Lecture 24 Heavy Metals (Lead, Arsenic) I....

ES/RP 532 Applied Environmental Toxicology Page 1 of 14

ESRP532 Lecture 24.doc Fall 2004

December 1, 2004

Lecture 24 Heavy Metals (Lead, Arsenic)

I. LeadA. Introduction: Since the 1960’s, great concern has been expressed over the presence of

lead in the environment;1. Gasoline additives, the organoleads, were recognized as the largest emission sources;2. The EPA recommended that the ambient standard (in the 1970’s) be set at 2 µg/m3. It

is now recognized that lead is capable of producing toxic effects in adults andchildren at exposures far lower than those producing gross clinical symptoms. Leadexposures that were considered “safe” only a decade ago are now recognized toproduce subtle toxicity (Mahaffey et al. 1992, pp. 360-391 in EnvironmentalToxicants, Human Exposures and Their Health Effects, M. Lippmann, ed., VanNostrand Reinhold)

B. Inorganic lead is ubiquitous in the environment; the “average” soil content of lead is ~15-25 ppm. This should be considered the “natural” background level, but accurate amountswill vary depending on anthropogenic sources of lead nearby the sample collection areas.1. Pb is a member of the Group IV elements (which includes C and Si) but it does not

bind with itself. Also, it has a stable +2 and +4 oxidation state.2. In freshwater, lead forms a number of complexes of low solubility with many anions,

including hydroxides, carbonates, sulfides, and less commonly sulfates.3. Lead also partitions favorably with humic and fulvic acids, forming moderately

strong chelates.4. At pH 10, Pb(OH)+ dominates all other species.5. Speciation shifts to favor chloride and hydroxide complexes in saltwater.

a. Approximately 75% of lead in rivers is in suspension and 25% in solution, but insaltwater, the corresponding ratio is approximately 50:50 (Moore, 1991,Inorganic Contaminants of Surface Water, Springer Verlag).

6. Alkyl lead compounds can be synthesized. Lead can also undergo methylation in theenvironment, which is mediated by bacteria in sediments to form (CH3)3Pb+ andrelated compounds.

C. Anthropogenic sources of lead include (one to two orders of magnitude greater than thatfrom natural sources) (Mahaffey et al.,1992):1. Manufacture and use of pesticides (the old lead arsenical compounds, long banned,

but residues persist in orchards);2. Refuse incineration;3. Coal combustion;4. Production of chemicals, caulking compounds, paint pigments, solder, cable covering,

ammunition, and storage batteries;5. Manufacture of glass and ceramics;6. Combustion of fuels containing lead additives.

a. Organolead compounds (alkyl leads) were added to gasoline, starting around 1923in the U.S. Typically, mixtures of tetramethyl lead, tetraethyl lead, andethylmethyl lead were added to gasoline in order to prevent detonation or



uncontrolled combustion of the gasoline/air mixture which is known as knocking(Connell, 1998, Basic Concepts of Environmental Chemistry, p. 259)

D. Of the various sources of lead, atmospheric emission from fuel containing lead additives,especially the organoleads (for ex., tetraethyl lead) were the biggest source.1. The average lead content of coal is 10 ppm, but in leaded gasoline, the concentration

was >1000 ppm2. In the 1970’s, the average annual lead concentration in air for most cities was 1-3

µg/m3a. 0.1 - 0.5 µg/m3 for non-urban locations;b.



b. Ambient lead measured in soil, rainwater runoff, and street dust: (Blais andMarshall, 1986, JEQ 15)1. Note that majority of lead species are bound to organic matter; only a small

proportion is actually alkyl leads

Pb Species (as mg/kg) in rainwater runoff, soils, and street dusts from an urban environmentSample Total

Pbmg/kg

Organic Boundmg/kg

Extractablemg/kg

TriethylPbµg/kg

DiethylPbµg/kg

First rainwater runoff;5 m from gas station,residential area

- 1.45 1.39 0.16 1.8

First runoff, 45 m fromgas station, urban area

2.6 0.37 - 0.40 0.47

First runoff;busy street intersection,urban area

17.9 17 8.5 0.28 0.36

Soil from a park;5 m from bust street,urban area

568 248 132 1.2 10

Soil from a potted tree;1 m from busy street,urban area

50 14 13 0.7 4

Street dust; busy street;urban

1669 1313 305 8 42

Street dust; 5 m from agas station; urban area

1062 377 447 29 166



c. Disposition in soil—(case study by Ou et al., 1995, ETAC 14:545-551.). Spikedsterile and nonsterile soils with triethyl lead; note that the Na-DDTA extractsrepresent organolead species, the phosphate buffer extracts represent nonleadedorganic species; the unaccounted for 14C may represent volatiles like ethanol orethane; it is not known if the 14CO2 is produced by organic metabolites or directmineralization of the alkyl groups; however, sterilization of the soils resulted insignificant decreases in mineralization.

Soil Depth(cm)

14CO2 Hexane-NaDDTA

PhosphateBuffer

Nonextractable14C

Recovery(% ofadded)

14C-triethyl lead0-15 15.4 22.1 9.4 27.8 74.715-30 16.0 20.7 6.0 23.8 66.530-45 16.2 20.7 3.0 28.5 68.414C-diethyl lead0-15 18.3 23.5 11.2 37.0 90.015-30 19.4 7.6 10.3 32.7 70.030-45 19.2 8.3 6.0 21.2 54.7

2. Studies of Greenland snow show deposition at remote distances from emissionsources (in this case leaded gasoline); deposition seems to follow the trend of leadedgasoline use; also there is an enrichment of organolead compounds relative toinorganic Pb compounds, but this varies by time of year. However, note that theamounts of organolead compounds are at least 2-3 orders of magnitude lower thaninorganic compounds (studies by Lobinski et al., 1994, ES&T, vol. 28, pp. 1459-71)

Historical use of lead in gasoline in the U.S. and in Europe



Organolead, inorganic lead (Pb+2), and diethyl lead in snow samples collected inGreenland snow during 1989. Note the concentration units for the inorganic leadcompared to the organic species. Notes also that there is a temporal variation indeposition.

Historical total organolead lead levels in in-depth snow cores from the Summit site.



3. One problem with atmospheric deposition is the occurrence of a lead burden inplants;a. Plants normally don’t absorb soil-borne lead compounds well; nevertheless, lead

is still absorbed and the amount absorbed is plant specific and may be affected bylead content in the soil.1. Lead salts tend to be quite insoluble and sorbed strongly to soil components;2. Acidity would tend to increase solubilization of lead.

b. However, the levels in both the atmosphere and thus on plants may be decreasingas a result of the phase-out of leaded gasoline (studies by Jones and Johnston,1991, ES&T vol. 25).1. Studies have found that lead levels are higher in foliar portions (than in roots,

stems, fruit), perhaps due to direct deposition;2. However, there is a portion that is readily washable from leaf surface,

especially when Pb is present at higher concentrations (for ex., when plantsare in closer proximity to a source)

F. Lead in food1. Lead contents in meat , milk, and poultry were generally below 0.3 ppm with some

exceptions; for ex. beef liver @ 0.4 ppm, shellfish up to 3 ppm; milk @ 0.02 -0.07ppm; most vegetables show concentrations



amounts. 150 day old monkeys retained 69.8% of an oral dose of lead nitrate, butadult monkeys retained 3.2%.

b. Organolead is very readily absorbed and stored in tissues high in lipid.c. Under steady state intake, about 40-70% of ingested lead can be excreted in the

urine; no biomagnification known (for ex. through the food chain).d. Three compartments for lead (data from a study where volunteers were given 156-

215 µg/day and studied for times up to 108-210 days):1. Blood lead amounts averaged 1900 µg (mostly associated with red blood

cells) and turned over in about 36 days;2. Soft tissue lead (contained ~600 µg Pb and turned over every 40 days)3. Bone lead (bone contained 200 mg; turned over every 104 days)

2. Diagnostic blood levelsa. Prior to 1970, 80 µg Pb/100 mL for adults; children @ 50-60 µg Pb/100 mL (i.e.,

µg/dL)b. Post 1970, both adults and children, level (based on disruption of heme synthesis)

set at 40 µg Pb/100 mLc. In 1985, CDC recommend that the intervention level be revised downward to 10

µg Pb/100 mL1. Lower standard was based on a scientific publication that indicated that

groups of pre-school children were at risk for long-lasting adverseneurobehavioral effects when blood lead concentration rose above 10µgPb/100 mL.

2. About 20 years ago, it was thought that children were most exposed to leadbecause of lead based paint chips and consequent hand-to-mouth ingestion.Research, however, shows that lead exposure is still unacceptably high inlarge cities. The soil lead data suggest that deposition of lead compoundsfrom gasoline are the main reason for this continued lead exposure in large,highly urbanized cities (Mielke, 1999, Lead in the inner cities. Am. Scientist87:62-73.a. Mielke (1999) has shown that as lead based paint was being phase out,

lead gasoline was in full production and use.



b. Soil analysis from around the foundation of buildings showed elevated Pblevels compared to soil between buildings. Furthermore, soil levelsdeclined as the soil was collected further from the street.

c. Note in the next figure (from Mielke 1999) that the heavier particles settlenear the street while smaller particles are carried by the wind until theymeet a barrier, such as a tree or a house to which they stick. Eventually,they are washed into the soil by rain. Lighter particles can be carried agreater distance and re eventually scavenged by precipitation and then fallto the ground. The first home in the figure represents a structure about 7meters from the street, while the second home represents a structure morethan 25 meters from the street.



3. The larger the city, the greater the soil lead concentration. Most of the lead is locatednear the foundation.

4. Children pick up more lead on their hands when they play outdoors than when theyplay indoors, suggesting that soil lead is the main exposure pathway for children.



5. Studies of the relationship between blood lead levels, soil lead, and the percentage ofpre-1940’s housing in a city (these would have the greatest levels of lead from lead-based paints) indicate that the correlation is not very good. This lack of concordancesuggests that the soil levels of lead are better indicators of blood lead levels than theresidence in a house with lead-based paint. (see next page)



6. Because children eat soil (as well as lead-based paint chips, etc), a soil standard wasproposed, but the Society for Environmental Geochemistry and Health recommendedthat the standard be flexible depending on the target blood level to be attained and the% of population to be protected.

Variation of soil lead guideline (ppm) with target blood lead concentration (PbB) and degree ofdesired protection (Wixson & Davies, 1994, Environ. Sci. Technol. 28:26A-31A)Target blood Pb Soil Lead Standard for % of Population with < Target Pb Level in

Blood (µg/dL) 95% 98% 99% 99.9%10 880 500 300 --15 2300 1860 1400 70020 3750 3000 2600 160025 5200 4250 3700 2500Assumptions: background PbB = 4 µg/dL

H. Ecotoxicological concerns1. Ingestion of lead shot by water fowl and direct toxicity due to accumulation of lead2. Bioaccumulation leading to transfer in the food chain3. Phytotoxicity does not seem to be on the radar screen

I. Treating lead intoxication: use of chelators like succimer; interesting note, someEgyptian scientists reported that garlic had natural chelators in it that gave a protectiveeffect against lead toxicity

II. ArsenicA. Not too long after G.W. Bush was took the oath of office in 2001, an ad ran on TV. The

ad has a little girl asking her dad for a glass of water with the question: Can I have morearsenic please?1. President Bush has been pilloried in the news because his administration made a

decision to roll back the arsenic standard from 10 ppb in drinking water to 50 ppb(circa March 2001). (Oh the good old days of not having to worry about terrorismand the gradual erosion of our civil liberties!)

2. The standard had stood throughout the previous administration without much fanfare.3. The National Academy of Sciences has been asked by EPA to reassess its old

standard of 50 ppb promulgated after a 1988 risk assessment.4. The National Academy of Sciences released its Arsenic in Drinking Water report in

1999, and although did not recommend a specific standard, did conclude thefollowing: “Upon assessing the available evidence, it is the subcommittee’sconsensus that the current EPA MCL for arsenic in drinking water of 50 µg/L doesnot achieve EPA’s goal for public health protection and therefore requires downwardrevision as promptly as possible.



a. The EPA goal was to ensure that the maximum risk at the MCL fell within the 10-4 to 10-6 range that the agency considers protective of the public health, thereforeachieving the overall purpose of the Safe Drinking Water Act.

5. The 50 ppb drinking water standard corresponded to an intake of 0.001 mg/kg perday.

B. There is not doubt that arsenic, especially in drinking water, has severe, noncarcinogeniceffects after subchronic exposures.1. Witness what is currently happening in Bangladesh with inhabitants in the low lying

areas drinking from shallow wells that are contaminated with natural levels ofarsenic.a. A common ailment are severe skin disorders of the extremities, starting with

hyperpigmentation and then progressing to palmar-plantar hyperkeratoses (seenext page).

b. Noncancer effects of chronic arsenic ingestion have been detected at arsenic doseson the order of 0.01 mg/kg per day and higher.

C. But the effect of most concern is carcinogenicity, especially of the skin, bladder, andlung.1. The evidence for carcinogenicity comes from human epidemiological studies rather

than from rat studies.2. First, arsenic is not really directly mutagenic, but it can affect DNA synthesis.

a. Indeed, at low doses it stimulates DNA synthesis but at high doses it inhibitssynthesis.

b. These experiments on DNA synthesis were done in human lymphocyte cellcultures. (Meng, Z. 1994. Effects of arsenic on DNA synthesis in human



lymphocytes. In Arsenic in the Environment. Pat II: Human Health andEcosystem Effects, J. O. Nriagu, ed. John Wiley & Sons, Inc.)

3. The main studies used to support the association between arsenic exposure indrinking water and cancer were conducted in Taiwan in a region with comparativelyhigh concentrations of As in drinking water. (for ex., Chen, C.-J. and L.-J. Lin.Human Carcinogenicity and atherogenicity induced by chronic exposure to inorganicarsenic. Pat II: Human Health and Ecosystem Effects, J. O. Nriagu, ed. John Wiley& Sons, Inc.)a. The age adjusted lung cancer mortality rates for females living in Taiwan drinking

water at levels of 0.6 ppm were 26.5, 40.9, and83.8 per 100,000 person-years.1. A significant increase in lung cancer mortality of 5.3 per 100,000 person-

years was observed in both men and women for every 0.1 ppm increase inwell-water arsenic level.

b. The NAS indicated that genotoxic effects of submicromolar concentrations ofarsenite on human and animal cells and one study of bladder-cell micronuclei inhumans with arsenic concentrations of 57-137 µg/L in urine indicate thatperturbations in cellular function related to plausible modes of carcinogenesismight be operating at arsenic exposure concentrations associated with the currentMCL.

D. One of the problems with the proposed lower MCL is that the exposure problem islargely related to natural levels of arsenic in water supplies. Thus, natural contaminationwould have to be regulated to a lower level, and it is pretty expensive to remove arsenic.1. The USGS has mapped arsenic concentrations in ground water. Locations with >50

ppb are located throughout the U.S. but are dominated by locations in the westernU.S.

E. Meanwhile, even under the rolled back standard, the 10 ppb was not to take effect until 5years down the road (i.e., 2006); the Bush administration wants to review the science onthe issue.

F. Another issue that involves concerns about arsenic exposure is the use of copper-chromated-arsenate (CCA) treated wood (pressurized wood, a.k.a. or wolmanizedlumber).1. The wood is used for outdoor applications including foundations, playground

equipment, fences, etc.2. Concerns were raised with the Consumer Product Safety Commission about rub off of

arsenic by children playing on CCA treated wood and subsequent exposure throughhand-to-mouth behavior.

3. CCA wood was recently (within the last two years) removed from the commercialmarket.

4. To further explore this issue from a skeptical perspective, as well as the issue relatedto arsenic in drinking water the pdf files of essays by Felsot (2001) fromAgrichemical & Environmental News.

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