Bone Lead Testing Facility

Research Collaborations

Current Research Projects

Linking the Effects of 9/11 to Kidney Disease
Collaborators: Mary Ann McLaughlin, MD (Icahn School of Medicine at Mount Sinai)
This study focuses on the prevalence and trajectory of kidney disease among participants of the WTC Health Program and evaluates kidney disease in a multi-factorial manner. Successful completion of the proposed research will address a critical knowledge gap regarding the risk of kidney damage among this group of patients, and the results will have the potential to impact prevention by informing screening guidelines. 

Past Research Projects

Exogenous Toxicants and Genetic Susceptibility in Amyotrophic Lateral Sclerosis
Collaborators: Lorene Nelson, Ph.D (Stanford University, CA), Stephen Van Den Eeden, Ph.D (Kaiser Permanente, Oakland CA)
The relationship between the development of Amyotrophic Lateral Sclerosis (ALS) and environmental exposures (including lead): investigated the etiologic role of deficient endogenous antioxidant defenses in ALS; evaluated the extent to which other neurodegenerative disorders aggregate among family members of ALS patients; and estimated the incidence of ALS

Exposure, Dose, Body Burden & Health Effects of Lead
Collaborators: Brian S. Schwartz, MD, MS (Johns Hopkins, Baltimore MD), Byung-Kook Lee, MD, MSc (Institute of Industrial Medicine, Soonchunhyang University, Chonan, Korea)
The relations among internal dose, bioavailable lead, body burden and health effects in lead workers: assessed changes in renal function, renal early biologic effects, blood pressure and neurobehavioral function in a population of workers with a broad range of lead exposures

Past adult lead exposure is associated with longitudinal decline in cognitive function.

Environmental Lead, Reproduction and Infant Development
Collaborator: Joseph Graziano, PhD, Columbia University
The effects of pre- and post-natal lead exposure and childhood cognitive, behavioral, hematopoietic and anthropomorphic development through age 12

Tibia lead levels and methodological uncertainty in 12-year-old children.

The relationship between blood lead, bone lead and child intelligence.

A Prospective Study of Prenatal and Childhood Lead Exposure and Erythropoietin Production.

Development and Malleability from Childhood to Adulthood
Collaborator: Sheppard G. Kellam, MD, Johns Hopkins University (Bayview Campus)
Assessed the possible role of lead exposure on the course of neuropsychological, cognitive, affective and social development of youths who were followed annually from ages 6-7; and assessed whether lead diminished their capacity for improvement through school-based intervention strategies

Bone Lead Standardization Project
Collaborator: Patrick J. Parsons, Ph.D. (New York State Department of Health, Wadsworth Center)
Created a body of standards for the in vivo measurement of lead in bone

L-shell x-ray fluorescence measurements of lead in bone: accuracy and precision.

An interlaboratory comparison of bone lead measurements via K-shell X-ray fluorescence spectrometry: validation against inductively coupled plasma mass spectrometry.

Skeletal Lead Mobilization during Pregnancy 
Collaborator: Stephen Rothenberg, PhD, Charles R. Drew University, Los Angeles
Professor Todd redesigned and refitted the commercially supplied, bone-lead measurement system at Drew University to improve its sensitivity to a level sufficient for measurement of environmentally exposed persons.

Maternal bone lead contribution to blood lead during and after pregnancy.

Seasonal variation in bone lead contribution to blood lead during pregnancy.

Neonatal lead poisoning from maternal pica behavior during pregnancy.

Increases in hypertension and blood pressure during pregnancy with increased bone lead levels.

Lead Exposure in South African Workers
Collaborator: Rodney Ehrlich, MD, University of Cape Town, South Africa
The first study of chronic lead exposure levels in both environmentally and occupationally exposed South Africans. Bone lead measurements were made on 600 battery workers and on groups of stevedores and adolescents. The collaboration was conducted with the Department of Community Health, The University of Cape Town and The Medical Research Council of South Africa.

Lead absorption and renal dysfunction in a South African battery factory.

Repeatability of tibia lead measurement by X-Ray fluorescence in a battery-making workforce.

Bone Lead Levels in Taiwanese occupationally and environmentally exposed adults and children
Collaborator: Saou-Hsing Liou, MD, PhD, School of Public Health, Taiwan

A pilot evaluation of tibia lead concentrations in Taiwan.

Age, Lead Exposure and Neurobehavioral Decline
Collaborator: Walter Stewart, PhD, Johns Hopkins University
Bioavailable (DMSA-chelatable) lead and cortical and trabecular bone lead were measured in workers exposed to organic and inorganic lead and in controls; measures were compared of exposure, bone lead and DMSA-chelatable lead as predictors of cognitive function and change in cognitive function.

Neurobehavioral function and tibial and chelatable lead levels in 543 former organolead workers.

Lead Exposure and Kidney Function in Genetically Susceptible Ethnic Minorities: A Pilot Study
Collaborators: Girish Nadkarni, PhD, Robert Wright, MD (Icahn School of Medicine at Mount Sinai); Andrea Baccarelli, MD, PhD (Columbia); Joel Schwartz, PhD (Harvard)

Hypothesis: cumulative lead exposure and APOL1 genotype interact (a gene-environment interaction) for the outcome of Chronic kidney disease (CKD).

Chronic kidney disease (CKD) affects up to 15% of the US population; persons of African ancestry (AAs) have threefold times the prevalence than people of European ancestry (EAs). High risk Apolipoprotein L1 (APOL1) genotypes, found nearly exclusively in AAs, are associated with a ten-fold higher risk of end stage renal disease (ESRD). However, not all individuals with APOL1 high risk genotype develop kidney disease, suggesting a role for environmental modifiers. There is an established link between cumulative heavy metal exposure, particularly lead, and incidence and progression of CKD. There are also substantial disparities in lead exposure between AAs and EAs due to differing environmental exposures. This raises the interesting hypothesis that cumulative lead exposure and APOL1 genotype may interact (a gene-environment interaction) for the outcome of CKD.