Domain-Specific Effects of Prenatal Exposure to PCBs, Mercury, and Lead on Infant Cognition: Results from the Environmental Contaminants and Child Development Study in Nunavik

By Boucher, Olivier; Muckle, Gina et al. | Environmental Health Perspectives, March 2014 | Go to article overview

Domain-Specific Effects of Prenatal Exposure to PCBs, Mercury, and Lead on Infant Cognition: Results from the Environmental Contaminants and Child Development Study in Nunavik


Boucher, Olivier, Muckle, Gina, Jacobson, Joseph L., Carter, R. Colin, Kaplan-Estrin, Melissa, Ayotte, Pierre, Dewailly, Eric, Jacobson, Sandra W., Environmental Health Perspectives


Introduction

Polychlorinated biphenyls (PCBs), methyl-mercury (MeHg), and lead (Pb) are ubiquitous environmental contaminants, to which exposure in utero has been linked to adverse effects on cognitive function in childhood (Grandjean et al. 1997; Jacobson and Jacobson 1996; Needleman et al. 1979). PCBs are persistent organochlorine industrial compounds that were banned in the 1970s and 1980s. Mercury (Hg) is an element that enters the food chain from both natural and anthropogenic sources and is converted to neurotoxic MeHg by aquatic biota. Environmental exposure to Pb, a metal that is used in numerous commercial products, has declined considerably with the conversion to unleaded gasoline but continues to be associated with poorer intellectual function even at low levels (Canfield et al. 2003; Lanphear et al. 2000).

As a growing number of environmental contaminants are recognized as teratogenic, a key issue is whether such exposures are associated with a global, undifferentiated pattern of cognitive impairment or whether exposure to each substance leads to a distinct profile of deficits based on its particular properties and mechanisms of action. Most studies of Pb have focused on postnatal exposure, primarily during the toddler period, and there is extensive evidence of long-term effects from postnatal Pb exposure on childhood IQ (e.g., Bellinger et al. 1992; Dietrich et al. 1993) and attention (e.g., Chiodo et al. 2004; Plusquellec et al. 2010). In childhood, prenatal PCB exposure has been linked primarily to reduced IQ and reading achievement (Jacobson and Jacobson 1996; Stewart et al. 2008), with some evidence suggesting vulnerability in response inhibition (Stewart et al. 2005). Effects of prenatal MeHg exposure in childhood have been examined in two large prospective studies--one in the Faroe Islands, where Hg was associated with poorer cognitive performance at 7 and 14 years of age (Debes et al. 2006; Grandjean et al. 1997); and the other, in the Seychelles Islands, where few adverse associations were found (Davidson et al. 2011; Myers et al. 1995, 2003). In the Faroese study, exposures were associated with diverse domains, including attention, fine motor function, visual spatial abilities, and memory. Consistent with these findings, we have recently reported an association between higher prenatal MeHg exposure and alterations in auditory attention and visual processing using neurophysiological assessments in school-age Inuit children (Boucher et al. 2010; Ethier et al. 2012). Given confounding between PCB and MeHg exposure, the effects of these two contaminants can be difficult to discriminate from each other (Grandjean et al. 2001).

Relatively few studies have examined effects of prenatal exposure to these contaminants on infant development. Among these contaminants, only PCBs have been consistently linked to a specific domain of infant cognitive function in multiple studies. In a cohort of infants exposed in utero to maternal consumption of PCB-contaminated fish, cord blood PCB concentrations were associated with poorer visual recognition memory on the Fagan Test of Infant Intelligence (FTII) at 7 months postpartum (Jacobson et al. 1985). This finding has been replicated at low levels of exposure in Oswego, New York (Darvill et al. 2000), and in infants whose mothers were exposed to high levels of exposure during an industrial accident in Taiwan (Ko et al. 1994). Two studies that examined the effects of prenatal exposure to MeHg in infancy linked that exposure to poorer psychomotor function on the Bayley Scales of Infant Development (BSID) at 30 and 36 months, respectively (Davidson et al. 2008; Lederman et al. 2008). Most of the evidence of cognitive impairment associated with prenatal Pb exposure comes from global developmental assessments, particularly the BSID (Bellinger et al. 1987; Dietrich et al. 1987; Hu et al. 2006), although one study has provided evidence for effects on sustained attention (Plusquellec et al.

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