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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 http://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

Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for lead. August 2007 [online]. Available from URL: http://www.atsdr.cdc.gov/toxprofiles/tp.asp?id=96&tid=22. 10/26/12

Alexander BH, Checkoway H, van Netten C, Muller CH, Ewers TG, Kaufman JD, et al. Semen quality of men employed at a lead smelter. Occup Environ Med 1996;53:411-416.

Apostoli P, Baj A, Bavazzano P, Ganzi A, Neri A, Ronchi L, et al. Blood lead reference values: the results of an Italian polycentric study. Sci Total Environ 2002;287:1-11.

Baghurst PA, Robertson EF, McMichael AJ, Vimpani FB, Wigg NR, Roberts RR. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Neurotoxicol 1987;8(3):395-401.

Becker K, Kaus S, Krause C, Lepom P, Schulz C, Seiwert M, et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Int J Hyg Environ Health 2002;205:297-308.

Bellinger D. Lead. Pediatrics 2004;113(4):1016-1022.

Bellinger D. Teratogen update: lead and pregnancy. Birth Defects Research (Part A). 2005;73:409-420.

Borja-Aburto VH, Hertz-Picciotto I, Rojas LM, Farias P, Rios C, Blanco J. Blood lead levels measured prospectively and risk of spontaneous abortion. Am J Epidemiol 1999;150(6):590-597.

Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. N Engl J Med 2003;348:1517-1526.

Centers for Disease Control and Prevention (CDC). Adult blood lead epidemiology and surveillance—United States, 2003-2004. MMWR Morb Mortal Wkly Rep 2006;55(32):876-879. Available at URL: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5532a2.htm. 10/26/12

Centers for Disease Control and Prevention (CDC). Blood lead levels—United States, 1999-2002. MMWR Morb Mortal Wkly Rep 2005;54(20):513-516. Available at URL: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5420a5.htm. 10/26/12

Centers for Disease Control and Prevention (CDC). Managing Elevated Blood Lead Levels Among Young Children. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta, Ga. 2002 [online]. Available at URL: http://www.cdc.gov/nceh/lead/CaseManagement/caseManage_main.htm. 10/26/12

Centers for Disease Control and Prevention (CDC). Preventing Lead Poisoning in Young Children. Atlanta (GA). 1991 [online]. Available at URL: http://wonder.cdc.gov/wonder/prevguid/p0000029/p0000029.asp 10/26/12

Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. Updated Tables, 2012a. [online] Available at URL: http://www.cdc.gov/exposurereport/. 10/26/12

Centers for Disease Control and Prevention (CDC). CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention Recommendations in "Low Level Lead Exposure Harms Children: A Renewed Call of Primary Prevention" . Atlanta (GA). 2012b. [online] Available at URL: http://www.cdc.gov/nceh/lead/ACCLPP/acclpp_main.htm. 10/26/12

Chiodo LM, Jacobson SW, Jacobson JL. Neurodevelopmental effects of postnatal lead exposure at very low levels. Neurotoxicol Teratol 2004;26:359-371.

Hu H, Aro A, Payton M, Korrick S, Sparrow D, Weiss ST, et al. The relationship of bone and blood lead to hypertension. JAMA 1996;275(15):1171-1176.

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Inorganic and Organic Lead Compounds. IARC Monogr Eval Carcinog Risks Hum 2006;87:1-471.

Jones RL, Homa DM, Meyer PA, Brody DJ, Caldwell KL, Pirkle JL, et al. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas, 1988-2004. Pediatrics 2009;123:e376-e385. doi:10.1542/peds:2007-3608.

Kim R, Rotnitzky A, Sparrow D, Weiss ST, Wager C, Hu H. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. JAMA 1996;275:1177-1181.

Korrick SA, Hunter DJ, Rotnitzky A, Hu H, Speizer FE. Lead and hypertension in a sample of middle-aged women. Am J Public Health 1999;89:330-335.

Lanphear BP, Dietrich K, Auinger P, Cox C. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Public Health Rep 2000;115:521-529.

Leggett RW. Age-specific kinetic model of lead metal in humans. Environ Health Perspect 1993;101(7):598-616.

Mantere P, Hänninen H, Hernberg S, Luukkonen R. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Scand J Work Environ Health 1984;10:43-50.

Manton WI, Angle CR, Stanek KL, Reese YR, Kuehnemann TJ. Acquisition and retention of lead by young children. Environ Res 2000;82:60-80.

Muntner P, Vupputyuri S, Coresh J, Batuman V. Blood lead and chronic kidney disease in the general United States population: results from NHANES III. Kidney Int 2003;63:1044-1050.

Nash D, Magder L, Lustberg M, Sherwin R, Rubin R, Kaufmann R, et al. Blood lead, blood pressure, and hypertension in perimenopausal and postmenopausal women. JAMA 2003;289(12):1523-1531.

O'Flaherty EJ. Physiologically based models for bone-seeking elements. IV. Kinetics of lead disposition in humans. Toxicol Appl Pharmacol 1993;118:16-29.

Payton M, Hu H, Sparrow D, Weiss ST. Low-level lead exposure and renal function in the Normative Aging Study. Am J Epidemiol 1994;140:821-829.

Pirkle JL, Kaufmann RB, Brody DJ, Hickman T, Gunter EW, Paschal DC. Exposure of the U.S. population to lead: 1991-1994. Environ Health Perspect 1998;106:745-750.

Schwartz BS, Lee BK, Lee GS, Stewar WF, Lee SS, Hwang KY, et al. Association of blood lead, dimercaptosuccinic acid-chelatable lead, and tibia lead with neurobehavioral test scores in South Korean lead workers. Am J Epidemiol 2001;153(5):453-464.

Schwartz J. Lead, blood pressure and cardiovascular disease in men. Arch Environ Health 1995; 50:31-37.

Soldin OP, Hanak B, Soldin SJ. Blood lead concentrations in children: new ranges. Clin Chim Acta 2003;327:109-113.

Smith DR, Osterloh JD, Flegal AR. Use of endogenous, stable lead isotopes to determine release of lead from the skeleton. Environ Health Perspect 1996;104(1):60-66.

Staessen JA, Roels H, Lauwerys RR, Amery A. Low-level lead exposure and blood pressure. J Hum Hypertens 1995;9:303-327.

Telisman S, Cvitkovic P, Jurasovic J, Pizent A, Gavella M, Rocic B. Semen quality and reproductive endocrine function in relation to biomarkers of lead, cadmium, zinc, and copper in men. Environ Health Perspect 2000;108(1):45-53.

Wilhelm M, Schulz D, Schwenk M. Revised and new reference values for arsenic, cadmium, lead, and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Int J Hyg Environ Health 2006;209:301-305.


 
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