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Contaminated fish consumption

To help public health professionals and others address the needs of persons living or working near hazardous waste sites, the information in this section is organized first by health effect (death, systemic, immunological, neurological, reproductive, developmental, genotoxic, and carcinogenic effects), and then by human and animal studies subdivided by type of exposure (e.g., occupational, contaminated fish consumption, inhalation, oral, and dermal). These data are discussed in terms of three exposure periods acute (14 days or less), intermediate (15-364 days), and chronic (365 days or more). [Pg.63]

Contaminated Fish Consumption. Limited information is available on hepatic end points in populations who consumed fish contaminated with PCBs and other chemicals in Triana, Alabama (Kreiss et al. 1981) and the Baltic Sea area (Svensson et al. 1994). No data were located on liver effects in fisheaters from the Great Lakes/St. Lawrence River basin. [Pg.131]

Contaminated Fish Consumption. Serum cholesterol, serum GGT, and blood pressure, but not serum HDL cholesterol or triglycerides, were positively correlated with serum PCB levels in 458 residents of Triana, Alabama (Kreiss et al. 1981). These associations were independent of age, sex, fish consumption, body mass index, and alcohol consumption. Consumption of contaminated fish was the only known source of PCB exposure, but PCB intake was not estimated. DDT was also increased in the serum of the people and in the fish, and serum DDT and serum PCB levels were highly correlated. [Pg.133]

Contaminated Fish Consumption. The neurochemical effects of exposure of rats to feed adulterated with 5 or 20% lyophilized salmon fillets from Lake Huron (LH) or Lake Ontario (LO) were examined by Seegal et al. (1998). The study was conducted in 88-day-old male and female rats that had been exposed in utero, during lactation, and postnatally until they were tested. Dopamine, serotonin, norepinephrine, and their metabolites, as well as ChAT activity were assayed in the frontal cortex, nucleus accumbens, caudate nucleus, hippocampus, and substantia nigra. Significant treatment-related effects included... [Pg.226]

Contaminated Fish Consumption. Mortality from liver cancer was not increased in the Svensson et al. (1995a) study of Swedish east coast (Baltic Sea) and west coast fisherman summarized in Section 3.2.8.2.2. [Pg.287]

Contaminated fish Consumption. There was no increased mortality from Hodgkin s lymphoma or non-Hodgkin s lymphoma in the Svensson et al. (1995a) study of Swedish east coast (Baltic Sea) and west coast fisherman summarized in Section 3.2.8.2.2. Mortality from multiple myeloma was increased in the fisherman from the east coast (SMR=3.08, 95% CI=1.24-6.35) and west coast (SMR=2.08, Cl=0.76. 53), as was mortality from leukemia was increased in the east coast fisherman (SMR=1.38, Cl=0.45-3.22). [Pg.295]

Florida, consumption of contaminated fish with 2-3 mg methylmercury/kg FW muscle ... [Pg.419]

The high BCF values observed for chlordecone (>60,000) indicate that the compound will be found in high concentrations in aquatic organisms that dwell in waters or sediments contaminated with chlordecone. Chlordecone has been detected in fish and shellfish from the James River, which empties into the Chesapeake Bay, at levels in the pg/g (ppm) range. There is currently a fish consumption advisory in effect for the lower 113 miles of the James River. Chlordecone residues were detected in foods analyzed from 1978-1982 and 1982-1986 as part of the Food and Drug Administration (FDA) Pesticide Residue Monitoring Studies. Chlordecone was detected in one of 27,065 food samples analyzed by 10 state laboratories, but was not detected in the more recent FDA Pesticide Residue Monitoring Studies from 1986 to 1991. No information on the specific foods in which residues were found or levels detected was located. [Pg.175]

An analysis of potential human exposure to contaminants in drinking water and foods was conducted in Ontario, Canada, in 1980. Mirex was detected only in edible fish taken from Toronto Harbor on Lake Ontario. The average mirex concentrations were 0.001 mg/kg (ppm) wet weight for white sucker, 0.01 mg/kg wet weight for rainbow trout, and 0.033 mg/kg wet weight for northern pike. Estimated human exposure levels, based on an average fish consumption of 0.53 kg/year for each fish species, were 0.0005 for white sucker, 0.0005 for rainbow trout, and 0.017 mg/year for northern pike, respectively (Davies 1990). [Pg.195]

Mirex contamination has triggered the issuance of several human health advisories nationwide. As of September 1993, mirex was identified as the causative pollutant in eight fish consumption advisories in three different states. This information is summarized below (RTI 1993) ... [Pg.197]

Spores may be transferred from soil and plants to the sea via rainwater, causing the prevalence in coastal waters of the same C. botulinum types as on the land. Such a correlation was observed in Great Britain, where the type B predominates both in soil and in bottom sediments. Similarly, 71% of fish and bottom-sediment samples collected in southern France were contaminated with type B, while C. botulinum type E was found only in 9.6% of samples (Each et al., 2002). However, it is commonly believed that non-proteolytic type E is characteristic for the marine environment. A distinguishing feature of type E strains is the ability to grow in low temperatures (about 3°C), which are typical for bottom layers of seas and oceans. Moreover, the bottom sediments provide anaerobic conditions for the outgrowth of Clostridium. Therefore, the marine environment promotes C. botulinum type E distribution. This has been further supported by the rate of fish and seafood contamination fish and seafood isolated in many countries are most frequently contaminated with C. botulinum type E (Dodds, 1993 a,b). Furthermore, epidemiological studies have shown that the majority of botulism cases linked to fish and seafood consumption reported between 1950 and 1996 in the U.S. were caused by C. botulinum type E (Centers for Disease Control and Prevention 1998). C. botulinum type F,... [Pg.202]

Pharmacokinetics has played a crucial and somewhat unusual role in the assessment of health risks from methylmercury. Some of the epidemiology studies of this fish contaminant involved the measurement of mercury levels in the hair of pregnant women, and subsequent measurements of health outcomes in their offspring (Chapter 4). Various sets of pharmacokinetic data allowed estimation of the level of methylmercury intake through fish consumption (its only source) that gave rise to the measured levels in hair. In this way it was possible to identify the dose-response relationship in terms of intake, not hair level. Once the dose-response relationship was established in this way, the EPA was able to follow its usual procedure for establishing an RfD (which is 0.1 ag/(kg b.w. day)). [Pg.255]

HI Maximum organic contaminant level Total trihalomethane (TTHM) (TTHM = the sum of the concentration of bromodichloromethane, dibromochloromethane and chloroform) Fresh water Salt water Fish consumption Acute 9,600 jjglL ns 5.1 Chronic ns ns ... [Pg.247]

Zhao et al. [105] have been calculated the hazard ratio (HR) of PFOS for fish consumption and the risks and potential effects of PFCs to health of coastal population in the Pearl River Delta. Due to the contamination levels of more consumed species (mandarin fish, bighead carp, grass carp and tUapia), the authors have concluded that the levels of PFCs in these fish species might pose an unacceptable risk to human health. [Pg.351]


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