Methylmercury risks

Risk assessment. The Gray model has not been used in human risk assessment. The author, however, suggests that the model would be useful to incorporate rat developmental toxicity data into the assessment of methylmercury risk. Specifically, the author suggests the model be used to convert the short-term exposure data from studies presently being used in risk assessments into continuous-exposure scenarios, which are more typical of the general public s likely exposure pattern. 

Charnley G. Assessing and managing methylmercury risks associated with power plant mercury emissions in the United States. MedGenMed 2006 9(8) 64. 

Clarkson, T.W. 1990. Human health risks from methylmercury in fish. Environ, Toxicol. Chem. 9 957-961. 

A Risk-Management Strategy for PCB-Contaminated Sediments (2001) Toxicological Effects of Methylmercury (2000)... 

Two of the more interesting uses of pharmacokinetic data in risk assessment involve the neurotoxic agents lead and methylmercury (Chapter 4). In the case of lead, epidemiological studies have typically involved the development of quantitative relationships between levels of lead in the blood and adverse health effects. Other measures of lead in the body have also been used. Levels in blood are now very easy to measure, and they do carry the strong advantage that they integrate cumulative exposures from many possible sources (water, food, paint, soil, air, consumer products). Current public health targets for lead are expressed as blood concentrations, typically in pg/dL (Chapter 4). 

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)). 

This is confusing. Why don t risk assessors simply decide what level of exposure is safe for each chemical, and risk managers simply put into effect mechanisms to ensure that industry reaches the safe level Why should different sources of risk be treated differently Why apply a no risk standard to certain substances (e.g., those intentionally introduced into food, such as aspartame) and an apparently more lenient risk-henefit standard to unwanted contaminants of food such as PCBs, methylmercury, and aflatoxins (which the FDA applies under another section of food law) Why allow technological limitations to influence any decision about health What is this risk-henefit balancing nonsense Aren t some of these statutes simply sophisticated mechanisms to allow polluters to expose people to risk ... 

O2 concentrations, such as found in marine wetlands. High biomethylation rates have also been observed in coastal sediments. Because methylmercury is transferred up the food chain, the marine fish that occupy high trophic levels have very high mercury concentrations. In some cases, such as for tuna and swordfish, concentrations are high enough to pose human health risks. 

Methylmercury intoxication affects mainly the central nervous system and results in paresthesias, ataxia, hearing impairment, dysarthria, and progressive constriction of the visual fields. Signs and symptoms of methylmercury intoxication may first appear several weeks or months after exposure begins. Methylmercury is a reproductive toxin. High-dose prenatal exposure to methylmercury may produce mental retardation and a cerebral palsy-like syndrome in the offspring. Low-level prenatal exposures to methylmercury have been associated with a risk of subclinical neurodevelopmental deficits. 

An understanding of the environmental fate of these elements is necessary in the total assessment of associated health risks. Mercury is known to cycle between the geosphere and biosphere (35). Once in the hydrosphere, it can be converted by sediment flora into highly toxic methylmercury whereupon it is incorporated into aquatic life and ultimately accumulates in human food chains (31). Limited bacterial conversion of inorganic to organic mercury has been shown to occur in soil humus (36) and in animal tissue as well (37). There is no evidence that alkylated mercury is generated from coal combustion directly if it did it would probably be dissociated to the elemental form (14). 

It can assess in utero exposure. Any substance in the maternal circulation can be transferred across the placenta to the developing fetus unless it is first metabolized and eliminated (Ginsberg et al. 2004). Risk assessment of the fetal period typically relies on maternal dose. However, biomonitoring of cord blood relative to maternal blood may be important to document whether there are substantial maternal-fetal differences in exposure. Evidence on methylmercury suggests that it concentrates in the fetus (Stern and Smith 2003), whereas an evaluation of 29 pesticides suggests similar concentrations across the maternal-fetal unit (Whyatt et al. 2003). 

EPA (U.S. Environmental Protection Agency). 2001. Methylmercury (MeHg) (CASRN 22967-92-6). Integrated Risk Information System, U.S. Environmental Protection Agency [online]. Available http //www.epa.gov/iris/subst/0073.htm [accessed Jan. 20, 2006]. 

Kedderis, G.L., and J.C. Lipscomb. 2001. Application of in vitro biotransformation data and pharmacokinetic modeling to risk assessment. Toxicol. Ind. Health 17(5-10) 315-321. Kershaw T.G., T.W. Clarkson, and P.H. Dhahir. 1980. The relationship between blood levels and dose of methylmercury in man. Arch. Environ. Health 35(l) 28-36. 

Stern, A.H., and A.E. Smith. 2003. An assessment of the cord blood Maternal blood methylmercury ratio Implications for risk assessment. Environ. Health Perspect. 111 (12) 1465-1470. 

This illustration shows how biomarker-based risk posed by methylmercury (5.8 pg/L as a blood equivalent of the RfD and 58 pg/L as a minimal effect concentration in human fish-eating populations, according to benchmark dose analysis) can be used directly to interpret population biomonitoring data. Pathway analyses conducted by others (Stern et al. 2001 Carrington... 

Carrington, C.D., and M.P. Bolger. 2002. An exposure assessment for methylmercury from seafood for consumers in the United States. Risk Anal. 22(4) 689-99. 

N.K. Mottet, C.M. Shaw, and T.M. Burbacher, Health risks from increases in methylmercury exposure. Environ, Health Perspect. 63 133-140, 1985. 

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