atomic no. 82, atomic wt. 207.21, metal, row 7, col. 8, val. 2-4, orbits 2-8-18-18

Uses of Lead

{Merck Index - © 1952 by Merck & Co., Inc.}

Lead. Pb; at. wt. 207.21; at. no. 82; valence 2-4. The most abundant ore of lead is galena, PbS. Contained in smaller quantities in the minerals cerussite, anglesite, pyromorphite. The final product of disintegration of each of the three radioactive series; the atomic weight of lead from radioactive elements vary according to its origin: from the radium series 206, the thorium series 208, the actinium series 207. Methods of extraction and purification: Riegel, Industrial Chemistry, p. 960, 5th ed., Reinhold Publishing Corp., New York, N. Y. Prepn. of lead of a high degree of purity: Richards, Wadsworth, J. Am. Chem. Sec. 38, 221 (1916).

Bluish-gray, soft, very malleable metal; lustrous when freshly cut; tarnishes on exposure to air. m. 327.4°; b. about 1619°: Fisher, Z. anorg. Chem. 219, 1 (1934); (Ref.) d204 11.364. Vapor pressure: Ingold, J. Chem. SOC.4 121, 2419 (1922). Hardness 1.5 on Moh's scale; Brinell hardness about 4. Soluble in hot conc. nitric acid; in boiling conc. hydrochloric or sulfuric acid; in acetic acid. Attacked by water containing air, nitrates, ammonium salts or carbon dioxide; superficially attacked by water containing sulfates and carbonates or by dil. hydrochloric or dil. sulfuric acid in the cold.

Toxicity: Acute: sweetish metallic taste, burning in mouth, severe thirst, inflammation of the G.I. tract with vomiting and diarrhea. Chronic: anorexia, "lead-line" on gum margin, nausea, vomiting, severe abdominal pain, paralysis, mental confusion, visual disturbances, anemia, convulsions.

Max. allowable concn. of fumes 0.15 mg./ cu. m. (This is WAY TOO MUCH — Tommy C. —)

Uses of Lead: Mainly in manuf. tetraethyl lead; for constructional purposes in manufacturing and handling sulfuric acid; in manufacturing phosphoric acid, chlorination or sulfonation processes, oil refining, gas production; manufacturing various chemical equipment: pipes, valves, stirrers, coils, kettles, pumps, evaporators, condensers; for lining tanks of various electroplating solutions; in manufacturing Babbitt metal, type metal, solder, cable covering, foil, matrices, storage batteries, plumbing-(water pipes, "goose necks", soldering joints, pipe joint compounds), weights; shot; Pewter; as a binder for porclain used to surface bath tubs and sinks, until the mid 1990's, (documented as a source of lead poisoning).

Lead Acetate.

Neutral or normal lead acetate; sugar of lead; salt of Saturn. Pb(C2HSO2)2 • 3H2O; mol. wt. 379.34. C4Hl2O7Pb; anhydrous salt 85.69%, H 14.31%. For the anhydrous: C 14.77%, H 1.86%, Pb 63.70%.

Sweet tasting, colorless crystals or white granules or powder; slight acetic odor; slowly effloresces.

Use: Dyeing and printing cottons; weighting silks; manuf. lead salts, chrome-yellow; also for various analytical procedures, e.g., detection of sulfide, determination of CrO3, MoO3. Rat poison.
Had been used to sweeten wine and other food products during the "Dark Ages".

Grades available: Reagent, N.F., technical.

Med. Use: Astringent on unbroken skin, mucous membranes, and in diarrhea.

Toxicity: Can cause lead poisoning.

Vet. Use: As Med. Use.

Warning! Avoid breathing dust. Wear dust mask approved by U.S. Bureau of Mines for this purpose. Wash thoroughly before eating or smoking.

Keep away from feed or food products.

Lead Antimonate: -- Use: As pigment in oil painting, staining glass, crockery and porcelain.

Lead Arsenate: -- Use: As constituent of various insecticides for larvae of gypsy moth, bell weevil, etc. Commercially available.

Toxicity: Chronic: lesions of skin and mucous membranes, scleroderma, bronzing, dry throat, hoarseness, coughing, Raynaud's disease, wrist drop, and difficulty in walking. Daily intake of 0.06 mg. of lead or 0.3 mg. arsenic over period of months believed sufficient for chronic poisoning.
Vet. Use: Has been reported useful in tapeworms of cattle, goats, sheep.

Lead Arsenite: -- Use: As insecticide like the arsenate.

Toxicity: More toxic and corrosive than lead arsenate.

Lead Borate: -- Use: Drier for varnishes and paints; with other metals (e.g., Ag) in galvanoplasty for production of conducting coatings on glass, pottery, porcelain, and chinaware.

Lead Carbonate: -- Use: Pigment in oil paints and water colors; in cements; for making putty and lead carbonate paper.

Lead Chloride: -- Use: Manuf. Pattison's white lead, Verona Yellow, Turner's Patent Yellow, lead oxychloride; as solder and flux.

Lead Chromate: -- Use: Pigment in oil and water colors; printing fabrics, decorating china and porcelain; in chemical analysis of organic substances.

Note: Basic lead chromates of various shades of color from brown-yellow to red are used as pigments.

Lead Chromate Red: Basic lead chromate; chrome or Persian red; Austrian cinnabar. -- Used as a pigment.

Lead Cyanide: -- Use: In metallurgy.

Lead Dioxide: Lead oxide brown; lead superoxide or peroxide. -- Use: Electrodes in batteries; oxidizer in manuf. of dyes; as discharge in dyeing with indigo; manuf. rubber substitutes; with amorphous phosphorus as ignition surface for matches; pyrotechny; manuf. pigments; in anal. chemistry.

Lead Ferrocyanide: -- Use: In metallurgy.

Lead Iodide: -- Use: Bronzing, gold pencils, mosaic gold, printing, photography.

Lead Linoleate: fused. -- Use: In varnishes by dissolving 1 part in 15-20 parts linseed oil at 120-150'.

Lead Molybdate: -- Use: In pigments.

Lead Monoxide: -- Use: In ointments, plasters; preparing soln. lead subacetate. Glazing pottery; glass flux for painting on porcelain and glass; lead glass; varnishes; with glycerol as metal cement; producing iridescent colors on brass and bronze; coloring sulfur-containing substances, e.g., hair, nails, wool, horn; manuf. artificial tortoise shell and horn; pigment for rubber; in manuf. boiled linseed oil; in assay of gold and silver ores.

Warning! Avoid breathing dust. Wear dust mask approved by U.S. Bureau of Mines for this purpose. Wash thoroughly before eating or smoking. Keep away from feed or food products.

Lead Nitrate: -- Use: Manuf. matches and special explosives; as mordant in dyeing and printing on -textiles; mordant for staining mother-of-pearl, horn; oxidizer in dye industry; sensitizer in photography; process engraving.

Med. Use: Formerly as an astringent and antiseptic for extern. use.

Vet. Use: Caustic in canker of horses.

Lead Oleate: -- Use: In varnishes; in extreme pressure lubricants.

Lead Oxide Red, Red lead: -- Use: Plasters and ointments; manuf. colorless glass; glaze for falence; flux for porcelain painting, protective paint for iron and steel; oil color for ship paints, varnishes; coloring rubber; cement for glass, gas and steam pipes; storage batteries; pencils for writing on glass; manuf. lead peroxide, matches.

Lead PhenoIsulfonate, Lead sulfocarbolate -- Med. Use: Formerly as an astringent and antiseptic in skin diseases and extem. ulcers.

Lead Phosphate: -- Use: Stabilizer for plastics.

Lead Resinate: -- Use: As drier in varnishes by dissolving 2-3 parts in 100 parts linseed oil at 120-150'.

Lead Silicofluoride: -- Use: In refining lead by electrolytic methods.

Lead Sodium Thiosulfate: -- Use: Manuf. matches.

Lead Stearate: -- Use: In extreme pressure lubricants; as drier in varnishes.

Lead Subacetate: -- Use: In sugar analysis to remove coloring matters, etc., from solns. before polarizing; for clarifying and decolorizing other solns. of organic substances.

Lead Subacetate Solution: -- Med. Use: Has been used as a local astringent.

Toxicity: May be absorbed from skin denuded of epidermis and cause systemic lead poisoning.

Vet. Use: In scratches, contusions, acute eczema, strained tendons, seborrhea.

Caution: Toxicity may result from absorption through the skin or licking.

Lead Sulfate: -- Use: Instead of white lead as pigment; with zinc in galvanic batteries; manuf. minium; in lithography; preparing rapidly drying oil varnishes; weighting fabrics.

Lead Sulfide: -- Use: Glazing earthenware.

Lead Tannate: -- Med. Use: Formerly used locally for chronic inflammations and extern. ulcers.

Lead Tartrate: -- Use: As addition to gasoline to prevent "knocking" in motors.

Caution: Acute or chronic poisoning may occur if inhaled or absorbed through skin.

Lead Tetroxide: -- Use: Reserve dyeing with aniline black; manuf. safety matches and cartridges.

Lead Vanadate, Lead metavanadate: -- Use: Mfg. other vanadium compds.

Link to Chemical Elements.com

" The Cancer Connection "

... free radical damage is frequently the trigger which leads to malignant changes in previously normal cells. Just as the first benefits to circulation of EDTA chelation therapy were discovered during treatment of heavy metal poisoning, so was the way in which this same treatment could help prevent, and indeed treat, cancer discovered.

Writing in a Swiss medical journal in 1976, Dr W Blumen described the strange but potentially very important discovery. In the late 1950s a group of residents of Zurich who lived adjacent to a major traffic route were treated for contamination by lead with EDTA chelation under the auspices of the Zurich Board of Health. These people had all inhaled large amounts of lead–laden fumes and were suffering from a range of symptoms identified as being related to lead poisoning, including stomach ache, fatigue, headache, digestive symptoms, etc. lead deposits were found to be present in their gum tissues and specific changes were found in their urine, linking their condition with high lead levels.

Some years later, in the early 1970s, people living in the same area were being investigated for the incidence of cancer, in an attempt to link the pollution with a higher cancer rate than average. This link was easily established as fully 11 per cent of the residents of the road had died of cancer over the period 1959 to 1972, a rate some 900 per cent above that expected when compared with people living in the same community but not directly affected by lead pollution. The forms of cancer most commonly related involved the lungs, colon, stomach, breast and ovary.

But what of the people previously treated with EDTA back in 1959?

Only one of the 47 people in that group had developed cancer. The cancer rate in people in the contaminated area who had not received EDTA was 600 per cent above that of the group who had had chelation.

Far and away the best protection from lead toxicity and its long–term effects is to avoid it altogether. However, this is of course not always within the control of the individual and a second best bet is to have the lead removed via chelation as a protective measure against its undoubted toxicity which can contribute towards the evolution of cancer.

Australian research scientist John Sterling, who has worked at the famous Issels clinic in Germany, mentions in a personal communication that Issels had noted a marked protective effect against cancer after use of EDTA chelation.

Animal studies ( using mice ) have shown that intravenous EDTA plays a preventive role against cancer, largely, it is thought, through removal of metallic ions which seem to be essential for tumour growth.

Walker and Gordon believe that the prevention offered to the citizens of Zurich was partly as a result of removal of metal ions and of lead ( which can chronically depress immune function ) and also due to the improvement in circulation which chelation produced. Tumours flourish in areas of poor oxygenation and the increase in the levels of this which chelation allows would, they believe, be sufficient to retard cancer development.

Halstead ( 1979 ) points to the significant increase in metal ions found as tissues age and the increased likelihood of cancer developing. There is also a proven link between high levels of certain metals in topsoil and cancer in the same regions. Interestingly, he confirms that most forms of chemotherapy involve drugs which have chelating effects either directly or as a result of breakdown of their constituents. He quotes experimental studies which show that in some forms of cancer such as Ehrlich's ascites tumour the use of EDTA was significantly able to strip the tumour cells of their heavy protective coat, allowing other mechanisms ( such as protein digesting enzymes ) to destroy the tumours.

At the very least EDTA chelation can be seen to offer a useful line of investigation in cancer prevention, and possibly treatment, in some forms of this disease.

Succimer lessens lead in blood, no gain in IQ
By Vasantha Arora
May 16, 2001 15:42 Hrs ( IST )

Washington: A drug is effective in lowering the level of lead in the bloodstream of exposed children, but they show no apparent gains in the intelligence quotient ( IQ ) and learning abilities as a result of the treatment.

This has been revealed in a study conducted by the National Institute of Environmental Health Sciences ( NIEHS ).

The children were given succimer, a drug that is known to reduce the blood level of lead. In addition, the research team attempted to end further exposure by cleaning the children's homes of residual lead. The researchers had hoped to find that these efforts would prevent or reduce lead–induced damage.

Compared to a control group, however, the treated children performed no better on tests of behavior, cognitive development and neuropsychological function.

In a press release, NIEHS director Kenneth Olden said, "The results of the trial show clearly that treatment after the fact does not undo the damage among five– year– olds. We must prevent these children from being exposed in the first place."

Prolonged exposure to lead causes an accumulation of the element in the body. That can result in a variety of mental and physical problems: reading and learning disabilities, speech and language handicaps, mental retardation, kidney disease and heart disease.

"We must prevent these children from being exposed in the first place," Olden said.

India Abroad News Service   —Reference—

[ In the "Natural World" organisms that regularly come in contact with toxic metals, have specific mechanisms for resistance. The genes for these systems are coded on transposons or plasmids. Humans don't have the full complement of these mechanisms, and drugs are used to treat overdoses of these metals. Chelating agents such as EDTA bind the metal many times, with great affinity, greater than that of the target enzyme. The complexes are stable and water soluble, readily excreted and do not enter the metabolism.   —Reference— ]

Symptoms of lead poisoning     Minnesota Department of Health – Lead

  • no desire to eat food
  • loss of recently acquired skills
  • drowsiness
  • irritability
  • headache
  • lack of energy
  • constipation
  • stomach cramps
  • trouble sleeping


J.clin.Path  (1961), 14, 548

The anaemia of lead poisoning


From the Department of Haematology, the University and Western Infirmary, Glasgow

SYNOPSIS: Three cases of lead poisoning with a hypochromic anaemia, despite adequate iron stores, are presented and discussed.

    The anaemia of lead poisoning is usually thought to be normochromic and normocytic, and punctate basophilia is regarded as a constant feature of the well–developed case

*   *   *

    Formerly the anaemia in lead poisoning was attributed to a shortened survival of cells in the circulation but more recently the importance of interference with haemoglobin synthesis has been recognized, and this is demonstrated in two of our three patients in whom an inability to use available iron despite active eyrthropoiesis was an important factor in the development of the anaemia. Only in the third did the haemolytic element predominate.

* * * *


    More than one mechanism has been blamed for the production of the anaemia of lead poisoning. The red cells may be rendered more ‘brittle’ by the lead ( Aub, Fairhill, Minot, and Reznikoff, 1925 ) and therefore may have a shorter life span than normal.


Received for publicatin 7 March 1961.


Original Paper

Miner Electrolyte Metab 1992;18:1–5


Elevated Lead Burden in
Chinese Patients without
Occupational lead Exposure

Ja-Liang Lin (a)
Paik-Seong Lim (b)


Studies were conducted in 10 healthy Chinese Controls, 10 patients with chronic renal failure without gout, 8 patients with gout complicated with chronic renal failure who subsequently developed gout. All the subjects had no history of occupational or accidental lead exposure. Total body lead burden was assessed by 24–hour urine collection measurements over a 72–hour period after intravenous administration of 1g of calcium disodium EDTA. The postinfusion urinary lead excretion of the healthy controls (90.2, range 57.2–161.5 ug/3 days/1.75m2) was higher than the values recently reported for healthy German controls. Similar to earlier studies, we failed to find elevated urinary lead excretion in patients with chronic renal failure without gout. Nevertheless, the EDTA mobilization test identified 2 patients with occult plumbism in this group of patients. Our study also clearly demonstrated that 4 of 6 patients with renal failure who developed gout de novo had underlying plumbism. The high prevalence of increased lead body burden in patients with chronic renal failure, in particular those associated with out, indicates that lead may contribute to a significant portion of chronic renal disease in our patients. In addition, our data suggest that chronic low–level environmental lead exposure may subtly affect renal function.


A causal relationship between gout and renal disease has been recognized since antiquity. However, this relationship had largely been forgotten or disclaimed by the turn of the 19th century. In the late 1960s the well–known epidemiological observations in Queensland [1] and the moonshine whisky belt of the USA [2] provided the most concrete confirmation and reawakened interest in this field. Until recently, its pathomechanism has not been clearly elucidated.

The high prevalence of gout in uremic populations with saturnism is remarkable. Emmerson [1] suggested that patients with renal failure who developed gout when serum creatinine had already been elevated almost invariably had underlying chronic saturnism. In addition he also stressed the diagnostic importance of the temporal relationship between the onset of gout and the occurrence of renal failure.   [ renal — of or near the kidneys ]

(a) Division of Nephrology Chang Gung Memorial Hospital, Taipei, Taiwan, ROC
(b) Division of Nephrology, Kuang Tien General Hospital, Sha Lu, Taichung, ROC

Whodunit?   Forget the Butler.   All Clues Lead to Lead.

Social scientists have always been fascinated by the startling rise in crime rates that took place in the 20th Century, and the equally precipitous drop-off that those same rates experienced in the 90s. Now researchers think they may have discovered what really did all the wrongdoing: The vast amounts of lead introduced into the post-WWII environment by leaded gasoline. And that’s not all...hormone disruptors may be getting in on all the illicit action, too.

The first of several recent studies to indicate that environmental pollutants may play a key role in overall levels of crime reached its conclusion quite by accident. Economic consultant Rick Nevin was hired by the Department of Housing and Urban Development (HUD) to conduct a cost-benefit analysis of removing lead paint from public housing projects. While the advantages of lead-free housing were clear (and clearly priceless in our view), Nevin was startled to find a fairly obvious relationship between the widespread use of leaded gasoline and the violent crime wave experienced by the country from approximately 1950 to 1990.

The use of leaded gasoline exploded in the boom following WWII, and by the time this use peaked in the mid-1970s, nearly everyone had some level of lead poisoning. Children were especially vulnerable. At the time lead was eliminated from gasoline, close to 80% of all children had levels of lead that would exceed today’s federal safety limit of 10 micrograms per deciliter of blood. Inner city children were especially hard hit, living as they often did in lead-painted housing and breathing air with high concentrations of automobile exhaust.

Nevin found that the much-discussed juvenile crime wave of the 1950s began just as the first generation of children significantly exposed to leaded gasoline became teenagers. In subsequent years, as lead contamination in the environment steadily increased, so did rates of violent crime. This trend suddenly reversed in the 1990s, which Nevin found coincided with the first generation of children to enjoy a substantially less lead-contaminated environment as a result of the lead gasoline phase-out reached their teens. Nevin also pointed out that nearly identical corresponding patterns could be noted in Great Britain, France, Australia and other countries.

The results of the research dovetail nicely with other studies on the effects lead has on human behavior. Fordham University law professor Deborah Denno, for example, studied some 3,000 different attributes to see if it was possible to identify determining factors for criminal behavior. Lead exposure was found to be the number one most reliable indicator.

Fortunately, lead levels have declined precipitously since the 1970s. According to the EPA, the number of children under age 6 with high blood lead levels has fallen from 4.7 million in 1978 to 300,000 today. As more and more lead paint is removed from homes, this number is expected to drop further, and lead poisoning, hopefully, will become a thing of the past.

But just as lead is fading out, a new behavioral threat may be emerging. According to new research from Japan, rising levels of hormone-disrupting chemicals in the environment may be causing more than endocrine damage to the human body. According to reports from the June 25th meeting of the Japan Society of Endocrine Disrupters Research, these substances may also be causing abnormal behaviors and triggering crimes of their own.

This recent meeting highlighted several studies that focused on such concerns. One project found that rats exposed to the common chemical Bisphenol-A had a more difficult time negotiating a maze than their unexposed peers and displayed behaviors that suggested they were suffering from some kind of Attention Deficit Hyperactivity Disorder. Another study found that female rats whose mothers had been exposed to the common endocrine-disrupting herbicide Glufosinate demonstrated extreme aggression towards other rats.

While more research is needed, such findings clearly point out that hormone-disrupting chemicals have great potential to become “the new lead. ” They are a class of materials that are just as dangerous and equally in need of severe restrictions, if not an outright ban.

For more on the HUD lead study see the journal Environmental Research 2000; 83: 1–22.


Lead-Poisoning Therapy with Succimer May Pose Hidden Risks — Preliminary Research



The following points are made by D.A. Schaumberg et al (J. Am. Med. Assoc. 2004 292:2750):

1) Although lead toxicity in humans has been recognized for centuries, the 20th century has left a legacy of unprecedented lead levels spread throughout the environment. Lead continues to pose a significant public health problem in spite of substantial reductions in lead exposure in the US in the recent past. Moreover, exposure has not been totally eliminated and most adults continue to have substantial body burdens of lead.[1]

2) Much of the lead taken into the body is incorporated into bone where it constantly interchanges with other tissues.[2] Recent studies suggest that accumulated lead exposure is related to several chronic disorders of aging including hypertension and cognitive decline,[1] disorders that have been associated with oxidative stress.[3-4] Several lines of evidence suggest that accumulated lead exposure could also increase the risk of another oxidative-stress-related disorder of aging, age-related cataract – the leading cause of blindness and visual impairment worldwide.[5]

3) The authors tested whether bone lead levels measured in both the tibia and patella were associated with age-related cataract in an ongoing study of men from the US who were drawn from the general population surrounding Boston. Participants were drawn from the Normative Aging Study (NAS), a longitudinal study of 2280 healthy male volunteers, begun in Boston in the 1960s. At the time of their initial enrollment, all NAS participants were free of heart disease, hypertension, diabetes mellitus, cancer, peptic ulcer, gout, recurrent asthma, bronchitis, or sinusitis. Study participants were predominantly white, and ranged in age from 48 to 93 years at the time of bone lead measurement. Every 3 to 5 years, participants underwent an extensive physical examination that included a standard ocular evaluation, not always including a dilated fundus examination, with notation of any abnormalities in the lens, optic nerve, and macula. Beginning in 1991 and continuing through 1999, NAS participants were invited to undergo bone and blood lead measurements.[2] At the time the present study was initiated, 795 (68%) of the 1171 NAS participants who were still being monitored had completed bone lead measurements.

4) Cataract assessment was done while masked to the lead level results. A participant was considered to have cataract if there was documentation for either eye of cataract surgery or a cataract graded clinically as 3+ or higher on a 4-point scale. The mean age of the study participants was 69 years and cataract was identified in 122 men.

5) The authors conclude these epidemiological data suggest that accumulated lead exposure, such as that commonly experienced by adults in the US, may be an important unrecognized risk factor for cataract. The authors suggest the research indicates that reduction of lead exposure could help decrease the global burden of cataract.

References (abridged):

1. Vig EK, Hu H. Lead toxicity in older adults. J Am Geriatr Soc. 2000;48:1501-1506

2. Hu H, Rabinowitz M, Smith D. Bone lead as a biological marker in epidemiologic studies of chronic toxicity. Environ Health Perspect. 1998;106:1-8

3. Romero-Alvira D, Roche E. High blood pressure, oxygen radicals and antioxidants: etiological relationships. Med Hypotheses. 1996;46:414-420

4. Mecocci P, Mariani E, Cornacchiola V, Polidori MC. Antioxidants for the treatment of mild cognitive impairment. Neurol Res. 2004;26:598-602

5. Thylefors B, Negrel AD, Pararajasegaram R, Dadzie KY. Global data on blindness. Bull World Health Organ. 1995;73:115-121

J. Am. Med. Assoc.  http://www.jama.com

Related Material:


The following points are made by R.L. Canfield et al (New Engl. J. Med. 2003 348:1517):

1) Lead is neurotoxic, and young children are at particular risk for exposure. Numerous studies indicate that blood lead concentrations above 10 micro-g per deciliter (0.483 micro-mol per liter) are associated with adverse outcomes on measures of intellectual functioning and social behavioral conduct. Such studies led to the identification of a blood lead concentration of 10 micro-g per deciliter or higher as a "level of concern" by the Centers for Disease Control and Prevention (CDC) and the World Health Organization.

2) It remains unclear whether lead-associated cognitive deficits occur at concentrations below 10 micro-g per deciliter. The CDC and WHO recognized that no evidence of a threshold existed for lead-associated deficits but noted an absence of research on the possible effects of blood lead concentrations below 10 micro-g per deciliter. Although some studies in which the average blood lead concentration was below 10 micro-g per deciliter have reported associations between the blood lead concentration and cognitive deficits, the analyses did not focus specifically on children whose concentrations remained below 10 micro-g per deciliter throughout life. Other evidence suggesting lead-related deficits at concentrations below 10 micro-g per deciliter relied on linear extrapolation or on data unadjusted for important potential confounders such as maternal intelligence and the quality of caregiving.

3) The authors examined associations between low-level exposure to lead and children's performance on intelligence tests at the ages of three and five years in a population that included many children whose blood lead concentrations remained below 10 micro-g per deciliter.

4) The authors conclude: "Blood lead concentrations, even those below 10 micro-g per deciliter, are inversely associated with children's IQ scores at three and five years of age, and associated declines in IQ are greater at these concentrations than at higher concentrations. These findings suggest that more U.S. children may be adversely affected by environmental lead than previously estimated."

New Engl. J. Med.  http://www.nejm.org

Related Material:


The following points are made by Vincent T. Breslin (J. Chem. Educ. 2001 78:1647):

1) Despite the ban on lead-based paints and leaded gasoline in the US in the 1970s and 1980s, 4.4 percent of American children aged 1 to 5 years still have blood lead levels high enough to cause irreversible damage to the developing nervous system. In addition, almost 12 percent of children in older housing in large urban areas have elevated blood lead levels, and African-American children living in the major US inner cities are affected disproportionately (approximately 22 percent). Lead exposure in young children results primarily from ingestion or inhalation of soil particles, drinking water, paint, and dust particles in and around the home and play areas.

2) Lead was used extensively as a corrosion inhibitor and pigment in both interior and exterior oil-based paints prior to 1978, and some paints were manufactured with lead concentrations of 50 percent by weight. Therefore, weathering of lead-based exterior paint and deposition of paint chips and dust on soils remains a significant source of lead to soils surrounding homes. Soil lead concentration at or above 500 micrograms per gram will result in a 1 to 5 percent probability that a child will have a blood lead concentration that equals or exceeds 10 micrograms per deciliter.

3) Drinking water is another source of ingested lead. Household plumbing fixtures, including metal pipes, faucets, and soldered joints, are possible sources of lead in drinking water. The lower the pH of the water and the lower the concentration of dissolved salts in the water, the greater is the solubility of lead in the water. Leaching of lead from plastic pipes has also been documented and has been attributed to the use of lead stearate, a stabilizer used in the manufacture of polyvinyl plastics.

J. Chemical Education  http://jchemed.chem.wisc.edu

Related Material:


The following points are made by Howard W. Mielke (American Scientist 1999 87:62):

1) Since the 1920s, millions of US children have been quietly poisoned by lead, and thousands of deaths are attributed to this over the long term.

2) Although childhood lead exposure in the US has diminished during the past 2 decades, the problem has not been solved. Instead, the demographics has shifted.

3) Over 50 percent (and perhaps even 70 percent) of children living in the inner city of New Orleans and Philadelphia have blood lead levels above the current guideline of 10 micrograms per deciliter [*Note #2]. In contrast, in the concrete "jungle" of Manhattan, where very little of the soil is exposed and almost all apartments and housing contain lead-based paints, only between 5 and 7 percent of children under the age of 6 have been reported to have blood-lead levels of 10 micrograms per deciliter or higher. It is of significance that in Brooklyn, across the river from Manhattan, where yards containing soil are common, the percentage of affected children is several times higher than in Manhattan.

4) The serious of the problem has been recognized by the US Centers for Disease Control and Prevention since the early 1990s, which has called pediatric lead poisoning "entirely preventable".

5) The author suggests that effective prevention assumes an accurate identification of the environmental reservoirs of lead, and that current policies to reduce lead exposure are based on the assumption that the greatest lead hazard comes from lead-based paints [*Note #3]. Most lead-based have now been removed from the market, and parents have been instructed to guard their children from eating paint flakes. However, for children, paint is now neither the most abundant nor the most accessible source of lead. The common problem is lead dust in the environment, with the soil a giant reservoir of tiny particles of lead. The greatest risk for exposure of inner city children is in the yards around houses and to a lesser extent in public playgrounds.

6) The author suggests that an accurate and complete appreciation of the distribution of lead in the environment can help shape policies that more effectively protect the health of children. The author concludes: "It took nearly 10 decades for lead to accumulate to its current levels in urban areas. With judicious planning, the problem can be resolved in much less time."

Notes by ScienceWeek:

Note #1: There is much data concerning certain syndromes, e.g., fetal alcohol syndrome, lead poisoning, etc. One research problem is that effects of low levels of environmental toxins on the developing nervous system can be subtle and not detected unless specific rather than general behavioral measures are applied.

Note #2: There is hardly a consensus concerning acceptable levels of lead in the whole blood of children. Some clinicians consider the danger point to be in the region of 50 micrograms per deciliter whole blood; other clinicians consider anything above 10 micrograms per deciliter as a cause for alarm. In terms of low-level effects on the developing central nervous system, general concentration cut-off points are perhaps arbitrary, since there is considerable individual variation in toxic susceptibility.

Note #3: In the US, lead was used in residential paint between 1884 and 1978, and leaded paint remains on the walls of many old buildings.

Source "ScienceWeek"

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