Lead Toxicity in Children: An Unremitting Public Health Problem.

BACKGROUND: Lead is a pervasive environmental contaminant. Lead accumulates in the body, impairing a molecular level various cellular processes. Lead exposure during childhood causes adverse and permanent neurodevelopmental consequences, sometimes even with "low" blood lead levels. Symptoms are frequently silent, making lead exposure an often unrecognized and underestimated threat for pervasive neurocognitive disorders. METHODS: We identified articles focusing on childhood exposure to lead and neurodevelopment via a search of the electronic database PubMed (National Library of Medicine), including journal articles published from 2007 to 2019. These articles were used to evaluate the effect of environmental lead exposure and analyze whether control efforts over the past decades have altered the prevalence of exposed children. CONCLUSIONS: Children are still being exposed to lead despite evidence of the adverse impact of exposure, even for children with blood lead levels below the currently recognized threshold for intervention. Legislative and educational efforts have reduced lead exposure but are not being followed universally. Primary prevention and identification of high-risk populations are the best cost-benefit interventions to fight this public health problem.

Evaluation of Two Fosphenytoin Loading Dose Regimens and Monitoring in Infants and Neonates Less Than Six Months of Age.

OBJECTIVES: The objectives of the study were to compare the free serum concentrations after different fosphenytoin loading dose strategies in patients younger than 6 months old and to investigate the frequency of seizure cessation following a loading dose of fosphenytoin. METHODS: This retrospective cohort study included neonates and infants admitted to a 150-bed children's hospital between August 1, 2014, and February 1, 2018. Patients were included if they were younger than 6 months old and had a postload free phenytoin serum concentration collected during the specified time frame. Patients were identified through a database query screening for the inclusion criteria. Patients were separated into 2 groups with the 15 mg/kg group as per protocol and the 20 mg/kg group as noted in common practice. Data collection included demographic information, fosphenytoin dose, time of administration of the fosphenytoin loading dose, time of sampling, free phenytoin serum concentration results, concomitant antiepileptic agents, albumin serum concentration, and total bilirubin serum concentration. RESULTS: Forty-one patients were included for analysis, 12 in the 15 mg/kg group and 29 in the 20 mg/kg group. The average free phenytoin concentration after the loading dose was 2.45 ± 0.54 mg/L in the 15 mg/kg group and 2.52 ± 0.66 mg/L in the 20 mg/kg group. Seizure cessation after the fosphenytoin loading dose was achieved in 3 of 12 (25%) patients in the 15 mg/kg group and in 13 of 29 (45%) patients in the 20 mg/kg group (p = 0.305). CONCLUSIONS: The study demonstrates that a traditional range of fosphenytoin loading dose (15-20 mg/kg) led to elevated postloading dose free phenytoin serum concentrations in the majority of patients with a seizure cessation rate of approximately 39%. The question remains as to what the optimal dose and target concentration should be in this patient population to achieve the best efficacy without risking associated toxicities.