little data in the medical literature to suggest that pesticide residues on food contribute to birth defects or other reproductive illnesses. However, these illnesses have been reported in a few occupational settings. Anecdotal reports from the public concerned about immune disorders and "sensitivity" have been difficult to assess as to their public health significance.
If Arizonans are like the general population of the U.S., then nearly 100% of them carry measurable amounts of DDT in their adipose (fat) tissue.
So far, studies that look for signs of harmful effects of DDT have not shown consistent results; yet, DDT was banned 20 years ago because of the harm it was doing to eagles and hawks. One study of women with breast cancer found higher levels of DDT than in controls. This finding was not confirmed in a larger subsequent study.
A recent study conducted in Mexico where DDT was used found that there were shortened periods of breast feeding as the levels of DDE (a metabolite of DDT) increased in women's breast milk (Gladen, 1994). Other organochlorine pesticides also reside in fat tissue. The advances in laboratory techniques over the past decades now permit scientists to find what were previously immeasurable amounts carried by humans.
There have been over 30 studies looking for reproductive effects of herbicides, including the phenoxy acid type that contains TCDD (dioxin). The results have been inconclusive.
Studies that could link birth defects to pesticides are extremely difficult to conduct without knowing the specific pesticides and amounts to which women are exposed, and such information is rarely available.
Other major problems include the lack of tests that could be used to measure the effects of pesticides in the general population. Except for DDT, there are no direct measurements of pesticides that are performed in the clinical setting, nor are there tracer substances or surrogates which could indicate exposure to pesticides. This remains a major limitation in studies of pesticide exposure and an area for further research.
Conclusion
This assessment is cursory, but the Committee used the scanty information available.
o Pesticides are used in large amounts. Current law, however, does not require the reporting of pesticides applied by the grower.
For that and other reasons, when the Committee performed this assessment, it was unable to obtain estimates of the amounts used on food crops in Arizona from the Arizona Department of Agriculture. This severely limited its ability to perform exposure and risk assessments for consumer exposure to pesticides.
o National studies of pesticide residues show that low levels of pesticides can be detected quite commonly on 38% of samples of food.
Imported foods tend to have slightly higher rates of violative residues compared to domestically-produced foods.
Residues of one or more pesticides can be found on many foods.
These is little evidence available that would suggest that these low levels are harmful. Our ability to detect low levels of pesticides has outpaced our ability to understand whether the levels are harmful. This is, and will continue to be, a difficult area in which to conduct epidemiologic studies.
o The trend in agribusiness is to move away from persistent organochlorine pesticides in favor of more powerful pesticides which are shorter-acting and do not persist in the environment or people.
The Committee proposes that studies of the effects of pesticides focus more on the effects experienced by humans, rather than by laboratory animals. The effects of low level exposure to consumers probably never will be measurable.
Instead, the Committee recommends greater emphasis on pesticide workers and farm workers who encounter far greater levels of pesticides on the job.
Microbial Contamination
Introduction
The Committee also looked at the risks to Arizonans from food-borne and water- borne illness and death resulting from microorganisms. These organisms include: viruses, bacteria, fungi, molds, protozoans, and pests.
Risks are also posed by allergens, and by growing, producing, delivering, and consuming food.
This analysis also includes risks posed by drinking water from public and private sources. The drinking water contamination may occur from the source to the tap and in bottled water.
This analysis does not consider chemical contaminants such as pesticides, hormones, drugs, or irradiated food. Nor does it consider many other risks that arise from individuals' life-styles and dietary choices such as obesity, caffeine, poor nutrition, and alcohol consumption.
Health Risks
Food-borne illness and death resulting from microorganisms and allergens are a common and preventable public health problem. Archer and Kuenber (1985) estimate that over 80 million food-borne and water-borne illnesses occur each year in the U.S.
The FDA (1993) has determined that about 9,000 deaths occur annually in the U.S. as a result of food-borne diseases.
The State of Arizona records food-borne illnesses and deaths when they are reported to them by the county health departments and physicians. Most illnesses, however, go unreported.
In 1993, the number of food-borne illness outbreaks reported to the State of Arizona was 53. The number of food-borne illness complaints was 1,656. There were no food-borne deaths reported.
If an analogy is made from statistical estimates for the U.S. for food-borne illness and death, there would be about 200,000 food-borne illnesses and about 138 food-borne deaths which occur in Arizona annually.
The estimated 200,000 food-borne illnesses may appear to be an excessive number. However, when we consider that the average person eats and/or drinks at least five to six different times per day, this amounts to more than 80 million times per year for Arizonans to subject themselves to the risk of food-borne illness and death.
The 200,000 cases of food-borne illnesses in Arizona are mostly illnesses which would cause minimal distress, such as simple diarrhea or other symptoms that would not alter an individual's normal daily activities.
The 138 deaths are estimates of the number of persons in which food-borne illness contributed to the cause of death. In other words, the illness was "the straw that broke the camel's back."
Many of these deaths are believed to occur to persons with other chronic illnesses. In most cases, "food-borne illness" would not be written on the death certificate as the underlying cause of death. Instead, the persons are usually listed as dying from their underlying chronic illness. These premature deaths could be postponed if the foods were uncontaminated.
Naturally-Occurring Toxins
Introduction
Through their diet, humans are exposed to a vast number of chemicals (Miller & Miller, 1986). By far the largest number of these chemicals are naturally-occurring substances, many of which are toxic.
Naturally occurring refers to chemicals that are not of synthetic origin and which are not intentionally or accidentally introduced into food. However, it should be stressed that a number of synthetic chemicals also are produced naturally.
For example, carcinogenic nitrosamines are of both synthetic and natural origin, as are a large number of hydrazines. Similarly, a number of phenolic antioxidants are of both synthetic or natural origin. In animal cancer bioassays, these natural and synthetic compounds have been shown to produce cancers with high dose exposures.
Health Risks
Some naturally-occurring toxins in foodstuffs are carcinogenic, including aflatoxins, which are produced from mold on grains, nuts, or seeds. While important in Africa, aflatoxins are not believed to be a significant hazard in the U.S. Other mycotoxins (poisons produced by mold) cause kidney and liver damage and probably are carcinogenic.
Data are not readily available to quantify the risk associated with naturally-occurring toxins. However, data from the poison control center in Tucson indicate that about 1,000 people asked for information after encountering plants in 1993. These cases represent all levels of poisoning from trivial to serious.
In addition, Scheuplein (1990) examined the relative distribution of cancer risk among seven different food categories. He concludes that almost all the risk of excess cancer incidence is due to naturally-occurring carcinogens present in ordinary food.
Conclusion
Clearly, more research needs to be done in the area of naturally-occurring carcinogens and toxicants. The problem becomes more complex because of the presence of anticarcinogens in various foods. The balance of carcinogenic to anti- carcinogenic chemicals will alter the impact of their dietary-associated carcinogenesis.
Because of the complexity of the overall problem of assessing the risk of naturally- occurring carcinogens and toxicants, it is difficult to perform a risk assessment on this issue.
Perhaps the greatest risk of cancer from the U.S. diet is the contribution of total calories. Present scientific evidence, particularly that obtained in animal models, suggests that over-eating contributes to dietary-associated cancers, as well as other health risks.
Increased public awareness of this fact, through educational programs, would be the most effective way to reduce the health risks associated with diet.
Antibiotics Used on Animals
Introduction
Animal growers treat their stock with antibiotics to keep the animals healthy. This widespread practice has raised concerns that some types of bacteria are becoming, or will become, resistant to the antibiotics, which will make it harder to treat bacterial diseases in humans.
So far, this concern is mostly theoretical. It has not been possible to establish a link between antibiotic-resistant bacterial diseases in humans and use of antibiotics in animals.
Dioxin in the Food Supply
Introduction
Dioxin is the layperson's term for polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans, including the highly toxic 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD).
Scientists from the EPA, other federal agencies, and the general scientific community have conducted a scientific reassessment of dioxin and related compounds in recent years. While the draft reassessments cannot be cited at this time, the information in this summary is consistent with the EPA highlights released to the public.
Sources of Dioxin
A variety of sources of dioxins have been identified and others may exist. The available information suggests that the presence of dioxin-like compounds in the environment has occurred primarily because of industrial practices and is likely to reflect changes in release over time.
The principal identified sources of environmental releases may be grouped into four major types:
o Combustion and incineration sources
o Chemical manufacturing and processing sources
o Industrial and municipal processes
o Reservoir sources
Because dioxin-like chemicals are persistent and accumulate in biological tissues, the primary means of human exposure is through ingestion of foods containing minute quantities of dioxin-like compounds. This results in widespread, low-level exposure of the general population to dioxin-like compounds.
The primary mechanism by which dioxin-like compounds enter the terrestrial food chain is via atmospheric deposition. Dioxin and related compounds enter the atmosphere directly through air emissions or indirectly, for example, through volatilization from land or water or from re-suspension of particles.
Deposition can occur directly on to soil or on to plant surfaces. It is unclear whether atmospheric deposition represents primarily current contributions of dioxin and related compounds from all media reaching the atmosphere, or it represents past emissions of dioxin and related compounds which persist and recycle in the environment.
Health Risks
While most individuals are exposed to persistent low-levels of dioxin in food, some individuals may be exposed to higher levels because of their proximity to point sources, or because of dietary practices.
The levels of dioxin and related compounds in the environment and in food in the U.S. are based on relatively few samples and must be considered uncertain. However, they seem consistent with levels measured in studies in Western Europe and Canada. The consistency of these levels across industrialized countries provides reassurance that the U.S. estimates are reasonable.
There is adequate evidence based on all available information, including studies with human populations and laboratory animals and from ancillary experimental data, to support the inference that humans are likely to respond with a broad spectrum of effects from exposure to dioxin and related compounds if exposures are high enough.
The effects from exposure to 2,3,7,8-TCDD are shared by other chemicals which have a similar structure and binding characteristics. Consequently, the biological system responds to the cumulative exposure to other dioxin-like chemicals rather than to the exposure to any single dioxin-like compound. While individual species vary in their sensitivity to any particular dioxin effect, the evidence indicates that humans, in general, are neither extremely sensitive nor insensitive to the individual effects of dioxin-like compounds.
With regard to carcinogenicity, a weight-of-the-evidence evaluation suggests that dioxin and related compounds are likely to present a cancer hazard to humans. The epidemiological data alone are not yet deemed sufficient to characterize the cancer hazard of this class of compounds as being "known." However, combining suggestive evidence of recent epidemiology studies with the unequivocal evidence in animal studies, and inferences drawn from mechanistic data, results in the characterization of dioxin and related compounds as likely to produce cancer in some humans under some conditions.
Despite the potential for dioxin and related compounds to cause a spectrum of responses in animals and humans, there is no clear indication of increased disease in the general population attributable to dioxin-like compounds. However, this lack of a clear indication should not be considered strong evidence for no effect of exposure to dioxin-like compounds; instead, it may be a result of the inability of our current data and scientific tools to directly detect effects at these levels of human exposure.
In Arizona, dioxin contamination has been a concern in the Globe area. From 1965 to 1969, the phenoxy herbicides 2,4-D 2,4,5-T and Silvex were aerially applied in the Globe Ranger District of the Tonto National Forest near Globe. This herbicide use project was designed to improve range land and to increase water runoff, resulting in increased water yields for downstream users.
Complaints regarding spray drift, deformed animals and human illness were received immediately after the 1969 spray treatment. The U.S. Forest Service convened two task forces and an interdepartmental panel of experts to assess the health and environmental consequences of the herbicide project. Silvex was detected in some environmental samples collected, and 2,3,7,8-TCDD was detected at 0.5 ppm in one sample of unused herbicide. However, laboratory methods had not yet been developed to analyze environmental samples for 2,3,7,8-TCDD in the low ppb or ppt ranges.
In 1985 and 1986 this area was again studied as part of the EPA National Dioxin Study to determine the extent of dioxin contamination in the United States. The results were reported in the proceedings of a national conference and were summarized in the following abstract:
------------------------------------------------------------- | At a later time, the ADEQ sampled water from various | | private wells and Kellner Creek, down-gradient from the | | former herbicide use area. The ADEQ also collected | | sediment from Kellner Creek and soil from Kellner Creek | | Campground for dioxin analysis. | -------------------------------------------------------------
Dioxin was not detected in any of these soil, sediment or water samples. However, the ADEQ detected dioxin at some of the same helicopter mixing and loading locations sampled and detected by the EPA in 1985 and 1986.
In the past, dioxin-like polychlorinated biphenyls (PCBs) have been widely-used in electrical equipment, such as transformers, and these types of equipment have been located in or near many commercial and industrial buildings. PCBs leaking from this equipment and dioxin-like compounds created during fires in PCB-filled transformers have constituted a potential source of dioxin exposure to the public.
There is no evidence of any such incidents taking place in Arizona. Further, compliance with federal regulations has resulted in the removal, recycling or retro- filling of all such equipment that posed a public health hazard.
Conclusion
There is no evidence that the population of Arizona has more or less exposure to dioxin-like compounds than the rest of the U.S. population. It is known, however, that essentially all adipose tissue samples from U.S. individuals fall within a predictable range because of the uniformity of dioxin levels in the food supply.
While the effect of this exposure level is not known for non-cancer end points, the Committee could make an estimate of the excess cancer risk based on annual dose- response models. This calculation would predict an upper bound of five cases per year in Arizona.