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Published on: November 11, 2014
Infant Parenteral Nutrition Remains a Significant Source for Aluminum Toxicity
Amanda R Hall1, Chris J Arnold2, Grant G Miller1
11 Department of Surgery, University of Saskatchewan, Saskatoon, Canada.
Insights
Aluminum contamination in infant parenteral nutrition (PN) is nearly three times the recommended limit. This study found significant links between aluminum levels and calcium gluconate and phosphate in PN, highlighting the need for further investigation to reduce infant exposure.
Area of Science:
- Neonatal Medicine
- Clinical Chemistry
- Toxicology
Background:
- Aluminum toxicity poses risks including anemia, bone defects, and liver disease.
- Aluminum is a common contaminant in parenteral nutrition (PN), particularly for infants.
- Assessing aluminum levels in infant PN is crucial for patient safety.
Purpose of the Study:
- To evaluate current aluminum contamination levels in infant PN.
- To identify potential sources and correlations of aluminum in PN formulations.
- To compare measured aluminum levels with established safety guidelines.
Main Methods:
- Collected 30 discarded infant PN samples from a neonatal intensive care unit.
- Analyzed aluminum content using inductively coupled plasma mass spectrometry.
- Compared aluminum levels with PN components using regression and ANOVA.
Main Results:
- Mean aluminum contamination was 14.02 mcg/kg/d, exceeding the <5 mcg/kg/d FDA guideline.
- Significant correlations found between aluminum and calcium gluconate (P < .0001) and phosphate (P = .05).
- No association observed between aluminum levels and infant weight in this cohort.
Conclusions:
- Infant PN exhibits aluminum contamination significantly above recommended levels.
- Calcium gluconate and phosphate are likely contributors to aluminum contamination.
- Further research is needed to pinpoint sources and reduce aluminum in infant PN.
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.
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.
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