Low-dose mercury exposure in early life: relevance of thimerosal to fetuses, newborns and infants

Abstract

This review explores the different aspects of constitutional factors in early life that modulate toxicokinetics and toxicodynamics of low-dose mercury resulting from acute ethylmercury (etHg) exposure in Thimerosal-containing vaccines (TCV). Major databases were searched for human and experimental studies that addressed issues related to early life exposure to TCV. It can be concluded that: a) mercury load in fetuses, neonates, and infants resulting from TCVs remains in blood of neonates and infants at sufficient concentration and for enough time to penetrate the brain and to exert a neurologic impact and a probable influence on neurodevelopment of susceptible infants; b) etHg metabolism related to neurodevelopmental delays has been demonstrated experimentally and observed in population studies; c) unlike chronic Hg exposure during pregnancy, neurodevelopmental effects caused by acute (repeated/cumulative) early life exposure to TCV-etHg remain unrecognized; and d) the uncertainty surrounding low-dose toxicity of etHg is challenging but recent evidence indicates that avoiding cumulative insults by alkyl-mercury forms (which include Thimerosal) is warranted. It is important to a) maintain trust in vaccines while reinforcing current public health policies to abate mercury exposure in infancy; b) generally support WHO policies that recommend vaccination to prevent and control existing and impending infectious diseases; and c) not confuse the 'need' to use a specific 'product' (TCV) by accepting as 'innocuous' (or without consequences) the presence of a proven 'toxic alkyl-mercury' (etHg) at levels that have not been proven to be toxicologically safe.