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EC number: 235-727-4
CAS number: 12626-81-2
Lead has been documented in observational human studies to produce toxicity in multiple organ systems and body function including the haemotopoetic sytem, kidney function, reproductive function and the central nervous system.
Documentation of repeated dose toxicity from lead exposure is
extensive and includes detailed evaluations of effects in
humans. Research in animals serves to support causality in epidemiology
studies and/or the elucidation of mechanisms of toxicity. The dose
response for health effects in human can usually be defined with
precision and indexed to internal measures of systemic exposure such as
the concentration of lead in blood. Effects assessment indexed to
external dose is thus not necessary.
In many instances the toxic manifestations of lead are mediated by
interaction of the lead ion with cellular proteins (e.g. metalloenzymes)
in place of essential trace minerals such as calcium, zinc or iron. As
such, the initial effects of lead upon the function of specific
metabolic, cellular, or organ system processes will be detectable as
increases or decreases in the activity of specific metalloenzymes. The
biological and clinical significance of such interactions requires
careful assessment of the extent of enzyme activity alteration and
whether or not the alteration alters metabolic pathways to an extent
that is of health significance.
The toxic effects of lead (by oral route) were observed when
administered to rats in doses of 0.05 mg/kg (substantial increases in
the weight coefficients of liver and kidneys...) with a short term
exposure 20 -30 days . The activity of aldolase increased and the level
of sulfhydryl groups decreased 5-10 days after intoxication (0<0.01).
The effect of the 0.005 mg/kg bw/day dose (LOEL) was expressed as a
trend in the increase of aldolase in the blood serum. By the 20th day of
intoxication the activity of aldolase normalized., and the activity of
other enzymes (B-galactosidase, B-glucosidase...) and cholesterol
content of the blood serum did not change. In animals which were exposed
to 0.0015 mg/kg of lead (NOEL), no deviation in functional state was
observed compared to the control group of animals.
For long term exposure -6 to 12 months- histological and histochemical
studies of gonads, liver and kidney showed disruptions in the funcional
and morphological conditions at doses of lead of 0.05 and 0.05 mg/kg
bw/day. The 0.0015 mg/kg dose of lead (which corresponds to 0.03 mg
lead/l. water) did not cause any changes. It can be considered that this
dose does not have an effect on the organism.
Studies on newborn mice exposed for 28 days at 2.5 mg/m3 of aerosolized
Pb(NO3)2 revealed that aerosolized lead is more immunosuppressive than
equivalent amounts of ingested lead. This is most likely due to the
greater absorption of inhaled lead and the subsequent cytotoxicity of
lead for cells in the draining lymph nodes.
Repeated dose toxicity: via oral route - systemic effects (target organ) urogenital: other
Demonstration of toxicty in humans is the basis for a recommended
classification of STOT RE1. Current classification is STOT RE2.
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