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Chapter 3

LEAD

INTRODUCTION

Throughout history lead has been mined, smelted, and used for a variety of purposes including plumbing (plumbum is Latin for lead), paint pigments, cosmetics, medicine, glazes, food sweeteners, and wine stabilizers. But the ill effects of lead have also been known for millennia. As early as the second century B.C., for instance, the Greek physician Nikander wrote of the "grave ills" caused by lead poisoning, including "feeble limbs" and low energy.

Lead is now recognized as the single most significant environmental health threat to American children.[1] Average blood-lead levels in Americans have plummeted over the past twenty years owing in large part to the federal government's bans on the use of lead in gasoline and residential paint.[2] The U.S. food industry has also helped, having halted the use of lead-soldered cans by 1992.[3] The result: while in 1976 the average level of lead in the typical American was 12.8 micrograms of lead per deciliter (µg/dL) of blood,[*] by 1988, it was about 2.8 µg/dL.[4] Today it is 2.3 µg/dL.[5] At the same time, scientific research has shown convincingly that low levels of lead exposure, once thought safe, are hazardous. Despite the dramatic reduction in sources of lead exposure, lead poisoning remains a reality for a disturbingly high number of people in this country -- particularly children.

Today, the effects of lead most often present themselves as chronic and debilitating, rather than acute and deadly. Lead poisons huge numbers of people of all ages and walks of life, but most vulnerable are the very young.[6] Although lead can affect adults, those most sensitive to lead's adverse effects -- and at highest risk -- are infants, children up to six years, and fetuses.[7] Unfortunately, most lead-exposed children do not present easily diagnosed symptoms.

The Third National Health and Nutrition Examination Survey (NHANES III, a nationwide, cross-sectional health survey studying persons aged one year or older) reported in 1997 that some 900,000 American children aged one to five years have blood-lead levels higher than the Centers for Disease Control's level of concern (10 µg/dL).[8] The toxicity of lead in relatively small doses is associated with learning disabilities, poor attention spans, and lowered IQ scores.[9] In addition, a variety of behavioral problems both subtle and serious stem directly from the presence of lead in our children.[10]

The political and economic dimensions of lead poisoning are profound. Though lead is no longer added to gasoline, paint, plumbing fixtures, or solder, very little has been done in most states to eliminate the hazards posed by lead in existing paint and plumbing systems and the reservoir of lead-contaminated soil and dust. For example, in 1995 the federal government estimated that 83 percent of the privately owned housing units built before 1980 contain some lead-based paint and that 19 percent of these residences, or twelve million homes, are occupied by families with children under the age of seven.[11]

Public concern about lead is rising. The number of children exposed to lead paint has caused an increase in lawsuits and high-priced awards in New York City, for instance. In the 1995 fiscal year, the city received 443 lead-paint claims on behalf of children exposed to lead in city-owned apartments, topping the 390 claims filed the previous year. These cases could cost the city $500 million in the next few years; $230 million was paid in 1994 to settle such claims against the city.[12] Both public and private landlords throughout the country have growing concern over lead-related litigation.

The good news is that lead poisoning is preventable, and there is much that parents can do to protect their children. This chapter describes scientific research on the health impacts of lead on children, suggested measures that concerned parents and others can take, model programs of local solutions that have worked throughout the nation, some regulatory safeguards currently in place, and government efforts that should be supported and improved.

HAZARDS OF LEAD

The first modern clinical study of lead's health effects was made in 1839 by Tanquerel des Planches, who published the results of a study of 1,207 persons with lead colic; more than 800 of these were painters or workers involved in the manufacture of white or red lead pigments.[13] As the century advanced, more studies were conducted, with the first description of childhood lead poisoning appearing in 1892, authored by an Australian doctor.[14] But it was only in the 1950s, in New York City, Chicago, Philadelphia, and other large cities that the first attempts were made to understand the true extent of lead poisoning in children.[15]

Knowing more about how lead adversely affects health has led the Centers for Disease Control (CDC) to reduce what it considers an acceptable blood-lead level three times over the past twenty years.[16] Until the early 1970s, the concentration of lead in the bloodstream considered to constitute poisoning was 60 µg/dL in children and 80 µg/dL in adults. Early in 1990, various federal agencies took a series of steps that lowered the acceptable lead level in blood. In 1991, the CDC followed suit by defining lead poisoning as a blood-lead level of 10 µg/dL or greater.[17]

Results from the 1994 Third National Health and Nutrition Examination Survey (NHANES III) were simultaneously encouraging and alarming. Between NHANES II reporting data from 1976 to 1980 and NHANES III reporting data from 1988 to 1991, the percentage of children aged one to five years suffering from lead poisoning decreased from 88.2 percent to 8.9 percent.[18] By Phase 2 of NHANES III reporting data from 1991 to 1994, the percentage of children under the age of six with unacceptable blood-lead levels had further declined to 4.4 percent.[19] This decline can be attributed to government and industry efforts to eliminate lead from gasoline and to reduce exposures from house paint, drinking water, and consumer products.[20] At the same time, this means that nearly one million children still have blood-lead levels at or above 10 µg/dL, the level which the CDC has determined to be of health concern.[21] According to the NHANES III-Phase 2 study, blood-lead levels were consistently higher for younger children than for older children, for older adults than for younger adults, for blacks than for whites, and for low-income families than for higher income families. Children residing in older housing are also more likely to have blood-lead levels greater than the CDC's level of concern.[22]

How Lead Poisons the Human Body

There are two ways by which most lead poisoning occurs: ingestion and, to a lesser extent (in the United States), inhalation. Once in the blood, lead is distributed primarily among blood, soft tissue (such as kidney, bone marrow, liver, and the brain), and mineralizing tissue (such as bone and teeth).[23] For adults, bones and teeth contain about 95 percent of the body's total burden of lead.[24] Bone and teeth store lead in different ways, which affect the rate at which the lead is resorbed into the rest of the body. When the body is under physiological stress such as pregnancy, lactation, or chronic disease, the normally inert lead can be mobilized, which will increase the lead level in blood. Because of these mobile lead stores, significant drops in a person's blood-lead level can take several months or sometimes years to materialize, even after complete removal from the source of lead exposure.[25]

The rate at which lead is absorbed by the body depends upon its chemical and physical form and on certain physiological characteristics of the exposed person, such as age and nutritional status. [26] For instance, the gastrointestinal tract of adults typically absorbs from 10 to 15 percent of the lead that is ingested; for pregnant women and children, this figure can be as high as 50 percent.[27] The quantity absorbed increases significantly under fasting conditions and with iron or calcium deficiency.[28] Inhaled lead deposited in the lower respiratory tract of adults and children is completely absorbed by the body.

For lead poisoning to develop, major acute exposures to lead need not occur. The body accumulates this metal over a lifetime, so even small doses, over time, can cause lead poisoning. It is the total body burden of lead that is related to the risk of adverse effects.[29] In exposure studies with adults, lead has a half-life in blood of approximately twenty-five days; in soft tissue, about forty days; and in the non-labile portion of bone (the "pools" from which lead is leached during times of physiological stress), more than twenty-five years. [30] Consequently, after a single exposure a person's blood-lead level may begin to return to normal; the total body burden, however, may still be elevated. The cumulative nature of lead necessitates that attention be paid to low levels of lead intake, for such levels add up to significant exposure over time.[31] Of course, acute poisoning can also occur after a single high-level exposure to lead.

Lead is devastating to the body for a variety of reasons. It inhibits production of heme for human hemoglobin necessary for oxygen transport. Lead also interferes with normal cellular calcium metabolism. It binds to most calcium-activated proteins, but with 100,000 times the affinity of calcium; once bound, it interferes with the normal actions of these proteins.[32] Because calcium and calcium-binding proteins serve as the messengers for many basic cellular processes, even small amounts of lead can do damage.

Health Effects

Death from encephalopathy or massive brain damage can occur in children with untreated blood-lead concentrations of 150 µg/dL and higher.[33] Approximately 10 percent of the concentration that can cause death can cause cognitive disturbances such as reduced attention span and memory, learning disabilities, and lowered IQs.[34] In addition, the cognitive effects of lead have been found in infants and children with blood-lead concentrations of 10 µg/dL,[35] and other studies have reported effects of lead at 10 to 15 µg/dL on growth rates, attained stature, birthweight, gestational age, auditory functioning, attention span, blood pressure, and some of the general metabolic pathways.[36] Some scientists have suggested that low-level chronic lead exposure in childhood may alter secretion of the human growth hormone, thus reducing the stature of children and increasing their chances for obesity, the effects of which persist into adulthood.[37]

Somewhat higher blood-lead concentrations disrupt the synthesis of heme, the essential and main component of red blood cells. Heme is responsible for the transport of oxygen in the blood. Some resulting effects described above -- cognitive dysfunction and behavioral disorders -- might well be irreversible.[38] With the review and concurrence of the Science Advisory Board, the EPA concluded that lead is a probable human carcinogen.[39] Emerging research indicates that no amount of lead is safe for a child. The EPA has established a goal of zero lead in drinking water, because "there are no clearly discernible thresholds for some of the non-cancer health effects associated with lead."[40]

The cumulative nature of lead buildup in the body (lead is stored in bone and released over time) requires that attention be paid to low levels of lead intake, for continuing exposure to low doses can add up to significant exposure over time.[41] This fact presents a special problem for pregnant women[42] by virtue of the danger to the fetus.[43] Lead ingested or inhaled by a pregnant woman is absorbed into the blood and can cross the placenta, thereby directly affecting the developing fetus. In addition, the physiological strain of events like pregnancy and nursing can mobilize preexisting lead stores in teeth and bones;[44] this lead re-enters the blood where it can be passed on to the fetus.[45]

SPECIAL VULNERABILITY OF CHILDREN

Children are in double jeopardy from the ill effects of lead, because their highest potential for exposure occurs when they are most physiologically susceptible. One of the reasons for the high exposure potential is behavioral patterns: children engage in more hand-to-mouth activity than adults, and so ingest more contaminants in dust or dirt.[46]

This high exposure comes at a time when children's bodies are building their vital organs and skeletal and neural structures.[47] Children readily absorb lead from their gastrointestinal tracts, and lead is particularly toxic to their developing nervous systems. In addition, children's bodies are not as efficient at sequestering circulatory lead in bones, and thus a higher fraction of the total lead burden becomes available to exert toxic effects on internal organs.[48] For fetuses, the risk is even greater. They have no metabolic or anatomical barrier to lead uptake, and thus no protection at crucial time periods when important organs like the central nervous system are developing.[49]

Children are generally at high risk of lead poisoning when their nutritional needs are the greatest and when nutrient deficiencies are likely to occur. Growing children are most in need of calcium, iron, zinc, and protein. The absence of these nutrients from a diet increases a child's chances for absorbing more lead.[50]

Unfortunately, when poisoned, most children do not present overt symptoms. Sometimes the symptoms of lead poisoning are nonspecific, ranging from irritability to stomach upset. As a result, the majority of cases go undetected.[51]

Children's Health Effects from Exposure to Lead

Though severe lead exposure (blood-lead levels greater than 80 µg/dL) can cause comas, convulsions, or death,[52] most recent studies have focused on the effects of lower levels (around 10 µg/dL), which do not cause distinctive symptoms. A 1993 National Academy of Sciences report summarized the health effects of lead exposure and found ill effects at blood-lead concentrations around 10 µg/dL in children.[53] Lower blood-lead levels have adverse effects on the central nervous system, kidneys, and hematopoietic system (responsible for the production of blood cells and platelets).[54] Many other effects begin at these low blood levels, including decreased stature or growth,[55] decreased hearing acuity,[56] and decreased ability to maintain a steady posture.[57]

Recent studies of children with low but elevated blood-lead levels strongly link lead with decreased intelligence and impaired neurobehavioral development.[58] Many carefully designed cross-sectional studies in several countries have been conducted over the past twenty years to examine the relationship between IQ levels and lead exposure. A study published in Epidemiology suggests that lead damage to children's developing brains could make the difference between their being on the low end of normal intelligence and dropping below normal.[59] The result could be a tripling of the number of youngsters who need specialized educational services. The study has been following more than 494 infants born in or near the lead smelting town of Port Pirie in Australia. By age seven, the visual-motor abilities of most children with relatively low levels of lead (defined as below 20 µg/dL) in their blood were adversely affected; such deficits could hamper a child's ability to read, write, and solve math problems by interfering with brain mechanisms involved in recognizing and copying shapes, visualizing objects in space, and forming nonverbal concepts.

One study by researcher Herbert H. Needleman examined the educational success of young adults relative to the amount of lead found in teeth they shed as first- and second-graders. In this study, dentine lead levels above 20 parts per million (ppm) were associated with a sevenfold risk of not graduating from high school and a six-fold risk of having a reading disability, as well as deficits in vocabulary, problems with attention and fine motor coordination, greater absenteeism, and lower class ranking.[60] Although dentine lead levels did not correspond in any simple way to blood-lead levels, the available preschool blood-lead levels of more highly exposed children averaged 34 µg/dL.[61] Increased dentine lead levels (greater than 16 ppm) have been linked to higher rates of learning disabilities in a 1990 Danish study.[62] A recent study examining the relationship between lead levels in the bone and delinquent behavior found that lead is correlated with antisocial behavior and delinquency in young boys, which is considered a foreshadowing of violent adult criminality.[63]

A recent Baltimore study showed that children with high blood-lead levels (mean 28 µg/dL) had a significantly higher rate of problem behaviors than comparable children with low lead levels (mean 9 µg/dL). The finding "lends support to a belief that undue lead exposure in early childhood may have a pervasive influence on the prevalence of juvenile delinquency in this country."[64]

Research begun in the 1980s also linked low levels of blood-lead to other maladies. These studies started screening of maternal blood-lead levels during the prenatal period, and monitoring continued for several years after birth. Results of these studies show a link between prenatal exposures and slower sensory-motor skills and delayed early cognitive development.[65] Research on maternal and umbilical cord blood-lead levels of 10 to 15 µg/dL indicates that babies exposed to lead are more likely to be born prematurely or have low birthweights.[66]

Children of Color

Despite the recent and large declines in blood-lead levels, young children of urban minority families are found to be at the greatest risk of lead poisoning. According to the most recent NHANES III-Phase 2 report, 8 percent of impoverished children are lead poisoned, compared to 1 percent of children from high-income families.[67] Among all children, 11.2 percent of African-American children are poisoned compared with 2.3 percent of white children.[68] Thirteen point seven percent of non-Hispanic black children one to five years of age living in housing built between 1946 and 1973 had blood-lead levels above the CDC's level of concern. In comparison, 1.4 percent of white children in the same age group living in housing built between 1946 and 1973 had blood-lead levels above the CDC's definition of poisoning.[69] The previous NHANES III-Phase I report indicated that among all low-income children, 28.4 percent of African-American children have blood-lead levels above the CDC's level of concern compared with 9.8 percent of white children.[70] Another earlier study found that twice as many black children whose annual family income is less than $6,000 have elevated blood-lead levels than white children with a similar family income.[71]

Poor, minority families live in some of the nation's oldest and most dilapidated dwellings, the hazard that has been identified by the Department of Housing and Urban Development (HUD), the CDC, and other agencies as the biggest source for lead exposure today. A recent study in Washington, D.C., found a "significantly high" concentration of lead present in soils near inner-city homes due to lead-based paint, with the majority (66 percent) of these dwellings occupied by African-Americans.[72]

Economic barriers put these groups at further risk. Parents of low-income families may be unemployed or in jobs that do not offer medical insurance; children of these families go without adequate medical care. Poor economic conditions also breed poor nutrition; without dietary elements -- such as calcium and iron -- the body's absorption of lead will increase. Language barriers and the fears of new immigrants sometimes stand in the way of helping minority communities reduce and prevent lead exposure. Lead screening and exposure reduction programs often lack effective outreach to communities that do not speak English or are underserved by medical care; therefore, educational programs may bypass these groups because they simply could not receive, read, or understand announcements.


Children of Color at Greatest Risk


Children under age six with blood-lead levels above the CDC's level of concern (10 µg/dL):
       African-American 11.2 percent
       Mexican-American    4.0  " 
       White, non-Hispanic    2.3  "

 

Children under age six with blood-lead levels above the CDC's level of concern residing in housing:
               Year Housing Built
Before 1946 1946-73
       Black, non-Hispanic 21.9 percent 13.7 percent
       Mexican-American 13.0  "    2.3  "
       White, non-Hispanic    5.6  "    1.4  "
NHANES III-Phase 2 (1991-94) CDC, 1997

Among all low-income children with blood-lead levels above the CDC's level of concern:
       African-American 28.4 percent
       White    9.8 percent
NHANES III-Phase I (1988-91)
Journal of the American Medical Association, 1994

SOURCES OF EXPOSURE TO LEAD

A common misconception is that the removal of lead from household paint and gasoline in the United States has been so successful that lead is no longer a health threat. Nothing could be further from the truth.

Ubiquitous and extremely toxic, lead continues to exist in large quantities in paint, dust, dirt, drinking water, food, and tableware. It has also been found in varnishes and pigment inks, hair dyes, anti-fouling paints, waterproofing materials, insecticides, solder, gasoline in certain foreign countries, pipes, plumbing fixtures, traditional folk remedies, and cosmetics.[73]

Once mined and introduced into the surface environment, lead persists. Over time, lead in various forms becomes available to the body as small particles. All of the 300 million metric tons of lead ever mined is still with us, largely in soil and dust. That explains in part why background concentrations of lead in modern North Americans are 300 times higher than they were in the native North American people before European settlement.[74] Currently, lead is used at a rate of over one million tons per year in the United States.[75]

Simultaneous exposure to multiple sources of lead is inevitable, thereby making it difficult to rank sources. For preschool children and fetuses, lead in paint is the greatest source of exposure. Lead in dusts and soils, and lead in drinking water are the next most significant sources of exposure. For adults not occupationally exposed to lead, tap water is probably the greatest source of exposure.[76]

Lead in Gasoline: A Global Problem

Although lead was banned from gasoline sold in the United States in 1995, leaded gasoline remains the largest single cause of lead poisoning globally. Almost fifteen million children in developing countries may be at risk from the adverse effects of lead due to exposure from gasoline. In developing countries, all urban children under age two and more than 80 percent of those age three to five are believed to have blood levels exceeding health standards set by the World Health Organization. With automobile use soaring in developing countries, airborne lead emissions are expected to grow substantially. Almost twenty countries have banned leaded gasoline, including the United States, Canada, Thailand, Brazil, and Argentina. Although Canada and the United States consume about half of all the gasoline used in the world, only 1.2 percent of worldwide emissions of airborne lead comes from these nations. A worldwide phase-out of lead from gasoline is critical for preventing an international epidemic of childhood lead poisoning.

Source: "Unleaded, Please," The Washington Post, July 5, 1997, p. A22.

Lead in Paint

Although federal legislation banned the use of leaded paint in residential buildings in 1978, we are still living with the legacy of this use -- the chipping and peeling old paint in buildings. According to the EPA, there are approximately 64 million privately owned and occupied homes built before 1980 that contain some lead-based paint, and 12 million of these homes are occupied by families with children under the age of seven.[77] This paint contained between 0.5 and 50 percent lead.[78] Lead-based paint used prior to 1950 is likely to contain much greater concentrations of lead than lead-based paint used between 1950 and 1978. Lead-based paint hazards are likely to be concentrated in housing that is in poor condition and has significant amounts of interior lead-based paint, and in housing that has been maintained or renovated with unsafe work practices, such as the dry sanding of lead-based paint surfaces.

When lead paint peels or is disturbed -- even during minor renovations -- lead-containing dust is produced. When children crawl and play on the floor, their hands and toys may become contaminated with lead dust, from which it is readily transferred to the hands and mouths of infants and toddlers. Since it is normal for infants and toddlers to explore their world by putting their hands on objects which they pick up into their mouths, they can easily ingest lead. Small children may chew on toys, furniture, or window ledges. If swallowed, even the tiniest lead particles are dangerous, for it takes only a very small amount of lead to hurt a child. Exterior paint is usually much higher in lead content, and thus more dangerous when it becomes accessible to the interior at windowsills.[79]

Chipped pieces of deteriorating leaded paint pose a danger to children, and children are also likely to be poisoned by inhaling and ingesting the finer particles that flake off as a result of the friction of the opening and closing of windows and doors. These heavy lead particles settle on windowsills, wood floors, and in carpeting and other low-lying areas where children play. Similarly, flakes and particles from exterior paint accumulate in the soil outside a house and endanger children. In addition, children can be poisoned by eating lead-based paint chips.

Lead in Soil

Although low levels of lead occur naturally in soil, it is the lead from sources such as paint, industrial sites and fuel exhaust that bring it to dangerous levels. The concentration of lead in soil adjacent to homes with lead-based paint can be as high as 10,000 ppm, and soil next to smelters can have lead levels of 60,000 ppm.[80] The soil near roads, highways, and garages may also contain high lead levels due to years of gasoline exhaust emissions.

The EPA has established health-based interim standards for soil lead concentrations and action recommendations for each standard. In areas that children are likely to use, soil lead concentrations between 400 and 5000 ppm necessitate controls that establish physical barriers with the degree of control being commensurate with the severity of the lead hazard. In areas that children are less likely to use, controls should be implemented when concentrations are between 2000 and 5000 ppm. Soil abatement (such as soil removal or permanent covering) is recommended when concentrations exceed 5000 ppm.[81]

In 1996, the EPA estimated that 23 percent, or 18 million, of the privately owned homes in the United States built before 1980 have soil lead levels in excess of 400 ppm.[82] An estimated 8 percent of private homes built before 1980 have soil lead levels above 2000 ppm and 3 percent of pre-1980 private homes were estimated to have soil lead concentrations above 5000 ppm. The EPA could not estimate soil lead levels in public housing because soil samples were not taken. The strongest predictor of soil lead was building age.

Lead in Water

Despite measures such as the Safe Drinking Water Act, waterborne lead remains a hazard. According to a 1993 EPA report, approximately 819 water systems serving 30 million people had excessive levels of lead.[83] Until a few decades ago, lead pipes were widely used for the service lines and connections that carry water from street mains to houses. Lead-based solder was used to join standard copper household water pipes until 1986, when solder containing more than 0.2 percent lead was outlawed for plumbing. Under federal law, new brass and bronze faucets can contain as much as 8 percent lead by weight. However, the successful settlement of a lawsuit filed under California's Proposition 65 resulted in the development of virtually lead-free faucets for 90 percent of the U.S. market. Contamination occurs when water rests in pipes and faucets for several hours or longer, allowing the metal to leach into the water, which means that lead content in the water is generally at its greatest when a faucet is first opened. Factors affecting the amount of lead leaching from plumbing include the water's relative pH and mineral content.[84] In 1988, the Lead Contamination Control Act prohibited the manufacture and sale of drinking water coolers containing lead and required states to establish programs to remove drinking water coolers containing lead from schools. Implementation of the law has been less than complete.[85]

Lead in Cans

In 1986, the EPA estimated that about 42 percent of the lead in food came from lead-soldered cans.[86] The amount in soldered cans decreased markedly throughout the 1980s. In 1980, 47 percent of food and soft drink cans were lead-soldered. By 1985, this figure had dropped to 14 percent and by 1990 less than 1 percent of food and soft drink cans were lead-soldered. By 1991, lead-soldered cans had been removed from use by food companies based in the United States, but imported cans of juice and food still contained lead solder.[87] By mid-1996, the FDA had effectively banned the use of lead solder in cans of imported foods.[88]

Lead in the Workplace

Certain occupations expose adults to lead, which they can unwittingly bring home on their clothes and shoes, and on their skin and hair. People employed in lead smelting, metal foundries, battery manufacturing, salvage, radiator repair, painting, and construction are at greatest risk for exposure to dangerous levels of lead. In fact, a recent study found that the children of lead-exposed construction workers were six times more likely to have blood-lead levels above 10 µg/dL than the children of neighbors employed in non-lead industries.[89] Others also at risk are those who plate metals, formulate or use paint, dyes, inks, and glazes, as well as those who are potters, welders, electricians, boat builders, and weapons buffs.[90] Improved safety controls in the workplace are needed to reduce lead exposure, both to workers and their families. In addition, simple measures such as leaving work shoes outside the house and laundering work clothing separately from other household fabrics can do much to reduce this risk.

Other Sources of Lead

Ceramic tableware is another potential source of lead exposure, because the decorative paints and glazes may contain lead, which can get into food.[91] Especially likely to leach lead are acidic foods such as citrus fruits, tomato-based foods, and applesauce when left on or in the tableware for an extended period of time.[92] The Food and Drug Administration (FDA) is responsible for placing limits on lead that can leach into food from ceramics.[93] The FDA has issued regulations requiring that decorative ceramicware bear a conspicuous stick-on label on a clearly visible surface and a permanent statement on the exterior surface of the base of the ceramicware stating that the piece is not for food use and that it may poison food. Alternatively, the regulation provides that a hole may be bored through the possible food-contact surface of the piece.[94] California's Proposition 65 sets lead-leaching limits far below the FDA guidelines. While it is still legal to sell a china pattern in California as long as it meets FDA standards, patterns that exceed Proposition 65 limits must bear a triangular yellow sticker and carry a health warning about exposure to lead. In 1992, six hundred patterns of china dinnerware met the Proposition 65 standard; by 1994, more than eight thousand patterns were in compliance.[95]

Lead exposure can stem from the use of folk remedies like azarcon and greta -- also known as liga, Maria Luisa, alarcon, coral, and rueda. Other lead-containing remedies and cosmetics include chuifong tukuwan, pay-loo-ah, ghasard, bali goli, kando, alkohl, kohl, surma, saoott, and cebagin.[96] Incidents of exposures to these medicines and cosmetics have been reported among groups from the Arab countries, India, Pakistan, China, and Latin America.[97]

Many hobbies can also result in exposure to lead. Molten lead can be used in casting toy soldiers, leaded solder is used in making stained glass (in the frames), leaded glazes are used in making pottery, and artists' paints may contain lead. Furniture refinishing may also result in lead exposure.[98]

Some households burn lead-painted wood in home stoves and fireplaces. These activities generate leaded fumes and ashes. Further contamination results from the disposal of the ashes in yards.[99]

In 1994, the Consumer Product Safety Commission (CPSC) announced the recall of twelve brands of crayons imported from China because they contained lead.[100] Since then no other incidents of lead in crayons have been reported.

In late June 1996, the CPSC determined that some vinyl miniblinds imported from China, Taiwan, Mexico, and Indonesia presented a lead poisoning hazard to children. Lead was added to stabilize the plastic, but exposure to sunlight and heat caused the formation of lead dust on the surface of the blinds. The amount of lead dust varied from blind to blind. The CPSC recommended that consumers remove the miniblinds in homes where children six and younger may be present. The CPSC found that, in some blinds, the levels of lead were so high that a child ingesting dust from less than one square inch of blind a day for about fifteen to thirty days could result in blood-lead levels at or above 10 µg/dL, the level determined to be hazardous to children. The manufacturers have changed the production process for miniblinds to eliminate lead, and new miniblinds without lead appeared in stores in late 1996.[101]

Later in 1996, the CPSC identified another potential lead poisoning hazard in paint on playground equipment. Testing by the CPSC and some state and local jurisdictions found that many school, park, and community playgrounds have metal or wood equipment with lead paint that deteriorates into lead-containing chips and dust over time due to exposure to sun, heat, and normal wear and tear.[102] The CPSC investigated older equipment in twenty-six playgrounds in thirteen cities in eleven states and found that sixteen playgrounds had equipment with lead levels in excess of the level identified by federal law (Title X). Based on the median level of lead found on older playground equipment tested, the CPSC determined that if a child ingested as little as one-tenth of a square inch of paint (about the amount that would fit on the tip of a pencil eraser) daily for fifteen to thirty days, his or her blood levels would exceed 10 µg/dL. As a result, the CPSC recommends a lead hazard assessment for playground equipment including -- as appropriate -- visual inspection, laboratory testing of paint, and permanent control measures such as replacing playground equipment or removal of lead paint. Remediation efforts must be directed to equipment with lead hazards -- most likely older playground structures.

In early 1997, the American Public Health Association, NRDC, the Alliance To End Childhood Lead Poisoning, and other organizations submitted a petition to the FDA to limit lead levels in calcium supplements and antacids.[103] The petition cites laboratory test results showing that twenty-two brands of supplements and antacids contain lead in amounts above California's Proposition 65 limit for lead exposure of 0.5 µg per day. Simultaneous to the petition, NRDC reached a settlement with one of the largest calcium supplement manufacturers to market virtually lead-free products. Calcium is an essential human nutrient that people should continue to take; it is now technically and economically feasible to manufacture calcium supplements with virtually no lead.

In 1997, scientists reported that some hair dyes contain lead at levels up to ten times the amount permitted to household paints.[104] While the form of lead in these dyes reportedly does not penetrate the scalp, the lead residue remaining on the hands of users, faucets, hair dryers, sinks and other surfaces may get on the hands of children and into their mouths. These dyes, containing lead acetate, are called "progressive" because they work by slowly changing the user's hair color over a period of several weeks.

WHAT YOU CAN DO

"Childhood lead poisoning is a man-made disease," Herbert L. Needleman has written. "Unlike other important illnesses, e.g., AIDS (acquired immune deficiency syndrome), cancer, or Alzheimer's disease, its nature is clear. Few mysteries surround it; the greater enigma is why lead has been permitted to persist in the human environment in the face of a mass of convincing data about where it is, what it does, and what is needed to get rid of it."[105]

Screen children for lead poisoning. How can adults tell if the children in their care are suffering from lead poisoning? Unfortunately, there are no outward symptoms clearly indicative of lead poisoning in the vast majority of cases, even those that would require immediate intervention.[106] When poisoned, children can sometimes exhibit a range of nonspecific symptoms -- headaches, stomach aches, cramps, or vomiting.[107]

For these reasons, the testing of blood-lead level is the only diagnostic test for lead exposure.[108] For chronic exposures, blood-lead levels often underrepresent the total body burden; nevertheless, it is the most widely accepted and commonly used measure of lead exposure. The CDC previously recommended that virtually all children be screened for lead poisoning, ideally commencing between six and twelve months of age and continuing, as needed, until age six.[109] The CDC reported that only about one-quarter of young children and one-third of poor children, who are at higher risk of lead exposure, had been screened under its universal screening recommendation.

Recently, the CDC proposed a departure from universal screening. The CDC now advises individual states to develop recommendations to ensure that any child with risk factors for lead poisoning be screened. This screening is recommended for one- and two-year-old children with risk factors for lead poisoning, such as living in housing built prior to 1950 or being a member of high-risk groups (Medicaid enrollee, poor, minority, or parents occupationally exposed to lead).[110]

Control lead-based paint hazards in your home. More than 80 percent of all housing in the United States built before 1978 contains some lead-based paint. In 1995, the Task Force on Lead-Based Paint Hazard Reduction and Financing estimated that five to fifteen million housing units contain lead hazards.[111] If managed properly, lead-based paint that is in good condition is usually not a hazard.

If you are buying a home or renting an apartment built before 1978, you should receive a pamphlet containing general information on lead-based paint hazards and disclosure of any known information about lead-based paint in the unit.

If you want to find out if your home contains lead-based paint or a lead hazard, you may hire a professional to inspect your home for lead paint and to evaluate for any lead hazards. Certified lead professionals offer two services: an inspection and a risk assessment. An inspection will determine the lead content of every painted surface in your home, but cannot tell you whether the paint poses a hazard or how to address any hazards that exist. A risk assessment will identify sources of serious lead exposure and options for controlling lead hazards.

Several states have developed certification or licensing programs for individuals who identify and assess lead-based paint for hazards. The EPA is developing a national training and certification program for lead-based paint professionals. Starting in 1999, all lead-based paint inspectors, risk assessors, and contractors must be trained and certified. For more information, contact the National Lead Information Center at 1-800-424-LEAD or your state's Childhood Lead Poisoning Prevention Program.

Parents, property owners, and contractors should take care not to inadvertently create lead dust hazards in the course of repainting or remodeling projects. Lead-based paint that is chipping or peeling, or is disturbed by a remodeling project, can easily produce lead dust hazards. Lead dust can be invisible to the naked eye and is difficult to clean up. It is important to put down plastic sheeting in the work area, to mist the paint and work area to control dust, and to clean up well at the end of the job with a wet mop and good detergent. When removing old paint, do not use any of the following unsafe practices:

  • open flame burning,
  • uncontrolled power sanding or sandblasting,
  • uncontrolled waterblasting,
  • use of heat gun operating at more than 1100 degrees Fahrenheit, or
  • extensive dry scraping.

Determine potential for lead contamination of your water supply. Plumbing is another potential source of lead exposure. Lead can contaminate your drinking water as a result of lead service lines, lead household pipes, lead solder, and lead-containing brass faucets. If you are concerned about lead in your drinking water, the first step is to have your tap water tested. Qualified labs are available to perform inexpensive lead measurement tests. (See the "What You Can Do" section in Chapter 7.) If you suspect lead contamination, or if test results indicate the presence of lead in harmful amounts, run the water, if it has been sitting in the pipes more than a few hours, at least 30 seconds before using it for drinking or cooking. (The purged water can be used for plants or dishes.) Never use hot water directly from the tap for drinking, cooking, or making infant formula. Some home water filters can remove lead from drinking water. Be sure the filter is certified by an independent testing organization such as NSF International (formerly the National Sanitation Foundation) as effective in lead removal.

In late 1992, NRDC and the Environmental Law Foundation filed a lawsuit against more than a dozen of the nation's principal manufacturers of drinking water faucets because their products leached lead into drinking water in violation of California's Proposition 65, which establishes the nation's strictest exposure standard for lead at 0.5 µg per day. By early 1996, all the defendants had agreed to technological changes resulting in the development of virtually lead-free faucets for 90 percent of the U.S. market. With this settlement, California's Proposition 65 has changed an entire industry. Extremely prominent warnings will be attached to products that do not comply. Though the agreement is enforceable only in California, the companies have said they will comply with its terms nationally as well. If you are installing new faucets in your home, ask the manufacturer whether they meet California's Proposition 65 limits for lead.

Prevent work-related exposure. The workplace is another potential source of lead exposure, particularly if you work in a radiator repair or construction, make pottery, or refinish furniture. Preventing worker exposure to lead is essential. Ideally, change clothes at work to avoid bringing lead particles home. If you wait until getting home to change, be aware that dust from clothes will reside on the car seat. Wiping car seats with a damp cloth will reduce lead levels. In any case, you should wash your leaded clothes separately from your other laundry to avoid spreading lead to other articles.[112]

Maintain a healthy diet and avoid lead-containing remedies. A diet high in calcium and iron is best for reducing a child's chances for being poisoned by lead once it is ingested. Make sure children consume adequate amounts of iron, calcium, and protein, for deficiencies in these nutrients increase the absorption of lead. [113]

Medication, particularly folk remedies, can be harmful to children because of its lead levels. Refrain from using remedies or cosmetics like alkohl, azarcon, bali goli, coral, ghasard, greta, liga, pay-loo-ah, and rueda.[114]

Seek medical treatment for lead-poisoned children. Once a child has been poisoned, the CDC recommends that children with blood-lead levels of 45 µg/dL or greater should be referred immediately for appropriate chelation therapy to remove lead from the bloodstream. To treat lead poisoning, doctors have at their disposal several drugs that are capable of binding or chelating lead, thus reducing its acute toxicity. Some practitioners prescribe chelation for children with blood-lead levels between 25 and 44 µg/dL, while others do not. Meanwhile, only minimal data exist about chelation therapy for children who have blood-lead levels below 45 µg/dL, so it is generally inadvisable at this level unless the patient is part of a clinical trial.[115]

It is not sufficient to provide treatment only; the patient and lead source must be permanently separated. (In fact, chelation is dangerous if the child is still exposed to lead.) The serious health risks posed by lead in the environment, combined with the fact that the poisoning of countless children goes undetected each year, means that prevention is critical. Thus, the creation of lead-safe environments for all people, particularly children, is an integral part of treatment.

MODEL PROGRAMS AND LOCAL SOLUTIONS

Successful prevention of lead poisoning requires controlling lead-based paint hazards as well as education and outreach to community members about childhood lead poisoning. Federal funding for abatement in low-income homes is critical. Also essential are local programs that train workers in safe lead remediation and inform citizens about lead. Below are several examples of effective programs to prevent childhood lead poisoning.

Lead Reduction Grants

The U.S. Department of Housing and Urban Development (HUD) operates the Lead-Based Paint Hazard Control Grant Program established by Title X of the Housing and Community Development Act of 1992. The purpose of the program is to reduce the exposure of young children to lead-based paint hazards in their homes. The program provides grants of one to four million dollars to state and local governments for lead control in privately owned, low-income owner-occupied and rental housing. As part of this effort, HUD also provides grants for conducting lead-based paint hazard control in low-income, privately-owned housing units on or near Superfund or "brownfield" sites. All grants are designed to stimulate the development of a trained and certified hazard evaluation and control industry. Since 1993, $335 million has been awarded to 70 grantees in twenty-six states. The work approved to date will lead to the control of lead-based paint hazards in more than 40,000 homes. These grants are a critical source of funding for lead remediation.

The EPA and the Department of Health and Human Services separately launched a program to deliver $3 million in grant funds to protect public health by reducing exposure to lead in low-income areas. The grant money is being used for five community-based projects to reduce lead exposure through education, outreach, and abatement training, which should result in the creation of jobs. The communities are Chicago, Illinois; Memphis, Tennessee; Milwaukee, Wisconsin; Missoula, Montana; and Alameda County, California. Unfortunately, this grant program will not receive further funding.

Community-Based Lead Poisoning Prevention

Federal grants for lead hazard control cannot solve the problem. In the long run, communities must develop the capacity to identify and control lead-based paint hazards. A critical element for success includes integrating the lead remediation projects into existing, ongoing housing advocacy efforts. Lead poisoning is the most critical among a range of environmental health issues that must be addressed in low-income communities. In addition, lead abatement training programs for community members must be targeted to the needs of the trainees. For example, lengthier programs that develop basic job skills in addition to providing specific information about lead are necessary for certain individuals. A one-week, information-based course will not be sufficient if the community intends the training program to help people on public assistance.

In Alameda County, California, a unique funding mechanism has been established to prevent lead poisoning. The county's assessment district levies an optional $10/unit tax on older homes and housing units certain to have lead hazards. Currently, four cities (Alameda, Berkeley, Emeryville, and Oakland) have elected to pay this tax. The money raised provides funding for economic development, community education, and loans or grants for lead remediation. A cornerstone of this program is the effort to integrate lead poisoning prevention and screening with the provision of other components of preventive medical care. In addition, county workers help assess the children's other needs and direct additional resources to the family. Because of the overall focus on well care for the child, this program should remain sustainable in the community.

Ideally, the efforts to reduce lead hazards should be within the context of providing healthy homes. For example, trained individuals from the community going into homes to inspect for lead could also test for other hazards such as carbon monoxide and radon, and could educate parents about other environmental health issues such as pediatric asthma and the associated risk factors. Dennis Livingston of Community Resources in Baltimore is a primary proponent of this critically important concept. Another feature advocated by Community Resources is the training of teenagers in the community to conduct risk evaluations for lead in homes and daycare centers.

In Cleveland, Ohio, exploratory efforts are underway for launching a Healthy Housing Partnership that builds on the education and intervention goals of the Lead-Safe Housing Program, by including asthma and other housing-related illnesses. Substandard housing conditions that contribute to lead poisoning, such as roof/plumbing leaks, are associated with environmental allergies and irritants that trigger childhood asthma exacerbations. For example, interventions that correct moisture problems and reduce household dust would not only reduce the deterioration of and therefore the exposure to lead-based paint but would also lower levels of mold and dust. A major focus of the proposed project will be to work through existing community-based organizations to train and assist building owners to integrate lead and asthma hazard-control considerations into their whole range of housing activities -- major renovation and repair, maintenance and cleaning, and tenant and homeowner education.[116]

CURRENT REGULATORY FRAMEWORK

As discussed above, the federal bans of leaded gasoline and lead-based paint have greatly reduced childhood lead poisoning. The removal of lead solder from food cans has also decreased children's exposure to lead. The FDA currently regulates the leaching of lead from ceramicware intended for food use. In 1992, Congress passed Title X of the Housing and Community Development Act, discussed below, intended to prevent childhood lead poisoning on a broad scale through lead reduction grants, training of workers for lead abatement, identification of lead-based paint hazards, and disclosure of information about lead-based paint in homes to prospective buyers or renters.

REFORMS NEEDED

Further government action remains essential as attention turns toward the remaining primary source of lead exposure: older housing in the United States. Reducing exposure to lead that may already be in the home or school will require tandem efforts from disparate groups, including property owners, landlords, tenants, parents, teachers, abatement contractors, home remodelers, and state and local agencies. Each needs to have the assurance that the others are working in a safe manner to control lead hazards. Without regulations stipulating abatement methods, efforts to clean up lead paint can increase lead exposure.

The enactment of the Residential Lead-Based Paint Hazard Reduction Act of 1992 (Title X of the Housing and Community Development Act of 1992) was an important step toward reducing lead hazards. Conceived as a transitional bill rather than as a final solution to lead-based paint hazards in housing, Title X's central purpose is to mobilize national resources to support expanded prevention efforts on a broad scale. Title X focuses attention and resources on situations believed to present lead exposure hazards. In addition to "inspections" to identify the presence of lead-based paint, Title X requires "risk assessments" to identify conditions causing lead exposures of concern. Property owners can reduce lead-based paint hazards through either short-term or long-term measures. Abatement is the elimination of lead-based paint hazards (not necessarily the removal of all lead-based paint) using strategies such as paint removal, enclosure, encapsulation, or component replacement. Interim controls temporarily reduce lead exposures through activities such as temporary containment, repairs, repainting, and specialized cleaning.

In order to build a quality abatement industry, Title X established requirements for contractor certification and licensing, trainer provider accreditation, laboratory licensing, and performance standards for testing and abatement products. In August 1996, the EPA issued regulations specifying the training and certification of individuals engaging in lead-based paint evaluation and reduction activities. The law also extends protection from lead poisoning to workers in the construction industry.

Title X imposes specific requirements and deadlines on federally owned, insured, and assisted housing to ensure that the federal government reduces lead hazards. The law also provides federal funding for reducing lead-based paint hazards in low-income private housing through a HUD competitive grants program.

Finally, through regulations effective in December 1997, the law requires disclosure of known information on lead-based paint before the sale or rental of most housing built before 1978. The EPA, under the terms of the statute, has published a pamphlet on lead hazards that must be provided to the purchaser or renter of pre-1978 housing. Home buyers have up to ten days to check the property for lead hazards at their own expense.

Ultimately, despite reductions in the use of lead in gasoline and paint, overall lead production continues to grow, and federal agencies have not addressed the impact of future increases of lead in the environment. One important and innovative proposal would have tackled this problem. In June 1993, Representative Ben Cardin (D-Md.) introduced legislation to provide a dedicated source of funds for abating lead-based paint hazards in housing and daycare centers. This legislation would have imposed an excise fee on lead ($0.45 per pound) as it is introduced in commerce (via primary and secondary smelters, and via the import of lead and lead-containing products). By increasing the price of lead, the fee would provide strong incentives for substitution and recycling. Safeguards in the trust fund legislation ensured that: benefits accrue to low-income families, federal funds are directed to the most serious hazard, abatement is done by properly trained and licensed contractors, and workers and occupants are fully protected. The bill was expected to generate thousands of jobs paying decent wages in areas with the highest unemployment levels. Unfortunately, the legislation failed to gain passage in 1994. The legislation embodies critical concepts for lead poisoning prevention. Some variation of the legislation may emerge for future congressional consideration.


Notes

* A microgram is one-millonth of a gram; a deciliter is one-tenth of a liter.

1. National Research Council, Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations. Washington, D.C.: National Academy Press, 1993, p. 1. Centers for Disease Control, Preventing Lead Poisoning In Young Children, October 1991.

2. Agency for Toxic Substances and Disease Registry, The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress, US Department of Health and Human Services, Public Health Service, 1988. Pirkle, J.L et al., "The Decline in Blood Lead Levels in the United States: the National Health and Nutrition Examination Surveys" (NHANES II, 1976 to 1980 and NHANES III, 1988 to 1991), JAMA, vol. 272, no. 4, July 27, 1994, pp. 284 - 291.

3. 58 Fed. Reg. 33863, June 21, 1993.

4. Pirkle et al., "The Decline in Blood Lead Levels in the United States."

5. CDC, "Update: Blood Lead Levels - United States, 1991-1994," Morbidity and Mortality Weekly Report, vol. 46, no. 7, February 21, 1997.

6. Brody, D. et al., "Blood Lead Levels in the US Population: Phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991)," JAMA, vol. 272, no. 4, July 27, 1994, pp. 277-283.

7. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States. Brody et al., "Blood Lead Levels in the US Population."

8. CDC, "Update: Blood Lead Levels - United States 1991- 1994,". Brody et al., "Blood Lead Levels in the U.S. Population."

9. National Research Council, Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations, p.24. Needleman, H. et al., "The Long-Term Effects of Exposure to Low Doses of Lead in Childhood," New Eng. J. of Medicine, vol. 322, January 11, 1990, pp.83-88. Needleman, H. et al., "Low-level Lead Exposure and the IQ of Children," JAMA, vol. 263, 1990, pp. 673-678.

10. Denno, D., "Considering Lead Poisoning as a Criminal Defense," Fordham Urban Law Journal, Fordham University, NY, volume XX, no. 3, 1993, page 377-400. Needleman, H. et al., "Bone Lead Levels and Delinquent Behavior," JAMA, vol. 275, no. 5, February 7, 1996, pp. 363-369.

11. U.S. EPA, Report on the National Survey of Lead-Based Paint in Housing - Base Report, April 1995.

12. Matthew Purdy, "New York Girding for Surge in Suits over Lead Damage," New York Times August 14, 1995.

13. National Research Council, Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations.

14. National Research Council, ibid.

15. National Research Council, ibid.

16. CDC, Preventing Lead Poisoning in Young Children. Pirkle et al., "The Decline in Blood Lead Levels in the United States."

17. CDC, Preventing Lead Poisoning in Young Children.

18. Pirkle et al., "The Decline in Blood Levels in the United States."

19. CDC, "Update Blood Lead Levels - United States, 1991-1994."

20. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States. Pirkle et al., "The Decline in Blood Levels in the United States."

21. CDC, "Update: Blood Lead Levels - United States, 1991-1994."

22. CDC, ibid.

23. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

24. Royce, S. and H. Needleman, eds., Case Studies in Environmental Medicine: Lead Toxicity, ATSDR, 1985.

25. Royce and Needleman, ibid.

26. Royce and Needleman, ibid.

27. Royce and Needleman, ibid.

28. Royce and Needleman, ibid.

29. Royce and Needleman, ibid.

30. Royce and Needleman, ibid.

31. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States. CDC, Preventing Lead Poisoning in Young Children.

32. National Research Council, Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations.

33. National Research Council, ibid.

34. National Research Council, ibid.

35. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

36. Schwartz, J. et al., "Relationship Between Childhood Blood-Lead Levels and Stature." Pediatrics, vol.77, 1986, pp. 281-288. Schwartz, J. and D. Otto, "Blood Lead, Hearing Thresholds, and Neurobehavioral Development in Children and Youth." Arch. Environ. Health, vol. 42, 1987, pp.153-160. Shukla, R. et al., "Fetal and Infant Lead Exposure: Effects on Growth in Stature," Pediatrics, vol. 84, 1989, pp. 604- 612. ATSDR, Toxilogical Profile for Lead, 1992.

37. Kim, R. et al., "A Longitudinal Study of Chronic Lead Exposure and Physical Growth in Boston Children," Environ. Health Pers., vol. 103, no. 10, October 1995, pp. 952-56. Denno, "Considering Lead Poisoning as a Criminal Defense."

38. National Research Council, Measuring Lead Exposure in Infants, Children, and Other Sensitive Populations, p.4.

39. 56 Fed. Reg. 26470, June 7, 1991.

40. 56 Fed. Reg. 26467-68, June 7, 1991.

41. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States. CDC, Preventing Lead Poisoning in Young Children.

42. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

43. ATSDR, ibid.

44. ATSDR, ibid.

45. ATSDR, ibid.

46. Brody et al., "Blood Lead Levels in the US Population."

47. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

48. ATSDR, ibid.

49. ATSDR, ibid.

50. ATSDR, ibid.

51. ATSDR, ibid.

52. CDC, Preventing Lead Poisoning in Young Children.

53. National Research Council, Measuring Lead Exposure in Infants, Children and Other Sensitive Populations.

54. CDC, Preventing Lead Poisoning in Young Children. ATSDR, Toxilogical Profile for Lead.

55. Shukla et al., "Fetal and Infant Lead Exposure." CDC, Preventing Lead Poisoning in Children. ATSDR, Toxicological Profile for Lead.

56. Schwartz and Otto, "Blood Lead, Hearing Thresholds, and Neurobehavioral Development in Children and Youth."

57. Bhattacharya, A. et al., "Postural Disequilibrium Quantification in Children with Chronic Lead Exposure: A Pilot Study," Neurotoxicology, vol. 9, 1988, pp. 327-40. CDC, Preventing Lead Poisoning in Children.

58. Mushak, P. et al., "Prenatal and Postnatal Effects of Low-Level Lead Exposure: Integrated Summary of a Report to the US Congress on Childhood Lead Poisoning." Environ. Res., vol. 50, 1989, pp.11-36. Brody et al., "Blood Lead Levels in the U.S. Population."

59. Baghurst, P. et al., "Exposure to Environmental Lead and Visual-Motor Integration at Age 7 Years: The Port Pirie Cohort Study," Epidemiology, vol. 6, No. 2, March 1995, pp. 104-109.

60. Needleman et al., "The Long-Term Effects of Exposure to Low Doses of Lead in Childhood."

61. Needleman, H. L. et al., "Deficits in Psychologic and Classroom Performance of Children with Elevated Dentine Lead Levels." New Eng. J. of Medicine, vol. 300, 1979, pp. 689-95.

62. CDC, Preventing Lead Poisoning in Young Children.

63. Needleman et al., "Bone Lead Levels and Delinquent Behavior."

64. Sciarillo, W. et al., "Lead Exposure and Child Behavior," American Journal of Public Health, vol. 82, no. 10, October 1992, pp. 1356-1360.

65. CDC, Preventing Lead Poisoning in Young Children. Bellinger, D. et al. "Longitudinal Analyses of Prenatal and Postnatal Lead Exposure and Early Cognitive Development," New Eng. J. of Medicine, vol. 316, 1987, pp.1037-43. Bellinger, D. et al., "Low-level Exposure and Children's Cognitive Function in the Preschool Years," Pediatrics, vol. 87, 1991, pp. 219-27. Dietrich, K. N. et al., "Low-Level Fetal Lead Exposure Effect on Neurobehavioral Development in Early Infancy," Pediatrics., vol. 80, 1987, pp. 721-30. Dietrich, K.N. et al., "Lead Exposure and Cognitive Development of Urban Preschool Children: the Cincinnati Lead Study Cohort at Age 4 Years," Neurotox. and Teratol., vol. 13, 1991, pp. 203-11. Ernhart, C.B. et al., "Intrauterine Exposure to Low Levels of Lead: The Status of the Neonate," Arch. Environmental Health, vol. 41, 1986, pp. 287-91.

66. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

67. CDC, "Update: Blood Lead Levels-United States, 1991-1994."

68. CDC, ibid.

69. CDC, ibid.

70. Brody et al., "Blood Levels in the U.S. Population."

71. Needleman, H. and D. Bellinger, "The Health Effects of Low-Level Exposure to Lead," Ann. Rev. Publ. Health, vol. 12, 1991, pp. 111-40.

72. Elhelu, M.A. et al., "Lead in Inner-City Soil and its Possible Contribution to Children's Blood Lead," Arch. Env. Health, vol. 50, no. 2, March/April 1995, pp. 165-169.

73. CDC, Preventing Lead Poisoning in Young Children.

74. National Research Council, Measuring Lead in Infants, Children, and Other Sensitive Populations.

75. Environmental Defense Fund, Legacy of Lead: America's Continuing Epidemic of Childhood Lead Poisoning: A Report and Proposal for Legislative Action, March, 1990. Bureau of Mines, Mineral Commodity Summaries, US Department of the Interior, 1989, pp. 90-91. Washington, DC:. (1988 data converted from metric tons to short tons; one metric ton equals about 2,200 pounds, while a US, or short ton, equals 2,000 pounds.)

76. National Research Council, Measuring Lead in Infants, Children and Other Sensitive Populations.

77. U.S. EPA, Report on the National Survey of Lead-Based Paint in Housing - Base Report.

78. Lead-Based Paint Hazard Reduction and Financing Task Force, Putting the Pieces Together: Controlling Lead Hazards in the Nation's Housing, 1995

79. National Research Council, Measuring Lead in Infants, Children, and Other Sensitive Populations. Environmental Law and Justice Clinic, Tenant's Handbook: Your Legal Right To Lead-Safe Housing, San Francisco: Golden Gate University School of Law, July 1995, p. 4.

80. ATSDR, The Nature and Extent of Lead Poisoning in the United States.

81. U.S. EPA, "Guidance on Residential Lead-Based Paint, Lead-Contaminated Dust, and Lead-Contaminated Soil," July 14, 1994.

82. U.S. EPA, Distribution of Soil Lead in the Nation's Housing Stock, May 1996.

83. U.S. EPA press release, "819 Cities Exceed Lead Levels for Drinking Water," May 11, 1993.

84. CDC, Preventing Lead Poisoning in Young Children

85. Mauss, E. et al., The Lead Contamination Control Act: A Study in Non-Compliance, Natural Resources Defense Council, June 1991.

86. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

87. National Research Council, Measuring Lead in Infants, Children, and Other Sensitive Populations. Can Manufacturers Institute, "Food and Soft Drink Can Shipments," Washington DC, 1992.

88. 60 Fed. Reg. 33106, June 27, 1995.

89. Whelan, E. et al., "Elevated Blood Lead Levels in Children of Construction Workers," Am. J. of Pub. Health, vol. 87, August 1997, pp.1352-1355.

90. CDC, Preventing Lead Poisoning in Young Children.

91. CDC, ibid.

92. Environmental Defense Fund, A Dish Owner's Guide to Potential Lead Hazards, 1991.

93. FDA, Compliance Policy Guide, Chapter 5, Subchapter 545, Section 545.450, December 12, 1995.

94. 59 Fed. Reg. 1638 January 12, 1994.

95. James Stratton, "Proposition 65: A Tenth Anniversary Update," Health and Environment Digest, vol. 9, no. 11, March 1996, pp. 93-95.

96. CDC, Preventing Lead Poisoning in Young Children.

97. CDC, ibid.

98. CDC, ibid.

99. CDC, ibid.

100. Office of Information and Public Affairs, CPSC, "News from CPSC: CPSC Announces Recall of Imported Crayons Because of Lead Poisoning Hazard," April 5, 1994.

101. CPSC, "News From CPSC: CPSC Finds Lead Poisoning Hazard for Young Children in Imported Vinyl Miniblinds," June 25, 1996.

102. CPSC, Staff Recommendations for Identifying and Controlling Lead Paint on Public Playground Equipment, October 1996.

103. NRDC et al., "Citizens' Petition to Initiate Rulemaking Concerning the Presence of Lead in Certain Dietary Calcium Supplements and Antacids," submitted to the U.S. Food and Drug Administration, January 27, 1997.

104. Mielke, H. et al., "Lead Based Hair Products: Too Hazardous for Household Use," J. Am. Pharm. Assoc., February 4, 1997.

105. Needleman, H. L., "The Persistent Threat of Lead: A Singular Opportunity," Am. J. of Pub. Health, vol. 79, no. 6, May 1989, pp. 643-645.

106. Stapleton, R. M., Lead Is A Silent Hazard. New York: Walker & Company, 1994.

107. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States.

108. Stapleton, Lead Is A Silent Hazard.

109. CDC, Preventing Lead Poisoning in Young Children.

110. CDC, Screening Young Children for Lead Poisoning: Guidance for State and Local Public Health Officials - Draft, February 1997.

111. Task Force, Putting the Pieces Together, June 1995.

112. CDC, Preventing Lead Poisoning in Young Children.

113. CDC, ibid. ATSDR, The Nature and Extent of Lead Poisoning in Children in the United States. Mahaffey, K.R., "Nutrition and Lead: Stratagies for Public Health," Environmental Health Perspectives, vol.103, supp. 6, September 1995, pp. 191-196.

114. CDC, Preventing Lead Poisoning in Young Children.

115. Royce and. Needleman, "Case Studies in Environmental Medicine: Lead Toxicity."

116. Greenberg, S., Healthy Housing Partnership Proposal - summary, Environmental Health Watch, September 1996.

last revised 11/25/1997

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