INTRODUCTION

We cannot study the neurotoxic effects of mercury during the primal period without updating a series of related hot topics:

• the maternal intake of sea-fish
• pollution in  human milk
• the use of dental amalgams
• the use of vaccines containing mercury derivatives

The paramount importance of these issues is obvious because the brain is the primary target tissue for mercury and there is a brain growth spurt during the primal period. At the age of one year (end of the primal period) the brain size of Homo Sapiens is 75% of the adult size.

CONSUMPTION OF SEA FISH

The enormous advantages for the offspring of the consumption of sea fish by the mother are not purely theoretical. A Danish study classified 8729 pregnant women according to their dietary habits, and particularly their fish intake.(1) The rates of prematurity varied from 1.9% in the group eating fish at least once a week to 7.1% in the zero consumption group. The same outcome was noted for low birth weight. Since prematurity and low birth weight increase mortality, morbidity and life long handicap, this study must be considered important. 'Today one can claim that low consumption of seafood is the best-known risk factor for preterm delivery'.(2) According to our own study, one of the effects of encouraging pregnant women to eat sea fish is to increase the average head circumference at birth, a valid marker of brain development from a statistical point of view.(3) We could not detect any significant effect in terms of birth weight and duration of pregnancy, probably because our dietary recommendations occurred too late (around 15 weeks gestation). We must emphasize that the authors of the Danish study assessed dietary habits that preceded to a great extent the beginning of pregnancy.(4)

In general the populations with high intakes of sea fish are in a favorable position by  all health criteria. Seafood consumption per person per year in a country can be calculated as total catch plus imports minus exports.(5) One can assume that fish consumption of pregnant women in a given country is closely related to the national consumption. Children at age 9 years in the Seychelles compare favorably with US norms in terms of neurocognitive, language, memory, motor, perceptual-motor, and behavioral functions. In this particular population mothers reported consuming fish on average 12 meals a week.(6) A series of studies have established that not only the rates of cardiovascular disease, but also the rates of certain psychiatric disorders are inversely correlated with the consumption of fish. A cross-national comparison of manic-depressive disorders (bipolar disorder) is highly demonstrative.(7)

In reality, when taking into account such easily accessible hard data, one might anticipate that pregnant women are encouraged to eat sea fish. It is not so. In many countries, pregnant women are much more familiar with recommendations that they should limit their consumption of fish because of concerns about mercury contamination. In the USA, a well-publicized January 2001 Federal Advisory(8) was followed by a sharp decline in fish consumption among pregnant women(9) while the rates of prematurity in North America are on the increase...

In order to interpret the current paradoxical situation, we must start from a preliminary and inevitable question: 'Do the advantages of sea fish consumption in pregnancy outweigh the risks associated with mercury pollution?'

WHAT HEALTH PROFESSIONALS SHOULD BE IN A POSITION TO EXPLAIN

Among humans, the sole source of exposure to the organic form called methyl mercury is the consumption of sea fish and sea mammals. Methyl mercury inhibits the division and migration of nerve cells and disrupts the cytoarchitecture of the developing brain.(10)

The origin of methyl mercury in the sea food chain is well understood. In nature, mercury vapor (Hg0), a stable gas, evaporates from the earth's surface (both soil and water) and is emitted by volcanoes and human activities (such as coal-burning power stations and municipal incinerators). After approximately one year, mercury vapor is converted to a soluble form (Hg2+) and returned to the earth in rainwater. It may be converted back to vapor form both in soil and in water by microorganisms and reemitted into the atmosphere. Thus, mercury may recirculate for long periods. Mercury attached to aquatic sediments is subject to microbial conversion to methyl mercury, whereupon it enters the aquatic food chain.

Two important points must be emphasized. The first one is that mercury levels depend on the rank of the fish in the sea food chain. At each step of the food chain, the mercury level is multiplied by a certain coefficient. This implies that small fish like anchovies, sardines, pilchards, herrings, the common mackerels, the small 'light' tuna, for example, may be considered safe in terms of mercury content. They are also the best in terms of long chain omega 3 polyunsaturated fatty acids, quality of proteins and mineral content. The mercury levels in such fish, if detectable, is not more than a small fraction of one 'part per million' (ppm). The fish with the highest mercury levels (in the region of one ppm) belong to species at the end of the food chain, like swordfish, tilefish, king mackerel and sharks. The levels are also high in carnivorous sea mammals. Tuna fish are in an intermediate situation: according to a FDA evaluation (December 2003) the levels in the Albacore 'white' canned tuna are 0.358 ppm versus 0.123 ppm in the smaller 'light' tuna.

It is noticeable that the US January 2001 federal advisory is derived from reports of subtle and small neuropsychological changes in children in the Faroe Islands, where the diet of the mothers was high in pilot-whale blubber and meat.(11) Similar findings have been reported in a small study of children in a New Zealand population eating sharks. (12) In countries such as the USA, we would expect public health organizations to focus on the Seychelles child development study, because fish in Seychelles contain much the same concentrations of methyl mercury as commercial fish usually consumed in North America and Western Europe. What is special to these islands (in the middle of the Indian Ocean) is that most people eat fish at every meal and that the neuro-intellectual, motor and behavioral functions of 9 year-old children have been well-documented as excellent.(6)

The second important point is that the kind of methyl mercury found in fish has been determined in 2003 for the first time.(13) Scientists working at the Stanford Synchrotron Radiation laboratory used a technique involving high-intensity X-rays to investigate the nature of mercury molecules in samples of swordfish, orange roughy and sand sole. It appeared that methyl mercury found in fish is mostly methyl mercury cysteine, while previous models of mercury toxicity had been based on methyl mercury chloride. This fact is of paramount importance, because cysteine is one of the few amino-acids that contains sulfur. Methyl mercury has a high affinity for sulfhydryls, reacting inside the cells with the sulfhydryl group on cysteine. This allows transport of mercury out of the cells. Cysteine (and N-acetyl cysteine) have been studied for their capacity to remove toxic metals from the body ('oral chelation'). These theoretical considerations will probably be supported by further research. We already know that tiny zebra fish larvae tolerate methyl mercury cysteine better than the chloride form.

Our current understanding of the molecular identity of mercury in fish should also attract the attention of anyone interested in species evolution. Mercury is not a man-made substance.  There has been methyl mercury in the sea food chain for hundreds of millions of years. That is why the issue of mercury pollution is radically different from the issue of pollution by man-made molecules that appeared during the twentieth century (PCBs, dioxins, etc.). During a long period of evolution fish had the time to adapt to the presence of methyl mercury in their environment. Combining mercury with cysteine, a substance that can remove toxic metals from the body, was the most logical strategy the evolutionary process could adopt. It is probable that the methyl mercury in cetaceans has a different molecular identity, because sea mammals appeared 'recently' (around 80 millions years ago) among the marine animal species.

From a practical point of view, we can claim today that the advantages of sea fish consumption in pregnancy outweigh by far the theoretical risks associated with mercury contamination. However it is wise to avoid the long-lived predatory fish such as swordfish and shark. A simple rule of thumb: 'Eat sardines. Don't eat sharks'.

BREAST-MILK LEVELS IN MERCURY

The levels of mercury in the mother's blood are generally about three times higher than the levels in milk. Furthermore exposure to mercury after birth occurs comparatively late in the development of human beings. These are the first reasons why exposure via breast-milk is probably less important than prenatal exposure.

Two major forms of mercury can enter breast milk. Methyl mercury does not enter breast milk at high rates because it is attached to red blood cells. But the small amount in breast milk is easily absorbed in the intestine of a nursing infant. The second form, inorganic mercury, enters breast milk easily but is not well absorbed in the baby's digestive tract.

From a series of German and Swedish studies (14,15,16) we can conclude that the mercury in human milk during the first weeks of breastfeeding is primarily inorganic mercury from dental amalgam fillings in the mother's mouth. However, after two months of lactation, mercury found in milk is primarily methyl mercury. A Swedish study conducted 6 weeks after birth (14) found no significant correlations between the levels of any form of mercury in milk and the levels of organic mercury in blood.

The results indicate that there is an efficient transfer of inorganic mercury from blood to milk and that amalgam fillings are the main source of mercury in milk. These data must be viewed in perspective. They lead to the conclusion that the advantages of breastfeeding outweigh the theoretical risks associated with mercury pollution, even for mothers with a large number of dental amalgam fillings. They also indicate that we cannot dissociate the questions raised by mercury in human milk and those related to the use of dental amalgams.

THE USE OF DENTAL AMALGAMS

Dental amalgams have been in use for over 150 years. They are inexpensive and thought to be more durable and easier to use than other types of fillings. The weight composition of these amalgams is typically 50 percent elemental mercury metal, combined with other metals such as silver and copper. Since their introduction, dental amalgams have been a source of controversy because of the assumed health risks of mercury. The 'amalgam wars' became heated around 1970 with the discovery that amalgams can release mercury vapor into the mouth in concentrations that are higher than those deemed safe by occupational health guidelines. It is now well established in humans that the continuous release of mercury vapor from amalgams is markedly increased for prolonged periods after chewing or tooth brushing and that the levels of mercury vapor in the mouth are correlated with the number of such fillings.(17,18,19,20)

The absorption and maternal-fetal distribution of mercury released from amalgams have been widely studied in sheep with radioactive mercury. A first study has demonstrated that mercury vapor is initially absorbed at lung, gastrointestinal, and jaw tissue sites. (21) In another study ewes had twelve amalgams placed in teeth at 112 days gestation.(22) Results demonstrated that mercury appears in maternal blood and amniotic fluid within 2 days, and that excretion of this mercury also begins within 2 days. Highest concentrations in the adult occur in kidney and liver, whereas in the fetus the highest concentrations appear in liver and pituitary gland. The placenta progressively concentrates the metal. In another study, lactating ewes nursed foster lambs, to dissociate prenatal exposure and postnatal exposure.(23) According to this study the liver is a primary fetal site of mercury concentration, and, after delivery, the lamb kidney receives additional mercury from mother's milk.

A synthesis of the relevant medical and scientific literature leads to the conclusion that dental amalgam usage as a tooth restorative material in pregnant women and children should be reconsidered and that placement and removal of amalgams in pregnant and lactating women will subject the fetus and neonate to unnecessary risk of mercury exposure."

THE USE OF VACCINES CONTAINING A MERCURY DERIVATIVE

In many countries, babies are exposed to ethyl mercury through vaccination. This organic form of mercury is the active ingredient of the preservative thimerosal, which has been used in many vaccines since the 1930s. In thimerosal the ethyl mercury radical is attached to the sulfur group of thiosalicylate. Although ethyl mercury has been known for a long time as a poison, and used as a fungicide, early toxicity studies of this preservative found no adverse health effects. However thimerosal was recently reevaluated in the USA by applying the guidelines for methyl mercury to ethyl mercury.(24) It has been calculated that infants undergoing the usual US program of vaccines from birth to six months of age would receive more than 0.1 ƒÊg of mercury per kilogram per day. Steps were rapidly taken to remove thimerosal from vaccines by switching to single-dose vials that do not require any preservative. Today, all routinely recommended licensed pediatric vaccines that are currently being manufactured for the US market contain no thimerosal or only trace amounts.

The attitudes are different in many other countries. In 2002 the Global Advisory Committee on vaccine safety of World Health Organization (WHO) stated that there is no evidence of toxicity in infants exposed to thimerosal in vaccines.(25) Personal comment: the sentence 'there is no evidence of toxicity' does not mean 'there is evidence of safety'! The committee took into account that the pharmacokinetic profile of ethyl mercury is substantially different from that of methyl mercury. They emphasized that the half-life of ethyl mercury is only a week, while it is about 50 days for methyl mercury. The current official conclusion of WHO is that there is no reason, on grounds of safety, to change the current immunization practices with thimerosal-containing vaccines, since the benefits outweigh any unproven risks.

The complexity of this issue is illustrated by the abundant correspondence that followed an article in The Lancet about mercury concentrations and metabolism in vaccinated children.(26) It was even mentioned that thimerosal might have irreversible genotoxic effects apart from those produced by mercury or ethyl mercury.(27)

In the countries where thimerosal-containing vaccines are still in use, we can understand the confusion of some parents. They have additional reasons to try to reduce the list of vaccines, or to postpone some of them, or to select trademarks that are thimerosal-free. They can wonder, for example, if the primal period is the ideal time to vaccinate against hepatitis B, which is mostly a sexually transmitted disease, or against diphtheria, in countries where the disease has disappeared, or even haemophilus influenza type B (2.81 cases per 100 000 in the UK in 2002 among children aged 1-4 years). Let us recall that thimerosal-containing vaccines include trademarks of diphteria - tetanus - pertussis vaccines, hepatitis B and Haemophilus influenzae type-B vaccines. It had been suggested that thimerosal-containing vaccines could be causally related to autism. This hypothesis is not supported by a study involving all children born in Denmark from January 1990 until December 1996 (nearly half a million).(28) The risk of autism and other autistic-spectrum disorders was the same among children vaccinated with thimerosal-containing vaccine and children vaccinated with thimerosal-free vaccine.

Until recently, Rh negative pregnant women were usually injected anti-D immunoglobulins associated with thimerosal. Today the main trademarks are thimerosal-free (e.g. RhoGAM, WINRho SDF, BayRho)

The last important issue is influenza vaccination of pregnant women. The majority of influenza vaccines contain thimerosal. However, some contain only trace amounts and are considered to be preservative-free. Manufacturers of preservative-free flu vaccine (Evans vaccines and Aventis Pasteur) use thimerosal early in the manufacturing process. The thimerosal gets diluted as the vaccine goes through the steps in processing. By the end of the manufacturing process there is not enough thimerosal left to act as a preservative and the vaccine is labeled 'preservative-free'. We must keep in mind a study (included in Primal Health Research data bank) of all child deaths from cancer in the UK during the period 1953 to 1959 (8059 cases matched with the same number of controls). Influenza vaccine in pregnancy appeared as a risk factor for cancer in childhood.(29)

This overview reveals that human beings are currently exposed to at least three sorts of mercury during their initial and crucial phases of development. The sources of two of them - inorganic mercury and ethyl mercury - are mostly iatrogenic. They can be eliminated.

REFERENCES

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2. Odent M. Risk factors for preterm delivery. Lancet 2003; 361: 436. -    

3. Odent MR, McMillan L, & Kimmel T. Prenatal care and sea fish. Eur J Obstetr Gynecol Reproduct Biol 1996; 68: 49-51. 

4. Odent M, Colson S, & De Reu P. Consumption of sea food and preterm delivery: Encouraging pregnant women to eat fish did not show effect. BMJ 2002; 324: 1279.

5. World Health Organization: Fish and fishery products: World apparent consumption based on food balance sheets (1961-1993). Rome, WHO Food and Agriculture Organization, 1996.

6. Myers GJ, Davidson PW, Cox C, et al. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Lancet 2003; 361: 1686-92.

7. Noaghiul S, & Hibbeln JR. Cross-National comparisons of seafood consumption and bipolar disorders. Am J Psychiatry 2003; 160: 2222-27.

8. Environmental Protection Agency, January 2001. (EPA-823-R-01-001).

9. Oken E, Kleinman KP, et al. Decline in fish consumption among pregnant women after national mercury advisory. Obstet. Gynecol. 2003; 102: 346-51.

10. Clarkson TW, Magos L, & Myers GJ. The toxicology of mercury: Current exposures and clinical manifestations. N Eng J Med 2003; 349: 1731-37.

11. Sorensen N, Murata K, et al. Prenatal methylmercury exposure as a cardiovascular risk factor at seven years of age. Epidemiology 1999: 10: 370-75.

12. Crump KS, Kjellstrom T, et al. Influence of prenatal mercury exposure upon scholastic and psychological test performance: Benchmark analysis of a New Zealand cohort. Risk Anal 1998; 18: 701-713.

13. Clarkson TW, Magos L, & Myers GJ. The toxicology of mercury: Current exposures and clinical manifestations. N Eng J Med 2003; 349: 1731-37.

14. Oskarsson A, Schultz A, et al. Total and inorganic mercury in breast milk in relation to fish consumption and amalgam in lactating women. Arch Env Health 1996; 51(3): 234-241.

15. Drasch G, Aigner S, et al. Mercury in human colostrum and early breast milk. Its dependence on dental amalgam and other factors. J Trace Elem Med Biol 1998; 12(1): 23-7.

16. Drexler H, & Schaller KH. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Environ Res 1998; 77(2): 124-9.

17. Patterson JE, Weissberg BG, & Dennison PJ. Mercury in human breath from dental amalgam. Bull Environ Contam 1985; 34: 459-68.

18. Svare CW, Peterson JW, et al. The effects of dental amalgams on mercury levels in expired air. J Dent Res 1981; 60: 1668-71.

19. Vimy MJ, & Lorscheider FL. Intra-oral air mercury released from dental amalgam. J Dent Res 1985; 64: 1069-71.

20. Vimy MJ, & Lorscheider FL. Serial measurements of intra-oral air mercury: estimation of daily dose from dental amalgam. J Dent Res 1985; 64: 1072-75

21. Hahn LJ, Kloiber MJ, et al. Dental 'silver' tooth fillings: A source of Hg exposure revealed by whole-body image scan and tissue analysis. FASEB J 1989; 3: 2641-2646.

22. Vimy MJ, Takahashi Y, & Lorscheider FL. Maternal-fetal distribution of mercury released from dental amalgam fillings. Am J Physiol 1990; 258: R939-R945.

23. Vimy MJ, Hooper DE, King WW, & Lorscheider FL. Mercury from maternal "silver" tooth fillings in sheep and human breast milk. A source of neonatal exposure Biol Trace Elem Res 1997; 56(2):143-152.

24. Ball LK, Ball R, & Pratt RD. An assessment of thimerosal use in childhood vaccines. Pediatrics 2001; 107: 1147-1154.

25. Vaccines and biologicals: recommendations from the Strategic Advisory Group of experts. Wkly Epidemiol Rec 2002; 77: 305-312.

26. Pichichero ME, Cernichiari E, et al. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: A descriptive study. Lancet 2002; 360: 1737-41.

27. Westphal GA, Asgari S, et al. Thimerosal induces micronuclei in the cytochalasin B-block micronucleus test with human lymphocytes. Arch Toxicol 2003; 77: 50-55.

28. Hviid A, Stellfield M, et al. Association between thimerosal-containing vaccine and autism  JAMA 2003; 290(13): 1763-66.

29. Gilman EA, Kinnier M, et al. Childhood cancers and their association with pregnancy drugs and illnesses. Paediatr and Perinatal epidemiol 1989; 3: 66-94.

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