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Seafood Safety 5 Occurrence of Chemical Contaminants in Seafood and Variability of Contaminant Levels ABSTRACT This chapter and the following one should be considered as a unit. Although the committee has not attempted a comprehensive quantitative assessment of the risks of chemical contaminants in seafood, this chapter performs the functions of the "hazard identification" portion of a chemical risk assessment–giving a broad overview of many different potential seafood contamination problems, as well as an extensive summary of available data for characterizing contaminant concentrations in aquatic organisms in the environment. Chapter 6 provides a discussion of the directions needed to improve quantitative risk assessment in this area [including a detailed treatment of the methods used to assess two specific hazards (polychlorinated biphenyls and methylmercury)] and, more broadly, covers the issues that are usually found under the headings "dose-response assessment," "exposure assessment," and "risk characterization," as well as some risk management considerations. The inorganic contaminants with the greatest potential for toxicity appear to be antimony, arsenic, cadmium, lead, mercury, selenium, and sulfites (used in shrimp processing). Among organic compounds, polychlorinated biphenyls, dioxins, several chlorinated hydrocarbon insecticides, certain processing-related contaminants (nitrosamines and possibly products of chlorination), and contaminants related to aquaculture pose sufficient potential risks for consumers to be worthy of additional study. In addition to providing a broad survey of data on chemical contamination of aquatic organisms and potential risks, this chapter undertakes an extensive set of analyses of the variability of concentrations of certain contaminants across geographic areas and the implications of this variability for control. In general, lognormal distributions appear to provide good descriptions of the pattern of variation of chemical contaminant concentrations among different geographic areas, and some contaminants (mostly organics) appear to be much more variable than others. The variability of contaminant concentrations among geographic areas is important because it indicates the potential for reduction of exposure through restrictions on the harvesting of aquatic organisms from specific sites. Based on analyses of data for inshore marine waters, for the most variable contaminants/sets of species, it would be possible theoretically to reduce the population dosage delivered by more than 50% by restricting harvesting/marketing from only the 5% most intensely contaminated sites. There is, therefore, considerable potential for management of the overall population dosage of contaminants by measures that would restrict harvesting in specific ways.
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Seafood Safety INTRODUCTION There is no area of the committee's work that poses greater challenges to both the scientific tools for understanding likely health hazards and the social tools for managing risks, than the diverse collection of chemical residues that find their way into the human diet partly by way of seafood. Moreover, the confusion between technical questions and social control problems is connected. The understanding of toxicology and environmental health has made important strides since the multitiered structure of federal food protection law was erected (principally by legislation in 1906, 1938, and 1958). Older concepts, which shaped the legislative framework within which food protection agencies attempt to function, suggested sharp distinctions between "poisons" and other substances, or between "safe" and "unsafe" levels of exposure to important categories of environmental toxicants.1 These ideas are gradually giving way to a more quantitative (although generally still highly uncertain) conception of risks, based on more detailed information about the mechanisms by which different substances interact with intricate biological systems and the diversity of those systems in different individuals in the large and disparate human population. To the extent that increased understanding indicates that certain categories of risks cannot be eliminated entirely, the tools for social control of these risks will have to be adapted to manage toxicant exposures and risks in the light of explicitly formulated trade-offs between the costs of forgoing certain portions of our food resources and the costs of potential adverse effects. The technical advances that have occurred in risk assessment in recent years have been applied most readily to issues of health protection by governmental institutions of relatively late vintage, operating under legislation adopted within the last 20 years – most notably, the different branches of the U.S. Environmental Protection Agency (EPA) and analogous state authorities. When the more modern techniques and assumptions for quantitatively assessing risks are applied to seafood contaminants, there are a number of areas of mismatch2 that give the appearance of inconsistency in the social and technical judgments on risks made by different agencies. Both this chapter and the next deal with aspects of chemical residues in aquatic organisms. In this chapter the committee focuses on the tasks that are usually thought of as part of the hazard identification portion of a quantitative chemical health risk assessment. Chapter 6 deals broadly with issues in the assessment of dose-response relationships, estimation of exposures, and characterization of risks. The committee has not, however, attempted a formal and comprehensive assessment of the risks of chemical residues in aquatic organisms. Aside from the fact that the available data on both contaminant3 levels and risks are inadequate for such a task at this time, the charge to the committee emphasized the review of the adequacy of current risk recognition, risk assessment, and risk management procedures in governmental agencies. In the next section of this chapter, the committee gives a broad overview of the types of toxic agents that are known or believed to be contaminants of seafood. Then, the various data bases available for characterizing the geographic and species distribution of chemical contaminants are reviewed, followed by the quantitative insights gleaned from these sources. The variability of contaminants by geography and species, which provides some of the most potentially important opportunities for reduction of exposures, is then considered. Finally, preliminary
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Seafood Safety conclusions and recommendations are offered, based on the material discussed in this chapter. Chapter 6 articulates basic concepts underlying the mechanisms of action of toxic substances and quantitative ideas about dose-time-response relationships. Then, a focused examination is provided of available Food and Drug Administration (FDA) risk assessment and risk management analyses for two types of residues — one a set of organic carcinogens, polychlorinated biphenyls (PCBs), and the other an organometallic residue with reproductive and neurological effects (methylmercury). These two important examples are used to fulfill the committee's charge to critique the adequacy of current governmental procedures for assessing risks and the opportunities for risk reduction. Finally, the balance of Chapter 6 provides a more general overview of what can be said very approximately about the quantitative risks of other contaminants in seafood. TOXIC AGENTS AND POTENTIAL TYPES OF HEALTH EFFECTS Metals and Other Inorganics The human and veterinary medical literature is replete with information regarding the toxicity of heavy metals. Based on this information, different metals can be classified as having major, modest, minor, or no potential for toxicity. Those with major potential for toxicity, in the committee's view, are antimony, arsenic, cadmium, chromium, lead, mercury, and nickel. Contaminants with a modest potential for toxicity include copper, iron, manganese, selenium, and zinc. Those of minor or no toxicity are aluminum, silver, strontium, thallium, and tin. This classification is based, among other parameters, on potency for producing effects and accessibility of the toxicant. Thus, such metals as nickel and chromium, known inhalant carcinogens, are among those of greatest toxicity, whereas selenium and tin are placed in the lesser categories. When considering the same metals as contaminants of an aquatic food source, however, their relative toxicities will certainly change. Criteria for identifying contaminants (hazard assessment, hazard analysis) of public health concern in the aquatic environment may vary but have been defined (PTI, 1987). These include (1) persistence, (2) bioconcentration potential, (3) toxicity to humans (or suspected toxicity), (4) sources of contaminants in the area of interest, and (5) high concentration in fish and shellfish from the area of interest. By applying such criteria, both nickel (except for its carbonyl form) and chromium (at least in its hexavalent form), inhalant carcinogens and elicitors of dermal hypersensitivity, would be suspect as contaminants of public health concern (Haines and Nieboer, 1988). However, both are poorly absorbed from the gastrointestinal tract, and there is little evidence that this route of exposure results in systemic toxicity (Beliles, 1978; Nieboer and Jusys, 1988). Similarly, the use of trin-butyltin (TBT) to control marine fouling of vessels and aquaculture sea pens has been followed by the accumulation of butyl- and elemental tins in the muscles of fish and invertebrates (Short and Thrower, 1987a,b). Organic tin compounds tend to be more toxic than inorganic salts, and organic forms in particular may be of public health concern. Although little information exists about the toxicity of tin to man, there is sufficient information regarding dosage levels without observable effect to eliminate the
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Seafood Safety probability of tin poisoning from contaminated seafood (WHO, 1980). Conversely, selenium is well recognized as toxic by ingestion and, at existing levels in some seafoods, may be a source of risk (Fan et al., 1988). Antimony has been recognized as both an occupational and an iatrogenic toxicant (Anonymous, 1988a,b; Groth et al., 1986). Recent seafood residue studies, however, either have failed to sample for this metal or indicate concentrations above detectable levels in few contaminated sites (Lowe et al., 1985; NOAA, 1987). Such findings and reasoning, coupled with estimates of ingestion levels, suggest a preliminary list of heavy-metal contaminants found in the edible portions of aquatic animals that may be detrimental to human health. The metals identified in this hazard analysis include arsenic, cadmium, lead, mercury, and selenium. Some toxicity information related to antimony is given later, in the section where current dosage is compared to "acceptable daily intake" levels and other recommended standards. Specific Trace Metals Arsenic Arsenic has a long history as a potent poison of humans and other animals. Previously used as a chemotherapeutic and homicidal drug, much information has been collected regarding its toxicity. It exists as the toxic trivalent form (arsenic trioxide, sodium arsenate, arsenic trichloride, etc.), as the less toxic pentavalent form (arsenic pentoxide, arsenic acid, lead arsenate, calcium arsenate, etc.), and as numerous organic forms (arsanilic acid, bimethyl arsenate, etc.). When ingested, inorganic arsenic may cause acute or chronic toxicity and is of primary concern as a carcinogen responsible for pulmonary carcinoma, hemangiosarcomas, and dermal basal cell and squamous cell carcinomas. Its toxicity is dependent on oxidation state and route of exposure. In its chronic manifestations, arsenic is responsible for gastroenteritis, nephritis, hepatomegaly, peripheral symmetrical neuropathy, and a number of lesions of the skin including plantar and palmar hyperkeratosis and generalized melanosis. Some of these lesions appear related to destruction of capillary endothelium, with consequent edema and even circulatory failure. At the molecular level the metal is known to uncouple phosphorylation; to react with sulfhydryl groups, thus upsetting cellular metabolism; to damage deoxyribonucleic acid (DNA) directly and to inhibit its repair (Buck, 1978). In addition, as sodium arsenate and arsenite it is teratogenic in lower animals (Earl and Vish, 1978). The metal, therefore, places at special risk pregnant and nursing mothers and their children. However, the predominant form of arsenic that exists in the edible portions of aquatic animals is the organic form, either arsenobetaine or arsenocholine. These forms have been named "fish arsenic" and no toxic effects from their ingestion have been reported in animals [at doses of 10,000 milligrams (mg) per kilogram (kg)] or in humans. Furthermore, there is no evidence of mutagenicity by arsenobetaine (Penrose, 1975; Tam et al., 1982). Although arsenobetaine constitutes the bulk of arsenic in fish, available studies are inadequate to conclude that the amounts of more toxic inorganic forms of arsenic (or organic forms that can be metabolized to inorganic arsenic in humans) are negligible in all fish. It is known, however, that the trivalent form (inorganic) is toxic to man and that long-term effects include dermal hyperkeratosis,
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Seafood Safety dermal melanosis and carcinoma, hepatomegaly, peripheral neuropathy, and in cases of inhalation, pulmonary carcinoma (ATSDR, 1989a; Goyer, 1986). Arsenic is used in the manufacture of pesticides, herbicides, and other agricultural products and is a by-product of mining and smelting operations (Buck, 1978). Cadmium Cadmium is unique among toxic metals because it is a relatively recent (50 years) contaminant of the aquatic environment. Its sources are solid waste dumping (pigment in paint) and cadmium-containing sewage sludge, the use of phosphatic fertilizers, electroplating and galvanizing manufacture, and mining (zinc, lead) wastewater (Sherlock, 1986; Sloan and Karcher, 1985). Cadmium is commonly found in its metallic form and as sulfides and sulfates. Invertebrates, both crustacea and bivalves, tend to accumulate metallic cadmium in large amounts by binding to various high-molecular-weight metallothioneine ligands. There is a differential affinity between crustacean muscle and hepatopancreas, the latter organ containing 10-20 times the concentration of the former. Because hepatopancreas may be considered a delicacy or marketed as "brown crab meat," the potential for ingesting large amounts of cadmium when eating lobsters or crabs is increased (McKenzie-Parnell et al., 1988; Sloan and Karcher, 1985). Cadmium may damage cells by its activity in the plasmalemma where it reacts with phosphate groups of the lipid bilayer to alter permeability, in the nucleus where it is mutagenic, on lysosomal membranes, and as an inhibitor of mitochondrial activity. Its ability to stimulate metallothioneine production in aquatic animals, however, does much to decrease its toxicity (Viarengo, 1985). Cadmium has been responsible for major human poisoning incidents as a contaminant of wastewater used for irrigation in Japan where the illness is known as itai-itai (ouch-ouch) disease. It is a chronic osteoporotic and osteomalacic condition that primarily affects multiparous females (Kobayashi, 1978). Although the highest accumulation of cadmium is found in bone, the liver and kidney also have a propensity for accumulating the metal, and the kidney is often seriously damaged in chronic occupational exposures (Lauwerys and De Wals, 1981). Clinically, patients suffer tubular dysfunction resulting in aminoaciduria, proteinuria, and glucosuria. Although the half-life of cadmium in kidneys of humans is uncertain, it may be as long as 30 years. Under such circumstances it has been conjectured that critical concentrations [kidney = 200 micrograms (µg) per gram (g) by age 50] could be used to establish maximum levels of daily exposure (Kjellström et al., 1977). What makes cadmium of dietary concern is that ordinary background dietary exposures were estimated to yield kidney concentrations of about one-quarter the hypothesized critical level. The segment of the population at greatest risk would appear to be older adults (ATSDR, 1989b). Studies in maternal-fetal tissues have provided evidence for accumulation and transplacental transfer of metals. In one study, placental cadmium levels were one to two times those in maternal or cord blood. It was observed also that erythrocyte cadmium levels were roughly three to five times plasma cadmium levels, and that maternal erythrocyte cadmium levels were somewhat higher (27%) than those of the fetus.
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Seafood Safety Lead Of all the heavy metals, lead probably has the longest history of environmental contamination and toxicity to humans (Green et al., 1978). For this reason, lead poisoning, or plumbism, has been intensely studied, and a large body of information is available for examination. Sources of lead found in the environment are multiple, and the metal is truly ubiquitous, being commonly found in food, water, and air. Evidence exists that lead in the environment has increased during the past 200 years, and it is not surprising that it can be found as a contaminant of aquatic animals (Shukla and Leland, 1973). Environmental lead is a product of storage battery, ammunition, solder, pigment, pipe, brass, and red lead manufacture. Tetraethyllead is a component of gasoline antiknock additives, although in recent years this use has been drastically reduced. There are at least five pools of lead in the body, two of which reside in the skeleton (90%) in cortical and trabecular bone. Lead in cortical bone is similar in half-life to cadmium (approximately 20 years). Other body compartments for lead include the kidney, lung, and central nervous system (Goyer, 1986). It is not surprising therefore that major lesions and clinical signs in humans suffering frank plumbism are referable to the blood (anemia), brain (convulsions, paralysis), and kidney (proteinuria). The condition in humans is best known because of its chronic toxicity to young children who ingest lead-base paint chips or lead in soil, house dust from paint, industrial dust, and automotive emissions. Oral ingestion of inorganic lead is without doubt the primary port of entry into humans. Of the lead ingested, only 5-15% is absorbed in adults but considerably more in children (Goyer, 1986). Recent studies suggest that very low levels ingested by pregnant women may result in learning and behavioral disabilities in neonates and preschool children (Waternaux et al., 1989). Excretion is primarily via the bile and the gastrointestinal tract. Organic lead compounds such as tetraethyllead may be absorbed in large quantities through the skin, but as toxicants these forms of lead are primarily a problem in the petroleum industry. All forms of lead toxicity are less frequent in adults; any occurrence is usually acute and occupationally related (Green et al., 1978). Lead's toxicological mode of action depends on its molecular configuration, inorganic lead being less toxic than and producing clinical signs different from tetraethyllead. Inorganic lead is an inhibitor of aminolevulinic acid dehydratase (ALAD) and heme synthetase, which leads to anemia (Hammond, 1978). The metal causes necrosis of neurons, myelin sheath degeneration, and especially, brain vascular damage with increased cerebrospinal fluid (CSF) pressure. These lead to encephalopathy and eventual mental retardation in children. Lead crosses the placental barrier, and there is a good correlation between maternal and fetal blood lead values (Van Gelder, 1978). Therefore, at primary risk from contaminated seafoods are the fetus and neonates. Mercury Mercury exists in elemental form, as monovalent (mercurous) or divalent (mercuric) salts, and methylated. The methylated form is the most toxic to humans (Harada, 1978). Methylmercury is formed in the environment from the divalent salts
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Seafood Safety by anaerobic bacteria. It is quite easily absorbed after ingestion and has a variable half-life of 60-120 days in man but is reported to have a half-life of up to 2 years in fish, where it is the predominant form (Al-Shahristani and Shihab, 1974; Stopford and Goldwater, 1975). The metal is known to produce c-mitosis and chromosomal alterations resulting in cellular damage, with the kidney and brain as target organs. Neuronal damage and axonal demyelination result in the clinical signs and symptoms of paresthesia, incoordination, tremor, and epileptic seizures. The metal also binds strongly to sulfhydral groups (mercaptans), thereby inactivating certain enzymes (Hammond, 1978). In its methylated form, mercury quite easily passes the placental barrier, placing the fetus at particular risk (Amin-Zaki et al., 1979). The relationship of clinical signs in humans to blood, hair, and urine mercury levels has been reviewed (Tollefson and Cordle, 1986). Children of symptom-free pregnant and nursing mothers with relatively low blood and hair levels may suffer from mental retardation. Selenium Selenium is an enigmatic metal because it functions both as an essential nutrient and, at slightly higher levels, as a poison. It is present in various enzymes, has been reported to possess anticarcinogenic effects in animals, is an antioxidant, and yet is a well-documented toxicant of domestic animals as well as a mutagen (Griffin, 1979; Schamberger, 1985; Schnell and Angle, 1983). As an animal toxicant it is a regional problem of the Southwest and Far West. Seleniferous (alkaline, oxidizing) soils give rise to high levels in selenium accumulator plants that are grazed by cattle, sheep, horses, and swine. Poisoned animals develop conditions known as "alkali disease" [subacute, <50 parts per million (ppm)] and "blind staggers" (acute, >100 ppm). Signs include anorexia, tooth and hair loss, watery diarrhea, lassitude, progressive paralysis, and eventual death (Harr and Muth, 1972). Selenium levels in water from seleniferous areas are often quite high so it is not surprising that selenium has been found as a contaminant of fresh and marine aquatic animals. Its source however is not solely natural. Anthropogenic contamination occurs and is the product of fossil fuel combustion (fly ash) and of paint, alloy, photoelectric battery, and rectifier manufacture (Fishbein, 1983; Sorensen et al., 1984). Selenium exists in a number of chemical forms, elemental selenium (Seo), selenide (Se2+), selenite (Se4+), and selenate (Se6+). These forms may bond with other metals or organic substances such as amino acids (Ewan, 1978). The selenates are most soluble and easily enter biological systems. In one study, approximately 15-30% of the selenium found in fish muscle was the selenate form (Cappon and Smith, 1981). The selenites and elemental selenium are relatively insoluble. This is not to say that selenite when ingested will not act as a toxicant, merely that its innate insolubility may affect its absorption and distribution within the body (Goyer, 1986). The biochemistry of selenium is poorly understood but has been reviewed recently (Reddy and Massaro, 1983). The mode of action of selenium as a toxicant at the cellular and biochemical levels is uncertain. The metal appears to damage endothelium selectively, resulting in edema and hemorrhage in both humans and animals. It is also responsible for toxic hepatitis with eventual fibrosis (not constituting cirrhosis) in chronic exposures.
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Seafood Safety Selenosis in animals is reported to produce infertility and congenital malformations (Harr, 1978). Selenosis in man appears to be a relatively rare occurrence, most often due to acute occupational exposure or chronic exposure to contaminated water or food sources. There appears to be very little information regarding the effect on man of chronically high levels of selenium in the diet and its potential risk (Wilber, 1983). Recently, however, levels have been reached in fish that have prompted health alerts in California (Fan et al., 1988). Organic Compounds In this section, some of the potential contaminants of seafood that have come to the committee's attention, and about which there are at least some minimal data, are surveyed. These include the chlorinated hydrocarbon pesticides that came into widespread use in the United States and elsewhere immediately after World War II (Hansen et al., 1985). Among the chlorinated hydrocarbon pesticides detected in seafood were benzene hexachloride (BHC) or hexachlorobenzene (HCB), chlordane, dieldrin, dichlorodiphenyltrichloroethane (DDT), endrin, heptachlor, lindane, nonachlor, octachlor, and pentachlorophenol. In addition, industrial chemicals and by-products such as PCBs and dioxins are routinely detected in seafood. Less frequently detected pesticides included chlorpyrifos, dacthal (DCPA), diazinon, ethylene dibromide (EDB), malathion, mirex, omethoate, pentachloroaniline, tecnazene, and trifluralin (FDA, 1988; Gunderson, 1988). In quite specific circumstances, such as in farm ponds in heavily agricultural areas, other chemicals — even those that are not known to bioconcentrate, such as atrazine — can be found in fish (Kansas DHE, 1988). Some pesticides detected are specific to various regions. The carboxylic acid herbicide 2,4-(dichlorophenoxy)acetic acid (2,4-D) has been found in oysters from the northern Chesapeake Bay and Alaskan bivalves (NOAA, 1988). Fish from the Arroyo Colorado and adjacent lower Laguna Madre in Texas contained measurable concentrations of pesticides such as ethion, carbophenothion, ethyl parathion, and methyl parathion (NOAA, 1988). The organic compounds classified here have been reviewed by Murphy (1980). Specific Organics Polychlorinated biphenyls (PCBs) Polychlorinated biphenyls include more than 200 different compounds ("congeners") that were used in various formulations as liquid insulators in electrical equipment, as encapsulating agents, in carbonless carbon paper, and in hydraulic fluids. The use of PCBs in "open" applications such as carbonless carbon paper was phased out in the early 1970s, and any new use for the remaining applications was stopped in the late 1970s with the passage of the Toxic Substances Control Act. The U.S. usage of approximately 500,000 tons of PCBs in 1930-1970 accounted for about half of the total world production. However, the unusually slow rate of environmental degradation of the more highly chlorinated PCBs in the environment and in higher organisms, and slow continued discharge of PCBs from old equipment and dump sites, have led to a
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Seafood Safety relatively slow rate of decline of PCB concentrations in fish from large freshwater bodies (e.g., the Great Lakes). The PCBs are a paradigmatic case for the phenomenon of bioconcentration. The more highly chlorinated congeners in particular tend to be both highly lipophilic and very slowly degraded by most organisms. Thus, PCBs that are passed "up" the food chain tend to become much more concentrated as predators are consumed by successively larger predators. In contrast, terrestrial animals that are used for human food are generally vegetarians (first-level consumers of the primary producing organisms). The principal potential health concerns from PCB exposure include carcinogenesis (on the basis of extensive animal evidence and some suggestive findings in human epidemiological studies), changes in human birth weights, and some loss of neurological performance in the offspring of mothers with relatively high dietary exposures or body burdens (Bertazzi et al., 1987; Brown, 1987; Cordle et al., 1982; Fein et al., 1984; Gladen et al., 1988; J.L. Jacobson et al., 1989, 1990; S.W. Jacobson et al., 1985; Rogan et al., 1986; Sunahara et al., 1987; Taylor et al., 1989). All carcinogens–in particular, the PCBs and dioxins–are not thought to act primarily by causing DNA mutations (Safe, 1989). This subject is discussed extensively in Chapter 6. Suffice it to say here that lack of knowledge of the precise mechanisms by which PCBs cause cancers makes quantitative assessment of their cancer risk more uncertain than is usual for other chemicals. The PCB mixtures that are delivered to humans via seafood are likely to be systematically different from the original mixtures that were used in animal testing because of more rapid degradation of some (particularly less chlorinated) congeners in the environment and in aquatic organisms. The selection for relatively persistent congeners in aquatic organisms might tend to increase human risk relative to that expected from a naive extrapolation; other factors might have the opposite effect. In any event, the numbers of cases that could be expected seem large enough to warrant exploration of further options for risk reduction. Dioxins 2,3,7,8-Tetrachlorodibenzo-p-dioxin (hereafter known as TCDD) is a contaminant of products made from trichlorophenol, including some chlorophenoxy herbicides. In humans, its effect has been linked to a severe dermatitis; fetal toxicity and numerous other effects have been observed in experimental animals at very low doses. In standard animal test systems, it is one of the most potent carcinogens known. Using its standard procedures for cancer potency estimation and certain consumption estimates, EPA estimated a lifetime cancer risk of approximately 1 in 100,000 from eating fish contaminated at the nominal detection level of 1 part per trillion (EPA, 1987). Using considerably different methodology for assessing the risk, FDA has advised that, for consumption patterns and species typical to the Great Lakes area, fish consumption should be limited if concentrations in the edible portion exceed 25 parts per trillion and should be banned if concentrations exceed 50 parts per trillion (Kociba et al., 1978).4 These profound differences in risk assessment indicate the tremendous uncertainty about the true potency of TCDD to cause human cancer.
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Seafood Safety Polycyclic aromatic hydrocarbons (PAHs) Polycyclic aromatic hydrocarbons are common environmental contaminants found in petroleum, soot, or tar from incomplete combustion, lubricants, and domestic sewage. Many are well-established carcinogens and are highly toxic. Their pervasiveness in the environment assures widespread contamination of aquatic organisms. Because they are poorly metabolized by bivalves and are easily accessible to these animals, they may pose important potential hazards to humans. Chlorinated hydrocarbon pesticides Like PCBs, the broad group of relatively lipid-soluble, persistent chlorinated hydrocarbons was largely phased out of production in the United States during the 1970s because of concerns for carcinogenicity and ecological effects. Fortunately, few members of the group have proved to be as persistent as PCBs in the environment. Like PCBs, however, the precise mechanisms of action of many chlorinated hydrocarbons in causing cancer appear not to be by direct or indirect reactions with DNA; accordingly, quantitative assessments of risk for this group are more uncertain than usual. DDT and metabolites: Both DDT and its metabolites [primarily dichlorodiphenyldichloroethane (DDE)] are persistent (slowly eliminated from organisms) lipophilic substances of uncertain health significance in humans, and are among the most widespread and frequently sampled of the chlorinated hydrocarbons. They are also persistent in ecosystems and bioaccumulate at higher levels of the food chain, resulting in toxicity to birds and aquatic organisms. The use of DDT was essentially banned in the United States in December 1972. Subacute effects of these chemicals at high doses in humans include central nervous system signs and, in rodents, liver toxicity and estrogenic effects. In addition, DDE has been observed to cause liver tumors in rodents. Dieldrin: Dieldrin (an epoxide of aldrin) is a cyclodiene insecticide that, like DDT, affects the central nervous system, but is more toxic and has caused human fatalities. It too is lipophilic and may be released from fat stores long after exposure, to cause toxicity. It has led to increased liver tumors when fed at relatively low levels to rodents. Chlordane: Chlordane is similar in molecular structure and mode of action to dieldrin, but is less toxic. Heptachlor and heptachlor epoxide compounds: Heptachlor and heptachlor epoxide are also chlorinated cyclodienes, and the epoxide is known to be stored in human fat. They have toxicity similar to dieldrin. Endosulfan: Endosulfan is a cyclodiene pesticide and a problem contaminant in estuaries near agricultural drainage areas due to its widespread use (NOAA, 1989). Endrin: Endrin is similar in its toxic effects to other cyclodiene pesticides and is more acutely toxic than DDT. Chlorinated benzenes and phenols: Lindane (γ-isomer of 1,2,3,4,5,6-hexachlorohexane), also known as benzene hexachloride (BHC), a mixture of α-, β-, and γ -isomers of 1,2,3,4,5,6-hexachlorocyclohexane depending on the manufacturer, is a neurotoxin but has also been found to cause aplastic anemia in humans.
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Seafood Safety Hexachlorobenzene has never been manufactured in the United States, but it is a ubiquitous fungicide and contaminant often found in other pesticides such as pentachloronitrobenzene (PCNB), which is used in the United States. Pentachlorophenol: Also known as PCP and penta, pentachlorophenol is a wood preservative, slimicide, and metabolite of the fungicide hexachlorobenzene. Like other polychlorinated phenols, it is contaminated with carcinogenic dioxins (NOAA, 1988). Mirex: Mirex is a pesticide used to control the fire ant in the southeastern United States. Like other organochlorine pesticides, it is lipophilic and has been reported to be a carcinogen on the basis of rodent studies. It may be a precursor of chlordecone (kepone), is persistent in the environment, and bioconcentrates in the food chain. Kepone: Kepone has produced appreciable toxicity in exposed workers. It can cause neurological lesions, liver damage, and reproductive failure and is similar in its bioconcentration properties to mirex. Toxaphene: Toxaphene is a very common domestically used insecticide of complex and often uncertain molecular structure. It is made by chlorinating a mixture of terpenes. It therefore may vary in toxicity from batch to batch depending on the proportion of its isomers. Fortunately, it is of relatively low persistence in the body. Carcinogenic activity is suspected. Carboxylic herbicides: The herbicides DCPA, 2,4-D, and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) are chlorophenoxy compounds commonly used in agriculture, and by government agencies and utility companies to control woody plants in rights of way and along roadsides. Although 2,4,5-T has been found to have teratogenic activity, there has long been discussion about whether this is attributable to small amounts of dioxin contaminants. Aside from teratogenesis, these agents can affect animals by impairing neurotransmission, resulting in muscle weakness, ventricular fibrillation, and neuritis. Atrazine: Atrazine is a herbicide commercially known as AAtrex. It is of low oral acute toxicity. However, its chronic effects are unknown. Structurally similar compounds have been shown to produce thyroid adenocarcinomas in rodents. Contamination Problems in Aquaculture Fish culture uses a variety of chemicals that represent potential threats to the health of the cultured animal, indigenous biota, and even the human consumer (Meyer and Schnick, 1989). A number of chemicals of potential toxicity to humans that are not registered for use in the United States are employed in other nations (Fox, 1990). These include furazolidone, nitrofurazone, carofur, chloramphenicol, and silvex–all of which are known or suspected carcinogens. Chemicals employed in aquaculture include (1) drugs used to treat disease (chemotherapy), (2) those introduced through construction materials, (3) chemicals to treat parasites (formaldehyde), (4) hormones used to alter reproductive viability, sex, and growth rates, and (5) water quality treatments (copper compounds). Of these groups, those of greatest potential concern are the chemotherapeutic drugs. Chemicals used in construction and hormones are not considered in this section because they are relatively nontoxic or have been considered under other headings (organics, pesticides).
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Seafood Safety could lead to nephrosis (Friberg et al., 1974). The NOAEL is 0.2 mg/day (0.0029 mg/kg/day) (CEC, 1978). Lead Occupational and environmental poisoning with lead is well documented (NRC, 1972, 1980a). A plethora of dose-response information is available that has been used by risk assessors to calculate an acute ADI. Neurodevelopmental effects in children are presently being used to assess acceptable dosage and blood levels, although there is considerable skepticism that a true threshold exists. The latter is a difficult task because precise exposure doses associated with effects are not well known (Tsuchiya, 1980). Reports concerning dose-response are conflicting for similar effects, and a wide range of interindividual variability is apparent. Half-life: The half-life is 5 years to decades for bones, depending on type and location. In blood, it is estimated at 21-28 days; in soft tissues, it is intermediate between these extremes. Lead accumulates in the skeletal system. Blood Median Acceptable Toxicant Concentration (MATC): The Centers for Disease Control (CDC) puts the level for young children at 25 parts per billion (ppb) (but see long-term effects). Blood LOAEL: The LOAEL is not well known in humans and varies according to the effect measured. It is a poor indicator of an individual's dose-response but is of value in assessing population exposure. Some LOAELs for varying effects are delta-aminolevulinic acid dehydratase 10-20 µg/100 mL; changes in peripheral nerve conduction velocity 51-60 µg/100 mL; chronic encephalopathy (children) 50-60 µg/100 mL; acute encephalopathy 80 µg/100 mL. Recent measurements of developmental impairment show differences between groups in the normal range (5-15 g/100 mL) (see below). Hair LOAEL: Hair is a poor estimator; there is no LOAEL. Percent Absorption: The absorption is very variable, with the best estimate being 10%. Children may reach 50%. True mean percentage absorption remains uncertain (Rabinowitz et al., 1974). Age, Sex, Reproductive Status, and Interindividual Variability of Response: Recent studies indicate that the brain of the fetus may be more sensitive to lead than that of the neonate; hence, CDC levels of 25 ppb in blood may not be acceptable (Waternaux et al., 1989). Pretoxic Indicator: delta-Aminolevulinic acid dehydratase inhibition in erythrocytes correlates negatively with lead blood levels (EPA, 1979). Free erythrocyte protoporphyrin (FEP) increases with blood lead levels but varies in relation to sex. Long-term Effects: Anemia due to inhibition of hemoglobin production and shortened life span of erythrocytes result. There is derangement of both the peripheral and the central nervous system (CNS), especially with regard to neurobehavioral problems. Slowed mental development in neonates has been measured by the Bailey Scales of Mental Development. Children with higher blood lead levels at 6 months (7.07 µg/100 mL, SD 1.18 µg/100 mL) have poorer scores at 18 months than those with lower blood levels (4.66 µg/100 mL, SD 0.50 µg/100 mL) (Waternaux et al., 1989). Irreversible
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Seafood Safety renal functional and morphological changes may occur (Tsuchiya, 1980). Kinetics: There are essentially two compartments (three possible): blood and soft tissue (10% of burden) and skeletal system (90% of burden). ADI: The ADI is estimated at 429 µg/day and the PTI at 6.1 µg/kg/day (FAO/WHO, 1972). Toxic Body Burden: The body burden that would be toxic to a 70-kg individual is 100-400 mg. Steady Daily Intake for Toxicity: The daily intake that would lead to toxicity is uncertain. Mercury As previously stated, the chemical form of the ingestible mercury in seafood is thought to be predominantly methylmercury. Both occupational and accidental environmental poisonings with the metal and its methyl or ethyl form have been extensively reported and reviewed in the literature. Observations of blood and other tissue LOAELs in affected individuals allow calculation of an acute ADI (Inskip and Piotrowski, 1985; Tollefson and Cordel, 1986). Half-life: Whole body half-life values reveal an interindividual variability and differences with regard to reproductive status. The half-life is estimated at 70 days but is more than 110 days in some individuals and is 45 days for lactating females (Al-Shahristani and Shihab, 1974; Greenwood et al., 1978). Blood LOAEL: In males and nonpregnant women the LOAEL in blood is 0.22-0.24 ppm; for pregnant women, 0.10 ppm; and due to fetal sensitivity, the maternal threshold is 0.05 ppm (Inskip and Piotrowski, 1985). A sound relationship exists between blood level and daily intake. Hair LOAEL: The LOAEL in hair for adults is 25-50 ppm; for pregnant women, 37 ppm; maternal threshold, 15-20 ppm. The threshold may be as low as 10 ppm (10 µg/g; blood 0.03 ppm) in cases of extended periods of exposure (Inskip and Piotrowski, 1985). Hair appears to better reflect existing body mercury levels than urine or blood and is more resistant to sudden change. Hair levels also appear related to fish intake (Airey, 1983; Ohno et al., 1984). The hair/blood ratio is consistent and helpful in estimating exposure. Percent Absorption: Gastrointestinal absorption is 95%. Age, Sex, Reproductive Status, and Interindividual Variability of Response: There is little evidence for systematic differences in response due to age or sex of adults. Pregnant women may have a greater sensitivity; however, they deliver full-term, normal-weight children whose blood levels may be twice that of the mother. Such children develop CNS signs, including cerebral palsy, and delayed motor activity and speech. Lesions may increase in severity over long periods (Amin-Zaki et al., 1979). Effects of mild exposure are unknown. Pretoxic Indicator: Porphyrinuria has been observed in early poisonings and is suggested as a possible indicator of exposure. Long-term Effects: In children exposed prenatally to mercury, mental retardation can occur. Kinetics: A single-compartment (possibly two-compartment) model is likely. There is
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Seafood Safety uncertainty as to how the methyl form complexes with tissue, but studies suggest binding to glutathione in human blood and rat brain. Of the total body burden, 3-7% is found in the brain (Naganuma et al., 1980). ADI: The ADI is 0.0033 mg/kg body weight. Estimates vary, however; even at this level there is an 8% risk of effect. Toxic Body Burden: The toxic body burden for a 70-kg individual is calculated to be 25 mg. Steady Daily Intake for Toxicity: The acute daily intake level is 300 µg; the chronic level is uncertain. Selenium Selenium as an ingestible toxicant remains enigmatic because of its known protective and deleterious effects. As previously noted, the metal may exist in a number of forms. Elemental selenium is not water soluble. The reduced form (-2) is selenide. The dioxide (+4) in water forms selenous acid whose salts are selenites, whereas the trioxide (+6) in water forms selenic acid whose salts are selenates. These substances appear to vary in toxicity and distribution in the body. Among other missing dose-response data for selenium, knowledge concerning the chemical forms found in seafood is incomplete. This lack results in an inability to calculate no-observed-adverse-effect levels (NOAELs), LOAELs, and frank effect levels (FELs). Although some dose-response data are available for inhalation toxicity in humans, very few are available concerning oral exposure. Recent studies of humans chronically exposed to selenium in endemic areas of the United States revealed no adverse health effects (Fan et al., 1988). The literature on selenium and its toxicity has been reviewed by Hogberg and Alexander (1986). Half-life: In humans, studies reveal three phases for selenite, which are 1 day, 8-20 days, and 65-116 days. Blood LOAEL: For nail changes the LOAEL is 0.179 µg/mL. Depending on the definition of selenosis, other reports indicate no signs with blood levels of 0.44 µg/mL. Blood FEL: The blood FEL is 1.3-7.5 µg/mL with a mean of 3.2 µg/mL. Tissue LOAELs: For nail changes as measured by hair concentration, the LOAEL is 0.828 µg/mL. Depending on the definition of selenosis, some report no signs with hair levels of 3.7 µg/mL. Hair FEL: The hair FEL is 4.1-100 µg/mL with a mean of 32.2 µg/mL. Percent Absorption: Absorption is estimated in humans to be from 40 to 80% for selenite and 75 to 97% for selenomethionine (Bopp et al., 1982). Age, Sex, Reproductive Status, and Interindividual Variability of Response: No information is available regarding the effect of human age, sex, reproductive status, or interindividual variability of response. Pretoxic Indicator: The use of increased glutathione peroxidase activity as an indicator of exposure is apparently of no value (Valentine et al., 1988). No biomarkers have been identified. Long-term Effects: The long-term effects are uncertain. Pathological nail changes, loss of hair, dermatitis, icterus, mottled teeth, and caries are some of the more obvious
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Seafood Safety ones. In a few instances, neurological upsets have been reported in adults. The target organ for chronic exposure in animals is the liver. This has not been documented in humans. Kinetics: Initially, selenium is distributed to most organs, but the percentage of distribution may depend on the chemical form. Selenium in humans appears to bind to plasma lipoproteins, cross the placenta, and enter milk. Transient accumulation occurs in blood, muscle, liver, and kidney, with greater retention in the brain, thymus, and reproductive organs. Excretion in humans is primarily by urine and exhalation. ADI: The ADI is uncertain. Yang et al. (1983) estimate 0.022 mg of organic selenium daily as a NOAEL for adult humans; the National Research Council (NRC, 1980b) gives the estimated safe and adequate daily dietary intake (ESADDI) for infants as 0.01-0.06 mg, for children 0.02-0.2 mg., and for adults 0.05-0.2 mg. Toxic Body Burden: No information is available. Steady Daily Intake for Toxicity: It has been estimated that 1 mg of selenium daily, as the selenite, would be toxic (Yang et al., 1983). Conclusions Thresholds of toxicity calculated for acute or short-term exposures, especially for mercury, may not reflect a threshold for chronic or long-term exposures. Recent assessment models have, therefore, included coefficients of cumulative toxicity (Inskip and Piotrowski, 1985; PTI, 1987). Such models, however, would be strengthened if data regarding chronic and cumulative toxicity could be generated. Models would be further strengthened by information regarding interindividual variability of response as a function of blood level. The existing dose-response data base with respect to human risk from seafoods contaminated with the trace metals arsenic, cadmium, lead, mercury, and selenium lacks sufficient information regarding the effects of chronic exposures, the sensitivity of certain subpopulations, and interindividual variability to make such an assessment. In the case of arsenic, although no sound human data exist, the primary form found in seafood is organic and appears to be of very low toxicity to animals. Therefore, identification of this trace metal as a potential hazard to humans may be premature. REFERENCES Airey, D. 1983. Total mercury concentrations in human hair from 13 countries in relation to fish consumptions and locations. Sci. Total Environ. 31:157-180. Al-Shahristani, H., and K.M. Shihab. 1974. Variation of biological half-life of methylmercury in man. Arch. Environ. Health 28:342-344. Amin-Zaki, L., M.A. Majeed, S.B. Elhassani, T.W. Clarkson, M.R. Greenwood, and R.A. Doherty. 1979. Prenatal methylmercury poisoning. Clinical observations over five years. Am. J. Dis. Child. 133:172-177. Anonymous. 1988a. Health and environmental effects profile for antimony oxides. NTIS/PB88-175039. Government Reports Announcements and Index, Issue 12. 129 pp. Anonymous. 1988b. Health effects assessment for antimony and compounds. NTIS/PB88-179445. Government Reports Announcements and Index, Issue 13. 46 pp. ATSDR (Agency for Toxic Substances and Disease Registry). 1989a. Toxicological Profile for Arsenic. ATSDR/TP-88/02. Prepared by Life Systems, Inc. for ATSDR, U.S. Public Health Service in
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Seafood Safety collaboration with U.S. Environmental Protection Agency. 125 pp. ATSDR (Agency for Toxic Substances and Disease Registry). 1989b. Toxicological Profile for Cadmium. ATSDR/TP-88/08. Prepared by Life Systems, Inc. for ATSDR, U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency. 107 pp. Beliles, R.P. 1978. The lesser metals. Pp. 547-616 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 2. Marcel Dekker, New York. Bertazzi, P.A., L. Riboldi, A. Pesatori, L. Radice, and C. Zocchetti. 1987. Cancer mortality of capacitor manufacturing workers. Am. J. Indust. Med. 11:165-176. Bevill, R.F., and W.G. Huber. 1977. Sulfonamides. Pp. 894-911 in L. Jones, N. Booth, and L. McDonald, eds. Veterinary Pharmacology and Therapeutics, 4th ed. Iowa State University Press, Ames. Booth, N.H. 1977. Drug and chemical residues in the edible tissues of animals. Pp. 1299-1342 in L. Jones, N. Booth, and L. McDonald, eds. Veterinary Pharmacology and Therapeutics, 4th ed. Iowa State University Press, Ames. Bopp, B.A., R.C. Sonders, and J.W. Kesterson. 1982. Metabolic fate of selected selenium compounds in laboratory animals and man. Drug Metab. Rev. 13:271-318. Brown, D. P. 1987. Mortality of workers exposed to polychlorinated biphenyls: An update. Arch. Environ. Health 42:333-339. Buck, W.B. 1978. Toxicity of inorganic and aliphatic organic arsenicals. Pp. 357-374 in F.W. Oehme, ed. Toxicity of the Heavy Metals in the Environment. Marcel Dekker, New York. Camber, C.I., M.H. Vance, and J. Alexander. 1956. How to use sodium bisulfite to control "blackspot" on shrimp. Univ. Miami Special Bull. No. 12, 4 pp. Cappon, C.J., and J.C. Smith. 1981. Mercury and selenium content and chemical form in fish muscle. Arch. Environ. Contam. Toxicol. 10:305-319. Cappuzo, J., A. McElroy, and G. Wallace. 1987. Fish and shellfish contamination in New England waters: An evaluation and review of available data on the distribution of chemical contaminants. Report submitted to Coast Alliance, Washington, D.C. 85 pp. CEC (Commission of the European Communities). 1978. Pp. 1-198 in Criteria (Dose/ Effect Relationships) for Cadmium. Pergamon Press. Oxford, England. Clark, J.R., D. Devault, R.J. Bowden, and J.A. Weishaar. 1984. Contaminant analysis of fillets from Great Lakes coho salmon, 1980 . J. Great Lakes Res. 10:38-47. Cordle, F., R. Locke, and J. Springer. 1982. Risk assessment in a federal regulatory agency: An assessment of risk associated with the human consumption of some species of fish contaminated with polychlorinated biphenyls (PCBs). Environ. Health Perspect. 45: 171-182. Duling, L. 1988. Fish contaminant monitoring program 1988 annual report. Report MI/DNR/SWQ-88/090. Michigan Department of Natural Resources, Surface Water Quality Division, Lansing. 300 pp. Earl, F.L., and T.J. Vish. 1978. Teratogenicity of heavy metals. Pp. 617-640 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 2. Marcel Dekker, New York. Ellis, K.J., D. Vartsky, I. Zanzi, S.H. Cohn, and S. Yasumura. 1979. Cadmium: In vivo measurement in smokers and nonsmokers. Science 205:323-324. EPA (Environmental Protection Agency). 1979. Ambient Water Quality Criteria for Lead. Water Planning and Standards. EPA 440/5-80-057. U.S. Environmental Protection Agency, Washington, D.C. 161 pp. EPA (Environmental Protection Agency). 1986. Pesticides Fact Sheet No. 109: Chlordane. EPA 540/FS 87/143. U.S. Environmental Protection Agency, Washington, D.C. 9 pp. EPA (Environmental Protection Agency). 1987. The National Dioxin Study: Tiers 3,5,6, and 7. EPA 440/4-87-003. Office of Water Regulations and Standards, Monitoring and Data Support Division, U.S. Environmental Protection Agency, Washington, D.C. 208 pp. EPA (Environmental Protection Agency). 1988a. Assessment of Dioxin Contamination of Water, Sediment and Fish in the Pigeon River System (a Synoptic Study) Report No. 001. U.S. Environmental Protection Agency, Region IV, Water Management Division, Atlanta, Georgia. 75 pp. EPA (Environmental Protection Agency). 1988b. Dioxin Levels in Fish Near Pulp and Paper Mills. Interim report dated October 25. U.S. Environmental Protection Agency, Office of Water Regulations and Standards, Washington, D.C. EPA (Environmental Protection Agency) 1988c. Integrated Risk Information System (IRIS). As, Cd, Pb, Hg and Se. DIALCOM, Inc., Washington, D.C.
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Seafood Safety Ewan, R.C. 1978. Toxicology and adverse effects of mineral imbalance with emphasis on selenium and other minerals. Pp. 445-490 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 2. Marcel Dekker, New York. Fan, A.M., S.A. Book, R.R. Neutra, and D.M. Epstein. 1988. Selenium and human health implications in California's San Joaquin Valley. J. Toxicol. Environ. Health 23:539-560. Fauvel, Y., G. Pons, and J.P. Legeron 1982. Ozonation de l'eau de mer et épuration des coquillages. Science et Peche, Nantes 320:1-16. FDA (Food and Drug Administration). 1982. Levels for Poisonous or Deleterious Substances in Human Food and Animals Feed. U.S. Food and Drug Administration, Washington, D.C. 13 pp. FDA (Food and Drug Administration). 1988. Compliance Program Guidance Manual. FY86 Pesticides and Industrial Chemicals in Domestic Food. Program No. 7304-004. U.S. Department of Health and Human Services, Public Health Service, U.S. Food and Drug Administration, Bureau of Foods, Washington, D.C. 48 pp. Fein, G.G., J.L. Jacobson, S.W. Jacobson, P.M. Schwartz, and J.K. Dowler. 1984. Prenatal exposure to polychlorinated biphenyls: Effects on birth size and gestational age. J. Pediatrics 105:315-320. Fishbein, L. 1983. Environmental selenium and its significance. Fundam. Appl. Toxicol. 3:411-419. Fowler, B.A. 1983. Pp. 1-281 in Biological and Environmental Effects of Arsenic, Vol. 6. Elsevier Science Publishers, Amsterdam, The Netherlands. Fox, A. 1990. Fishery chemicals used in foreign countries. Intracenter memorandum, January 16. National Fisheries Research Center, Seattle, Wash. Friberg, L., M. Piscator, G.F. Nordberg, and T. Kjellström. 1974. Cadmium in the Environment, 2nd ed. CRC Press, Cleveland, Ohio. Vol. I, 209 pp; Vol. II, 248 pp. Friberg, L., C.-G. Elinder, T. Kjellström, and G.F. Nordberg. 1985. Cadmium and Health. A Toxicological and Epidemiological Appraisal. CRC Press, Boca Raton, Fla. 307 pp. Fukayama, M.Y., H. Tan, W.B. Wheeler, and C.I. Wei. 1986. Reactions of aqueous chlorine and chlorine dioxide with model food compounds. Environ. Health Perspect. 69:267-274. Fukushima, M. A. Ishizaki, K. Nogawa, M. Sakamoto, and E. Kobayashi. 1974. Epidemiological studies on renal failure of inhabitants in "itai-itai" disease endemic district (Part 1). Some urinary findings of inhabitants living in and around the endemic district of the Jinzu River basin. Jap. J. Pub. Health 21:65-73. Gadbois, D.F., and R.S. Maney. 1983. Survey of polychlorinated biphenyls in selected finfish species from United States coastal waters. Fish. Bull. (USFWS) 81:389-396. Gladen, B. C., W.J. Rogan, P. Hardy, J. Thullen, J. Tinglestad, and M. Tully. 1988. Development after exposure to polychlorinated biphenyls and dichlorodiphenyldichloroethene transplacentally and through human milk. J. Pediatr. 113:991-995. Gossett, R.W., H.W. Puffer, R.H. Arthur, Jr., J. Alfafara, and D.R. Young. 1982. Pp. 29-37 in W. Bascon, ed. Levels of Trace Organic Compounds in Sportfish from Southern California. Coastal Water Research Project Biennial Report. Southern California Coastal Water Research Project 1981-1982, Long Beach, Calif. Gossett, R.W., H.W. Puffer, R.H. Arthur Jr., and D.R. Young. 1983. DDT, PCB and Benzo(a)pyrene levels in white croaker (Genyonemus lineatus ) from southern California. Mar. Poll. Bull. 14:60-65. Goyer, R.A. 1986. Toxic effects of metals. Pp. 582-635 in C. Klassen, M. Amdur, and J. Doull, eds. Casarett and Doull's Toxicology, 3rd ed. Macmillan, New York. Green, V.A., G.W. Wise, and J.C. Callenbach. 1978. Lead poisoning. Pp. 123-141 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 1. Marcel Dekker, New York. Greenwood, M.R., T. W. Clarkson, R. A. Doherty, A. H. Gates, L. Amin-Zaki, S. Elhassani, and M. A. Majeed. 1978. Blood clearance half-times in lactating and non-lactating members of a population exposed to methylmercury. Environ. Res. 16:48-54. Griffin, A.C. 1979. Role of selenium in the chemoprevention of cancer. Adv. Cancer Res. 29:419-422. Groth, D.H., L.E. Stettler, J.R. Burg, W.M. Busey, G.C. Grant, and L. Wong. 1986. Carcinogenic effects of antimony trioxide and antimony ore concentrate in rats. J. Toxicol. Environ. Health 18:607-626. Guarino, A.M., S.M. Plakas, R.W. Dickey, and M. Zeeman. 1988. Principles of drug absorption and recent studies of bioavailability in aquatic species. Vet. Human Toxicol. 30:41-44. Gunderson, E. L. 1988. FDA Total Diet Study, April 1982-April 1984, Dietary intakes of pesticides,
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Seafood Safety selected elements and other chemicals. J. Assoc. Off. Anal. Chem. 71:1200-1209. Haines, A.T., and E. Nieboer. 1988. Chromium hypersensitivity. Pp. 497-532 in J. Nrigau and E. Nieboer eds. Chromium in the Natural and Human Environment. John Wiley & Sons, New York. Hall, R.A., E.G. Zook, and G.M. Meaburn. 1978. National Marine Fisheries Service Survey of Trace Elements in the Fishery Resource. NOAA Technical Report NMFS SSRF-721, National Technical Information Service No. PB 283 851, March. 313 pp. Hammond, P.B. 1978. Metabolism and metabolic action of lead and other heavy metals. Pp. 87-99 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 1. Marcel Dekker, New York. Hansen, J.C., H.C. Wulf, N. Kromann, and K. Alboge. 1985. Cadmium concentrations in blood samples from the East Greenlandic population. Dan. Med. Bull. 32:277-279. Harada, M. 1978. Methyl mercury poisoning due to environmental contamination (Minamata disease). Pp. 261-302 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 1. Marcel Dekker, New York. Harr, J.R. 1978. Biological effects of selenium. Pp. 393-426 in F.W. Oehme, ed. Toxicity of Heavy Metals in the Environment, Part 2. Marcel Dekker, New York. Harr, J.R., and O.H. Muth. 1972. Selenium poisoning in domestic animals and its relationship to man. Clin. Toxicol. 5:175-186. Hattis, D. 1972. The FDA and nitrite—A case study of violations of the Food, Drug, and Cosmetic Act with respect to a particular food additive. Presented in hearings before the Select Committee on Nutrition and Food Needs of the United States Senate, September 21, pp. 1692-1720. Hattis, D. 1987. A pharmacokinetic mechanism-based analysis of the carcinogenic risk of ethylene oxide. National Technical Information Service, No. NTIS/PB88-188784. MIT Center for Technology, Policy and Industrial Development, No CTPIC 87-1 , August. 176 pp. Hattis, D. 1989. Letter report from Dr. Dale Hattis, MIT, to W. Munns, Environmental Research Laboratory, Narragansett, R.I., December 28. 4 pp. Hawke, J.P., S.M. Plakas, R. Vernon Minton, R.M. McPhearson, T.G. Snider, and A.M. Guarino. 1987. Fish pasteurellosis of cultured striped bass (Morone saxatilis) in coastal Alabama. Aquaculture 65:193-204. Hogberg, J., and J. Alexander. 1986. Selenium. Pp. 482-520 in L. Friberg, J. Parizek, and V. Vouk, ed. Handbook on the Toxicology of Metals, 2d end. Elsevier Science Publishers, Amsterdam, The Netherlands. Huber, G. 1977a. Penicillins. Pp. 912-928 in L.M. Jones, N.H Booth, and L.E. McDonald, eds. Veterinary Pharmacology and Therapeutics, 4th ed. Iowa State University Press, Ames. Huber, G. 1977b. Tetracyclines. Pp. 929-939 in L.M. Jones, N.H. Booth, and L.E. McDonald, eds. Veterinary Pharmacology and Therapeutics, 4th ed. Iowa State University Press, Ames. Huber, G. 1977c. Streptomycin, chloramphenicol and other antibiotic agents. Pp. 940-971 in L.M. Jones, N.H. Booth, and L.E. McDonald, eds. Veterinary Pharmacology and Therapeutics, 4th ed. Iowa State University Press, Ames. Inskip, M.J., and J.K. Piotrowski. 1985. Review of the health effects of methylmercury. J. Appl. Toxicol. 5:113-133. Jacobson, J.L., H.E. Humphrey, S.W. Jacobson, S.L. Schantz, M.D. Mullin, and R. Welch. 1989. Determinants of polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), and dichlorodiphenyl trichloroethane (DDT) levels in the sera of young children. Am. J. Publ. Health 79:1401-1404. Jacobson, J.L., S.W. Jacobson, and H.E. Humphrey. 1990. Effects of in utero exposure to polychlorinated biphenyls and related contaminants on cognitive functioning in young children. J. Pediatr. 116:38-45. Jacobson, S.W., G.G. Fein, J.L. Jacobson, P.M. Schwartz, and J.K. Dowler. 1985. The effect of intrauterine PCB exposure on visual recognition memory. Child Develop. 56:853-860. Kansas DHE (Department of Health and Environment). 1988. A Survey of Pesticides in Tuttle Creek Lakes, Its Tributaries and the Upper Kansas River. Water Quality Assessment Section, Bureau of Water Protection, Kansas Department of Health and Environment, Topeka, Kansas. 29 pp. Kjellström, T., and G.F. Nordberg. 1985. Kinetic model of cadmium metabolism. Pp. 179-197 in L. Friberg, C.G. Elinder, T. Kjellström, and G.F. Nordberg, eds. Cadmium and Health: A Toxicological and Epidemiological Appraisal, Vol. 1 Exposure, Dose and Metabolism. CRC Press, Boca Raton, Fla.
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Representative terms from entire chapter: