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F344/N rats, and “clear evidence of carcinogenicity” of PCE for both sexes of B6C3F 1 mice. IARC reevaluated the evidence of carcinogenicity of PCE in 1987 using data from the NTP study and concluded that there was sufficient evidence that PCE is carcinogenic to animals (IARC, 1987). Other studies on PCE included those by Rampy et al. (1978) and Theiss et al. (1977). Rampy et al. (1978) exposed male and female Sprague-Dawley rats to PCE by inhalation (300 or 600 ppm) 6 hours/day, 5 days/week for 12 months. Animals were subsequently observed for 18 months. Pathological changes in the liver or kidney were not observed. Theiss and coworkers studied the ability of PCE to induce lung adenomas in A/St male mice (Theiss et al., 1977). Animals 6 to 8 weeks old were given 80, 200, or 400 mg/kg of PCE in tricaprylin (intraperitoneally) three times a week. Each group received 14, 24, or 48 injections. Treated animals did not exhibit a significant increase in the average number of lung tumors when compared to controls. IV. DERIVATION OF CANCER POTENCY Basis for Cancer Potency Perchloroethylene has been observed to induce mononuclear cell leukemia in male and female rats and liver tumors in male and female mice (NTP, 1986). CDHS (1992) decided that the tumor incidence data from this study were suitable for use in developing a quantitative risk assessment. Methodology Results from the 1986 NTP inhalation study were used as the basis for estimating the carcinogenic risk of PCE to humans. In this bioassay, PCE was 99.9% pure, and animals were exposed 6 hours/day, 5 days/week for 103 weeks. The mice in the 100 and 200 ppm dose groups were exposed to a timeweighted-average (TWA) of 16 and 32 ppm, respectively (e.g., 100 ppm × 6 hours/24 hours × 5 days/7 days). Similarly, rats in the 200 and 400 ppm dose groups were exposed to a TWA of 33 and 66 ppm, respectively. The CDHS staff used the metabolized dose, adjusted to continuous lifetime exposure, to calculate the carcinogenic potency of PCE (CDHS, 1992). There are several uncertainties using this approach: 1) It was assumed that oxidative metabolism leads to the production of carcinogenic metabolites but the ultimate carcinogen(s) has not been well characterized. The metabolism of PCE is not well quantified in humans, and 20-40% of the absorbed PCE has not been accounted for. 2) The pharmacokinetic models used do not account for individual differences in metabolism and storage. The body burden depended on factors such as age, sex, exercise or workload, body mass, adipose tissue mass, pulmonary dysfunctional states, and individual differences in the intrinsic capacity to metabolize PCE. Two pharmacokinetic models, the steady-state and the PB-PK approaches were used. They incorporated an 18.5% estimated applied dose as the fraction of the dose that is metabolized in humans. For the low-dose PCE risk assessment, the Crump multistage polynomial (Crump, 1984) was chosen. 483
This model, rather than a time dependent form of the multistage model, was chosen because most tumors were discovered only at the time of sacrifice, and survival in this study was relatively good. The cancer potency values derived using the two different pharmacokinetic approaches using the 1986 NTP rat and mouse studies ranged from 0.12 - 0.95 (mg/kg-d) –1 . When expressed as a function of human applied dose the values obtained ranged from 0.0025 to 0.093 (mg/kg-d) –1 . Using an estimated human weight of 70 kg, estimated breathing rate of 20 m 3 /day and the PCE conversion factor of 1 ppb = 6.78 µg/m 3 , the cancer unit risk values for PCE ranged from 0.2 - 7.2 × 10 –5 (ppb) –1 . After considering the quality of the cancer bioassays and the uncertainty of human metabolism, CDHS (1992) decided that the best value for the PCE cancer unit risk was 4.0 × 10 –5 (ppb) –1 [5.9 × 10 -6 (µg/m 3 ) -1 ]. This value is derived from the tumor incidence data for the most sensitive species, sex, and tumor site, male mouse hepatocellular adenomas or carcinomas (NTP, 1986). V. REFERENCES Blair A, Decoufle P and Grauman D. 1979. Causes of death among laundry and dry-cleaning workers. Am J Pub Health 69:508-511. Blair A, Stewart PA, Tolbert PE, Grauman D, Moran FX, Vaught J and Rayner J. 1990. Cancer and other causes of death among a cohort dry cleaners. Br J Ind Med 47:162-168. Brown D and Kaplan S. 1987. Retrospective cohort mortality study of dry cleaner workers using perchloroethylene. J Occup Med 29:535-541. California Department of Health Services (CDHS) 1991. Health Effects of Tetrachloroethylene (PCE) . Berkeley, CA. Crump KS. 1981. Statistical aspects of linear extrapolation. In: Proceedings of the Third Life Sciences Symposium, Health Risk Analysis, Gatlinburg, Tennessee, October 27-30, 1980. Richmond CR, Walsh PJ and Copenhaver ED, eds. The Franklin Institute Press, Philadelphia, PA, pp. 381-392. Duh RW and Asal NR. 1984. Mortality among laundry and dry-cleaning workers in Oklahoma. Am J Pub Health 74:1278-1280. Kaplan SD. 1980. Dry-Cleaner Workers Exposed to Perchloroethylene: A Retrospective Cohort Mortality Study. PB81-231367. National Institute of Occupational Safety and Health, Washington, DC. Katz RM and Jowett D. 1981. Female laundry and dry-cleaning workers in Wisconsin: a mortality analysis. Am J Pub Health 71:305-307. Ludwig HR, Meister MV, Roberts DR and Cox C. 1983. Worker exposure to perchloroethylene in the commercial dry cleaning industry. J Am Ind Hyg Assoc 44:600-605. Lynge E and Thygesen L. 1990. Primary liver cancer among women in laundry and dry cleaning work in Denmark. Scand J Work Environ Health 16:108-112. 484
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Air Toxics Hot Spots Program Risk A
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Prepared by: John D. Budroe, Ph.D.
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This document is one of five docume
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TABLE OF CONTENTS PREFACE i INTRODU
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N-Nitrosodimethylamine 401 N-Nitros
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Hot Spots Unit Risk and Cancer Pote
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Additional ATES and PETS documents
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data. If several data sets (dose an
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US EPA Calculation of Carcinogenic
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exposure to a concentration of 1 µ
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incidences for each of the dose lev
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computes the surface area of a sphe
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Comparison of Hot Spots Cancer Unit
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Gold, L., de Veciana, M., Backman,
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Animal Studies Rats Woutersen et al
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ased on sufficient evidence of carc
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ACETAMIDE CAS No: 60-35-5 I. PHYSIC
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Methodology Expedited Proposition 6
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cancer mortality. However, US EPA (
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Table 2. Lung adenoma incidence in
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Table 3 (continued). Acrylamide-ind
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Robinson M, Bull RJ, Knutsen GL, Sh
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Also, a trend was observed correlat
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eported. Cause-specific expected de
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Bio/Dynamics Inc. conducted a study
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examination. Interim sacrifices wer
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Table 8. Tumor incidence in male an
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Gaffey WR and Strauss ME. 1981. A m
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(technical grade; 98% pure) by gava
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International Agency for Research o
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still alive in the low-dose control
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ANILINE CAS No: 62-53-3 I. PHYSICAL
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fibrosarcomas, stromal sarcomas, ca
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ARSENIC (INORGANIC) CAS No: 7440-38
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elationship between arsenic exposur
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al. (1988) did not induce lung tumo
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A risk assessment was also conducte
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Chen C, Chuang Y, You S, Lin T and
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Schrauzer G, White D, McGinness J,
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Table 1: Summary of epidemiologic s
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had at least one animal demonstrati
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mesothelioma, recommended lifetime
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National Institute for Occupational
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BENZENE CAS No: 71-43-2 I. PHYSICAL
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Animal Studies Available experiment
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Table 3: Summary of NTP bioassay re
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Table 4: Summary of benzene low-dos
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Maltoni C, Conti B and Cotti G. 198
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a benign tumor of the kidney. No ba
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al. (1968) found no tumors in lifet
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following relationship, where C(t 1
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Miakawa M. and Yoshida O. 1975. Pro
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human population and that BPDE-DNA
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demonstrated the tumor initiating a
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Table 4: Bronchoalveolar tumors fro
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Table 5: IARC groupings of PAHs, mi
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Table 6 (continued): IARC Group 3 P
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Potency Equivalency Factors (PEF) f
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This was rounded to a PEF of 0.1. 1
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experiment (Takayama et al., 1985)
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Deutsch-Wenzel RP, Brune H, Grimmer
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Krewski D, Thorslund T and Withey J
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U.S. Environmental Protection Agenc
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Sorahan et al. (1983) studied cance
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Lijinsky W. 1986. Chronic bioassay
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the drinking water (Schroeder and M
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Table II. Effective dose, upper-bou
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BIS(2-CHLOROETHYL)ETHER CAS No: 111
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IV. DERIVATION OF CANCER POTENCY Ba
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BIS(CHLOROMETHYL)ETHER CAS No: 542-
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Table 1. Bis(chloromethyl)ether-ind
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Drew RT, Laskin S, Kuschner M and N
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ates for the 1968 U.S. male populat
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Table 1: Incidence of primary tumor
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National Institute of Occupational
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was less than 0.05 when controlling
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up period. The final cohort include
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If the cadmium-exposed workers incl
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on personnel records (20%); (3) eva
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were exposed to a continuous (23.5
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procedure (NLIN), the parameters we
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International Agency for Research o
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Two reports were published on cance
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Mendel rats, respectively), and sub
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Eschenbrenner A and Miller E. 1946.
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III. CARCINOGENIC EFFECTS Human Stu
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cancers, were less than expected. T
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and no cases of cancer (although cl
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There was a statistically significa
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NTP (1982a) also conducted an carci
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Several pathologists have independe
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hepatocellular adenoma/carcinoma tu
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carcinogenic potency may decline in
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Cochrane W, Singh J and Miles W. 19
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North Atlantic Treaty Organization,
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CHLORINATED PARAFFINS (average chai
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ased on dose-response data for beni
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chloroform in drinking water with k
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Overall, the present epidemiologica
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female dogs received toothpaste bas
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Calculated q 1 * values from the ab
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Hogan MD, Chi Py, Hoel DG and Mitch
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Table 1. Study design summary for N
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V. REFERENCES California Environmen
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toluidine. Followup of this subcoho
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feeding studies on by NCI (1979) us
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CHROMIUM (HEXAVALENT) CAS No: 18540
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expected rate may be inflated becau
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Oral Borneff et al. (1968) exposed
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CREOSOTE (COAL TAR-DERIVED) CAS No:
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from an inhalation exposure study (
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Table 1. Study design summary for N
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Table 1. Experimental design for ca
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Hazardous Substance Data Bank (HSDB
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Table 1: Tumor induction in Fischer
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Table 1. Experimental design of 2,4
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Additional analysis of these data b
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Jackson RJ, Greene CJ, Thomas JT, M
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Table 1. Tumor incidence in rats ex
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Girard R, Tolot F, Martin P and Bou
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exposed more than 16 years before t
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interpretation of dose extrapolatio
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1, 1-DICHLOROETHANE CAS No: 75-34-3
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Table 1b. Study design for carcinog
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National Cancer Institute (NCI) 197
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mice, hepatocellular carcinoma inci
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V. REFERENCES California Department
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DAB/day by gavage for the life of t
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2,4-DINITROTOLUENE CAS No: 121-14-2
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Ellis et al.(1979) (also reported b
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Final Statement of Reasons for OAL,
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to the small sample size and short
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In an inhalation study, Torkelson e
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V. REFERENCES American Conference o
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EPICHLOROHYDRIN CAS No: 106-89-8 I.
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espiratory tumors were noted in the
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Table 4. Epichlorohydrin-induced fo
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Konishi Y, Kawabata A, Denda A, Ike
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exposed to arsenicals for 20 months
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espectively (all statistically sign
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ETHYLENE DICHLORIDE CAS No: 107-06-
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Several factors have been suggested
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myelogenous leukemias (4 and 8 year
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statistically significant. CDHS not
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combined with the incidence in the
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incidence of primary brain tumors.
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Table 6 (continued): Organ/Sex Mali
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An Upper 95% Confidence Limit (UCL)
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ETHYLENE THIOUREA (ETU) CAS No: 96-
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male and female rats. Tumor inciden
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FORMALDEHYDE CAS No: 50-00-0 I. PHY
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presented an extension of a previou
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Methodology In developing a spectru
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Casanova M, Morgan KT, Steinhagen W
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Tobe M, Kaneko T, Uchida Y, Kamata
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Table 1. Hexachlorobenzene-induced
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50 pups (F 1 ) of each sex were ran
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Ertürk E, Lambrecht RW, Peters HA,
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Table 1. Liver hepatoma incidence i
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1988). An airborne unit risk factor
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HYDRAZINE CAS No: 302-01-2 I. PHYSI
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Methodology Inhalation A linearized
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LEAD AND LEAD COMPOUNDS (INORGANIC)
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and other occupational carcinogens
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y inhalation is similar for rats an
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Goyer RA. 1992. Nephrotoxicity and
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LINDANE (g-Hexachlorocyclohexane) C
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Using these relationships, a human
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METHYL TERT-BUTYL ETHER (MTBE) CAS
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Tumor incidences according to the r
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kidney changes indicative of chroni
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Interspecies scaling for oral doses
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Table 4 (continued): Dose Response
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Experimental Pathology Laboratories
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Animal Studies Male and female HaM/
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Gold L, Sawyer C, Magaw R, Backman
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Using the statistical tests (one-ta
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Table 1: Methylene chloride-induced
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Significant treatment-related incre
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National Toxicology Program (NTP) 1
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noted; however, the study duration
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Crump KS, Howe RB, Van Landingham C
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Table 1. Michler’s ketone-induced
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NICKEL AND NICKEL COMPOUNDS CAS No:
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the high exposure group was 14.0. A
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male and 121 female rats, was expos
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2.1 - 2.6 × 10 -4 (µg/m 3 ) -1 .
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The increased incidence of bladder
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A linearized multistage procedure w
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N-NITROSO-N-METHYLETHYLAMINE CAS No
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propylamine in drinking water at 0.
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N-NITROSODIETHYLAMINE CAS No: 55-18
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Table 2. Treatment groups, concentr
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California Department of Health Ser
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animals and the second generation t
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ationale for selection of the OEHHA
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A unit risk value based upon air co
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N-NITROSODIPHENYLAMINE CAS No: 86-3
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Methodology Dosage estimates of NDP
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Crump KS, Howe RB. 1984. The multis
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Table 1. P-Nitrosodiphenylamine-ind
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N-NITROSOMORPHOLINE CAS No: 59-89-2
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N-NITROSOPIPERIDINE CAS No: 100-75-
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Table 3. N-Nitrosopiperidine-induce
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Crump KS, Howe RB, Van Landingham C
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testicular tumors were noted in the
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PARTICULATE MATTER FROM DIESEL-FUEL
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etired railroad workers who had had
Page 441 and 442: employment (χ 2 test for trend: p
Page 443 and 444: elevated smoking-adjusted risk esti
Page 445 and 446: Table 1 (continued): Reference Miln
Page 447 and 448: Table 1 (continued): Reference Damb
Page 449 and 450: Table 1 (continued): Reference Burn
Page 451 and 452: Table 1 (continued): Reference Raff
Page 453 and 454: Table 1 (continued): Epidemiologica
Page 455 and 456: Table 1 (continued): Epidemiologica
Page 457 and 458: Table 1 (continued): Reference Wegm
Page 459 and 460: Animal Studies Section 6.1 (Animal
Page 461 and 462: The variability, or heterogeneity,
Page 463 and 464: estimate for those studies for whic
Page 465 and 466: Figure 1: Estimates of Relative Ris
Page 467 and 468: q 1 * = Excess relative risk × CA
Page 469 and 470: Table 3: Number of Workers in the E
Page 471 and 472: u nexposed workers at zero concentr
Page 473 and 474: for each µg/m 3 of diesel exhaust
Page 475 and 476: Table 4: Values from Unit Risk for
Page 477 and 478: their findings that a reasonable es
Page 479 and 480: Garshick E, Schenker M, Woskie S an
Page 481 and 482: Lewis T, Green, FH MW, Burg J and L
Page 483 and 484: Rothman K. 1986. Modern epidemiolog
Page 485 and 486: PENTACHLOROPHENOL CAS No: 87-86-5 I
Page 487 and 488: The default lifespan for mice is 10
Page 489 and 490: documented. An excess risk from ski
Page 491: B6C3F 1 mice and F344/N rats were e
Page 495 and 496: POLYCHLORINATED BIPHENYLS (PCBs) CA
Page 497 and 498: several benign adenomatous lesions
Page 499 and 500: Ito et al. (1973) exposed groups of
Page 501 and 502: could not be characterized by chlor
Page 503 and 504: exposure (all pathways and mixtures
Page 505 and 506: National Toxicology Program 1993. T
Page 507 and 508: Table 1. Potassium bromate-induced
Page 509 and 510: 1,3-PROPANE SULTONE CAS No: 1120-71
Page 511 and 512: IV. DERIVATION OF CANCER POTENCY Ba
Page 513 and 514: PROPYLENE OXIDE CAS No: 75-56-9 I.
Page 515 and 516: oxide. In the NTP carcinogenicity s
Page 517 and 518: 1,1,2,2-TETRACHLOROETHANE CAS No: 7
Page 519 and 520: assumed a body weight of 70 kg and
Page 521 and 522: total); an untreated control group
Page 523 and 524: TOLUENE DIISOCYANATE CAS No: 26471-
Page 525 and 526: Animal Studies The National Toxicol
Page 527 and 528: Mortillaro PT and Schiavon M. 1982.
Page 529 and 530: male or female rats. Increases in h
Page 531 and 532: TRICHLOROETHYLENE CAS No: 79-01-6 I
Page 533 and 534: A mortality analysis of a cohort of
Page 535 and 536: elative to that of the controls whi
Page 537 and 538: applied or metabolized. The range o
Page 539 and 540: Katz RM and Jowett D. 1981. Female
Page 541 and 542: 10,000 ppm 2,4,6-trichlorophenol in
Page 543 and 544:
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Bionetics Research Laboratories. 19
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control; females: 6/10 exposed, 0/1
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over controls (p < 0.04). Other tum
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was increased (100/314 exposed vs.
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Table 3. Cancer potency estimates f
Page 555 and 556:
Crouch E. 1983. Uncertainties in in
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VINYL CHLORIDE CAS No: 75-01-4 I. P
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Table 1 (continued): A Summary of E
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al., 1983). Histopathology of all o
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Table 3: Tumor incidences in 100 pp
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experiment, animals were exposed to
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Experiment BT1 Most previous risk a
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No statistical analyses of mortalit
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Table 11 gives unit risk estimates
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Bertazzi PA, Villa A, Foa V, Saia B
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Nicholson WJ, Hammond EC, Seidman H
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immunotoxicity, reproductive toxici
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scheme. TEFs for two major noncance
Page 581 and 582:
NATO/CCMS (1988a) Pilot Study on In
Page 583 and 584:
Table 2 Toxicity Equivalency Factor
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Table 4 A Comparison of CTEF- and I
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Office of Environmental Health Haza
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Group 4: The agent is probably not
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TECHNICAL SUPPORT DOCUMENT FOR DESC
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US EPA IRIS Inhalation Unit Risk an
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TECHNICAL SUPPORT DOCUMENT FOR DESC
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as appropriate, and revise IRIS fil
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Chemical Exposure Route Study Type
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Page 603 and 604:
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Methyl tert-butyl ether p. 5: Added
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