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Draft Briefing Paper 08-1-95

Summary of the Problem

In general, toxicity arising from exposure to lead in the environment has been considered a pediatric disease. Occupational lead toxicity which affects adults is still a major problem in industry throughout the world. Recent data on the health effects of lead focus on that adverse health effects have been observed in young children continually exposed to low levels of lead and that the population potentially at risk from low-level lead exposure and toxicity has been expanded beyond the young child to include the fetus, adults, and the aging.

Canadian Recommendations1

• Establishment and implementation of regulations and standards for lead in the air, water, food, soil and gasoline at federal and provincial levels;
• Development of a set of specific health-based multimedia guidelines and strategies for prevention and reduction of lead exposure both adult population and child population;
• Emphasis on the prevention of neurobehavioural effects in the younger children with control of blood lead level below 10 µg/L in children.

Lead in the Environment

Lead occurs from natural or anthropogenic (man-made) sources in the environment. Common sources of lead exposure come from occupational settings (plumbers, pipe fitters, lead miners, auto mechanics, glass manufacturers, shipbuilder, printers, plastic manufacturers, lead smelters and refiners, police officers, steel welders or cutters, construction workers, manufacturers of rubber, gas station attendants, battery manufacturers and bridge reconstruction workers), the general environment (lead-based paint, soil/dust, plumbing leachate, roadway, glazed and leaded gasoline), or hobbies (glazed pottery making, target shooting, lead soldering, painting, preparing lead shot, stained-glass making, car or boat repair, home remodeling, folk remedies, "health" food, cosmetics and "moonshine" whiskey).2 Soil is a major sink for anthropogenic lead (e.g., contamination from industrial emissions, coal ash, flaking paint (particularly in and around house or building), sewage sludge, mining and smelting as well as fallout from automobile emissions).3-5 The recent withdrawal of leaded gasoline from the market in Canada will reduce the importance of automobile emissions contributing to soil contamination.

The general population is exposed to lead in ambient air, in many food, in drinking water, and in dust. Certain sensitive groups of the population are at the greatest risk of experiencing adverse health effects from lead exposure. These include preschool age children (less than 6 years old), pregnant women and their fetuses, the elderly, smokers, alcoholics, and people with genetic diseases affecting heme synthesis, nutritional deficiencies, neurological or renal dysfunction, and white males between 40-59 years of age.6

The most significant exposure pathways that contribute to the current body burden of lead include air inhalation, inhalation or direct ingestion of settled dust, and the ingestion of food and water. Direct inhalation of lead accounts for only a small part of the total human exposure, and Health & Welfare Canada estimated that approximately 23% of an urban adult's daily lead intake and 1-2% of a child's come from inhalation of lead.7 However, inhalation of lead contaminated dust is common. The direct ingestion of dust or soil, resulting from swallowing lead deposited in the upper respiratory tract or through normal mouthing activity and pica (abnormal tendency to eat substances not normally eaten), is one of great potential importance, especially for children.8-11 The ingestion of food and water is another major pathway for general population exposure to lead. The global daily intake of lead estimated by UNEP12 was 80 µg/d for food and 40 µg/d for drinking water. A daily intake of 16.5 µg/d (both food and water) in the diet of Canadian infants was observed.13

Childhood Exposure

Children may be exposed to lead from a variety of sources. Recently, more than 1.2 million children in the U.S.(<6 years of age) have been estimated to have blood lead levels that exceed 15 µg/dl as a result of living in deteriorated housing with lead paint; 188,000 children may have blood lead levels that exceed 25 µg/dl; 240,000 children may have elevations in blood lead to toxic ranges due to tap water lead; and as many as 11.7 million children (<7 years of age) are exposed to lead in dust and soil from a variety of sources.6,14 In addition, FDA estimated that in 1990, 2-year-old children received 16% of their total lead exposure from food (5 µg/d), 1% from soil, 7% from water, and 75% from dust. Other significant sources of lead in childhood exposure include lead in paint, food and drinking water. 14-15 Occasionally, children may be exposed to lead from unexpected sources, such as electric urn, stove-top kettle, cosmetics, ceramic glaze, formula preparation with lead-contaminated renovation, folk medicines, and aural, nasal, or gastrointestinal foreign bodies.16-19 A more recent concern has also been raised regarding the potential risk from the paint removal or "deleading" process which may result in a significant, albeit transient, increase in blood lead.20-22

The major source of lead exposure for fetus is from pregnant women. 1984 blood lead prevalence projection techniques from NHANES II data to determine numbers of white and black women of childbearing age and pregnant women in the U.S. 4.4 million women of childbearing age and 403,200 pregnant women are estimated to have blood lead levels >10 µg/dl.23 Over the next 10 years, the projected cumulative numbers of fetus at risk of health effects from lead exposure will be over 4 million and about 20 million over the next 50 years.

Measurement of Lead in Humans

Exposure assessment for an individuals who is exposed to lead may be through biological monitoring. One of the best way to evaluate the exposure to lead from all sources is to determine the concentrations of lead in blood. Measured blood levels can then be correlated with adverse health effects observed in exposed individuals. Research has shown that elevated lead levels in dust or soil may cause elevated blood lead concentrations, especially in children.

There are two general approaches to evaluating the levels of inorganic and organic forms of lead in tissues or fluids.24 The first involves measurement of the concentrations of lead in a body fluid (blood, urine) or in a tissue (teeth, bone). The blood lead level is by far the most popular and useful of the direct measurement of lead, and reflects current exposure due to the short half-life of blood lead (28-36 days ).25 However, lead in this body fluid is not a reliable indicator of body burden. Because the greatest proportion of absorbed lead is deposited in bone, this compartment is best suited for determining body burden in adults.26

The alternative approach is to measure the concentration of a heme precursor in blood (protoporphyrin IX) or in urine (d-aminolaevulinic acid (ALA)) or to measure inhibition of ALA dehydratase (ALAD) in blood. Lead interferes with heme biosynthesis by altering the activity of three enzymes: ALA synthetase (ALAS), ALAD and ferrochelatase. Enzyme inhibition occurs at very low level of lead (3-5 µg/dl) and the net result is the increase in the blood and urine concentrations of ALA.27 Consequently, these parameters are more accurate to reflect the biologically active fraction of circulating lead. Particularly, erythrocyte protoporphyrin (EP), which is a reliable indicator of past chronic exposure since erythrocytes retain EP acquired from bone for their lifetime, is used for screening asymptomatic children for lead toxicity.28

Health Effects in Humans

In the early this century, concern has been focused on occupational toxicity and overt clinical illness: severe anemia, neuropathy or encephalophathy, colic and renal failure, at high blood lead levels of >70-80 µg/dl in both adults and children. In the early 1970s, subclinical toxicity in both occupational workers and general population had been recognized at blood lead concentrations of 40-60 µg/dl for adults and below 25 µg/dl for children. In the 1980s, many studies reported effects of lead on children's intelligence quotient (IQ), academic achievement, and behavior at very low blood lead levels. The Centers for Disease Control Advisory Committee has, recently, concluded that lead toxicity may be found at levels of 10 µg/dl and that effects may occur at levels below that.29 The Centers for Disease Control has lowered their definition of what they consider to be elevated blood lead levels and lead toxicity no less than three times in the past 22 years: 30 µg/dl in 1970, 25 µg/dl in 1985 and 10 µg/dl in 1992. Today preventive strategies should focus on the millions of children at risk.30

Hematological Effects. Lead effects on the hematological system have long been recognized. And moderate anemia is a common feature of clinic lead poisoning. The lead-induced anemia is produced principally by two mechanisms: an interference with heme synthesis and increased rate of erythrocyte destruction, resulting in reduced circulating hemoglobin.6,31-32 Little is known regarding the dose-response relationship between blood lead levels and hemoglobin concentration. Anemia has been reported to occur in children at the range of blood lead levels of 40-130 µg/dl and in adults at >50 µg/dl.33 Lead-induced anemia was a biologically and clinically important consequence of lead absorption, even at low levels of exposure 15.

Neurological effects. Lead may affect both the peripheral and central nervous system. High concentration lead exposure is associated with encephalopathy in both adults (PbB 100-120 µg/dl) and children (PbB 80-100 µg/dl).31,34-37 The most common clinical feature in adults is a peripheral neuropathy.6,38-41 Neurobehavioural toxicity had shown in adults at blood level between 30-60 µg/dl39.42-44 Since the low dose effects of interest have been seen in human studies, particularly in children, neurobehavioural toxicology has become a relatively new discipline.

Renal effects. Long-term, relatively high dose exposure to lead has been considered to be one of the causes of chronic nephropathy, which may progress to renal failure. The reliability of the diagnosis for lead nephropathy is mainly based on medical history, increased lead body burden, pathological lesions (such as interstitial nephritis, tubular atrophy, interstitial fibrosis and dilation of tubules, etc.), associated pathologies (e.g., hypertension, gout, neurological disorders and haematological disorders), and renal dysfunction manifested as aminoaciduria, glucosuria, phosphaturia, azotemia, increased sodium, decreased uric acid excretion and reduction in glomerular filtration rate6.45-48 The acute lead-induced nephropathy is likely to be reversible and occurs in children (usually at blood lead level >80 µg/dl) whose exposure are by the oral route, and occasionally in lead workers.6,45

Cardiovascular effects. Long-term, high-dose exposure to lead was reported early this century to be associated with cardiovascular disease, particularly hypertension.49 Several recent epidemiological studies from the Second National Health and Nutrition Examination Survey (NHANES II), the British Regional Heart Study (BRHS), and numerous other smaller-scale studies have clearly concluded that a small but positive association exists between blood lead levels and increase in blood pressure, even at relatively low levels (as low as 7 µg/dl for middle-aged men).50-59 In addition, an estimated mean increase of about 1.5-3.0 mmHg in systolic blood pressure appears to occur for every doubling of blood lead concentration in adult males and less than 1.0-2.0 mmHg for adult females.60 The evidence is most convincing in adult men aged 40-59 years old and for systolic rather than diastolic pressure. Cardiovascular events other than hypertension, including electrocardiographic abnormalities, degenerative changes in cardiac muscle, altered vessel compliance, myocarditis and atherosclerosis, etc., have also been observed.61

Reproductive effects. Lead-induced effects on human reproductive functions have been clearly observed, especially in men at high blood lead levels. With the recent understanding of being an internal source from bone in which lead stores persist for decades, lead can affect the next generation (as a delayed transgenerational toxin) even after maternal exposure has long stopped. Higher blood lead levels were associate with the increase of abnormal spermatozoa, spontaneous miscarriages, stillbirth and low birth weight.62-64

Child growth and development. In 1979, Needleman et al. published a pioneering paper on the behavioral effects of low-level lead exposure in children.65-68 Since then, well-designed and well-executed investigations have been conducted for the effects of lead on children's IQ, academic achievement, and behavior throughout the world.69-73

The developing nervous system of the child makes the child more sensitive to lead exposure. The dose-response relationships for neurobehavioral effects may not only occur at blood lead levels of 10-15 µg/dl but at cord blood lead levels of 6-7 µg/dl. Based on these new data, EPA (1990)60 concluded that "a blood lead concentration of 10-15 µg/dl, and possibly lower, remains the level of concern for impaired neurobehavioral development in infants and children." Thus, this low level "ought to avoided in pregnant women, fetus, infants and young children, although it is recognized that pregnant women per se are not necessarily a population risk."

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