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Lead MSDS, Sources, Testing, Toxicity, and Health InformationLead MSDS (Material Safety Data Sheet), plus common sources, methods of testing, and health information for this toxic heavy metal is below. If you own a home built prior to 1978 you are more likely to have lead-based paint inside. If lead-based paint deteriorates and becomes paint chips or airborne dust it will greatly increase your exposure risks, with childhood Lead poisoning of particular concern.  It is estimated that more than 20 million homes may have lead-based paint chips and thus high levels of easily respirable dust with lead in it. Of these 20+ million homes contaminated with lead, many millions of them are also home to one or more children - a high risk group for the toxic effects of Lead exposure. The below Lead MSDS and answers to frequently asked questions about lead will help you identify other sources of the toxic element in or around your home and help you assess any risk of lead poisoning and help you to mitigate the health hazard. Lead from Deadly Radon Gas and Air Purifiers for Lead ControlDid you know that Radon Gas is the second leading cause of Lung Cancer and that when Radon undergoes radioactive decay it can produce Lead atoms and radiation inside your lungs? The toxic Radon decay products can also cling to tiny dust particles and be inhaled deeply into the lungs. This and the health hazards of cigarette smoke, may be one reason why smokers in homes with elevated Radon levels have a much higher risk of Lung Cancer. Everyone should have their home tested for Radon gas because it is the only way to tell if your home has elevated levels. Radon is odorless and invisible and can vary greatly from one property to the next based on geological variations. So even if your neighbor has low levels it does not mean that your home will too, and visa versa. While even the best air purifier cannot efficiently capture Radon gas directly, a high quality HEPA air cleaner will efficiently capture tiny dust particles which can act as carriers for the Radon decay products. An efficient HEPA air purifier for Lead dust may also help to reduce health risk as a result of decomposing lead-based paint chips, but not entirely or on a wholehome basis. Air cleaning is no substitute for source control measures such as thorough lead-based paint removal. Hiring a lead removal expert is a good idea in most cases. If you are interested in air cleaning for any residual particles and most other household indoor air pollutants, the best air cleaner for lead, dust, and chemical gases is the top-rated IQAir HealthPro Plus HEPA air purifier. IQAir HealthPro Plus HEPA Air Purifiers: Powerfully Efficient Air Cleaning of Solids and GasesPublic Health Statement for LeadCONTENTS:
What happens to lead when it enters the environment?
How might I be exposed to lead? Where lead is likely to be a hazard How can lead affect my health? How likely is lead to cause cancer?
How does lead affect children?
How can families reduce the risk of exposure to lead? Checking your family and home for lead What you can do to protect your family Are you planning to buy or rent a home built before 1978 Remodeling or renovating a home with lead-based paint Is there a medical test to show whether I've been exposed to lead?
Has the federal government made recommendations to protect human health from Lead?
HIGHLIGHTS:Exposure to lead can happen from breathing workplace air or dust, eating contaminated foods, or drinking contaminated water. Children can be exposed from eating lead-based paint chips or playing in contaminated soil. Lead can damage the nervous system, kidneys, and reproductive system. Lead has been found in at least 1,280 of the 1,662 National Priority List sites identified by the Environmental Protection Agency (EPA).
What is Lead?Lead is a naturally occurring bluish-gray ductile metal found in small amounts in the earth's crust. Lead can be found in all parts of our environment. Much of it comes from human activities including burning fossil fuels, mining, and manufacturing. Lead has many different uses. It is used in the production of batteries, ammunition, metal products (solder and pipes), and devices to shield X-rays. Because of health concerns, lead from gasoline, paints and ceramic products, caulking, and pipe solder has been dramatically reduced in recent years. Did you know the following facts about lead? FACT: Lead exposure can harm young children and babies even before they are born.If you think your home might have lead hazards, read on to learn about lead and some simple steps to protect your family. Synonyms for Lead:
Sources of Lead:What happens to Lead when it enters the environment?
How might I be exposed to Lead?
Where Lead is Found*In general, the older your home, the more likely it has lead-based paint. *
Where Lead is Likely to be a Hazard*Lead from paint chips, which you can see, and lead dust, which you can't always see, can be serious hazards.*
Note: Lead-based paint that is in good condition is usually not a hazard.
Household Product listing Lead as an ingredient:
Household Product listing Lead Acetate as an ingredient:
Household Product listing Lead Oxide as an ingredient:
Industrial Processes with risk of exposure to Lead:
Activities with risk of exposure to Lead:
How can Lead affect my health?Diseases associated with exposure to Lead:
Half-life of Lead:The Half-life of Lead is the time required to reduce by one half the amount of Lead absorbed by the body. Half-life can be calculated accurately only for those substances eliminated linearly, independent of concentration. For linearly eliminated substances, it takes approximately 3.5 half-lives to eliminate 90% of the substance.
How likely is lead to cause cancer?We have no conclusive proof that lead causes cancer in humans. Kidney tumors have developed in rats and mice that had been given large doses of some kind of lead compounds. The Department of Health and Human Services (DHHS) has determined that lead and lead compounds are reasonably anticipated to be human carcinogens and the EPA has determined that lead is a probable human carcinogen. The International Agency for Research on Cancer (IARC) has determined that inorganic lead is probably carcinogenic to humans and that there is insufficient information to determine whether organic lead compounds will cause cancer in humans. back to topHow does lead affect children?Small children can be exposed by eating lead-based paint chips, chewing on objects painted with lead-based paint, or swallowing house dust or soil that contains lead. Children are more vulnerable to lead poisoning than adults. A child who swallows large amounts of lead may develop blood anemia, severe stomachache, muscle weakness, and brain damage. If a child swallows smaller amounts of lead, much less severe effects on blood and brain function may occur. Even at much lower levels of exposure, lead can affect a child's mental and physical growth. Exposure to lead is more dangerous for young and unborn children. Unborn children can be exposed to lead through their mothers. Harmful effects include premature births, smaller babies, decreased mental ability in the infant, learning difficulties, and reduced growth in young children. These effects are more common if the mother or baby was exposed to high levels of lead. Some of these effects may persist beyond childhood. Health Effects of Lead*Childhood lead poisoning remains a major environmental health problem in the U.S..* *Even children who appear healthy can have dangerous levels of lead in their bodies.*
How can families reduce the risk of exposure to lead?
Checking Your Family and Home for Lead*Get your children and home tested if you think your home has high levels of lead.* *Just knowing that a home has lead-based paint may not tell you if there is a hazard.* To reduce your child’s exposure to lead, get your child checked, have your home tested (especially if your home has paint in poor condition and was built before 1978), and fix any hazards you may have.
Note: Home test kits for lead are available, but studies suggest that they are not always accurate. Consumers should not rely on these tests before doing renovations or to assure safety. What You Can do to Protect Your Family
Are You Planning to Buy or Rent a Home Built Before 1978?Many houses and apartments built before 1978 have paint that contains lead (called lead-based paint). Lead from paint, chips, and dust can pose serious health hazards if not taken care of properly. Federal law requires that individuals receive certain information before renting or buying a pre-1978 housing:
Remodeling or Renovating a Home with Lead-Based Paint*If not conducted properly, certain types of renovations can release lead from paint and dust into the air.* Many houses and apartments built before 1978 have paint that contains lead (called lead-based paint). Lead from paint, chips, and dust can pose serious health hazards if not taken care of properly.
Is there a medical test to show whether I've been exposed to lead?
A blood test is available to measure the amount of lead in your blood and to estimate the amount of your recent exposure to lead. Blood tests are commonly used to screen children for lead poisoning. Lead in teeth or bones can be measured by X-ray techniques, but these methods are not widely available. Exposure to lead also can be evaluated by measuring erythrocyte protoporphyrin (EP) in blood samples. EP is a part of red blood cells known to increase when the amount of lead in the blood is high. However, the EP level is not sensitive enough to identify children with elevated blood lead levels below about 25 micrograms per deciliter (µg/dL). These tests usually require special analytical equipment that is not available in a doctor's office. However, your doctor can draw blood samples and send them to appropriate laboratories for analysis. Low Cost Heavy Metals and Lead Test Kit
If you are concerned about other toxic chemicals (such as Formaldehyde), toxic black mold, toxins from cigarette smoke, or if you would like to know which of over 400 volatile organic compounds may be contaminating your indoor air, I recommend this professional-grade indoor air quality test kit direct from the manufacturer (much cheaper than what the experts usually charge). back to top
Has the federal government made recommendations to protect human health from Lead?
The Centers for Disease Control and Prevention (CDC) recommends that states test children at ages 1 and 2 years. Children should be tested at ages 3-6 years if they have never been tested for lead, if they receive services from public assistance programs for the poor such as Medicaid or the Supplemental Food Program for Women, Infants, and Children, if they live in a building or frequently visit a house built before 1950; if they visit a home (house or apartment) built before 1978 that has been recently remodeled; and/or if they have a brother, sister, or playmate who has had lead poisoning. CDC considers a lead level of 10 µg/dL to be a level of concern for children. EPA limits lead in drinking water to 15 µg per liter.
References
Agency for Toxic Substances and Disease Registry (ATSDR). 2005. Toxicological Profile for lead. (Draft for Public Comment). Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. The Environmental Protection Agency: "Lead in Paint, Dust, and Soil"
Where can I get more information about Lead?ATSDR can tell you where to find occupational and environmental health clinics. Their specialists can recognize, evaluate, and treat illnesses resulting from exposure to hazardous substances. You can also contact your community or state health or environmental quality department if you have any more questions or concerns. For more information, contact:
The National Lead Information Center (NLIC) provides the general public and professionals with information about lead hazards and their prevention. NLIC operates under a contract with the U.S. Environmental Protection Agency (EPA), with funding from EPA, the Centers for Disease Control and Prevention, and the Department of Housing and Urban Development. Contact the National Lead Information Center for detailed information or questions. By Phone: call and speak with a specialist Monday through Friday, 8:00 am to 6:00 pm eastern time (except Federal holidays) at 1(800) 424-LEAD [5323]. By Recorded Message: the NLIC telecommunications systems has the capability to receive recorded messages in English and Spanish 24-hours a day, seven days a week at 1(800) 424-LEAD [5323]. By FAX: 585-232-3111 By Mail: 422 South Clinton Avenue, Rochester, NY 14620 The NLIC's above hotline distributes a basic information packet on lead that includes the EPA brochure Lead Poisoning and Your Children, three fact sheets, and a list of state and local contacts for additional information. Callers who have more specific questions are referred to the Clearinghouse (800-424-LEAD) and can speak directly with an information specialist. Information specialists provide on-phone technical assistance. CDC Childhood Lead Poisoning Prevention Program This program promotes state and local screening efforts and develops improved treatments for lead exposure. Safe Drinking Water Hotline 1-800-426-4791 The Safe Drinking Water Hotline provides the general public, regulators, medical and water professionals, academia, and media, with information about drinking water and ground water programs authorized under the Safe Drinking Water Act. The Hotline is operated under contract by Booz Allen Hamilton, Incorporated, and housed in its Crystal City, Virginia, offices.
Lead MSDS InformationLead Material Safety Data Sheetacc. to OSHA and ANSI
Complete Lead Toxicology and Chemical InformationFULL RECORD CASRN: 7439-92-1 This record contains information for lead in its zero valence state only. For general toxicity and environmental fate of lead ions and lead compounds, refer to the LEAD COMPOUNDS record; for compound-specific information, to the appropriate individual record, e.g., lead iodide, lead phosphate, etc. For other data, click on the Table of Contents Human Health Effects: Evidence for Carcinogenicity: CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Sufficient animal evidence. Ten rat bioassays and one mouse assay have shown statisticlly significant increases in renal tumors with dietary and subcutaneous exposure to several soluble lead salts. Animal assays provide reproducible results in several laboratories, in multiple rat strains with some evidence of multiple tumor sites. Short term studies show that lead affects gene expression. Human evidence is inadequate. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient. /Lead and compounds/ A3; Confirmed animal carcinogen with unknown relevance to humans. /Lead, elemental, and inorganic compounds, as Pb/ Human Toxicity Excerpts: TOXIC BY INGESTION & INHALATION OF DUST OR FUME. SEVERE POISONING IS PRODUCED THROUGH EXPOSURE TO FUMES FROM LEAD FURNACES IF FUMES ARE ALLOWED TO ESCAPE & FROM DUST FROM DROSSING. MOST ... LEAD EXPOSURE STUDIES INVOLVE LEAD OXIDE DUST OR THE FUME OF METALLIC LEAD. SOME REPORTS HAVE INDICATED THAT THE DUSTS OF CERTAIN INSOLUBLE LEAD COMPOUNDS, SUCH AS THE SULFIDE & CHROMATE, WERE LESS HAZARDOUS THAN MORE SOLUBLE FORMS OF LEAD. ONE OF 2 /EPIDEMIOLOGICAL/ STUDIES ON METALLIC LEAD WORKERS SHOWED NO EXCESS OF CANCER DEATHS. THE OTHER SHOWED A SLIGHT (ALTHOUGH SIGNIFICANT) EXCESS OF DEATHS DUE TO CANCERS OF DIGESTIVE SYSTEM & RESP SYSTEM AMONG SMELTER WORKERS BUT NOT AMONG WORKERS IN LEAD-ACID BATTERY FACTORY. AS 60% OF MEMBERS OF SMELTER WORKERS COHORT WERE HIRED AFTER 1950, FURTHER FOLLOW-UP OF THIS COHORT IS WARRANTED, IN ORDER TO DETERMINE MORE RELIABLY IF THERE IS AN EXCESS RISK. Cases of lead poisoning due to retained bullets are reported only rarely but represent potentially life-threatening reactions. ... Almost all cases in USA have involved the dissolution of a single bullet over several mo to more than 20 yr. ... Bullets in joint spaces are ... more likely to cause toxic complications than are bullets lodged in soft tissues. LEAD METAL FOREIGN BODIES IN EYE OR ... ORBIT IN HUMANS ... HAVE BEEN CONSIDERED TO CAUSE LITTLE REACTION & RARELY ANY TOXIC EFFECT. CLINICAL EXPERIENCES WITH VARIOUS INTRAOCULAR FOREIGN BODIES PRESENTED IN DETAIL WITH HISTOLOGIC STUDIES ... INDICATED THAT LEAD METALLIC FOREIGN BODIES CAUSED MINIMAL INFLAMMATORY REACTION, MAINLY MECHANICAL INJURY. ... /IN ANOTHER REPORT IT WAS/ CONCLUDED THAT LEAD FRAGMENTS IN PATIENTS WERE WELL TOLERATED IN THE EYE & IN THE ORBIT & THAT THEY SHOULD NOT BE REMOVED UNLESS THEY WERE IN THE ANTERIOR CHAMBER. ... /A/ CASE /IS DESCRIBED/ IN WHICH ... A SMALL LEAD SHOT WAS ALLOWED TO REMAIN IN THE VITREOUS, THE VISION RETURNED TO NORMAL AS BLOOD IN THE VITREOUS ABSORBED OR SETTLED IN THE COURSE OF A YEAR. ... IN ONE CASE, WHICH APPEARS TO HAVE BEEN QUITE EXCEPTIONAL ... A PATIENT WITH A LEAD SHOT BEHIND ONE GLOBE HAD IMPAIRED VISION IN THAT EYE. THIS WAS ASSUMED TO BE DUE TO A TOXIC EFFECT OF LEAD. WHETHER THIS INTERPRETATION WAS CORRECT OR NOT, A SIGNIFICANT IMPROVEMENT OF VISION WAS REPORTED WHEN SYSTEMIC & TOPICAL TREATMENT WITH 2,3-DIMERCAPTOPROPANSULFONATE SODIUM WAS STARTED 5 YEARS AFTER THE INJURY. In a cross-sectional study, the neurobehavioral effects of low-level lead exposure were evaluated in a group of 59 lead workers compared with 59 matched controls. The groups were not significantly different in age, education level, sleep pattern, or use of alcohol. The mean blood lead level in the exposed group was 2.37 umol/l (50 ug/100 ml) which was similar to the previous three years (2.36, 2.36, and 2.32 umol/l, respectively). The mean duration of exposure was 8109 hrs. Visual sensory function was affected, and perhaps as a consequence sustained attention and psychomotor tasks were performed more slowly by the lead exposed group. Cognitive functions were also impaired, with sensory store and short term memories, and learning abilities all showing deficits in lead workers. Multiple linear regression analysis relating to lead workers test performance and their lead exposure showed that performance on the sensory store memory test alone was significantly related to exposure. The activities of erythrocyte (rbc) arginase, pyrimidine 5'- nucleotidase (P5N), and deoxypyrimidine 5'-nucleotidase (dP5N) were compared in 16 lead workers and 14 age-matched controls as correlates of blood lead (PbB) and unextracted zinc protoporphyrin (EP). Subjects with blood lead of 0.9-2.5 uM (19-52 ug/dl) had 6.5 + or - 0.6 IU of pyrimidine 5'-nucleotidase activity with uridine monophosphate (UMP) as substrate, significantly less (p< 0.001) than the 12.0 + or - 0.7 IU activity of controls with blood lead 0.3-0.6 uM (6-12 ug/dl). Erythrocyte pyrimidine 5'-nucleotidase was significantly correlated with blood lead (r= 0.75). There were no significant differences in erythrocyte arginase or deoxypyrimidine 5'-nucleotidase activity. In a cross-sectional study of 20 gun-metal foundry workers (mean age 47 yr) the subclinical neurophysiological effects of exposure to lead, zinc, copper, and tin were evaluated by "short-latency" somatosensory evoked potential (SSEP). Controls were age and height-matched males without occupational exposure to lead. Range of employment was 1-16 yr (mean 10 yr). In exposed workers, mean blood lead was 42 ug/dl, mean zinc plasma 95 ug/dl, mean copper plasma 105 ug/dl, and mean urinary tin 28 ug/l. In workers, the interpeak latency of SSEP in the cervico-spino-bulbar region (N9(Erb)-N13 latency) was significantly prolonged (p< 0.05), and the MCV and SCV in the forearm were significantly slowed (0.01< p< 0.05) when compared with controls. The yield of urinary lead following challenge with Ca-EDTA was positively related to SSEP latency in the cervico-spino-bulbar region and inversely related to hematocrit (p< 0.05). The interpeak latency in the upper central nervous system (N13-20 latency) was inversely related to zinc concentration in erythrocytes. Latency up to the Erbs point was inversely related to urinary zinc. MCV and SCV in the palm were positively related to erythrocyte zinc concentration and plasma copper concentration, respectively (p< 0.05). It appears that zinc antagonizes the central and peripheral neurophysiologic dysfunction caused by lead, and similarly copper antagonizes the peripheral sensory nerve dysfunction. Battery workers (N= 18), who were exposed to high airborne lead levels, /were compared/ with cement workers (N= 18), who were exposed to ambient lead levels. Blood lead urinary lead, semen lead, and zinc protoporphyrin concentrations were markedly elevated (p< 0.001) in battery workers. Battery workers had a significantly shifted (p< 0.025) frequency distribution of sperm count (median count, 45 vs 73x10x6 cells/cc, respectively). ... These results suggest a direct toxic effect of increased lead absorption on sperm production or transport in man. Lead containing particles in ambient air have an aerodynamic diameter of approx 0.1-1.0 um, & the predicted deposition in the airway is about 35%. This is questionable for smaller particles (< 0.1 um) which are mainly deposited by diffusion. Actual measurements of deposition in human volunteers gave results that differed considerably depending on the physical & chemical properties of the inhaled aerosol. ... A deposition of approx 25% /was observed/ after exposure to particles with a mass median aerodynamic diameter of 0.25 um. ... A deposition in the resp tract of about 60% /was observed/ in persons close to a motorway, where particles were about 0.03 um in diameter. This figure is consistent with lab expt carried out by the same authors, in which subjects inhaled radioactively labeled particles of about the same size. When volunteers inhaled lead particles near urban roads where the particle size was larger (0.2-2.0 um), deposition was about 50%. Based on available data, it seems reasonable to conclude that the rate of deposition of airborne lead in the general population is approx 30-50%, depending on particle size & ventilation rates. There is no evidence that inhaled lead /as a trace substance in the environment/ has local effects on the respiratory system in man ... . Dissolution of lead from lead soldered joints in water pipes frequently occurs where water is soft or acidic. /SRP: Thereby contributing to long term chronic exposure to the general population./ Most lead poisoning in children occurs between ages 1 and 5 years. There is a higher incidence of child-related lead poisoning during the warmer months. Chronic exposure to lead has been found to produce infertility, germinal epithelium damage, oligospermia and testicular degeneration, decreased sperm motility, and prostatic hyperplasia. There is convincing evidence that lead is transferred to neonates via maternal milk. It appears that maternal milk might be a source of lead for the neonates, particularly when metal levels are elevated in the mother. Arthralgia, often associated with muscle aches and pain, is a frequent symptom in lead poisoning. Although generally thought to appear mainly in chronic poisoning, joint pain is often reported even by persons exposed briefly (weeks) who have relatively low blood lead concentrations. It is a symptom that ... frequently indicates that the blood lead concentration is on the rise. ... The EPA concluded that blood levels in the range of 50-70 ug/dl are associated with a 5-point reduction in IQ, even among asymptomatic children and after controlling for potential confounding factors. /Researchers/ reported on a cohort of 132 young adults whose levels of dentine lead were measured in primary school. Young people whose childhood dentine levels were greater than 20 ppm were found to be at a markedly higher risk of dropping out of high school and having reading disabilities, than the low-lead exposure group, whose dentine lead levels had been less than 10 ppm. Other measures of performance affected included vocabulary and grammatical reasoning, absenteeism, hand-eye coordination (poorer) and reaction time (slowed). The earliest subjective symptoms /of lead poisoningin working adults/ are diffuse and include weariness at the end of the day. The patient is moody and irritable and may fall asleep watching television. Often he loses his interest in leisure-time activities. Such mild symptoms frequently occur with blood-lead levels below 80 ug/100 ml. ... 49 long-term lead-exposed workers were compared to 27 low-exposed workers through a number of psychologic tests. After controlling for age, the exposed group performed worse on tests measuring memory, learning, and reaction time, while impaired performance was not detected in reasoning, perceptual speed, and psychomotor ability. ... /Researchers/ found impaired performances on tests of verbal concept formation, perceptual performance, and memory in a lead-exposed group with present lead concentrations between 40 and 60 ug/100 ml. A study of 260 infants prospectively followed from birth suggests that the expected stature of a child born to a mother with a prenatal blood lead concentration over 7.7 ug/dL is about 2 cm shorter at 15 mos of age if, potentially, the infant also incurred a 10 ug/dL blood level increase during the 3- to 15-month interval of life. Moderate effects on follicle stimulating hormone and luteinizing hormone have been correlated with lead levels over about 50 ug/dL. The relative risk of preterm delivery at exposure levels of 14 ug/dL or greater was 8.7 times the risk at levels of up to 8 ug/dL in one prospective study. A Cincinnati study noted a half-week's reduction in gestation for every 10 ug/dL increment in blood lead. Lead has an adverse effect on fetuses, particularly in the later stages of development. Distribution of lead in fetal tissues was examined in a case in which a woman was exposed during pregnancy. The female worker was exposed to lead dust for 8 hr daily when conception occurred. ... Measurements of lead content were started after the end of the exposure and continued for 6 months until normal values were obtained. Because of half-life of nearly 20 days for lead elimination from blood, the estimated body burden at the end of exposure was about 1200 ppb. The fetal tissue samples contained between 0.4 (brain) and 7.9 (liver) ug Pb/g dry weight. The fetal lead was stored mainly in bone, blood, and liver. Goyer found inclusion bodies in renal biopsies of two lead industry workers who had excess lead exposure, but only subclinical signs of lead toxicity in the form of weakness, nausea, some abdominal colic, and blood lead values of about 100 ug/dl. Finnish men were biologically monitored for lead exposure. The cases (213 spontaneous abortions) and controls (300 births) were identified from medical registers in Finland. The results did not show a statistically significant relationship between spontaneous abortion and paternal lead exposure among all the study subjects. However, a significant increase in the risk of those women whose husbands had been monitored (blood lead equal to or greater than 1.5 umol/l) during or close to the time of spermatogenesis was observed. Small increases in blood pressure have been related to adults with PbB levels down to 7 ug/dl. ... PbB concentrations in excess of 60 ug/100 g ... have been associated with peripheral neuropathy, gastrointestinal disturbances and anemia. ... Nerve conduction velocities ... /decreases/ in workers with maximal blood leads between 50 and 70 ug/100 g. Food and Environmental Agents: Effect on Breast-Feeding: Reported Sign or Symptom in Infant or Effect on Lactation: Lead: Possible neurotoxicity. /From Table 7/ Medical Surveillance: ... Comparative advantages of /the biological indicator/ delta-aminolevulinic acid dehydratase in typical (variable) occupational exposure conditions included: the highest sensitivity at low and relatively high lead (Pb) exposure levels; better reflection of biologically active Pb as opposed to blood lead (particularly compared to delta-aminolevulinic acid and coproporphyrin); higher specificity compared to other indicators of Pb effect; and generally higher reliability with regard to biologically and methodologically induced variations. ... Populations at Special Risk: SRP: Law enforcement officers are subject to potential intoxication while firing weapons in an indoor firing range. Lead toxicity is of special concern to workers, such as miners and smelters, automobile finishers, foundry and storage battery workers, typesetters, sheet metal workers, and spray painters. Lead ... may also be a contaminant in moonshine whiskey. Probable Routes of Human Exposure: ... MOST SEVERE HAZARD OCCURS IN SPRAYING OF MOLTEN LEAD ... GRINDING OR POWER SANDING ... SOLDER & POURING OF LEADED IRON & STEEL ... MIXING & WEIGHING OF LEAD POWDERS. PRINCIPAL TYPES OF PRIMARY INDUSTRIES WITH OCCUPATIONAL EXPOSURE ... ARE LEAD SMELTING & REFINING, STORAGE BATTERY MANUFACTURE, WELDING & STEEL CUTTING & PRINTING. HIGHEST EXPOSURES ... OCCUR IN SMELTING & REFINING OF LEAD. MOLTEN LEAD & LEAD ALLOYS ARE BROUGHT TO HIGH TEMP, RESULTING IN VAPORIZATION OF LEAD. Emergency Medical Treatment:
Antidote and Emergency Treatment: Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Lead and related cmpds/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious. Use hyperventilation to help control increased intracranial pressure. Start an IV with lactated Ringer's to support vital signs. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Lead and related cmpds/ The treatment of lead poisoning is based on the prompt termination of exposure and on the use of chelating agents. The first requirement is categoric. The second is determined by the severity of poisoning; at present, the greatest issue is whether a symptomatic patients should be treated or not. The most commonly used therapeutic chelating agents are CaEDTA, BAL, and D-penicillamine can be given ... . /SRP: DMSA should also be considered./ It is not easy to judge which method is superior. ... /Lead/ Animal Toxicity Studies: Evidence for Carcinogenicity: CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Sufficient animal evidence. Ten rat bioassays and one mouse assay have shown statisticlly significant increases in renal tumors with dietary and subcutaneous exposure to several soluble lead salts. Animal assays provide reproducible results in several laboratories, in multiple rat strains with some evidence of multiple tumor sites. Short term studies show that lead affects gene expression. Human evidence is inadequate. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient. /Lead and compounds/ A3; Confirmed animal carcinogen with unknown relevance to humans. /Lead, elemental, and inorganic compounds, as Pb/ Non-Human Toxicity Excerpts: Lead particles have been well tolerated in the eyes of dogs & rats. ... Lead particles in the anterior chamber in rabbits became coated with purulent exudate & sometimes were extruded through the cornea at the limbus. In the vitreous humor in rabbits a similar purulent reaction was observed, causing the vitreous to shrink & the retina to separate. LEAD POWDER SUSPENDED IN CORN OIL WAS ADMIN TO MALE & FEMALE FISCHER 344 RATS BY STOMACH TUBE (10 MG TWICE/MO FOR 12 MO). CONTROL RATS WERE GIVEN 0.5 ML OF CORN OIL BY STOMACH TUBE ACCORDING TO SAME SCHEDULE. ONE LYMPHOMA & 4 LEUKEMIAS WERE FOUND IN 5/47 LEAD-TREATED RATS; THIS DID NOT DIFFER SIGNIFICANTLY FROM THE INCIDENCE OF 3 LYMPHOMAS IN 29 CONTROLS. NO OTHER NEOPLASMS WERE REPORTED IN TREATED OR CONTROL RATS. LEAD POWDER SUSPENDED IN TRIOCTANOIN WAS ADMIN IM TO 25 MALE & 25 FEMALE FISCHER RATS AS 9 MONTHLY INJECTIONS OF 10 MG, THEN 3 MONTHLY INJECTIONS OF 5 MG. EQUAL NUMBER OF VEHICLE CONTROLS WERE USED. 1 TREATED FEMALE DEVELOPED FIBROSARCOMA AT SITE OF IMPLANTATION ... THE LYMPHOMA RATE WAS SAME IN TREATED AS IN CONTROL ANIMALS. TWELVE SHEEP WERE EXPOSED TO FINELY POWDERED METALLIC LEAD IN THEIR DIET (DOSES, 0.5 TO 16 MG/KG BODY WT) DURING ENTIRE ... PREGNANCY; BLOOD LEVELS WERE ABOUT 0.4 MG/L, WITHOUT RESULTING IN DEATH. NINE ANIMALS SERVED AS CONTROLS. RATE OF LAMBING WAS 18% IN EXPOSED (27% ABORTIONS) & 100% IN UNEXPOSED SHEEP (NO ABORTIONS). NO MALFORMATIONS WERE REPORTED. ... /IT WAS CONCLUDED THAT/ CHRONIC LEAD POISONING IN SHEEP CAUSED ABORTION, MISCARRIAGE & TRANSITORY STERILITY. THERE WAS NO SIGNIFICANT EXCESS OF CHROMOSOME DAMAGE IN CULTURED LEUKOCYTES OBTAINED FROM 9 COWS ACCIDENTALLY INTOXICATED WITH MIXTURE OF HEAVY METALS & SHOWN TO HAVE TOXIC LEVELS OF LEAD IN LIVER & KIDNEYS. Waterfowl can become poisoned by ingesting 6-8 buckshot from frequently hunted shorelines. Natural sources of lead such as galena or soils are not particularly toxic but can add to the total body burden. In waterfowl, lead shot ingestion causes anorexia, loss of wt, weakness, lethargy, diarrhea, coma, & quiet death. ... Progressive tachycardia /has been observed/ in geese as the birds became more & more ill. Some geese developed ECG abnormalities. In geese chronically poisoned with lead shot, microscopic degenerative lesions appear in the myocardium before any ECG abnormalities are manifested. Lesions include upper GI impaction with plant materials, emaciation, distended gallbladder, flabby hemorrhagic heart, discolored friable liver, & enteritis. Lesions in mallard ducks given lead shot include destruction of proventricular epithelium, bone medullary osteocytes, & pectoral muscle cells. Renal proximal tubules contain intranuclear inclusions. Mallard ducks also may develop encephalopathy & peripheral neuropathy. Metallic lead in the form of weights or foil can cause poisoning, as also can shot; duck frequently dredge up shot from the mud at the bottom of ponds. Lead shot in muscle is usually encapsulated, & systemic poisoning from it is unlikely. Nevertheless, lead shot dropped by anglers on river banks is a serious cause of poisoning in swans. ... Vegetation in the neighborhood of a smelter engaged in melting down old battery plates had a lead content of up to 3200 ppm. ... Vegetation near a busy highway may contain 500 ppm of lead due to contamination by exhaust fumes. It should be noted that in these cases the lead is only a surface contaminant; significant quantities of the element cannot be taken up by vegetation from lead-bearing soil, although the latter has itself caused poisoning in small animals. Birds (fowls, ducks, geese & pigeons) are all susceptible to lead poisoning. They show anorexia & ataxia, followed by excitement & loss of condition. Egg production, fertility, & hatchability decrease; & mortality may be high. It is doubtful whether the term "toxic dose" has any real meaning when it is applied to a substance such as /elemental/ lead /in its ionic form/, as it is affected by so many different factors. Among these are environment, nutrition, disease & age, the last of these being considerably more important, as young animals are considerably more sensitive than old ones. There is also a seasonal variation. Over half the cases of lead poisoning in cattle in Scotland occur in the spring. Similar effects have been noted for dogs. ... Even more important is the fact that lead is both cumulative & ubiquitous. All living creatures are continually absorbing it, & the "toxic" dose is only the amount necessary to bridge the gap between this normal intake & a potentially dangerous level. ... Three or four lead shots will kill a duck, 10 a goose. The acute oral lethal single dose of lead in ... calves /is/ 50-600 mg/kg as lead or lead salts. ... Solid lead is not as toxic as /the/ more soluble salts, which are more readily absorbed. Eleven pregnant squirrel monkeys were perorally exposed to lead during the latter two-thirds of pregnancy (mean blood lead 0.54 ug/ml (2.61 umol/l), range 0.39-0.82 ug/ml (1.88-3.96 umol/l), at a dosing regime producing no maternal toxic symptoms. Lesions similar to lead encephalopathy and growth retardation of the fetal cerebrum were seen in some of the offspring, as well as neurological and behavioral symptoms at adult age. Cerebral lead levels in offspring (an abortion, stillborns, a sacrificed full-term fetus, and a neonatal death) were between 0.1-0.7 ug/g. Pre- and perinatal mortality, and prematurity, was increased, and the size of the offspring at birth was reduced. The head circumference tended to be reduced postnatally. ... Animal studies indicate that relatively high levels of lead exposure interfere with resistance to infectious disease. ORAL ADMIN OF LEAD TO RATS INHIBITED ACTIVITY OF DELTA-AMINOLEVULINIC ACID DEHYDRATASE. EDTA TREATMENT OF RATS GIVEN LEAD CAUSED REACTIVATION OF LIVER DELTA-AMINOLEVULINIC ACID DEHYDRATASE. Studies have been conducted with nestling kestrels in which oral intubations were administered daily for the first 10 days post-hatching. A high mortality from metallic lead was observed with 525 mg/kg, reduced growth was observed with 125 mg/kg, and altered physiology was observed with 25 mg/kg. /From table/ Ecotoxicity Values: LC50 Japanese quail (Coturnix japonica), males or females, 14 days old, oral (5-day ad libitum in diet) >5,000 ppm; at 1000, 2236 & 5000 onset of toxic signs began at 7, 7 & 7 days and remissed at 11, 11 & 12 days, respectively, no mortality was observed; control references were dieldrin & dicrotophos; corn oil diluent was added to diet at ratio of 2:98 by wt; (extreme concentrations: 1,000-5,000 ppm) /Lead metal, 100%/ Metabolism/Pharmacokinetics: Absorption, Distribution & Excretion: Only 1 to 2% of ingested lead is absorbed from the GI tract because it can form rather insoluble compounds, even within the gut. Acid conditions favor dissolution of lead & its compounds. ... Metallic lead shot or bullets lodged in tissues do not dissolve readily because tissue pH is not low enough. The absorption rate of deposited lead depends on various factors, particularly on the physiochemical form of lead in particles. There is ... no evidence of lead accumulation in the lung, & any lead compound once deposited is eventually absorbed or transferred to the gastrointestinal tract. Only a very minor fraction of particles over 0.5 um in mean maximal external diameter are retained in the lung but are then cleared from the respiratory tract & swallowed. ... The percentage of particles less than 0.5 um retained in the lung increases with reduction in particle size. About 90% of lead particles in ambient air that are deposited in lung are small enough to be retained. Absorption of retained lead through alveoli is relatively efficient & complete. A group of 109 male workers occupationally exposed to both antimony (as Sb2O3) and lead in the glass-producing industry were examined for levels of these metals in whole blood and urine. The workers were divided into four groups based on specific work activities: melter (n= 32), batch mixer (n= 45), craftsman (n= 8), and glass washer (n= 24). Blood and urine samples were collected at the end of a shift. Concentrations of lead in the blood ranged from 70 to 680 ug/l. Median values for melters, batch mixers, craftsmen, and glass washers were 220, 340, 275, and 170 ug/l, respectively. A significant difference (p< 0.05) was found only between the batch mixers and glass washers. The urinary lead values ranged from 7 to 110 ug/l with median values for melters, batch mixers, craftsmen, and glass washers of 35, 43, 24, and 42 ug/l, respectively. A significant difference was found between only the batch mixers and craftsmen (p< 0.05). Exposure rates for lead were not given. ... Two human volunteers were given 212Pb intravenously. There was no lead in the feces during the first 24 hr, whereas the urine contained 4.42% of the dose. The figures for the second 24 hours, however, were 1.5% and 1.42%, respectively, which indicates that the fecal route may contribute as much as the urinary one to total excretion. Other possible routes for lead excretion include sweat, milk, hair, nails, desquamating epithelia, and teeth. As much as 90% of ingested lead is not absorbed and is excreted in the feces. The urine is the primary vehicle for excretion of absorbed lead, but a smaller proportion may be excreted in the bile. An inverse relationship was found between diets containing metallic lead of particle sizes </= 250 um and absorption in rats. Biological Half-Life: The first half-time of lead in blood after the cessation of exposure is 35-40 days, while for the lead in long bones, the half-time is around 20 yr. Mechanism of Action: The ability of a number of metals and organic chemicals to induce metallothionein synthesis in primary cultures of rat hepatocytes was tested to determine whether metallothionein induction in vivo results from a direct effect of the agent on the liver or as a result of an indirect, physiological response to the agent. Hepatocytes were exposed to metals (zinc, cadmium, mercury, manganese, lead, cobalt, nickel, and vanadium) or org cmpd. Ethanol, urethane, L-2-oxothiazolidine-4-carboxylate, or dexamethasone and were assayed for metallothionein by the cadmium/mercury radioassay. Cell viability was monitored by protein synthesis activity and cellular potassium ion concn. Increases in metallothionein concn were noted for zinc (22 fold), mercury (6.4 fold), cadmium (4.8 fold), cobalt (2.4 fold), nickel (22 fold), and dexamethasone (4.5 fold). However, even at max tolerated concn, manganese, lead, vanadium, ethanol, urethane, and L-2-oxothiazolidine-4-carboxylate did not increase metallothionein. Thus, zinc, cadmium, mercury, cobalt, nickel, and dexamethasone induce metallothionein in vitro and are direct inducers of metallothionein synthesis in hepatic tissue. In contrast, manganese, lead, ethanol, urethane, and L-2-oxothiazolidine-4-carboxylate, which did not increase the metallothionein content of hepatocytes, apparently do so in vivo by an indirect mechanism. Interactions: Female Swiss mice were exposed to lead in the drinking water at concentrations ranging from 0 to 1000 ppm for 105 or 280 day periods of time. The effect of lead on urethane induced pulmonary adenoma formation was evaluated in the 105 day study. Urethane induced sleeping times observed following ip injection of urethane (1.5 mg/g) after 3 weeks of lead exposure were not altered by lead indicating that lead did not affect the rate of urethane elimination. Pulmonary adenoma formation was evaluated 84 days later. Lead exposure did not affect the number of tumors produced, nor did it alter the mean tumor diameter in the lead treatment groups. Immunosuppressive activity of lead did not enhance urethane induced adenoma formation. In the 280 day study, leukemia was observed in all treatment groups. Mortality was greater in the lead exposed mice. Mice exposed to 50 or 1000 ppm lead had 41.6% and 58.3% more deaths associated with the virus. The median survival time was also reduced in the lead exposed mice. Immunosuppressive effects of lead increased expression of the murine lymphocytic leukemia virus. Cultured C6 rat glioma cells were exposed to lead acetate (0, 1, 10, or 100 uM) for 3-4 days. Cells were analyzed for changes in viability and intracellular lead, iron, and copper concentrations after lead treatment was discontinued. Lead uptake did not affect intracellular iron or copper concentrations. Unlike C6 cells, however, astroglia showed elevations of intracellular iron or copper after lead treatment. C6 cells appear to be an adequate model for selected events in glial toxicosis, such as lead stimulated protein synthesis in oligodendroglia and lead uptake in astroglia, but not lead induced alterations of intracellular copper and iron in astroglia. The distribution of iv admin lead (50 nmol/kg) was studied by means of autoradiography and impulse counting in pregnant C57BL mice (day 18 of gestation) treated orally with dithiocarbamates. Diethyldithiocarbamate, disulfiram or thiram (2X1 mmol/kg) or vehicle (gelatin) alone, was given by gavage 2 hr before & immediately after injection of lead. All the dithiocarbamates changed the distribution pattern of lead. Disulfiram had the greatest effect at 24 hr after lead. The pattern of changes in lead distribution is consistent with the formation in the body of lipid sol. Lead-dithiocarbamate complexes that pass biological barriers more easily than inorganic lead (to brain, fetus, melanocytes, etc), probably are followed by a dissociation of the complexes in the tissues. Chelating agents, zinc salts, and selenium preparations have been utilized with some success in attempts to reduce absorption and/or increase the excretion of absorbed lead. ... Both selenium and vitamin E have been shown to be involved in decreasing the toxic effect of lead in rats. Pharmacology: Interactions: Female Swiss mice were exposed to lead in the drinking water at concentrations ranging from 0 to 1000 ppm for 105 or 280 day periods of time. The effect of lead on urethane induced pulmonary adenoma formation was evaluated in the 105 day study. Urethane induced sleeping times observed following ip injection of urethane (1.5 mg/g) after 3 weeks of lead exposure were not altered by lead indicating that lead did not affect the rate of urethane elimination. Pulmonary adenoma formation was evaluated 84 days later. Lead exposure did not affect the number of tumors produced, nor did it alter the mean tumor diameter in the lead treatment groups. Immunosuppressive activity of lead did not enhance urethane induced adenoma formation. In the 280 day study, leukemia was observed in all treatment groups. Mortality was greater in the lead exposed mice. Mice exposed to 50 or 1000 ppm lead had 41.6% and 58.3% more deaths associated with the virus. The median survival time was also reduced in the lead exposed mice. Immunosuppressive effects of lead increased expression of the murine lymphocytic leukemia virus. Cultured C6 rat glioma cells were exposed to lead acetate (0, 1, 10, or 100 uM) for 3-4 days. Cells were analyzed for changes in viability and intracellular lead, iron, and copper concentrations after lead treatment was discontinued. Lead uptake did not affect intracellular iron or copper concentrations. Unlike C6 cells, however, astroglia showed elevations of intracellular iron or copper after lead treatment. C6 cells appear to be an adequate model for selected events in glial toxicosis, such as lead stimulated protein synthesis in oligodendroglia and lead uptake in astroglia, but not lead induced alterations of intracellular copper and iron in astroglia. The distribution of iv admin lead (50 nmol/kg) was studied by means of autoradiography and impulse counting in pregnant C57BL mice (day 18 of gestation) treated orally with dithiocarbamates. Diethyldithiocarbamate, disulfiram or thiram (2X1 mmol/kg) or vehicle (gelatin) alone, was given by gavage 2 hr before & immediately after injection of lead. All the dithiocarbamates changed the distribution pattern of lead. Disulfiram had the greatest effect at 24 hr after lead. The pattern of changes in lead distribution is consistent with the formation in the body of lipid sol. Lead-dithiocarbamate complexes that pass biological barriers more easily than inorganic lead (to brain, fetus, melanocytes, etc), probably are followed by a dissociation of the complexes in the tissues. Chelating agents, zinc salts, and selenium preparations have been utilized with some success in attempts to reduce absorption and/or increase the excretion of absorbed lead. ... Both selenium and vitamin E have been shown to be involved in decreasing the toxic effect of lead in rats. Environmental Fate & Exposure: Probable Routes of Human Exposure: ... MOST SEVERE HAZARD OCCURS IN SPRAYING OF MOLTEN LEAD ... GRINDING OR POWER SANDING ... SOLDER & POURING OF LEADED IRON & STEEL ... MIXING & WEIGHING OF LEAD POWDERS. PRINCIPAL TYPES OF PRIMARY INDUSTRIES WITH OCCUPATIONAL EXPOSURE ... ARE LEAD SMELTING & REFINING, STORAGE BATTERY MANUFACTURE, WELDING & STEEL CUTTING & PRINTING. HIGHEST EXPOSURES ... OCCUR IN SMELTING & REFINING OF LEAD. MOLTEN LEAD & LEAD ALLOYS ARE BROUGHT TO HIGH TEMP, RESULTING IN VAPORIZATION OF LEAD. Natural Pollution Sources: LEAD RARELY OCCURS IN THE ELEMENTAL STATE, BUT EXISTS ... IN A NUMBER OF ORES ... ALSO OCCURS IN VARIOUS URANIUM & THORIUM MINERALS, ARISING FROM RADIOACTIVE DECAY. Pb derived from the decay of radon. /Inorganic lead/ Metallic lead is naturally occurring and is the end product of three natural radioactive elements uranium (206), thorium (208), and actinium (207)(1). Milk Concentrations: Other possible routes for lead excretion include ... milk.... Environmental Standards & Regulations: Acceptable Daily Intakes: Tolerable intake of lead for preschool children should be less than the 3 mg/wk recommended provisionally for adults. ... /Inorganic lead/ 0.007 mg/kg (WHO) /Lead; from table/ CERCLA Reportable Quantities: Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b). RCRA Requirements: D008; A solid waste containing lead may or may not become characterized as a hazardous waste when subjected to the Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so characterized, must be managed as a hazardous waste. Atmospheric Standards: National primary and secondary ambient air quality standard for lead and its compounds, measured as elemental lead is: 1.5 ug/cu m, maximum arithmetic mean averaged over a calendar quarter. /Lead and its compounds, as Pb/ Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Lead compounds are included on this list. /Lead compounds/ Clean Water Act Requirements: Toxic pollutant designated pursuant to section 307(a)(1) of the Clean Water Act and is subject to effluent limitations. /Lead and inorganic and organic lead compounds/ Designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. Federal Drinking Water Standards: EPA 15 ug/l (Action Level) State Drinking Water Guidelines: (AZ) ARIZONA 20 ug/l (ME) MAINE 10 ug/l FDA Requirements: The FDA action level of lead is 7.0 ug/ml of leaching soln for pottery (ceramics) flatware (avg of 6 units); 5.0 ug/ml of leaching soln for small hollowware (any one of 6 units); 2.5 ug/ml of leaching soln for large hollowware (any one of 6 units); 7.0 ug/ml of leaching soln if product intended for use by adults for silver-plated hollowware (avg of 6 units); and 0.5 ug/ml of leaching soln if product intended for use by infants and children for silver-plated hollowware (one or more of 6 units). /Inorganic lead/ Chemical/Physical Properties: Molecular Formula: Pb Molecular Weight: 207.2 Color/Form: Bluish-white, silvery, gray metal. Highly lustrous when freshly cut, tarnishes upon exposure to air. Cubic crystal structure. Boiling Point: 1740 deg C Melting Point: 327.4 deg C Density/Specific Gravity: 11.34 @ 20 deg C/4 deg C Heat of Vaporization: 206 cal/g @ 1740 deg C Vapor Pressure: 1.77 mm Hg @ 1000 deg C Viscosity: Viscosity of molten lead (327.4 deg C) 3.2 centipoises, (400 deg C) 2.32 cP, (600 deg C) 1.54 cP, (800 deg C) 1.23 cP. Other Chemical/Physical Properties: VAPOR PRESSURE: 10 MM HG AT 1162 DEG C; 100 MM HG AT 1421 DEG C; 400 MM HG AT 1630 DEG C Very soft and malleable, easily melted, cast, rolled, and extruded. Density (at mp) 10.65 g/cu cm. Heat capacity (20 deg C): 0.031 cal/g/deg C. Resistivity (microohm-cm) at 20 deg C: 20.65; at 100 deg C: 27.02; at 320 deg C: 54.76; at 330 deg: 96.74. Standard electromotive force (aq) Pb/Pb2+ +0.126 v. Coefficient of linear expansion (0-100 deg C) 29X10-6, (20-300 deg C) 31.3X10-6, (-183 deg C to +14 deg C) 27X10-6; thermal conductivity varies from 0.083 at 50 deg C to 0.077 at 225 deg C. Hardness 1 on Mohs' scale; Brinell hardness (high purity Pb) 4.0. Reacts with hot concd nitric acid, with boiling concd hydrochloric or sulfuric acid. Attacked by pure water, weak organic acids in the presence of oxygen. Resistant to tap water, hydrofluoric acid, brine, solvents. Chemical Safety & Handling: Fire Potential: Flammable in the form of dust when exposed to heat or flame. Toxic Combustion Products: When heated ... it emits highly toxic fumes of lead. Explosive Limits & Potential: Moderately explosive in the form of dust when exposed to heat or flame. Hazardous Reactivities & Incompatibilities: CAN REACT VIGOROUSLY WITH OXIDIZING MATERIALS. Ground mixtures of sodium carbide and ... lead ... can react vigorously. ... Trituration in a mortar of disodium acetylide with finely divided lead may be violent, carbon being liberated. ... Reaction with chlorine trifluoride at ambient or slightly elevated temp is violent, ignition often occurring. Mixtures of trioxane with 60% hydrogen peroxide solution are detonable by heat or shock, or spontaneously after contact with metallic lead. The latter may be ... /due/ to the heat of oxidation of lead. ... Reacts violently or explosively with fused ammonium nitrate below 200 deg C. ... Lead containing dry-box gloves may ignite in nitric acid environment. Finely divided lead produced by reduction of the oxide with furfural vapor at 290 deg C is pyrophoric and chemically reactive. A solution of sodium azide in copper pipe with lead joints formed copper azide and lead azide, both detonating compounds. REACTS WITH HOT CONCN NITRIC ACID, BOILING CONCN HYDROCHLORIC & SULFURIC ACIDS Strong oxidizers, hydrogen peroxide, acids. Incompatible with NaN3; Zirconium ... Hazardous Decomposition: When heated to decomposition it emits highly toxic fumes of lead. Immediately Dangerous to Life or Health: 100 mg/cu m Protective Equipment & Clothing: Wear appropriate personal protective clothing to prevent skin contact. Wear appropriate eye protection to prevent eye contact. Recommendations for respirator selection. Max concn for use: 0.5 mg/cu m. Respirator Class(es): Any air-purifying respirator with a high-efficiency particulate filter. Any supplied-air respirator. Recommendations for respirator selection. Max concn for use: 1.25 mg/cu m. Respirator Class(es): Any supplied-air respirator operated in a continuous flow mode. Any powered, air-purifying respirator with a high-efficiency particulate filter. Recommendations for respirator selection. Max concn for use: 2.5 mg/cu m. Respirator Class(es): Any air-purifying, full-facepiece respirator with a high-efficiency particulate filter. Any supplied-air respirator that has a tight-fitting facepiece and is operated in a continuous-flow mode. Any powered, air-purifying respirator with a tight-fitting facepiece and a high-efficiency particulate filter. Any self-contained breathing apparatus with a full facepiece. Any supplied-air respirator with a full facepiece. Recommendations for respirator selection. Max concn for use: 50 mg/cu m. Respirator Class(es): Any supplied-air respirator operated in a pressure-demand or other positive-pressure mode. Recommendations for respirator selection. Max concn for use: 100 mg/cu m. Respirator Class(es): Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode. Recommendations for respirator selection. Condition: Emergency or planned entry into unknown concn or IDLH conditions: Respirator Class(es): Any self-contained breathing apparatus that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode. Any supplied-air respirator that has a full facepiece and is operated in a pressure-demand or other positive-pressure mode in combination with an auxiliary self-contained breathing apparatus operated in pressure-demand or other positive-pressure mode. Recommendations for respirator selection. Condition: Escape from suddenly occurring respiratory hazards: Respirator Class(es): Any air-purifying, full-facepiece respirator with a high-efficiency particulate filter. Any appropriate escape-type, self-contained breathing apparatus. Preventive Measures: Control of exposure to toxic materials in ceramics is important because of the large variety of toxic materials /including lead tetroxide/. Dust control is of paramount importance. This is accomplished by good local exhaust ventilation, careful handling and storage of materials and proper clean-up techniques. The area should have general dilution ventilation, but also local exhaust systems for dry clay and glaze mixing, liquid glaze spraying and for the kiln emissions. All dry clays and glazes should be stored in sealed containers (not in ripped open paper bags). Plastic garbage cans with lids, on wheels, or similar containers can be used. All materials should be handled in a manner that prevents the creation of dusts. Premixed liquid glazes should be used and work done with materials in the wet form as much as possible. Good housekeeping is essential to keep the dust level down. There must be no dry sweeping or vacuuming in the studio, as this will resuspend settled dust that can be inhaled by the artists. Wet mopping, wet wiping and wet vacuuming or high efficiency particulate air (HEPA) filtered vacuuming is recommended. Protective equipment such as respirators, heat resistant gloves, eye protection, emergency showers and fire extinguishers are recommended around kilns. Proper studio design is important to insure that adequate ventilation, proper storage areas, handwashing sinks, safety equipment and other facilities are provided and safety hazards are avoided. Personal hygiene is also important. Artists should not eat, drink or smoke in the studio. Clothes should be washed daily. Hands and particularly nails should be washed frequently throughout the day, especially before eating, drinking, smoking or leaving the studio for the day. Cloakroom accommodation should be provided for personal protective equipment with separate accommodation for clothing taken off during working hours. Washing accommodation, including bathing accommodation with warm water, should be provided and used. Time should be allowed for washing before eating. Arrangements should be made to prohibit eating and smoking in the vicinity of lead processes and suitable messrooms should be provided. SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. All contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning. The worker should wash daily at the end of each work shift. Work clothing that becomes wet or significantly contaminated should be removed or replaced. Workers whose clothing may have become contaminated should change into uncontaminated clothing before leaving the work premises. Stability/Shelf Life: TARNISHES ON EXPOSURE TO AIR; ATTACKED BY PURE WATER, WEAK ORG ACIDS IN PRESENCE OF OXYGEN; RESISTANT TO TAP WATER, HYDROFLUORIC ACID, BRINE, SOLVENTS Cleanup Methods: Environmental considerations: Water spill: Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). Adjust pH to neutral (pH= 7). Use mechanical dredges of lifts to remove immobilized masses of pollutants & precipitates. Environmental considerations: Land spill: Dig a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be contained with a flexible impermeable membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water. ... Described treatment of wastewater from a tetraethyl lead manufacturing process. Two major categories of waste were inorganic lead wastewaters and organic lead wastewaters. After sedimentation in a holding basin to recover solid lead and lead oxide, the inorganic lead waste fraction (66.1 mg/l) was effectively treated by coagulation with ferric and ferrous sulfate. /Inorganic lead/ Disposal Methods: Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number D008, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste. Precipitation is the preferred treatment process for removing toxic heavy metals from electroplating waters. Precipitation processes include hydroxide, lime and/or sulfide treatment. Chemical reduction is used to treat complex metals such as nickel, copper, hexavalent chromium waste, soluble lead, silver, metal containing cyanide, and mercury. Adsorption has shown potential for treating and polishing aqueous metal bearing wastes. Activated carbon, activated alumina, and iron filings are all applicable adsorbents. Alkaline chlorination and incineration are effective cyanide destruction treatments. Evaporation, ion-exchange, reverse osmosis, electrodialysis, and electrolytic recovery are waste reduction and recovery techniques applicable to metal bearing hazardous streams. The following wastewater treatment technologies have been investigated for lead: Concentration process: Biological treatment. /Lead/ The following wastewater treatment technologies have been investigated for lead: Concentration process: Chemical precipitation. /Lead/ The following wastewater treatment technologies have been investigated for lead: Concentration process: Reverse osmosis. /Lead/ The following wastewater treatment technologies have been investigated for lead: Concentration process: Activated carbon. /Lead/ The following wastewater treatment technologies have been investigated for lead: Concentration process: Miscellaneous sorbents. /Lead/ Occupational Exposure Standards: OSHA Standards: The employer shall assure that no employee is exposed to lead at concentrations greater than 50 ug/cu m averaged over an 8-hr period. If an employee is exposed to lead for more than 8 hr in any work day, the permissible exposure limit, as a TWA for that day, shall be reduced according to the following formula: Maximum permissible limit (in ug/cu m)= 400 divided by the number of hours worked in the day. /Lead, inorganic, as Pb/ Threshold Limit Values: 8 hr Time Weighted Avg (TWA): 0.05 mg/cu m. /Lead, elemental, and inorganic compounds, as Pb/ Excursion Limit Recommendation: Excursions in worker exposure levels may exceed three times the TLV-TWA for no more than a total of 30 min during a work day, and under no circumstances should they exceed five times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Lead, elemental, and inorganic compounds, as Pb/ A3; Confirmed animal carcinogen with unknown relevance to humans. /Lead, elemental, and inorganic compounds, as Pb/ Biological Exposure Index (BEI): Determinant: lead in blood; Sampling Time: not critical; BEI: 30 ug/100 ml. [Note: Women of child bearing potential, whose blood Pb exceeds 10 ug/dl, are at risk of delivering a child with a blood Pb over the current Centers for Disease Control guideline of 10 ug/dl. If the blood Pb of such children remains elevated, they may be at increased risk of cognitive deficits. The blood Pb of these children should be closely monitored and appropriate steps should be taken to minimize the child's exposure to environmental lead.] /Lead, elemental/ NIOSH Recommendations: Recommended Exposure Limit: 10 hr Time-Weighted avg: 0.1 mg/cu m. Air concentrations should be maintained so that worker blood lead remains less than 0.06 mg PB/100 g of whole blood. Immediately Dangerous to Life or Health: 100 mg/cu m Other Occupational Permissible Levels: Australia: 0.15 mg/cu m (as Pb) (1990); Federal Republic of Germany: 0.1 mg/cu m total dust (as Pb), short-term level 1 mg/cu m, 30 min, once per shift, Pregnancy group B, a risk of damage to the developing embryo or fetus must be considered to be probable, to minimize the potential risk, a BAT value of 30 ug/dl blood has been evaluated specifically for women under 45 years old (1991); Sweden: 0.1 mg/cu m, total dust, 0.05 mg/cu m, respirable dust (1989); United Kingdom: 0.15 mg/cu m (1991). Manufacturing/Use Information: Major Uses: Main uses are in the manufacture of storage batteries, ammunition, nuclear and x-ray shielding devices, cable covering, ceramic glazes, noise control materials, bearing, brass and bronze, casting metals, solders, pipes, traps, and bends. Construction material for tank linings, piping, and other equipment handling corrosive gases and liqs used in the manuf of sulfuric acid, petr refining, halogenation, sulfonation, extraction, condensation; for x-ray and atomic radiation protection; manuf of tetraethyllead, pigments for paints, and other organic and inorganic lead compds; bearing metal and alloys; storage batteries; in ceramics, plastics, and electronic devices; in building construction; in solder and other lead alloys; in the metallurgy of steel and other metals. Lead and lead compounds was used in solder applied to water distribution pipes and to seams of cans used for food, in some traditional remedies, in bottle closures for alcoholic beverages and in ceramic glazes and crystal tableware. Manufacturers: ASARCO, Incorporated, Hq, 180 Maiden Lane, New York, NY 10038 (212) 510-2000. Production sites: Glover, MO 63646; Denver CO 80216 The Doe Run Co., hq, 1801 Park 270 Drive, Suite 300, St. Louis, MO 63146 (314) 453-7100. Production site: Boss, MO 65440 Cominco Alaska Incorporated, (wholely owned subsidiary of Cominco Ltd.,Toronto, Canada) Hecla Mining Company, Coeur d'Alene, ID Pegasus Gold, Inc., Spokane, WA. Methods of Manufacturing: The lead mineral in most crude ores is separated from the gangue and other valuable minerals. Occasionally, the ores are sufficently rich in lead and low in impurities to be smelted directly. The primary operation of ore dressing are crushing, grinding, and concentration (beneficiation). The first step is a size reduction of the mined ore to liberate the desired minerals from interlocking gangue. Primary (gyratory or jaw) and secondary (gyratory or roll) crushers are employed. Wire-mesh screens bypass the finer material & return the oversize for recrushing. Further comminution is accomplished by wet grinding in horizontal, cylindrical mills containing steel balls, rods, or flint pebbles. Autogenous grinding is employed occasionally. Classifiers that depend on differences in settling rates in air or water are used in closed circuit with grinding mills to recirculate oversize for regrinding. Gravity concentration ... /such as/ the separation of ore from gangue using jigs, heavy-medium separation, or tables, is applicable to lead ores. These techniques are often combined with the more widely used flotation process. Flotation ... makes it possible to selectively separate ... the gangue ... /&/ other valuable minerals from the lead ore, such as sphalerite (zinc sulfide). For flotation the ore is ground to a size sufficiently fine that the surface forces of adhesion to the bubbles, supplied for buoyancy, overcome the force of gravity. ... The ground & sized ore is discharged from classifiers to a conditioning tank in which the slurry is mixed with the required chemicals, & then passed to the flotation cells in which air is forced up through the slurry, forming bubbles to which the galena adheres. The floated galena is trapped in the top froth & eventually skimmed. ... The lead concentrate skimmed from the cell is dewatered & thickened to a moisture content of 50%. Vacuum filtering further decreases the moisture to 15% ... . ... /The/ series of processes ... /used to/ produce commercial grade of lead /from lead concentrate include/ blast-furnace smelting (sintering ... /&/ smelting) ... drossing (soda process ... /&/ continuous drossing) ... refining (pyrometallurgical methods ... /&/ electrolytic refining) ... /& the/ imperial smelting process (none in the USA). General Manufacturing Information: The Bureau of Mines is investigating a leach-electrolysis technique to produce lead from galena concentrates without sulfur emissions. The concentrate is leached with a hot FeCl3-NaCl solution to obtain a filtrate containing more than 99% of the lead & a residue of elemental sulfur & gangue material. Pure PbCl2 crystallizes out of the leach solution on cooling & is electrolyzed in a relatively low temp fused-salt cell to yield lead metal & chlorine gas. New developments in the refining of lead in general have focused on improvements & adaptions of the traditional pyrometallurgical & electrorefining processes, & esp on the conversion of batch processes into continuous processes. Completely continuous refining operations are the goal of these efforts. The recovery of lead from scrap is an important source for the lead demands of the USA & rest of the world. In the USA, 50% of the lead requirements are satisfied by recycled lead products. The ratio of secondary to primary lead increases with increasing lead consumption for batteries. The well-organized collecting channels forecast a stable & growing future for lead. ... The principal types of scrap are battery plates, drosses, skimmings, & industrial scrap such as solders, babbitts, cable sheathing, etc. Some of this material is reclaimed by kettle melting & refining. ... Most scrap is a combination of metallic lead & its alloying constituents mixed with compounds of these metals, usually oxides & sulfates. ... Most recycled lead derives from scrap lead batteries since >50% of the lead consumed in the USA is in the form of lead batteries. About 90% is reclaimed; hence, the bulk of the recycling industry is centered on the processing of lead battery scrap. At present, battery scrap is converted to impure lead or lead alloys by pyrometallurgical processes employing blast, reverberatory, or rotary furnaces. In many plants, a furnace combination is used. ... The overall recovery of the metallic components of scrap in plants having both reverberatory & blast furnaces is over 95%. ... The decisions being made by the operators of secondary smelters as to which procedures will be designed into new plants or installed in updating old plants are strongly influenced by the introduction of new grid alloys, such as calcium alloys, low-antimony alloys (2-3%), & strontium alloys, to replace the traditional 5-7% antimonial alloys, & by air pollution standard requirements. The projected world and USA demand for lead in the year 2000, including that supplied from recycled lead, is est at approx 9X10+6 and 2.2X10+6 tonnage/yr, respectively. This is an annual growth rate of about 3% for the world & 1.5% for the USA. The demand in the developing nations is expected to grow at a faster rate than in the industrialized nations. If these estimates are correct, the lead industry in the USA would have to increase by 50 to 60%. The cumulative demand for primary lead in the world from 1973 to 2000 has been est at 140X10+6 tons. The est world reserves of 150X10+6 tons are sufficient to supply this demand. The economics of USA lead prodn, both primary & recycled, are markedly influenced by government regulations concerning lead concn in air. Compliance with those standards has been costly, and if more limiting standards are imposed, can result in a reduction of present smelter capacity & set limits on future expansion. Stricter regulations concerning lead emissions and ambient air lead levels, as well as the need to reduce capital and operating costs have lead to the development of alternative lead smelting processes to replace the sinter-blast furnace combination. Four processes have reached the stage of being promoted for commercial use, namely: Kivcet, QSL, Isamelt, and Boliden Kaldo. These processes have the potential advantages of meeting proposed in-plant hygiene requirements, utilizing the heat of combustion and thereby reducing energy costs, reduction in capital and operating costs through the use of high intensity vessels, and the production of low volumes of process gas of high SO2 content through the use of large amounts of oxygen. 1997 Production by state: Missouri, 412,000 metric tons; Montana, 9,230 metric tons; and Colorado, Idaho, Illinois, New York, and Tennessee (combined), 26,600 metric tons. 1997: Lead recovered from new scrap, 63,700 metric tons; old scrap, 1,040,000 metric tons, of which 991,000 metric tons comes from batteries. The princpal U.S. lead producers, ASARCO, Inc. and The Doe Run Co., account for 75% of domestic mine production and 100% of primary lead production. Both companies employ sintering/blast furnace operations at their smelters and pyrometallurigical methods in their refineries. The most important ore mineral is galena, PbS (87% Pb), followed by anglesite, PbSO4 (68% Pb), and cerussite, PbCO3 (77.5% Pb). The latter two minerals result from the natural weathering of galena. Although lead is a relatively rare element, the occurrence of concentrated and easily accessible lead ore deposits is unexpectedly high. Formulations/Preparations: Grade: high purity (less than 10 ppm impurity); pure (99.9+); powdered (99% pure); pig lead; paste. Forms available: ingots, sheet, pipe, shot, buckles or straps, grids, rod, wire, etc; paste; powder; single crystals. Low bismuth, low silver, pure lead. 99.995% lead (ASTM B29-92) (for chemical applications requiring low bismuth and silver contents). Specifications (max allowable metal, wt%: Sb, As, Sn, 0.0005 each; Cu, 0.0010; Ag, 0.0010; Bi, 0.0015; Zn, 0.0005; Te, 0.0001; Ni, 0.0002; Fe, 0.0002. Refined pure lead. 99.97% lead (ASTM B29-92) (for lead battery applications). Specifications (max allowable metal, wt%: Sb, As, Sn, 0.0005 each; Cu, 0.0010; Ag, 0.0025; Bi, 0.025; Zn, 0.0005; Te, 0.0001; Ni, 0.0002; Fe, 0.001. Pure lead. 99.94% lead (ASTM B29-92). Specifications (max allowable metal, wt%: Sb, As, Sn, 0.001 each, 0.002 total; Cu, 0.0015; Ag, 0.005; Bi, 0.05; Zn, 0.001; Ni, 0.001; Fe, 0.001. Chemical copper-lead. 99.90% lead (ASTM B29-92) (for applications requiring corrosion protection and formability). Specifications (max allowable metal unless range is given, wt%: Sb, As, Sn, 0.001 each, 0.002 total; Cu, 0.040-0.080; Ag, 0.020; Bi, 0.025; Zn, 0.001; Ni, 0.002; Fe, 0.002. Impurities: ASTM requires pig lead to be 99.85 to 99.90% pure; impurities consist of silver, copper, arsenic, antimony, tin, zinc, iron, and/or bismuth. After softening /lead bullion/, the impurities that may still remain in the lead are silver (about 0.2%), gold (about 0.006%), copper, tellurium, platinum metals, & bismuth (up to 0.1%). Although these concentrations may be tolerable for some lead applications, their market value encourages separation & recovery. Consumption Patterns: Transportation-automotive batteries, gasoline additives, 70%; construction, ammunition, electrical uses, TV glass, and paint, 25%; ceramics, type metal, ballast or weights, and tubes or containers, 5% (1986) COMPONENT OF LEAD OXIDE BATTERIES, 36.5%; COMPONENT OF ANTIMONIAL LEAD BATTERIES, 29.1%; CHEM INT FOR LEAD ALKYLS, 11.1%; CHEM INT FOR PIGMENTS, 5.7%; AMMUNITION, 4.1%; SOLDER, 2.6%; SHEET LEAD, 1.4%; CABLE COVERING, 1.4%; OTHER METAL PRODUCTS, 6.3%; OTHER, 1.8% (1982) Lead consumption in the USA by product in approx metric tons for 1979: ammunition, 52,884; bearing metal, 12,230; brass & bronze, 15,569; cable covering, 15,623; caulking lead, 4,055; casting metals, 9,365; pipes, traps, bends, 2,942; sheet lead, 6,545; solders, 40,429; storage battery grids, posts, etc, 309,838; storage battery oxides, 337,412; terne metal, 4,722; pigments, 82,788; antiknock additives, 186,947. Lead consumption in the USA by product in approx metric tons for 1978: ammunition, 55,776; bearing metal, 9,510; brass & bronze, 16,502; cable covering, 13,851; caulking lead, 9,909; casting metals, 3,611; pipes, traps, bends, 10,479; sheet lead, 12,626; solders, 68,391; storage battery grids, posts, etc, 412,568; storage battery oxides, 466,714; terne metal, 3,778; pigments, 91,643; antiknock additives, 178,333. Lead consumption in the USA by product in approx metric tons for 1977: ammunition, 61,961; bearing metal, 10,873; brass & bronze, 15,148; cable covering, 13,705; caulking lead, 8,725; casting metals, 5,428; pipes, traps, bends, 10,555; sheet lead, 15,205; solders, 58,320; storage battery grids, posts, etc, 416,709; storage battery oxides, 441,387; terne metal, 1,491; pigments, 90,703; antiknock additives, 211,295; annealing, weights, galvanizing ballast, 21,478; other uses, 35,812. Lead consumption in the USA by product in approx metric tons for 1976: ammunition, 66,659; bearing metal, 11,851; brass & bronze, 14,207; cable covering, 14,452; caulking lead, 11,317; casting metals, 6,085; pipes, traps, bends, 12,509; sheet lead, 22,170; solders, 57,447; storage battery grids, posts, etc, 348,221; storage battery oxides, 397,859; terne metal, 1,447; pigments, 95,792; antiknock additives, 217,507; annealing, weights, galvanizing ballast, 24,401; other uses, 29,351. By class of products, 1997: Metal products, 7.8%; Storage Batteries, 86.9%; Miscellaneous, including other oxides, 5.3%. By product, 1997: Ammunition, shot and bullets, 3.46%; Bearing metals, 0.16%; Brass and bronze, billets and ingots, 0.28%; Cable covering, power and communication, 0.31%; Caulking lead, building construction, 0.087%; Casting metals 1.14%; Pipes, traps and extruded products, 0.12%; Sheet lead, 1.19%; Solder, 0.60%; Storage batteries, 86.9%; Other metal products, 0.47%; Other oxides, 4.18%; Miscellaneous uses, 0.53%. U. S. Production: Between 1960 & 1978, mine prodn in the USA ... increased from 232,00 to 541,000 tonnage. The large increase occurred from 1968 to 1970 with the coming on stream of mines & smelters in the newly developed Missouri lead belt. Domestic mine prodn in 1978 accounted for 70% of the USA primary lead prodn. (1977) 1.31X10+12 G (1978) 541,000 metric tons (mine production); 776,000 metric tons (refined production with some secondary lead included) (1982) 1.09X10+12 G (1986) 1.26x10+12 g 1997: Recoverable lead from mines (after smelting and refining), 448,000 metric tons; Primary lead (refined; domestic ores and base bullion), 343,000 metric tons; Secondary lead (lead content), 1,110,000 metric tons. U. S. Imports: (1977) 2.30X10+11 G (1982) 9.50X10+10 G (1986) 1.20X10+10 g 1997: Lead in ore and concentrates, 17,800 metric tons; Lead in base bullion, 25 metric tons; lead in pigs, bars, and reclaimed scrap, 265,000 metric tons. (lead content) U. S. Exports: (1977) 8.90X10+9 G (1982) 5.56X10+10 G (1986) 1.40X10+10 g 1997: Lead ore and concentrates, 42,200 metric tons; Lead materials, excluding scrap, 104,000 metric tons. (lead content) Laboratory Methods: Clinical Laboratory Methods: MICRODETERMINATION OF LEAD IN BLOOD & URINE BY ANODIC STRIPPING VOLTAMMETRY EQUIPPED WITH MERCURY ELECTRODE. NO INTERFERENCE WAS FOUND WITH COEXISTING IONS FOUND IN URINE. /TOTAL LEAD/ High performance liquid chromatography assay of RBC UMPase activity is a sensitive and rapid assay that appears to meet criteria for a reliable clinical laboratory index of blood lead concentrations. /Total lead/ Lead concentrations (ug/g wet weight) in human bone (tibia) were measured noninvasively in vivo employing an x-ray fluoresence technique. Forty-five workers who had been chronically exposed to lead (mean duration of employment 20.9 yr) were found to have a mean bone lead content of 52.9 ug/g wet weight (range 0-198 ug/g). Blood lead, urinary lead excretion after EDTA chelation, zinc protoporphyrin, and unstimulated urinary lead excretion were also evaluated. The correlation coefficients (r) between bone lead measurements (as assayed by x-ray fluoresence) and blood lead, zinc protoporphyrin, or unstimulated urinary lead were 0.44 (p=0.004), 0.39 (p=0.015), and 0.40 (p=0.01) respectively. The correlation coefficient between x-ray fluoresence (XRF) findings and lead excretion following Ca-EDTA administration was 0.69 (p<0.001). /Total lead/ Biological indicator of exposure to lead or lead compounds. Analyte: Lead. Matrix: blood or tissue. Method: Inductively-coupled argon plasma-atomic emission spectroscopy. Wavelength: 220.4 nm. Precision: 0.85. This method is useful for monitoring the blood of workers exposed to several metals simultaneously. This is a simultanous multielemental analysis, but is not compound-specific. /Total lead/ Biological indicator of exposure to lead & lead compounds. Analyte: Lead(II)-APDC (ammonium pyrrolidine dithiocarbamate) complex. Matrix: blood or urine. Technique: atomic absorption, air/acetylene. Quality control: commercial controls, pooled urine or blood, urine corrected for creatinine. Extraction: APDC-MIBK (methyl isobutyl ketone). Range: 5 to 150 ug/100 g blood; 5 to 150 ug/100 ml urine. Precision: 0.05. This procedure quantitates Pb(2+) in blood or urine to assess body burden, injury to the hematopoietic system, & to comply with Federal regulations. Blood lead is the preferred biological indicator of lead absorption. The optimum working range is 0.1 to 1.5 ug Pb/g or per ml urine. Interferences: Phosphate, EDTA, & oxalate can sequester lead and cause low lead readings. /Total lead/ Sampling Procedures: Airborne particulate lead is sampled with a high-volume air sampler (as high as 2 cu m/min) for a period of 24 hr and analyzed by atomic absorption spectrometry. Gross particulate loading is determined by weighing the filter before and after sample collection. Additional supplemental samplers include the following: 1) dichotomous sampler - to fractionate samples into two size ranges, since there are distinct differences in the effects of small and large particles on humans; 2) tape sampler - to monitor airborne particulates for shorter time intervals (for source and transport studies). Analyte: Lead. Matrix: Air. Sampler: Filter (0.8-um cellulose ester membrane). Flow rate: 1 to 4 l/min. Vol: min, 200 l at 0.05 mg/cu m; max, 1200 l. Stability: stable. Shipment is routine. Range studied: 0.13 to 0.4 mg/cu m; 0.15 to 1.7 mg/cu m (fume). Overall precision: 0.072; 0.068 (fume). The working range is 0.25 to 0.5 mg/cu m for a 400 l air sample. The method is applicable to elemental lead, including lead fume, & all other aerosols containing lead. This is an elemental analysis, not compound specific. Special References: Special Reports: CHISOLM JJ JR, D BARLTROP; RECOGNITION & MANAGEMENT OF CHILDREN WITH INCR LEAD ABSORPTION; ARCHIVES OF DISEASES IN CHILDHOOD 54: 249-62 (1979). REVIEW WITH DISCUSSION ON MANAGEMENT & RECOGNITION OF INCREASED LEAD ABSORPTION IN CHILDREN USEPA; Ambient Water Quality Criteria Doc: Lead (1980) EPA 440/5-80-057 USEPA; Air Quality Criteria for Lead (1977) EPA 600/8-77-017 USEPA; Intermedia Priority Pollutants Guidance Document Lead (1982) Nat'l Research Council Canada; Effects of Chromium in the Canadian Envir (1976) NRCC No.15017 WHO; Environ Health Criteria: Lead (1977) USEPA; Air Quality Criteria for Lead I-IV (1986) EPA-600/8-83/028aF McInnes G; Airborn Lead Concentrations and the Effect of Reductions in the Lead Content of Petrol (1986) National Academy of Sciences; Lead in the Human Environment (1980) USEPA; Health Effects Assessment for Lead (1984) PB86-134665 DHHS/ATSDR; The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress (7/88) WHO; Environmental Health Criteria 119: Principles and Methods for the Assessment of Nephrotoxicity Associated with Exposure to Chemicals (1991) DHHS/FDA; Guidance Document for Lead in Shellfish (1993) U.S. Dept Health & Human Services/Agency for Toxic Substances & Disease Registry; Toxicological Profile for Lead (Update) (1993) ATSDR/TP-92/12 Synonyms and Identifiers: Related HSDB Records: 6923 [LEAD COMPOUNDS] Synonyms: CI pigment metal 4 CI 77575 KS-4 LEAD Lead flake Lead metal Lead S2 Olow (Polish) Pb-S 100 PLUMBUM Formulations/Preparations: Grade: high purity (less than 10 ppm impurity); pure (99.9+); powdered (99% pure); pig lead; paste. Forms available: ingots, sheet, pipe, shot, buckles or straps, grids, rod, wire, etc; paste; powder; single crystals. Low bismuth, low silver, pure lead. 99.995% lead (ASTM B29-92) (for chemical applications requiring low bismuth and silver contents). Specifications (max allowable metal, wt%: Sb, As, Sn, 0.0005 each; Cu, 0.0010; Ag, 0.0010; Bi, 0.0015; Zn, 0.0005; Te, 0.0001; Ni, 0.0002; Fe, 0.0002. Refined pure lead. 99.97% lead (ASTM B29-92) (for lead battery applications). Specifications (max allowable metal, wt%: Sb, As, Sn, 0.0005 each; Cu, 0.0010; Ag, 0.0025; Bi, 0.025; Zn, 0.0005; Te, 0.0001; Ni, 0.0002; Fe, 0.001. Pure lead. 99.94% lead (ASTM B29-92). Specifications (max allowable metal, wt%: Sb, As, Sn, 0.001 each, 0.002 total; Cu, 0.0015; Ag, 0.005; Bi, 0.05; Zn, 0.001; Ni, 0.001; Fe, 0.001. Chemical copper-lead. 99.90% lead (ASTM B29-92) (for applications requiring corrosion protection and formability). Specifications (max allowable metal unless range is given, wt%: Sb, As, Sn, 0.001 each, 0.002 total; Cu, 0.040-0.080; Ag, 0.020; Bi, 0.025; Zn, 0.001; Ni, 0.002; Fe, 0.002. EPA Hazardous Waste Number: D008; A waste containing lead may (or may not) be characterized a hazardous waste following testing by the Toxicant Extraction Procedure as prescribed by the Resource Conservation and Recovery Act (RCRA) regulations. /Lead/ For more information consult the Lead MSDS above. Top of Page Return to Home Page of Home Air Purifier Expert from Lead MSDS Information Best Indoor Air Quality Test Kit |
