LEAD

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.

MOLECULAR FORMULA

ERG GUIDE NUMBER

151-SUBSTANCES - TOXIC (NON-COMBUSTIBLE)

SYNONYM REFERENCE

(Ariel GlobalView, 2002;(ATSDR , 1997; Hathaway et al, 1996; HSDB , 2002; RTECS , 2002)

USES/FORMS/SOURCES

USES

The metal is widely used for its malleability, density, low melting point, corrosion resistance, chemical stability and opacity to x-rays and atomic radiation. It is a poor electrical conductor but a good sound and vibration absorber. Despite its usefulness, lead is toxic to humans (Lewis, 2001; Budavari, 2000; (ATSDR, 1999); ACGIH, 1996a).
At least half, and perhaps as much as 70%, of the worldwide lead usage is for the production of lead-acid batteries used in automobiles and other industrial applications (Bingham et al, 2001; (ATSDR, 1999)).
Other uses of lead include an ingredient in pigments for paints, enamels, ceramic glazes, and glass, and as an ingredient in plastics and rubbers. Lead is used in metallurgy to make lead alloys, such as those used to make alloys for bearings. It has been used to make solder, foils, caulking, coverings for cable, and ammunition. Lead has been widely used in storage batteries and as shielding for x-ray and atomic radiation (Lewis, 2001; Baselt, 2000; Budavari, 2000; (ATSDR, 1999); Sittig, 1991).
In the construction industry it has been used to dampen vibration. Lead is often used to line tanks, piping and other equipment used in the production of sulfuric acid. It is used in petroleum refining and other chemical processes. Tetraethyl lead, an organic lead, has been used widely as an anti-knock agent in gasoline, though its use has been phased out by the Environmental Protection Agency (Lewis, 2001; Budavari, 2000; (ATSDR, 1999); Sittig, 1991).

FORMS

Elemental lead exists as a highly lustrous, heavy, silvery-gray metal with a cubic crystal structure that assumes a bluish tint as it tarnishes in air. It is quite soft and malleable (Lewis, 2001; Budavari, 2000) .
It is predominantly found in a number of ores, the most common of which is lead sulfide, also known as galena (Bingham et al, 2001; (ATSDR, 1999)).
Lead is available in a wide range of solid forms such as sheets, ingots, rod, pipe, shot, buckles or straps, grids, wire, paste, single crystals, or powder. Grades include high purity (less than 10 ppm impurity), pure (99.9+%), powdered (99% pure), low bismuth, low silver, pure lead (99.995%), refined pure (99.97%), chemical copper-lead (99.90%), pig lead, or paste (HSDB , 2002; Lewis, 2001).

SOURCES

Lead is a naturally-occurring metallic element found in the earth's crust at about 15-30 mg/kg. Lead does not generally occur in pure elemental form, but exists in several mineral ores including galena (lead sulfide), anglesite (lead sulfate), cerussite (lead carbonate), mimetite (lead chloroarsenate), and pyromorphite (lead chlorophosphate) (Bingham et al, 2001; Budavari, 2000; Lewis, 2000; (ATSDR, 1999); ACGIH, 1996a).
In 1996, 93% of domestically mined lead was produced in Missouri and Alaska, contributing to a total domestic production of 436,000 metric tons. Approximately 268,000 metric tons of lead metal and 14,800 metric tons of lead scrap and waste were imported during that same year ((ATSDR, 1999)).
Pure lead is derived through the roasting and reduction of galena, anglesite, and cerussite, that is then purified through the following methods: desilvering (Parkes process); electrolytic refining (Betts process); pyrometallurgical refining (Harris process); or the Betterton- Kroll process (for the removal of bismuth) (Ashford, 1994; Lewis, 2001).
ROUTE OF EXPOSURE

Exposure to lead in the general population occurs from inhalation of contaminated air and dust of various types or ingestion of food and water containing lead with a fairly even split between ingestion and inhalation exposure routes. About 5-15% of ingested lead is absorbed by adults with less than 5% retained. Children, however, absorb approximately 50% of ingested lead and retain about 30% (Lewis, 2000).

SOURCES OF LEAD EXPOSURE

Autoclave tapes (Davis, 1987)
Automobile storage battery casing; battery repair shops (Wong A, Castro Jr G & Duarte JG et al, 1994; MMWR, 1989; Dolcourt et al, 1981)
Automobile fumes (Reith et al, 2003; Morgan et al, 2001; Landrigan, 1982)
Bone meal or dolomite supplements (Jones et al, 1999; Miller, 1987)
Bootleg whiskey (moonshine, corn liquor) (Reith et al, 2003; Morgan et al, 2001; Morgan et al, 2001; Landrigan, 1982)
Brewing kettle (imported samovar from Iran; used for reconstitution of powdered infant formula) (Shannon, 1998)
Calcium supplements (Ross et al, 2000)
Candle with lead-containing wicks (Sobel et al, 2000)
Ceramic-coated capacitor manufacturing (Kaye et al, 1987)
Ceramic glazes (found on pottery, earthenware, bone china, and porcelain) (Shiri et al, 2007; Anon, 2004; Reith et al, 2003; Morgan et al, 2001; Vance et al, 1990; Phan et al, 1998; Roberge et al, 1994; Matte et al, 1994; Chassaing et al, 1991; Zuckerman et al, 1989; Bradley et al, 1987; Landrigan, 1982; Natelson & Fred, 1976)
Clay pots used for tamarind jelly (contained 58,000 mcg lead/g) (Fuortes & Bauer, 2000)
Contaminated animal feed from mining waste (Lund & Brown, 1989)
Contaminated flour from a stone mill repaired with molten lead (Kokori et al, 1999; Jones et al, 1999; Dona et al, 1999; Carton et al, 1987; Kocak et al, 1989)
Contaminated infant formula from water boiled in imported kettle from Iran (Frankel et al, 1992; Shannon, 1998).
Cosmetics (traditional, Surma, Kohl, or Kajal mascara/eyeliner may contain 17.3 to 79.5% lead; from Saudi Arabia, India, Pakistan, and Iran) (Al-Ashban et al, 2004; Reith et al, 2003; Morgan et al, 2001; Jones et al, 1999; Kulshrestha, 1996; Nir et al, 1992; Healy & Aslam, 1986; Pontifex & Garg, 1985; Landrigan, 1982)
Crystal (may contain 24% to 32% lead oxide) (Graziano & Blum, 1991; Appel et al, 1992)
Dental films stored in lead-lined table-top containers ((Anon, 2001))
Firing ranges (Beaucham et al, 2014; Stromness et al, 2000; Shannon, 1999; Chau et al, 1995; Ozonoff, 1994; Brewer, 1989; Valway et al, 1989; Fisher-Fischbein et al, 1987; Norotny et al, 1987; Goldberg et al, 1991; Fischbein, 1992a; Tripathi et al, 1990)
Folk remedies or traditional medicines (see below for more specific terms) (Reith et al, 2003; Morgan et al, 2001; Landrigan, 1982; Bose et al, 1983)
Gold ore processed using artisanal techniques (Burton, 2012)
Hair spray (older brands) (Raasch et al, 1983; Curry et al, 1986; Landrigan et al, 1975)
Heroin (Parras et al, 1987)
Hongdans (lead tetraoxide) traditional chinese medicine (Lin et al, 2012)
Home battery manufacture (Reith et al, 2003; Morgan et al, 2001; Landrigan, 1982)
Homemade traditional alcoholic beverage (tsipouro) (Kokori et al, 1999)
Illicit methamphetamine (may contain lead acetate as an impurity or direct contamination) (Allcott et al, 1987; Norton et al, 1989; CDC, 1989)
Imported candy wrappers (cellophane) (Fuortes & Bauer, 2000)
Ink (Cohen et al, 1986)
Ingested bullets or pellets (McNutt et al, 2000; Lyons & Filston, 1994; Gellert et al, 1993; Greensher et al, 1974)
Ingested fish sinkers (Fergusson et al, 1997).
Jewelry (low-cost children's and costume jewelry imported and sold in the US) (Weidenhamer & Clement, 2007; Berkowitz & Tarrago, 2006)
Lead-contaminated flour (lead used to repair grindstones for flour mills) (Dona et al, 1999; Kocak et al, 1989; Carton et al, 1987)
Lead-contaminated ground paprika (lead tetroxide or red lead) used in home-made sausages (Kakosy et al, 1996)
Lead-contaminated spices used in food preparation (Swanuri marili; Kharchos suneli [zafron]; Kozhambu) (Woolf & Woolf, 2005)
Lead-contaminated water used in infant formulas (Liebelt et al, 1992)
Lead crystal alcoholic beverage decanters (Appel et al, 1992).
Lead curtain weights (Blank & Howieson, 1983; Hugelmeyer et al, 1988)
Lead pipes (Reith et al, 2003; Morgan et al, 2001; Landrigan, 1982)
Lead shot ingestion (McKinney, 2000; Selbst et al, 1986; Greensher et al, 1974)
Lead stabilizers (eg; lead sulfate, lead stearate) as additives in plastics to coat or insulate wire and cables in the formulation of polyvinyl chloride plastic (Coyle et al, 2005)
Litargirio (a yellow or peach-colored powder used as a antiperspirant/deodorant or as a folk remedy in the Hispanic community) (Anon, 2005)
Lozeena (Iraq) food coloring, orange powder (Jones et al, 1999)
Necklace with beads; medallion pendant (Anon, 2004a; Jones et al, 1999)
Nipple shields for breastfeeding (Kokori et al, 1999)
Paint chips and dust (on houses, toys and furniture) (Reith et al, 2003; Morgan et al, 2001; ATSDR , 1997; Budavari, 1996; ACGIH, 1996a; Landrigan, 1982)
Plastic wire coating (from chewing the plastic insulation stripped off electrical wires; plastic coating lead content 10,000 to 39,000 mcg lead/g of coating) (CDC, 1993; Franco et al, 1994)
Pool cue chalk (mostly contained less than 30 ppm lead; however, 3 kinds of chalk contained lead concentrations in excess of 6000 ppm [Master green, Pioneer green and tangerine])(Dargan et al, 2000; Miller et al, 1995; Miller et al, 1996)
Radiator mechanics (Tribe, 1997; Goldman et al, 1987; Lussenhop et al, 1989)
Renovation/modernization of old homes (Curran & Nunez, 1989; Gonzalez & Ungaro, 1982)
Retained bullets (Akhtar et al, 2003; Madureira et al, 2001; DeMartini et al, 2001; McQuirter et al, 2001; Murdock et al, 1999; Viegas & Calhoun, 1986; Aly et al, 1993; Farber et al, 1994; Meggs et al, 1994; John & Boatright, 1999)
Silver jewelry workers (Kachru et al, 1989)
Soil contaminated with lead (Reith et al, 2003; Budavari, 1996; ACGIH, 1996a; ATSDR , 1997; Prpic-Majic et al, 1992).
Toy necklace (a medallion pendant contained 38.8% lead (388,000 mg/kg), 3.6% antimony, and 0.5% tin; from India, recalled in the US) (VanArsdale et al, 2004; Anon, 2004a)
Wine (metallic lead sheets enclosing many European wine bottles) (Rovira et al, 1989; Nriagu, 1985; Elias, 1985)
Wine leachate from bathtubs (homemade red wine) (Mangas et al, 2001)

CALCIUM SUPPLEMENTS

In one study, four commercial calcium preparations labeled as being "natural" (i.e., oyster shell) had measurable lead content (approximately 1 mcg/d for 800 mg/d of calcium, 2 mcg/d for 1500 mg/d of calcium, and up to 10 mcg/d for renal dosage). However, no lead was found in the calcium acetate or polymer products (Ross et al, 2000).
Calcium supplements from bone meal may have lead concentrations of up to 12.8 mcg/g, although no cases of lead toxicity have been reported from ingestion (Miller, 1987).

DIET

In many countries, the intake of lead from diet can approach or exceed the PTWI (Provisional Tolerable Weekly Intake; 25 mcg/kg body weight or 1500 mcg/person). In Brazil, lead was detected in medicinal herbs prepared with the leaves, fruits or barks of the plants, casara buckthorn, horse chestnut, centella asiatic, celastraceae and ginkgo biloba. Three horse chestnut samples contained 153, 156, and 1480 mcg lead/gram, with the estimated lead intake through the consumption of horse chestnut reaching 440% of PTWI (Caldas & Machado, 2004).

DUST/FUMES

CANDLES WITH A METALLIC WICK: In a study of lead exposure from candles, it was shown that approximately 10% (n=86) of candles with metallic wicks contain lead. After burning these candles for 3 hours, they would produce air lead concentrations ranging from 15.2 to 54.0 mcg/m(3) in 24 hours. This is 10.1 to 36.0 times the US EPA standard of 1.5 mcg/m(3) (Sobel et al, 2000).
FIRES: In a case-controlled evaluation of victims (n=66) of severe smoke inhalation following a closed-space fire, patients with severe smoke inhalation had a statistically significant 2-fold increase in whole blood lead level (mean lead level among cases was 6.64 mcg/dL vs 2.89 mcg/dL among controls). The authors, however, noted that these findings were unlikely to be of clinical significance. Currently, treatment recommendations for adults are based on blood lead levels of 40 mcg/dL or greater. Based on these findings, widespread testing for lead intoxication in adult victims of smoke inhalation is not necessary. It was suggested, that repeated acute adult exposures (e.g., firefighters) or pediatric exposures may require further evaluation (Lahn et al, 2003).
SECOND HAND TOBACCO SMOKE: In a cross-sectional analysis of data from the Third National Health and Nutrition Examination Survey (NHANES III), a stratified multistage clustered probability design was used to select a representative sample of the US population. A dataset of 5592 children was used to estimate 37 million children between the ages of 4 to 16 years. The study found that children with high cotinine levels, due to second hand tobacco smoke exposure, were more likely to have high blood lead levels (>/= to 10 mcg/dL) than those with low cotinine levels. It has been estimated that main stream tobacco smoke contains 60 ng of lead per cigarette, and that sidestream smoke contains 5 to 10 ng of lead per cigarette (Mannino et al, 2003).

The adjusted linear regression model indicated that geometric mean blood lead levels were 38% higher (95% CI) in children with high cotinine levels as compared with low cotinine levels. The study suggested that second-hand smoke could be associated with elevated blood lead levels with the strongest association being in younger children.

GOLD ORE PROCESSING: In 2010, children (n=463 less than 5 years of age) of 4 villages in Zamfara state in rural northwestern Nigeria developed massive childhood lead poisoning after exposure to lead contaminated gold ore-processing in family compounds. It was found that approximately 25% (118 of 463) of children under the age 5 died within a year of lead exposure. An initial blood tests revealed 8 children with BLLs of 168 to 370 mcg/dL. BLLs of 59% of surviving children were then collected; 97% of these BLLs were at least 45 mg/dL and 85% surpassed the portable sampling devices' maximum detection limit of 65 mcg/dL (Burton, 2012; Dooyema et al, 2012).

FOLK REMEDIES

Folk/traditional medicines may be found in the following locations: Korea, Pakistan, India, China, Mexico and the Middle East (Anon, 2004b; Shrestha & Greenberg, 2002; Traub et al, 2002; van Vonderen et al, 2000; Jones et al, 1999; Spriewald et al, 1999; Dolan et al, 1991; Mitchell-Heggs et al, 1990; Smitherman & Harber, 1991; McElvaine et al, 1990; Markowitz et al, 1994; Chi et al, 1994; Perharic et al, 1994).

Alarcon (almost pure lead tetroxide) (Jones et al, 1999; Bose et al, 1983)
Albayalde (lead carbonate) (Mexico; most prevalent among migrant workers in south Texas, Florida, and California) (Jones et al, 1999; Cueto et al, 1989; CDC, 1993)
Amratanshta (India) (Frith et al, 2005)
Azarcon (a bright orange powder containing approximately 92% to 97% lead tetroxide) (Jones et al, 1999; Bose et al, 1983)
Bala goli (India) (Jones et al, 1999)
Bao ning dan (a Chinese herbal pill) (Auyeung et al, 2002)
Bruhat Vata Chintamani Rasa (India) (Meiman et al, 2015)
Coral (almost pure lead tetroxide) (Jones et al, 1999; Bose et al, 1983)
Deshi Dewa (a white powder from Asia) (Kulshrestha, 1996)
EX and ADISSA (Ayurvedic medications from India) (Shrestha & Greenberg, 2002)
Ghasard (India) (Jones et al, 1999)
Greta (Lead oxide) (Mexico; most prevalent among migrant workers in south Texas, Florida, and California) (Jones et al, 1999; Cueto et al, 1989; CDC, 1993)
Hau ge fen (a Chinese herbal tea) (Markowitz et al, 1994)
Hongdans (containing lead tetraoxide) traditional chinese medicine (Lin et al, 2012)
Kandu (India) (Jones et al, 1999)
Liga (almost pure lead tetroxide) (Jones et al, 1999; Bose et al, 1983)
Maharasanadi Kashayam (India) (Frith et al, 2005)
Mahayogaraj Guggulu (India; in one case, it contained 7052 mg/kg of lead (1.75 mg per tablet) and 12,756 mg/kg of mercury (3.5 mg per tablet)) (Frith et al, 2005; Meiman et al, 2015)
Maha yogran guggulu (India; contains 6.47% lead by weight) (Saryan, 1991).
Maria Luisa (almost pure lead tetroxide) (Jones et al, 1999; Bose et al, 1983)
Nzu (Salted Nzu) (U.S. Food and Drug Administration, 2009)
Pay-loo-ah (among Hmong Laotian refugees; a bright orange-red powder, containing 1% to 90% lead and 70% to 80% arsenic) (Jones et al, 1999; CDC, 1983)
Rueda (almost pure lead tetroxide) (Jones et al, 1999; Bose et al, 1983)
Pushap and Sharti (Indian Ayurvedic herbal formulations) (van Vonderen et al, 2000; Spriewald et al, 1999; Dundabin et al, 1992)
Satrinj and bint dahab (traditional medications available in Oman, contain 98% and 90% lead oxide, respectively) (Woolf et al, 1990)
Tibetan herbal vitamin tablets (Moore & Adler, 2000)

Litargirio (also known as litharge or lead monoxide, is a yellow or peach-colored powder) is used as an antiperspirant/deodorant and a folk remedy for burns and fungal infections of the feet. It is also used in the manufacture of batteries, glass, ceramics, or rubber products and as a paint pigment. Litargirio is manufactured and/or packaged by Dominican Republic laboratories and is available locally in botanicas (shops selling herbs) or bodegas ( grocery stores) in the Hispanic community. In one report, the litargirio sample contained 790,000 ppm (79%) lead (Anon, 2005).
Nzu, found in African specialty stores, is marketed as a traditional remedy for treatment of morning sickness in pregnant women. Nzu appears as a ball of clay or mud and is typically sold in small plastic bags with handwritten labels identifying it as "Nzu" or "Salted Nzu". Laboratory analysis of a sample of Nzu, by the Texas Department of State Health Services (DSHS), found that it contained high concentrations of lead and arsenic (U.S. Food and Drug Administration, 2009).
Hongdan (red lead) is a traditional Chinese medicine containing lead tetraoxide. In one study, 16 Hongdans samples had an average lead content of 817,000 mg/kg. Two Chinese children (a 3-year-old boy and a 6-month-old girl) with lead toxicity after using Hongdan (a lead concentration of 214,000 mg/kg) with talcum baby powder had blood lead concentrations of 303 mcg/L and 385 mcg/L, respectively (Lin et al, 2012)

LEAD BULLETS

Lead intoxication from retained bullets or shrapnel has been reported. Almost all cases involve lodging of the missile in or near a joint. Inflammatory changes from development of arthritis or re-injury have often precipitated symptoms. Synovial fluid is a better solvent for lead than serum or bone and synovial lead levels can be much higher than blood levels (Akhtar et al, 2003; Madureira et al, 2001; DeMartini et al, 2001; McQuirter et al, 2001; John & Boatright, 1999; Farber et al, 1994; Aly et al, 1993; Meggs et al, 1994; John & Boatright, 1999; Viegas & Calhoun, 1986; Roberts et al, 1983; DiMaio & Garriott, 1980; Dillman et al, 1979; Switz et al, 1976) .
Fifteen emergency department patients with radiographic evidence of retained lead bullets or shrapnel had statistically significant increased blood lead levels (mean 17 mcg/dL) compared to matched controls (mean 7 mcg/dL). Time since initial exposure ranged from 1 to 45 years. Actual composition of retained bullets was not determined (Farrell et al, 1999).
One study of 240 emergency department patients reported that persons with extra-articular retained missiles (EARMS) had significantly higher whole blood lead levels than matched controls. A positive correlation between whole blood lead levels and a history of recent fractures (the last 30 days) was found. This can be explained by the fact that bone lead stores are released into the circulation during instances of bone injury and remodeling. In addition, no correlation between whole blood lead levels and the number of reported symptoms of lead toxicity in persons with or without EARMS was observed. Overall, elevated lead levels were not clinically significant and did not change patient management in 96% of the patients (Nguyen et al, 2005).
In one study, changes in blood lead levels in subjects (n=451) were evaluated during the first year after a gunshot wound with a retained bullet. It was shown that blood lead concentrations increased significantly with time after injury up to 3 months, with number of retained fragments (p<0.0005), and with increasing age (p<0.0005). Blood lead increase as a function of fragmentation was 29.5% higher among subjects who had suffered a torso bone fracture (chest, abdomen, and pelvic regions) than in subjects without a fracture (p<0.0005). Higher blood lead levels were noted in subjects with bullets or fragments lodged near bone (p<0.0005) or near joints (p=0.032). In addition, logistic models correctly reported a blood lead elevation of equal to greater than 20 mcg/dL in 81% and 85% of subjects at 3 and 6 months postinjury, respectively. At 3 months and 12 months, the prevalence of elevated blood lead were 11.8% and 2.6%. respectively. Continued surveillance of blood lead levels after gunshot injury for these patients was recommended (McQuirter et al, 2004).
INDOOR FIRING RANGES: In a study of 41 states that participated in Adult Blood Lead Epidemiology and Surveillance (ABLES) program (years: 2002 to 2012), it was found that 2056 persons had BLLs 10 mcg/dL or greater (1271 with BLLs 10 to 24 mcg/dL; 785 with BLLs of 25 mcg/dL or greater) after exposure to lead at work (631 were employed in police protection and 1425 were employed in other amusement and recreation industries, including indoor firing ranges). In addition, 2673 persons were exposed to lead in non-work-related target shooting and had elevated BLLs (1290 with BLLs of 25 mcg/dL or greater and 1388 with BLLs of 10 to 24 mcg/dL) (Beaucham et al, 2014).

LIPSTICKS

In 2010, testing of 400 lipsticks by the US FDA revealed a maximum lead concentration of 7.19 ppm. Based on this concentration, average (2/3 of a 3-g tube/year) and high (2.5 3-g tubes/year) lipstick use by a child will not increase BLLs and at least 90 tubes of lipstick is needed to be ingested over a year to increase a child's BLL by 1 mcg/dL (Monnot et al, 2015).

OCCUPATIONAL EXPOSURE

In an industrial setting, exposure to lead mainly occurs from inhalation of dust or fumes (Budavari, 1996; ACGIH, 1996a; ATSDR , 1997) Lead dust carried home from work on contaminated clothing or equipment can contaminate the home, causing elevated blood lead levels in family members (Baker et al, 1977; Nunez et al, 1993).
Occupational exposure to lead may occur in the following settings:

Autoclave indicator strips (use the color change of white lead carbonate to black lead sulfide to indicate adequacy of sterilization) (Davis, 1987)
Bricklaying (by using a special brick mortar, containing 71% lead oxide, formulated to resist acid in an accumulation tank at a paper mil) (CDC, 1991a)
Capacitor manufacturing (Kaye et al, 1987)
High voltage tower conservators (Krawczyk et al, 2006)
Construction and repair of lead-painted bridges (CDC, 1995; CDC, 1993; Rae et al, 1991; Marino et al, 1989)
Dye factory (Ger et al, 1994)
Leaded or stained glass production, laboratories, or ceramics (ACGIH, 1991)
Lead recycling plant (Chao & Wang, 1994)
Precious metals refinery (Kern, 1994)
Producing lead carbonate (Ger et al, 1994)
Radiator repair (inhalation of lead fumes generated during soldering joints and dust generated by blasting the radiator cores) (Nunez et al, 1993; CDC, 1991b; Goldman et al, 1987)
Wire and cable company (lead stearate stabilizer) (Ger et al, 1994)
Working with lead naphthenate (a metallic soap used as a drying agent in paint and as a high pressure lubricant) (Goldberg et al, 1987)

TAKE-HOME LEAD POISONING - All industries in which lead is used (eg; furniture refinishing and construction) present occupational hazards. Industrial lead dust, carried on the clothes of parents, is an exposure source for children (Baker et al, 1977). Employers in these industries should arrange personal exposure monitoring and surface wipe sampling for lead and implement workplace improvements, including a respiratory protection program; use of HEPA vaccum-attached power sanders; use of a high-efficiency toxic dust HEPA vacuum; daily clean uniforms; separate storage lockers, changing area with showers, and lunch room; warning signs; safety training addressing take-home lead; and a lead medical surveillance program (Centers for Disease Control and Prevention, 2001).

In one report, family members of workers exposed to lead had elevated BLLs (Centers for Disease Control and Prevention, 2001).

PAINT

Lead in paint is usually in the form of lead carbonate. It enters the body when paint chips are eaten, when paint is sucked, when the dust of the paint is picked up on the hands of toddlers, during house renovation, or when painted metal is cut with an acetylene torch.
Since 1977, household paint must contain no more than 0.06% (600 ppm) lead by dry weight. Overt lead poisoning usually occurs in housing built before World War II. A chip of old or industrial paint the size of a thumbnail may contain 50 to 200 mg of lead. For comparison, the average dietary intake of lead in children is only 20 to 80 mcg/day (Anon, 1987).
In a lead screening of 5168 children aged 1 to 3 years in Salt Lake County, Utah, high serum lead levels (>20 mcg/dL) were found in 7 (0.1%) children. In 5 of the 7 cases, the source of exposure was traced to deteriorating lead-based paint in their homes (CDC, 1997).
Lead-containing pigments that have been used in paints include (Joly et al, 1987):

calcium plumbate
ceruse (basic lead carbonate)
chromium yellows
lead phosphite
lead cyanamide
metallic lead
minium
molybdenum reds

The solubility of lead-based pigments in gastric fluid determines the hazard after ingestion. Pigments with partial solubility include lead minimum, basic lead carbonate, and metallic lead. Other pigments that are practically insoluble in gastric fluid include lead chromate, lead silicochromate, lead sulfochromate, and lead sulfochromomolybdate (Joly et al, 1987).
Alkyl paints may contain drying agents, such as lead naphthenate or lead octoate. Usual concentrations are 0.1 to 0.3% (Joly et al, 1987).

WATER SUPPLY

FLINT, MICHIGAN: In 2014, residents of Flint, Michigan were exposed to lead after their water supply was changed from Detroit-supplied Lake Huron water to Flint River water. Flint has aging water distribution system with old lead pipes and lead plumbing. In addition, the city water has high levels of chloride, high chloride-to-sulfate mass ratio, and no corrosion inhibitors. Authorities detected high rates of lead leaching into drinking water and very high water lead levels (WLLs). A retrospective study evaluated blood lead levels (BLLs) of 1473 children (age, less than 5 years) from Flint before (2013) and after (2015) water source change. The incidence of elevated blood lead levels (EBLL) before and after the water source change were 2.4% to 4.9% (P less than .05), respectively. Children from disadvantaged neighborhoods had the greatest EBLL increases. The change in EBLL outside of Flint was not statistically significant (0.7% to 1.2%; P greater than .05) (Hanna-Attisha et al, 2016).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

USES: Lead is a soft metal that is used in a variety of industrial processes. It has been used in paint and gasoline, but the use of lead in house paint and gasoline has been outlawed for decades in the United States (US). Folk medications may also contain large amounts of lead salts. Soil may have large amounts of lead contamination from industrial processes or old paint. Some products manufactured outside the US (eg, pottery, jewelry, toys, makeup) may contain lead.

TOXICOLOGY: Lead exerts its toxic effects through a variety of mechanisms and effects many organ systems. It binds sulfhydryl groups, impacting various enzymes, receptors and proteins. Lead interferes with metabolic pathways in mitochondria, and in systems that regulate cellular energy and metabolism. It causes activation/inactivation of many enzymes via its competing effects with other cations, notably calcium, ferrous iron, and zinc. Lead inhibits several enzymes involved in heme synthesis, and impairs erythrocyte membrane stability, causing anemia.

EPIDEMIOLOGY: There are several thousand cases of lead poisoning reported to poison centers in the US every year. However, severe toxicity is very uncommon and deaths are rare. In children with chronic lead poisoning, ingestion of lead paint chips and dust in older dilapidated housing is the most common source of exposure. Inhalational exposure is the most common cause of adult/occupational lead toxicity.

WITH POISONING/EXPOSURE

MILD TO MODERATE TOXICITY: The primary concerns of mild to moderate toxicity from lead exposure in young children are neurodevelopmental, specifically lower intelligence quotient scores and behavioral problems. Population studies suggest that mild cognitive impairment develops at low levels of lead exposure (blood lead concentrations of 10 mcg/dL). Intermittent vomiting, anorexia and abdominal pain may also develop. In mild to moderate exposures in adults, concerns include hypertension, spontaneous abortion and sperm abnormalities, and more subtle neurocognitive effects. Fatigue, mild somnolence, headache, insomnia, abdominal pain, constipation, mild anemia, myalgias and arthralgias, and mild weakness may also develop.
SEVERE TOXICITY: Acute ingestions of very large amounts of lead are rare, but may cause abdominal pain, nausea, vomiting, anemia (usually hemolytic), toxic hepatitis, and encephalopathy. In children, severe toxicity manifests as encephalopathy (ie, coma, seizures, ataxia, incoordination, cranial nerve palsies, increased intracranial pressure, bizarre behavior or altered mentation), persistent vomiting, and anemia. More severe subacute or chronic exposures in adults can lead to symptoms such as fatigue, malaise, irritability, anorexia, insomnia, weight loss, decreased libido, arthralgias, myalgias, hypertension, crampy abdominal pain, nausea, constipation or diarrhea (less commonly), impaired concentration, headache, diminished visual-motor coordination, tremor, encephalopathy, a peripheral motor neuropathy (especially affecting the upper extremities causing wrist drops), a normochromatic or microcytic anemia (the hallmark of which is basophilic stippling), nephrotoxicity (a reversible acute tubular dysfunction and chronic interstitial fibrosis), hyperuricemia, and associated gout.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Avoid any skin contact.
Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases.
Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

ACUTE CLINICAL EFFECTS

SUMMARY

TOXICOLOGY: Lead exerts its toxic effects through a variety of mechanisms and effects many organ systems. It binds sulfhydryl groups, impacting various enzymes, receptors and proteins. Lead interferes with metabolic pathways in mitochondria, and in systems that regulate cellular energy and metabolism. It causes activation/inactivation of many enzymes via its competing effects with other cations, notably calcium, ferrous iron, and zinc. Lead inhibits several enzymes involved in heme synthesis, and impairs erythrocyte membrane stability, causing anemia.
EPIDEMIOLOGY: There are several thousand cases of lead poisoning reported to poison centers in the US every year. However, severe toxicity is very uncommon and deaths are rare. In children with chronic lead poisoning, ingestion of lead paint chips and dust in older dilapidated housing is the most common source of exposure. Inhalational exposure is the most common cause of adult/occupational lead toxicity.
MILD TO MODERATE TOXICITY: The primary concerns of mild to moderate toxicity from lead exposure in young children are neurodevelopmental, specifically lower intelligence quotient scores and behavioral problems. Population studies suggest that mild cognitive impairment develops at low levels of lead exposure (blood lead concentrations of 10 mcg/dL). Intermittent vomiting, anorexia and abdominal pain may also develop. In mild to moderate exposures in adults, concerns include hypertension, spontaneous abortion and sperm abnormalities, and more subtle neurocognitive effects. Fatigue, mild somnolence, headache, insomnia, abdominal pain, constipation, mild anemia, myalgias and arthralgias, and mild weakness may also develop.
SEVERE TOXICITY: Acute ingestions of very large amounts of lead are rare, but may cause abdominal pain, nausea, vomiting, anemia (usually hemolytic), toxic hepatitis, and encephalopathy. In children, severe toxicity manifests as encephalopathy (ie, coma, seizures, ataxia, incoordination, cranial nerve palsies, increased intracranial pressure, bizarre behavior or altered mentation), persistent vomiting, and anemia. More severe subacute or chronic exposures in adults can lead to symptoms such as fatigue, malaise, irritability, anorexia, insomnia, weight loss, decreased libido, arthralgias, myalgias, hypertension, crampy abdominal pain, nausea, constipation or diarrhea (less commonly), impaired concentration, headache, diminished visual-motor coordination, tremor, encephalopathy, a peripheral motor neuropathy (especially affecting the upper extremities causing wrist drops), a normochromatic or microcytic anemia (the hallmark of which is basophilic stippling), nephrotoxicity (a reversible acute tubular dysfunction and chronic interstitial fibrosis), hyperuricemia, and associated gout.

CARDIOVASCULAR

HYPERTENSIVE EPISODE: EXPOSURE: Blood pressure was significantly elevated in a group of lead-exposed workers when compared to a cohort of unexposed workers (de Kort et al, 1987). Increase of diastolic pressure has been found in workers exposed to low levels of lead for up to 45 years, and higher diastolic value has been found in workers with blood lead levels over 40 mcg/dL without any effect on the systolic measurement (Harbison, 1998a).

DERMATOLOGIC

SYSTEMIC DISEASE: ACUTE EXPOSURE: Dermal application of lead acetate solution on eczematous skin has resulted in intoxication (Triebig, 1984).

ENDOCRINE

DISORDER OF ENDOCRINE SYSTEM: ACUTE EXPOSURE: Neuroendocrine dysfunction as been implicated as a contributing factor in the decreased stature of children with high blood lead levels (Schwartz et al, 1986).
VITAMIN D DEFICIENCY: ACUTE EXPOSURE: Decreased concentrations of 1,25 dihydroxy vitamin D have been associated with low level lead exposure (Rosen et al, 1980).
DECREASED BODY GROWTH: ACUTE EXPOSURE: Lead-induced short stature may be due to diminished growth hormone secretion (Huseman et al, 1992)
CATECHOLAMINE LEVEL ELEVATED: ACUTE EXPOSURE: Plasma epinephrine and norepinephrine levels were significantly elevated in 15 lead exposed children compared with controls (deCastro, 1990). These findings may relate to hypertension and hyperactivity associated with lead exposure.

GASTROINTESTINAL

GASTROINTESTINAL TRACT: ACUTE EXPOSURE: Abdominal pain, vomiting, constipation, diarrhea and anorexia are common in patients with chronic toxicity. A metallic taste in the mouth and weight loss may also develop (Lin et al, 2012a; Nair et al, 2011; Smith, 2007). CHRONIC EXPOSURE: Abdominal pain and anorexia have been reported subsequent to lead absorption from gunshot wounds. Lead poisoning has been reported from 3 months to 40 years after gunshot wounds (Harbison, 1998).

GENITOURINARY

RENAL TUBULAR DISORDER: Tubular injury noted by proteinuria, glycosuria, and aminoaciduria has been described (a Fanconi-like syndrome). Acute renal failure has been reported in a child (Khan et al, 1983).

Elevated urinary levels of N-acetyl-3-D-glucosaminidase, beta-2-microglobulin, alpha-1-microglobulin, and glutathione S-transferase may serve as early markers of subclinical renal injury (El-Safty et al, 2004; Kumar & Krishnaswamy, 1995; Lin et al, 1993; Kumar & Krishnaswamy, 1995).

TOXIC NEPHROPATHY: CHRONIC EXPOSURE: Lead nephropathy after chronic lead exposure has been well described. Interstitial nephritis, reduced glomerular filtration rate, and nonspecific proximal tubular dysfunction are typical(Niamane et al, 2002; Wedeen et al, 1986; Verschoor et al, 1986).
DECREASED SPERM COUNT: ACUTE EXPOSURE: Decreased sperm count and motility, increases in abnormal sperm, and infertility have been reported with occupational exposure (Assennato et al, 1987; Fisher-Fischbein et al, 1987; Lerda, 1992).

HEENT

HEARING LOSS: Mild hearing loss has been associated with increased blood lead levels in children and adults (Schwartz & Otto, 1987; Schwartz & Otto, 1991; Rybak, 1992).
BURTON'S LINES: Lead sulfide precipitates in gum margins causing dark gray-blue-black lines (Camuglia et al, 2008; Aly et al, 1993; ILO, 1983). Present in older children and adults; rarely in children <5 years as the sulfide comes from bacteria rarely found in the mouths of young children (Aly et al, 1993; ILO, 1983).

HEMATOLOGIC

ANEMIA: ACUTE EXPOSURE: Anemia has been reported in patients with lead poisoning (Beigmohammadi et al, 2008; Traub et al, 2002; Moore & Adler, 2000). Early in the course of poisoning, and particularly in children, lead-induced anemia is microcytic and hypochromic, but in the chronic stage, it often changes to normochromic and normocytic. It seems that the more acute the poisoning is, the more important is the shortening of erythrocyte life span; in chronic poisoning, the heme synthesis inhibition is more significant (Zenz, 1994).
HEMOLYTIC ANEMIA: ACUTE EXPOSURE: Severe lead intoxication accompanied by hemolytic anemia has been reported (Miwa et al, 1981). Hemolysis has also been reported following acute ingestion of red lead (lead oxide) (Nortier, 1980).
MICROCYTIC ANEMIA: ACUTE EXPOSURE: Microcytic anemia is fairly common in patients with lead poisoning (Anon, 2004b; Lavoie & Bailey, 2004; Mangas et al, 2001).
IRON DEFICIENCY: ACUTE EXPOSURE: Children with high blood lead concentrations are more likely to have biochemical iron deficiency than anemia (Rajkumar et al, 1987). Screening for iron deficiency in children with elevated blood lead should not be based solely on elevation in FEP, but also on dietary and socioeconomic risk factors (Carraccio et al, 1987; Linakis & Shannon, 1989).

HEPATIC

INJURY OF THE LIVER: ACUTE EXPOSURE: Liver injury has been reported following acute ingestion of 7 g of lead acetate (Karpatkin, 1961; Sixel-Dietrich et al, 1985).
LIVER ENZYMES ABNORMAL: ACUTE EXPOSURE: Elevated liver enzymes and total bilirubin have been reported in patients with lead poisoning (Nair et al, 2011; Beigmohammadi et al, 2008; Auyeung et al, 2002).

MUSCULOSKELETAL

MUSCLE PAIN: ACUTE EXPOSURE: Myalgia and arthralgia are common symptoms in adults (Mangas et al, 2001; Kakosy et al, 1996; Grimsley & Adams-Mount, 1994).

NEUROLOGIC

TOXIC ENCEPHALOPATHY: ACUTE EXPOSURE: Fatalities and serious long term effects from lead poisoning result from acute encephalopathy with increased intracranial pressure. The encephalopathic syndrome includes depressed sensorium, headache, vomiting, ataxia, extreme irritability, papilledema, impaired consciousness, coma, seizures, and lateralizing neurologic signs (Fluri et al, 2007; Kokori et al, 1999; Wiley et al, 1995). Brain MRI of one patient with lead poisoning revealed hyperintense lesions in the basal ganglia (Fluri et al, 2007). Patients may be misdiagnosed as having amyotrophic lateral sclerosis since lead poisoning may mimic the clinical features of a motor neuron disease (Fluri et al, 2007).
ENCEPHALOPATHY: CHRONIC EXPOSURE: Encephalopathy induced by lead is accompanied by severe cerebral edema, increase in cerebral spinal fluid pressure, proliferation and swelling of endothelial cells in capillaries and arterioles, proliferation of glial cells, neuronal degeneration, and focal cortical necrosis (Lewis, 1996).
HEADACHE: ACUTE EXPOSURE: More obscure symptoms of lead poisoning include: malaise, fatigue, headache, and irritability (Astudillo et al, 2003; Traub et al, 2002; Mangas et al, 2001).
COGNITIVE DEVELOPMENT PEDIATRIC: ACUTE EXPOSURE: Children with BLLs of 10 mcg/dL or greater are more likely to have learning and behavioral effects than children with levels of less than 10 mcg/dL ( CDC, 1997).
COGNITIVE FUNCTION ADULTS: ACUTE EXPOSURE: Neurobehavioral tests in lead workers show deficits in cognitive function including decrease in memory, attention, concentration, and psychomotor performance (Schwartz et al, 2000; Mangas et al, 2001; Valciukas et al, 1986).
ASTHENIA: ACUTE EXPOSURE: Weakness, malaise, somnolence and fatigue have been reported following lead exposure (Frith et al, 2005; Shrestha & Greenberg, 2002; Mangas et al, 2001).
PARALYSIS: ACUTE EXPOSURE: Peripheral nervous paralysis (or lead palsy) typically affects extensor muscles and is characterized by selective involvement of motor neurons, with little or no sensory abnormalities (Zenz, 1994).

PSYCHIATRIC

AGGRESSIVE BEHAVIOR: ACUTE EXPOSURE: An association between air lead concentrations and aggressive and violent behavior has been reported (Stretesky & Lynch, 2001).

VITAL SIGNS

HYPERTENSION: Blood pressure was significantly elevated in a group of lead-exposed workers when compared to a cohort of unexposed workers (de Kort et al, 1987).

CHRONIC CLINICAL EFFECTS

SUMMARY

The hazard of exposure to lead is particularly serious in small companies or operations, often employing no more than three or four workers, engaged in radiator repair, leaded or stained glass production, laboratories, or ceramics.
Lead poisoning in adults is usually occupational or hobbies related due to inhalation of lead containing dust, fumes or vapors. Upon inhalation, absorption takes place easily from the respiratory tract and symptoms develop relatively quickly as compared to oral ingestion.
Subtle neurological/neurophysiological effects have been demonstrated in workers with blood lead levels below 60 microgram per 100 milliliter of blood.
The onset of symptoms of chronic lead poisoning often is gradual. The major organ systems affected are the nervous system, red blood cells, and kidneys.
Signs and symptoms include:

Abdominal tenderness
Anemia
Anxiety
Disturbance of the gastrointestinal tract (includes constipation, anorexia, and rarely excruciating colic)
Facial pallor
Forgetfulness and/or poor concentration
Glomerular sclerosis
Hypotension
Insomnia
Interstitial fibrosis
Irreversible vascular sclerosis
Lassitude
Motor weakness (which may lead to paralysis of the extensor muscles of the wrist and ankles)
Pallor of the eye grounds
Tubular cell atrophy
Weight loss and/or malnutrition

Lead poisoning diagnosis is supported when lead content of blood is greater than 50 mcg/dL, and if urine is greater than 80 mcg/dL.
Lead poisoning has been misdiagnosed as chronic fatigue syndrome in some patients, due to the presenting signs and symptoms.
PEDIATRIC: Children have been considered a risk group for lead toxicity, mainly due to the neurophysiological or neuro-cognitive deficits that may result.
Signs and symptoms for children include weight loss, weakness, and anemia. Encephalopathy occurs frequently in children who have ingested inorganic lead compounds.

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

PREHOSPITAL: Activated charcoal may be used after an acute ingestion. For dermal, eye or inhalational exposures, treatment is standard decontamination including removal of contaminated clothing and washing the exposed area with soap and water.

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance;give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID

EYE EXPOSURE: Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection.

Contact lens use is not recommended when working with this chemical. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.

DERMAL EXPOSURE: Promptly flush the contaminated skin with soap and water. If this chemical penetrates the clothing, promptly remove the clothing and flush the skin with water. If irritation persists after washing, get medical attention.
INHALATION EXPOSURE: Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE: If this chemical has been swallowed, get medical attention immediately.
TARGET ORGANS: Eyes, gastrointestinal tract, central nervous system, kidneys, blood, and gingival tissue (National Institute for Occupational Safety and Health, 2007; Chemsoft(R) , 2000).

GENERAL

Essential to the successful treatment of all cases of lead poisoning is removal of the patient from the source of exposure.

INHALATION EXPOSURE

INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

DERMAL EXPOSURE

DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

EYE EXPOSURE

DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

ORAL EXPOSURE

ACUTE INGESTION

There are no data on adsorption of inorganic lead to activated charcoal, however salts of some other heavy metals are adsorbed.
PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION

Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).

ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).

Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

ADULT

The minimum lethal human dose to this agent has not been delineated.
Acute lead poisoning is rare; it is estimated that ingestion of 10 to 30 grams of a lead salt would result in death after 1 to 2 days (Baselt, 2000).

PEDIATRIC

A 4-year-old child died one week after treatment with Chinese herbal formulations that contained up to 7.5 mg/dose. At the time of death, the child's lead levels were measured at 3 mg/kg in the brain and 17 mg/kg in the liver (Baselt, 2000).
A 2-year-old boy died after drinking apple juice out of a glazed earthenware container over the duration of several weeks. Blood lead levels at the time of death were 0.4-2.2 mg/kg lead in the brain, 13 mg/kg lead in the liver, and 18 mg/kg lead in the kidney (Baselt, 2000).
A 2-year-old girl died after ingesting paint (containing 5-35% lead) and playing in areas with lead dust concentrations of 6,732 mcg/ft(2). Blood lead levels at the time of diagnosis were 391 mcg/dl, and despite a reduction to 72 mcg/dl and treatment, she died of diffuse cerebral edema two days after being admitted to the hospital (CDC, 2001).
A 20-month-old boy died from severe lead toxicity after eating paint chips containing 0.2-33.1% lead, and exposure to lead in house dust at levels up to 31,128 mcg/ft(2) (CDC, 1991).

MAXIMUM TOLERATED EXPOSURE

ADULT

The maximum tolerated human exposure to this agent has not been delineated.
The normal upper limit for blood lead is considered to be approximately 0.40 mg/L (Baselt, 2000).
Adults are at increased risk of developing symptoms and signs with levels above 40 mcg/dL (OSHA) although effects at lower levels have been observed (Wang et al, 1985).
Lead in excess of 0.07 mg per 100 cc (70 mcg/dL) in whole blood frequently indicates severe lead poisoning. Lead excretion in urine generally exceeds 0.1 mg/L of urine (Lewis, 1996).
Workers with blood lead levels of 40 to 60 mcg/100 mL blood may have subtle neurologic effects (Hathaway et al, 1996).
Abdominal pain, anemia, basophilic stippling of red blood cells, elevated blood lead concentrations, and elevated urinary lead excretions during chelation were noted in some of the 8 patients ingesting liquid lead-based ceramic glazes (Vance et al, 1990).
Lead affects heme synthesis, as is evidenced by a decrease in delta- aminolevulinic acid dehydrase (ALA-D) activity in lead-exposed individuals. No threshold has been found for inhibition of ALA-D activity down to a blood lead concentration of 12 mcg/dl (ACGIH, 1996a).
A 59-year old woman complaining of joint pain, insomnia, and irritability was found to have a blood lead level of 0.90 mg/L (Baselt, 2000).
CASE REPORT: A man suffered the symptoms of severe lead poisoning as a result of drinking a homemade red wine. The patient used a highly corroded enamel bathtub to crush and store the wine. His PbB level was 98 mcg/dL two weeks after admission and prior to chelation therapy (Mangas et al, 2001).
Toxicity of lead salts vary by compound. Please refer to the data on chemical of interest for information specific to a compound.
CASE REPORT: A 41-year-old man developed lead poisoning symptoms after taking Ayurvedic medications (EX and ADISSA) from India to treat oligospermia. A blood lead level of 78 mcg/dL was obtained on admission; it was estimated that a total of 1.26 grams of lead was ingested during the course of his therapy (Shrestha & Greenberg, 2002).
CASE SERIES: Three patients with lead poisoning had varying degrees of exposure to a Chinese herbal pill (Bao ning dan). The authors reported that blood lead concentrations did not correlated with clinical severity. One patient had the highest blood lead level after taking the pills for only 3 days. Although the second patient took the pills for 2 months, she had the lowest blood lead concentration. She developed liver derangement and severe anemia. The third patient was asymptomatic; however, she had the longest exposure to the pills (Auyeung et al, 2002).
CASE REPORT: A 45-year-old male with a history of schizophrenia developed severe lead poisoning (BLL 391 mcg/dL) after ingesting 206 22-caliber lead bullets. He recovered following aggressive GI decontamination and chelation therapy (McNutt et al, 2000).

PEDIATRIC

Children with BLLs of 10 mcg/dL or greater are more likely to have learning and behavioral effects than children with levels of less than 10 mcg/dL ( CDC, 1997). In one study, authors reported that BLLs, even those below 10 mcg/dL, are inversely associated with children's IQ scores at 3 and 5 years of age. In addition, associated declines in IQ were greater at these levels than at higher levels (Canfield et al, 2003).
For lead paint on children's toys, the Consumer Product Safety standard is 600 ppm (Fuortes & Bauer, 2000).
CASE REPORT: A 17-year-old girl developed only nausea and abdominal pain after ingesting 20 g of lead nitrate (12.6 g or 6 mmol of lead). Her blood lead concentration was 20.4 mcmol/L (447 mcg/dL) 90 minutes after ingestion. Following chelation therapy with calcium disodium EDTA for 5 days, she recovered completely (Mikler et al, 2009).
CASE REPORT: A case of severe lead poisoning (blood lead level 173 mcg/L) in a middle-school-age child with a 5-year-long habit of pica, including ingesting paint and plaster from the walls has been reported. Although he was thought to be "asymptomatic", he had severe neurodevelopmental toxicity (a high level of motor activity, short attention span, poor scholastic performance, and poor impulse control/aggressive behavior). Radiographic films of the long bones showed lines of increased density (lead lines) in the metaphyseal plate of the distal femur and proximal tibia and fibula (Chin & Charlton, 2004).
CASE REPORT: A 4-month old child became comatose after developing a blood lead level of 1.37 mg/L but recovered with treatment (Baselt, 2000).
CASE REPORT: A 5-year-old Indian boy with static encephalopathy, seizures, and developmental delay from neonatal asphyxia developed persistent anemia (hemoglobin 9.2 g/dL) without basophilic stippling after taking Tibetan herbal vitamin tablets (3 times daily) for 4 years. His blood lead level was 86 mcg/dL (Moore & Adler, 2000).
CASE SERIES : Two children were asymptomatic after the ingestion of single lead foreign objects which resulted in markedly elevated blood lead levels (patient 1: venous lead level (VLL) of 89 mcg/dL at 48-hour post ingestion; patient 2: VLL of 48 mcg/dL at 36-hour post ingestion). These objects were removed by endoscopy (Holstege et al, 2001).
SURVEY- SECOND-HAND TOBACCO SMOKE AND BLOOD LEAD LEVELS: In a survey of over 5592 children, higher levels of serum creatinine were related to higher mean blood lead levels in 4 to 12 year old children.

The following table lists the lowest observed effect levels of lead (BLL) in children (Mushak et al, 1989).

BLL (mcg/dL)	NEUROLOGICAL EFFECTS	HEME SYNTHESIS EFFECTS	OTHER EFFECTS
10-15	Deficits in neurobehavioral development; electrophysiological changes	ALA-D inhibition	Reduced gestational age and weight at birth; reduced size up to age 7-8 years
15-20	.	EP elevation	Impaired vitamin D metabolism; pyrimidine-5'-nucleotidase inhibition
25	Lower IQ, slower reaction time	.	.
30	Slowed nerve conduction velocity	.	.
40	.	Reduced hemoglobin; elevated coproporphyrin and urinary ALA	.
70	Peripheral neuropathies	Frank anemia	.
80-100	Encephalopathy	.	Colic, other GI effects; renal effects

NEONATES

CASE REPORT: Severe congenital lead poisoning (cord blood lead 7.6 mcmol/L or 157.5 mcg/dL; BLL of 11.8 mcmol/L) has been reported in a preterm infant born to a woman using lead-contaminated herbal tablets (maternal BLL of 5.2 mcmol/L or 107.7 mcg/dL on admission; maternal BLL 2.3 mcmol/L 12 hours before birth). This neonatal BLL has been the highest recorded for a surviving infant. The infant recovered following chelation therapy (Tait et al, 2002).
CASE REPORT: A healthy-appearing neonate with a cord blood lead of 126 mcg/dL (Hct of 48) was born to a woman with chronic lead toxicity and a maternal BLL of 57.6 mcg/dL (Hct of 15). The authors suggested that a threefold difference in hematocrit between mother and child, presence of fetal hemoglobin, and mobilization of bone lead during parturition, may have contributed to differences among maternal, cord and fetal blood lead levels of healthy neonate (Mirkin et al, 2000b).
CASE REPORT: A neonate with congenital lead intoxication (BLL 17-37 mcg/dL; hemoglobin 12.2 g/dL; Hct 35.1%) was treated with IV calcium EDTA and oral DMSA. The authors recommended prenatal screening in mothers who are at high risk for elevated BLL, such as recent immigrants from areas with a high prevalence of lead exposure or those with other children with elevated BLL (Guzman et al, 2000).

Carcinogenicity Ratings for CAS7439-92-1 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Lead

A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A3 ; Listed as: Lead and inorganic compounds, as Pb

A3 :Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.

EPA (U.S. Environmental Protection Agency, 2011): B2 ; Listed as: Lead and compounds (inorganic)

B2 : Probable human carcinogen - based on sufficient evidence of carcinogenicity in animals.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 3 ; Listed as: Lead, organic compounds

3 : The agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans. This category is used most commonly for agents, mixtures and exposure circumstances for which the evidence of carcinogenicity is inadequate in humans and inadequate or limited in experimental animals. Exceptionally, agents (mixtures) for which the evidence of carcinogenicity is inadequate in humans but sufficient in experimental animals may be placed in this category when there is strong evidence that the mechanism of carcinogenicity in experimental animals does not operate in humans. Agents, mixtures and exposure circumstances that do not fall into any other group are also placed in this category.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2B ; Listed as: Lead

2B : The agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans. This category is used for agents, mixtures and exposure circumstances for which there is limited evidence of carcinogenicity in humans and less than sufficient evidence of carcinogenicity in experimental animals. It may also be used when there is inadequate evidence of carcinogenicity in humans but there is sufficient evidence of carcinogenicity in experimental animals. In some instances, an agent, mixture or exposure circumstance for which there is inadequate evidence of carcinogenicity in humans but limited evidence of carcinogenicity in experimental animals together with supporting evidence from other relevant data may be placed in this group.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2A ; Listed as: Lead compounds, inorganic

2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.

NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Lead and compounds (as Pb)
MAK (DFG, 2002): Category 3B ; Listed as: Lead and its inorganic compounds except lead arsenate

Category 3B : Substances for which in vitro or animal studies have yielded evidence of carcinogenic effects that is not sufficient for classification of the substance in one of the other categories. Further studies are required before a final decision can be made. A MAK value can be established provided no genotoxic effects have been detected. (Footnote: In the past, when a substance was classified as Category 3 it was given a MAK value provided that it had no detectable genotoxic effects. When all such substances have been examined for whether or not they may be classified in Category 4, this sentence may be omitted.)

NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): R ; Listed as: Lead and Lead Compounds

R : RAHC = Reasonably anticipated to be a human carcinogen

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS7439-92-1 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD:

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

LD50- (ORAL)GUINEA_PIG:
- 1330 mg/kg ((OHM/TADS, 2002))
LDLo- (INTRAPERITONEAL)GUINEA_PIG:
- 100 mg/kg ((OHM/TADS, 2002))
LDLo- (INTRAPERITONEAL)RAT:
- 1 g/kg (RTECS, 2004)
TCLo- (INHALATION)GUINEA_PIG:
- 20 mg/kg for 6H for 30D - intermittent -- effects on the immunologic system (RTECS, 2004)
- 200 mcg/kg for 6H for 26W - intermittent -- effects on the immunologic system (RTECS, 2004)
TCLo- (INHALATION)HUMAN:
- 10 mcg/m(3) -- gastritis, changes to the liver (RTECS, 2004)
TCLo- (INHALATION)RAT:
- female, 3 mg/m(3) for 24H at 1-21D of pregnancy -- biochemical and metabolic effects on the offspring (RTECS, 2004)
- female, 10 mg/m(3) for 24H at 1-21D of pregnancy -- fetotoxicity, developmental abnormalities of the blood and lymphatic system (including spleen and marrow) in the offspring (RTECS, 2004)
TD- (ORAL)PRIMATE:
- female breeding Rhesus monkeys, 5 or 10 mg/kg/day lead acetate in water for 13-27W (prior to conception to 5.5M postpartum) -- 19-year cohort study showed a strong association between early lead exposure and inguinal hernia and endometriosis later in life (Krugner-Higby et al, 2003)
TD- (ORAL)RAT:
- 50 mg/kg, and 200 mg/kg of lead acetate for 12W on alternate days - significant decrease in neurotransmitter activity (acetylcholinestrase, norepinephrine, dopamine, serotonin) (Sidhu & Nehru, 2003)
TDLo- (ORAL)HUMAN:
- 450 mg/kg for 6Y -- flaccid paralysis without anesthesia, hallucinations/ distorted perceptions, muscle weakness (RTECS, 2004)
TDLo- (ORAL)MOUSE:
- female, 6,300 mg/kg at 1-21D of pregnancy -- affected female fertility index, preimplantation mortality (RTECS, 2004)
- female, 300 mg/kg for 1-2D of pregnancy -- affected fertility (RTECS, 2004)
- female, multigenerations, 1,120 mg/kg -- fetotoxicity, fetal death (RTECS, 2004)
- female, 4,800 mg/kg at 1-16D of pregnancy -- cytological changes in the embryo or fetus (including somatic materials) (RTECS, 2004)
- 6,879 mg/kg for 5W - continuous -- pigmented or nucleated erythrocytes, other changes to the blood and cell counts (RTECS, 2004)
TDLo- (ORAL)RAT:
- 1,050 mcg/kg for 30W - intermittent -- degenerative changes of the brain and coverings, alteration of classical conditioning, changes to metabolic system (RTECS, 2004)
- female, multigenerations, 790 mg/kg -- fetotoxicity, fetal death (RTECS, 2004)
- female, 1,110 mg/kg for 1-22D of pregnancy -- developmental abnormalities of the blood and lymphatic system (including spleen and marrow) in the offspring, effect on growth statistics (RTECS, 2004)
- female, 520 mg/kg for 7-22D of pregnancy and 10D after birth -- biochemical and metabolic effects on the offspring (RTECS, 2004)
- female, 1,140 mg/kg at 14D prior to mating and 21D after birth -- behavorial effects on offspring (RTECS, 2004)

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS7439-92-1 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

Lead

TLV:

TLV-TWA: 0.05 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A3
Codes: BEI
Definitions:

A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): CNS and PNS impair; hematologic eff
Molecular Weight: 207.20

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Lead and inorganic compounds, as Pb

TLV:

TLV-TWA: 0.05 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A3
Codes: BEI
Definitions:

A3: Confirmed Animal Carcinogen with Unknown Relevance to Humans: The agent is carcinogenic in experimental animals at a relatively high dose, by route(s) of administration, at site(s), of histologic type(s), or by mechanism(s) that may not be relevant to worker exposure. Available epidemiologic studies do not confirm an increased risk of cancer in exposed humans. Available evidence does not suggest that the agent is likely to cause cancer in humans except under uncommon or unlikely routes or levels of exposure.
BEI: The BEI notation is listed when a BEI is also recommended for the substance listed. Biological monitoring should be instituted for such substances to evaluate the total exposure from all sources, including dermal, ingestion, or non-occupational.

TLV Basis - Critical Effect(s): CNS and PNS impair; hematologic eff
Molecular Weight: Varies

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS7439-92-1 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS7439-92-1 (National Institute for Occupational Safety and Health, 2007):

Listed as: Lead and compounds (as Pb)
REL:

TWA: 0.050 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: Not Listed
Note(s): See Appendix C; [*Note: The REL and PEL also applies to other lead compounds (as Pb) -- see Appendix C.]

IDLH:

IDLH: 100 mg Pb/m3 (as Pb)
Note(s): Not Listed

OSHA PEL Values for CAS7439-92-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Lead, inorganic (as Pb); see 29 CFR 1910.1025
Table Z-1 for Lead, inorganic (as Pb); see 29 CFR 1910.1025:

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3:

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7439-92-1 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7439-92-1 (U.S. Environmental Protection Agency, 2010):

Listed as: Lead (D008)
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity
Listed as: Lead
Final Reportable Quantity, in pounds (kilograms):

10 (4.54)

Additional Information:
Listed as: Lead and compounds

Additional Information:
Listed as: Lead compounds

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7439-92-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS7439-92-1 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS7439-92-1 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS7439-92-1 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Lead Compounds
Effective Date for Reporting Under 40 CFR 372.30:
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28: 100

See 40 CFR 372.28: Lower thresholds for chemicals of special concern

Listed as: Lead Compounds: Includes any unique chemical substance that contains lead as part of that chemical's infrastructure
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as: Lead (this lower threshold does not apply to lead when contained in a stainless steel, brass or bronze alloy)
Effective Date for Reporting Under 40 CFR 372.30:
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28: 100

See 40 CFR 372.28: Lower thresholds for chemicals of special concern

Listed as: Lead
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS7439-92-1 (49 CFR 172.101 - App. B, 2005):

Listed as Lead compounds, soluble, n.o.s.
Severe Marine Pollutant: No

EPA TSCA Inventory for CAS7439-92-1 (EPA, 2005):

Listed as: Lead

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS7439-92-1 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

29 CFR section 1910.1025 contains the OSHA Lead standard applicable to work areas where there may be a potential for lead exposure. Please refer to this section for detailed requirements regarding protective equipment, housekeeping, monitoring, and other requirements for lead use in industry.

HANDLING

When handling lead, take all precautions to avoid exposure such as wearing appropriate protective clothing and equipment. The atmospheric concentration of lead in the workplace, including lead dust, should be strictly controlled (ITI, 1995).

Wear personal protective clothing and equipment to prevent skin and eye contact or respiratory exposure (NIOSH , 2002; Sittig, 1991). Contact lenses should not be worn when working with lead (NIOSH , 2002).

Clothing that becomes significantly contaminated should be removed and replaced (NIOSH , 2002).

If lead contacts the skin, promptly wash affected areas with soap and water. If it contacts the eyes, immediately flush them with excess water, occasionally lifting the lower and upper lids (NIOSH , 2002).

Persons should wash any exposed areas at the end of the work shift (NIOSH , 2002; Sittig, 1991). Employees should leave contaminated clothing or equipment in the workplace at the end of each shift and should wash after each shift to prevent lead from being introduced into the employees' homes (ATSDR , 1997; HSDB , 2002; NIOSH , 2002).

When possible, use wet or other methods of handling to minimize suspension of airborne dusts. Sweeping or vacuuming should not be used as a clean up method, as this will resuspend settled dusts. Wet mopping, wet wiping and wet vacuuming or high efficiency particulate air (HEPA) filtered vacuuming is recommended (HSDB , 2002; ITI, 1995).

Rubber gloves containing lead may ignite on contact with nitric acid (HSDB , 2002; Lewis, 2000; Urben, 1999).

Smoking or eating should not be permitted in work areas (ITI, 1995).

STORAGE

ROOM/CABINET RECOMMENDATIONS

Lead should be stored under refrigerated conditions (NTP, 2001).
Local exhaust ventilation should be employed in areas where point source emissions exist (HSDB , 2002).
Separate storage areas should be provided for personal protective clothing and equipment used in lead-contaminated facilities to ensure that there is no direct contact by persons who handle, dispose of, or decontaminate the clothing (HSDB , 2002).

INCOMPATIBILITIES

Store lead away from oxidizing materials (e.g., perchlorates, peroxides, permanganates, chlorates, and nitrates), as violent reactions may occur on contact (Lewis, 2000) NTP, 2001; (OHM/TADS , 2002; Sittig, 1991).
Fire or explosions may result from the reactions of lead with the following elements and compounds (HSDB , 2002; IPCS , 1994; Lewis, 2000) NTP, 2001; (Pohanish & Greene, 1997; Urben, 1999; Sittig, 1991):
- ammonium nitrate
- chlorine trifluoride
- hydrogen peroxide
- potassium
- sodium
- trioxane + hydrogen peroxide
Lead is incompatible with (Budavari, 2000; HSDB , 2002; Lewis, 2000; NFPA, 2002a; NIOSH , 2002) NTP, 2001; (Urben, 1999):
- acids
- boiling, concentrated hydrochloric acid
- boiling, concentrated sulfuric acid
- disodium acetylide
- hot, concentrated nitric acid
- hydrogen peroxide
- sodium acetylide
- sodium azide
- sodium carbide
- strong oxidizers
- zirconium
Sodium azide and lead react to form lead azide, an explosive compound (NFPA, 2002a).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

For workplace personal protective equipment requirements and more specific information on respiratory protection and other protective measures relating to lead, refer to the OSHA Lead standard found at 29 CFR section 1910.1025.

Wear personal protective clothing and equipment to prevent skin and eye contact or respiratory exposure (NIOSH , 2002; Sittig, 1991).

Clothing that becomes significantly contaminated should be removed and replaced (NIOSH , 2002).

If lead contacts the skin, any affected areas should be washed with soap and water (NIOSH , 2002).

Persons should wash any exposed areas at the end of the work shift (NIOSH , 2002; Sittig, 1991).

Employees should leave contaminated clothing or equipment in the workplace at the end of each shift and should wash after each shift to prevent lead from being introduced into the employees' homes (ATSDR , 1997; HSDB , 2002; NIOSH , 2002).

EYE/FACE PROTECTION

Use adequate eye protection to prevent contact of lead with the eyes (NIOSH , 2002; Sittig, 1991).

Contact lenses should not be worn when working with lead (NIOSH , 2002).

If lead contacts the eyes, immediately flush them with excess water, occasionally lifting the lower and upper lids (NIOSH , 2002).

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

When working with or around lead powder, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge with a dust filter (NTP, 2001).

Wear a mechanical filter respirator when handling lead (ITI, 1995).

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7439-92-1.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

ENGINEERING CONTROLS

When possible, use wet or other methods of handling to minimize suspension of airborne dusts. Sweeping or vacuuming should not be used, as this will resuspend settled dusts (HSDB , 2002; ITI, 1995).

Local exhaust ventilation should be employed in areas where point source emissions exist (HSDB , 2002).

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.
- Containers may explode when heated.
- Runoff may pollute waterways.
Solid lead will not burn. However, it is moderately flammable when exposed to heat or flame when in the form of dust (Lewis, 2000; OHM/TADS , 2002; Sittig, 1991).
When heated to decomposition, lead emits highly toxic fumes (OHM/TADS , 2002).
This substance may react violently on contact with oxidizing materials (Lewis, 2000).
On contact with hydrogen peroxide or active metals (e.g., sodium, potassium), lead may cause fire or explosions (IPCS , 1994).
Reactions of lead and chlorine trifluoride at ambient or slightly elevated temperatures can be violent, often resulting in ignition (HSDB , 2002; Urben, 1999).
Lead reacts violently or explosively with fused ammonium nitrate below 200 degrees C (HSDB , 2002; Urben, 1999).
Finely divided lead, produced through the reaction of lead oxide with furfural vapor at 290 degrees C, is pyrophoric and chemically reactive (HSDB , 2002; Urben, 1999).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS7439-92-1 (NFPA, 2002):

Not Listed

INITIATING OR CONTRIBUTING PROPERTIES

Rubber gloves containing lead may ignite on contact with nitric acid (HSDB , 2002; Lewis, 2000; Urben, 1999).

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Water spray, fog or regular foam.
Move containers from fire area if you can do it without risk.
Dike fire control water for later disposal; do not scatter the material.
Use water spray or fog; do not use straight streams.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers.
Cool containers with flooding quantities of water until well after fire is out.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.
For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

NFPA Extinguishing Methods for CAS7439-92-1 (NFPA, 2002):

Not Listed

If lead is involved in a fire, use an extinguishing agent appropriate for the surrounding fire (Sittig, 1991).

Dry chemical, carbon dioxide, foam, or Halon extinguishing agents may be used (NTP, 2001; (Sittig, 1991).

Do not use water to extinguish fires involving lead (Sittig, 1991).

COMBUSTION TOXICITY

When heated to decomposition, solid lead will emit highly toxic lead fumes (ILO, 1998; IPCS , 1994; Lewis, 2000; OHM/TADS , 2002).

EXPLOSION HAZARD

Lead dust is moderately explosive if exposed to heat or an ignition source (Lewis, 2000; OHM/TADS , 2002).

Sodium azide and lead react to form lead azide, an explosive compound (NFPA, 2002a).

Copper azide and lead azide, both explosive compounds, were formed when a solution of sodium azide was stored in copper piping with lead joints (HSDB , 2002).

Trioxane and hydrogen peroxide mixtures explode on contact with lead; this may be due to the heat of the oxidation of lead (Lewis, 2000; Urben, 1999).

Powdered lead can react explosively with fused ammonium nitrate (Urben, 1999).

On contact with hydrogen peroxide or active metals (e.g., sodium, potassium), lead may cause fire or explosions (IPCS , 1994).

Lead reacts violently or explosively with fused ammonium nitrate below 200 degrees C (HSDB , 2002; Urben, 1999).

DUST/VAPOR HAZARD

Lead dust is toxic through inhalation, and acts as a cumulative poison, affecting the central nervous system, blood, reproductive system, and kidneys, among other systems. When inhaled, it is easily absorbed from the respiratory tract. Symptoms of exposure to lead dust include: loss of appetite, anemia, malaise, anemia, hypertension, insomnia, headache, irritability, arthralgia, muscle and joint pain and weakness, tremors, flaccid paralysis without anesthesia, hallucinations, distorted perceptions, gastritis, and changes to the liver (ATSDR, 1999; (Bingham et al, 2001; Lewis, 2000; Lewis, 2001).

Lead dust is moderately flammable or explosive if exposed to heat or an ignition source (Lewis, 2000; OHM/TADS , 2002).

Vapors form at 550-600 degrees C and combine with oxygen to form lead oxide (IPCS , 1994).

When heated to decomposition, solid lead will emit highly toxic lead fumes (IPCS , 1994; Lewis, 2000; OHM/TADS , 2002). Severe poisoning can result from lead fumes produced from lead furnaces (HSDB , 2002).

REACTIVITY HAZARD

Lead may react vigorously or violently on contact with oxidizing materials (Lewis, 2000; OHM/TADS , 2002).

On contact with hydrogen peroxide or active metals (e.g., sodium, potassium, magnesium, zinc), lead may cause fire or explosions (IPCS , 1994; Lewis, 2000; Sittig, 1991).

Reactions of lead and chlorine trifluoride at ambient or slightly elevated temperatures can be violent, often resulting in ignition (HSDB , 2002; Lewis, 2000) NTP, 2001; (Urben, 1999).

Lead reacts violently or explosively with fused ammonium nitrate below 200 degrees C (HSDB , 2002; Lewis, 2000) NTP, 2001; (Pohanish & Greene, 1997; Urben, 1999).

Finely divided lead, produced through the reaction of lead oxide with furfural vapor at 290 degrees C, is pyrophoric and chemically reactive (HSDB , 2002; Urben, 1999).

Sodium azide and lead react to form lead azide, an explosive compound (NFPA, 1997).

Copper azide and lead azide, both explosive compounds, were formed when a solution of sodium azide was stored in copper piping with lead joints (HSDB , 2002).

Trioxane and hydrogen peroxide mixtures explode on contact with lead; this may be due to the heat of the oxidation of lead (Lewis, 2000; Urben, 1999).

Rubber gloves containing lead may ignite on contact with nitric acid (HSDB , 2002; Lewis, 2000; Urben, 1999).

Powdered lead is incompatable with sodium acetylide (Lewis, 2000; Urben, 1999).

Mixtures of ground lead and sodium carbide can react vigorously (HSDB , 2002; NFPA, 2002a).

Lead is incompatible with sodium azide, disodium acetylide, and zirconium (HSDB , 2002; Lewis, 2000) NTP, 2001).

NFPA (2002) reports that alloys of lead and 10-70% zirconium will ignite when struck with a hammer.

Lead reacts with hot, concentrated nitric acid, and boiling, concentrated hydrochloric and sulfuric acids (Budavari, 2000) NTP, 2001).

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.
Keep unauthorized personnel away.
Stay upwind.
Keep out of low areas.

Evacuate all workers from area of lead spill (Sittig, 1991).

AIHA ERPG Values for CAS7439-92-1 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS7439-92-1 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Lead
TEEL-0 (units = mg/m3): 0.05
TEEL-1 (units = mg/m3): 0.15
TEEL-2 (units = mg/m3): 0.25
TEEL-3 (units = mg/m3): 100
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS7439-92-1 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS7439-92-1 (National Institute for Occupational Safety and Health, 2007):

IDLH: 100 mg Pb/m3 (as Pb)
Note(s): Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Do not touch damaged containers or spilled material unless wearing appropriate protective clothing.
- Stop leak if you can do it without risk.
- Prevent entry into waterways, sewers, basements or confined areas.
- Cover with plastic sheet to prevent spreading.
- Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers.
- DO NOT GET WATER INSIDE CONTAINERS.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
In case of a spill, personnel without proper protective equipment should be kept away from the spill area (Sittig, 1991).
When possible, use wet or other methods of handling to minimize suspension of airborne dusts. Sweeping or vacuuming should not be used as a clean up method, as this will resuspend settled dusts. Wet mopping, wet wiping and wet vacuuming or high efficiency particulate air (HEPA) filtered vacuuming is recommended (HSDB , 2002; ITI, 1995).
Spilled solutions containing lead should be contained and then covered with an appropriate sorbent and then placed in a suitable container for later disposal or reclamation (Sittig, 1991; OHM/TADS , 2002).

SMALL LEAK/SPILL

Add lime to precipitate basic lead carbonate. A complexing agent (i.e., ethylenediamine tetraacetic acid) can be added then absorbed on carbon (OHM/TADS , 2002).

LARGE LEAK/SPILL

Add lime to precipitate basic lead carbonate. A complexing agent (i.e., ethylenediamine tetraacetic acid) can be added then absorbed on carbon (OHM/TADS , 2002).

WASTE TREATMENT OPTIONS

RECYCLING/RECLAMATION

Lead should be reclaimed, recycled, or salvaged for reuse whenever possible (ITI, 1995; OHM/TADS , 2002) Sittig; 1991).
An estimated 90-95% of the lead consumed in the United States is recyclable (ATSDR, 1999).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

CHEMICAL TREATMENT

Lead may be treated with nitric acid to form lead nitrate, then precipitated as lead sulfide. The sulfide can be sent to a recovery plant to reclamation (Sittig, 1991).
In wastewaters containing lead, allow the lead to settle in a holding tank and recover the solids; treat the inorganic fraction with ferric sulfate and ferrous sulfate (HSDB , 2002).
Precipitation is a recommended method for removing heavy metals, including lead, from wastewaters. This process includes treatment with hydroxide, lime, and/or sulfide (HSDB , 2002).
Reverse osmosis treatment has been investigated for removal of lead from wastewaters (HSDB , 2002).
The use of activated carbon and other sorbents has been investigated for removal of lead from wastewaters (HSDB , 2002).
Consult the latest U.S. Environmental Protection Agency's rules and regulations, relative to the Residential Lead-Based Paint Hazard Reduction Act (Title X) and related authorities, for guidance on lead-based paint clean-up and disposal.

BIOREMEDIATION

Biological concentration treatment has been investigated for removal of lead from wastewaters (HSDB , 2002).
The aerobic bacteria, Pseudomonas pseudoalcaligenes, showed a high biosorption potential for lead suggesting a possible application in the removal and recovery of lead from industrial effluents. At pH 5.0 with an initial lead concentration of 100 mg/L, p. pseudoalcaligenes was able to reach a biosorption capacity of 271.1 mg lead (Leung et al, 2001).
The CHL004 strain of p. aeruginosa is able to remove lead from solidified media and soil (ATSDR, 1999).

PHYSICAL TREATMENT

Incineration of materials contaminated with lead in special, high-temperature incineration facilities is recommended (NTP, 2001).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

ENVIRONMENTAL EXPOSURE

Metallic lead is a naturally-occurring element that enters the environment from weathering of soils, rocks, and sediments containing lead-bearing minerals such as galena (lead sulfide), cerrusite (lead carbonate) and anglesite (lead sulfate). Lead's estimated natural concentration in the earth's crust is 16 ppm. Natural sources for atmospheric lead include volcanic dusts, silicated dusts, sea salt aerosols, forest fires and radioactive decay of uranium and thorium minerals. Once released, lead cycles between air, water, sediment and soil through various natural processes. Soil and sediment act as sinks for immobile lead compounds and complexes (HSDB, 2005; (ATSDR, 1999)).
Human activities release far more lead into the environment through atmospheric emissions than natural sources. Lead can enter the environment at any point during such industrial processes as mining, smelting and refining of metallic lead; manufacturing and disposal of lead or lead-containing products (e.g., fuels containing antiknock lead compounds); smelting furnaces in the steel and grey iron industries, battery manufacture and reclamation; fossil fuel combustion (e.g., coal-fired power plants); and cement and ceramic production. Emissions from gasoline-powered vehicles were once considered the largest source of atmospheric lead, though lead emissions have decreased steadily since EPA phased out use of leaded gas in the early 1970s (HSDB, 2005; (ATSDR, 1999); IPCS , 1994).
The predominant source of atmospheric lead is emissions from human activities and industrial sources, including smelters, automobile exhausts, and industrial dusts and fumes. The atmospheric contribution of lead from natural geologic sources is minimal(HSDB, 2005; (ATSDR, 1999)).

OCCUPATIONAL EXPOSURE

Workers may be exposed to lead via dust or fume inhalation and dermal contact during its production, handling, and use. Potential worker exposure to toxic lead levels is of special concern for industries that perform lead smelting and refining; automobile refinishing; foundries and storage battery manufacturing; welding and steel cutting; glass blowing; lead crystal, cement, paint, and ceramic production; and printing and typesetting (HSDB, 2005; (ATSDR, 1999)).
Exposure to high lead levels in dust and fumes at indoor firing ranges is a potential health concern for law enforcement officers (HSDB, 2005)

GENERAL POPULATION EXPOSURE

The major exposure pathways for the general population are inhalation of atmospheric lead and ingestion of lead from food, water, and soil. Ingestion of lead-contaminated food and water pose the largest exposure source. Food may become contaminated through growth in a contaminated environment, or bioconcentration through the food chain, or through storage in or contact with lead-soldered cans, certain ceramic-glazed pottery, and lead crystal. Drinking water may become contaminated from corrosion of lead pipes. Inhalation of dust and ingestion of lead in paint chips are exposure pathways of special concern for children. Dermal absorption of lead is also considered a potentially important exposure pathway (HSDB, 2005; (ATSDR, 1999)).

ENVIRONMENTAL FATE AND KINETICS

In the atmosphere, lead largely exists as dusts or particles of lead oxide, lead carbonate, and organic alkyl lead compounds. Particle size determines transport distance for airborne lead particulate, with small particles sometimes transported thousands of kilometers. Larger particles (those with diameters >2 micrometers) settle closer to the emission source (HSDB, 2005; (ATSDR, 1999); IPCS , 1994).
Lead and its compounds are removed from the atmosphere primarily by wet deposition with precipitation, accounting for as much as 40-70% of lead deposition. Dry deposition is also an important removal mechanism ((ATSDR, 1999)).
((ATSDR, 1999)).
- Photolysis and photochemical reactions with hydroxyl radicals or ozone can degrade organic lead compounds in the atmosphere (HSDB, 2005; (ATSDR, 1999); IPCS , 1994).

WATER

SURFACE WATER
- Atmospheric fallout along with runoff and wastewater are the major sources for lead's entry to surface water. Small amounts of lead are released to surface water through leaching from natural ores and soil. Lead exists in surface water in either a particulate form or dissolved form. Sorption is considered the principal fate process whereby lead is removed from water and accumulates in sediment. Organic matter content in water is among the most important factors controlling sediment adsorption. Other factors include ligand availability, pH, redox conditions, salinity, iron concentration, and the nature of dissolved particulate matter in the water column and sediment (HSDB, 2005; (ATSDR, 1999)).
- The quantities of dissolved lead forms that remain in solution depend on the water's dissolved salt content and pH; e.g., about 30 mcg/L in hard water (pH>5.4) and about 500 mcg/L in soft water (pH<5.4). Dissolved lead ions typically form ligands and low-solubility complexes with major anions in water (e.g., sulfide, hydroxide, carbonate, phosphate). These ligands and complexes then precipitate and accumulate in sediment. Organolead complexes chiefly form in the presence of humic material, which can retain bound lead even at relatively low pH. Lead can also accumulate in sediment by forming insoluble precipitates with hydrous oxides of iron, aluminum, and manganese; or by absorption to clay minerals and organic matter (HSDB, 2005; (ATSDR, 1999)).
- Estuarine studies show lead can cycle between its dissolved and particulate phases as well as pass between the aqueous and sediment environment compartments (HSDB, 2005).
- Some organic lead compounds can volatilize from water, although this process is considered negligible due to lead's low vapor pressure and insolubility. Some organic lead compounds may undergo photolysis and some naturally-occurring compounds (methyl iodide, glycine betaine) can oxidatively methylate lead [Pb(0) and Pb(+2)] (HSDB, 2005; (ATSDR, 1999)).
GROUND WATER
- Lead typically does not leach to groundwater unless conditions are acidic. Rapid leaching of soil lead has reportedly occurred at some highly contaminated sites and landfills (HSDB, 2005; OHM/TADS, 2005; (ATSDR, 1999)).

SOIL

TERRESTRIAL
- Most lead enters surface soil by atmospheric deposition and accumulates at a rate proportional to the atmospheric deposition rate. Lead can enter agricultural soils as an impurity in some fertilizers and insecticides (HSDB, 2005; (ATSDR, 1999)).
- Lead can persist in soil for a long period of time by forming low-solubility compounds with salt ions (e.g., sulfate, oxide, sulfide, and phosphates); or by adsorbing to organic matter, clay, and minerals; or by forming fairly stable complexes with organic and inorganic materials. Soil pH, organic matter content, soil type, cation exchange capacity, and metal concentrations all influence lead's mobility in soil. Lead compounds and complexes become more soluble (mobile) in acidic soil solutions or in the presence of reduced organic matter (HSDB, 2005; OHM/TADS, 2005).
- Studies at an outdoor shooting range in Michigan found lead concentrations in the subsurface vadose zone proportional to those in the surface soil horizon. Mobilization was attributed to the transformation of metallic lead to soluble PbCO3 and PbSO4 (HSDB, 2005).
- Lead may be taken up by some plants, then return to the soil as the plants decay. Lead mainly remains in the upper 2-5 cm, if soil pH is 5 or higher and organic matter content is at least 5% ((ATSDR, 1999)).

ABIOTIC DEGRADATION

The principal transport processes for lead in the environment include precipitation from the atmosphere to soil and water, uptake by plants and animals, and final reentry to the atmosphere (HSDB, 2005; (ATSDR, 1999)).

In the ambient atmosphere, lead usually exists in particulate form, as an oxide, carbonate, sulfate, or organic lead compound. Lead can travel long distances in the atmosphere depending on particle size. Wet and dry deposition, washout, and gravitational settling are important processes for removing particulate lead from the atmosphere. Organic lead compounds may undergo photodegradation in the atmosphere and photolysis and hydrolysis in surface water (HSDB, 2005; (ATSDR, 1999); IPCS , 1994).

The major sources of lead's entry to surface water are atmospheric fallout and surface runoff. In surface water, lead exists in either dissolved or particulate form. Dissolved lead commonly forms insoluble compounds in water by combining with carbonate or sulfate ions, which then absorb to ferric hydroxide, precipitate out, and accumulate in sediments. Sorption is considered the principal fate process whereby lead is removed from water to enter sediment (HSDB, 2005; (ATSDR, 1999)).

BIODEGRADATION

Benthic microorganisms can biomethylate lead, causing it to remobilize from sediment and reenter the aqueous environment (HSDB, 2005).

The aerobic bacterium, Pseudomonas pseudoalcaligenes, has shown a high biosorption potential for lead suggesting a possible application in lead removal and recovery from industrial effluents. At pH 5.0 and an initial lead concentration of 100 mg/L, P. pseudoalcaligenes reached a biosorption capacity of 271.1 mg lead (Leung et al, 2001).

The CHL004 strain of P. aeruginosa can remove lead from solidified media and soil ((ATSDR, 1999)).

BIOACCUMULATION

HUMANS

Lead had a reported half-life in the human body (whole) of 1460 days (OHM/TADS, 2005).

FISH

Lead tissue residues were sampled in various marine organisms (teleost and elasmobranch fish species, bivalve and cephalopod mollusc species, crustaceans) from the Adriatic and Ionian seas. Results included the following(Marcotrigiano & Storelli, 2003):
- Fish muscle: ND (non-detect) to 0.40 (average 0.08) mcg/g (wet wgt)
- Fish liver: 0.03-1.73 (average 0.47) mcg/g (wet wgt)
- Cephalopod flesh: 0.09-1.82 (average 0.61) mcg/g (wet wgt)
- Cephalopod digestive gland: 0.06-2.66 (average 0.88) mcg/g wet weight
- Bivalve flesh: ND-1.70 (average 0.65) mcg/g (wet wgt)
- Crustacean flesh: ND-0.07 (average 0.02) mcg/g (wet wgt)
Lead tissue residues were sampled in various marine organisms (teleost and elasmobranch fish species, bivalve and cephalopod mollusc species, crustaceans) from the Adriatic and Ionian seas. Results included the following(Marcotrigiano & Storelli, 2003): Fish muscle: ND (non-detect) to 0.40 (average 0.08) mcg/g (wet wgt) Fish liver: 0.03-1.73 (average 0.47) mcg/g (wet wgt) Cephalopod flesh: 0.09-1.82 (average 0.61) mcg/g (wet wgt) Cephalopod digestive gland: 0.06-2.66 (average 0.88) mcg/g wet weight Bivalve flesh: ND-1.70 (average 0.65) mcg/g (wet wgt) Crustacean flesh: ND-0.07 (average 0.02) mcg/g (wet wgt)
- Fish muscle: ND (non-detect) to 0.40 (average 0.08) mcg/g (wet wgt)
- Fish liver: 0.03-1.73 (average 0.47) mcg/g (wet wgt)
- Cephalopod flesh: 0.09-1.82 (average 0.61) mcg/g (wet wgt)
- Cephalopod digestive gland: 0.06-2.66 (average 0.88) mcg/g wet weight
- Bivalve flesh: ND-1.70 (average 0.65) mcg/g (wet wgt)
- Crustacean flesh: ND-0.07 (average 0.02) mcg/g (wet wgt)
- Lead levels were either low or not detected in most fish samples.
- Lead concentrations in fish livers all exceeded fish muscle lead levels.
- Flesh from three of four bivalve species had detectable lead levels.
- Lead levels in crustacean flesh were relatively low.

PLANTS

AQUATIC
- Plants may take up lead directly from contaminated soils, sediment and air, as well as from surface deposition of particulate matter. Reported lead concentrations for a variety of edible plants were 0.0033 to 0.045 mcg/g (wet wgt) ((ATSDR, 1999)).
TERRESTRIAL
- Some plants can take up and accumulate available lead from soil nutrient solutions and soil itself to a lesser degree (HSDB, 2005).

MAMMALS

Lead accumulates in mammalian bones (OHM/TADS, 2005).
A 1-year study conducted in a West Slovakian lowland reported significantly higher median lead concentrations in liver and kidneys from brown hares (Lepus europaeus) collected in winter versus spring and summer. Differences were attributed to higher lead levels in older plants contaminated by aerogenous emissions. Other results included the following(Massanyi et al, 2003):
- Median lead concentrations in male livers (0.216 mg/kg-wet wt) were significantly higher than female liver concentrations (0.127 mg/kg-wet wt).
- Adult liver and kidney lead concentrations were not significantly different from juvenile levels.
- Lead, mercury, and cadmium levels in kidneys were significantly correlated.

OTHER

INVERTEBRATES
- A lead residues field study in Louisiana reported a bioaccumulation factor (BAF) for red swamp crayfish (Procambarus clarkii) of 1.7 and a BAF for alligator weed (Alternanthera philoxiroides) of 14.8. Study results showed no biomagnification of lead from alligator weed to crayfish (Naqvi et al, 1993).

BIOCONCENTRATION FACTOR

Lead bioconcentrates and bioaccumulates in both aquatic and terrestrial organisms. Some aerobic bacteria show a high biosorption potential for lead. Higher trophic-level organisms can be poisoned from eating lead-contaminated prey (Leung et al, 2001; (ATSDR, 1999)).
Lead can bioconcentrate in aquatic and terrestrial plants and animals; biomagnification, however, is not expected to occur. Lower level aquatic organisms (e.g., algae) tend to have greater lead concentrations than organisms higher on the food chain (e.g., carnivorous fish). High trophic-level organisms may experience lead poisoning from eating lead-contaminated food or prey (HSDB, 2005; (ATSDR, 1999)).
Some reported bioconcentration factors (BCFs) are relatively high: e.g., freshwater algae (92,000 in Senenastrum capricornutum), oysters (6,600 in Crassostrea virginica), and rainbow trout (726 in Salmo gairdneri). Median bioconcentration factors are usually lower; e.g., fish (42); oysters (536); insects (500); algae (725); and mussels (2,750)((ATSDR, 1999)).
Reported BCFs for four freshwater invertebrate species range from 499-1,700. By comparison, BCFs of 42 and 45 for brook trout and bluegill, respectively, indicate fish tend to bioaccumulate less lead than invertebrates (HSDB, 2005).
Lead bioaccumulation in some saltwater organisms may pose a potential human health concern. Reported BCFs for edible marine species include mussels (2,570), oysters (1,400), and hard clams (17.5) (HSDB, 2005).

ENVIRONMENTAL TOXICITY

ECOTOXICITY STUDIES

The LC50 (oral) for lead (metal 100%) was >5000 ppm for 14-day-old male and female Japanese quail (Coturnix japonica) in a 5-day ad libitum dietary study. While no mortality occurred, toxic symptoms began at 7 days at dietary levels of 1000, 2236, and 5000 ppm; symptom remission occurred at 11, 11, and 12 days, respectively (HSDB, 2005).
A field study performed near a large non-ferrous smelter in Belgium attributed adverse effects on condition and health in Great tit (Parus major) nestlings to heavy metal exposure. Sampling occurred along a pollution gradient (0-4000 m) over three consecutive breeding seasons. Nestlings' excrement from nest sites closest to the smelter had significantly higher concentrations of lead and other heavy metals. Other results included the following (Janssens et al, 2003):

Mean lead fecal levels (28.8 mcg/g-dry wt) were nearly 30 times higher at the closest nest vs. the most distant nest (1.1 mcg/g-dry wt).
Nestling body mass and condition showed significant reduction at the most contaminated nest site.
Nestlings' legs showed deformities in three nests near the smelter.

Lead is potentially toxic to all aquatic organisms, with organic lead compounds tending to be more toxic than inorganic lead compounds. Lead becomes more toxic to fish as dissolved oxygen levels decrease. Toxicity to aquatic organisms increases in acidic or soft water (HSDB, 2005; OHM/TADS, 2005; (ATSDR, 1999)).

ECOTOXICITY VALUES

INVERTEBRATES

LC50 - STONEFLY (Acroneuria): 64 ppm as Pb for 336H -- static sulfate, freshwater (OHM/TADS, 2005)
LC50 - MAYFLY (Ephemerella): 16 ppm as Pb for 168H -- static sulfate, freshwater (OHM/TADS, 2005)
LC50 - CADDISFLY (Hydrospyche): 32 ppm as Pb for 168H -- static sulfate, freshwater (OHM/TADS, 2005)
TLm - TUBIFICID WORMS: 49 ppm for 24H -- pH 6.5, freshwater (OHM/TADS, 2005)

CRUSTACEANS and MOLLUSCS

LC50 - COCKLE: >500 ppm as Pb for 48H -- static nitrate, saltwater (OHM/TADS, 2005)
LC50 - PRAWN: 375 ppm for 48H -- aerated, saltwater (OHM/TADS, 2005)
LC50 - PINK SHRIMP: 375 ppm as Pb for 48H -- static nitrate, saltwater (OHM/TADS, 2005)
LC50 - COCKLE: 7500 ppm for 48H -- aerated, saltwater (OHM/TADS, 2005)
TLm - EASTERN OYSTER: 0.5 ppm for 2016H, saltwater (OHM/TADS, 2005)

BACTERIA and PROTOZOA

LC50 - PROTOZOA (Tetrahymena pyriformis): 42 ppm as Pb for 96H -- static soft, freshwater (OHM/TADS, 2005)
TOXIC - AEROBIC BACTERIA: 1 ppm -- freshwater (OHM/TADS, 2005)
TOXIC - FLAGELLATES INFUSION: 0.5 ppm -- freshwater (OHM/TADS, 2005)

FISH

LC50 - RAINBOW TROUT, juvenile: 0.14 ppm as Pb for 96H -- flow-through, nitrate, freshwater (OHM/TADS, 2005)
NOEC - RAINBOW TROUT, juvenile: 0.012 ppm as Pb for >1Y -- soft, flow-through, nitrate, freshwater (OHM/TADS, 2005)
NOEC - RAINBOW TROUT, juvenile: 0.018 ppm as Pb for >1Y -- hard, flow-through, nitrate, freshwater (OHM/TADS, 2005)
TLm - SALMON: 0.41 ppm for 24H -- 1000-3000 ppm dis. solids, freshwater (OHM/TADS, 2005)
TLm - STICKLEBACK: 0.53 ppm for 24H -- 1000-3000 ppm dis. solids, freshwater (OHM/TADS, 2005)
TLm - SUNFISH: 1.4 ppm for 48H -- tap water, freshwater (OHM/TADS, 2005)
TLm - SUNFISH: 2.0 ppm for 24H -- tap water, freshwater (OHM/TADS, 2005)
TLm -MINNOW: 2.4 ppm for 96H -- soft freshwater (OHM/TADS, 2005)
TOXIC or LETHAL - MINNOW: 0.4 ppm for 26H -- distilled freshwater (OHM/TADS, 2005)
TOXIC or LETHAL - STICKLEBACKS: 1 ppm for 204H -- freshwater (OHM/TADS, 2005)
TOXIC or LETHAL - TROUT: 1.4 ppm for 18H -- soft freshwater (OHM/TADS, 2005)

PLANTS

IL50 - EURASION WATERMILFOIL: 363 ppm -- root weight, freshwater (OHM/TADS, 2005)
IL50 - EURASION WATERMILFOIL: 808 ppm -- stem weight, freshwater (OHM/TADS, 2005)
IL50 - EURASION WATERMILFOIL: 767 ppm -- root length, freshwater (OHM/TADS, 2005)
IL50 - EURASION WATERMILFOIL: 725 ppm -- stem length, freshwater (OHM/TADS, 2005)

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

207.2

DESCRIPTION/PHYSICAL STATE

Lead is a blue-gray metallic element with a cubic crystal structure. It is lustrous when cut, but tarnishes when exposed to air. A very soft metal, lead is very ductile and has a high density (ACGIH, 1996a; Budavari, 2000; Lewis, 2000; NIOSH , 2002).

All forms of lead are solid. Significant vapor occurs only at temperatures >500 degrees C (ACGIH, 1996a).

No information found at the time of this review.

VAPOR PRESSURE

1.77 mmHg (at 1000 degrees C) (ACGIH, 1996a; Budavari, 2000) NTP, 2001)

approximately 0 mmHg (NIOSH , 2002)

10 mmHg (at 1162 degrees C) (ATSDR , 1997; HSDB , 2002)

100 mmHg (at 1421 degrees C) (ATSDR , 1997; HSDB , 2002)

400 mmHg (at 1630 degrees C) (ATSDR , 1997; HSDB , 2002)

1 mmHg (at 973 degrees C) (Lewis, 2000)

1 mmHg (at 987 degrees C) (OHM/TADS , 2002)

5 mmHg (at 1099 degrees C) (OHM/TADS , 2002)

10 mmHg (at 1167 degrees C) (OHM/TADS , 2002)

100 mmHg (at 1417 degrees C) (OHM/TADS , 2002)

"significant" above 500 degrees C (ACGIH, 1996a)

SPECIFIC GRAVITY

OTHER TEMPERATURE AND/OR PRESSURE

11.34 (at 20/4 degrees C) (Budavari, 2000; Lewis, 2000; ITI, 1995; NIOSH , 2002; OHM/TADS , 2002)
11.3437 (at 16 degrees C) (NTP, 2001)
11.35 (at 20 degrees C) (ACGIH, 1996a)

TEMPERATURE AND/OR PRESSURE NOT LISTED

11.35 (Lewis, 2001)
11.343 (Bingham et al, 2001)

DENSITY

OTHER TEMPERATURE AND/OR PRESSURE

10.65 g/cm(3) (at melting point) (Budavari, 2000)
11.35 g/cm(3) (at 20 degrees C) (ACGIH, 1996a)
11.3437 g/cm(3) (at 16 degrees C) (Clayton & Clayton, 1994)

TEMPERATURE AND/OR PRESSURE NOT LISTED

11.35 g/cm(3) (Ashford, 1994)

FREEZING/MELTING POINT

FREEZING POINT

621 degrees F (NIOSH , 2002)

MELTING POINT

327 degrees C (Ashford, 1994)
327.4 degrees C (Budavari, 2000; ITI, 1995; Lewis, 2001)
327.5 degrees C (ACGIH, 1996a; Bingham et al, 2001) NTP, 2001; (OHM/TADS , 2002)
327.43 degrees C (Lewis, 2000)

BOILING POINT

1740 degrees C; 3164 degrees F (ACGIH, 1996a; Bingham et al, 2001; Budavari, 2000; ITI, 1995; Lewis, 2000; NIOSH , 2002) NTP, 2001)

1755 degrees C (Lewis, 2001)

1770 degrees C (Ashford, 1994)

1744 degrees C (OHM/TADS , 2002)

FLASH POINT

Not Applicable (NIOSH , 2002)

EXPLOSIVE LIMITS

LOWER

Not Applicable (NIOSH , 2002)

UPPER

Not Applicable (NIOSH , 2002)

SOLUBILITY

IN WATER

Lead is attacked by pure water, but is resistant to tap water (Budavari, 2000).
Lead dissolves slowly in water containing a weak acid, but will not dissolve in plain water (Lewis, 2001). It is least soluble at pH 8-10 (OHM/TADS , 2002).
Lead is insoluble in water (Bingham et al, 2001; NIOSH , 2002) NTP, 2001).
At pH >5.4, the total solubility of lead is calculated to be 20 mcg/L in hard water, and approximately 500 mcg/L in soft water (ATSDR, 1999).
At pH 7-8, total solubility is 0.001-0.01 mg/L (OHM/TADS , 2002).

IN ORGANIC SOLVENTS

Lead is resistant to solvents (Budavari, 2000).
Lead is slightly soluble in alcohol (Bingham et al, 2001).

OTHER

Lead will react with concentrated, boiling hydrochloric or sulfuric acids (Budavari, 2000).
Lead reacts with hot concentrated nitric acid. It may be attacked by weak organic acids in the presence of oxygen, but resists hydrofluoric acid (Budavari, 2000).
Lead is soluble in dilute nitric acid and acetic acid. It is slowly soluble in hydrochloric acid and is also soluble in alkali solutions. At room temperature, lead is attacked by chlorine and fluorine (ITI, 1995; Lewis, 2001; Lewis, 2000).
Lead is soluble in nitric acid and hot, concentrated sulfuric acid (ATSDR , 1997).
Lead is soluble in nitric acid at 221 g/100 mL/50 degrees C. It is soluble in glycerin (Bingham et al, 2001).
Lead resists brine (Budavari, 2000).
Many forms of inorganic lead can dissolve sufficiently in bodily fluids to be toxic, especially when inhaled in finely divided form (ACGIH, 1996a).

OTHER/PHYSICAL

THERMAL CONDUCTIVITY

Varies from 0.083 (at 50 degrees C) to 0.077 (at 225 degrees C) (Budavari, 2000)

VISCOSITY

3.2 cP (at 327.4 degrees C) (molten lead) (Budavari, 2000)
2.32 cP (at 400 degrees C) (molten lead) (Budavari, 2000)
1.54 cP (at 600 degrees C) (molten lead) (Budavari, 2000)
1.23 cP (at 800 degrees C) (molten lead) (Budavari, 2000)

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