High Lead Levels Remain Due to Bone Storage
Lead that is in the blood is only a fraction of the lead that is in a person’s body. That lead also collects in a person’s bones has been known since before the 1940s when x-rays were able to detect lead deposits in bone (Warren, 2001, p. 14). In fact, 95% of the lead not immediately excreted is retained in the bones (Warren, 2001, p. 15-16). It was incorrectly assumed in the late nineteenth century into the turn of the century that lead in bones stayed safely in the bones (Warren, 2001, p. 10), when in fact certain metabolic changes can cause lead from bones to return into other areas of the body (Warren, 2001, p. 16).
One problem with remediation and lead bone deposits is that lead levels in the bloodstream can lower after remediation and then end up rising again. This can be due to incomplete remediation, but it can also be due to the lead from bone deposits. Researchers Roberto Gwiazda, Carla Campbell, and Donald Smith pioneered a method of estimating, without huge risk to the patient, the amount of lead from bones that is responsible for the rise in blood lead levels post-remediation (2005, p. 104). They did this by using isotropic analysis of lead ratios in blood and feces pre and post intervention to determine where the lead is coming from postintervention (Ibid). This was managed by clever deduction of the lead isotropic ratios present and influx and efflux, and does rely on underlying assumptions such as the lead isotropic levels in the bones not changing between time points and that feces lead levels can be used as an approximator of lead consumed (Gwiazda et al., 2005, p. 105). (Recall from Warren pg 15 that lead consumed is either excreted immediately or put straight into the bones.)
One large drawback is that this only works if the isotropic influx and efflux ratios are notably different (Ibid). Due to that problem, only three cases were analyzed in the study, so the results are highly preliminary (Gwiazda et al., 2005, p. 107). The researchers found that in all three of their cases the majority of the lead in the blood after remediation was from the bones (Gwiazda et al., 2005, p. 108). They therefore concluded that any remediation efforts need to be followed up on many months later to allow for the lead to buffer out of the bones of patients (Gwiazda et al., 2005, p. 109). This study supports the wide-ranging effects of the work of Dr. Carol Angle and Dr. Matilda McIntire by further examining how lead can affect the body once a person is exposed, as they began working on in the 1970s with their studies on blood enzymes, as seen in previous pages.
These study findings, if substantiated by more results in the future, help to explain a troubling phenomenon with remediation that has occurred for decades. Researchers have continuously been finding that lead levels in children do not lower as expected after remediation. In the 1980s, Julian Chisolm and colleagues experienced this with preschool children in Baltimore, finding that “‘Children’s PbB [blood lead] reequilibriated with their new level of environmental lead exposure…after approximately three months’” (as cited by Markowitz and Rozner, 2013, p. 129). In fact, a later study with Chisolm and colleague Mark Farfel in the 1990s found that some lead abatement practices actually increased children’s blood lead levels after six months (Markowitz and Rozner, 2013, p. 148). If the results of the Gwiazda et al. study hold up however, it is possible that the troubles of Chisolm, Farfel, and countless others with lead abatement are that children’s lead levels rose due to their bone’s lead leaching out not due to lead from their environment leaching in. This would have to be studied on a longer time scale in order to verify it, however. This would be happy news for defenders of lead remediation in that it means that some of these techniques may have worked long-term all along, but unfortunate for those who oppose primary prevention as it shows how integral to the body lead becomes once a person has been exposed.
Gwiazda, R., Campbell, C., & Smith, D. (2005). A Noninvasive Isotopic Approach to Estimate the Bone Lead Contribution to Blood in Children: Implications for Assessing the Efficacy of Lead Abatement. Environmental Health Perspectives, 113(1), 104-110. https://doi.org/10.1289/ehp.7241
Markowitz, G. E., & Rosner, D. (2013). Milbank Memorial Fund(Eds.), Lead wars the politics of science and the fate of America's children. Berkeley: University of California Press; New York : Milbank Memorial Fund.
Warren, C. (2001). Brush with Death: A Social History of Lead Poisoning. Baltimore: Johns Hopkins University Press.