Document 9DOVrGgZMGoavB7Gn28YBpe5

, (COMMISSION DER EUROpAlSCHEN CEMEIN8CHAFTEN COMMISSION DES c o mmu n a u t E* e u r o p Ee n n e s 14 UNITED STATES ENVIRONMENTAL PROTECTION AGENCY INTERNATIONAL SYMPOSIUM Environmental health aspects of lead Die gesundheitlichen Aspekte der Umweltverschmutzung durch Biel Les problfemes sanitaires posSs par le plomb present dans I'environnement ILZRO'S RESEARCH TO DEFINE LEAD'S IMPACT ON MAH COLE JEROME F, and LYNAM DONALD R. International Lead Zinc Research Organization Inc. NEW YORK, USA Amsterdam, October 2 - 6, 1972 N40701 Summary The International lead Zinc Research Organization (ILZRO) has sponsored ; a comprehensive program of research on the environmental health aspects ' of lead. These projects have included studies of the character and concentrations of atmospheric lead and also of the impact of environ* mental lead On public health. 'v ^ Specific emphasis has been placed on determing the dynamics of absorption of lead by man and animals from the environment; and also an assessing the biological impact of exposure to lead. It was concluded, that, although man's activities ha^e caused a generalized ecologic trans^ location of lead and that detrimental effects to health are caused only by exposure to lead far in excess of the concentrations to which the public is continuously exposed. . .1 y`tf .. .i't-Uv ' DUP050057916 introduction; . V V. vW-`. * ...... The lnternatibnal Lead Zinc Research Org]ahization^ InG; t(ILZRO): is' earcharm of thd' world-wWe lead andainp * industry/' ILZRO's member coiftpanies account for more than three-fourths' of the world's lead; and zinc production?^ ''^out8^de;:thd'*:Coiimuhiat''hid^ `of nations';: *' ; ' Sitice its inception ILZRO, aione and in cooperation with' other Industriai^.VSv andgoverqmental groups, has sponsored a* broad program of research in order V;. to further our understanding of the? effect of lead on health* This research : has been .responsive to the potential Iprobleatsiassociated with the use of lead andt its. products and indicates the industry's interest inprotectingits employees, the general public and the:environment T ?' * ' - head in the Environment .. / ` V`- Sources , *. .* . ` Leadlis ahatural constituent of soils and thus has always found its way'NUitp ; the food man eats, the? beverages he drinks, and the air- he ^breathes * Supeii^; imposed upon the naturally-o.ccurrjfejg lead',, however, is a quantity caused by - ?^ man's industrial and social activities* i Of course, among the best known SQufce| of additional lead are emissions from the smelting of non-ferrous metals, the; C manufacture of lead products, and the usage of lead alkyl antiknock additives?' in gasoline* - ' Lead in Air ?. . One of the. earliest and the most extensive study of the size distribution of? atmospheric lead aerosols was conducted by Stanford Research Institute under ILZRO sponsorship (1),(2)* This study utilizeda Goetz aerosol spectrometer to determine the size distribution of lead aerosols at sites in Los Angeles, Chicago, Philadelphia, Cincinnati, San Francisco Bay area along with remote sites in Oklahoma and Arizona* The results indicated that the size diatribe utions of lead at the different locations were fairly constant (mass median \ equivalent diameter of 0*12 micrometer to 0.31 micrometer) even when remote locations were compared with urban areas* Recently, however, ;Lawther, et. K. ?; al.' (3) have commented that sampling devices dependent upon inertial impaction,^ such as the Goetz aerosol spectrometer, mAy underestimate the size pf normally aglomerated atmospheric lead particulate^* Also, because,. of the irregularity * of shape of the particles and the greater influence of diffusion rather than .v. inertial forces on the movement of. particles of this size, models relating . mash median equivalent diameter to lung deposition may not apply to atmos~;> V pheric lead particles* The recently completed f,A Survey of Air and Population Lead Levels in Selected American Communities11, better known as the "Seven-City Study" provides much v-? information of the concentrations of lead in the atmosphere of urban and non- ? urban areas in the United States (4). This study was carried out by the - Kettering Laboratory of the University. .QfJCincinnati and was jointly sponsored by the Agencythe American Petroleum Institute and ILZRO* . .. . 1 DUP050057917 Air lead concentrations were measured continuously for one year at 59 sampling sites located in and hear Cincinnati, Philadelphia, Los Angeles, Washington* New York, Chicago, Houston and Los Alamos* The yearly means and confidence' * intervals of? lead concentrations are summarized for each station in Table 1. The lowest mean annual atmospheric concentration occurred at a site in, the" desert community of Los Alamos, New Mexico (0.14 jig/nr*) and the highest mean annual concentration was found at an urban site in Los Angeles (4.55 pg/ia?). The data for the non-urban area in Okeana and Los Alamos represent an almost "background" situation while the data from Los Angeles represent levels found in an.urban situation with a very heavy concentration of automobiles along with atmospheric and topographical factors conducive to the achievement of high levels of air pollution. ; One of the purposes of the Seven-City Study was to determine if a change in % concentration of airborne lead had occurred at a series of reference Ideations'^ * designated in 1961-62 (5)> v< f ". `. The data showed higher lead concentrations at most of the sampling sites in ^ . f the later study. However, data obtained from the U. S, Environmental Pro tection Agency National Air Surveillance Network (NASN) cast doubt on our yy /,o'V;- ability to conclude that there has been an upward trend in airborne lead . ', ; ^ concentration over the 8-year period. -Figure 1 shows the NASN data for the v : years 1960-69 at the same site in Los Angeles as one of the 11Three Cityy.: Survey" and "Seven-City Study" sites. Obviously the year-to-year variability r in air lead concentrations, as demonstrated by the NASN data, preclude the possibility of defining a trend, either upward or downward, with only two points. , ' Lead in Crops The impact of airborne lead concentrations on foods was investigated in another major program sponsored by ILZRO and conducted by the University of California ; at Riverside (6),(7) and (8). The lead content of 27 varieties of consumer crops and plants was determined in samples collected at various distances;from highways with heavy traffic. The results of the study demonstrated that leed.::y ;V.-;y` accumulations on plants were caused principally by aerial deposition and not* - \ to any great extent, by absorption of lead from soil. Increases of leadihy surface soil were restricted to distances from the highway of less than 50 . i- meters and occurred only in the surface (0 to 7.5 cm. depth). Lead 'in soil t>yyy. was not related to distance from* the highway at depths in the soil mrofile of .'.y yy 50 cm. it was concluded that lead froii automobile exhaust exists aiSstinple; f v >v surface deposits on vegetation, that the highest lead concentrationslin veg-. etation were those plant portions which have the highest surface to volume ratio, and that the concentration of lead on vegetation is a function of distance from the highway. Despite the influence of proximity to t he highway on the iead content on croA ^, , the lead content of the portions of crops normally eaten were generally below 1.0 /ig/Gm on a`fresh weight basis. The few exceptions were grown quite close to the roadways and in nearly all instances washing reduced the lead content y to below 1 /ig/0m. >. 2 DUP050057918 A number of fresh and frozen foods and one canned food tomatoeswere purchased from markets in the study area. The results of this survey are shown in Table 2. It was concluded that these foods have estimated normal values and consequently are not considered to represent a significant source of lead contamination. Lead in Water In- the field of water pollution ILZROVs only major project has been to define the current practices for the control of lead effluent from battery manufacturing* A survey of lead-acid battery plants, varying . in size of production from 250 tcj greater than 12,000 batteries per day wad conducted* The survey indicated that cheMcal precipitation . with hydrated lime or sodium hydroxide was the most common treatment practice* It was concluded that jlead concentrations in waste water from battery manufacturing plants can be reduced to 1.0 ppm with only nominal expense and care; the concentration can be reduced to 0*5 ppm kith good design and operation; and concentrations of 0.3 to 0.2 ppm can be obtained only with very good design and extraordinary careful operations. Biological Effects of Exposure to Lead Several projects have been sponsored to determine the effects of lead on biological organisms. The scope of these various projects has spanned a range from the subcellular effects of lead to effects on the organism of our major concern, man. j Subcellular and Cellular Effects : The purpose of these projects have been twofold: (1) to provide a better understanding of the mechanisms of lead*s toxicity and (2) to determine the concentrations of lead required to produce biological effects. The effects of lead on certain enzymes, nerve cells and im mature red blood cells (reticulocytes) have been investigated. One study has been aimed at the determination of the effect of lead on certain enzymes (10), (11). Though lead is known as a sulfhydryl enzyme r inhibitor, it's affinity toward monovalent sulfur ligands in proteins and enzymes is actually considerably smaller than that of many other elements, e.g., silver, mercury, or cadmium. Concentrations of 10 to 10*"^ M lead far.in excess of concentrations present in tissues and body fluids in states of lead intoxication in vivo, are required to inhibit mono- thipl sulfhydryl enzymes. j Figure 2 shows that lipoamide dehydrogenase, an oxidative, FAD-dependaht, di-thiol enzyme, was found to te inhibited by lead at lower concentrat ions in vitro. Fifty percent inhibition was caused by 6*5 x 10"^ M lead, but no inhibition was noted at a concentration less than 1.0 X 10 M. This inhibition was reversed by EDTA and partial protection was afforded ` by adding substrate and co-enzymes to the medium after lead was added, suggesting that lead binds to the active dithiot center of lipoamide dehydrogenase. 3 DUP050057919 In another study the effect of lead on mitochondrial oxidative phosphorylation was investigated-. (12). It was found that the threshold of beef heart mlto- ehonodrial respiration is 24 x 10~& M lead and 119 x 10. M lead is required to completely shut off mitochrondrial oxidative activity. It was found that . the concentration of lead required to inhibit oxidative phosphorylation.was much reduced by the absence of inorganic phosphate in the incubation medium,. Since intracelluar inorganic phosphate is present in tissue, inhibition of mitochondrial respiration requires relatively high concentrations of lead. Through the use of a recording Fragilograph, it was found that lead-incubated human red cells* were divided into osmotically sensitive and osmotically resistant populations. This differentiation of red cells, however, occurred only After incubation with very high lead concentrations (10~^ and 10r^ M of lead) which are well above normal physiological levels. In another study at the cellular level it was shown that , unlike mercuric and thallium Salts, lead acetate produced no morphological damage to tissue cultures of newborn rat and mouse cerebellum, spinal cord, and spinal ganglia (13). The highest concentration of lead acetate tested was 10*" M. There was, however, a constant and marked degenerative reaction of macrophages followed by hypertrophy of glial cells, ' It was further found that there was no evidence of absorption of lead by the nerve cell in vitro from a leadcontaining medium. Heavy uptake was, however, observed in macrophages, menigeal cells, and to a less extent by the glial cells. This different absorption of lead may explain the differences in the morphological damage effects noted. Further studies examined the effect of the addition of sera from lead poisoned humans and laboratory animals to mature myelinated cultures of the nervous system. The exposure produced partial or complete degeneration and breakdown of the myelin sheath, which in most instances was accompanied by.complete preservation of the nerve cell bodies and axons, but not of the glial cells.V From the in vitro work it appears that lead has no direct effect on myelin and nerve cells, but rather than the excessive absorption of lead by mesenchymal tissue and the moderate absorption by glial cells is responsible for the break* down of myelin sheath. This work, however, produced two unexplained but intriguing results: * * 1) The effects of sera from lead| poisoned animals and patients on myelinated nervous system Cultures was not correlated to the actual concentration of lfead in these sera. Therefore, it is possible that the observed myelin disturbances was not due to the actual presence of lead hut rather to other = substances secondarily present in these sera. 2) Lead appeared to facilitate the development and differentiation of nervous tissue in young cultures, although the mechanism and meaning of this observation is not clear. Though the above investigations of the celluar and sub-ceiluar effects of lead were undertaken to provide a better understanding of the toxic mechanisms of lead, one study had a, perhaps, more direct purpose. Microorganisms from an actlviated sludge plant were used to determine inhibitory effects of lead on 4 DUP050057920 secondary sewage treatment plantp (9). The results of the study which included turbidity, BOD, and bacteria count experiments, indicated that lead in concentrations ranging from 0.1 to 20 ppm has little, if any effect on the growth of the microorganisms during the usual sludge digestion period. A lead concentration of 100 ppm definitely inhibits the activated sludge microorganisms and could completely disrupt an activated sludge process. Lead in concentrations of 50 ppm appears to inhibit the growth rate but probably would not upset an activated sludge system* Effects of Lead on Animals Because of the practical difficulties in conducting some types of experimental work on humans, several projects have been aimed at defining the effect of lead on laboratory animals, in one such study, rabbits and guinea pigs were exposed for their entire lives (periods up to 4 years) to urban air. This air contained a mean concentration of 2.46 ug/m^ (14); (15). Another group of animals was exposed for an equivalent length of time to air which has been passed through prefilters and absolute filters. The lead content of the liver, lung, kidney, heart, gastrointestinal tract, pelt, spleen, muscle and bone was determined. Of these, only bone showed a statist tically significant difference in lead content with that of both the rabbits and guinea pigs being higher than their respective controls. . Mortality and longevity were identical in the exposed and nan-exposed colonies and no effect on rate of gaining weight was attributable to exposure. Exposure of rats to 10 ugPb/m^ continuously and intermit* . tently in an inhalation chamber for a year produced similar results (16), (17). Animals were sacrificed periodically and lead content of the total body, bone, kidney and blood was determined. It was determined that lead in blood and solft tissue reaches equilibrium much more rapidly on continuous exposure than does bone and, consequently, total body lead. ; content. In yet another experiment rats arid monkeys were exposed to an average ' v ; of 21.5 ugPb/m^ ih a chamber for `a twelve month period (18). Figure 3 A shows the blood lead concentration of the animals exposed to lead versus unexposed animals both during the exposure and post-exposure periods. It is clear that the exposed animals clearly showed an elevated blood lead- concentration in both monkeys and rats though the magnitude of the difference is apparently species dependent. In both species, however* . the blood lead concentration appeared to stabilize after 4 months of : exposure indicating an approach to an equilibrium condition.. 1\ An increase in the lead content of tissues other than blood also occurred in animals as a result of exposure to airborne lead. Measurements were' made in the rats after six and twelve months of exposure and. also in some rats six months after exposure was terminated. In bone, kidney, and liver tissues of exposed ratsf the concentration of lead was ten or more times as great as that of control animals. There was .less increase, in lung tissues. There were no striking differences between the levels found at six and twelve months as; shown in Table 3. This indicates that a stable condition had been attained by 6 months in the rats, but is in some disagreement with earlier data which appeared to show a continuing : increase in bone lead and total body lead content in rats during 12 months exposure to lOug/m^ (16). j DUP050057921 Delta**aminolevulinic acid dehydrase (Al A-D) activity in red cells was deter mined but . the natural level of activity in the rhesus monkey? is apparently too low to permit meaningful results. Natural levels of activity in.rats, however, were higher and it was shown that after 12 months exposure, the activity of . this enzyme in red cells was only about one-third that of the unexposed controls. .The effect was reversible/however, and within one month after termination r of exposure, the activity of ALA-D in red cells had returned*to normal. Despite the depression of the ALA-D activity in red cells of exposed rats, there was no difference between exposed and control animals in ALA-D activity in liver and brain tissues obtained at the twelve month autopsy. Examination of the animals also included routine blood studies selected to disclose the general well-be^ag and clinical status of the animals. Routine clinical chemistry examinations of the* rats and monkeys did not reveal any' deviation of either the control or exposed groups with regard to hematology and histopathology. Both groups, then(appeared to be equally healthy with ; the exposed animals seemingly unaffected in any detrimental way by exposure to 21.5 for a twelve month period. v'^: Another study was directed at determining the effect of lead exposure on / neurological behavior in rhesus monkeys (19). Animals were divided into the following dose groups receiving the following daily dosages of lead: 0,0.05, 0.50, and 5.00 mgPb per kilogram of body weight. During thirty-three months of testing, total blood lead, blood!ALA-D activity and urinary delta- aminolevulinic acid (ALA) were determined to monitor, the level of systemic intoxication. In add!ton, two standarized hehavorial tests, a conditioned / behavior performance test and a delayed response performance test were . conducted weekly; No performance decrement was shown in any of the exposure.; groups in either test.. The only significant indicators of lead intoxication. ' were elevated blood lead and urinary ALA, as expected. Red cell ALA-D . Activity was measured, but as indicated previously, is naturally top 'low'to serve as a useful indicator in this species. All other physiological . /'/../'/V pwrameters yielded nb. evidence of toxic effects due to chronic lead ingestion > even at. a level of 5 mgPb/kg body weight. It is of interest. that this ; " ''; / dosage produced a perhaps, unexpectedly, low stable blood lead concentration ; ;pf 40-60 /ig/100G afteif reaching in excess of 80 /lg/lOOG early in the .experiment.. .; ' . Effects of Lead oh Nan ` Several ILZRO projects have been aimed| at defining the impact of lead directly ./ on man. One experiment utilized .human! volunteers exposed to airborne lead . . ' ; in a respiratory chamber, Su^jpcts wet^exposed tolO^g/m^and 20jig/m3' a '*, of lead in air for increasing/lengths time during successive 16 week periods. . ! The subjects1 intake of lead in food and drink and output in urine and feces-' were carefully measured. A slight elevation of blood .leadand urinary'lead.;*^*>*/' was noted in the subject exposed to 10jjig/m? but this was attributed; to an / unexplained increase in his intake of lead in food during the: latter part of; ' the exposure period. Two subjects exposed to 20 jig/m?. for as long a$ 84 hours . / per week for 16 weeks produced/equivocal results. It was apparent that/the practical limitations as to the'number of subjects available and the fact that exposure, while lenghty, was required to be intermittent prevented a true ; , ; . assessment of the effect of the affects of continuous exposure to.these` f v concentrations of lead in air; / 1 f 6 DUP050057922 tte were fortunate, however, in that, with the co-sponsorship of the American i?etroleum Institute and the U.S. Environmental Protection Agency, we.were able tq initiate a new project in which it wad possible to expose 14 hunuin; volunteers simultaneously and almost continuously (23 hours/day) for tip to 4 months v<18), (20). ; JThe mean concentrationlo| airborne lead in the chamber was ;LQf. 9 i id 1 jUjj;/m- ad determined by daily sampling and analysis. In addition there vdS some indication that an additional 10-15% lead passed the particulate filter. While -thi/ti. lead.whs not characterized, it may have been organic lead which wad'.not chahged..to lead oxide particulate in the particulate generating flame and. Which^becatiii of the recirculation of air in the chamber, may have built ufr^ver/'ihb, C df the exposure period. Studies of particles collected, ort electron microscope grids indicated that the mean geometric diameter of the particles produced, in the f|ame ^as about 0.05 micrometers. of lead in the blood of eight men who remained. in the study throughout the four month exposure period and 16 week post exposure 4 period is shown in figure It is clear that exposure to this concentration oflear in air, under, these Conditions, produced a significant elevation of lead in the. blood Of the exposed, subjects> The increase in blood .lead . . concentration appeareijgto be limited to the first 10 weeks of exposure suggesting that a etablG situaHpi^$rith regard to bldod lead had been attained within . the limits of the experiment. / Tnb activity of rbd cell ALA-D was also estimated in both exposed. end unexposbd men. A significant reduction in the activity of ALA-jb inthe;red- cells of. these meti Vas nctad Shortly after exposure; commenced and was maintained throughput the exposure period. Orinary excretion of lead was also elevate^ in exposed .. tt'.is noteworthy that the volunteers^ showed a significant weight gain during the exposure pferiqjf* Whether this increase in weight was due to inactivity ;. while in th^ chamber^ to greater food intake, or to both is hot.clear, fecal excretion of lead from the exposed mbn was* higher than from controls, however, Suggesting that food intake iuay havejbeen jjt factor. Whether or not greater !; >|Spd intake by the exposed;iitfoup may* have,Tin-part, |peounted.for the increase f iH; blood lead concehtratibh is alyo not clear. .Other .studies of,the human volunteers* which included comprehensive studies of serum chemistry, hematology, urinalysis * and excretion pf heme predjirsers, . including AtAi. ittrfche urine were normal and were unchanged during exposure; At. present a similar experiment with a lower exposurelevdl has been completed. However, the data have not yet been fully analyzed;. " ~ .:*r' > |n interpreting, the results Vtf-? these'experiments one must be mindful of the;". Comments of .fcawther, et: al(3) regarding experiments of this type. It lias ^een pointed out that electron micrographs of atmospheric lead particles show them to be quite different from particles produced burning tetraetji^ lead iji a propane flame, which was the me^ns of generating lead particles. in; all. |he inhalation chamber project*; It;may be -that exposure ,torl!the^ more-;or; less . , regularly shaped particles in these experiments, essentially .OnacCis^ * by extraneous `'smpky11 material may create exaggerated situation with regard p iuiig depoffition and absorption. 7 DUP050057923 The final data which will be discussell are the biological data arising from the "Seven-City Study." Blood samples were obtained from groups of volunteers in each of the eight cities in which air-lead measurements were made. Total fecal output was also obtained from some of these women in each cityv In add ition^ smoking history was obtained. ` With the exception of some volunteers in Los Alamos, and in the case of special studies in Cincinnati, Philadelphia and Alpine County, California, volunteers were exclusively women. In order to be included in the study the women'must have resided for at least 5 years within about a 1 mile radius of one or more of the air sampling stations. Women were selected because it was believed that they would be less likely to be . occupationally exposed to lead and would be more likely to spend a greater portion'of each day in and near their homes than men, i.e., within a one mile radius of one or more of the air sampling stations. The mean blood lead, fecal lead data.,, and the annual mean air lead concentration at the station(s) nearest their homes are shown in Table 4, it was found that smokers exhibit a statistically significant greater blood lead concentration than non-smokers and previous smokers. However, there was no significant regression of age on blood lead concentration (age 20 to 79) of fecal lead content on blood lead concentration or of air lead concentration and blood lead concentration from 0.17 to 3.39 ug/m3. Figure 5 shows the lack of a relationship between air lead concentration and blood lead concentration from, 0.17 to 3.39 ug/m3* In addition an attempt was made to determine if the blood lead, concentration of selected populations had changed over the period from the Three Cities Survey to the Seven City Study. In Cincinnati, 45 policemenv showed a mean blood lead in May, 1962 of 23.5 jig/lOPG and in March, 1971 they showed a mean of 17.9 fig/wr9 a statistically significant decrease, (P^O.OO). in Pennypack, Pennsylvania, the mean blood lead concentration of 23 persons in April 1961 was 12.4 pg/100G and in April was 13.8 *ig/100Gf not a statistically significant change (P0.09). i Another special survey conducted in Alpine County, California--a rural mount ain area--showed a two month air lead; concentration of 0.03 jig/m . The average blood lead concentration of 37 males and females, in 1961 was reported as lljutg/ 100G, while the mean blood lead concentration of 39 different persons in 1971 was 17.7/ig/100G. While this was an apparent statistically significant difference (P*0.002), it was concluded that the 4961 Alpine County blood lead concentration, which cons tituted the lowes t point of .(the controvers ial Goldsmith-Hexter regression was in error. This conclusion was ba^ed on the belief that neither a higher. nor lower air lead concentration prevailed in Alpine County in 1961 than in 1971 and that the 1961 Alpine County blood leads were determined by a labor- atory which exhibited highly erratic results (21). \^ . Summary It is apparent that raan*s use of lead has caused a generalized ecological translocation of lead. Further it has been shown that lead, at higher concentrations than to which the population is continuously exposed, does cause an increase in blood and bone lead concentration in man and animals. There is some evidence that lower airborne concentrations may cause some elevation in the bone lead concentration of laboratory animals. * On the 'other hand, there is no evidence that harmful effects of lead occur at other than concentrations well in excess of those to which the public is continuously exposed. v ; 8 DUP050057924 ILZRO's research into the environmental impact of lead Is continuing and hopefully It will continue to provide useful data of benefit to both the industry and the general public. 9 DUP050057925 References 1.; ILZRO Project, Lh-69, Variations of Atmospheric Lead Concentrations tod Type with Particle Size, Stanfotd-Research Institute, Monlb Park, . ; California, Final Report, November 1, 1963, 2. * Robinson, E. and Ludwig, F.L.: Particle Size Distributions of Urban Lead Aerosols,. J. Air Poll* Con, Assoc*, 17:664-8, 1967* -'\3*~ Lawther, P.J., et, al*: Airborne Lead and its Uptake by inhalation, Preprint of paper presented at a conference on '/Lead in the Environment, Zoological Society of London, Janqary 27, 1972. 4; . ILZRO Project, LH-115, Seven-City Study (Survey of Air and Population Lead Levels in Selected American Communities), University of Cincinnati, Ohio, Progress Report, April, 1972. 5.' The Working Group on Lead Contamination: Survey of Lead in the Atmosphere of Three Urban Communities, U.S.P.H.S., .Publication No. 999-AP-12. 6.- . ILZRO Project LH-109, Relationship Between Lead in Motor Vehicle Exhaust and Consumer Crops, University of California at Riverside, California, Final Report, February 20, 1970* 1 7* Schuck, E.A. and Locke, J.K.: Relationship of Automotive Lead particulates to Certain Consumer Crops. Environmental Sci. Technoi. 4: 324-30, 1970. j v: ; 8. Page, A.L., et* al.: Lead Quantities in Plants, Soil, and Air Near Soimej iajor highways in Southern California. Hilgradia, 41:1^31, '197.1,1 t 9. ILZRO Project LH-188, Evaluation of Lead Plant Wastewater Treatments Methods, IIT Research Institute, Chicago, Illinois, Final Report, February 15r 1972* . < * . , . : ' 10. ILZRO Project LH-94, Biological Basis of Lead Intoxication, Harvard University, Boston, Massachusetts,! Progress Report,. 11. Ulmer,. D.D. and Vallee, B.L.; Effects of Lead on Biochemical Systems. Paper presented at 2nd Annual Conference yn Trade Substances^ in , Environmental Health, Columbia, Mb. , July 16-18, 1968'. 12.. ILZRO Project LH-159, Effect of Lead on the Respiratory Activity of irythopoietic Cells, Ohio State Research Foundation, Columbus, Ohio, : V Pinal Report, June, 1971. ` . ' \'v /' 13. ILZRO Project LH-I17, Effects of Lead on Tissue. Culture of the - Central Nervous System, Columbia University,..New York,, Progress Report,;; February, * 1967 . '/ /v- DUP050057926 14* ILZRO Project LH-118, Lead Burdens in Laboratory Animals, Wayne State University, Detroit, Michigan, Final Report, February 3, 1969, 15 Smith, R.G., et. al.: Study of lead Levels in Experimental Animals. Environ, Sci. Teehnol. 4:333-8, 1970. IS, ILZRO Project LH-110, Rate of Uptake of Lead by Rats During Continuous inhalation of Lead Oxide Particles, University of Cincinnati, Ohio, Progress Report, April 8,.1968.1 17. ILZRO Project LH-111, Relative Quantities of Lead in Rats Following Continuous vs. Intermittent inhalation of Lead Oxide Particles, University of Cincinnati, Ohioj IProgress Report, April 8, 1968. 18, . itZRO Project LH-151, Atmospheric Contaminants in Animals and Man, Albany Medical College, Albany, Mew Xork, Final Report (Part I), , June, 1972.- # Is. iLZRO Project LH-114, The Effects of Chronic Plumbism on neurophysiological Behavior in the Fhesus Monkey, Industrial Bio-Test Laboratories, Inc, , ^lorthbrook, Illinois, Progress Report, August 24, 1972. 20 Griffin, T.B. et. al.: A Comparative Study of Inhalation of Lead Particulates in Animals and Man, Paper presented at the 11th Annual Meeting, Society of Toxicology, Williamsburg, Virginia, March, 1972. 21 Tepper, L.B.: Letter to L, Carothers, U.S, Environmental Protection Agency as part of testimony before EPA Hearings on Fuels and Fuel Additives,, . 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H P <2 DUP050057928 TABLE 2 , \ -- : LEAD CONTENT OF VARIOUS FRESJf AND FROZEN FOODS PURCHASED FROM LOCAL MARKETS type of food - ;Pb Content* As receive*! pgPb/gm Water wa Freskfoods fceiery /Collards 'Spinach ' ' Romaine lettuce Outer leaves . : , / inner leaves ' : 'Artichokes . outer leaves inner leaves broccoli flower - /stalk ' .- Carrots,. peels V inner portion Potatoes feeels ? d inner portion :t>0as ; i^ods with peas pods Frozen foods ./Deans Peas Carrots Spinach Strajvberries : Potatoes . 0.02 ' 0.50 JO. 25 1 0.18 0.01 0.04 B.D. 0.30 0.04 0.06 B.D. 0.11 0.02 0.02 0.02 . p.D. B.D. b.D. * 0.07 0.02 0.01 . '' B.D. 6.25 040; 0.10 B.D. 0. 04 B.D. 0.19 0.04 . 0.05 B.D. 0.02 Q. 02 B. D. ' ?-P. --* ' Results are expressed as pg Pb per grain of Jifesh or frozen vegetables as received. B.D. indicates below the limit of detectability, or less than 0.01 jxgPb/gm. . \ DUP050057929 tABLE 3. AVERAGE TISSUE 1EVE1S WITH STANDARD DEVIATIONS OF LEAD Group bone Tissue Kidney Liver ' Vi ' * Lung 6 Mouths Expo6uA& Conttol fexposed 0.36 +0.12 4.4? + 1,14 0.19 + 0.04. 2.30 + 0.47 0.24 + 0.06 3.63 + 0,98 0.11 + 0.04 0.72 i 0.53 12 Months ExposuAz-' Control` Exposed 0.43+6.14 5,13 + 1.36 0.21 + 0.04 2.03 + 0160 - 0.27 + 0.06 2.83 +0.53 0.12 +M 6. .- 0. 3 0.43 + 6.17 6 Uotvtiu Recover * Control Exposed 0.50 + 0.19 5.42 + 1.09 0.22 + 0.03 0.45 + 0.15 0.27 + 0,07 0.14 0.05 0.71 + 0.20 0.14+6.05 DUP050057930 0$ 2 1 r uI I<UD J8S rH gft Ocs Q MEAN AIR* BLOOD AND FECAL CONCENTRATIONS--SEVEN CITY STUDY ? Feces were collected fro m !80 women at each location. 5I s 1 si t. s* >* II l' to I *-> DUP050057931 MEAN ANNUAL AIR LEAD -jig/m* DUP050057932 LEAD CONCENTRATION, M jjg Pb fOO mi BLOOD/ FI0URr: 3 BLOOD LEAD OF ANIMALS EXPOSED TO AIRBORNE LEAD DUP050057934 BLOOD LEAD OF MEN EXPOSED TO 10.9 jig /c u m AIRBORNE LEAD jug Pb / 100 ml BLOOD LEAD fH AIR JJG/M LEAD IN BLOOD MG/100 G bb m * tT RM> LOS ALAMOS o k k an a HOUSTON PORT WASHINGTON LOMmi*"'**- # RITTENHOUSf SQ. BRIDGEPORT GREENWICH VILLAGE o PASADENA O DUP050057936