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0277 Lead and compounds (inorganic); CASRN 7439-92-1
Human health assessment informat ion on a chemical substance is included in the IRIS database only after a comprehensive review of toxicity data , as outlined in the IRIS assessment development process . Sections I (Health Hazard Assessment s for Noncarcinogenic Effects) and II (Carcinogenicity Assessment for Lifetime Exposure) present the conclusions that were reached during the assessment development process. Su pporting information and explanations of the methods used to derive the values given in IRIS are provided in the guidance documents located on the IRIS website

. STATUS OF DATA FOR Lead and compounds (inorganic) File First On-Line 03/01/1988



### _I. Chronic Health Hazard Assess ments for Noncarcinogenic Effects _I.A. Reference Dose for Chronic Oral Exposure (RfD) Substance Name — Lead an d compounds (inorganic) CASRN — 7439-92-1 Section I.A. Last Revised — 07/08/2004 In general, the oral Reference Dose (RfD) is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily exposure to the human population (including sensitive subgroups) that is likely to be without an ap preciable risk of deleterious effects during a lifetime. The RfD is Search IRIS by Keyword

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 Reference Dose for Chronic Oral Exposure ( RfD )

Category (section) Status Last Revised Oral RfD Assessment (I.A.) discussion 07/08/2004 Inhalation RfC Assessment (I.B.) no data Carcinogenicity As sessment (II.) on-line 11/01/1993 

## Integrated Risk Information System file://rtifile02/ehe/Projects/0213199-EPA_SPPD_(Base)/0213199.000.003- Pulp_Paper/Technical_Record/Dockets/Sector%2 0EPA-HQ-OAR-2007-0544/Promulgation/Ready%20to% 20u p load/039_IRIS_Asst_Lead_and_Cm p ds.mht Last u p dated on Frida y, Jul y 20 , 2012 

## Pa g e 1 of 12 Lead and compounds (inor g anic) (CASRN 7439-92-1) | IRIS | US EPA

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...based on the assumption that thresholds exist for certain toxic effects such as cellular necrosis and is expressed in units of mg/kg-day. Plea se refer to the guidance documents at http://www.epa.gov/ir is/backgrd.html for an elaboration of these concepts. Since RfDs can be derived for the noncarcinogenic health effects of subs tances that are also carc inogens, it is essential to refer to other sources of information concerning the carcinogenicity of this chemical substance. If the U.S. EPA has evaluated this substance for pote ntial human carcinogenicity, a summary of that evaluation will be contained in Section II of this file. __I.A.1. Oral RfD Summary Health effects associated with exposure to in organic lead and compounds include, but are not limited to, neurotoxicity, develo pmental delays, hypertension, impa ired hearing acuity, impaired hemoglobin synthesis, and male reproductive im pairment. Importantly, many of lead's health effects may occur without overt signs of toxicity. Lead has particularly signific ant effects in children, well before the usual term of chronic exposure ca n take place. Children under 6 years old have a high risk of exposure because of their more freq uent hand-to-mouth behavior (Centers for Disease Control and Prevention (CDC), 1991: http://www.cdc.gov/nceh/lead/public ations/books/plpyc/contents.htm ). EPA considered providing an RfD for inorganic lead in 1985, and concluded th at it was inappropriate to develop an RfD, as documented onlin e in the following statement in 1988: A great deal of information on the health effects of lead has been obtained through decades of medical observation and scientif ic research. This information has been assessed in the development of air and water quality criteria by the Agency's Office of Health and Environmental Assessment (OHEA) in support of regulatory decision-making by the Office of Air Quality Planning an d Standards (OAQPS) and by the Office of Drinking Water (ODW). By comparison to most other environmental toxicants, the degree of uncertainty about the health effects of lead is quite low. It appears that some of these effects, particularly changes in the levels of certain blood enzymes and in aspects of children's neurobehavioral developm ent, may occur at blood lead levels so low as to be essentially without a threshold. The Agency's RfD Work Group discussed inorganic lead (and lead compounds) at two meetings (07/08/1985 and 07/22/1985) and considered it inappropriate to develop an RfD for inorganic lead. EPA is not providing a review of current literature co ncerning the health effects of lead at this time (June, 2004), given the ongoing effort of the CD C to re-evaluate the blood lead level of concern (CDC, 2004: http://www.cdc.gov/nceh /lead/spotLights/changeBLL.htm ). A screening-level review of the more recent toxicology literature pertinent to noncancer effects associated with oral exposure to Lead and compounds (inorganic) was conducted by an EPA contractor in September 2002, and identified one or more significant new studies si nce the 1985 assessment. IRIS users may request the references for those studies from th e IRIS Hotline at hotline.iris@epa.gov or (202)566-1676. Current knowledge of lead pharma cokinetics indicates that risk values derived by standard procedures would not truly indicate the potential risk, because of the difficulty in accounting for pre-existing body burdens of lead. Lead bioaccumul ates in the body, primarily in the skeleton. Lead body burdens vary significantly with age, health status, nutritional state, maternal body burden during gestation and lactat ion, etc. For this reason, and because of the continued apparent lack of threshold (CDC, 2004: http://www.cdc.go v/nceh/lead/spotLights/changeBLL.htm ), it is still inappropriate to develop re ference values for lead. The purpose of this 2004 update is to assist IRIS users in finding relevant risk information and risk assessment methods that have been developed with in EPA for media-specific applications. Most of these methods focus on blood lead levels, throug h the development of several media-specific lead exposure levels for risk management and regulato ry purposes. Further information on these lead 

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...risk assessment methods and tools is described in Section 1.A.4. __I.A.2. Principal and Supporting Studies (Oral RfD) Not applicable. __I.A.3. Uncertainty and Modifying Factors (Oral RfD) Not applicable. __I.A.4. Additional Studies/Comments (Oral RfD) As noted above, EPA is not providing a review of current literature at this time. In addition to information developed by CDC and the Agency for Toxic Substances and Disease Registry (ATSDR), described below, EPA has developed a number of le ad exposure limits in support of regulatory decision-making, and has developed methods to assessrisk from lead in situations not covered by these limits, also described below. The CDC identified 10 μg/dL as the blood lead le vel of concern in childre n in their 1991 report "Preventing Lead Po isoning in Young Children" (http://www.cdc.gov/nceh/lead/ publications/books/ plpyc/contents.htm ), and provided risk management options for categori es of blood lead levels higher than 10 μg/dL. In view of the fact that health effects were an d continue to be identified belo w the level of concern, the CDC convened an Advisory Committee on Childhood Lead Poisoning Prev ention to consider whether the level of concern should be changed. The Advisory Committee's progress reports can be found at http://www.cdc.gov/nceh/lead/ACCLPP/acclpp_main.htm . At this time, CDC has not changed the blood lead level of concern for three reasons (March 23, 2004, http://www.cdc.gov/nceh/lead/ spotLights/changeBLL.htm : "No effective clinical interventions are known to lower blood lead levels for children with levels less than 10 μg/dL or to reduce the risks for adverse developmental effects." "Children cannot be accurately classified as having blood lead levels above or below 10 μg/dL because of the inaccuracy i nherent in laboratory testing." "Finally, there is no evidence of a thre shold below which adverse effects are not experienced. Thus, any decision to establish a new level of concern would be arbitrary and provide uncertain benefits." In addition to the ongoing CDC effort, the ATSDR is mandated by Congress under CERCLA (1980) and SARA (1986) to develop toxicological profiles for all hazardous waste sites on the National Priorities List (NPL) (PB/99/166704, NTIS PB-99-66704; http://www.atsdr.cdc.gov/toxprofiles/tp13.html ). Lead is the most common toxic metal at these sites. The ATSDR Toxicological Profile for Lead was last updated in 1999. EPA has developed a number of lead exposure leve ls in support of regulatory decision-making, which limit the amount of lead that can be pr esent in various environmental media. Under the National Primary Drinking Water Regulations, EP A established a Maximum Contaminant Level (MCL) for lead in drinking water due to any source. Un der the Toxic Substances Control Act (TSCA) as amended by the Residential Lead-B ased Paint Hazard Reduction Act, EPA established standards for lead in paint, house dust, and outdoor soil. The following links provide more information: Action level for lead in drinking water: http://www.epa.gov/safewater/mcl.html#mcls Regulation for lead in paint housedust, and outdoor soil: http://www.epa.gov/oppt/lead/pubs/leadhaz.htm National ambient air quality st andard: http://www.epa.gov/ttn/naaqs/ 

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...Note that additional relevant info rmation will be found by following links provided at these websites, such as dose-response relationships relating blood lead levels to change s in IQ (children) and hypertension (men). Due to the likelihood of simultaneous exposure to various sources of lead, EPA recommends a caseby-case evaluation of the relative contributions of relevant lead exposures in a particular setting. The Superfund Program has guidelines for identifying lead-contaminated soil (http://www.epa.gov/superfund/p rograms/lead/products.htm ), and facilitates site-specific risk assessments at contaminated waste sites on the Na tional Priority List, where the major sources of soil contamination are activities su ch as disposal of mining and ma nufacturing wastes contaminated with lead and deposition of lead from air, ratherthan presence of lead-b ased paint in residences (see: http://www.epa.gov/superfun d/programs/lead/trwhome.htm ). The Superfund Program uses the Integrated Exposure Uptake Biokinetic (IEU BK) Model for Lead in Children. The IEUBK Model provides estimates of the risk of elevated blood lead associated with particular combinations of relevant sources of lead exposure . This interactive mode l is described in more detail and provided for downloading at http://www.epa.gov/ superfund/programs/lead/products.htm . Note that the IEUBK model was used in direct support of th e lead-based paint regulation cited above. The Superfund Program has also developed an Adul t Lead Model, for use when lead exposures to adults, especially pregnant women, are of greater concern. This model is de scribed and provided for downloading at http://www.epa.gov/ superfund/programs/lead/adult.htm

. EPA maintains a lead resources page (http://w ww.epa.gov/opptintr/lead/pubs/resources.htm ). Links are provided to many ot her EPA offices, government ag encies, and other organizations involved in efforts to reduce expo sure to lead in the environment. __I.A.5. Confidence in Risk Values Not applicable. __I.A.6. EPA Documentation an d Review of the Oral RfD Agency Completion Date - 05/26/2004 __I.A.7. EPA Contacts (Oral RfD) Please contact the IRIS Hotline for all questions conc erning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (fax), or hotline.iris@epa.gov (email address).

_I.B. Reference Concentration for Chronic Inhalation Exposure (RfC) Substance Name — Lead an d compounds (inorganic) CASRN - 7439-92-1 In general, the Reference Concentration (RfC) is an estimate (with uncertai nty spanning perhaps an order of magnitude) of a daily inhalation exposu re of the human population (including sensitive subgroups) that is likely to be without an apprecia ble risk of deleterious effects during a lifetime. The RfC considers toxic effects for both the resp iratory system (portal-of -entry) and for effects peripheral to the respiratory system (extraresp iratory effects). The inhalation RfC (generally expressed in units of mg/m3) is analogous to the oral RfD and is likewise based on the assumption that thresholds exist for certain toxi c effects such as cellular necrosis. 

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...Inhalation RfCs are derived according to the Interim Methods for Deve lopment of Inhalation Reference Doses (EPA/600/8-88/066F, 1989) and subsequently, according to Methods for Derivation of Inhalation Reference Concentrat ions and Application of Inhalation Dosimetry (EPA/600/8-90/066F, 1994). Since RfCs can also be derived for the noncarcinogenic health effects of substances that are carcinogens, it is esse ntial to refer to other sources of information concerning the carcinogenicity of this chemical substance. If the U.S. EPA has evaluated this substance for potential human carc inogenicity, a summary of that evaluation will be contained in Section II of this file. __I.B.1. Inhalation RfC Summary No RfC is available. See Section I.A. for additional information. __I.B.2. Principal and Supporting Studies (Inhalation RfC) Not applicable. __I.B.3. Uncertainty and Modifying Factors (Inhalation RfC) Not applicable. __I.B.4. Additional Studies/Comments (Inhalation RfC) Not applicable. __I.B.5. Confidence in the Inhalation RfC Not applicable. __I.B.6. EPA Documentation and Review of the Inhalation RfC Agency Completion Date -- Not applicable. __I.B.7. EPA Contacts (Inhalation RfC) Please contact the IRIS Hotline for all questions conc erning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (fax), or hotline.iris@epa.gov (email address).



### _II. Carcinogenicity Assessment for Lifetime Exposure
Substance Name — Lead an d compounds (inorganic) CASRN — 7439-92-1 Section II Last Revised — II.A. introductory pa ragraph revised 07/08/2004. II.A.1 - II.D. last revised 11/01/1993 Section II provides information on three aspects of the carcinogenic assessment for the substance in question; the weight-of-eviden ce judgment of the likelihood that the substance is a human carcinogen, and quantitative estimates of risk fr om oral exposure and fr om inhalation exposure. The quantitative risk estimates are presented in three ways. The slope factor is the result of application of a low-dose extrapol ation procedure and is presented as the risk per (mg/kg)/day. The unit risk is the quantitative estimate in terms of either risk per μg/L drinking water or risk per 

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...μg/cu.m air breathed. The third form in which risk ispresented is a concentration of the chemical in drinking water or air associated with cancer risks of 1 in 10,000, 1 in 100,000, or 1 in 1,000,000. The rationale and methods used to develop the carc inogenicity information in IRIS are described in the Risk Assessment Guidelines of 1986 (EPA /600/8-87/045) and in the IRIS Background Document. IRIS summaries developed since the publication of EPA's more recent Proposed Guidelines for Carcin ogen Risk Assessment also utilize those Guidelines where indicated (Federal Register 61(79):17960-18011, April 23, 1996). Users are referred to Section I of this IRIS file for information on long-ter m toxic effects other th an carcinogenicity. _II.A. Evidence for Human Carcinogenicity Note that the National Toxicology Program's Report on Carcinogens Review Committee has recommended that lead and lead compounds be considered "reasonably anticipated to be human carcinogens" (http://ntp

- server.niehs.nih.gov/NewHomeRoc/roc11Bkgrnd2003.html ; July 2003). Also, the International Agency fo r Research on Cancer (IARC) ha s undertaken a re evaluation of lead's carcinogenicity (htt p://monographs.iarc.fr/ENG/ Monographs/vol87/index.php ). __II.A.1. Weight-of-Evidence Characterization Classification — B2; probable human carcinogen
Basis — Sufficient animal evidence. Ten rat bioassays and one mouse assay have shown statistically significant increases in renal tumors with dietary and subcutaneous exposure to several soluble lead salts. Animal assays provide reproducib le results in several laboratories, in multiple rat strains with some evidence of mult iple tumor sites. Short term stud ies show that lead affects gene expression. Human evidence is inadequate. __II.A.2. Human Carcinogenicity Data Inadequate. There are four epidemio logic studies of occupational co horts exposed to lead and lead compounds. Two studies (Dingwall-Fordyce and Lane , 1963; Nelson et al., 1982) did not find any association between exposure and cancer mortality. Selevan et al. (1985), in their retrospective cohort mortality study of primary lead smelter work ers, found a slight decrease in the total cancer mortality (SMR=95). Apparent excesses were obse rved for respiratory cancer (SMR=111, obs=41, p>0.05) and kidney cancer (SMR=204, obs=6, p>0.05). Cooper and Gaffey (1975) and Cooper (1985 update) performed a cohort mortality study of battery plant workers and lead smelter workers. They found statistically significant excesses for total cancer mortality (SMR=113, obs=344), stomach cancer (SMR=168, obs=34), and lung cancer (SMR=124, obs=109) in the battery plant workers. Although similar excesses were observed in the smelter workers, they were not statistically significant. Cooper and Gaffey (1975) felt it was possible th at individual subjects were monitored primarily on the basis of obvious signs of lead exposure, while others who showed no symptoms of lead poisoning were not monitored.
All of the available studies lacked quantitative exposure informatio n, as well as information on the possible contribution from smokin g. All studies also included expo sures to other metals such as arsenic, cadmium, and zinc for which no adjustment was done. The cancer excesses observed in the lung and stomach were relatively small (<2 00). There was no consistency of site among the various studies, and no study showed any dose-r esponse relationship. Thus, the available human evidence is considered to be inadequate to refute or demons trate any potential carcinogenicity for humans from lead exposure. __II.A.3. Animal Carcinogenicity Data Sufficient. The carcinogenic potential of lead salt s (primarily phosphates an d acetates) administered via the oral route or by injection has been demo nstrated in rats and mi ce by more than 10 

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...investigators. The most characteristic cancer respon se is bilateral renal carc inoma. Rats given lead acetate or subacetate orally ha ve developed gliomas, and lead subacetate also produced lung adenomas in mice after i.p. ad ministration. Most of these inve stigations found a carcinogenic response only at the highest dose. The lead comp ounds tested in animals are almost all soluble salts. Metallic lead, lead oxide and lead tetraalkyls have not been tested adequately. Studies of inhalation exposure have not b een located in the literature. Azar et al. (1973) admi nistered 10, 50, 100, and 500 ppm lead as lead acetate in dietary concentrations to 50 rats/sex/group for 2 year s. Control rats (100/s ex) received the basal laboratory diet. In a second 2-ye ar feeding study, 20 rats/group were given diets containing 0, 1000, and 2000 ppm lead as lead acetate. No rena l tumors were reported in the control groups or in treated animals of either sex receiving 10 to 100 ppm. Male rats fed 500, 1000, and 2000 ppm lead acetate had an increased renal tumor incidenc e of 5/50, 10/20, and 16/20, while 7/20 females in the 2000 ppm group developed renal tumors. The Azar et al. (1973) study is limited by the lack of experimental detail. The possibility of environmental contamination from le ad in the air or drinking wate r was not mentioned. The strain of rats used was not specified in the study, but the Health Effect s Assessment for Lead (U.S. EPA, 1984) indicates the rats were Wistar strain. The weight gain at 1000 and 2000 ppm was reported to be depressed, but details were not given. Kasprzak et al. (1985), in investigating the intera ction of dietary calcium on lead carcinogenicity, fed 1% lead subacetate (8500 ppm Pb) to male Sprague-Dawley rats in the diet for 79 weeks. Of the rats surviving (29/30) in this treatment grou p beyond 58 weeks, 44.8% had renal tumors. Four rats had adenocarcinomas; the remaining nine had adenomas. Bilateral tumors were noted. No renal tumors were noted among the controls. As part of a study to determine interactions be tween sodium nitrite, ethyl urea and lead, male Sprague-Dawley rats were given lead acetate in their drinking water for 76 weeks (Koller et al., 1986). The concentration of lead was 2600 ppm. No kidney tumors were detected among the 10 control rats. Thirteen of 16 (8 1%) lead-treated rats had renal tubular carcinoma; three tumors were detected at 72 weeks and the remainder detected at the termination of the study. Van Esch and Kroes (1969) fed basic lead acetate at 0, 0.1%, and 1.0% in the diet to 25 Swiss mice/sex/group for 2 years. No renal tumors developed in the control group, but 6/25 male mice of 0.1% basic lead acetate group had renal tumors (adenomas and carcinomas combined). In the 1.0% group, one female had a renal tumor. The au thors thought that the low incidence in the 1.0% group was due to early mortality. Hamsters given lead subacetate at 0.5% and 1% in the diet had no significant renal tumor response (Van Esch and Kroes, 1969). __II.A.4. Supporting Data for Carcinogenicity Lead acetate induces cell transformation in Syrian hamster embryo cells (D iPaolo et al., 1978) and also enhances the incidence of simian adenovirus induction. Lead oxide showed similar enhanced adenovirus induction (C asto et al., 1979).
Under certain conditions lead co mpounds are capable of inducing chromosomal aberrations in vivo and in tissue cultures. Grandjean et al. (1983) showed a relationship between sister chromatid exchange and lead exposure in exposed worker s. Lead has been shown, in a number of DNA structure and function assays, to affect the molecu lar processes associated with the regulation of gene expression (U.S. EPA, 1986b). 

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..._II.B. Quantitative Estimate of Carcinogenic Risk from Oral Exposure Not available. Quantifying lead's cancer risk involves many unc ertainties, some of which may be unique to lead. Age, health, nutritional state, body burden, an d exposure duration influence the absorption, release, and excretion of lead. In addition, curre nt knowledge of lead ph armacokinetics indicates that an estimate derived by stan dard procedures would not truly describe the potential risk. Thus, the Carcinogen Assessment Group recommends that a numerical estimate not be used.

_II.C. Quantitative Estimate of Carcinogenic Risk from Inhalation Exposure Not available.

_II.D. EPA Documentation, Review, and Contacts (Carcinogenicity Assessment) __II.D.1. EPA Documentation Source Document — U.S. EPA, 1984, 1986, 1989 U.S. EPA, 1989 has received OHEA and SAB review. The 1986 Air Quality Criteria Do cument for Lead has received Agency and External Review. __II.D.2. EPA Review (Car cinogenicity Assessment) Verification Date — 05/04/1988 Screening-Level Literature Review Findings — A screening-level review of the more recent toxicology literature pertinent to the cancer as sessment for Lead and compounds (inorganic), conducted by an EPA contractor in September 2002, did not identify any critical new studies. IRIS users who know of important new studies may provide that inform ation to the IRIS Hotline at hotline.iris@epa.gov or (202)566-1676. __II.D.3. EPA Contacts (Carcinogenicity Assessment Please contact the IRIS Hotline for all questions conc erning this assessment or IRIS, in general, at (202)566-1676 (phone), (202)566-1749 (fax), or hotline.iris@epa.gov (email address).



### _III. [reserved] _IV. [reserved] _V. [reserved]

_ VI. Biblio g ra p h y 

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...Substance Name — Lead an d compounds (inorganic) CASRN — 7439-92-1 Section V.I. Last Revised — 07/08/2004 _VI.A. Oral RfD References None.

_VI.B. Inhalation RfC References None.

_VI.C. Carcinogenicity Assessment References Anderson, E.L., and CAG (Carcinogenic Assessment Group). 1983. Quantitative approaches in use to assess cancer risk. Risk Analysis. 3: 277-295. Azar, A., H.J. Trochimowicz and M.E. Maxfield. 1973 . Review of lead studies in animals carried out at Haskell Laboratory - Two year feeding study an d response to hemorrhage study. In: Barth D., A. Berlin, R. Engel, P. Recht and J. Smeets, Ed. En vironmental health aspects of lead: Proceedings International Symposium; October 1972; Amster dam, The Netherlands. Commission of the European Communities, Luxemberg. p. 199-208. Casto, B.C., J. Meyers and J.A. DiPaolo. 1979. E nhancement of viral transformation for evaluation of the carcinogenic or mutagenic potential of inorganic metal salts. Cancer Res. 39: 193-198. Cooper, W.C. 1985. Mortality among employees of lead battery plants and lead producing plants, 1947-1980. Scand. J. Work Environ. Health. 11: 331-345. Cooper, W.C. and W.R. Gaffey. 1975. Mortality of lead workers. In: Pr oceedings of the 1974 Conference on Standards of Occupational Le ad Exposure, J.F. Cole , Ed., February, 1974. Washington, DC. J. Occup. Med. 17: 100-107. Dingwall-Fordyce, I. and R.E. Lane. 1963. A follow-up study of lead workers. Br. J. Ind. Med. 20: 313-315. DiPaolo, J.A., R.L. Nelson and B.C. Casto. 1978 . In vitro neoplastic transformation of Syrian hamster cells by lead acetate and its relevance to environmental ca rcinogenesis. Br. J. Cancer. 38: 452-455. Grandjean, P., H.C. Wulf and E. Niebuhr. 1983. Sist er chromatid exchange in response to variations in occupational lead exposure. Environ. Res. 32: 199-204. Kasprzak, K.S., K.L. Hoover and L.A. Poirier. 198 5. Effects of dietary ca lcium acetate on lead subacetate carcinogenicity in kidneys of male Sprague- Dawley rats. Ca rcinogenesis. 6(2): 279- 282. Koller, L.D., N.I. Kerkvliet and J.H. Exon. 1986. Ne oplasia induced in male rats fed lead acetate, ethyl urea and sodium nitrate. Toxicol. Pathol. 13: 50-57. 

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...Nelson, D.J., L. Kiremidjian-Schumacher and G. Stot zky. 1982. Effects of cadmium, lead, and zinc on macrophage-mediated cytotoxicity toward tumor cells. Environ. Res. 28: 154-163. Selevan, S.G., P.J. Landrigan, F.B. Stern and J.H. Jones. 1985. Mortality of lead smelter workers. Am. J. Epidemiol. 122: 673-683.
U.S. EPA. 1984. Health Effects Assessment for Lead. Prepared by the Office of Health and Environmental Assessment, Environm ental Criteria and Assessment Office, Cincinnati, OH, for the Office of Emergency and Remedial Response, Washington, DC. EPA/540/1-86/055. NTIS PB85- 163996/AS.
U.S. EPA. 1986a. Guidelines for Carcinogen Risk Assessment. En vironmental Protection Agency, Washington, DC. 51 FR 33992-34003. U.S. EPA. 1986b. Air Quality Criter ia Document for Lead. Volumes III, IV. Prepared by the Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office, Research Triangle Park, NC, for the Office of Air Qualit y Planning and Standards. EPA-600/8-83/028dF. U.S. EPA. 1989. Evaluation of the potential carcin ogenicity of lead and lead compounds: In support of reportable quantity adjustments pursuant to CERCLA Sectio n 102. Prepared by the Office of Health and Environmental Assessment, Washington, DC. EPA/600/8-89/045A. (External Review Draft). Van Esch, G.J. and R. Kroes. 1969. The induction of renal tumors by feeding of basic lead acetate to mice and hamsters. Br. J. Cancer. 23: 265-271.



### _VII. Revision History
Substance Name — Lead an d compounds (inorganic) CASRN — 7439-92-1 File First On-Line 03/01/1988

Date Section Description 09/26/1988 II. Carcinog en summary on-line 02/01/1989 IV.B.1. Effect leve l corrected in discussion 06/01/1989 II.D.3. Primary contact changed 06/01/1989 IV.A.1. Reference corrected - changed number for part in CFR 12/01/1989 II.A.3. Last paragraph - Correct Van Esch 1969 citation 12/01/1989 VI. Bibliography on-line 07/01/1990 I.A. Changed contact J. Cohen's office and telephone number 07/01/1990 IV.F.1. EPA contact changed 02/01/1991 I.A. Message revised to include new EPA document 02/01/1991 I.A. EPA contacts changed 05/01/1991 II.A. Text edited 01/01/1992 IV. Regulatory actions updated 

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### _VIII. Synonyms
Substance Name — Lead an d compounds (inorganic) CASRN — 7439-92-1 Last Revised — 07/08/2004
7439-92-1 Lead Lead and compounds plumbum 06/01/1992 IV.B.2. MCL monito ring reqs. and BAT corrected 07/01/1993 II.D.3. Secondary contact's phone number changed 07/01/1993 VI.C. References alphabetized correctly 11/01/1993 II.D.1. U.S. EPA 1987 replaced with 1989; rev. state. revised 11/01/1993 VI.C. U.S. EPA 1987 deleted; U.S. EPA 1989 added 04/01/1997 III., IV., V. Drinking Water Health Advisories, EPA Regulatory Actions, and Supplementar y Data were removed from IRIS on or be fore April 1997. IRIS users were direct e to the appropriate EPA Program Offices for this information. 12/03/2002 I.A., II.D.2. Screening-Level Literature Review Findings message has been added.
07/08/2004 I.A., I.B., II. Previous reference value discussions re placed with links to EPA websites containing regulatory information and other websites with risk assessment information; cancer discussion retained , added links to agencies conducting reviews of lead carcinogenicity.

IRIS Home Chronic HealthHazards for NonCarcinogenic Effects Reference Dose for Chronic Oral Exposure (RfD)

Oral RfD Summary Principal and Supporting Studies Uncertainty and Modifying Factors Additional Studies/Comments Confidence in the Oral RfD EPA Documentation and Review

Reference Concentration for Chronic Inhalation

Exposure (RfC)

Inhalation RfC 

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...Summary Principal and Supporting Studies Uncertainty and Modifying Factors Additional Studies/Comments Confidence in the Inhalation RfC EPA Documentation and Review Carcinogenicity Assessment for Lifetime Exposure Evidence for Human Carcinogenicity

Weight-ofEvidence Characterization Human Carcinogenicity Data Animal Carcinogenicity Data Supporting Data for Carcinogenicity Quantitative Estimate of Carcinogenic Risk from Oral Exposure Summary of Risk Estimates Dose-Response Data Additional Comments Discussion of Confidence Quantitative Estimate of Carcinogenic Risk

from Inhalation Exposure Summary of Risk Estimates Dose-Response Data Additional Comments Discussion of Confidence EPA Documentation, Review and, Contacts Bibliography Revision History Synonyms 

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