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Lead and compounds (inorganic); CASRN 7439-92-1

Human health assessment information 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 Assessments for Noncarcinogenic Effects) and II 

(Carcinogenicity Assessment for Lifetime Exposure) present the conclusions that were reached 

during the assessment development process. Supporting 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 Assessments for Noncarcinogenic Effects 

_I.A. Reference Dose for Chronic Oral Exposure (RfD) 

Substance Name — Lead and 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 appreciable risk of deleterious effects during a lifetime. The RfD is 

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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 Assessment (II.) on-line 11/01/1993

Integrated Risk Information System

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Last updated on Friday, July 20, 2012

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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. Please refer to the guidance documents at 

http://www.epa.gov/iris/backgrd.html for an elaboration of these concepts. Since RfDs can be 

derived for the noncarcinogenic health effects of substances that are also carcinogens, 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 potential 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 inorganic lead and compounds include, but are not 

limited to, neurotoxicity, developmental delays, hypertension, impaired hearing acuity, impaired 

hemoglobin synthesis, and male reproductive impairment. Importantly, many of lead's health 

effects may occur without overt signs of toxicity. Lead has particularly significant effects in children, 

well before the usual term of chronic exposure can take place. Children under 6 years old have a 

high risk of exposure because of their more frequent hand-to-mouth behavior (Centers for Disease 

Control and Prevention (CDC), 1991: 

http://www.cdc.gov/nceh/lead/publications/books/plpyc/contents.htm). 

EPA considered providing an RfD for inorganic lead in 1985, and concluded that it was inappropriate 

to develop an RfD, as documented online 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 scientific 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 and 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 development, 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 concerning the health effects of lead at this time 

(June, 2004), given the ongoing effort of the CDC 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 since the 1985 assessment. IRIS users may request 

the references for those studies from the IRIS Hotline at hotline.iris@epa.gov or (202)566-1676. 

Current knowledge of lead pharmacokinetics 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 bioaccumulates in the body, primarily in the skeleton. Lead 

body burdens vary significantly with age, health status, nutritional state, maternal body burden 

during gestation and lactation, etc. For this reason, and because of the continued apparent lack of 

threshold (CDC, 2004: http://www.cdc.gov/nceh/lead/spotLights/changeBLL.htm), it is still 

inappropriate to develop reference 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 within EPA for media-specific applications. Most of 

these methods focus on blood lead levels, through the development of several media-specific lead 

exposure levels for risk management and regulatory 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 lead exposure limits in support of regulatory 

decision-making, and has developed methods to assess risk from lead in situations not covered by 

these limits, also described below. 

The CDC identified 10 μg/dL as the blood lead level of concern in children in their 1991 report 

"Preventing Lead Poisoning in Young 

Children" (http://www.cdc.gov/nceh/lead/publications/books/plpyc/contents.htm), and provided 

risk management options for categories of blood lead levels higher than 10 μg/dL. In view of the 

fact that health effects were and continue to be identified below the level of concern, the CDC 

convened an Advisory Committee on Childhood Lead Poisoning Prevention 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 inherent in laboratory testing." 

"Finally, there is no evidence of a threshold 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 levels in support of regulatory decision-making, 

which limit the amount of lead that can be present in various environmental media. Under the 

National Primary Drinking Water Regulations, EPA established a Maximum Contaminant Level (MCL) 

for lead in drinking water due to any source. Under the Toxic Substances Control Act (TSCA) as 

amended by the Residential Lead-Based 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 standard: http://www.epa.gov/ttn/naaqs/

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Note that additional relevant information will be found by following links provided at these websites, 

such as dose-response relationships relating blood lead levels to changes 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/programs/lead/products.htm), and facilitates site-specific risk 

assessments at contaminated waste sites on the National Priority List, where the major sources of 

soil contamination are activities such as disposal of mining and manufacturing wastes contaminated 

with lead and deposition of lead from air, rather than presence of lead-based paint in residences 

(see: http://www.epa.gov/superfund/programs/lead/trwhome.htm). The Superfund Program uses 

the Integrated Exposure Uptake Biokinetic (IEUBK) 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 model 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 the lead-based paint regulation cited above. 

The Superfund Program has also developed an Adult Lead Model, for use when lead exposures to 

adults, especially pregnant women, are of greater concern. This model is described and provided for 

downloading at http://www.epa.gov/superfund/programs/lead/adult.htm. 

EPA maintains a lead resources page (http://www.epa.gov/opptintr/lead/pubs/resources.htm). 

Links are provided to many other EPA offices, government agencies, and other organizations 

involved in efforts to reduce exposure to lead in the environment. 

__I.A.5. Confidence in Risk Values 

Not applicable. 

__I.A.6. EPA Documentation and 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 concerning 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 and compounds (inorganic) 

CASRN - 7439-92-1 

In general, the Reference Concentration (RfC) is an estimate (with uncertainty spanning perhaps an 

order of magnitude) of a daily inhalation exposure of the human population (including sensitive 

subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime. 

The RfC considers toxic effects for both the respiratory system (portal-of-entry) and for effects 

peripheral to the respiratory system (extrarespiratory 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 toxic effects such as cellular necrosis. 

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Inhalation RfCs are derived according to the Interim Methods for Development of Inhalation 

Reference Doses (EPA/600/8-88/066F, 1989) and subsequently, according to Methods for 

Derivation of Inhalation Reference Concentrations 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 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 potential human carcinogenicity, 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 concerning 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 and compounds (inorganic) 

CASRN — 7439-92-1 

Section II Last Revised — II.A. introductory paragraph 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-evidence judgment of the likelihood that the substance is a human 

carcinogen, and quantitative estimates of risk from oral exposure and from inhalation exposure. 

The quantitative risk estimates are presented in three ways. The slope factor is the result of 

application of a low-dose extrapolation 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 is presented 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 carcinogenicity 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 Carcinogen 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-term toxic effects other than 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 for Research on Cancer (IARC) has undertaken a reevaluation of 

lead's carcinogenicity (http://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 reproducible results in several laboratories, in multiple rat 

strains with some evidence of multiple tumor sites. Short term studies show that lead affects gene 

expression. Human evidence is inadequate. 

__II.A.2. Human Carcinogenicity Data 

Inadequate. There are four epidemiologic studies of occupational cohorts 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 workers, found a slight decrease in the total cancer 

mortality (SMR=95). Apparent excesses were observed 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 that 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 information, as well as information on the 

possible contribution from smoking. All studies also included exposures 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 (<200). There was no consistency of site among the 

various studies, and no study showed any dose-response relationship. Thus, the available human 

evidence is considered to be inadequate to refute or demonstrate any potential carcinogenicity for 

humans from lead exposure. 

__II.A.3. Animal Carcinogenicity Data 

Sufficient. The carcinogenic potential of lead salts (primarily phosphates and acetates) administered 

via the oral route or by injection has been demonstrated in rats and mice by more than 10 

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investigators. The most characteristic cancer response is bilateral renal carcinoma. Rats given lead 

acetate or subacetate orally have developed gliomas, and lead subacetate also produced lung 

adenomas in mice after i.p. administration. Most of these investigations found a carcinogenic 

response only at the highest dose. The lead compounds 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 been located in the literature. 

Azar et al. (1973) administered 10, 50, 100, and 500 ppm lead as lead acetate in dietary 

concentrations to 50 rats/sex/group for 2 years. Control rats (100/sex) received the basal 

laboratory diet. In a second 2-year feeding study, 20 rats/group were given diets containing 0, 

1000, and 2000 ppm lead as lead acetate. No renal tumors were reported in the control groups or 

in treated animals of either sex receiving 10 to100 ppm. Male rats fed 500, 1000, and 2000 ppm 

lead acetate had an increased renal tumor incidence 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 lead in the air or drinking water was not mentioned. The strain 

of rats used was not specified in the study, but the Health Effects 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 interaction 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 group 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 between 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 (81%) 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 authors 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 (DiPaolo et al., 1978) and 

also enhances the incidence of simian adenovirus induction. Lead oxide showed similar enhanced 

adenovirus induction (Casto et al., 1979). 

Under certain conditions lead compounds 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 workers. Lead has been shown, in a number of DNA 

structure and function assays, to affect the molecular 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 uncertainties, some of which may be unique to lead. 

Age, health, nutritional state, body burden, and exposure duration influence the absorption, 

release, and excretion of lead. In addition, current knowledge of lead pharmacokinetics indicates 

that an estimate derived by standard 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 Document for Lead has received Agency and External Review. 

__II.D.2. EPA Review (Carcinogenicity 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 assessment 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 information 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 concerning 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. Bibliography 

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Substance Name — Lead and 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 and response to hemorrhage study. In: Barth D., A. 

Berlin, R. Engel, P. Recht and J. Smeets, Ed. Environmental health aspects of lead: Proceedings 

International Symposium; October 1972; Amsterdam, The Netherlands. Commission of the 

European Communities, Luxemberg. p. 199-208. 

Casto, B.C., J. Meyers and J.A. DiPaolo. 1979. Enhancement 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: Proceedings of the 1974 

Conference on Standards of Occupational Lead 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 carcinogenesis. Br. J. Cancer. 38: 

452-455. 

Grandjean, P., H.C. Wulf and E. Niebuhr. 1983. Sister 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. 1985. Effects of dietary calcium acetate on lead 

subacetate carcinogenicity in kidneys of male Sprague- Dawley rats. Carcinogenesis. 6(2): 279-

282. 

Koller, L.D., N.I. Kerkvliet and J.H. Exon. 1986. Neoplasia 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. Stotzky. 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, Environmental 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. Environmental Protection Agency, 

Washington, DC. 51 FR 33992-34003. 

U.S. EPA. 1986b. Air Quality Criteria 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 Quality Planning and Standards. EPA-600/8-83/028dF. 

U.S. EPA. 1989. Evaluation of the potential carcinogenicity of lead and lead compounds: In support 

of reportable quantity adjustments pursuant to CERCLA Section 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 and compounds (inorganic) 

CASRN — 7439-92-1 

File First On-Line 03/01/1988 

Date Section Description

09/26/1988 II. Carcinogen summary on-line

02/01/1989 IV.B.1. Effect level 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 and 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 monitoring 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 Supplementary

Data were removed from IRIS on or before April 1997. IRIS users were directe

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 replaced 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 Health 

Hazards 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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