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Trace Elements in Abiotic and Biotic Environments
In humans, the central nervous system is the main target organ for Pb toxicity.
Ingestion of high amounts of Pb from the environment by children, particularly
when anemic, has been associated with reduced intelligence and impaired motor
function.
Infants and young children are more vulnerable than adults to the toxic effects
of Pb, and they also absorb Pb more readily. Even short-term, low-level exposures of Pb by young children are considered to have an effect on neurobehavioral
development. The most critical effect of low-level Pb exposure is on intellectual
development in young children and, Pb crosses the placental barrier and accumulates in the fetus. For children, the weight of evidence is greatest, and evidence across studies is most consistent, for an association of blood Pb levels with
impaired neurodevelopment, specifically reduction of intelligence quotient (IQ).
The developing brain was identified as the most vulnerable organ for Pb exposure.
Under certain conditions, such as pregnancy and osteoporosis, bone resorption
can result in increased concentrations of Pb in blood. Lead readily crosses the
placenta and is transferred into breast milk.
The toxic effects of Pb have been principally established in studies on people
exposed to Pb in the course of their work. Short-term exposure to high levels of
Pb can cause brain damage, paralysis (lead palsy), anemia, and gastrointestinal
symptoms. Long-term exposure can cause damage to the kidneys, reproductive, and
immune systems, in addition to effects on the nervous system.
Neurotoxicity, cardiovascular effects, and renal toxicity were identified as the
critical effects. Lead toxicity results in central nervous system, hematological and
cardiovascular systems, and kidney damage. Lead interferes with the activity of several enzymes involved in the biosynthesis of heme. Signs of acute Pb intoxication
include dullness, restlessness, irritability, poor attention span, headaches, muscle
tremor, abdominal cramps, kidney damage, hallucinations, loss of memory, and
encephalopathy. Signs of chronic Pb toxicity include tiredness, sleeplessness, irritability, headaches, joint pain, and gastrointestinal symptoms.
For adults, the adverse effect, greatest and most consistent, is a Pb-associated
increase in blood pressure. As with the Pb-associated reduction in IQ, the increase
is small when viewed as the effect on an individual’s blood pressure, but important
when viewed as a shift in the distribution of blood pressure within a population.
Pocock et al. (1983) showed a linear increase in blood Pb in thousands of men
in the United Kingdom exposed to various levels of Pb in drinking water. Blood Pb
in adult males increased by 6.22 μg/L for every additional 1 μg Pb/day taken from
drinking water. If drinking water contains 5 μg/L, then the contribution to blood Pb
from drinking water is 31 μg/L
According to WHO (2011c), anemia occurs at blood Pb levels in excess of 0.4 mg/L
in children, and 0.5 mg/L in adults. International Agency for Research on Cancer
(IARC) classified inorganic Pb as probably carcinogenic to humans (Group 2A,
evidence inadequate in humans, sufficient in animals) (IARC 2013).
Based on the dose–response analyses, Joint FAO/WHO Expert Committee on
Food Additives (JECFA) estimated that the previously established provisional tolerable weekly intake (PTWI) of 25 μg/kg bw is associated with a decrease of at least
3 IQ points in children and an increase in systolic blood pressure of approximately