Aluminum toxicity is associated with anemia, impaired bone metabolism, neurologic defects, and parenteral nutrition (PN)–associated liver disease” Hall et al (2016).
Background: Aluminum toxicity is associated with anemia, impaired bone metabolism, neurologic defects, and parenteral nutrition (PN)–associated liver disease. This element is a ubiquitous contaminant of PN components, especially in infant formulations. We assessed the current levels of aluminum contamination in infant PN at a level III neonatal intensive care unit.
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Materials and Methods: Thirty samples of PN prepared in the same hospital for infants aged <30 days (mean [SD] weight, 1.54 [0.71] kg) were collected from discarded solution. Each sample was analyzed for aluminum content via inductively coupled plasma mass spectrometry. The components of PN (from label) and measured aluminum content were then compared using linear regression and 1-way analysis of variance.
Results: The mean (SD) aluminum contamination of infant PN was 14.02 (6.51) mcg/kg/d. Only 3 samples were <5 mcg/kg/d. Aluminum levels and infant weight were not associated. Linear regression revealed a significant correlation between aluminum and both calcium gluconate (P < .0001) and phosphate (P = .05), with a trend between aluminum and potassium (P = .07).
Conclusions: Aluminum contamination in infant PN remains almost 3 times higher than the advised maximum exposure (<5 mcg/kg/d, Food and Drug Administration 2004). Unexpectedly, an association between infant weight and aluminum exposure was not apparent, likely due to the homogeneity of our population. Isolating the source of aluminum contamination is difficult, as multiple components appear to be involved. Calcium gluconate is likely still a major contributor, but further investigations into individual components are warranted to promote the reduction of aluminum in infant PN.
Hall, A.R., Arnold, C.J., Miller, G.G. and Zello, G.A. (2016) Infant Parenteral Nutrition Remains a Significant Source for Aluminum Toxicity. JPEN. 16th March. .
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