Monday, November 24, 2014

Postnatal Growth Following Prenatal Lead Exposure and Calcium Intake

By: Assistant Editor Lydia Furman, MD

Photo by F. Lamiot via Wikimedia Commons (edited)
Lead is a ubiquitous environmental toxin, with well appreciated deleterious effects on the neurodevelopment of young children. But what do we know about the physical growth of lead-exposed infants and children? Dr. Hong and colleagues prospectively examine the effect of maternal lead levels during early and late pregnancy on postnatal growth at birth and at 6, 12 and 24 months (doi: 10.1542./peds.2014-1658).

Lead does cross the placenta, so prenatal exposure clearly has potential to reach the developing fetus; however there is limited evidence to date of any impact on postnatal growth beyond the neonatal period (Schell et al, Am J Human Bio, 2009).

Certainly no lead level is considered “safe.” With a new focus on primary prevention, the CDC has established 5.0 micrograms/dL or greater as the lead level that identifies children who are in the highest 2.5 percent of US children based on the National Health and Nutrition Examination survey (NHANES) data on blood lead levels in children.

Previously the CDC used a “level of concern” of 10 micrograms/dL; however it became clear that even at these “low” levels there were negative effects on neurodevelopment as assessed at 24 months with the Bayley Scales of Infant Development (Tellez-Rojo et al, Pediatrics, 2006), on intelligence as assessed at age 6 years (Canfield et al, New England Journal of Medicine, 2003 and Jusko et al, Environmental Health Perspectives, 2007), and on reading readiness at kindergarten entry (McLaine et al, Pediatrics, 2013). With the new population-based 2.5 percentile level of 5.0 micrograms/dL, clinicians, public health departments and parents hope to have the opportunity to intervene earlier and prevent deleterious effects.

But with less than 5.0 micrograms/dL as a non-actionable level for children, any direct effect of prenatal lead levels higher than this on child growth would be surprising. Hong and colleagues studied a cohort of 1,150 pregnant women whose mean lead level of 1.25 micrograms/dL was actually much lower.  Their unexpected results are a call to action for public health servants, policy makers and child advocates.

The authors further asked whether dietary intake of calcium has any impact on lead’s effects, and measured women’s diets carefully using dietary interviewers and 24 hour recall. Mothers’ mean daily calcium intake at study entry was 541 mg/24 hours; when pregnancy dietary intake of calcium was below the mean, this intensified the negative effect of maternal lead levels on infant growth, particularly birth weight.

The authors make a convincing case for biological plausibility of both the interrelationship between maternal dietary calcium intake during pregnancy and maternal blood lead levels, and the consequent demonstrated effect on infant growth. This article sets the stage for additional public health work, both to promote increased dietary calcium during pregnancy, and to continue the fight to reduce exposure of mothers and children to environmental toxins, including lead.

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