汞在新建水库食物网中生物累积与风险评价研究进展

汞是唯一参与全球循环的液态重金属。1974年,自美国学者Smith首次报道水库中鱼类总汞含量高于邻近自然湖泊以来,水库中鱼类汞升高的风险成为新建水库环境影响评价中的重要内容之一。汞在水库生态系统生物组分和非生物组分中含量升高的现象先后在世界各国报道,包括加拿大、美国、芬兰、泰国和巴西等。通过对系列的野外研究进行回顾,表明了水库形成后生态系统中汞的甲基化过程发生了变化。水库形成对汞在食物网中的鱼类、底栖生物、浮游生物的累积产生影响。水库中汞的生物累积、迁移转化主要与被淹没土壤和植物腐解过程有着直接或间接的关系。水库形成后,总汞、甲基汞和甲基汞比例在生态系统食物网各组分中的变化并不一致。蓄水后,水体中总汞变化较小,甲基汞和甲基汞比例上升明显;浮游生物尤其是浮游动物中总汞升高,但甲基汞和甲基汞比例升高更为明显;与浮游动物类似,底栖水生昆虫中总汞升高,甲基汞和甲基汞比例升高也更为明显;鱼类作为食物网顶级消费者,甲基汞比例一般在80%以上,在水库形成后鱼类总汞和甲基汞均明显升高,但甲基汞比例变化已经不大。这些变化揭示了水库形成后甲基汞在食物网传递的两个主要可能途径,一是微型生物食物网。通过悬浮颗粒物、浮游植物、浮游动物这一环节,甲基汞和甲基汞比例有明显的增加。第二个途径是底层生物食物网。通过悬浮颗粒物、细菌、碎屑食性底栖水生昆虫、肉食型底栖水生昆虫环节,甲基汞和甲基汞比例明显增加。这两种途径均能导致以水生昆虫、小鱼、甲壳类等为食的肉食性鱼类汞含量增加。水库形成后,生态系统中汞的甲基化发生了明显的"加速"过程。这种"加速"过程最直接的因素是成库后大量土壤淹没使得汞的甲基化平衡被打破。这个过程主要有两方面的影响。一方面是直接影响,被淹没土壤和植被在腐解过程中主动或被动地将甲基汞释放到水库生态系统中;另一方面是间接影响,被淹没土壤和植被的腐解使水库底部形成厌氧环境,有利于无机汞从被淹没土壤和植被中溶出,为甲基化反应提供充裕的、可供甲基化的无机汞,同时腐解产生的大量营养物质为微生物提供丰富食物来源,使硫酸盐还原菌大量繁殖,促进无机汞的甲基化。在我国,有关汞在新建水库食物网中生物累积和风险评价的研究有待进一步加强。     

Total mercury in commercial fishes and estimation of Brazilian dietary exposure to methylmercury

BackgroundMercury, in particular its most toxic form methylmercury, poses a risk to public health. Dietary methylmercury exposure is mainly by fish, and it can vary with fish contamination and by dietary habits of the population. This study aimed to quantify total mercury levels in different fish from Brazil and to estimate Brazilian exposure to methylmercury by fish consumption.MethodsTotal mercury occurrence was investigated in 18 different fish species by atomic absorption spectrometry with thermal decomposition and gold amalgamation. Dietary exposure to methylmercury was estimated by a deterministic method for different groups considering consumption by sex, different Brazilian geographical regions and habitat (rural or urban).ResultsCarnivorous fish showed higher levels of mercury (0.01 to 0.93 mg/kg) compared to non-strictly carnivorous fish (<0.01 to 0.30 mg/kg). Farmed fishes showed significantly lower levels compared to wild fish. Mean Brazilian fish consumption achieves FAO/WHO health recommendation of about two portions of fish per week. However, there is a large difference between fish consumption at urban and rural homes and among Brazilian geographic regions. These differences in consumption impacted estimated methylmercury intake that was higher in the Northern (1.85 μg/kg bw week) and in the Northeastern (0.72 μg/kg bw week) regions and also by rural population (1.08 μg/kg bw week). These values were compared with the toxicological reference dose for neurotoxicity of 1.6 μg/kg bw week.ConclusionEven though total levels of mercury in fish were lower than Brazilian and international legislations, in the Northern Brazilian region methylmercury intake overpassed the toxicological reference dose for neurotoxicity and in rural areas it achieved 68% of this reference dose.     

Mercury as a risk factor for cardiovascular diseases

Mercury is a heavy metal that exists naturally in the environment. Major sources include the burning of fossil fuels (especially coal) and municipal waste incineration. Mercury can exist in several forms, with the most hazardous being organic methylmercury. In waterways (lakes, rivers, reservoirs, etc.), mercury is converted to methylmercury, which then accumulates in fish, especially in large predatory fish. Fish and fish products are the major--if not the only--source of methylmercury in humans. Mercury has long been recognized as a neurotoxin for humans, but in the last 10 years, its potentially harmful effects on cardiovascular diseases (CVD) have raised a cause for concern, mostly due to the proposed role of mercury in oxidative stress propagation. Some epidemiological studies have indeed found an association between increased levels of mercury in the body and risk of CVD. There are several plausible mechanisms to explain the association; these are discussed in this review. We also review the epidemiological studies that have investigated the association between mercury and CVD.     

Dynamic accumulation and redistribution of methylmercury in the lens of developing zebrafish embryos and larvae

Neurotoxic methylmercury compounds are widespread in the environment and human exposure worries many communities worldwide. Despite numerous studies addressing methylmercury toxicity, the detailed mechanisms underlying its transport and accumulation, especially during early developmental stages, remain unclear. Zebrafish larvae are increasingly used as a model system for studies of vertebrate development and toxicology. Previously, we have identified the lens epithelium as the primary site for cellular mercury accumulation in developing zebrafish larvae (Korbas et al. in Proc Natl Acad Sci USA 105:12108–12112, 2008). Here we present a study on the dynamics of methylmercury accumulation and redistribution in the lens following embryonic and larval exposure to methylmercury l-cysteineate using synchrotron X-ray fluorescence imaging. We observed highly specific accumulation of mercury in the lens that continues well after removal of fish from treatment solutions, thus significantly increasing the post-exposure loading of mercury in the lens. The results indicate that mercury is redistributed from the original target tissue to the eye lens, identifying the developing lens as a major sink for methylmercury in early embryonic and larval stages.     

Assessing and managing methylmercury risks associated with power plant mercury emissions in the United States

Until the Clean Air Mercury Rule was signed in March 2005, coal-fired electric utilities were the only remaining, unregulated major source of industrial mercury emissions in the United States. Proponents of coal-burning power plants assert that methylmercury is not a hazard at the current environmental levels, that current technologies for limiting emissions are unreliable, and that reducing mercury emissions from power plants in the United States will have little impact on environmental levels. Opponents of coal-burning plants assert that current methylmercury exposures from fish are damaging to the developing nervous system of infants, children, and the fetus; that current technology can significantly limit emissions; and that reducing emissions will reduce exposure and risk. One concern is that local mercury emissions from power plants may contribute to higher local exposure levels, or "hot spots." The impact of the Mercury Rule on potential hot spots is uncertain due to the highly site-specific nature of the relationship between plant emissions and local fish methylmercury levels. The impact on the primary source of exposure in the United States, ocean fish, is likely to be negligible due to the contribution of natural sources and industrial sources outside the United States. Another debate centers on the toxic potency of methylmercury, with the scientific basis of the US Environmental Protection Agency's (EPA's) recommended exposure limit questioned by some and defended by others. It is likely that the EPA's exposure limit may be appropriate for combined exposure to methylmercury and polychlorinated biphenyls (PCBs), but may be lower than the available data suggest is necessary to protect children from methylmercury alone. Mercury emissions from power plants are a global problem. Without a global approach to developing and implementing clean coal technologies, limiting US power plant emissions alone will have little impact.     

Population-Based Fish Consumption Survey and Probabilistic Methylmercury Risk Assessment

A fish consumption survey was developed and administered by telephone to 820 Wyoming fishing license holders. Survey respondents provided the frequency, species, and quantity of Wyoming-caught and store-bought fish consumed for license holder and household members. Deterministic and probabilistic methylmercury exposure distributions were estimated by multiplying fish consumption by species-specific mercury concentrations for each household member. Risk assessments were conducted for children, women of childbearing age, and the rest of the population by comparing methylmercury exposure distributions to levels of concern. The results indicate that probabilistic risk assessment likely provides a more realistic view of the risk to the study population. The results of this study clearly indicate that: (1) there is no level of fish consumption that is without risk of methylmercury exposure, (2) fish advisories may be warranted for children and women of childbearing age, and (3) that store-bought fish generally contribute more to methylmercury exposure than do Wyoming-caught fish.     

锌对染汞孕鼠胚胎毒性的影响及其机理研究

目的:探讨妊娠期补锌对染汞孕鼠胚胎发育毒性的保护作用.方法:建立孕鼠动物模型,应用不同剂量的氯化甲基汞(0.01、0.05、2.00mg/kg·d)及5.00mg/kg·d硫酸锌于妊娠6～9天连续灌胃.蒸馏水灌胃为对照组,观察孕鼠及胚胎的汞毒性及硫酸锌的影响.应用ICP-MS法测定各组胎鼠脑组织汞含量;Western blot法检测各组胎鼠脑bcl-2蛋白表达情况;TUNEL法检测各组胎鼠脑细胞凋亡情况.结果:各组均未发现死胎、吸收胎及畸形胎;0.01、0.05mg/kg·d氯化甲基汞对孕鼠及胎鼠生长发育没有明显的抑制作用;2.00mg/kg·d氯化甲基汞可以明显抑制孕鼠体重增长及胎鼠身长、体重及尾长的增长(P＜0.05),但对孕鼠产仔数、胎窝总重及胎盘总重没有明显的影响,0.05mg/kg·d、2.00mg/kg·d 氯化甲基汞组胎鼠脑组织汞含量较对照组明显升高(P＜0.05),bcl一2蛋白表达明显下降(P＜0.05),脑细胞凋亡较对照组明显升高(P＜0.05);应用硫酸锌预处理后,氯化甲基汞对孕鼠及胚胎的毒性作用明显降低(P＜0.05),胎鼠脑组织汞含量较染汞组明显降低(P＜0.05),bcl-2蛋白表达明显升高(P＜0.05),胎鼠脑细胞凋亡明显降低(P＜0.05).结论:孕期补锌可以降低氯化甲基汞对孕鼠胚胎的毒性作用,其机制与锌通过升高bel-2蛋白的表达而抑制细胞凋亡有关.     

Effect of subchronic administration of ethanol and methylmercury in combination on the tissue distribution of mercury in rats

The effect of oral administration for 14 weeks of 8 g.kg-1.day-1 ethanol and 0.5 mg.kg-1.day-1 methylmercuric chloride in combination to rats fed isocaloric diets has been investigated. Ethanol, in contrast to published studies, failed to influence the tissue distribution of methylmercury and its inorganic mercury metabolite in brain and kidney, and did not inhibit the increase in kidney weight induced by methylmercury. Ethanol and methylmercury, in combination and individually, reduced the renal but not the hepatic activity of gamma-glutamyltransferase, but did not affect the renal and biliary concentration of reduced glutathione. Further study is required to determine the circumstances under which ethanol can influence the tissue distribution of methylmercury and its inorganic mercury metabolite.     

Accumulation of mercury in estuarine food chains

To understand the accumulation of inorganic mercury and methylmercury at the base of the estuarine food chain, phytoplankton (Thalassiosira weissflogii) uptake and mercury speciation experiments were conducted. Complexation of methylmercury as methylmercury-bisulfide decreased the phytoplankton uptake rate while the uptake rate of the methylmercury-cysteine and -thiourea complexes increased with increasing complexation by these ligands. Furthermore, our results indicated that while different ligands influenced inorganic mercury/methylmercury uptake by phytoplankton cells, the ligand complex had no major influence on either where the mercury was sequestered within the phytoplankton cell nor the assimilation efficiency of the mercury by copepods. The assimilation efficiency of inorganic mercury/methylmercury by copepods and amphipods feeding on algal cells was compared and both organisms assimilated methylmercury much more efficiently; the relative assimilation efficiency of methylmercury to inorganic mercury was 2.0 for copepods and 2.8 for amphipods. The relative assimilation is somewhat concentration dependent as experiments showed that as exposure concentration increased, a greater percentage of methylmercury was found in the cytoplasm of phytoplankton cells, resulting in a higher concentration in the copepods feeding on these cells. Additionally, food quality influenced assimilation by invertebrates. During decay of a T. weissflogii culture, which served as food for the invertebrates, copepods were increasingly less able to assimilate the methylmercury from the food, while even at advanced stages of decay, amphipods were able to assimilate mercury from their food to a high degree. Finally, fish feeding on copepods assimilated methylmercury more efficiently than inorganic mercury owing to the larger fraction of methylmercury found in the soft tissues of the copepods.     

The chemical forms of mercury and selenium in whale skeletal muscle

Human exposure to potentially neurotoxic methylmercury species is a public-health concern for many populations worldwide. Both fish and whale are known to contain varying amounts of methylmercury species. However studies of populations that consume large quantities of fish or whale have provided no clear consensus as to the extent of the risk. The toxicological profile of an element depends strongly on its chemical form. We have used X-ray absorption spectroscopy to investigate the comparative chemical forms of mercury and selenium in fish and whale skeletal muscle. The predominant chemical form of mercury in whale is found to closely resemble that found in fish. In the samples of skeletal muscle studied, no involvement of selenium in coordination of mercury is indicated in either whale or fish, with no significant inorganic HgSe or HgS type phases being detected. The selenium speciation in fish and whale shows that similar chemical types are present in each, but in significantly different proportions. Our results suggest that for equal amounts of Hg in skeletal muscle, the direct detrimental effects arising from the mercury content from consuming skeletal muscle from whale and fish should be similar if the effects of interactions with other components in the meat are not considered.     

Accumulation of methylmercury and inorganic mercury in the brain

Differences in metabolism between different mercury species are well recognized. Conclusions that only a minor demethylation of methylmercury takes place in the brain are based primarily on results from short term studies. Results from a number of studies on humans exposed for many years to methylmercury have shown high concentrations of inorganic mercury in the brain in relation to total mercury. Similar evidence is available from studies on monkeys exposed for several years to methylmercury. The results indicate that a significant accumulation of inorganic mercury takes place with time despite the fact that the demethylation rate is slow. Differences in biological halftimes between different mercury species will explain the results. Some data do still need confirmation using different analytical methods. There is reason to believe that the one-compartment model for methyl mercury cannot be used without reservations. Inorganic mercury has a complicated metabolism. After exposure to metallic mercury vapor, inorganic mercury, probably bound to selenium, accumulates in the brain. A fraction of the mercury is excreted, with a long biological halftime. Studies on rats and monkeys indicate that inorganic mercury penetrates the blood-brain barrier only to a very limited-extent.     

Consensus document on the prevention of methylmercury exposure in Spain: Study group for the prevention of Me-Hg exposure in Spain (GEPREM-Hg)

The beneficial effects of fish consumption in both children and adults are well known. However, the intake of methylmercury, mainly from contaminated fish and shellfish, can have adverse health effects. The study group on the prevention of exposure to methylmercury (GEPREM-Hg), made up of representatives from different Spanish scientific societies, has prepared a consensus document in a question and answer format, containing the group’s main conclusions, recommendations and proposals. The objective of the document is to provide broader knowledge of factors associated with methylmercury exposure, its possible effects on health amongst the Spanish population, methods of analysis, interpretation of the results and economic costs, and to then set recommendations for fish and shellfish consumption. The group sees the merit of all initiatives aimed at reducing or prohibiting the use of mercury as well as the need to be aware of the results of contaminant analyses performed on fish and shellfish marketed in Spain. In addition, the group believes that biomonitoring systems should be set up in order to follow the evolution of methylmercury exposure in children and adults and perform studies designed to learn more about the possible health effects of concentrations found in the Spanish population, taking into account the lifestyle, eating patterns and the Mediterranean diet.     

Temperature, growth and dietary effects on fish mercury dynamics in two Ontario lakes

A bioenergetics-based model was used to investigate the effects of temperature, growth and dietary exposure on methylmercury dynamics in walleye (Stizostedion vitreum) and yellow perch (Perca flavescens) from two lakes sampled in northwestern Ontario. Orange Lake was smaller, warmer, had slower fish growth and higher mercury concentrations in yearling yellow perch and walleye (three fold difference in 40 cm walleye) than Trout Lake. The model was applied to test the hypothesis that higher water temperatures in Orange Lake increased metabolic needs, food consumption and mercury uptake in fish. The effects of different growths rates in the lakes were also considered. Temperature/metabolic effects and growth effects on internal methylmercury dynamics in walleye and perch were predicted to occur but be of secondary importance. Different dietary exposure to methylmercury was likely the dominant source of variation in fish mercury concentrations between the two lakes.     

The structures of solvated methylmercury(II) chlolade,bromide and iodide in pyridine solution; Implications for aqueous solution

The structures of solvated methylmercury(II) halides in pyridine solution were determined by a large angle X-ray scattering technique. Near-linear CH₃HgX (X = Cl, Br and I) species solvated by two weakly-coordinated pyridine molecules are indirectly interpreted. Additional mercury-pyridine interactions, through van der Waals forces, are found at the sum of the van der Waals radii. The HgX bond distances in the methylmercury(II) halides are found to be 2.325(8), 2.480(3) and 2.649(3) Å for chloride, bromide and iodide, respectively. The HgC bond distances are assumed to be ∼2.08 Å. This interaction is indicated in the radial distribution functions. The bond distance between mercury and the two solvating pyridine molecules is ∼2.8 Å, e.g., 2.84(2) Å in methylmercury(II) bromide. The additional mercury interactions with roughly two pyridine molecules at the sum of van der Waals radii are revealed at around 3.15 Å. Comparison between Raman stretching vibrations and the solvated structures of methylmercury(II) complexes found in various solvents indicates a lower limit in solvent donor property for the formation of solvate bonds to mercury for the methylmercury(II) halides.     

Effects of Inorganic Mercury and Methylmercury on the Ionic Currents of Cultured Rat Hippocampal Neurons

1. The effects of inorganic Hg²⁺ and methylmercuric chloride on the ionic currents of cultured hippocampal neurons were studied and compared. We examined the effects of acute exposure to the two forms of mercury on the properties of voltage-activated Ca²⁺ and Na⁺ currents and N-methyl-D-aspartate (NMDA)-induced currents.2. High-voltage activated Ca²⁺ currents (L type) were inhibited by both compounds at low micromolar concentrations in an irreversible manner. Mercuric chloride was five times as potent as methylmercury in blocking L-channels.3. Both compounds caused a transient increase in the low-voltage activated (T-type) currents at low concentrations (1 M) but blocked at higher concentrations and with longer periods of time.4. Inorganic mercury blockade was partially use dependent, but that by methylmercury was not. There was no effect of exposure of either form of mercury on the I–V characteristics of Ca²⁺ currents.5. Na⁺- and NMDA-induced currents were essentially unaffected by either mercury compound, showing only a delayed nonspecific effect at a time of overall damage of the membrane.6. We conclude that both mercury compounds show a relatively selective blockade of Ca²⁺ currents, but inorganic mercury is more potent than methylmercury.     

Mercury Toxicity and the Mitigating Role of Selenium

Mercury is a well-known environmental toxicant, particularly in its most common organic form, methylmercury. Consumption of fish and shellfish that contain methylmercury is a dominant source of mercury exposure in humans and piscivorous wildlife. Considerable efforts have focused on assessment of mercury and its attendant risks in the environment and food sources, including the studies reported in this issue. However, studies of mercury intoxication have frequently failed to consider the protective effects of the essential trace element, selenium. Mercury binds to selenium with extraordinarily high affinity, and high maternal exposures inhibit selenium-dependent enzyme activities in fetal brains. However, increased maternal dietary selenium intakes preserve these enzyme activities, thereby preventing the pathological effects that would otherwise arise in their absence. Recent evidence indicates that assessments of mercury exposure and tissue levels need to consider selenium intakes and tissue distributions in order to provide meaningful risk evaluations.     

Toenail mercury concentration as a biomarker of methylmercury exposure

The aim of the study was to assess the value of toenail mercury as an alternative biomarker of methylmercury exposure compared with blood and hair. Blood, hair and toenail total mercury concentrations were determined simultaneously in a southern urban sea n = 35 and an eastern rural lake n = 37 group and separately in a central Finnish rural lake n = 39 group. A questionnaire based index was used for estimating frequency of exposure taking into account high vs low mercury fish. Total mercury concentration was determined by cold vapour atomic absorption spectrophotometry. The mean Fish Consumption Frequency Index varied from 4.7 to 9.9 on a scale of 1-20. The blood, hair and toenail mercury mean concentrations ranged from 2.9 to 14.6 g l-1, 0.45 to 1.57 mg kg-1 and 0.20 to 0.54 mg kg-1, respectively. In the combined southern and eastern groups n = 72 sampled simultaneously, the correlations between blood and hair mercury were r = 0.92 and that of blood and toenails r = 0.78 p 0.0001 . In the central Finnish group the correlations were more moderate. In the three groups all three biomarkers correlated highly with the fish consumption index, r = 0.43-0.76 p 0.0001 . Men consumed high mercury fish more frequently than women, 8.6 vs 6.6 n.s. . The mean mercury levels of blood and hair were two fold, but toenail mercury levels were only 30 higher in men compared with those of the women. The relative sensitivity slope of the sources decreased in the order, blood hair toenails. In conclusion, toenails, an easily accessible tissue for the estimation of methylmercury exposure, have been shown to be closely correlated with the well established samples for biomarkers, viz. blood and hair mercury.     

Toenail mercury concentration as a biomarker of methylmercury exposure

The aim of the study was to assess the value of toenail mercury as an alternative biomarker of methylmercury exposure compared with blood and hair. Blood, hair and toenail total mercury concentrations were determined simultaneously in a southern urban sea n = 35 and an eastern rural lake n = 37 group and separately in a central Finnish rural lake n = 39 group. A questionnaire based index was used for estimating frequency of exposure taking into account high vs low mercury fish. Total mercury concentration was determined by cold vapour atomic absorption spectrophotometry. The mean Fish Consumption Frequency Index varied from 4.7 to 9.9 on a scale of 1-20. The blood, hair and toenail mercury mean concentrations ranged from 2.9 to 14.6 g l-1, 0.45 to 1.57 mg kg-1 and 0.20 to 0.54 mg kg-1, respectively. In the combined southern and eastern groups n = 72 sampled simultaneously, the correlations between blood and hair mercury were r = 0.92 and that of blood and toenails r = 0.78 p 0.0001 . In the central Finnish group the correlations were more moderate. In the three groups all three biomarkers correlated highly with the fish consumption index, r = 0.43-0.76 p 0.0001 . Men consumed high mercury fish more frequently than women, 8.6 vs 6.6 n.s. The mean mercury levels of blood and hair were two fold, but toenail mercury levels were only 30 higher in men compared with those of the women. The relative sensitivity slope of the sources decreased in the order, blood hair toenails. In conclusion, toenails, an easily accessible tissue for the estimation of methylmercury exposure, have been shown to be closely correlated with the well established samples for biomarkers, viz. blood and hair mercury.     

Methylmercury distribution, metabolism, and neurotoxicity in the mouse brain

Methylmercury distribution, biotransformation, and neurotoxicity in the brain of male Swiss albino mice were investigated. Mice were orally dosed with [203 Hg]methylmercury chloride (10 mg/kg) for 1 to 9 days. Methylmercury was evenly distributed among the posterior cerebral cortex, subcortex, brain stem, and cerebellum. The The anterior cerebral cortex had a significantly higher methylmercury concentration than the rest of the brain. The distribution of methylmercury's inorganic mercury metabolite was found to be uneven in the brain. The pattern of distribution was cerebellum greater than brain stem greater than subcortex greater than cerebral cortex. The order of the severity of histological damage was cerebral cortex greater than cerebellum greater than subcortex greater than brain stem. There was no correlation between methylmercury distribution in the brain and structural brain damage. However, there was a relationship between the distribution of methylmercury's inorganic mercury metabolite and structural damage in the anterior cerebral cortex (positive correlation) and the anterior subcortex (negative correlation). There was also a positive correlation between the fraction of methylmercury's metabolite of the total mercury present and structural brain damage in the anterior cerebral cortex. This study suggests that biotransformation may have a role in mediating methylmercury neurotoxicity.     

Efficacy of Translators for Establishing Mercury Total Maximum Daily Loads

In Oregon's Willamette River, methylmercury levels in fish triggered health advisories and the need for a mercury Total Maximum Daily Load (TMDL). A translator was used to relate surface water total mercury (C_THg) to dissolved methylmercury concentrations (C_DMeHg). The USEPA's Spreadsheet-based Ecological Risk Assessment for the Fate of Mercury (SERAFM) was used to elucidate the annual relationship between mercury loads, C_THg, and C_DMeHg, to investigate whether C_THg is a reasonable predictor for C_DMeHg, and to consider how load reductions may be affected by the differing annual trajectories of total and methylmercury concentrations. Modeling and observations suggest that C_THg and C_DMeHg are not directly proportional, that C_THg is an inconsistent predictor of C_DMeHg, that a single point estimate translator could easily misjudge their relationship, and that C_DMeHg may be more responsive to environmental factors than to load alone. While a translator is convenient for relating C_THg and C_DMeHg for regulatory purposes, it may not, due to environmental factors unrelated to loading, be the most efficacious means for this purpose. TMDLs relying on a translator are advised to conduct co-located total and methylmercury sampling with sufficient frequency to provide information on the watershed-specific annual relationship between total mercury and methylmercury.