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

AX5-67
Reference
Chang et al.
(1997)
Tsao et al.
(2000)
Carmignani
et al. (2000)
Table AX5-5.3. Studies of the Effects of Lead Exposure on Blood Pressure and Adrenergic System
Species/
Tissue
Pb Exposure Measured Parameters
Age/
Weight n Dosage Duration Pb Level CVS Other Reference Species/Tissue
Wistar rats 190–200 g 20 Pb acetate
0.5% in
drinking
water
Wistar rats 190–200 g 70 Pb acetate
0–2% in
drinking
water
2 mo Blood 29.1 ±
1.9 µg/dL
aorta; 1.9 ±
0.2 µg/g
2 mo Blood, heart,
aorta, kidney
Male SD rats 3 mo 24 60 ppm 10 mo Blood 22.8 ±
1.2 µg/dL
BP Plasma
catecholamines +
aorta; β receptor
binding assay and
cAMP generation
BP, β agoniststimulated
cAMP
production
(10 µM
isoproterenol
in vitro)
BP, HR,
cardiac
contractility
(dP/dt), blood
flow
pl NEpi, cAMP β
receptor densities
Plasma NE, Epi,
dopamine, monoamine
oxidase (MAO)
activity, histology
— Pb exposure caused
HTN, elevated plasma
NE (unchanged
plasma Epi).
↓ isoproterenolstimulated
plasma
cAMP, ↓ β receptor
density in aorta.
— Pb exposure raised BP
and pl NE + lowered
aorta and heart β
receptor density, basal
and stimulated cAMP
productions +
increased kidney β
receptor density and
basal and stimulated
cAMP productions.
— Pb exposure raised BP
and dp/dt, lowered
carotid blood flow, (no
change in HR) raised
plasma NE and Epi
and MAO (all tissues)
lowered plasma NOx
+ ↓aorta media
thickness,
↑lymphocyte
infiltration in
periaortic fat,
nonspecific change in
kidney (congestion,
edema, rare prox.
tubular cell necrosis).