Major adverse impacts on public health can be divided into four categories (1) brain and nervous system damage, and particularly mental development impairment in children; (2) reproductive system interference including effects such as premature infant and low births; (3) circulatory system damage such as O2 absorption decrease and increase in blood pressure; and (4) kidneys malfunctioning.
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These various health effects have been recognized for several decades in the case of relatively high lead exposure. Lead intoxication is a widespread problem. One of every nine children under six years of age has blood lead levels high enough to be at risk. In 1970, an estimated 3 million children in older, inner-city neighborhoods were likely to be affected, but areas children in suburban and rural areas were at risk too.
The most sensitive target of lead poisoning is the nervous system. In children, neurologic deficits have been documented at exposure levels once thought to cause no harmful effects. Exposure to lead can have a wide range of effects on a child’s development and behavior. Even when exposed to small amounts of lead levels, children may appear inattentive, hyperactive and irritable. Children with greater lead levels may also have problems with learning and reading, delayed growth and hearing loss. At high levels, lead can cause permanent brain damage and even death.
Lead inhibits the body’s ability to make hemoglobin by interfering with several enzymatic steps in the heme pathway. Ferrochelatase, which catalyzes the insertion of iron into protoporphyrin IX, is sensitive to lead. A decrease in the activity of this enzyme results in an increase of the substrate, erythrocyte (EP), in the red blood cells. Lead can induce two types of anemia. Acute high-level lead poisoning has been associated with hemolytic anemia. In chronic lead poisoning, lead induces anemia by diminishing red blood cell survival.
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Lead toxicity has endocrine effects. A strong inverse correlation exists between blood lead levels and levels of vitamin D. Because the vitamin D-endocrine system is responsible in a large part for the maintenance of extra-and intra-cellular calcium homeostasis, it is likely that lead impairs cell growth and maturation and tooth and bone development.
Long-term lead exposure has a direct nephropathy effect on the kidney. Impairment of proximal tubular function manifests a fanconi-like syndrome. There is also evidence of an association between lead exposure and hypertension, an effect that may be mediated through renal mechanisms. Gout may develop as a result of lead-induced hyperuricemia, with selective decreases in the fractional excretion of uric acid before a decline in creatine clearance. Renal failure accounts for 10% of deaths in patients with gout
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An increased frequently of miscarriages and stillbirths among women working in the lead trades are reported. Increasing evidence indicates that lead not only affects viability of fetus, but development as well. Developmental consequences of prenatal exposure to low levels of lead include reduced birth weight and premature birth. However, most studies in humans have failed to show a relationship between lead levels and congenital malformations.
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