Exposure fish consumption

States have made substantial recent progress in the adoption, and EPA approval, of toxic pollutant water-quahty standards. Furthermore, virtually all states have at least proposed new toxics criteria for priority toxic pollutants since Section 303 (c) (2) (B) was added to the CWA in February of 1987. Unfortunately, not all such state proposals address, in a comprehensive manner, the requirements or Section 303 (c) (2) (B). For example, some states have proposed to adopt criteria to protect aquatic hfe, but not human health other states have proposed human health criteria that do not address major exposure pathways (such as the combination of both fish consumption and drinking water). In addition, in some cases final adoption or proposed state toxics criteria that would be approved by EPA has been substantially delayed due to controversial and difficult issues associated with the toxic pollutant criteria adoption process. 

Relevance. A key criterion in the selection of biological indicators is relevance to human and ecological health and to the development of policy. Fish are directly relevant, for example, given that consumption of fish is the primary pathway for exposure to MeHg. The concentration of MeHg in fish is also a key variable in the issuance of fish-consumption advisories. 

Human intake of total mercury from the diet normally ranges between 7 and 16 pg daily (Schumacher et al. 1994 Richardson et al. 1995). Fish consumption accounts for much of this exposure in the form of methylmercury 27% of the intake, and 40% of the absorbed dose. Intake of inorganic mercury arises primarily from foods other than fish, and is estimated at 1.8 pg daily with 0.18 pg absorbed daily (Richardson etal. 1995). In certain areas of India, blood mercury concentrations of people who ate fish were three to four times higher than non-fish eaters (Srinivasen and Mahajan 1989). In some countries, mercury in dental amalgams accounts for 2.8 pg daily, equivalent to as much as 36% of the total mercury intake and 42% of the absorbed dose (USPHS... 

In humans, total PCB concentrations in maternal milk were elevated (>1.1 mg/kg milk fat) in 4 of 122 cases in the New Bedford Harbor vicinity, Massachusetts (Korrick and Altshul 1998). At least one female was occupationally exposed, as judged by the congener profile and history. PCB exposures from fish consumption were likely, but not from residence adjacent to a PCB-contami-nated site. In all four cases, their newborns were full-term and healthy (Korrick and Altshul 1998). 

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). 

In addition to individuals who are occupationally exposed to 3,3 -dichlorobenzidine (see Section 5.5), there are several groups within the general population that have the potential for exposures to 3,3 -dichloro-benzidine at levels above those of the general population. These groups include individuals living in proximity to sites where 3,3 -dichlorobenzidine was produced or sites where 3,3 -dichlorobenzidine was disposed, and individuals living near one of the 32 NPL hazardous waste sites where 3,3 -dichloro-benzidine has been detected in some enviromnental media (HazDat 1998). 3,3 -Dichlorobenzidine was not detected in fish samples obtained from rivers near nine textile dyestuff manufacturers known to use 3,3 -dichlorobenzidine-based pigments (Diachenko 1979), nor were there any fish consumption advisories for 3,3 -dichlorobenzidine in 1996. Therefore, recreational and subsistence fishers are not at risk. 

More recently, several authors studied the possible association between fish consumption and levels of PFCs in human blood [138], as well as the evaluation of the risk associated with fish consumption [73, 139]. In recognition of the potential for human exposure to PFCs via fish consumption, the Minnesota Department of Health has issued fish consumption advisories for contaminated sections of the Mississippi River (Minnesota Department of Health 2007). This advisory suggests that people limit their intake of fish to no more than one meal a week if PFOS levels in fillet exceed 38 ng/g. 

In the late 1950s the subtle and serious consequences of methyl mercury exposure became evident in Minamata, Japan. Initially, early signs of uncoordinated movement and numbness around the lips and extremities, followed by constriction in visual fields in fishermen and their families, baffled health experts. Developmental effects were clearly evident in infants who exhibited subtle to severe disabilities. This spectrum of adverse effects was finally related to methyl mercury exposure from consumption of contaminated fish. Minamata Bay was contaminated with mercury and methyl mercury from a factory manufacturing the chemical acetaldehyde. Mercury was used in the manufacturing process, which also resulted in both mercury and methyl mercury being discharged into Minamata Bay. The fish in the bay accu-... 

The primary human exposure to methyl mercury is from consumption of contaminated fish. The most sensitive population is the developing fetus or infant due to the effects of methyl mercury on the nervous system (neurotoxic) and developmental effects. Exposure limits and fish consumption advisories are directed at pregnant women, women of childbearing age, and children. All agencies also recognize that fish consumption has many nutritional benefits and is an important part of many people s diet. Nevertheless, the widespread distribution of mercury and subsequent bioaccumulation of methyl mercury requires that many agencies have developed recommendation for levels of mercury in fish. Below is a list of some of these recommendations, but it is very important to consult the local fish consumption advisories. 

Much of our current understanding of these impacts arose from research on wildlife and human populations within the Great Lakes basin. Despite being banned in North America more than 25 years ago, the toxicological risks from PCB exposure are still a present-day concern. For example, current PCB concentrations in fish in the Great Lakes are sufficiently large as to drive the need for fish consumption advisories for sport fish and to restrict commercial fisheries. 

Persky, V., M. Turyk, H.A. Anderson, L.P. Hanrahan, C. Falk, D.N. Steenport, R. Chatterton, Jr., and S. Freels. 2001. The effects of PCB exposure and fish consumption on endogenous hormones. Great Lakes Consortium. Environ. Health Perspect. 109(12) 1275-... 

Myers, G.J., P.W. Davidson, C. Cox, C.F. Shamlaye, D. Palumbo, E. Cernichiari, J. Sloane-Reeves, G.E. Wilding, J. Kost, L.S. Huang, and T.W. Clarkson. 2003. Prenatal methyl mercury exposure from ocean fish consumption in the Seychelle child development study. Lancet 361(9370) 1686-1692. 

The main sources of exposure to mercury for the general population are from the diet and dental amalgam.21,28 The main dietary source of mercury is fish and this has led to interest in potential exposure to mercury on the neurological development of children from populations with high fish consumption.29 There is no statutory control of mercury in most food in the UK, but the levels of mercury in fish are controlled by European Commission Decision 93/351/EEC which sets an average limit for mercury in fish of 0.5 mg/kg or 0.5 ppm (part per million).30 This average limit is, however, increased to 1.0 mg/kg or 1 ppm for the edible parts of the predatory and bottom-dwelling species listed in the Annex to the Decision. 

Dickman, M.D., Leung, K.M.C., 1998. Mercury and organochlorine exposure from fish consumption in Hong Kong. Chemosphere 37, 991-1051. 

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. 

This annex aims to illustrate qualitative uncertainty analysis through a case-study that involves estimation of exposure to a persistent, bioaccumulative and lipid-soluble group of chemicals to which humans are exposed mainly through fish consumption, which is referred to here as PBLx. Examples of appropriate communication of the outcome to various target audiences are also considered. 

This is an example exposure assessment that illustrates quantitative representations of uncertainty and variability at the higher tiers of an exposure assessment. This case-study is based on human exposures to a persistent, bioaccumulative and lipid-soluble compound through fish consumption. This compound is fictional and referred to here as PBLx, but it has properties that correspond to those of known persistent compounds. Specific goals of this case-study are to illustrate (1) the types of uncertainty and variability that arise in exposure assessments, (2) quantitative uncertainty assessment, (3) how distributions are established to represent variability and uncertainty, (4) differences among alternative variance propagation methods, (5) how to distinguish uncertainty from variability and (6) how to communicate the results of an uncertainty analysis. 

In order to illustrate the use of the variance propagation methods described above, we have selected for the case-study a simple three-input exposure model. The three inputs for this model include water concentration, fish BCF and fish consumption rates. The model output is dose expressed in micrograms per day averaged over a one-year exposure period. This model has the form ... 

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