Mercury exposure during early human development

Sammanfattning: People are exposed to methylimercury (MeHg) mainly via consumption of fish, especially large predatory fish species. Inhaled mercury vapour (Hg0) released from dental amalgam fillings is the main source of exposure to inorganic mercury (I-Hg). In the body, a small fraction of MeHg is demethylated to inorganic He while most Hg0 is oxidized to Hg2+. Both MeHg and Hg2+ are neurotoxic, especially for the developing brain. The aim of the present thesis was to increase the knowledge about the exposure to MeHg and I-Hg in Swedish women of childbearing age, the transport to the fetus and infant and to evaluate possible associations between Se, an antioxidant reported to protect against Hg toxicity; and the different forms of Hg. Hg exposure during pregnancy was studied by determination of total Hg in maternal hair and MeHg and I-Hg in maternal blood. Fetal exposure was assessed by MeHg and I-Hg in cord blood. Infant exposure was assessed by MeHg and I-Hg in infant blood and total Hg in breast milk. The concentrations of MeHg and I-Hg were determined by cold vapour atomic fluorescens spectrophotometry (CVAFS). Se concentrations in scrum or whole blood were analysed by graphite furnace atomic absorption spectrophotometry (GFAAS). The exposure to I-Hg was mainly as Hg0 from dental amalgam fillings with low exposure from oilier sources. The concentration of I-Hg in cord blood was about the same as in maternal blood and increased with increasing number of maternal dental amalgam fillings. This shows that a substantial fraction of Hg0 passes the placenta to the fetus before being oxidized to Hg2+. Also, I-Hg accumulated in the placenta in relation to the number of amalgam filings. The use of amalgam in dentistry is decreasing. MeHg exposure was highly dependent on fish consumption in general, but consumption of freshwater fish and certain marine species e.g. swordfish and tuna contributed more to the exposure. MeHg in cord blood increased with increasing maternal fish consumption. It was almost twice the concentration in maternal blood, supporting an active transport of MeHg across the placenta. Although, the average exposure to MeHg was relatively low, there was quite a range. A small fraction of women recruited because of high fish consumption had Hg concentrations exceeding the RfD (U.S. EPA) and PTWI (JECFA), corresponding to a daily intake of0. 1-0.2 µg MeHg/kg bw. Thus, there seems to be a fairly narrow margin of safety for increased risk of neurodevelopmental effects in fetus of women with high fish consumption unless they decrease their intake of certain fish species before being pregnant. It can be concluded that the recently updated dietary advisories on fish consumption for pregnant and lactating women and women planning pregnancy are justified and necessary as long as MeHg levels in fish are elevated. There was a good compliance to the dietary advisories regarding fish consumption during pregnancy but it is important that the advisories reach all women planning pregnancy, so they can decrease their consumption of certain fish species to avoid early fetal exposure. However, it is also important to emphasize the benefits of fish consumption. It is not known to what extent the positive effects of fish consumption may outweigh the negative effects of MeHg. Infant exposure to I-Hg and MeHg was lower than the prenatal exposure. Total Hg concentrations in breast milk decreased during the first three months postpartum. I-Hg seems to be more easily transported to breast milk than MeHg. Still, MeHg in breast milk may contribute more to infant exposure, because of higher gastrointestinal absorption. Infant blood MeHg decreased until 13 weeks of age indicating that infants are able to excrete MeHg taken up during fetal life, contrary to previous believes. No associations between Se and the different forms of Hg were observed in the placenta and Se did not affect the accumulation or transport of I-Hg or MeHg in placenta. The concentration of Se in serum decreased during the course of pregnancy. Probably, this can partly be explained by a prioritized fetal transport and need of Se for placental functions.