Air Quality Criteria for Lead Volume II of II - (NEPIS)(EPA) - US ...

AX6-123
Table AX6-4.5 (cont’d). Renal Effects of Lead in Children
Reference, Study
Location, and Period Study Description Pb Measurement Findings, Interpretation
Europe
McDonald and Potter
(1996)
Boston, MA
1991
Moel and Sachs (1992)
Chicago, IL
1974-1989
Bernard et al. (1995b)
Czech Republic
Study date not
provided
454 pediatric hospital patients who were diagnosed with
Pb poisoning between 1923 and 1966 were traced
through 1991.
Mortality study, comparison with U.S. population.
62 participants with blood Pb >100 µg/dL, diagnosed and
chelated between 1966 and 1972, together with 19 agematched
control siblings with initial blood Pbs less than
40 µg/dL. Mean age at follow-up = 22 yrs.
Renal outcomes = serum creatinine, uric acid, and ∃ 2microglobulin,
fractional excretion of ∃2-microglobulin,
urinary protein:creatinine ratio, and tubular reabsorption
of phosphate.
144 children living close to a Pb smelter (exposed groups
1 and 2).
51 controls living in a rural area presumed to be
relatively unpolluted with Pb.
Mean age = 13.5 yrs.
Renal outcome measures included urinary albumin, RBP,
NAG, Clara cell protein, and ∃2-microglobulin.
Retinol binding protein
73.8 µg/g creatinine (controls)
109.4 µg/g creatinine (exposed group 1)
117.8 µg/g creatinine (exposed group 2)
∃2-microglobulin
60.3 µg/g creatinine (controls)
89.1 µg/g creatinine (exposed group 1)
66.4 µg/g creatinine (exposed group 2)
NAG
1.56 IU/g creatinine (controls)
2.32 IU/g creatinine (exposed group 1)
1.46 IU/g creatinine (exposed group 2)
Multiple linear adjusting for age and gender.
Mean initial blood Pb
150.3 µg/dL (highly poisoned
as children)
Data for siblings not available
as levels