22 Volume 85 • Number 5 A D VANC EME N T O F T H E SCIENCE sure, from 40–70% of circulating lead can come from stores in the bones (Smith et al., 1996). How and when lead is re-released into the bloodstream depends on the concentration of lead in the outer layers of the bone and the body’s demand for calcium (Dowd et al., 2001; Stojsavljević et al., 2019). Lead accumulates in the inert and labile components of cortical and trabecular bone. The inert component is closer to the center of the bone, which can store lead for decades. The labile component is located toward the outer layers of the bone and can easily exchange lead from bone to blood (Stojsavljević et al., 2019). Lead stored in the inert component can mobilize to the labile component with time or in situations where the body releases calcium from the bone, such as when a child suers a broken bone. The mechanism by which lead is exchanged between blood and bone mimics that of calcium exchange. Lead can bind to hydroxyapatite (a calcium phosphate mineral that serves as a calcium reserve for the body) and fluctuates according to the concentration of calcium found in the blood (Dowd et al., 2001; Pounds et al., 1991; Saisa-ard et al., 2014). Deficiencies in calcium, phosphorus, and vitamin D result in higher lead bone storage and more frequent re-release (Jones, 2011). Bone growth in children creates multiple opportunities for lead to be reintroduced into the bloodstream. The largest growth spurt occurs during puberty when there is a greater demand for hydroxyapatite formation (Stagi et al., 2013). Females reach full height at approximately 15 years and continue to build bone mass until 21 years. Males grow until approximately 18 years and build bone mass up to 12 months after reaching full height (Jones, 2011). Also, lead is released during states of high bone turnover such as following bone fractures or in children with conditions that prevent bone mass formation (e.g., osteoporosis, conditions that limit physical activity) (Janz, 2002). Age-based dierences, individual dierences in stored bone-forming nutrients, and bone injuries can all explain BLL spikes in some older children. Summary Current practices for BLL testing in children that rely on one or two BLL tests administered to only the youngest children (i.e., 0–5 years) are not aligned with knowledge regarding the complexity of lead absorption, transport, and disposition in the body throughout childhood and adolescence. In the respiratory system, lead deposition and absorption rates are complex and depend on many changing factors, including lead particulate size, length, frequency of exposure, respiratory rate, where in the lungs lead particulates are deposited, and importantly, individual dierences in the development of the lungs and alveoli. Ingested lead is influenced by complex interactions of chemical, biological, biophysicochemical, and behavioral factors related to dietary intake, dietary deficiencies, and maturity of the GI tract. These interactions of factors can be additive, antagonistic, or synergistic. Once in the bloodstream, lead absorption by RBCs is influenced by common (ALAD) genetic variants and by ongoing fluctuations in calcium, iron, and zinc levels. Additional age-dependent factors facilitate and oppose the distribution of lead into tissues and rerelease of lead into the circulatory system. Current approaches for BLL testing in children inadvertently do not take into account the likely fluctuations in child BLLs described previously in this article. As Sobin et al. (2022) discussed, a revision of current practices is needed to ensure feasibility for monitoring highest-risk children. Suggested revisions include: • Acceptance of capillary samples for final determination of lead poisoning, with electronic documentation of “clean” collection methods submitted by workers. • New guidance specifying analysis of capillary samples by inductively coupled plasma mass spectrometry or graphite furnace atomic absorption spectrometry with documented level of detection ≤0.2 µg/dL. • Adaptation of universal testing and monitoring guidance that is census tract-specific for children from birth to 10 years. These changes to current practices can immediately increase our national capacity for inclusive and equitable detection and monitoring of BLLs, particularly for dangerous lowerrange BLLs in children in the U.S. Corresponding Author: Michelle Del Rio, Assistant Professor, Department of Environmental and Occupational Health, Indiana University–Bloomington, 2719 East 10th Street, Innovation Center, Room 254, Bloomington, IN 47405. Email: midelrio@iu.edu. Agency for Toxic Substances and Disease Registry. (2017). Lead (Pb) toxicity: Who is at risk of lead exposure? https://www.atsdr.cdc.gov/ csem/leadtoxicity/who_at_risk.html Ahlfeld, S.K., & Conway, S.J. (2014). Assessment of inhibited alveolar-capillary membrane structural development and function in bronchopulmonary dysplasia. Birth Defects Research. Part A, Clinical and Molecular Teratology, 100(3), 168–179. https://doi. org/10.1002/bdra.23226 Allegaert, K., van den Anker, J.N., Naulaers, G., & de Hoon, J. (2007). 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