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

AX6-105
Table AX6-4.3 (cont’d). Renal Effects of Lead in the Patient Population
Reference, Study
Location, and
Period Study Description Pb Measurement Findings, Interpretation
Europe (cont’d)
Colleoni and
D’Amico (1986)
Italy
(~1982-1985)
Colleoni et al. (1993)
Italy
Study date not
provided
Craswell et al. (1987)
Germany and
Australia
Study date not
provided
12 consecutive patients with CRI (mean serum
creatinine = 3.3 mg/dL) and gout, renal diagnosis
consistent with chronic interstitial nephritis in all; 7 had
history of occupational Pb exposure.
12 controls with chronic glomerulonephritis and no
history of Pb exposure or gout.
Pb excretion in the 48 hrs after administration of 1.5 g
EDTA im.
All 115 patients on hemodialysis at the time of the study;
41 women.
Blood Pb data from prior study of 383 healthy controls in
same geographical area served as comparison.
See discussion below under Australia.
Mean EDTA chelatable Pb
(µg/48 hrs)
180 (CRI, no gout)
505 (CRI & gout)
Mean blood Pb
(corrected for hemoglobin)
19.9 µg/dL (patients)
14.7 µg/dL (controls)
Significantly higher EDTA chelatable Pb in the
group with CRI and gout compared to CRI alone.
EDTA chelatable Pb significantly correlated with
serum creatinine in patients with CRI and gout but
not CRI alone. Authors conclude that Pb is cause of
CRI with gout but renal insufficiency alone not
responsible for increased Pb body burden (absence
of evidence for reverse causation).
Limitations = small sample size, limited data
analysis.
Significantly higher mean blood Pb in hemodialysis
patients compared to healthy controls. 13% had
blood Pb levels >30 µg/dL. Blood Pb level was not
associated with duration of hemodialysis. Mean Pb
levels higher in smokers and in relation to alcohol
ingestion. Pb not detectable in dialysis fluids.
Limited data analysis.