125 Ballant<strong>in</strong>e, L., Murphy, T. G. & Simoneaux, B.J. (1985) Metabolism of 14 C atraz<strong>in</strong>e <strong>in</strong> orally dosed rats. Unpublished report No. ABR-85104 dated 6 February 1985, from Ciba-Geigy Corp., Greensboro, North Carol<strong>in</strong>a, USA.. Submitted to WHO by Syngenta Crop Protection AG. Basler, A. & Rohrborn, G. (1978) SCE test <strong>in</strong> vivo: chromosome aberrations <strong>in</strong> bone marrow cells. Unpublished report No. 175-77-1 ENV D from University of Düsseldorf, Germany. Blondell, J. & Dellarco, V. (2003) Review of atraz<strong>in</strong>e cancer epidemiology. Unpublished report No. D295200 dated 28 October 2004 from United States Environmental Protection Agency, Health Effects Division (7509C). Boobis, A.R., Cohen, S.M., Dellarco, V., McGregor, D., Meek, M.E., Vickers, C., Willcocks, D., Farland, W. (2006) IPCS framework for analyz<strong>in</strong>g the relevance of a cancer mode of action for humans. Crit. Rev. Toxicol., 36, 78–192. Brusick, D.J. (1994) An assessment of the genetic toxicity of atraz<strong>in</strong>e: relevance to human health and environmental effects. Mutat. Res., 317, 133–144. Brusick, D. (2000) An assessment of the genetic toxicology database for atraz<strong>in</strong>e 1994–2000. Unpublished report dated 21 June 2000, pp 1–15. Submitted to WHO by Syngenta Crop Protection AG. Butler, M.A. & Hoagland, R.E. (1989) Genotoxicity assessment of atraz<strong>in</strong>e and some major metabolites <strong>in</strong> the Ames test. Bull. Environ. Contam. Toxicol., 43, 797–804. Catenacci, G., Barbieri, F., Bersani, M., Feriolo, A., Cottica, D. & Maroni, M. (199). Biological monitor<strong>in</strong>g of human exposure to atraz<strong>in</strong>e. Toxicol. Lett., 69, 217–222. Ceresa, C. (1988a) G 34048 - micronucleus test, mouse. Unpublished report No. 871373 dated 31 August 1988, from Ciba-Geigy Ltd, Basle, Switzerland, Submitted to WHO by Syngenta Crop Protection AG. Ceresa, C. (1988b) G 30027 - micronucleus test, mouse. Unpublished report No. 871546 dated 31 May 1988, from Ciba-Geigy Ltd, Basle, Switzerland. Submitted to WHO by Syngenta Crop Protection AG. Chau, R.Y., McCormick, G.C. & Arthur, A.T. (1990) Hydroxyatraz<strong>in</strong>e - 13-week feed<strong>in</strong>g study <strong>in</strong> dogs. Unpublished report No. 892076 dated 20 March 1990, from Ciba-Geigy Corp., Research Department, Pharmaceuticals Division, Summit, New Jersey, USA, Submitted to WHO by Syngenta Crop Protection AG. Chollet, M.C., Degraeve, N., Gilot-Delhalle, J., Colizzi, A., Moutschen, J. & Moutschen-Dahmen, M. (1982). Mutagenic efficiency of atraz<strong>in</strong>e with and without metabolic activation. Mutation Res. 97, 237–238. Abstract presented at the 1st Meet<strong>in</strong>g of the Belgian Environmental Mutagen Society, Brussels, 24 October 1981. Chow, E. & Hart, E. (1995) Two-year dietary chronic toxicity/oncogenicity study with G-34048 technical <strong>in</strong> rats. Unpublished report No. F-00125 dated 27 January 1995, from Environmental Health Center, Farm<strong>in</strong>gton, Connecticut, USA.. Submitted to WHO by Ciba-Geigy Ltd. Connor, K., Howell, J., Chen, I., Liu, H., Berhane, K., Sciarretta, C., Safe, S. & Zacharewski, T. (1996) Failure of chloro-s-triaz<strong>in</strong>e-derived compounds to <strong>in</strong>duce estrogen receptor-mediated responses <strong>in</strong> vivo and <strong>in</strong> vitro. Fundam. Appl. Toxicol., 30, 93–101. Connor, K., Howell, J., Safe, S., Chen, I., Liu, H., Berhane, K., Sciarretta, C., & Zacharewski, T. (1998) Failure of chloro-s-triaz<strong>in</strong>e-derived compounds to <strong>in</strong>duce estrogenic responses <strong>in</strong> vivo and <strong>in</strong> vitro. In: Ballant<strong>in</strong>e, L.G., McFarland, J.E. & Hackett, D.S., eds, Triaz<strong>in</strong>e herbicides: risk assessment. Wash<strong>in</strong>gton, DC, Oxford University Press,.pp 424–431. Cooper, R.L., Stoker, T.E., Goldman, J.M., Parrish, M.B. & Tyrey, L. (1996) Effect of atraz<strong>in</strong>e on ovarian function <strong>in</strong> the rat. Reprod. Toxicol., 10, 257–264. Cooper, R.L., Laws, S.C., Das, P.C., Narotsky, M.G., Goldman, J.M., Tyrey, E.L. & Stoker, T.E. (<strong>2007</strong>) Atraz<strong>in</strong>e and reproductive function: mode and mechanism of action studies. Birth Defects Res. B Dev. Reprod. Toxicol., 80, 98–112. Cooper, R.L., Stoker, T.E., Tyrey, L., Goldman, J.M. & McElroy, W.K. (2000) Atraz<strong>in</strong>e disrupts the hypothalamic control of pituitary-ovarian function. Toxicol. Sci., 53, 297–307. ATRAZINE 37–138 JMPR <strong>2007</strong>
126 Cumm<strong>in</strong>gs, A.M., Rhodes, B.E. & Cooper, R. L. 2000. Effect of atraz<strong>in</strong>e on implantation and early pregnancy <strong>in</strong> four stra<strong>in</strong>s of rats. Toxicol. Sci., 58, 135–143. Das, P.C., McElroy, W.K. & Cooper, R.L. (2000) Differential modulation of catecholam<strong>in</strong>es by chlorotriaz<strong>in</strong>e herbicides <strong>in</strong> pheochromocytoma (PC12) cells <strong>in</strong> vitro. Toxicol. Sci., 56, 324–331. Das, P.C., McElroy, W.K. & Cooper, R.L. (2001) Alteration of catecholam<strong>in</strong>es <strong>in</strong> pheochromocytoma (PC12) cells <strong>in</strong> vitro by the metabolites of chlorotriaz<strong>in</strong>e herbicide. Toxicol. Sci., 59, 127–137. Das, P.C., McElroy, W.K. & Cooper, R.L. (2003) Potential mechanisms responsible for chlorotriaz<strong>in</strong>e-<strong>in</strong>duced alterations <strong>in</strong> catecholam<strong>in</strong>es <strong>in</strong> pheochromocytoma (PC12) cells. Life Sci., 73, 3123–3138. Davidson, I.W.F. (1988) Metabolism and k<strong>in</strong>etics of atraz<strong>in</strong>e <strong>in</strong> man. Unpublished report No. 101947 dated 1989, from Bowman Gray School of Medic<strong>in</strong>e, Department of Pysiology/ Pharmacology, North Carol<strong>in</strong>a, USA. Submitted to WHO by Syngenta Crop Protection AG. De Roos, A.J., Zahm, S.H., Cantor, K.P., Weisenburger, D.D., Holmes, F.F., Burmeister, L.F. & Blair, A. (2003) Integrative assessment of multiple pesticides as risk factors for non-Hodgk<strong>in</strong>’s lymphoma among men. Occup. Environ. Med., 60, E11. De Veer, I., Moriske, H.J., & Ruden, H. (1994) Photochemical decomposition of organic compounds <strong>in</strong> water after UV-irradiation: <strong>in</strong>vestigation of positive mutagenic effects. Toxicol. Lett., 72, 113–119. Della Croce, C., Morichetti, E., Intorre, L., Soldani, G., Bert<strong>in</strong>i, S. & Bronzetti, G. (1996) Biochemical and genetic <strong>in</strong>teractions of two commercial pesticides with the monooxygenase ystem and chlorophyll<strong>in</strong>. J. Environ. Pathol. Toxicol. Oncol., 15, 21–28. Deparade, E. (1986) G-30027 - Salmonella/mammalian microsome mutagenicity test. Unpublished report No. 861172 dated 5 December 1986, from Ciba-Geigy Ltd, Basle, Switzerland. Submitted to WHO by Syngenta Crop Protection AG. Deparade, E. (1987) G 28273 - Salmonella/mammalian-microsome mutagenicity test. Unpublished report No. 871372 dated 10 November 1987 from Ciba-Geigy Ltd, Basle, Switzerland. Submitted to WHO by Syngenta Crop Protection AG. Deparade, E. (1988) G 34048 - Salmonella/mammalian-microsome mutagenicity test. Unpublished report No. 871376 dated 15 February 1988 from Ciba-Geigy Ltd, Basle, Switzerland.. Submitted to WHO by Syngenta Crop Protection AG. Deparade, E. (1989) G 30033 - Salmonella and Escherichia/liver-microsome test. Unpublished report No. 891236 dated 18 December 1989 (amended 21 December 1993) from Ciba-Geigy Ltd, Basle, Switzerland. Submitted to WHO by Syngenta Crop Protection AG. Deparade, E. (1990) G 28279 - Salmonella and Escherichia/liver-microsome test. Unpublished report No. 891243 dated 18 January 1990 (amended 21 December 1993) from Ciba-Geigy Ltd, Basle, Switzerland. Submitted to WHO by Ciba-Geigy Ltd. Devos, S., De Bosscher, K., Staels, B., Bauer, E., Roels, F., Berghe, W., Haegeman, G., Hooghe, R. & Hooghe- Peters, E.L. (2003) Inhibition of cytok<strong>in</strong>e production by the herbicide atraz<strong>in</strong>e. Search for nuclear receptor targets. Biochem. Pharmacol., 65, 303–308. Devos, S., Van Den Heuvel, R., Hooghe, R. & Hooghe-Peters, E.L. (2004) Limited effect of selected organic pollutants on cytok<strong>in</strong>e production by peripheral blood leukocytes. Eur.Cytok<strong>in</strong>e Netw., 15, 145–151. Dooley, G.P., Prenni, J.E., Prentiss, P.L., Cranmer, B.K., Andersen, M.E. & Tessari, J.D. (2006) Identification of a novel hemoglob<strong>in</strong> adduct <strong>in</strong> Sprague Dawley rats exposed to atraz<strong>in</strong>e. Chem. Res. Toxicol., 19, 692–700. Duchosal, F., Vogel, O., Chevalier, H.J., Luetkemeier, H., & Biedermann, K. (1990a) 28-Day oral toxicity (feed<strong>in</strong>g) study with G 28279 tech. <strong>in</strong> the rat. Unpublished report No. RCC 252090 dated 21 September 1990 from RCC AG, It<strong>in</strong>gen, Switzerland. Duchosal, F., Vogel, O., Wilson, J.T., Luetkemeier, H., & Biedermann, K. (1990b) 28-Day oral toxicity (feed<strong>in</strong>g) study with G 30033 tech <strong>in</strong> the rat. Unpublished report No. RCC 252088 / CG 891235 dated 21 September 1990 from RCC AG, It<strong>in</strong>gen, Switzerland. ATRAZINE 37–138 JMPR <strong>2007</strong>
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Pesticide residues in food — 2007
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TABLE OF CONTENTS Page List of part
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Dr Vicki L. Dellarco, Office of Pes
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Abbreviations used 3-MC ACTH ADI ai
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MRL MS MS/MS MTD NMR NOAEC NOAEL NO
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Introduction The toxicological mono
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AMINOPYRALID First draft prepared b
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5 higher renal excretion in the gro
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7 Table 4. Recovery of radioactivit
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9 Table 7. Pharmacokinetic paramete
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11 (c) Exposure by inhalation Five
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13 Table 9. Acute toxicity of amino
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15 The data from urine analysis rev
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17 18, monthly for palpable masses.
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19 Table 12. Body weights of rats f
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21 Table 15. Results of assays for
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23 in both groups, feed consumption
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25 neurotoxicity after 12 months. B
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27 The same five time-mated NZW rab
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29 Mortality was increased in all g
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31 Levels relevant to risk assessme
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33 References Brooks, K.J. (2001a)
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35 Consulting, The Dow Chemical Com
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ATRAZINE First draft prepared by Ru
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39 in the early 1990s; this reflect
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41 Maximum concentrations in the bl
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43 In a study on comparative metabo
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45 Table 1. Metabolism of atrazine
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47 Figure 2. Proposed metabolic pat
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49 to intact skin; and that no read
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51 the highest dose, and food consu
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53 mice (evaluated as roughly equiv
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55 Table 5. Incidence of mammary tu
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57 Table 6. Selected findings from
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59 was decreased when compared with
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61 Table 9. Selected findings of a
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63 proestrus at the expense of days
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65 Table 10. Selected studies of ge
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67 End-point Test object Concentrat
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69 Table 12. Relevant findings in a
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71 Table 14. Relevant findings in a
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73 respectively) and in males at th
- Page 90 and 91: 75 Table 15. Relevant findings in a
- Page 92 and 93: 77 All dams survived until the end
- Page 94 and 95: 79 250 and 500 ppm. Body-weight gai
- Page 96 and 97: 81 In an assay for reverse mutation
- Page 98 and 99: 83 on pubertal development in femal
- Page 100 and 101: 85 parameters (decreased pH, specif
- Page 102 and 103: 87 Table 20. Relevant findings in a
- Page 104 and 105: 89 0, 75, 150 or 300 mg/kg bw per d
- Page 106 and 107: 91 The NOAEL was 25 ppm, equal to 1
- Page 108 and 109: 93 In a study on the effect of atra
- Page 110 and 111: 95 Delayed parturition was seen at
- Page 112 and 113: 97 observed in the pair-fed group.
- Page 114 and 115: 99 examined, offspring in the atraz
- Page 116 and 117: 101 antagonize E2-induced luciferas
- Page 118 and 119: 103 increase in steroidogenesis is
- Page 120 and 121: 105 The immune system of adult mice
- Page 122 and 123: 107 In a later review of cancer epi
- Page 124 and 125: 109 In a 25-day study in rabbits tr
- Page 126 and 127: 111 developmental toxicity were 10
- Page 128 and 129: 113 regulation in male offspring in
- Page 130 and 131: 115 (d) Diaminochlorotriazine (DACT
- Page 132 and 133: 117 Developmental target/critical e
- Page 134 and 135: 119 • The failure to ovulate resu
- Page 136 and 137: 121 The relationship between increa
- Page 138 and 139: 123 Table A2. Comparison of paramet
- Page 142 and 143: 127 Dunkelberg, H., Fuchs, J., Heng
- Page 144 and 145: 129 Heneweer, M., van den Berg, M.
- Page 146 and 147: 131 Lindsay, L.A., Wimbert, K.V., G
- Page 148 and 149: 133 Morseth, S.L. (1996d) Chronic (
- Page 150 and 151: 135 Rudzki, M.W., Batastina, G., &
- Page 152 and 153: 137 Tennant, A.H., Peng, B. & Klige
- Page 154 and 155: AZINPHOS-METHYL First draft prepare
- Page 156 and 157: 141 methylation and oxidation of me
- Page 158 and 159: 143 Table 1. Acute oral toxicity of
- Page 160 and 161: 145 Table 2. Cholinesterase activit
- Page 162 and 163: 147 at the highest dose. In both sp
- Page 164 and 165: 149 Table 6. Cholinesterase activit
- Page 166 and 167: 151 Table 8. Fertility of F 0 and F
- Page 168 and 169: 153 Table 10. Fertility parameters
- Page 170 and 171: 155 Groups of 22 mated Sprague-Dawl
- Page 172 and 173: 157 after completion of the feeding
- Page 174 and 175: 159 reduced motor activity in males
- Page 176 and 177: 161 sensitivity with that of labora
- Page 178 and 179: 163 measures to prevent worker expo
- Page 180 and 181: 165 when brain cholinesterase activ
- Page 182 and 183: 167 Critical end-points for setting
- Page 184 and 185: 169 Eiben, R., Schmidt, W., & Loese
- Page 186 and 187: 171 Myhr, B.C. (1983) Evaluation of
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175 Figure 1. Chemical structures o
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177 In a comparative study, the abs
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179 Figure 2. Main pathways of biot
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181 (iv) Dermal sensitization In a
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183 observed in rats at the highest
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185 Mortality was not affected by t
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187 the group at 100 ppm, reduction
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189 and five females per group were
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191 10-12%) than those of controls
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193 Comments Biochemical aspects Or
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195 Toxicological evaluation Althou
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197 Metabolism in animals Toxicolog
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199 Harrison, M.P. (1984a) Cyhaloth
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DIFENOCONAZOLE First draft prepared
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203 a sex difference nor any marked
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205 demonstrated that the highest t
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207 Figure 3. Proposed metabolic pa
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209 of the study were unremarkable.
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211 Table 3. Results of studies of
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213 The no-observed-adverse-effect
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215 lower than those of rats in the
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217 hepatocellular enlargement. In
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219 i.e. males lost 15.4% and femal
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221 and 357. This reduced food cons
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223 There was very high mortality a
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225 Table 6. Treatment-related hist
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227 Rats Groups of 80 CRL:CD(SD)®
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229 Table 7. Histopathology finding
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231 D. Temporal association. The fe
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233 2.5 Reproductive toxicity (a) M
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235 t estes weights in the males at
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237 continued to be lower than thos
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239 Corpora lutea in each ovary wer
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241 S1 + S2, not ossified — —
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243 in the control group and in the
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245 physically examined for changes
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247 Table 16. Results of studies of
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249 can occur in untreated mice, in
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251 Study of reproductive toxicity
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253 Table 19. Results of studies of
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255 Table 21. Results of studies of
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257 of the test article on microsom
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259 Ophthalmoscopic examinations pe
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261 the radioactivity was re-elimin
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263 In a single-dose study of neuro
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265 Estimate of acceptable daily in
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267 Clapp, M.J.L., Killick, M.E., H
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269 Herbold, B. (1983c) THS 2212 tr
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271 Pinto, P. (2006b) Difenoconazol
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DIMETHOMORPH First draft prepared b
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275 Five different treatment groups
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277 To investigate the significance
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279 and the E : Z isomer ratio was
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281 Table 10. Tissue distribution o
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283 (e) Dermal sensitization The de
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285 females at the highest dose, to
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287 The NOAEL was 10 mg/kg bw per d
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289 concentrations in females were
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291 health, moribundity and mortali
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293 0-9%, mean, 3.5%; only one out
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Table 26. Organ weights adjusted to
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297 cell hyperplasia. The testes tu
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299 unscheduled DNA synthesis, the
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301 Figure 3. Cumulative percentage
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303 Rabbits In a dose-range finding
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305 (b) Potentiation of hexobarbito
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307 0.2% or less of the administere
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309 eye-opening, pinna unfolding or
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311 Lowest relevant inhalation NOAE
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313 Gardner, J.R. (1989) CME 151 te
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315 van de Waart, E.J. (1991b) Eval
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318 Committee on Pesticide residues
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320 (a) Ocular irritation Rabbits T
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322 weights were decreased in males
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324 toxicity was 5 mg/kg bw per day
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326 respectively; range for histori
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328 Table 4. Incidence of Leydig-ce
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330 and/or bilateral) was noted in
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332 No treatment-related signs of m
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334 Table 6. Incidence of selected
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336 or teratogenic potential at the
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338 and progesterone. The concentra
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340 the doses used in the 1-year st
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342 No neurotoxic effects were seen
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344 Lowest relevant reproductive NO
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346 Keller, D.A. (1992c) Oncogenici
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PROCYMIDONE First draft prepared by
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351 Rats Groups of five male and fe
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353 Table 1. Pharmacokinetic parame
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355 Seven doses C max (µg equivale
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357 Three groups of five male and f
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359 The excretion of radioactivity
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361 Figure 1. Proposed metabolic pa
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363 water consumption were determin
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365 finding. Histopathology reveale
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367 The NOAEL was 500 ppm, equivale
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369 The NOAEL was 100 mg/kg bw per
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371 at 2000 ppm. Histopathology rev
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373 b Each test was conducted in tr
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375 experimental period. Rats were
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377 hypospadias, testicular atrophy
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379 a single dose, which produced o
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381 The anti-androgenic activities
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383 but only at 6000 ppm after 13 w
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385 The results are summarized in T
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387 males (all litters) in the grou
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389 procymidone (18-27% of the admi
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391 Procymidone induced liver tumou
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393 The Meeting concluded that the
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395 Toxicologically significant com
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397 Harada, T. (1983) A review on m
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399 Murakami, M., Yoshitake, A. & H
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401 Tarui, H. (2005b) In vitro meta
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404 Explanation Profenofos is the I
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406 The metabolism of ring-labelled
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408 2. Toxicological studies 2.1 Ac
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410 Rabbits Groups of two male and
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412 Groups of five male and five fe
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414 control group and in the test g
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416 of the rabbits at the highest d
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418 The NOAEL for brain acetylcholi
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420 Table 2. Histopathological find
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422 1 out of 70; lowest dose, 3 out
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424 body‐weight gains (3-10% decr
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426 treated groups for body-weight
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428 (b) Short-term studies of neuro
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430 represented as equally as possi
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432 pound and the equitoxic mixture
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434 Inhibition of brain acetylcholi
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436 Toxicological evaluation Erythr
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438 Neurotoxicity/delayed neurotoxi
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440 Harris, S.B. (1982) A teratolog
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442 Puri, E. (1982a) Autoradiograph
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PYRIMETHANIL First draft prepared b
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447 Table 1. Excretion profile in r
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449 Table 3. Half-life of pyrimetha
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451 Table 4. Identification of meta
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453 SN 614 277. The presence of the
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455 2. Toxicological studies 2.1 Ac
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457 treated rabbits showed slight e
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459 still evident in the liver; how
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461 In a 90-day feeding study, grou
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463 per day or 800 mg/kg bw per day
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465 The dosing solutions were prepa
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467 mortality and morbidity. Change
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469 2.4 Genotoxicity Pyrimethanil w
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471 mean body‐weight gains. After
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473 Analysis of dosing solutions in
- Page 490 and 491:
475 In a 7-day feeding study, group
- Page 492 and 493:
477 at 200 mg/kg bw. These clinical
- Page 494 and 495:
479 s ystemic toxicity was 400 ppm
- Page 496 and 497:
481 Acute toxicity Rat, LD 50 , ora
- Page 498 and 499:
483 Grosshans, F. (2003) Pyrimethan
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485 Markham, L.P. (1989d) Technical
- Page 502 and 503:
ZOXAMIDE First draft prepared by I.
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489 The excretion of radioactivity
- Page 506 and 507:
491 Table 3. Mean concentration of
- Page 508 and 509:
493 Table 4. Distribution of metabo
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495 were also found in the urine, a
- Page 512 and 513:
497 owing to the absence of a dose-
- Page 514 and 515:
499 The NOAEL was 30 000 ppm, equiv
- Page 516 and 517:
501 Table 9. Haematological finding
- Page 518 and 519:
503 Table 11. Body weight, food con
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505 daily for signs of moribundity,
- Page 522 and 523:
507 Table 14 Results of studies of
- Page 524 and 525:
509 phase. The study was certified
- Page 526 and 527:
511 Table 16. Spleen weights and hi
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513 FOB/motor activity assessment,
- Page 530 and 531:
515 Excretion was primarily in the
- Page 532 and 533:
517 days 14 to 21. Increased relati
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519 Lowest relevant inhalation NOAE
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521 Morrison, R.D. & Gillette, D.M.
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ANNEX 1 Reports and other documents
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525 31. Pesticide residues in food:
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527 67. Pesticide residues in food
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529 101. Pesticide residues in food