Introduction
Lead is a chemical element with symbol Pb and atomic number 82. It is used in several ways, from bullet to lead-acid batteries. But its main use in the last decades was in fuel, as
tetraethyllead , a compound with the formula (CH
3CH
2)
4Pb. It has been mixed with gasoline since the 1920s to allow a rising in the engine compression, which improved vehicle performance.
Lead pollution from engine exhaust is dispersed into the air and into the vicinity of roads and easily inhaled or even eaten from children. Lead fuel was banned in the US in 1970s, while in Italy and in the EU it has not been saled since 2000 due to a community law, even if new car used unleaded fuel from 1990. At the moment all world countries have banned leaded fuel with the exception of Afghanistan, Myanmar and North Korea, while Algeria, Yemen and Iraq are dual countries, that means both leaded and unleaded fuel are sold.
The disappearing of this kind of fuel modified parameter of lead toxicity. Before 1970, childhood lead poisoning was defined by a blood-lead concentration greater than 60 mcg/dl. The level considered acceptable in the US was set at 40 mcg/dl in 1970 and reduced to 25 mcg/dl in 1985. In 1991 was established the current level of 10 mcg/dl.
Lead damages the nervous system and causes brain disorders and blood disorders. Like other heavy metals, lead is a neurotoxin that accumulates both soft tissues and bones. Children are more exposed to lead effects because they are growing, their central nervous system is in formation and the intake of lead per unit body is higher than for adult.
Harmful effect of leaded gasoline 2012
Environmental lead exposure: a public health problem of global dimensions 2000
Biochemical effects
Concerning the neurons, lead interferes with the releas of neurotransmitters , mostly glutamate, which is important in many functions including learning, by blocking NMDA receptors . The targeting of NMDA receptors is thought to ben one of the main causes for lead's toxicity to neurons. A John Hopkins report found that in addition to inhibiting the NMDA receptor, lead exposure decreased the amount of the gene for the receptor in part of the brain. In addition, lead has been found in animal studies to cause programmed cell death in brain cells.
In the central nervous system instead lead causes the axon of nervous cells to degenerate and lose their myelin coats. Lead is able to pass through the endothelial cells at the blood brain barrier because it can substitute the calcium ions and be uptaken by Calcium-ATPase pumps. In a child's developing brain, lead interferes with synapse formation in the cerebral cortex, neurochemical development, and organization of ion channels.
In kidney instead lead interacts with 25(OH)D-1α hydroxylase and lead poisoning inhibits excretion of the waste product urate and causes a predisposition for gout, in which urate builds up. This condition is known ad saturnine gout.
In the cardiovascoular system lead inhibits the body's ability to make hemoglobin by interfering with several enxymatic steps in the heme pathway. Specifically, lead decreases heme biosynthesis by inhibiting d-aminolevulinic acid dehydratase (ALAD) and ferrochelatase acrtivity. Ferrochelatase, wich caralyzes the insertion of iron into protoporphyrin IX, is quite sensitive to lead. A decrease in activity of this enzyme result in an increase of the substrate, erythrocyte protoporphyrin (EP), in the red blood cells, also found in the form of the ZPP-bound to zinc rather than iron). Also associated with lead exposure is an increase in blood and plasma d-aminolevulinic acid (ALA) and free erythrocyte protoporphyrins (FEP).
In the endocrine system, studies of children with high lead exposure have found that a strong invers correlation exists between blood lead level and Vitamin D levels. Lead impedes vitamin D conversion into 1,25 dihydroxyvitamin D, which is largely responsible for the maintenance of extra and intracellular calcium homeostasis. Diminished 1,25 dihydroxyvitamin D may impair cell growth, maturation and tooth and bone development. In general, these adverse effects seem to be restricted to children with chronically high blood lead level and chronic nutritional deficiuncy, especially with regard to calcium, phosphorous and vitamin D, Lead have minimal, if any, effect on thyroid function.
Effects of lead exposure on hippocampal metabotropic glutamate receptor subtype 3 and 7 in developmental rats, 2009
ENVIRONMENTAL POLICY AS SOCIAL POLICY? THE IMPACT OF CHILDHOOD
LEAD EXPOSURE ON CRIME, 2007
Lead exposure during synaptogenesis alters NMDA receptor targeting via NMDA receptor inhibition, 2011
Social effects
An american study proved that childhood lead exposure can lead to psychological deficits that are associated with aggressive and criminal behavior. But on the other side, the removal of leaded fuel from gasoline in the US in 1970, and the consequent reduction in childhood exposure in the late 1970s and early 1980s is responsible for significant declines in violent crime in the 1990s. In fact lead has irreversible degenerative effect on the central nervous system.
High lead exposures during childhood are associated with lower IQ as an adult. The IQ scores of children with blood lead level of 10 mcg/dl were points lower than for children with lead levels of 1 mcg/dl. In detail, each increase of 10 mcg per deciliter in the lifetime average blood lead concentration was associated with a 4,6-point decrease in IQ, and IQ declined by 7,4
points as lifetime average blood lead concentrations increased from 1 to 10 mcg per
deciliter.
Children with blood lead level grather than 10 mcg/dl are even in danger of developmental disabilities.
Intellectual Impairment in Children with Blood Lead Concentrations below 10 µg per Deciliter 2003
ENVIRONMENTAL POLICY AS SOCIAL POLICY? THE IMPACT OF CHILDHOOD
LEAD EXPOSURE ON CRIME 2007
The long-term effects of exposure to low doses of lead in childhood 1990
