Biomonitoring Summary
Lead
CAS No. 7439-92-1
Lead
CAS No. 7439-92-1
Lead
CAS No. 7439-92-1
General Information
Elemental lead is a soft, malleable, dense, blue-gray metal that occurs naturally in soils and rocks. Lead is most often mined from ores or recycled from scrap metal or batteries. Elemental lead can be combined with other elements to form inorganic and organic compounds, such as lead phosphate and tetraethyl lead. Lead has a variety of uses in manufacturing: storage batteries, solders, metal alloys (e.g. brass, bronze), plastics, leaded glass, ceramic glazes, ammunition, antique-molded or cast ornaments, and for radiation shielding. In the past, lead was added to gasoline and residential paints and used in soldering the seams of food cans. Lead was used in plumbing for centuries and may still be present.
Before the 1980's, the main source of lead exposure for the general U.S. population was aerosolized lead emitted from combustion engines that used leaded gasoline. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops. Since lead has been eliminated from gasoline, adult lead exposures tend to be limited to occupational (e.g., battery and radiator manufacturing) and recreational sources. However, the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al., 2000). Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery; stained glass framing; pewter utensils and drinking vessels; older plumbing systems with leaded pipes or lead soldered connections; lead-based painted surfaces undergoing renovation or demolition; imported children's trinkets and toys; lead-containing folk remedies and cosmetics; bullet fragments retained in human tissue; lead-contaminated dust in indoor firing ranges; and contact with soil, dust, or water contaminated by mining or smelting operations. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR, 2007; CDC, 1991).
Lead is absorbed into the body after fine lead particulates or fumes are inhaled, or after soluble lead compounds are ingested. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient. In the blood, absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone. Approximately half of the absorbed lead may be incorporated into bone, which is the site of approximately 90% of the body lead burden in most adults. The skeleton acts as a storage depot, and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al, 1996). Lead can cross the placenta and enter the developing fetal brain. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton, with a half-life of years to decades. Approximately 70% of lead excretion occurs via the urine, with lesser amounts eliminated via the feces; scant amounts are lost through sweat, hair, and nails (Leggett, 1993; O'Flaherty, 1993).
The toxic effects of lead result from its interference with the physiologic actions of calcium, zinc, and iron, through the inhibition of certain enzymes, and through binding to ion channels and regulatory proteins. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR, 2007). Large amounts of lead in the body can cause anemia, kidney injury, abdominal pain, seizures, encephalopathy, and paralysis. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects. BLLs and associated toxic effects differ in children and adults. For instance, BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger 2004; CDC, 1991; Nash et al., 2003; Schwartz, 1995; Staessen et al., 1995). In 1991, the Centers for Disease Control and Prevention (CDC) established a BLL of 10 µg/dL or higher as the level of concern in children. Recent studies suggest that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al., 2003; Lanphear et al., 2000). Many animal studies have established the multiple neurotoxic effects of lead (ATSDR, 2007).
In occupationally exposed adults, subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al., 1984; Schwartz et al., 2001), with overt encephalopathy, seizures, and peripheral neuropathy generally occurring at much higher levels (e.g., higher than 100-200 µg/dL). BLLs higher than 40 µg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al., 1996; Muntner et al., 2003; Payton et al., 1994). Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al., 2003; Schwartz, 1995; Staessen et al., 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al., 1996; Korrick et al., 1999). High dose occupational lead exposure, usually with BLLs greater than 40 µg/dL, may alter sperm morphology, reduce sperm count, and decrease fertility (Alexander et al., 1996; Telisman et al., 2000). At low environmental exposures, lead in women may be associated with hypertension during pregnancy, premature delivery, and spontaneous abortion (Baghurst et al, 1987; Bellinger 2005; Borja-Aburto et al., 1999).
Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH, respectively. Both drinking water and ambient air standards for lead have been established by the U.S. EPA. IARC considers inorganic lead compounds probable human carcinogens, and organic lead compounds not classifiable with respect to human carcinogenicity. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at https://www.atsdr.cdc.gov/toxprofiles/index.asp.
Biomonitoring Information
Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. BLLs reflect both recent intake and equilibration with stored lead in other tissues, particularly in the skeleton. Urine levels may reflect recently absorbed lead, though there is greater individual variation in urine lead than in blood and greater potential for contamination.
The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U.S. adult residents. Overall, the national prevalence rate for adults with BLLs 25 µg/dL or higher was 7.5 per 100,000 adults; the prevalence rate has declined annually since 1994 (CDC, 2006). A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC, 2005). The U.S. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC, 2012). A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.07 µg/dL (Becker et al., 2002), almost double the geometric mean of 1.75 µg/dL in U.S. adults in the 1999-2000 NHANES sample. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.S. adults in the 1999-2000 NHANES sample (Apostoli et al., 2002a).
In NHANES 1999-2002 in children 1-5 years old, both the geometric mean (1.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.6%) were lower than those from NHANES 1991-1994, when the geometric mean BLL was 2.7 µg/dL and 4.4% of children had BLLs of 10µg/dL or higher (CDC, 2012a; Pirkle et al., 1998). More recently, Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.6% in NHANES1988-1991 to 1.4% in NHANES 1999-2004, which is an 84% decline. Temporal declines in children's BLLs have been found in other developed countries (Wilhelm et al., 2006). Surveillance data reported by U.S. state childhood lead programs also show a decline in the percentage of children younger than 6 years of age who had BLLs of 10 µg/dL or higher. Data submitted through state public health programs from 2006 showed that 1.21% of approximately 3.3 million children tested had BLLs of 10 µg/dL or higher. However, BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors, including minority race or ethnicity; urban residence; residing in housing built before the 1950's; and low family income (CDC, 1991; CDC, 2002; Jones et al., 2009). For example, approximately 11,000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample; the geometric mean BLL was 3.2 µg/dL in males and 3.0 µg/dL in females (Soldin et al., 2003). Recently, the CDC has adopted its expert advisory panel recommendation to use a reference level based on the 97.5 percentile blood lead estimate in U.S. children ages 1-5 years old. This value will be used to identify children with excessive lead exposure (CDC, 2012b). The terminology "blood lead level of concern" will no longer be used.
Biomonitoring studies on levels of lead provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of lead than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.
References
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