Toxic Effects of Lead and Mercury

James Roberts, MD, MPH

Disclosures

December 31, 2009

Heavy metals are toxic to humans. Two of the most common and widely studied of these metals are lead and mercury, both of which are highly toxic to the developing brain and nervous system.

Excessive exposure can begin in the intrauterine period, leading to adverse effects at birth. Prenatal exposure is more common with mercury, whereas lead poisoning is more common during the first few years of life.

This article provides an overview of lead and mercury toxicity, including sources of exposure, adverse effects, treatment, and prevention. The primary goals are to impart an understanding of the toxicology of these metals[1] and to help the physician be prepared to counsel families on ways to prevent adverse effects from lead and mercury toxicity.[2] The article also discusses relevant medical literature for further study.

Lead

Lead is a dense, highly malleable metal that is resistant to corrosion. It was once used extensively in building construction, plumbing, and paint and is still added to some paint used on steel structures, such as bridges and railways.[3]

Lead has no known health benefits and has adverse effects throughout the body. It can damage the kidneys, nervous system, and reproductive system and can cause high blood pressure. Lead is especially harmful to fetuses and young children, whose brains are in development.

Elevated blood levels of lead in children are a major preventable health problem. The higher the dose and the longer the duration of exposure, the greater the likelihood of damage. Elevated levels can lead to learning disabilities, behavioral problems, and mental retardation. Extremely high levels may lead to seizures and coma and can be fatal.[4]

History of Lead Poisoning

Lead poisoning has occurred since at least the time of the Roman Empire. The Romans had indoor plumbing that contained lead, and they used lead in much of their cookware. Romans who worked in lead mines were also exposed.

Modern-day lead poisoning in Western countries was described around the turn of the 20th century. Most reports on lead poisoning in the medical literature of the late 1800s and early 1900s described severe encephalopathy with seizures and coma due to ingestion of lead-based paint chips.[5]

By the 1920s, many countries, including Great Britain, Poland, and Cuba, had banned lead-based paint -- at least for use indoors or on baby furniture. US paint manufacturers dramatically decreased the amount of lead in their products in the early 1950s. The Environmental Protection Agency (EPA) did not, however, ban lead paint for home use until 1978. This delay occurred despite growing evidence of harm from lead at even lower levels than what would cause clinically detectable encephalopathy.

Sources of Lead

Since the ban on lead, old paint is now the primary source of lead exposure. Children can be exposed when they ingest paint chips or dust or soil that has been contaminated by lead-based paint.[1]

Exposure increases when paint is disturbed, such as when windows or doors are opened and closed. Painting over lead-based paint does not solve this problem. Inhalation of dust containing lead pain is another method of transmission. Dust from deteriorating paint tends to settle on windowsills and floors, where young children are likely to crawl or place their hands. This is especially problematic because young children tend to repeatedly place their hands in their mouths. Toys and other household objects also may gather dust and wind up in a child's mouth.

Soil also can be contaminated by fumes from leaded gasoline, which the United States phased out in the 1970s and 1980s.[1] However, contaminated soil continues to present a hazard.[2]

Another potential source of lead is the water supply. Water can be contaminated by lead pipes and solder in water-distribution systems and household plumbing. Although public water supplies are monitored for lead, no such system exists for well water.[4]

Children's toys and jewelry are another potential source of lead. The US Consumer Product Safety Commission maintains a list of products that have been recalled due to high lead levels and for other reasons.

Less-common sources of lead include fishing weights, bullets, car batteries, and various imported cosmetics and traditional remedies.[1] In addition, a variety of professions and hobbies involve lead exposure, including home remodeling, ceramics, furniture refinishing, and making stained glass. Not only can these types of exposure affect adults, but lead on hands and clothing can be transferred to children.[1]

Symptomatic Lead Poisoning

If levels of lead in blood are high enough -- generally above 70 μg/dL -- clinical signs and symptoms of lead poisoning and possibly acute encephalopathy may be present. Early symptoms of lead poisoning include abdominal pain and constipation. Acute lead encephalopathy is characterized by irritability, lethargy, coma, seizures, and in some cases, death.[6,7]

In 1943, Byers and Lord[8] reported that children who survived severe lead encephalopathy subsequently had significant learning problems, decreased attention span, and reduced intelligence. In other words, they were never able to "recover" from their lead exposure.

Modern Epidemiology of Lead Poisoning

Mean blood lead levels in US children steadily decreased in the 1970s and 1980s as lead was removed from paint and gasoline. As a result, symptomatic lead poisoning as described above has largely disappeared.

However, it is critical to point out that lead has effects at far lower levels than previously thought. Complex epidemiology studies have demonstrated similar cognitive and behavioral problems in cases of subclinical levels of lead in blood, thus reinforcing Byers and Lord's original findings.[9,10,11,12,13]

For example, in 1979 Needleman and colleagues[9] found a link between elevated levels of lead and cognitive and behavioral abnormalities. Children with high dentine lead levels had lower reading scores, greater inattentiveness, and lower IQ than those with low levels. Subsequent population testing has estimated a loss of 2-4 IQ points as blood lead levels increase from 10 μg/dL to 20 μg/dL.[10,11,12,13]

Epidemiologic data led the Centers for Disease Control and Prevention (CDC) to establish the current action level of 10 μg/dL in 1991.[1] The prevalence of elevated blood levels of lead in the United States has decreased substantially since then from about 8.6% in 1988-1991 to about 1.4% in 1999-2004.[14]

Who Should Be Screened

Children who live in older housing should be screened for lead poisoning. "Older housing" generally refers to structures built before 1978, although the greatest risk is from housing constructed before 1950. In addition, children in lower socioeconomic strata are at greater risk for lead poisoning. Therefore, children who are insured by government programs (Medicaid is the primary proxy) should be screened for lead poisoning with a blood lead test.

Blood lead screening is generally done on the first birthday and repeated around the second birthday. A capillary (fingerstick) blood lead test is sufficient for the first screen, but a venous sample should be obtained for confirmation if the result on the capillary screen is greater than 10 μg/dL.

What Is a "Normal" Blood Lead Level?

Healthcare providers are used to being able to classify values as either normal or abnormal. Hence, medical students and practitioners frequently ask what constitutes a normal lead level.

The answer is "none" -- no blood lead level is normal because lead serves no physiologic function in the human body. Practitioners should not confuse this fact with the CDC designation of a blood lead level of 10 μg/dL as the "action level."[1] The setting of an action level does not imply that a blood lead level less than 10 μg/dL -- or even less than 5 μg/dL-- is normal. Instead, a level below above 10 μg/dL indicates a point at which public health measures should be implemented.

Blood Lead Levels Below 10 μg/dL

More recently, studies have examined the effect on IQ of blood levels of lead lower than 10 μg/dL. Researchers have found that the steepest rate of decline in IQ occurs when levels increase from 3 to 8 μg/dL.[15,16,17] The data suggest that no threshold exists for the adverse effects of lead. Despite these preliminary data, the CDC's action level has not changed since 1991.[1]

Blood Lead Levels of 10 μg/dL or Higher

According to CDC guidance, follow-up monitoring and education should be provided when a child's blood lead level is 10 μg/dL or higher.

Providers should attempt to identify the probable source of lead through an environmental history.[18] As noted above, the most common source is old housing with deteriorating paint or dust from the paint.[19,20]

Steps to reduce exposure include testing paint and dust to identify sources of lead, regularly wet-mopping floors and wet-wiping window wells and window sills, and regularly washing children's hands and toys. If repainting or renovations need to be done in a home built before 1978, lead-safe working methods must be followed and pregnant women and children should not be present. Scraping old paint has the potential to release even more lead into the home.[21]

All tap water used for drinking and cooking should come from the cold tap. If the municipal water supply is safe but pipes leading to the home contain lead, the tap should run for 1 or 2 minutes before the water is used for these purposes. Reboiling water should be avoided.[22]

The CDC recommends adequate dietary intake of iron and calcium for persons with elevated blood levels of lead. Sufficient iron is believed to prevent lead absorption because iron and lead compete for absorption sites in the gut. Study results in humans, however, have been inconsistent on whether dietary iron intake affects levels of lead in blood. The evidence on whether dietary calcium affects blood lead levels is also somewhat conflicting. No evidence exists to suggest that supplementation with either iron or calcium reduces these levels, which is why the CDC guidelines emphasize dietary intake of these minerals.

Children with elevated blood lead levels are at increased risk for iron deficiency, although whether this deficit is entirely related to lead or to a confounder based on socioeconomic status is not well-defined.Children with elevated levels of lead also may be at increased risk for calcium deficiency.[18]

For more information on ways to reduce lead exposure, see the Website of the CDC.[1]

Providers should schedule an initial follow-up visit after 3 months, with additional follow-up testing as recommended by the CDC. Because the half-life of lead in blood is approximately 30 days, testing at the 3-month mark may show a reduction in blood levels if the source of contamination has been sufficiently addressed. Failure of the blood lead level to decrease may indicate either continuing exposure or a high level of bone lead, which will reequilibrate when levels begin to decrease.

The length of time needed for blood lead levels to move out of the high-risk zone depends on peak blood lead levels, as well as length of time of elevation. One study found that blood lead levels between 10 and 14 μg/dL take about 9 months to decline to less than 10 μg/dL. The length of time for decline increased for each successive category of peak blood levels: 14 months for 15-19 μg/dL, 21 months for 20-24 μg/dL, and 24 months for 25-29 μg/dL.[23]

Blood Lead Levels of 20 μg/dL or Higher

If levels of lead in the blood reach 20 μg/dL or higher, or stay at 15 μg/dL or higher over an extended period, more intensive management is needed. The state should step in at this point to conduct a home visit and to assess the environment.[18]

Blood Lead Levels of 45 μg/dL or Higher

Persons with a blood lead level of 45 μg/dL or higher should receive chelation according to CDC guidelines.[18] Chelation therapy involves the administration of dimercaptosuccinic acid (DMSA), also known as succimer. The lead binds to the drug and is excreted in the urine.

The CDC does not recommend chelation for blood levels below 45 μg/dL. Although a randomized, controlled trial of chelation for levels in the range of 20-44 μg/dL found that chelation made the level decrease more rapidly initially, the eventual decline over time was similar because of the rebound effect on lead levels following chelation. More important, chelation had no affect on cognition in this group.[24,25]

Summary

Although the prevalence of elevated blood lead levels has decreased nationwide, children remain at risk for lead poisoning. Prevention, both primary and secondary, is the most important way to reduce the morbidity associated with lead poisoning.

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