This Policy Statement was reaffirmed September 2022.: An extensive literature documents the existence of pervasive and persistent child health, development, and health care disparities by race, ethnicity, and socioeconomic status (SES). Disparities experienced during childhood can result in a wide variety of health and health care outcomes, including adult morbidity and mortality, indicating that it is crucial to examine the influence of disparities across the life course. Studies often collect data on the race, ethnicity, and SES of research participants to be used as covariates or explanatory factors. In the past, these variables have often been assumed to exert their effects through individual or genetically determined biologic mechanisms. However, it is now widely accepted that these variables have important social dimensions that influence health. SES, a multidimensional construct, interacts with and confounds analyses of race and ethnicity. Because SES, race, and ethnicity are often difficult to measure accurately, leading to the potential for misattribution of causality, thoughtful consideration should be given to appropriate measurement, analysis, and interpretation of such factors. Scientists who study child and adolescent health and development should understand the multiple measures used to assess race, ethnicity, and SES, including their validity and shortcomings and potential confounding of race and ethnicity with SES. The American Academy of Pediatrics (AAP) recommends that research on eliminating health and health care disparities related to race, ethnicity, and SES be a priority. Data on race, ethnicity, and SES should be collected in research on child health to improve their definitions and increase understanding of how these factors and their complex interrelationships affect child health. Furthermore, the AAP believes that researchers should consider both biological and social mechanisms of action of race, ethnicity, and SES as they relate to the aims and hypothesis of the specific area of investigation. It is important to measure these variables, but it is not sufficient to use these variables alone as explanatory for differences in disease, morbidity, and outcomes without attention to the social and biologic influences they have on health throughout the life course. The AAP recommends more research, both in the United States and internationally, on measures of race, ethnicity, and SES and how these complex constructs affect health care and health outcomes throughout the life course.

The classical laboratory tests for exposure to organophosphorus toxicants (OP) are inhibition of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activity in blood. In a search for new biomarkers of OP exposure, we treated mice with a biotinylated organophosphorus agent, FP-biotin. The biotinylated proteins in muscle were purified by binding to avidin-Sepharose, separated by gel electrophoresis, digested with trypsin, and identified from their fragmentation patterns on a quadrupole time-of-flight mass spectrometer. Albumin and ES1 carboxylesterase (EC 3.1.1.1) were found to be major targets of FP-biotin. These FP-biotinylated proteins were also identified in mouse plasma by comparing band patterns on nondenaturing gels stained for albumin and carboxylesterase activity, with band patterns on blots hybridized with Streptavidin Alexa-680. Two additional FP-biotin targets, AChE (EC 3.1.1.7) and BChE (EC 3.1.1.8), were identified in mouse plasma by finding that enzyme activity was inhibited 50–80%. Mouse plasma contained eight additional FP-biotinylated bands whose identity has not yet been determined. In vitro experiments with human plasma showed that chlorpyrifos oxon, echothiophate, malaoxon, paraoxon, methyl paraoxon, diazoxon, diisopropylfluorophosphate, and dichlorvos competed with FP-biotin for binding to human albumin. Though experiments with purified albumin have previously shown that albumin covalently binds OP, this is the first report of OP binding to albumin in a living animal. Carboxylesterase is not a biomarker in man because humans have no carboxylesterase in blood. It is concluded that OP bound to albumin could serve as a new biomarker of OP exposure in man.

OBJECTIVES: To develop predictive models for death or neurodevelopmental impairment (NDI) after neonatal hypoxic-ischemic encephalopathy (HIE) from data readily available at the time of NICU admission (“early”) or discharge (“cumulative”). METHODS: In this retrospective cohort analysis, we used data from the Children’s Hospitals Neonatal Consortium Database (2010–2016). Infants born at ≥35 weeks’ gestation and treated with therapeutic hypothermia for HIE at 11 participating sites were included; infants without Bayley Scales of Infant Development scores documented after 11 months of age were excluded. The primary outcome was death or NDI. Multivariable models were generated with 80% of the cohort; validation was performed in the remaining 20%. RESULTS: The primary outcome occurred in 242 of 486 infants; 180 died and 62 infants surviving to follow-up had NDI. HIE severity, epinephrine administration in the delivery room, and respiratory support and fraction of inspired oxygen of 0.21 at admission were significant in the early model. Severity of EEG findings was combined with HIE severity for the cumulative model, and additional significant variables included the use of steroids for blood pressure management and significant brain injury on MRI. Discovery models revealed areas under the curve of 0.852 for the early model and of 0.861 for the cumulative model, and both models performed well in the validation cohort (goodness-of-fit χ²: P = .24 and .06, respectively). CONCLUSIONS: Establishing reliable predictive models will enable clinicians to more accurately evaluate HIE severity and may allow for more targeted early therapies for those at highest risk of death or NDI.

Ferroptosis is a type of programmed cell death caused by phospholipid peroxidation that has been implicated as a mechanism in several diseases resulting from ischemic-reperfusion injury. Most recently, ferroptosis has been identified as a possible key injury mechanism in neonatal hypoxic-ischemic brain injury (HIBI). This review summarizes the current literature regarding the different ferroptotic pathways, how they may be activated after neonatal HIBI, and which current or investigative interventions may attenuate ferroptotic cell death associated with neonatal HIBI.