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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 6 Soil and Food as Potential Sources of Exposure at Hazardous-Waste Sites AT TIMES IT IS DIFFICULT TO identify completely the routes of exposure when ill health effects are suspected from hazardous-waste sites. The same problem of determining precisely who is exposed to what compounds and in what concentrations exists for exposure through ingestion of soil as it does for exposure through domestic water consumption, in that direct ingestion is not likely to constitute the sole route. Soil ingestion suffers from an additional complexity. Except among small children, it is unusual for soil to be ingested directly, although adults do ingest modest amounts of soil nonetheless (Calabrese et al., 1990). Unless a chemical is extremely potent, the exposure is unusually direct as with certain occupations, or there is extensive dust contamination of food and residences (the contaminated dust being available to be resuspended in the air and inhaled), contamination due chiefly to exposure to soil is unusual. However, contaminated soil and domestic water can act as vehicles for contamination of plant or animal foods that are subsequently ingested—as is the case for mercury and pesticide contamination of fish and heavy metal or pesticide contamination of fruits and vegetables. The questions of the effects of pesticide residues on foods and the subsequent health risks for children are the subject of study by another National Research Council committee, and they will not be considered here.
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 This chapter reviews the health effects linked to exposure to contaminants in soil or food, other than those resulting from direct pesticide applications to crops. These include home gardening in contaminated soil, some exposures involving work with soil, and consumption of fish from contaminated waters. Although heavily exposed persons could have a high risk of disease, in general, small numbers of persons have been exposed directly or indirectly through ingestion of foods that have absorbed contaminants from soil or water, or through avocational or vocational exposures to contaminated materials. Studies of soil and food contamination usually encompass many individuals with relatively low or negligible exposure in the “exposed” group. Accordingly, low estimates of risk, as well as low attributable risks in the general population, can be discerned, although some highly exposed individuals can incur serious risks, especially when contaminated soil has been used as topsoil in building construction. CHEMICAL EXPOSURE THROUGH FISH AND OTHER FOODS In accordance with Figure 1-1 of this report, animal studies on the consumption of contaminated fish are relevant to this discussion. Animals experimentally exposed to fish contaminated with polychlorinated biphenyl (PCB) congeners and other pollutants display a range of neurologic, immunologic, and enzymatic impairments. Hertzler (1990) reports that rats fed different concentrations of Lake Ontario salmon consistently evidence lower activity, rearing, and other behaviors, when compared to rats fed ocean salmon or rat chow. Studies of the levels of two common pesticides, Mirex and PCBs in rat brain and fish, found dose-related neurobehavioral effects. Cleland et al. (1989) similarly report that mice fed diets of Lake Ontario salmon had reduced immune function, including lowered immunoglobulin, which correlated with elevated PCB levels in the ingested salmon. An earlier study by Cleland et al. (1987) produced both hepatomegaly and suppression of important detoxifying enzymes in mice fed Lake Ontario coho salmon, compared to unexposed control mice. Regarding environmental contamination of finfish and shellfish and other freshwater species, inadequate harvest management and control is in effect for environmental chemicals such as mercury, lead, cadmium, PCBs, dioxin, and pesticides, according to a recent report of the Institute of Medicine (1991). Regional agricultural or industrial pollution varies considerably and can be substantial in some small areas. One fifth of the fish and shellfish eaten in the United States comes from recreational or subsistence fishing, and is not sub-
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 ject to health-based control or monitoring. One study reported that regular fish eaters have dichlorodiphenyl trichloroethane (DDT) and PCB levels significantly higher than those who are not regular fish eaters (Fiore et al., 1989). In addition, well over half of the U.S. supply of seafood is imported (Institute of Medicine, 1991). Seafood may also be contaminated by bacterial, viral, and other biologic agents (Teitelbaum, 1990). Whether these may be affected by environmental agents is unclear. MERCURY CONTAMINATION In 1953, a severe neurological disorder was first recognized among persons living in several villages near Minamata Bay, Japan. Mercury-containing effluent from a vinyl chloride production process emptied into the bay from a nearby chemical factory was responsible for the contamination of fish and shellfish consumed by inhabitants of small villages along the shore. The onset of Minamata disease usually began with a progressive numbness in the fingers and toes and often in the lips and tongue (Kurland et al., 1960). This was followed by lack of muscle coordination, clumsiness, difficulty in swallowing, deafness, and blurring of vision. Spasticity and muscle rigidity often were present. Most cases ended in death or severe, permanent disability. The incidence of the disease for the period 1953-1960 in the total of about 10,000 inhabitants varied from 4 percent for those in a village near the industrial facility to 0.2 percent for those in a distant village. Cats and fish-eating birds were affected, and laboratory animals fed fish and shellfish from Minamata Bay also developed the disease (Tsubaki and Irukayama, 1977). In the U.S., mercury contamination of fish is especially prevalent in the Great Lakes region; for example, the State of Michigan has issued advisories based on its monitoring of mercury and other contaminants in sport fish (Institute of Medicine, 1991). Since 1983, levels of methylmercury exceeded levels of concern in about 3 out of 4 of the 60 Michigan inland lakes tested. Because of methylmercury contamination the state advised pregnant women, nursing mothers, women who intended to have children, and children over age 15 to eat no large-mouth bass, walleye, northern pike, or muskie from these lakes and to eat no more than one meal per month of rock bass, crappie, and yellow perch over 5 inches in length (Institute of Medicine, 1991). No advisory was issued for men who may wish to reproduce, despite evidence that sperm may be vulnerable to subtle effects as well (NRC, 1989).
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 CADMIUM CONTAMINATION The mining and refining of metals such as zinc, copper, lead, and cadmium from ore have given rise to substantial cadmium pollution in several areas of the world. Cadmium emissions in water from mines upstream of farming areas and deposition of atmospheric emissions from zinc smelters have resulted in pollution of soil. Basic foodstuffs, such as rice and wheat, constitute major hazards when they are grown in such polluted areas. The best-known example is the case of contaminated rice grown in cadmium-polluted areas of Japan (Friberg et al., 1985a). River water used for irrigation had been polluted by cadmium-containing wastes from a nearby mine. In 1946, Itai-Itai byo, the “ouch-ouch disease,” was first identified. Its symptoms were later recognized to be the result of osteomalacia—a softening of the bones caused by a deficiency of vitamin D or of calcium and phosphorous—from chronic cadmium poisoning that developed through the consumption of the contaminated rice (Friberg et al., 1985b). Nakagawa et al. (1990) recently found that both definitely diagnosed and suspected Itai-Itai subjects showed a significantly lower cumulative survival rate than the controls. In the past three decades, a number of epidemiologic studies demonstrated that cadmium soil pollution is associated with a number of diseases. A dose-response relationship between cadmium in rice and the prevalence of tubular proteinuria (an excess of serum proteins in the urine) has been demonstrated (Nogawa and Ishizaki, 1979). Further, pH of the water supply can directly or indirectly affect the levels of a number of heavy metals, including mercury, lead, and cadmium that may leach into domestic water (Graham et al., 1990). DDT The widespread distribution and recycling of DDT, a heavily used pesticide in the 1950s and 1960s, illustrates how hazards to humans can remain in the food chain. High levels of metabolites of DDT in fish caught for subsistence eating near Triana, Alabama, in 1978 were mirrored in similarly high levels in the persons eating those fish. An initial study of 12 residents showed blood levels of metabolites of DDT among the highest ever recorded (Anonymous, 1979). A subsequent cross-sectional study of residents of Triana and the surrounding rural area used a questionnaire and blood and urine analysis for DDT residues. It found a positive association of elevated serum triglyceride with DDT (Kreiss et al., 1981). There were no associations with other health effects. Other studies of residents also detected
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 elevated levels of PCB, presumably ingested from fish as well (Kreiss, 1985). Levels were linked with elevations in blood pressure and a host of other indications of altered systemic effects, as discussed in the following chapter. The route of exposure was believed to be to DDT, PCB, and related chemicals derived from industrial waste dumped into a stream. The case was the subject of intense litigation, and after its settlement, no efforts were made to obtain additional health data. This highlights a general problem, which will be discussed further in the next report of the committee. DIOXIN Recent research shows that humans who regularly consume fish from certain regions of the U.S. have higher levels of dioxin than those who do not regularly eat fish (Kuehl et al., 1989; Schwartz et al., 1983). A European study (Svennsson et al., 1991) has shown a statistically significant association between reported amount of fish eaten (from polluted waters) and plasma levels of dioxin. Fries and Paustenbach (1990) reviewed potential food sources of dioxins. They conclude that beef is a more important pathway than milk for dioxins. On the matter of the toxicity to humans from dioxin, the published literature is uneven. In animals, dioxin remains one of the most potent carcinogens ever studied. In humans, the evidence remains mixed, although the burden of proof has recently shifted. A study of the largest cohort of exposed workers ever studied finds that workers exposed to dioxin have increased death rates from overall cancer, as well as from soft-tissue sarcoma and non-Hodgkin's lymphoma (Fingerhut et al., 1991). Many of the previous studies of this problem have been plagued with errors in classification of exposed and unexposed groups, according to some reports, and hence have been biased toward a finding of no effect. Thus, Zack and Gaffey (1983) reported no increase in cancer in a series of studies on a subgroup of the same workers in which the positive finding has just been noted by Fingerhut et al. (1991). However, their study excluded workers in maintenance and repair from the exposed study group; these workers are, in fact, likely to have had high intermittent exposures when repairing product machinery. Studies of agricultural and forest workers directly exposed to pesticides have also found elevations in non-Hodgkin's lymphoma and other cancers (Alavanja et al., 1989; Wigle et al., 1990). The net result of these studies has been to strengthen the case for considering that dioxin, a common contaminant of some pesticides, does increase the
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 risk of cancer in humans. Although a number of issues remain to be resolved, the risk involved for humans is likely to be substantially less than that predicted by animal studies. Bailar (1991) notes that while the results on the Fingerhut et al. (1991) study are equivocal, they do effectively shift the burden on proof. “The hypothesis that low exposures [to dioxin] are entirely safe for humans is distinctly less tenable now than before” (Bailar, 1991, p. 262). PCBS Reports of increasing incidence of tumors in fish in the Great Lakes and other bodies of water (Baumann, 1984) were regarded as indicators of a potential human hazard, especially to groups such as sport fishermen and their families. Subpopulations that consume fish taken from contaminated waters, such as Lake Michigan and near Triana, Alabama, have mean serum polychlorinated biphenyl (PCB) levels several times those found in other general population groups in ranges that extend into concentrations found in industrial populations involved in capacitor manufacture (Kreiss, 1985). Because of concerns over prenatal exposure to PCBs and related contaminants, 236 children born to women who had consumed Lake Michigan fish were assessed at four years of age (Jacobson et al., 1990a,b). Prenatal exposure (indicated by umbilical cord serum PCB level) was associated with lower weight (Jacobson et al., 1990a). The children with the greatest exposure weighed 1.8 kilograms less on the average than did the least exposed children. In addition, tests showed a dose-response relationship for prenatal exposure that led to poorer short-term memory function on verbal and quantitative tests. The effects were not attributable to a range of confounding factors, including lead exposure. In 1985, Rogan et al. (1988) examined 117 children born to women affected by the 1979 mass poisoning of cooking oil with thermally degraded PCBs in Taiwan, and 108 exposed controls. The exposed children were shorter and lighter than the controls, and had more frequent abnormalities of gingiva, skin, nails, teeth, and lungs. The exposed also showed higher frequency of delay of developmental milestones, deficits on developmental testing, and abnormalities of behavioral assessment. EXPOSURE TO PCBS THROUGH OTHER ROUTES PCBs were widely used in the U.S. for two decades, and are now restricted. Manufacture is prohibited, but exposure continues from PCBs used in the past, primarily in electric capacitors. Capacitor
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 fires can produce emissions of PCBs, along with dioxin (2,3,7,8-tetrachlorodibenzodioxin, a common contaminant of incomplete combustion of PCBs). Further, PCBs are a major contaminant at Superfund sites, as noted in Chapter 3. As an indicator of the types of effects that might be sought in those potentially exposed to PCBs from hazardous waste sites, data from those exposed to PCBs under other circumstances are potentially relevant. Kilburn et al. (1989) studied 14 firemen 6 months after exposure to PCBs and their by-products generated in a transformer fire. Comparison with other firemen not involved in the fire showed that those exposed had significant neurobehavioral (cognitive function) impairment. No relationship, however, was found between the firemen's serum or fat levels of PCBs such as Arochlor 1258 and their type or degree of neurobehavioral impairment. These levels varied widely and were within the ranges described for environmentally exposed populations. There were improvements in some signs after a detoxification program. It is possible that much of this symptomatology was related to toxic by-products of PCBs generated in the fire. After an office building electrical transformer fire in Binghamton, New York, in 1981, a medical surveillance program was established for 482 fire fighters, police, clean-up workers and others involved (Fitzgerald et al., 1989). Of those followed, 33 percent had never worked in the building but were in the vicinity and were included as a low-exposure control. Over a three-year period there was no reduction in fertility, fetal loss, or excess cancer incidence in comparison to that expected from New York state rates. However, there was an excess of reported unexplained weight loss, muscle pain, frequent coughing, skin color changes, and nervousness or sleep problems in the heavily exposed compared to the low-exposure group. Many of the subjects knew their exposure status and possible health effects, so recall bias could not be excluded as an explanation for these differences. Nevertheless, there were higher mean serum PCB levels measured immediately after the fire in those who subsequently reported excessive weakness, skin color changes, or loss of appetite compared to those without such symptoms. In a case report, Shalat et al. (1989) described three kidney adenocarcinomas in men who worked for a public utility company and were exposed to PCBs. The authors commented on the relatively young age of the subjects (34, 43, and 56) but gave no details of the population from which the cases were drawn, or the time period of observation. In a series of studies, Rogan and his colleagues at the National Institute of Environmental Health Sciences (NIEHS) have studied the
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 effects of transplacental exposure to PCBs and DDE (dichlorodiphenyl dichloroethene). The routes of exposure are unknown, but believed to include contaminated soil. In a study of 912 infants born in North Carolina, samples of placenta, maternal and cord serum, and milk/ colostrum were obtained and analyzed for PCB and DDE levels (Rogan et al., 1986). No relationship was found between birth weight, head circumference, or neonatal jaundice and PCB or DDE levels. However, higher PCB levels were associated with hypotonicity and hyporeflexia and higher DDE levels with hyporeflexia. In a subsequent follow-up of 858 of these children, examinations were conducted at 6 months and 1 year (Gladen et al., 1988). Psychomotor testing using a scale of infant development was related to the estimated PCB and DDE body burden of the mother at birth. Low psychomotor development index (PDI) scores were related to higher transplacental exposure to PCBs at 6 and 12 months of age, but no relationship was found for the mental index (MDI) score. For high DDE levels there was no relationship to the PDI at either 6 or 12 months, while for the MDI higher transplacental exposure to DDE was associated with higher scores at 6 months, but there was no association at 12 months. No association was found for breast milk PCB or DDE levels and either score. There is evidence that prenatal exposure to PCBs shortens gestational age (Taylor et al., 1984). In a review, Tilson et al. (1990) point to the similarity of effects from perinatal exposure to PCBs in a variety of species (rodents, rhesus monkeys, and humans). However, humans appear to be the most sensitive species to show adverse effects on development and behavior in the young in terms of measured levels of PCBs. It is also worth noting that such effects were detected after exposure of mothers to PCBs at levels below both the relevant standards for occupational exposure and those for food contamination. DIRECT EXPOSURE FROM DUMPS ARSENIC ATSDR (1989) conducted a human exposure study to determine whether adults or children living near an abandoned arsenic production site who frequented the area had elevated levels of urinary arsenic, and if so whether time spent at the site was correlated with elevated urinary arsenic levels. The only indication of unusual exposure was the finding that three children had elevated levels of urine arsenic. These levels fell after residents were cautioned to stay away from contaminated and potentially contaminated areas.
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 The Anaconda Company Smelter in Montana operated from 1884 to 1980, extracting copper from ore. Wastes from the smelter contaminated the area surrounding it, including the upwind town of Anaconda (population 10,000) and the closer, downwind community of Mill Creek (population 100). The site was listed on the National Priorities List final list in 1983 (EPA, 1990). Binder et al. (1987) conducted a population-based survey of the Anaconda area, studying the relation of arsenic soil contamination levels with urinary arsenic levels in children. It was known that the children had elevated arsenic levels when the smelter was operating, and they were interested in seeing whether new exposure data would verify several exposure models that predicted that the children would have continuing significant and measurable exposure to arsenic. Soil levels (measured in 1985) of arsenic ranged from 140-1950 ppm (mean = 715 ppm) for Mill Creek, 27-345 ppm (mean = 144 ppm) for Anaconda, to 19-146 ppm (mean = 44 ppm) for Livingston, the control community that was demographically similar to Anaconda but had no history of mining or smelting industries; housedust levels were also measured. Urinary arsenic levels of the Mill Creek children were significantly higher than the Livingston children for both March (66.1 µg/l to 10.6 µg/l) and July (54 µg/l to 16.6 µg/l). Surprisingly, the urinary arsenic levels for Anaconda and Opportunity (6 kilometers from the smelter stack) were not significantly higher than Livingston, thereby contradicting the prediction of the exposure models. EPA (1990) decided to temporarily relocate all Mill Creek residents between 1986 and 1987; by 1988 all residents were permanently relocated. LEAD EXPOSURE Mined and processed since antiquity, lead remains a ubiquitous, persistent environmental pollutant that is also one of those most common at Superfund sites. Lead enters the environment through a broad range of pathways, reflecting the diverse uses to which industrial societies have put this heavy metal. These range from automobile and industrial emissions to paint pigments and solder. In addition, lead enters drinking water through old lead pipes, common in many older northeastern cities, through leaching of lead solder applied to water pipes in homes prior to 1988, or through brass faucets that contain some lead. Once lead is emitted into the air, it ultimately settles by means of wet and dry deposition as soil dust and into waterways, where it can be recycled through the environment and into humans. Natural sources of lead provide a minimal contribution to the total
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 human burden. Levels of lead in the atmosphere now are estimated to be 10 to 20 thousand times higher in some urban areas compared to more remote regions of the globe. Lead deposited on soils can bind to a number of other naturally occurring materials, including other dusts, clays, hydrous oxides, and humic and fulvic acids. Soil is logically the most common repository, or sink, for airborne lead, but it cannot be considered a permanent sink. As with other soil contaminants, once lead pollutes soil, opportunities are enhanced for lead to be absorbed and recycled into the human food chain through grazing animals, home gardening, and general agricultural activity. Also, lead exposure can occur directly from soil exposure to young children who play outdoors, mouth objects on the ground, or engage in extensive pica. In addition, millions of children are at risk of exposure to lead dust from old lead paint in their homes and schools. The amount of lead that can be toxic to a young child is quite small. The average toddler should consume no more than 100 micrograms per day of lead, according to the World Health Organization. In the 1970s, a person running her hand along a table top could acquire more than that amount on her fingertip because of deposits from ambient air. Because such small amounts of lead can be toxic, efforts are continuing to reduce exposures. ATSDR is conducting a number of studies involving mining wastes. A study of residential surface soils in Leadville, Colorado, located near the California Gulch Superfund site, found that more than 60 percent of the residential soil levels were higher than 1000 ppm and more than 80 percent had levels higher than 500 ppm (CDOH et al., 1990). Soil lead levels of more than 500-100 ppm are associated with increased in blood lead concentrations, especially in young children (CDC, 1985). The Leadville study found that 41 percent of the children had blood lead levels greater than 10 µg/dl and 15 percent had greater than 15 µg/dl. The authors note that the Bunker Hill Superfund site in Idaho had similar findings of 41 percent of the children having levels of 10 µg/dl and above, and 14 percent had greater than 15 µg/dl; the Silver Creek (Utah) mine tailings exposure study found a mean blood lead level of 7.8 µg/dl compared to the 4.0 µg/dl of their control population (CDOH, 1990). EPA uses a level of 1.4 µg/dl as its estimate of background blood level. This indicated that at all these sites, children have elevated levels of lead. Studies of community residents living near metal smelters have found that their blood lead levels correlate directly with the distance that they live from these facilities (Landrigan et al., 1975; Baker et al., 1977), as have studies of children living near major highways (Mahaffey, 1983). For those Superfund sites that involve previously operating
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 waste incinerators, similar patterns of exposure may also have occurred. ATSDR issued a health advisory for the Caldwell incinerator, located in Lenore, North Carolina, based on a health assessment that found significant elevations of blood lead both in workers at the small incinerator and in residents of the community (ATSDR, 1990). In addition, more than half of the 80 workers had advanced neuropathies. Although this advisory has not been published in the literature that this report generally reviews, we cite it here as an illustration of the fact that such community effects have been documented. Soil lead levels in these circumstances can be an important reservoir for continuous re-exposure of the population. MIXED CHEMICAL EXPOSURE Under many circumstances, the route of exposure is unclear. This applies to potential chemical exposures from many toxic-waste sites. One example is a study of residents near a landfill site in Hamilton Ontario, used from the early 1950s until 1980 for disposal of solid and liquid industrial wastes (Hertzman et al., 1987). The study of residents was preceded by a study of workers to help focus on relevant symptomatology. Both groups exhibited mood, narcotic, skin, and respiratory disorders. Although perception of exposure could explain the results of the study, it was the authors' conclusion that the adverse effects seen were more likely than not the result of chemical exposure. DETECTION OF CONTAMINANTS Where residents near hazardous-waste sites have engaged in home gardening, residues in their foods need to be carefully evaluated. In order to evaluate these residues, background levels need to be determined. The Food and Drug Administration (FDA) Market Basket Survey consists of four samples of grocery products purchased annually in each of four regions of the U.S., and prepared for eating. In the Total Diet Study, 234 different food items are collected and analyzed four times each year in three cities in each of four regions. Analyses are conducted on chemical residues in this market basket, in some cases evaluating contaminants in samples as small as three raisins, and extrapolated to the general food supply. Comparisons are made between the residues measured and the Acceptable Daily Intakes (ADI) established for individual contaminants. The ADI is established by panels of scientific experts at the FDA and other international organizations and are estimated to be the daily amount of a chemical that can be safely
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 ingested, without substantially increasing an individual's lifetime risk. The FDA Total Diet Study includes very few seafood samples. Those included, such as haddock, pollock and fish sticks, are among the products least likely to include significant lipophilic pesticide or other chemical contamination (Institute of Medicine, 1991). A number of analysts have questioned the validity of applying such a limited sampling strategy to generalizations about the nation 's overall food supply (Institute of Medicine, 1991). ADIs are set for individual compounds; the cumulative effect cannot be calculated by such means. In addition, the market basket survey cannot estimate contributions from either imported or home grown produce. PESTICIDE CONTAMINATION OF FOOD Accidental or illegal pesticide contamination of food can result in acute epidemics of illness. This is demonstrated by a study of one such episode in California in 1985 (Goldman et al., 1990). Aldicarb, a carbamate pesticide, can be incorporated into the flesh of fruits, and was found to be the source of an extensive outbreak of illness associated with contaminated watermelons. As in restaurant food-poisoning episodes, detection of the contamination was aided by the fact that watermelon was consumed by a group of persons, which made it easier to trace the cause of the multiple illnesses. Several hazardous-waste sites contain pesticide residues and therefore could be potential sources of foodborne exposure if they were to contaminate nearby areas. To the committee's knowledge, such episodes have not been reported. For example, the Hardeman County, Tennessee site (discussed in Chapter 5) contained pesticide wastes, but the studies focussed on groundwater as the route of exposure (Clark et al., 1982; Harris et al., 1984). While it is probable that chronic exposure of the general population to pesticides is mainly through the food chain (Kutz et al., 1991), accurate exposure assessment of this route is difficult (McKone and Ryan, 1989). ANIMALS AS SENTINELS Studies on animals provide a useful additional source of information with which to evaluate chemical contamination in soil. Rowley et al. (1983) studied the natural vole population at Love Canal. Voles were trapped in three areas: I-the immediate Love Canal area, II-very close to Love Canal, and III-an area about one kilometer away, whose vole population served as the control. They found significant differences in mortality. The mean life expectancy after weaning for
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 voles in areas I and II being 23.6 and 29.2 days, respectively, compared to 48.8 days for the control animals from area III. Liver and adrenal weights in females and seminal vesicle weights in males were also significantly reduced in area I compared to area III voles. Also, levels of contaminants such as hexachlorocyclohexane and other chlorinated hydrocarbons were detected in voles from areas I and II, but not in those from the control area. Another relevant study in this regard was recently completed by Hayes et al. (1990). They conducted a case-control study of Military Working Dogs (MWD) that served in Vietnam during the war, compared with control dogs that served in the continental U.S. during the same time period. They found a statistically significant elevation in the risk of testicular tumors for MWD from Vietnam. Other laboratory studies have also detected a link between exposure to some of the chemicals used in Vietnam, which include dioxin as a contaminant, and a variety of cancers. These studies of wildlife may be useful indicators of potential exposure at hazardous waste sites, especially for those sites that have previously been used as playgrounds or sites for other recreational activities involving extensive contact with soil. For further exploration of this topic, see the recent National Research Council report on the use of animals as sentinals of environmental health hazards (NRC, 1991). CONCLUSIONS Soil provides a usually unrecognized source of exposure to contaminants. Models indicate that adults may be exposed directly or indirectly, through the food chain, and that children incur greater exposures per unit of body weight. Home gardening and ingestion of subsistence or recreational fish can be important sources of these contaminants, according to a number of sources. In addition, commercial shellfish and finfish may also be contaminated. Epidemiologic studies of hazardous-waste sites need to incorporate consideration of soil as a route of exposure. REFERENCES Alavanja, M.C.R., A. Blair, S. Merkle, J. Teske, B. Eaton, and B. Reed. 1989. Mortality among forest and soil conservationists. Arch. Environ. Health 44: 94-101 Anonymous. 1979. High serum concentrations of DDT residues: Triana, Alabama. Morbid. Mortal. Week. Rep. 28: 123-124 ATSDR (Agency for Toxic Substances and Disease Registry). 1989. The Crystal Chemical
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ENVIRONMENTAL EPIDEMIOLOGY: Volume 1 Company Arsenic Exposure Study, Houston Texas Atlanta, Ga.: Epidemiology & Medicine Branch, Agency for Toxic Substances and Disease Registry ATSDR (Agency for Toxic Substances and Disease Registry). 1990. Public Health Advisory for Caldwell Systems, Inc., Caldwell County, Lenore, North Carolina. July 25, 1990 Bailar, J.C. 1991. How dangerous is dioxin? N. Engl. J. Med. 324: 260-262 Baker, E.L., Jr., C.G.Hayes, P.J. Landrigan, J.L. Handke, R.T. Leger, W.J. Houseworth, and J.M. Harrington. 1977. A nationwide survey of heavy metal absorption in children living near primary copper, lead, and zinc smelters. Am. J. Epidemiol. 106: 261-273 Baumann, P.C. 1984. Cancer in wild freshwater fish populations with emphasis on the Great Lakes. J. Great Lakes Res. 10: 251-253 Binder, S., D. Forney, W. Kaye, and D. Paschal. 1987. Arsenic exposure in children living near a former copper smelter. Bull. Environ. Contam. Toxicol. 39: 114-121 Calabrese, E.J., E.J. Stanek, C.E. Gilbert, and R. M. Barnes. 1990. Preliminary adult soil ingestion estimates: Results of a pilot study Regul. Toxicol. Pharmacol. 12: 88-95 CDC (Centers for Disease Control). 1985. Preventing Lead Poisoning in Young Children: A Statement by the Centers for Disease Control, January 1985. DHHS Publication No. 99-2230. Atlanta: U.S. Department of Health and Human Services, Public Health Service CDOH (Colorado Department of Health), University of Colorado at Denver, and Agency for Toxic Substances and Disease Registry. 1990. Leadville Metals Exposure Study. [n.p.] : State of Colorado. Clark, C.S., C.R. Meyer, P.S. Gartside, V.A. Majeti, B. Specker, W.F. Balisteri, and V.J. Elia. 1982. An environmental health survey of drinking water contamination by leachate from a pesticide waste dump in Hardeman County, Tennessee Arch. Environ. Health 37: 9-18 Cleland, G.B., J.F. Leatherland, and R. A. Sonstegard. 1987. Toxic effects in C57B1/6 and DBA/2 mice following consumption of halogenated aromatic hydrocarbon-contaminated Great Lakes coho salmon (Oncorhynchus kisutch Walbaum) Environ. Health Perspect. 75: 153-157 Cleland, G.B., P.J. McElroy, and R.A. Sonstegard. 1989. Immunomodulation in C57B1/6 mice following consumption of halogenated aromatic hydrocarbon-contaminated coho salmon (Oncorhynchus kisutch) from Lake Ontario J. Toxicol. Environ. 24: 477-486 EPA (U.S. Environmental Protection Agency). 1990. National Priorities List Sites: Montana. EPA/540/4-90/027. Washingon, D.C.: United States Environmental Protection Agency. Fingerhut, M.A., W.E. Halperin, D.A. Marlow, L.A. Picitelli, P.A. Honchar,, M.H. Sweeney, A. L. Greifa, P.A. Dill, K. Streenland, and A.J. Suruda. 1991. Cancer mortality in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin N. Engl. J. Med. 324: 212-218 Fiore, B.J., H.A. Anderson, L.P. Hanrahan, L.J. Olson, and W.C. Sonzogni. 1989. Sport fish consumption and body burden levels of chlorinated hydrocarbons: A study of Wisconsin anglers Arch. Environ. Health 44: 82-88 Fitzgerald, E.F., A.L. Weinstein, L.G. Youngblood, S.J. Standfast, and J.M. Melius. 1989. Health effects three years after potential exposure to the toxic contaminants of an electrical transformer fire. Arch. Environ. Health 44: 214-221 Friberg, L., C.-G. Elinder, T. Kjellstorm, and G.F. Nordberg, eds. 1985a. Cadmium and Health: A Toxicological and Epidemiological Appraisal, I. Exposure, Dose and Metabolism Boca Raton: CRC Press.
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Representative terms from entire chapter: