For many years, tetraethyl lead was added to gasoline to act as a lubricant and improve its octane rating.
However, there has been an explosion of knowledge during the last two decades with regard to the adverse health impact of long-term exposures to low levels of ambient lead.
In response to this growing body of data, most industrialized countries and several developing countries have or will soon prohibit the use of leaded gasoline entirely.
The toxic properties of lead at high concentrations have been known since ancient times as lead has been mined and smelted for more than 40 centuries. Precautions in its use have been widespread for centuries, but it has only been recently that its adverse impacts at very low levels have been fully appreciated.
The seminal work in this area is the 1979 report by Dr. Herbert Needleman and his colleagues which showed that children with high levels of lead accumulated in their baby teeth experienced more behavioral problems, lower IQ's and decreased ability to concentrate.
More recent evidence indicates that it is not only the length and severity of exposure to lead that results in the health damage but the age at which exposure occurs. The newborn child is the most prone to injury from overexposure to lead.
Based on the growing body of data showing adverse effects from lead, in 1985 the US EPA reduced the maximum allowable lead content in leaded gasoline to 0.1 grams per gallon. As part of that rulemaking, EPA uncovered evidence linking lead in the blood and high blood pressure.
A subsequent study, in which 249 children were monitored from birth to two years of age, found that those with prenatal umbilical-cord blood lead levels at or above 10 micrograms per deciliter consistently scored lower on standard intelligence tests than those at lower levels.
More recently, British researchers reviewed every epidemiologic study on lead and IQ published since 1979 that had over 100 children and measured IQ as a function of blood or tooth lead levels. Based on a meta-analysis of all the data, they concluded that a doubling of body lead burden from 10 to 20 µg/dl in blood levels was associated with a mean fall of about 1 to 2 IQ points.
Over the past century, a range of clinical, epidemiological and toxicological studies have continued to define the nature of lead toxicity, to identify young children as a critically susceptible population, and to investigate mechanisms of action of lead toxicity. A full discussion of lead toxicity, clinical manifestations and mechanisms of action can be found in the 1995 Environmental Health Criteria Document for Lead, published by the International Program on Chemical Safety (IPCS).
In summary, lead affects many organs and organ systems in the human body with subcellular changes and neurodevelopmental effects appearing to be the most sensitive. The most substantial evidence from cross sectional and prospective studies of populations with lead levels generally below 25 µg/deciliter of blood relates to decrements in intelligence quotient (IQ).
As noted by the IPCS, existing epidemiological studies do not provide definitive evidence of a threshold. Below the range of about 10 - 15 µg/deciliter of blood, the effects of confounding variables and limits in the precision in analytical and psychometric measurements increase the uncertainty attached to any estimate of effect. However, there is some evidence of an association below this range. Animal studies provide support for a causal relationship between lead and nervous system effects, reporting deficits in cognitive functions at lead levels as low as 11-15 µg/deciliter of blood which can persist well beyond the termination of lead exposure.
- impaired sensory motor function
- impaired renal function
- a small increase in blood pressure has been associated with lead exposure
- some but not all epidemiological studies show a dose dependent association of pre-term delivery and some indices of fetal growth and maturation at blood lead levels of 15 µg/deciliter or more.
Lead and its compounds may enter the environment at any point during mining, smelting, processing, use, recycling or disposal. In countries where leaded gasoline is still used, the major air emission is from mobile and stationary combustion of gasoline. Areas in the vicinity of lead mines and smelters are subject to high levels of air emissions.
Airborne lead can be deposited on soil and water, thus reaching humans through the food chain and in drinking water. Atmospheric lead is also a major source of lead in household dust.
Because of the concerns highlighted above, a global consensus has emerged to phase out the use of lead in gasoline.
- In December 1994, at the Summit of the Americas, heads of state from a number of countries pledged to develop national action plans for the phase out of leaded gasoline in the Western Hemisphere.
- Since 1996, the use of leaded gasoline has been banned in the United States.
- In May 1996, the World Bank called for a global phase out of leaded gasoline and offered to help countries design feasible phase out schedules and incentive frameworks.
- A key recommendation of the Third "Environment for Europe" Ministerial Conference held in Sofia, Bulgaria in October 1995 called for the reduction and ultimate phase out of lead in gasoline.
- In June 1996, the second United Nations Conference on Human Settlements, called Habitat II, included the elimination of lead from gasoline as a goal in its agenda.
- In May 1997, environmental ministers from the Group of Seven plus Russia endorsed the phase out of leaded gasoline in the 1997 Declaration of Environmental Leaders of the Eight on Children's Environmental Health.
| 
