Chemosphere 139 (2015) 667–668
Contents lists available at ScienceDirect
Chemosphere journal homepage: www.elsevier.com/locate/chemosphere
Letter to the editor The neurological effects of prenatal and postnatal exposure to mercury need to include ethylmercury
Hsi et al. (2014) is a study deserves the attention of environmental scientists interested in early-life exposure and neurodevelopment effects of Hg, and Chemosphere is commended for featuring such an important paper. Hsi et al. measured total and methyl-mercury in all relevant (non-invasive) tissues (including meconium, hair, fingernail, and toenail) in order to link it to neurodevelopment in young children. However, in relation to both pre- and postnatal periods, they did not include ethylmercury exposure in Thimerosal-containing vaccines (TCVs) likely to have been taken by mothers (during pregnancy) and or by the child during the ‘‘neonatal, infant, and toddler periods’’. They rightly pointed out that prenatal and postnatal exposure represented by low-level hair-Hg in children may affect growth and development. However, an important source of exposure related to TCVs, still used in China and possibly in Taiwan, was not considered in the model. Their diligent study would make an even better contribution if we were informed of this type of exposure during pregnancy and postnatal or had they included it in the statistical model. TCVs such as the hepatitis-B vaccine (HBV) are administered on the very first postnatal day and are followed by other TCVs with respective booster shots (Dórea, 2007). There is a possibility that TCVs other than HBV and DTP could be taken by pregnant mothers and children, like seasonal flu and H1N1, depending on the season. These additional exposures could elevate ethylmercury (etHg) exposure beyond the 118.5 expected from the regular infant immunization schedule during the first six months (Dórea, 2007). Why does it matter? Major studies addressing etHg exposure and neurodevelopment started to appear only in the last ten years (Dórea, 2010), and only in high-income countries (the USA, the UK, and Italy). For the most part, these results were inconclusive and in some cases conflicting (Dórea, 2010). More recent studies that include etHg in the statistical strategy to assess neurodevelopment consistently showed that TCV can negatively influence test results. Real-life scenarios are likely to have more than one neurotoxic exposure relevant to the early life (pregnancy and lactation) period. In studies from different parts of the world, controlled variables were age of neurodevelopment test evaluation and sources of environmental neurotoxic (fish-meHg, polluted mining environment) exposure (Dórea et al., 2012, 2014; Marques et al., 2014) such as in Brazil. The source of environmental exposure in Korea was second hand smoke (Lee and Ha, 2012), while in Poland controlled variables were second hand smoke, and cord-blood concentrations of Hg and Pb (Mrozek-Budzyn et al., 2012).
http://dx.doi.org/10.1016/j.chemosphere.2014.06.045 0045-6535/Ó 2014 Elsevier Ltd. All rights reserved.
It is pertinent to mention that additionally to etHg, TCVs are adjuvanted with Al to increase antigenicity. TCVs carry considerable amounts of Al (1.0–1.5 mg mL 1) and Thimerosal 0.01% with an Al:Hg ratio of 50 (Wang et al., 2012); even in Thimerosal-free individual doses the Al concentration remains the same. In such cases, it is impossible to disentangle any specific effect (from etHg or from Al), but these circumstances make populations such as the one studied by Hsi et al. exposed to multiple hits (methylmercury, ethylmercury, aluminum), which increases the chances of developmental delays as measured by BSDI II (Marques et al., 2014). Finally, Table 6 did not list the number of children in the subgroups of high and low fish-eaters. Although it is not in dispute that meHg is negatively correlated with neurological development, it is possible that measured biomarkers of exposure may be due to unaccounted sources of Hg in the rice-based diet commonly consumed in China (Rothenberg et al., 2013) but not discussed by Hsi et al. Finally, in view of the health benefits of fish consumption, we need to be sensitive about all forms (ethylmercury and methylmercury) of Hg as well as all sources of exposure (TCVs, fish, and rice) that might pose risks of neurodevelopmental delays.
References Dórea, J.G., 2007. Exposure to mercury during the first six months via human milk and vaccines: modifying risk factors. Am. J. Perinatol. 24, 387–400. Dórea, J.G., 2010. Making sense of epidemiological studies of young children exposed to thimerosal in vaccines. Clin. Chim. Acta 411, 1580–1586. Dórea, J.G., Marques, R.C., Isejima, C., 2012. Neurodevelopment of Amazonian infants: antenatal and postnatal exposure to methyl- and ethylmercury. J. Biomed. Biotechnol., 132876. Dórea, J.G., Marques, R.C., Abreu, L., 2014. Milestone achievement and neurodevelopment of rural Amazonian toddlers (12 to 24 months) with different methylmercury and ethylmercury exposure. J. Toxicol. Environ. Health Part A 77, 1–13. Hsi, H.C., Jiang, C.B., Yang, T.H., Chien, L.C., 2014. The neurological effects of prenatal and postnatal mercury/methylmercury exposure on three-year-old children in Taiwan. Chemosphere 100, 71–76. Lee, B.E., Ha, E.H., 2012. Response to commentary ‘‘Co-exposure and confounders during neurodevelopment: we need them in the bigger picture of secondhand smoke exposure during pregnancy’’. Environ. Res. 112, 235. Marques, R.C., Bernardi, J.V.E., Dórea, J.G., Moreira, M.F.R., Malm, O., 2014. Perinatal multiple exposure to neurotoxic (lead, methylmercury, ethylmercury, and aluminum) substances and neurodevelopment at six and 24 months of age. Environ. Pollut. 187, 130–135. Mrozek-Budzyn, D., Majewska, R., Kieltyka, A., Augustyniak, M., 2012. Neonatal exposure to Thimerosal from vaccines and child development in the first 3 years of life. Neurotoxicol. Teratol. 34, 592–597. Rothenberg, S.E., Yu, X., Zhang, Y., 2013. Prenatal methylmercury exposure through maternal rice ingestion: insights from a feasibility pilot in Guizhou Province, China. Environ. Pollut. 180, 291–298. Wang, L., Lei, D., Zhang, S., 2012. Acellular pertussis vaccines in China. Vaccine 30, 7174–7178.
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Letter to the editor / Chemosphere 139 (2015) 667–668
José G. Dórea Faculty of Health Sciences, Universidade de Brasília, C.P. 04322, 70919-970 Brasília, DF, Brazil Tel.: +55 61 3368 3575; fax: +55 61 3368 5853. E-mail address: [email protected] Available online 4 July 2014
Contents lists available at ScienceDirect
Chemosphere journal homepage: www.elsevier.com/locate/chemosphere
Letter to the editor The neurological effects of prenatal and postnatal exposure to mercury need to include ethylmercury
Hsi et al. (2014) is a study deserves the attention of environmental scientists interested in early-life exposure and neurodevelopment effects of Hg, and Chemosphere is commended for featuring such an important paper. Hsi et al. measured total and methyl-mercury in all relevant (non-invasive) tissues (including meconium, hair, fingernail, and toenail) in order to link it to neurodevelopment in young children. However, in relation to both pre- and postnatal periods, they did not include ethylmercury exposure in Thimerosal-containing vaccines (TCVs) likely to have been taken by mothers (during pregnancy) and or by the child during the ‘‘neonatal, infant, and toddler periods’’. They rightly pointed out that prenatal and postnatal exposure represented by low-level hair-Hg in children may affect growth and development. However, an important source of exposure related to TCVs, still used in China and possibly in Taiwan, was not considered in the model. Their diligent study would make an even better contribution if we were informed of this type of exposure during pregnancy and postnatal or had they included it in the statistical model. TCVs such as the hepatitis-B vaccine (HBV) are administered on the very first postnatal day and are followed by other TCVs with respective booster shots (Dórea, 2007). There is a possibility that TCVs other than HBV and DTP could be taken by pregnant mothers and children, like seasonal flu and H1N1, depending on the season. These additional exposures could elevate ethylmercury (etHg) exposure beyond the 118.5 expected from the regular infant immunization schedule during the first six months (Dórea, 2007). Why does it matter? Major studies addressing etHg exposure and neurodevelopment started to appear only in the last ten years (Dórea, 2010), and only in high-income countries (the USA, the UK, and Italy). For the most part, these results were inconclusive and in some cases conflicting (Dórea, 2010). More recent studies that include etHg in the statistical strategy to assess neurodevelopment consistently showed that TCV can negatively influence test results. Real-life scenarios are likely to have more than one neurotoxic exposure relevant to the early life (pregnancy and lactation) period. In studies from different parts of the world, controlled variables were age of neurodevelopment test evaluation and sources of environmental neurotoxic (fish-meHg, polluted mining environment) exposure (Dórea et al., 2012, 2014; Marques et al., 2014) such as in Brazil. The source of environmental exposure in Korea was second hand smoke (Lee and Ha, 2012), while in Poland controlled variables were second hand smoke, and cord-blood concentrations of Hg and Pb (Mrozek-Budzyn et al., 2012).
http://dx.doi.org/10.1016/j.chemosphere.2014.06.045 0045-6535/Ó 2014 Elsevier Ltd. All rights reserved.
It is pertinent to mention that additionally to etHg, TCVs are adjuvanted with Al to increase antigenicity. TCVs carry considerable amounts of Al (1.0–1.5 mg mL 1) and Thimerosal 0.01% with an Al:Hg ratio of 50 (Wang et al., 2012); even in Thimerosal-free individual doses the Al concentration remains the same. In such cases, it is impossible to disentangle any specific effect (from etHg or from Al), but these circumstances make populations such as the one studied by Hsi et al. exposed to multiple hits (methylmercury, ethylmercury, aluminum), which increases the chances of developmental delays as measured by BSDI II (Marques et al., 2014). Finally, Table 6 did not list the number of children in the subgroups of high and low fish-eaters. Although it is not in dispute that meHg is negatively correlated with neurological development, it is possible that measured biomarkers of exposure may be due to unaccounted sources of Hg in the rice-based diet commonly consumed in China (Rothenberg et al., 2013) but not discussed by Hsi et al. Finally, in view of the health benefits of fish consumption, we need to be sensitive about all forms (ethylmercury and methylmercury) of Hg as well as all sources of exposure (TCVs, fish, and rice) that might pose risks of neurodevelopmental delays.
References Dórea, J.G., 2007. Exposure to mercury during the first six months via human milk and vaccines: modifying risk factors. Am. J. Perinatol. 24, 387–400. Dórea, J.G., 2010. Making sense of epidemiological studies of young children exposed to thimerosal in vaccines. Clin. Chim. Acta 411, 1580–1586. Dórea, J.G., Marques, R.C., Isejima, C., 2012. Neurodevelopment of Amazonian infants: antenatal and postnatal exposure to methyl- and ethylmercury. J. Biomed. Biotechnol., 132876. Dórea, J.G., Marques, R.C., Abreu, L., 2014. Milestone achievement and neurodevelopment of rural Amazonian toddlers (12 to 24 months) with different methylmercury and ethylmercury exposure. J. Toxicol. Environ. Health Part A 77, 1–13. Hsi, H.C., Jiang, C.B., Yang, T.H., Chien, L.C., 2014. The neurological effects of prenatal and postnatal mercury/methylmercury exposure on three-year-old children in Taiwan. Chemosphere 100, 71–76. Lee, B.E., Ha, E.H., 2012. Response to commentary ‘‘Co-exposure and confounders during neurodevelopment: we need them in the bigger picture of secondhand smoke exposure during pregnancy’’. Environ. Res. 112, 235. Marques, R.C., Bernardi, J.V.E., Dórea, J.G., Moreira, M.F.R., Malm, O., 2014. Perinatal multiple exposure to neurotoxic (lead, methylmercury, ethylmercury, and aluminum) substances and neurodevelopment at six and 24 months of age. Environ. Pollut. 187, 130–135. Mrozek-Budzyn, D., Majewska, R., Kieltyka, A., Augustyniak, M., 2012. Neonatal exposure to Thimerosal from vaccines and child development in the first 3 years of life. Neurotoxicol. Teratol. 34, 592–597. Rothenberg, S.E., Yu, X., Zhang, Y., 2013. Prenatal methylmercury exposure through maternal rice ingestion: insights from a feasibility pilot in Guizhou Province, China. Environ. Pollut. 180, 291–298. Wang, L., Lei, D., Zhang, S., 2012. Acellular pertussis vaccines in China. Vaccine 30, 7174–7178.
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Letter to the editor / Chemosphere 139 (2015) 667–668
José G. Dórea Faculty of Health Sciences, Universidade de Brasília, C.P. 04322, 70919-970 Brasília, DF, Brazil Tel.: +55 61 3368 3575; fax: +55 61 3368 5853. E-mail address: [email protected] Available online 4 July 2014
