Professor of Pediatrics
Director of Pediatric Resident Education
Johns Hopkins University School of Medicine
Phi Beta Kappa, magna cum laude — University of Illinois, Champaign-Urbana (1974–78)
M.D. — Northwestern University Medical School, Chicago (1978–82)
Internship/Residency, Pediatrics — Children's Hospital of Los Angeles, USC School of Medicine (1982–84)
Residency, Pediatrics — Riley Children's Hospital, Indiana University (1984–85)
Robert Wood Johnson Fellowship in General Academic Pediatrics — Johns Hopkins Hospital (1986–88)
Assistant Professor of Pediatrics, University of Southern California School of Medicine (1988–1990)
Medical Director, Harriet Lane Pediatric Primary Care Clinic, Johns Hopkins (1990–2003)
Director, Pediatric Primary Care Educational Program, Johns Hopkins Children's Center (1991–present)
Assistant Professor (1991–97), Associate Professor (1998–2005), Professor of Pediatrics (2005–present) — Johns Hopkins School of Medicine
Network Director, CORNET, Continuity Research Network, Ambulatory Pediatric Association (2002–present)
Director of Pediatric Resident Education, Johns Hopkins (2003–present)
Dr. Serwint served as Co-Investigator at the Johns Hopkins clinical site of the TLC trial under Principal Investigator J. Julian Chisolm, MD, at the Kennedy Krieger Institute in Baltimore. The Hopkins site received $593,962 in total direct costs for the clinical center proposal (NIEHS RFP #NO1-ES-9231, 1993–1999).
Serwint published the iron status analysis for the TLC population (J Pediatr, 1999), comparing iron markers in 787 African American children from the TLC screening cohort (BLL 20–44 µg/dL) against 222 African American urban children from NHANES III with BLL <10 µg/dL.
Cohort distinction: The analysis used the TLC screening cohort (N=787), not the randomized cohort (N=780). These are overlapping but distinct populations with different selection criteria.
Ferritin threshold: Iron depletion was defined as ferritin <10 µg/L. This threshold is below WHO (<12 µg/L), current clinical practice (<15 µg/L), and neurodevelopmental research thresholds (<20–25 µg/L). No analysis was performed at these higher thresholds.
Reported findings: Iron depletion (ferritin <10 µg/L) was 11% in TLC vs. 13% in NHANES III (P=.46). Iron deficiency anemia (ferritin <10 + hemoglobin <11 g/dL) was 3% in TLC vs. 4% in NHANES III (P=.52). Arithmetic mean ferritin was 27.2 ± 18.4 µg/L (TLC) vs. 27.0 ± 20.4 µg/L (NHANES III) (P=.904).
Erythrocyte indices: TLC children had statistically significantly lower MCV (75.4 vs. 78.0 fL, P<.001) and higher RDW (14.3% vs. 13.5%, P<.001) compared to NHANES III controls. These microcytic indices are consistent with iron-restricted erythropoiesis in some children, even where ferritin means were comparable.
Comparator limitation: The comparison was between lead-exposed children (BLL 20–44 µg/dL) and lower-exposed children (BLL <10 µg/dL)—not against healthy, unexposed controls. The NHANES III comparator group had significantly higher parental education (77.2% vs. 60.2% completing high school) and employment (61.2% vs. 36.0%).
The paper concluded that laboratory investigation or empirical treatment for iron deficiency is not justified based on moderately elevated blood lead levels alone.
Serwint JR, Damokosh AI, Berger OG, Chisolm JJ Jr, Gunter EW, Jones RL, et al. No difference in iron status between children with low and moderate lead exposure. J Pediatr. 1999;135(1):108–110. PMID: 10393615.
Source: Curriculum Vitae of Janet Rose Serwint, M.D. (dated April 1, 2007)