Translate this page to any language by choosing a language in the box below.

Mercury/Methyl Mercury

What to do if you have a mercury spill

The heavy metal, mercury (Hg), is a known toxicant that is generated by anthropogenic activities. One of the most significant consequences of mercury pollution is that aquatic organisms can absorb mercury, convert it to methyl mercury and accumulate it in their tissues leading to increasing concentrations in the food chain. This means if you eat a lot of fish, particularly larger fish which are higher up the food chain, you may be ingesting a fair amount of methyl mercury.

Chronic mercury poisoning due to organic mercury ingestion is primarily a central nervous system problem, whereas inorganic mercury poisoning is essentially a renal problem. This is due to their differences in disposition and metabolism, i.e. the lipid solubility of organic mercury, its easy transport across the blood-brain barrier and its conversion in the brain (as well as in other cells) to the highly toxic mercuric ion by catalase. Moreover, unlike mercurous and mercuric ions, metallic mercury and methyl mercury (MeHg) are able to cross the placenta and be concentrated in the fetus, making them highly neurotoxic for the fetus. The NIEHS supports grants investigating the possible deleterious effects of inorganic (mercuric) and/or organic mercury on the brain, kidney and immune system in epidemiological as well as mechanistic studies.

Two studies supported by NIEHS are especially relevant since they are examining the effects of chronic low level MeHg in children exposed because of a marine diet. Both cohorts have been exposed to MeHg primarily pre- as well as post-natally.

This cohort resides in the Seychelles Island and is homogenous for a variety of cultural and socioeconomic factors that normally are confounders of the neurocognitive tests being used to measure effects. The project is a longitudinal study in which the MeHg exposure of a cohort of children has been followed prenatally to the current age of 66 months. The study established that the amount of MeHg found in mother's hair during pregnancy correlates well with the Hg level in prenatal brain as determined by the autopsy of the brains of 22 stillborns. The MeHg exposure levels, as measured in maternal hair at delivery, range from 0.5-27 ppm with a median of 6.8 ppm. The battery of tests done on these children (McCarthy Scales, Woodcock Johnson Achievement Test, Preschool Language Scale, Bender Gestalt, Achenbach Child Behavior Checklist, Children's Ravens, Digit Symbol),while better at picking up mental deficiency than neurocognitive deficits, are similar to the ones used in longitudinal lead studies. Thus far, the investigators have not measured any detrimental outcomes at age 5 � years that correlate with low level MeHg exposure, (Clarkson; P01ES05197)

Grandjean (R01ES061123) is performing a longitudinal study in a cohort residing in the Faeroe Islands that is also homogenous for a number of factors that can be confounders for the outcome measures being used. Exposure was measured by MeHg concentrations in cord blood and maternal hair. The children have been followed to the current age of 82-84 months. The Hg in maternal hair ranged from 0.2-40 ppm with a median of 4.5 ppm in hair and 22.9ug/g in cord blood. While several of the test instruments were the same as those used in the Seychelles, others used only in the Faroes study were chosen because they were more suited to older children (California Verbal Learning Test, Boston Naming Test, WISC Block Design, Digit Learning, Mood Scale Tactual Performance, Computerized Psychological Test, Finger Tapping, Hand Eye Coordination, Continuous Performance Test, Evoked Potential). The tests measured neurocognitive developmental deficits rather than mental deficiency. Whereas most of the test scores for the cohort are within the normal range, the results show a change in long-term recall measurements that correlates well with MeHg levels in cord blood but not as well with maternal hair Hg. The investigators maintain that the types of subtle changes they see on their test results indicate an effect of Hg in several areas of the brain.

There may be several reasons for the different results in the two studies:

• Some of the measurement instruments are different. The ones in which an effect was found in the Faeroes cohort were not used in the Seychelles.
• The oldest children in the Seychelles study are 5 � years old while in the Faeroes Island study they are 7 years of age. The tests used in the Faeroes are better suited to older children and it is easier to do neurocognitive testing in school age children.
• The diet in the Faeroes may expose the children to another known neurotoxicant, PCBs, depending on how much whale blubber their mothers consumed during pregnancy. There is no PCB exposure in the Seychelles. PCB exposure may be contributing to some of the Faeroes test results. In fact, the investigators show excellent correlation between PCB exposure and adverse performance on the Boston Naming Test in the Faeroes study.
• Using cord blood Hg as the correlative exposure indicator in the Faeroes study may miss high first trimester fetal exposure to Hg thereby influencing the results.

In order to resolve the issue of whether low-level MeHg exposure causes developmental delays, the Seychelles study will be continued so that the cohort can be tested at age 7 years with some of the same instruments used in the Faeroes study and a new cohort on the Faeroes will be examined for the relationship between PCB exposure and neurocognitive function.

Back to top