4
Health Risks Associated with Seafood Consumption

This chapter reviews the potential risks associated with chronic exposure to particular seafoodborne contaminants and risks associated with certain more acute seafoodborne hazards. The discussion includes consideration of the extent to which seafood consumption might increase consumers’ risk of adverse health impacts due to exposure to toxicants, depending upon the critical dose-response relationships for the contaminant, the distribution of contaminant body burden in the population, and the extent to which the body burden is due to seafood consumption rather than to other sources and pathways of exposure. The chapter concludes with a discussion of the interaction between nutrients and contaminants—in particular, selenium and methylmercury—in seafood, and measures that consumers can take to reduce exposure to contaminants that may be present in seafood.

ENVIRONMENTAL CHEMICALS

Consumers seeking the health benefits associated with the consumption of seafood are concerned about potential health risks associated with the presence of chemical contaminants, both those occurring naturally and those resulting from human activities, in seafood. These contaminants include inorganic compounds such as methylmercury and other metals, as well as persistent organic pollutants (POPs) such as dioxins and polychlorinated biphenyls (PCBs). Of these, methylmercury is the contaminant that has elicited the most concern among consumers.



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks 4 Health Risks Associated with Seafood Consumption This chapter reviews the potential risks associated with chronic exposure to particular seafoodborne contaminants and risks associated with certain more acute seafoodborne hazards. The discussion includes consideration of the extent to which seafood consumption might increase consumers’ risk of adverse health impacts due to exposure to toxicants, depending upon the critical dose-response relationships for the contaminant, the distribution of contaminant body burden in the population, and the extent to which the body burden is due to seafood consumption rather than to other sources and pathways of exposure. The chapter concludes with a discussion of the interaction between nutrients and contaminants—in particular, selenium and methylmercury—in seafood, and measures that consumers can take to reduce exposure to contaminants that may be present in seafood. ENVIRONMENTAL CHEMICALS Consumers seeking the health benefits associated with the consumption of seafood are concerned about potential health risks associated with the presence of chemical contaminants, both those occurring naturally and those resulting from human activities, in seafood. These contaminants include inorganic compounds such as methylmercury and other metals, as well as persistent organic pollutants (POPs) such as dioxins and polychlorinated biphenyls (PCBs). Of these, methylmercury is the contaminant that has elicited the most concern among consumers.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Methylmercury Mercury is a heavy metal that is present in the environment as a result of both human activities (referred to as anthropogenic sources) and natural processes. The primary anthropogenic source is the combustion of fossil carbon fuels, particulary from coal-fired utility boilers; other sources include municipal, medical, and hazardous waste incineration (NRC, 2000). The natural sources include volcanic emissions and the weathering of rock containing mercury ore. Mercury can be deposited locally or travel long distances in the atmosphere and contaminate sites far from its point of release. Further, the complex biogeochemistry of mercury fate and transport creates uncertainty in efforts to apportion the relative contributions of these processes to global mercury pollution. The US Environmental Protection Agency (US EPA) estimated that 50 to 75 percent of the total yearly input of mercury into the environment is anthropogenic (US EPA, 1997), while the United Nations Environment Programme (UNEP) suggests that this source accounts for more than half of the inputs (UNEP, 2002). Mercury exists in the environment in several different forms, including metallic, inorganic, and organic, and interconversion between forms can occur. The form of mercury of greatest concern with regard to seafood consumption is methylmercury (MeHg). Methylmercury results when mercury in other forms is deposited in water bodies and biotransformed through the process of methylation by microorganisms. It bioaccumulates up the aquatic trophic food chain as smaller organisms are consumed by larger organisms. Because methylmercury is persistent, this bioaccumulation process results in large long-lived predatory species, such as certain sharks, swordfish, and tuna, or freshwater species such as bass, walleye, and pickerel having the highest concentrations (Kraepiel et al., 2003). Methylmercury levels can also be high in marine mammals such as whales, and in animals that feed on marine life, such as polar bears and sea birds. Consumption of aquatic life is the major route of human exposure to methylmercury. The seafood choices a consumer makes, and the frequency with which different species are consumed, are thus important determinants of methylmercury intake. Because of the global dispersion of methylmercury and migration of species, the extent of regional variation in body burdens among different aquatic animals is less striking than the regional variations in certain other water contaminants, such as PCBs or dioxin-like compounds (DLCs). This implies that the location in which an aquatic animal was caught might provide relatively little information about its methylmercury content. Methylmercury is not lipophilic (lipid soluble) and is thus present in the largest concentrations in the muscle tissue of aquatic animals rather than in fat or oils. Approximately 95 percent of ingested methylmercury is absorbed across the gastrointestinal tract into the blood. The half-life

OCR for page 121
Seafood Choices: Balancing Benefits and Risks of methylmercury in blood in humans is estimated to be 50 days, and the whole-body half-life to be 70–80 days, although the residence time of mercury in the brain appears to be considerably longer (NRC, 2000). Hair is frequently used as an exposure biomarker for methylmercury. Hair is a route of methylmercury excretion, and approximately 80 to 90 percent of the total mercury found in hair is in the methylated form. Hair mercury is a good biomarker in fish-consuming populations. Autopsy studies suggest that maternal hair mercury level correlates reasonably well with the level of mercury in the fetal brain (Cernichiari et al., 1995). Mercury Burdens in the US Population The first nationally representative estimates of blood and hair mercury levels were provided by the National Health and Nutrition Examination Survey (NHANES) of 1999–2000. Among women 16–49 years old, the geometric mean hair mercury level was 0.2 parts per million (ppm), with 75th, 90th, and 95th percentiles of 0.42, 1.11, and 1.73 ppm, respectively (McDowell et al., 2004). The geometric mean blood mercury level was 1.02, with 75th, 90th, and 95th percentiles of 2.07, 4.84, and 7.13 ppm, respectively (Mahaffey et al., 2004). The prevalence of levels in excess of 5.8 µg/L (benchmark dose lower bound [BMDL] adjusted for uncertainty and for population variability) was 5.66 percent. Levels were 50 percent higher among older women (30–49 years) compared to younger women, and levels were highest among women who self-identified as “Other” racial/ethnic category (Asians, Native Americans, Pacific Islanders). Mercury burdens were strongly associated with the amount of self-reported fish consumption (Mahaffey et al., 2004). Among women reporting eating 5–8 fish meals per month, these figures were 2.56, 4.54, 8.80, and 11.60 ppm, respectively. Levels were seven times greater among women who reported eating nine or more fish meals in the previous 30 days, compared to women who reported no consumption. Among these relatively high fish-consumers, the 50th, 75th, 90th, and 95th percentiles for blood mercury were 3.02, 6.68, 12.00, and 13.40 ppm, respectively. Data on blood and hair mercury levels in adult men in the United States were not collected as part of NHANES until 2003, and no data for this group has been reported. Therefore, estimates must be made based on mercury biomarker data reported as part of large cohort studies. Urine and blood mercury levels of 1127 Vietnam-era pilots were measured for a study of the health effects of exposure to dental amalgam (Kingman et al., 1998). The mean blood mercury level in this group of men was 3.1 ppm, with a range up to 44 ppm, but the contribution of fish consumption to blood mercury levels is unknown because data were not collected on fish intake.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks An important limitation of NHANES as a source of data on population exposures to methylmercury is that the sampling plan used to identify the 3637 women who contributed data in the 1999–2002 survey is likely to have missed subgroups of high fish-consumers, including sport fishers and subsistence fishers. Examples of such groups include individuals living in areas that provide ready access to seafood (e.g., island populations) (Ortiz-Roque and Lopez-Rivera, 2004), fishers (Burge and Evans, 1994; Bellanger et al., 2000), groups for whom fish or marine mammals are an especially important component of overall diet, and individuals who consume a high-fish diet for its cardioprotective effects. For example, one report described a case series of 116 patients who consumed large quantities of fish and had their blood tested; almost all (89 percent) had blood mercury levels greater than 5 µg/L, ranging up to 89 µg/L (Hightower and Moore, 2003). Evidence from the Third National Report on Human Exposure to Environmental Chemicals (CDC, 2005b) suggests that population exposures to mercury might have decreased between 1999–2000 and 2001–2002. Among women 16–49 years of age, the geometric mean declined from 1.02 µg/L (95% CI 0.825-1.270) to 0.833 (95% CI 0.738-0.940). An even greater decline was evident at the high end of the distribution, as the level corresponding to the 95th percentile in the earlier survey was 7.10 (95% CI 5.30-11.30) compared to 4.6 (95% CI 3.7-5.9) in the later survey. Because of the short time period covered by these data, however, the possibility that the observed time trend reflects sampling variability cannot be rejected. Health Effects in Critical Target Organs Organs of the central nervous and cardiovascular systems are considered to be the critical target organs with regard to methylmercury. Neurological Toxicity The tragic epidemic of frank neurological disease that was identified in the late 1950s in Minamata, Japan, first brought to the world’s attention the devastating effects of methylmercury on the developing fetal brain. Children exposed in utero to high levels of MeHg presented with cerebral palsy, mental retardation, movement and coordination disorders, dysarthria, and sensory impairments.The neuropathological lesions associated with Congenital Minamata Disease (mercury poisoning) were diffuse, occurring throughout the brain. In individuals exposed only in adulthood, the lesions were highly focal, clustering in regions that matched clinical presentation (e.g., motor disorders = precentral gyrus and cerebellum, constriction of visual fields = calcarine fissure of occipital cortex). The major molecular mechanisms of MeHg neurotoxicity include inhibition of protein and macromolecular synthesis, mitochondrial dysfunction, defective calcium and ion flux, disruption of neurotransmitter homeostasis, initiation

OCR for page 121
Seafood Choices: Balancing Benefits and Risks of oxidative stress injury, microtubule disaggregation, and post-translational phosphorylation (Verity, 1997). The diffuse injury associated with prenatal exposure is attributable to the ability of MeHg to arrest mitotic cells in metaphase, disrupting the exquisitely choreographed processes of cell proliferation, differentiation, and migration. The result is a brain in which there are reduced cortical cell densities, islands of heterotopic neurons in cerebral and cerebellar white matter, anomalous cytoarchitecture, disturbance in laminar pattern of cerebral cortex, absence of granule and Purkinje cells in the cerebellum, incomplete myelination in the hypoplastic corpus callosum, glial proliferation (“bizarre astrocytes in the white matter”), and limited gyral differentiation (Choi, 1989). No cases of Congenital Minamata Disease have been reported in the United States, where the primary concern has been whether chronic exposure to MeHg, as the result of seafood consumption among the general population, is associated with subtle adverse health outcomes. Therefore, several risk assessments have been conducted in the past decade in which the goal was to identify a fetal mercury burden that can be interpreted as being without appreciable risk. The basis for most risk assessments for MeHg exposure has been one or more of the three major epidemiologic studies available: the New Zealand study (Kjellstrom et al., 1986), the Faroe Islands study (Grandjean et al., 2001), and the Seychelles study (Myers et al., 2003) (see Box 4-1). The New Zealand and Faroe Islands studies, but not the Seychelles study, have generally been regarded as providing evidence of harm from MeHg exposures at which clinical effects are not evident, although it should be noted that benchmark dose analyses of the data from the 9-year evaluation of children in the Seychelles study cohort produced BMDLs in the range of 17–23 ppm (Van Wijngaarden et al., 2006), only slightly higher than the BMDLs based on the New Zealand and Faroe Islands studies data. In view of the perceived discrepancies in the findings of the three studies, the choice of critical study has stimulated considerable controversy. Some risk assessors chose the Faroe Islands study (US EPA, 2001; NRC, 2000), while others chose the Seychelles study (ATSDR, 1999). In an effort to use all of the best available data, the Joint Expert Committee on Food Additives and Contaminants (JECFA), a joint committee of the World Health Organization (WHO) and the Food and Agricultural Organization of the United Nations (FAO), averaged the effect estimates reported for the Faroes and Seychelles studies; including the New Zealand study did not significantly change the results (FAO/WHO JECFA, 2003). In all these assessments, however, the final result was a single number interpreted as a reference level for intake for the most sensitive subgroup, the fetus, as shown in Table 4-1. These reference levels differ largely because of differences in the uncertainty factors applied. These levels were derived on the basis of health effects observed, rather than

OCR for page 121
Seafood Choices: Balancing Benefits and Risks BOX 4-1 Three Major Epidemiological Studies on Methylmercury These three studies were conducted among geographically disparate island populations with a high availability of seafood (tuna is an important export product of Seychelles, approximately one-third of the Faroese workforce is employed in the fishing industry, and both aquaculture and marine fishing feature in the economy of New Zealand). Cohen (2004) summarized these three cohorts in reviews. Seychelles Child Development Study The Seychelles Child Development Study (SCDS) is an ongoing collaboration between the Ministry of Health of Seychelles, a small archipelago country in the Indian Ocean, and the University of Rochester, New York. “Initially the objectives focused on two primary questions. Firstly, could clinical neuro-development effects be found in children after exposure to methylmercury (MeHg) in utero from a maternal diet high in fish and, secondly, what is the lowest level of foetal [sic] exposure to cause such effects?” (Shamlaye, 2004). Seychelles was determined to be a favorable location for this study for a number of reasons: the Seychellois regularly consume fish (an average of 12 meals per week), and the number of annual births allowed for recruitment of a large cohort of mothers and children in a short period of time (Shamlaye, 2004; Myers et al., 2003). The Seychelles Child Development Study enrolled 779 mother-infant pairs between 1989 and 1990, of which 717 were eligible for analysis. Among the tests administered at 107 months were the Wechsler Intelligence Scale for Children—Third Edition, the Boston Naming Test, the California Verbal Learning Test, the Bruininks-Oseretsky Test of Motor Proficiency, a Continuous Performance Test, the Developmental Test of Visual-Motor Integration, the Grooved Pegboard, and selected subtests of the Woodcock-Johnson Tests of Achievement. The children were evaluated (i.e., cognitive, language, motor, adaptive behavior, and social-emotional development) at 6, 19, 29, 66, and 107 months. Maternal hair samples were also collected at enrollment. The information provided here, along with the results from the study, can be accessed in the Special Issue of the Seychelles Medical and Dental Journal, Volume 7, Issue 1, 2004. [Online]. Available: http://www.seychelles.net/smdj/ [accessed July 7, 2005]. Also, in 2000, Clarkson et al. recruited a new cohort of mother-infant pairs in Seychelles, and this project is due for completion in 2006. Faroe Islands Study The Faroe Islands Study, conducted in this North Atlantic Ocean archipelago located between Scotland, Norway, and Iceland, consisted of a cohort of

OCR for page 121
Seafood Choices: Balancing Benefits and Risks 1022 consecutive singleton births from 1986–1987. The objective of this study was to investigate possible neurobehavioral effects of prenatal exposure to neurotoxicants, such as methylmercury. The Faroese are high consumers of seafood, including pilot whale, which exposes them to high levels of methylmercury. The study team analyzed maternal hair mercury concentrations and cord blood mercury concentrations at birth and conducted neurobehavioral examinations on 917 of the children just before school entry (about 7 years of age) and at 14 years of age. The detailed examinations, which lasted about 5 hours for each child, took place mostly in the National Hospital in Torshavn, the capital of the Faroes Island. The examination included finger tapping; hand-eye coordination; reaction time on a continuous performance test; Wechsler Intelligence Scale for Children—Revised Digit Span, Similarities, and Block Design; Bender Visual Motor Gestalt Test; Boston Naming Test; and California Verbal Learning Test. The parent accompanying the child (usually the mother) was also asked to fill out a self-administered questionnaire on the child’s past medical history, current health status, and social factors (Grandjean, 1997). New Zealand Study The New Zealand Study involved the screening of 11,000 children born in 1978, over 900 of whose mothers consumed fish more than four times per week during pregnancy. As with the other cohorts, the objective of this study was to investigate the association between prenatal mercury exposure and subsequent development during childhood (Crump, 1998). Maternal hair samples were collected at birth to assess mercury exposure during pregnancy. At 4 years of age, the Denver Developmental Screening Test and a set of neurological screening tests were completed on 74 children, 38 with “high” maternal hair mercury levels (> 6µg/g) and 36 with “low” maternal hair mercury levels, matched on maternal demographic characteristics, age, hospital where the birth took place, and date of birth. Maternal interviews about the ages at which the child achieved developmental milestones were also conducted (Kjellstrom et al., 1986). At 6 years of age, 238 children were evaluated. A child with a high maternal hair mercury was matched with three children with low hair mercury levels, but similar in gender, maternal ethnic group, age, smoking habits, location of residence, and number of years living in New Zealand (Kjellstrom et al., 1989). The tests administered included the Test of Oral Language Development, the Weschlar Intelligence Scale for Children-Revised, and the McCarthy Scales of Children’s Abilities.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks TABLE 4-1 Reference Levels for Fetal Exposure to Methylmercury Source Reference Level JECFA provisional tolerable weekly intake 1.6 µg/kg body weight/week US EPA reference dose 0.1 µg/kg body weight/day Agency for Toxic Substances and Disease Registry minimal risk level 0.3 µg/kg body weight/day SOURCES: FAO/WHO JECFA, 2003; US EPA, 2001; ATSDR, 1999. the general population, and are risk management guidelines rather than estimates of threshold of effect. While such numbers can be used to estimate the number of individuals at potential risk (i.e., for whom the margin of exposure is less than 10-fold), they convey nothing about the quantitative characteristics of the dose-response relationship, i.e., for the risk associated with each unit increase in mercury burden above the reference level. A variety of hypotheses have been proposed to explain the apparent discrepancy between the results of the Seychelles and Faroe Islands studies. The National Research Council (NRC) committee did not consider that any of them is clearly supported by the evidence, however. The issues evaluated include differences between populations in the temporal characteristics of exposure (presumed to be stable among the Seychellois, but potentially episodic among the Faroese due to occasional consumption of pilot whale), reliance on different biomarkers of exposure (cord blood mercury vs. maternal hair mercury), population differences in vulnerability to methylmercury, the influence of other aspects of nutrition on methylmercury toxicity, and differences in the neuropsychological tests administered and the ages at which children were assessed. Consideration has also been given to the possibility of residual confounding in one or both studies, particularly with regard to the high exposures of the Faroese to PCBs and other POPs. Although considerable debate has ensued seeking to identify the reasons for the apparent discrepancies among the three major studies of fetal MeHg neurotoxicity, their magnitude might be less dramatic than commonly supposed. As the analyses of the National Research Council Committee on the Toxicological Effects of Methylmercury showed, the BMDLs calculated for the three major studies vary by much less than the 10-fold (one order of magnitude) uncertainty factor applied to the BMDL to achieve the Reference Dose (RfD) (NRC, 2000). Figure 4-1 shows a qualitative effort to assess the degree of concordance among studies of the “no observed adverse effect levels” (NOAEL) estimated for each study on the basis of benchmark dose analysis. An estimate of 10 to 20 ppm appears to be reasonably accurate. Interestingly, this is the range identified by WHO (1990) based solely on the relatively poor-quality data available from a mass poisoning episode

OCR for page 121
Seafood Choices: Balancing Benefits and Risks FIGURE 4-1 Integration of data from the New Zealand, Faroe Islands, and Seychelles studies of prenatal methylmercury neurotoxicity. Two ranges are provided for the NOAEL from the New Zealand study. The estimate labeled (1) was derived when the data for a child with a very high maternal hair mercury level (86 ppm) were included in the analyses. The estimate labeled 2 was derived when the data for this child were excluded. This child’s mercury level was more than fourfold higher than the level for any of the 236 other children in this cohort. NOTE: NOAEL = No observed adverse effect level. SOURCE: Personal communication, Clarkson et al., University of Rochester, March 2005. that occurred in Iraq in the 1970s (Personal communication, Clarkson and colleagues, University of Rochester, March 2005). Ryan (2005) conducted an analysis of data from the three previously described studies using maximum likelihood and Bayesian hierarchical models to derive an estimate of the slope of the dose-response relationship between children’s neurodevelopment and their prenatal methylmercury exposure. This analysis, presented to the Committee on Nutrient Relationships in Seafood (Ryan, 2005), suggested that children’s IQ scores decline by 0.1 to 0.25 points for each ppm increase in maternal hair mercury level. The point estimates were nearly identical in the three studies (results for the New Zealand study differed considerably depending on whether one particular observation was included or excluded) (see Figure 4-2). The point estimates of the slopes for the other neurodevelopmental endpoints measured in the three studies, some of which were common across studies, were also surprisingly similar (Figure 4-3).

OCR for page 121
Seafood Choices: Balancing Benefits and Risks FIGURE 4-2 Point estimates and 95 percent confidence intervals, based on regression analyses, for the changes in full scale IQ (“coefficients”) associated with each ppm increase in maternal hair mercury reported in the three studies. A coefficient with a negative sign indicates that the IQ scores for children within a study cohort decreased with increasing hair mercury level. Two estimates are provided for the New Zealand study, one based on the inclusion of the child with a maternal hair mercury level of 86 ppm and one based on the exclusion of this child. SOURCE: Ryan, 2005. These analyses, therefore, suggest that although the findings of the Seychelles study appear discrepant from those of the Faroe Islands and New Zealand studies if one focuses only on the p-values of the reported analyses, at a deeper, quantitative level that focuses on the rates of decline in scores as mercury burden increases, the findings of the three studies are remarkably concordant. Part of the challenge in characterizing the health risks associated with increased MeHg exposure in seafood is related to the fact that this source also provides nutrients that might have health effects which mitigate those of MeHg. Thus, studies tend not to provide a “pure” estimate of MeHg toxicity but an estimate that represents the balance between the putative harm caused by the contaminant and the putative benefits provided by the

OCR for page 121
Seafood Choices: Balancing Benefits and Risks FIGURE 4-3 Coefficients for achievement and cognition-related endpoints from the three studies. The symbols Q, C, and B denote the three endpoints that are common to two or more studies, namely IQ (Q), California Verbal Learning Test (C), and Boston Naming Test (B), respectively. X’s indicate endpoints that were unique to one of the studies. Coefficients reflect the change in test score for each ppm increase in maternal hair mercury. A coefficient with a negative sign indicates that a test score decreased as maternal hair mercury level increased. New Zealand estimates are based on including the child with a maternal hair mercury level of 86 ppm. The Faroe Islands median hair:cord blood ratio of 200 (Budtz-Jorgensen, 2004b) was used to convert the Faroe Islands results to units of hair mercury. SOURCE: Ryan, 2005. nutrients in seafood. This issue is critical, however, because the goal in giving advice regarding seafood consumption should be to enable people to obtain the greatest benefit for the least risk. An illustration of the delicacy of this balance is provided by a study of 135 mother-infant pairs in Boston (Oken et al., 2005). Mothers reported consuming an average of 1.2 fish servings per week during the second trimester of pregnancy (range 0–5.5 servings/week), and had a mean hair

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Fries GF. 1995a. A review of the significance of animal food products as potential pathways of human exposures to dioxins. Journal of Animal Science 73(6):1639–1650. Fries GF. 1995b. Transport of organic environmental contaminants to animal products. Reviews of Environmental Contamination and Toxicology 141:71–109. Fyfe M, Kelly MT, Yeung ST, Daly P, Schallie K, Buchanan S, Waller P, Kobayashi J, Therien N, Guichard M, Lankford S, Stehr-Green P, Harsch R, DeBess E, Cassidy M, McGivern T, Mauvais S, Fleming D, Lippmann M, Pong L, McKay RW, Cannon DE, Werner SB, Abbott S, Hernandez M, Wojee C, Waddell J, Waterman S, Middaugh J, Sasaki D, Effler P, Groves C, Curtis N, Dwyer D, Dowdle G, Nichols C. 1998. Outbreak of vibrio parahaemolyticus infections associated with eating raw oysters—Pacific Northwest, 1997. Morbidity and Mortality Weekly Report 47(22):457–462. [Online]. Available: http://www.cdc.gov/mmwr/preview/mmwrhtml/00053377.htm [accessed April 11, 2006]. Ganther HE, Goudie C, Sunde ML, Kopecky MJ, Wagner P, Oh S-H, Hoekstra WG. 1972. Selenium: Relation to decreased toxicity of methylmercury added to diets containing tuna. Science 175(26):1122–1124. Geyer HJ, Rimkus GG, Scheunert I, Kaune A, Schramm K-W, Kettrup A, Zeeman M, Muir DCG, Hansen LG, Mackay D. 2000. Bioaccumulation and occurrence of endocrine-disrupting chemicals (EDC), persistent organic pollutants (POPs), and other organic compounds in fish and other organisms including humans. In: Hutzinger O, Beek B, eds. Bioaccumulation, New Aspects and Developments. The Handbook of Environmental Chemistry, Vol. 2, Part J. Berlin, Germany: Springer Verlag. Pp. 1–166. Global Aquaculture Alliance. 2004. Responsible Aquaculture Program. [Online]. Available: http://www.gaalliance.org/resp.html [accessed April 3, 2006]. Gombas DE, Chen Y, Clavero RS, Scott VN. 2003. Survey of Listeria monocytogenes in Ready-to-Eat Foods. Journal of Food Protection 66(4):559–569. Grandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K, Murata K, Sorensen N, Dahl R, Jorgensen PJ. 1997. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicology and Teratology 19(6):417–428. Grandjean P, Weihe P, Burse VW, Needham LL, Storr-Hansen E, Heinzow B, Debes F, Murata K, Simonsen H, Ellefsen P, Budtz-Jorgensen E, Keiding N, White RF. 2001. Neurobehavioral deficits associated with PCB in 7-year-old children prenatally exposed to seafood neurotoxicants. Neurotoxicology and Teratology 23(4):305–317. Gregus Z, Gyurasics A, Csanaky I, Pinter Z. 2001. Effects of methylmercury and organic acid mercurials on the disposition of exogenous selenium in rats. Toxicology and Applied Pharmacology 174(2):177–187. Guallar E, Sanz-Gallardo I, Veer PV, Bode P, Aro A, Gomez-Aracena J, Kark JD, Riemersma RA, Martin-Moreno JM, Kok FJ. 2002. Mercury, fish oils, and the risk of myocardial infarction. New England Journal of Medicine 347(22):1747–1754. Hanekamp JC, Frapporti G, Olieman K. 2003. Chloramphenicol, food safety and precautionary thinking in Europe. Environmental Liability 11:209–221. [Online]. Available: http://www.richel.org/theodoc/pdf/Chloramphenicol.pdf [accessed May 1, 2006]. Harris WS, Windson SL, Dujovne CA. 1991. Effects of four doses of n-3 fatty acids given to hyperlipidemic patients for six months. Journal of the American College of Nutrition 10(3):220–227. Hefle SL. 1996. The chemistry and biology of food allergens. Food Technology 50(3):86–92. Higashi GJ. 1985. Foodborne parasites transmitted to man from and other aquatic foods. Food Technology 39(3):69–74. Hightower JM, Moore D. 2003. Mercury levels in high-end consumers of fish. Environmental Health Perspectives 111(4):604–608. Hites RA. 2004. Polybrominated diphenyl ethers in the environment and in people: A meta-analysis of concentrations. Environmental Science and Technology 38(4):945–956.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Hites RA, Foran JA, Carpenter DO, Hamilton MC, Knuth BA, Schwager SJ. 2004. Global assessment of organic contaminants in farmed salmon. Science 303(5655):226–229. Hlady W, Klontz K. 1996. The epidemiology of Vibrio infections in Florida, 1981–1993. Journal of Infectious Diseases 173(5):1176–1183. Huisman M, Koopman-Esseboom C, Lanting CI, van der Paauw CG, Tuinstra LG, Fidler V, Weisglas-Kuperus N, Sauer PJ, Boersma ER, Touwen BC. 1995. Neurological condition in 18-month-old children perinatally exposed to polychlorinated biphenyls and dioxins. Early Human Development 43(2):165–176. Humphrey H. 1988. Human exposure to persistent aquatic contaminants. In: Schmidtke NW, ed. Toxic Contamination in Large Lakes. Chelsea, MI: Lewis Publishers. Pp. 227–238. Hungerford JM. 2005. Committee on Natural Toxins and Food Allergens: Marine and freshwater toxins. Journal of the Association of Official Analytical Chemists International 88(1):299–324. Huss HH, Ababouch L, Gram L. 2004. Assessment and Management of Seafood Safety and Quality. Technical Paper No. 444. Rome, Italy: Food and Agricultural Organization. [Online]. Available: http://www.fao.org/DOCREP/006/Y4743E/y4743e06.htm [accessed March 30, 2006]. ICEID (International Conference on Emerging Infectious Diseases). 2006. Consumption of Risky Foods Declines. Atlanta, GA: International Conference on Emerging Infectious Diseases. [Online]. Available: http://www.asm.org/ASM/files/LeftMarginHeaderList/DOWNLOADFILENAME/000000002017/risky%20foods.pdf [accessed April 11, 2006]. IFT (Institute of Food Technologists). 2006. Antimicrobial Resistance: Implications for the Food System, Summary. IFT Expert Report. [Online]. Available: http://members.ift.org/NR/rdonlyres/17A8181C-143C-4D94-8885-9093C4AFC533/0/OnePagerSummary.pdf [accessed August 26, 2006]. IISD (International Institute for Sustainable Development). 1998. Report of the first session of the INC for an international legally binding instrument for implementing international action on center persistent organic pollutants (POPS): 29 June–3 July 1998. Earth Negotiations Bulletin 15(10):1. [Online]. Available: http://www.iisd.ca/download/pdf/enb1510e.pdf [accessed March 13, 2006]. Ikemoto T, Kunito T, Tanaka H, Baba N, Miyazaki N, Tanabe S. 2004. Detoxification mechanism of heavy metals in marine mammals and seabirds: Interaction of selenium with mercury, silver, copper, zinc, and cadmium in liver. Archives of Environmental Contamination and Toxicology 47(3):402–413. Ikonomou MG, Rayne S, Addison RF. 2002. Exponential increases of the brominated flame retardants, polybrominated diphenyl ethers, in the Canadian Arctic from 1981 to 2000. Environmental Science and Technology 36(9):1886–1892. IOM (Institute of Medicine). 1991. Seafood Safety. Washington, DC: National Academy Press. IOM. 2003. Dioxins and Dioxin-Like Compounds in the Food Supply: Strategies to Decrease Exposure. Washington, DC: The National Academies Press. ISSC (Interstate Shellfish Sanitation Conference). 2001. Vibrio Management Committee Meeting, Biloxi, MS, November 8–9, 2001. [Online]. Available: http://issc.org/Archives/old-newsletters/Nov-2002/VMCNOV.htm [accessed April 28, 2006]. ISSC. 2002. Vibrio vulnificus Risk Management Plan for Oysters. [Online]. Available: http://www.issc.org/Vibrio_vulnificus_Education/1/II%20A%20Vibrio%20vulnificus%20Risk%20Management%20Plan.doc [accessed March 2, 2006]. ISSC. 2003a. Guide for the Control of Molluscan Shellfish 2003. National Shellfish Sanitation Program, Interstate Shellfish Sanitation Conference. [Online]. Available: http://www.cfsan.fda.gov/~ear/nss2-toc.html [accessed April 20, 2006].

OCR for page 121
Seafood Choices: Balancing Benefits and Risks ISSC. 2003b. Florida Vibrio vulnificus Risk Reduction Plan for Oysters. [Online]. Available: http://www.issc.org/Vibrio_vulnificus_Education/1/II%20B%20a%20Florida%20Vibrio%20Vulnificus%20Risk%20Reduction%20Plan%20for%20Oy.rtf [accessed April 28, 2006]. Jackson GJ. 1975. The new disease status of human anisakiasis and North American cases: A review. Journal of Milk and Food Technology 38(12):769–773. Jacobson JL, Jacobson SW. 1996. Dose-response in perinatal exposure to polychlorinated biphenyls (PCBs): The Michigan and North Carolina cohort studies. Toxicology and Industrial Health 12(3–4):435–445. Jacobson JL, Jacobson SW. 2003. Prenatal exposure to polychlorinated biphenyls and attention at school age. Journal of Pediatrics 143(6):780–788. Jacobson JL, Jacobson SW, Humphrey HE. 1990. Effects of in utero exposure to polychlorinated biphenyls and related contaminants on cognitive functioning in young children. Journal of Pediatrics 116(1):38–45. Jensen CD, Spiler GA, Wookey VJ, Wong LG, Whitman JH, Scala J. 1988. Plasma lipids on three levels of fish oil intake in healthy human subjects. Nutrition Reports International 38:165–171. Jensen TK, Grandjean P, Jorgensen EB, White RF, Debes F, Weihe P. 2005. Effects of breast feeding on neuropsychological development in a community with methylmercury exposure from seafood. Journal of Exposure Analysis and Environmental Epidemiology 15(5):423–430. Johansson N, Basun H, Winblad B, Nordberg M. 2002. Relationship between mercury concentration in blood, cognitive performance, and blood pressure, in an elderly urban population. BioMetals 15(2):189–195. Kamrin MA. 2004. Bisphenol A: A scientific evaluation. Medscape General Medicine 6(3):7. Kimbrough RD. 1987. Human health effects of polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs). Annual Review of Pharmacology and Toxicology 27: 87–111. Kimbrough RD, Squire RA, Linder RE, Strandberg JD, Montalli RJ, Burse VW. 1975. Induction of liver tumor in Sherman strain female rats by polychlorinated biphenyl aroclor 1260. Journal of the National Cancer Institute 55(6):1453–1459. Kingman A, Albertini T, Brown LJ. 1998. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. Journal of Dental Research 77(3):461–471. Kjellstrom T, Kennedy S, Wallis S, Mantell C. 1986. Physical and Mental Development of Children with Prenatal Exposure to Mercury from Fish. Stage I: Preliminary Tests at Age 4. Solna, Sweden: National Swedish Environmental Protection Board. Kjellstrom T, Kennedy S, Wallis S, Stewart A, Friberg L, Lind B, Wutherspoon T, Mantell C. 1989. Physical and Mental Development of Children with Prenatal Exposure to Mercury from Fish. Stage II: Interviews and Psychological Tests at Age 6. Solna, Sweden: National Swedish Environmental Protection Board. Kodavanti PR, Ward TR. 2005. Differential effects of commercial polybrominated diphenyl ether and polychlorinated biphenyl mixtures on intracellular signaling in rat brain in vitro. Toxicological Sciences 85(2):952–962. Koeman JH, Peeters WH, Koudstaal-Hol CH, Tjioe PS, de Goeij JJ. 1973. Mercury-selenium correlations in marine mammals. Nature 245(5425):385–386. Koeman JH, van de Ven WS, de Goeij JJ, Tjioe PS, van Haaften JL. 1975. Mercury and selenium in marine mammals and birds. Science of the Total Environment 3(3):279–287. Kohn MA, Farley TA, Ando T, Curtis M, Wilson SA, Jin Q, Monroe SS, Baron RC, McFarland LM, Glass RI. 1995. An outbreak of Norwalk virus gastroenteritis associated with eating raw oysters. Implications for maintaining safe oyster beds. Journal of the American Medical Association 273(6):466–471.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Kong KY, Cheung KC, Wong CK, Wong MH. 2005. Residues of DDTs, PAHs and some heavy metals in fish (Tilapia) collected from Hong Kong and mainland China. Journal of Environmental Science and Health. Part A: Toxic/Hazardous Substances and Environmental Engineering 40(11):2105–2115. Koonse B, Burkhardt W, Chirtel S, Hoskins GP. 2005. Salmonella and the sanitary quality of aquacultured shrimp. Journal of Food Protection 68(12):2527–2532. Kosta L, Byrne AR, Zelenko V. 1975. Correlation between selenium and mercury in man following exposure to inorganic mercury. Nature 254(5497):238–239. Kraepiel AM, Keller K, Chin HB, Malcolm EG, Morel FM. 2003. Sources and variations of mercury in tuna. Environmental Science and Technology 37(24):5551–5558. Kulkarni P. 2005. The Marine Seafood Export Supply Chain in India: Current State and Influence of Import Requirements. Winnipeg, Manitoba, Canada: International Institute for Sustainable Development. [Online]. Available: http://www.tradeknowledgenetwork.net/pdf/tkn_marine_export_india.pdf [accessed May 2, 2006]. Lange WR, Snyder FR, Fudala PJ. 1992. Travel and ciguatera fish poisoning. Archives of Internal Medicine 152(10):2049–2053. Law RJ, Alaee M, Allchin CR, Boon JP, Lebeuf M, Lepom P, Stern GA. 2003. Levels and trends of polybrominated diphenylethers and other brominated flame retardants in wildlife. Environment International 29(6):757–779. Lehane L. 1999. Ciguatera Fish Poisoning: A Review in a Risk-Assessment Framework. Canberra, Australia: National Office Animal and Plant Health, Agriculture, Fisheries and Forestry. [Online]. Available: http://www.affa.gov.au/corporate_docs/publications/pdf/animalplanthealth/chief_vet/ciguatera.pdf [accessed April 3, 2006]. Lehrer SB. 1993. Seafood allergy. Introduction. Clinical Reviews in Allergy 11(2):155–157. Longnecker MP, Wolff MS, Gladen BC, Brock JW, Grandjean P, Jacobson JL, Korrick SA, Rogan WJ, Weisglas-Kuperus N, Hertz-Picciotto I, Ayotte P, Stewart P, Winneke G, Charles MJ, Jacobson SW, Dewailly E, Boersma ER, Altshul LM, Heinzow B, Pagano JJ, Jensen AA. 2003. Comparison of polychlorinated biphenyl levels across studies of human neurodevelopment. Environmental Health Perspectives 111(1):65–70. Luksemburg W, Wenning R, Maier M, Patterson A, Braithwaite S. 2004. Polybrominated diphenyl ethers (PBDE) and polychlorinated dibenzo-p-dioxins (PCDD/F) and biphenyls (PCB) in fish, beef, and fowl purchased in food markets in northern California U.S.A. Organohalogen Compounds 66:3982–3987. Lunder S, Sharp R. 2003. Tainted Catch: Toxic Fire Retardants Are Building Up Rapidly in San Francisco Bay Fish—And People. Washington, DC: Environmental Working Group. [Online]. Available: http://www.ewg.org/reports_content/taintedcatch/pdf/PBDEs_final.pdf [accessed September 12, 2005]. Luten JB, Ruiter A, Ritskes TM, Rauchbaar AB, Riekwel-Booy G. 1980. Mercury and selenium in marine- and freshwater fish. Journal of Food Science 45:416–419. Mahaffey KR, Clickner RP, Bodurow CC. 2004. Blood organic mercury and dietary mercury intake: National Health and Nutrition Examination Survey, 1999 and 2000. Environmental Health Perspective 112(5):562–570. McDowell MA, Dillon CF, Osterloh J, Bolger PM, Pellizzari E, Fernando R, Montes de Oca R, Schober SE, Sinks T, Jones RL, Mahaffey KR. 2004. Hair mercury levels in US children and women of child-bearing age: Reference range data from NHANES 1999–2000. Environmental Health Perspectives 112(11):1165–1171. McKerrow JH, Sakanari J, Deardorff TL. 1988. Anisakiasis: Revenge of the sushi parasite. New England Journal of Medicine 319(18):1228–1229.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Mead PS, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, Griffine PM, Tauxe RV. 1999. Food-related illness and death in the United States. Emerging Infectious Diseases 5(5):607–625. [Online]. Available: http://www.cdc.gov/ncidod/eid/vol5no5/mead.htm [accessed January 12, 2006]. Mead PS, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, Griffine PM, Tauxe RV. 2006. Food-related illness and death in the United States. Emerging Infectious Diseases 5(5):607–625. Meironyté D, Norén K, Bergman A. 1999. Analysis of polybrominated diphenyl ethers in Swedish human milk: A time-related trend study, 1972–1997. Journal of Toxicology and Environmental Health, Part A 58(6):329–341. Mendelsohn ML, Mohr LC, Peeters JP. 1998. Biomarkers: Medical and Workplace Applications. Washington, DC: Joseph Henry Press. Mocarelli P, Gerthoux PM, Brambilla P, Marocchi A, Beretta C, Bertona M, Cazzaniga M, Colombo L, Crespi C, Ferrari E, Limonta G, Sarto C, Signorini, Tramacere PL. 1999. Dioxin health effects on humans twenty years after Seveso: A summary. In: Ballarin-Denti A, Bertazzi PA, Facchetti S, Mocarelli P, eds. Chemistry, Man, and Environment: The Seveso Accident 20 Years On: Monitoring, Epidemiology and Remediation. Pp. 41–52. Moreland KB, Landrigan PJ, Sjödin A, Gobeille AK, Jones RS, McGahee EE, Needham LL, Patterson DG. 2005. Body burdens of polybrominated diphenyl ethers among urban anglers. Environmental Health Perspectives 113(12):1689–1692. Morton RA, Burklew MA. 1970. Incidence of ciguatera in barracuda from the west coast of Florida. Toxicon 8(4):317–318. Myers GJ, Davidson PW, Cox C, Shamlaye CF, Palumbo D, Cernichiari E, Sloane-Reeves J, Wilding GE, Kost J, Huang LS, Clarkson TW. 2003. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Lancet 361 (9370):1686–1692. National Fish Meal and Oil Association. 2002. Certificate of Analysis and Pesticide Scans. Provided to the FDA by Thionville Laboratories, Inc. [Online]. Available: http://www.fda.gov/ohrms/dockets/dailys/02/Jul02/070202/99p-5332_sup0003_01_vol1.pdf [accessed August 28, 2006]. Nguon K, Baxter MG, Sajdel-Sulkowska EM. 2005. Perinatal exposure to polychlorinated biphenyls differentially affects cerebellar development and motor functions in male and female rat neonates. Cerebellum 4(2):112–122. NRC (National Research Council). 1999. Hormonally Active Agents in the Environment. Washington, DC: National Academy Press. NRC. 2000. Toxicological Effects of Methylmercury. Washington, DC: National Academy Press. NRC. 2006. Health Risks from Dioxin and Related Compounds: Evaluation of the EPA Reassessment. Washington, DC: The National Academies Press. Ocean Nutrition Canada. 2004. Manufacturing: MEG-3. [Online]. Available: http://www.ocean-nutrition.com/inside.asp?cmPageID=158/ [accessed May 11, 2006]. O’Neil CE, Lehrer SB. 1995. Seafood allergy and allergens: A review. Food Technology 49(10):103–116. O’Neil C, Helbling AA, Lehrer SB. 1993. Allergic reactions to fish. Clinical Reviews in Allergy 11(2):183–200. Oken E, Wright RO, Kleinman KP, Bellinger D, Hu H, Rich-Edwards JW, Gillman MW. 2005. Maternal fish consumption, hair mercury, and infant cognition in a US cohort. Environmental Health Perspectives 113(10):1376–1380.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Olsen SJ, MacKinon LC, Goulding JS, Bean NH, Slutsker L. 2000. Surveillance for foodborne disease outbreaks—United States, 1993–1997. Morbidity and Mortality Weekly Report 49(Surveillance Summary 1):1–51. [Online]. Available: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss4901a1.htm [accessed March 31, 2006]. Olson RE. 1986. Marine fish parasites of public health importance. In: Kramer DE, Liston J, eds. Seafood Quality Determination. Amsterdam, the Netherlands: Elsevier Science Publishers. Pp. 339–355. Ortiz-Roque C, Lopez-Rivera Y. 2004. Mercury contamination in reproductive age women in a Caribbean island: Vieques. Journal of Epidemiology and Community Health 58(9):756–757. Otwell S, Garrido L, Garrido V, Benner R. 2001. Farm-raised Shrimp: Good Aquacultural Practices for Product Quality and Safety. Florida Sea Grant Publication SGEB-53. Gainesville, FL: Florida Sea Grant University. [Online]. Available: http://www.uhh.hawaii.edu/~pacrc/Mexico/files/manual/08_shrimp_farming_methods.pdf [accessed May 3, 2006]. Parizek J, Ostadalova I. 1967. The protective effect of small amounts of selenite in sublimate intoxication. Experientia 23(2):142–143. Passos CJ, Mergler D, Gaspar E, Morais S, Lucotte M, Larribe F, Davidson R, de Grosbois S. 2003. Eating tropical fruit reduces mercury exposure from fish consumption in the Brazilian Amazon. Environmental Research 93(2):123–130. Patandin S, Lanting CI, Mulder PG, Boersma ER, Sauer PJ, Weisglas-Kuperus N. 1999. Effects of environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42 months of age. Journal of Pediatrics 134(1):33–41. Paulsson K, Lundbergh K. 1989. The selenium method for treatment of lakes for elevated levels of mercury in fish. Science of the Total Environment 87–88:495–507. Paustenbach D, Galbraith D. 2005. Biomonitoring: Measuring Levels of Chemicals in People—and What the Results Mean. New York, NY: American Council on Science and Health. [Online]. Available: http://www.acsh.org/docLib/20050721_biomonitoring.pdf [accessed March 28, 2006]. Peele C. 2004. Washington State Polybrominated Diphenyl Ether (PBDE) Chemical Action Plan: Interim Plan. Olympia, WA: Washington State Department of Ecology, Department of Health. [Online]. Available: http://www.ecy.wa.gov/pubs/0403056.pdf [accessed March 22, 2006]. Ralston NVC. 2005 (April 11). Selenium Modulation of Toxicants in Seafood. Presented to the Committee on Nutrient Relationships in Seafood: Selections to Balance the Benefits and Risks, Washington, DC, Institute of Medicine. Rayne S, Ikonomou MG, Antcliffe B. 2003. Rapidly increasing polybrominated diphenyl ether concentrations in the Columbia River system from 1992 to 2000. Environmental Science and Toxicology 37(13):2847–2854. Rice DC. 2000. Identification of functional domains affected by developmental exposure to methylmercury: Faroe Islands and related studies. Neurotoxicology 21(6):1039–1044. Rice DC. 2004. The US EPA reference dose for methylmercury: Sources of uncertainty. Environmental Research 95(3):406–413. Rice, DC. 2005 (February). Brominated Flame Retardants: A Report to the Joint Standing Committee on Natural Resources, 122nd Maine Legislature. Prepared by the Bureau of Health and Department of Environmental Protection. [Online]. Available: http://mainegov-images.informe.org/dep/rwm/publications/legislativereports/pdf/bromfeb2005.pdf#search=%22rice%20brominated%20flame%20retardants%3A%20a%20report%20to%20the%20joint%20standing%20committee%20on%20natural%20resources%22 [accessed August 26, 2006]. Rim H. 1982. Clonorchiasis. In: Hillyer G, Hopla C, eds. CRC Handbook Series in Zoonoses, Volume II. Boca Raton, FL: CRC Press Inc. Pp. 17–32.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Rissanen T, Voutilainen S, Nyyssonen K, Lakka TA, Salonen JT. 2000. Fish oil-derived fatty acids, docosahexenoic acid and docosapentaenoic acid, and the risk of acute coronary events—The Kuopio Ischaemic Heart Disease Risk Factor Study. Circulation 102(22):2677–2679. Robson MG, Hamilton GC. 2005. Pest control and pesticides. In: Frumkin H, ed. Environmental Health: From Global to Local. San Fransisco: John Wiley and Sons, Inc. Pp. 544–580. Rodgers RPC, Levin J. 1990. A critical reappraisal of the bleeding time. Seminars in Thrombosis and Hemostasis 16(1):1–20. Rodrick GE, Cheng TG. 1989. Parasites: Occurrence and significance in marine animals. Food Technology 43(11):98–102. Roegge CS, Schantz SL. 2006. Motor function following developmental exposure to PCBS and/or MEHG. Neurotoxicology and Teratology 28(2):260–277. Roegge CS, Wang VC, Powers BE, Klintsova AY, Villareal S, Greenough WT, Schantz SL. 2004. Motor impairment in rats exposed to PCBs and methylmercury during early development. Toxicological Sciences 77(2):315–324. Rogan WJ, Chen A. 2005. Health risks and benefits of bis(4-chlorophenyl)-1,1,1-trichloroethane (DDT). Lancet 366(9487):763–773. Ross G. 2004. The public health implications of polychlorinated biphenyls (PCBs) in the environment. Ecotoxicology and Environmental Safety 59:275–291. Ryan LM. 2005. Effects of Prenatal Mercury Exposure on Childhood IQ: A Synthesis of Three Studies. Report to the US Environmental Protection Agency. Ryan JJ, Patry B, Mills P, Beaudoin NG. 2002. Recent trends in levels of brominated diphenyl ethers (BDEs) in human milks from Canada. Organohalogen Compounds 58:173–176. SACN (Scientific Advisory Committee on Nutrition). 2004. Advice on Fish Consumption: Benefits and Risks. London, England: The Stationery Office. Saint-Phard D, Gonzalez P, Sherman P. 2004. Unsuspected mercury toxicity linked to neurologic symptoms: A case series. Archives of Physical and Medical Rehabilitation 85:E25 (abstract). Sakanari JA, Moser M, Deardorff TL. 1995. Fish Parasites and Human Health: Epidemiology of Human Helminthic Infections. California Sea Grant College, University of California. Salonen JT, Seppanen K, Nyyssonen K, Korpela H, Kauhanen J, Kantola M, Tuomilehto J, Esterbauer H, Tatzber F, Salonen R. 1995. Intake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men. Circulation 91(3):645–655. Salonen JT, Seppanen K, Lakka TA, Salonen R, Kaplan GA. 2000. Mercury accumulation and accelerated progression of carotid atherosclerosis: A population-based prospective 4-year follow-up study in men in eastern Finland. Atherosclerosis 148(2):265–273. Sampson HA. 1992. Food hypersensitivity: Manifestations, diagnosis, and natural history. Food Technology 46:141–156. Santerre CR. 2004. Farmed salmon: Caught in a numbers game. Journal of Food Technology 58(2):108. [Online]. Available: http://seafood.ucdavis.edu/organize/santerresalmon.pdf [accessed April 27, 2006]. Schantz SL, Gardiner JC, Gasior DM, Sweeney AM, Humphrey HE, McCaffrey RJ. 1999. Motor function in aging Great Lakes fisheaters. Environmental Research 80(2 Part 2): S46–S56. Schantz SL, Gasior DM, Polverejan E, McCaffrey RJ, Sweeney AM, Humphrey HE, Gardiner JC. 2001. Impairments of memory and learning in older adults exposed to polychlorinated biphenyls via consumption of Great Lakes fish. Environmental Health Perspectives 109(6):605–611.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Schantz SL, Widholm JJ, Rice DC. 2003. Effects of PCB exposure on neuropsychological function in children. Environmental Health Perspectives 111(3):1–27. Schecter A, Päpke O, Tung K-C, Staskal D, Birnbaum L. 2004. Polybrominated diphenyl ethers contamination of United States food. Environmental Science and Technology 38(20):5306–5311. Schecter A, Papke O, Tung KC, Joseph J, Harris TR, Dahlgren J. 2005. Polybrominated diphenyl ether flame retardants in the U.S. population: Current levels, temporal trends, and comparison with dioxins, dibenzofurans, and polychlorinated biphenyls. Journal of Occupational and Environmental Medicine 47(3):199–211. Seychelles Medical and Dental Journal. 2004. Special Issue: Volume 7, Number 1. [Online]. Available: http://www.seychelles.net/smdj/ [accessed January 12, 2006]. Shamlaye C, Davidson PW, Myers GJ. 2004. The Seychelles Child Development Study: Two decades of collaboration. Seychelles Medical and Dental Journal, Special Issue 7(1):92–99. [Online]. Available: http://www.seychelles.net/smdj/SECIVB.pdf [accessed March 9, 2006]. Sjödin A, Jones RS, Focan J-F, Lapeza C, Wang RY, McGahee EE III, Zhang Y, Turner WE, Slazyk B, Needham L, Patterson DG Jr. 2004a. Retrospective time-trend study of polybrominated diphenyl ether and polybrominated and polychlorinated biphenyl levels in human serum from the United States. Environmental Health Perspectives 112(6):654–658. Sjödin A, Päpke O, McGahee E III, Jones R, Focant J-F, Pless-Mulloli T, Toms L-M, Wang R, Zhang Y, Needham L, Herrmann T, Patterson D Jr. 2004b. Concentration of polybrominated diphenyl ethers (PBDEs) in house hold dust from various countries—inhalation a potential route of human exposure. Organohalogen Compounds 66:3817–3822. Smith AG, Gangolli SD. 2002. Organochlorine and chemicals in seafood: Occurrence and health concerns. Food and Chemical Toxicology 40:767–779. Stern AH, Smith AE. 2003. An assessment of the cord:maternal blood methylmercury ratio: Implications for risk assessment. Environmental Health Perspectives 111(12):1465–1470. Stewart PW, Reihman J, Lonky EI, Darvill TJ, Pagano J. 2003. Cognitive development in preschool children prenatally exposed to PCBs and MeHg. Neurotoxicology and Teratology 25(1):11–22. Stoker TE, Laws SC, Crofton KM, Hedge JM, Ferrell JM, Cooper RL. 2004. Assessment of DE-71, a commercial polybrominated diphenyl ether (PBDE) mixture, in the EDSP male and female pubertal protocols. Toxicological Sciences 78(1):144–155. Taylor SL, Bush RK. 1988. Allergy by ingestion of seafood. In: Tu AT, ed. Handbook of Natural Toxins, Volume 3, Marine Toxins and Venoms. New York: Marcel Dekker. Pp. 149–183. Taylor SL, Nordlee JA. 1993. Chemical additives in seafood products. Clinical Reviews in Allergy 11(2):261–291. Ulbrich B, Stahlmann R. 2004. Developmental toxicity of polychlorinated biphenyls (PCBs): A systematic review of experimental data. Archives in Toxicology 78(5):252–268. UNEP (United Nations Environment Programme). 2002. Global Mercury Assessment. Geneva, Switzerland: UNEP Chemicals. [Online]. Available: http://www.chem.unep.ch/mercury/Report/GMA-report-TOC.htm [accessed March 1, 2006]. UNEP Global Environmental Facility. 2003. Regionally Based Assessment of Persistent Toxic Substances. Global Report 2003. Geneva, Switzerland: United Nations. [Online]. Available: http://www.chem.unep.ch/pts/gr/Global_Report.pdf [accessed April 26, 2006]. US EPA (United States Environmental Protection Agency). 1987. National Dioxin Study. Tiers 3, 5, 6, and 7. EPA-440/4-87-003. Washington, DC: Office of Water Regulations and Standards. US EPA. 1991. Guidelines for developmental toxicity risk assessment. Federal Register 56: 63798-63826. [Online]. Available: http://www.epa.gov/ncea/raf/pdfs/devtox.pdf [accessed April 26, 2006].

OCR for page 121
Seafood Choices: Balancing Benefits and Risks US EPA. 1994. Exposure and Human Health Reassessment of 2,3,7,8-tetrachlorodibenzo-p-dioxin ((TCDD) and Related Compounds. National Academy of Sciences (NAS) Review Draft. Washington, DC: National Center for Environmental Assessment. US EPA. 1995. The Use of the Benchmark Dose Approach in Health Risk Assessment. EPA/630/R-94-007, Washington, DC: Office of Research and Development. US EPA. 1997. Mercury Report for Congress. Volume 1. Executive Summary. EPA-452/R-97-003. Washington, DC: Office of Air Quality Planning and Standards and Office of Research and Development. [Online]. Available: http://www.epa.gov/ttn/oarpg/t3/reports/volume1.pdf [accessed January 12, 2006]. US EPA. 2000a. Exposure and Human Health Reassessment of 2,3,7,8-tetrachlorodibenso-p-dioxin (TCDD) and Related Compounds. Draft Final Report. Washington, DC: US EPA. [Online]. Available: http://cfpub.epa.gov/ncea/cfm/part1and2.cfm?ActType=default [accessed March 2, 2006]. US EPA. 2000b. Guidance for Assessing Chemical Contaminant Data for Use in Fish Advisories. Volume II: Risk Assessments and Consumption Limits. Third Edition. Washington, DC: Environmental Protection Agency. [Online]. Available: http://www.epa.gov/ost/fish-advice/volume2/index.html [accessed March 2, 2006]. US EPA. 2000c. Exposure and Human Health Reassessment of 2,3,7,8-tetrachlorodibenso-p-dioxin (TCDD) and Related Compounds. Part III: Dioxin: Draft Integrated Summary and Risk Characterization for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds. [Online]. Availabe: http://cfpub.epa.gov/ncea/cfm/part1and2.cfm?ActType=default [accessed August 26, 2006]. US EPA. 2001. Water Quality Criterion for the Protection of Human Health: Methylmercury. Chapter 4: Risk Assessment for Methylmercury. Washington, DC: Office of Sciences and Technology, Office of Water, EPA. [Online]. Available: http://www.epa.gov/waterscience/criteria/methylmercury/merc45.pdf [accessed September 12, 2005]. US EPA. 2003. 2001 Toxics Release Inventory Data Release Questions and Answers. [Online]. Available: http://www.epa.gov/tri/tridata/tri01/external_qanda_for_revision.pdf [accessed March 13, 2006]. US EPA. 2005. The Inventory of Sources and Environmental Releases of Dioxin-Like Compounds in the United States: The Year 2000 Update. [Online]. Available: http://www.epa.gov/ncea/pdfs/dioxin/2k-update/ [accessed March 13, 2006]. US EPA. 2006. Health Effects of PCBs. [Online]. Available: http://www.epa.gov/pcb/pubs/effects.html [accessed March 2, 2006]. USDA (United States Department of Agriculture). 2005. National Nutrient Database for Standard Release 18. [Online]. Available: http://www.nal.usda.gov/fnic/foodcomp/Data/SR18/sr18.html) [accessed May 11, 2006]. Van den Berg M, Birnbaum L, Bosveld AT, Brunstrom B, Cook P, Feeley M, Giesy JP, Hanberg A, Hasegawa R, Kennedy SW, Kubiak T, Larsen JC, van Leeuwen FX, Liem AK, Nolt C, Peterson RE, Poellinger L, Safe S, Schrenk D, Tillitt D, Tysklind M, Younes M, Waern F, Zacharewski T. 1998. Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife. Environmental Health Perspectives 106(12):775–792. Van Wijngaarden E, Beck C, Shamlaye CF, Cernichiari E, Davidson PW, Myers GJ, Clarkson TW. 2006. Benchmark concentrations for methyl mercury obtained from the 9-year follow-up of the Seychelles Child Development Study. Neurotoxicology 27(5):702–709. Verity MA. 1997. Pathogenesis of methyl mercury neurotoxicity. In: Yasui M, Strong MJ, Ota K, Verity MA, eds. Mineral and Metal Neurotoxicology. Boca Raton, FL: CRC Press. Pp. 159–167. Viberg H, Fredriksson A, Eriksson P. 2003. Neonatal exposure to polybrominated diphenyl ether (PBDE 153) disrupts spontaneous behaviour, impairs learning and memory and decreases hippocampal cholinergic receptors in adult mice. Toxicology and Applied Pharmacology 192(2):95–106.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Virtanen, JK, Voutilainen S, Rissanen TH, Mursu J, Tuomainen TP, Korhonen MJ, Valkonen VP, Seppanen K, Laukkanen JA, Salonen JT. 2005. Mercury, fish oils, and risk of acute coronary events and cardiovascular disease, coronary heart disease, and all-cause mortality in men in eastern Finland. Arteriosclerosis, Thrombosis and Vascular Biology 25(1):228–233. Vreugdenhil HJ, Lanting CI, Mulder PG, Boersma ER, Weisglas-Kuperus N. 2002a. Effects of prenatal PCB and dioxin background exposure on cognitive and motor abilities in Dutch children at school age. Journal of Pediatrics 40(1):48–56. Vreugdenhil HJ, Slijper FM, Mulder PG, Weisglas-Kuperus N. 2002b. Effects of perinatal exposure to PCBs and dioxins on play behavior in Dutch children at school age. Environmental Health Perspectives 110(10):A593–A598. Vreugdenhil HJ, Mulder PG, Emmen HH, Weisglas-Kuperus N. 2004. Effects of perinatal exposure to PCBs on neuropsychological functions in the Rotterdam cohort at 9 years of age. Neuropsychology 18(1):185–193. Vupputuri S, Longnecker MP, Daniels JL, Guo X, Sandler DP. 2005. Blood mercury level and blood pressure among US women: Results from the National Health and Nutrition Examination Survey, 1999–2000. Environmental Research 97(2):195–200. Walkowiak J, Wiener JA, Fastabend A, Heinzow B, Kramer U, Schmidt E, Steingruber HJ, Wundram S, Winneke G. 2001. Environmental exposure to polychlorinated biphenyls and quality of the home environment: Effects on psychodevelopment in early childhood. Lancet 358(9293):1602–1607. Watanabe C. 2002. Modification of mercury toxicity by selenium: Practical importance? Tohoku Journal of Experimental Medicine 196(2):71–77. Weil M, Bressler J, Parsons P, Bolla K, Glass T, Schwartz B. 2005. Blood mercury levels and neurobehavioral function. Journal of the American Medical Association 293(15):1875–1882. Weinstein MR, Litt M, Kertesz DA, Wyper P, Ross D, Coulter M, McGreer A, Facklam R, Ostach C, Willey BM Borczyk A, Low DE, and the Investigative Team. 1997. Invasive infection due to a fish pathogen: Streptococcus iniae. New England Journal of Medicine 337(9):589–594. Whanger PD. 1985. Metabolic interactions of selenium with cadmium, mercury, and silver. Advances in Nutritional Research 7:221–250. WHO (World Health Organization). 1990. Environmental Health Criteria 101: Methylmercury. Geneva, Switzerland: WHO. [Online]. Available http://www.inchem.org/documents/ehc/ehc/ehc101.htm [accessed March 9, 2006]. WHO. 2001. Consultation on Risk Assessment of Non-Dioxin-Like PCBs. 2001 (September 3–4). Presented at the Federal Institute for Health Protection of Consumers and Veterinary Medicine (BgVV), Berlin, Germany. [Online]. Available: http://www.who.int//pcs/docs/consultation_%20pcb.htm [accessed March 17, 2006]. WHO. 2003. Diet, Nutrition, and the Prevention of Chronic Diseases. Geneva, Switzerland: WHO. [Online]. Available: http://www.who.int/hpr/NPH/docs/who_fao_expert_report.pdf [accessed March 2, 2006]. Willett, WC. 2006. Fish: Balancing health risks and benefits. American Journal of Preventive Medicine 29(4):320–321. Winneke G, Walkowiak J, Lilienthal H. 2002. PCB-induced neurodevelopmental toxicity in human infants and its potential mediation by endocrine dysfunction. Toxicology 181–182:161–165. Yokoo EM, Valente JG, Grattan L, Schmidt SL, Platt I, Silbergeld EK. 2003. Low level methylmercury exposure affects neuropsychological function in adults. Environmental Health 2(1):8.

OCR for page 121
Seafood Choices: Balancing Benefits and Risks Yoneda S, Suzuki KT. 1997. Detoxification of mercury by selenium by binding of equimolar Hg-Se complex to a specific plasma protein. Toxicology and Applied Pharmacology 143(2):274–280. Yoshizawa K, Rimm EB, Morris JS, Spate VL, Hsieh C-C, Spiegelman D, Stampfer MJ, Willett WC. 2002. Mercury and the risk of coronary heart disease in men. New England Journal of Medicine 347(22):1755–1760.