Appendix 2-5: Rejected ecotox bibliography for Chlorpyrifos

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in vitro effects of different concentrations (1-100 mu M) of Mancozeb (fungicide) and Metribuzin (herbicide), on the proliferative responses of human and rat spleen lymphocytes stimulated by concanavalin A (ConA, mitogen), the Th1- (IL-2, INF gamma) and Th2- (IL-4) cytokine secretion and on the intracellular oxidative status. The results showed that Mancozeb significantly reduced ConA lymphocyte proliferation in a dose-dependent manner in both humans and rats. It also decreased IL-2, INF gamma and IL-4 secretion with a a shift away to Th1 phenotype. Metribuzin at low concentrations (1-10 mu M) resulted in activation of ConA stimulated lymphocyte proliferation and cytokine production in both human and rat spleen cells. However, at high concentrations (25-100 mu M), Metribuzin induced a dose-dependent inhibition of lymphocyte proliferation and cytokines. Changes in intracellular levels of reduced Glutathione, hydroperoxides and carbonyl proteins and in the activities of catalase and SOD were observed after Mancozeb and Metribuzin exposure reflecting oxidative stress and DNA damage specially at high concentrations. In conclusion, Mancozeb and Metribuzin had significant immunomodulatory properties with oxidative stress induction at high concentrations. (C) 2011 Elsevier Inc. All rights reserved.
Keywords: Mancozeb, Metribuzin, Rat splenocytes, Human lymphocytes, Cytokines,
ISI Document Delivery No.: 823UU

878. Mee Kin, Chai and Guan Huat, Tan. Headspace solid-phase microextraction for the evaluation of pesticide residue contents in cucumber and strawberry after washing treatment . 2010 Dec 1-; 123, (3): 760-764.

Rec #: 5120
Notes: Chemical of Concern: CPY
Abstract: The headspace solid-phase microextraction was developed to examine the organophosphorus (diazinon, malathion, chloropyrifos, quinalphos, profenofos) and organochlorine (chlorothalonil, +_-endosulfan and +_-endosulfan) pesticide residues in vegetable (cucumber) and fruit (strawberry) samples. The effects of washing by different solutions were evaluated for the reduction of organophosphorus and organochlorine pesticide residues contents. Gas chromatography with electron capture detection was used to analysis the investigated pesticides. The results showed that washing by a non-toxic solution can decrease the concentration of pesticide residues in the fruit and vegetable samples. The data further indicated that acetic acid was the most effective solution in removing the residues of the investigated pesticides from the fruit and vegetable samples when compared to sodium carbonate, sodium chloride and tap water. The amount of pesticides removed by solution washing is related to their water solubility and vapour pressure properties. HS-SPME/ Pesticide residues/ Washing

879. Meeker, J D ; Ravi; Barr, D B; Hauser, R, and Meeker, J D. Circulating Estradiol in Men Is Inversely Related to Urinary Metabolites of Nonpersistent Insecticides. 2008 Feb; 25, (2): 184-191.

Rec #: 46169
Notes: Chemical of Concern: CPY
Abstract: Abstract: Background: Estradiol plays an important role in male reproductive health as a germ cell survival factor. Chlorpyrifos and carbaryl, nonpersistent insecticides to which the general population are commonly exposed, were recently shown to inhibit estradiol metabolism in vitro which could lead to altered hormone balance. Methods: Subjects (N=322) were the male partners in couples presenting to a Massachusetts infertility clinic from years 2000-2003. 3,5,6-Trichloro-2-pyridinol (TCPY), the major urinary metabolite of chlorpyrifos and chlorpyrifos-methyl, and 1- and 2-naphthol (1N and 2N), urinary metabolites of carbaryl and naphthalene, were measured in a spot urine sample from each subject. Estradiol, sex hormone binding globulin (SHBG), and prolactin were measured in serum collected from subjects during the same clinic visit. Results: Using multiple linear regression, an interquartile range (IQR) increase in TCPY was associated with a 1.36pg/mL decline (95% confidence interval=-2.91 to -0.22) in estradiol concentration. When estradiol and TCPY were divided into quintiles, there was a dose-dependent increase in the odds of being in the lowest estradiol quintile with increasing TCPY quintiles. Conclusion: On a population level, these reductions in estradiol levels are of potential public health importance because of widespread exposure to TCPY and its parent insecticides.
Keywords: Infertility
Keywords: survival factor
Keywords: Germ cells
Keywords: Naphthalene
Keywords: Carbaryl
Keywords: Globulins
Keywords: Metabolites
Keywords: Hormones
Keywords: Estradiol
Keywords: Sex hormones
Keywords: Public health
Keywords: Chlorpyrifos
Keywords: Prolactin
Keywords: Insecticides
Keywords: Urine
Keywords: Population levels
Keywords: X 24330:Agrochemicals
Keywords: Toxicology Abstracts
Date revised - 2008-04-01
Language of summary - English
Pages - 184-191
ProQuest ID - 20543574
SubjectsTermNotLitGenreText - Estradiol; Metabolites; Insecticides; Chlorpyrifos; Carbaryl; Public health; Urine; Sex hormones; Prolactin; Germ cells; Infertility; Hormones; Population levels; Naphthalene; Globulins; survival factor
Last updated - 2011-12-13
British nursing index edition - Reproductive Toxicology [Reprod. Toxicol.]. Vol. 25, no. 2, pp. 184-191. Feb 2008.
Corporate institution author - Meeker, J D; Ravi; Barr, D B; Hauser, R
DOI - MD-0007976063; 8103556; 0890-6238 English

880. Meggs, W. J. and Brewer, K. L. Toxicant Exposures and the Obesity Epidemic.

Rec #: 76739
Notes: Chemical of Concern: CPY
Abstract: MESH HEADINGS: Adult
MESH HEADINGS: Chlorpyrifos/adverse effects
MESH HEADINGS: Environmental Exposure/*adverse effects
MESH HEADINGS: Insecticides/*adverse effects
MESH HEADINGS: Obesity/*epidemiology eng

881. Mehrani, H. and Golmanesh, L. Changes in mRNA and protein levels of nicotinic acetylcholine receptors in Diazoxon exposed pC12 cells. 2008; 22, (5): 1257-1263.

Rec #: 65099
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: Effects of diazoxon on the gene and protein expression of nicotinic acetylcholine receptors (nAChR) were evaluated in PC12 cells. Cells were exposed to 100 mu M diazoxon for 48 h in the presence versus absence of nAChR agonists or antagonists. Diazoxon significantly inhibited AChE activity in the cells. At the mRNA level, transcripts of the alpha(4) and beta(2) subunits of nAChR were significantly reduced in cells exposed to diazoxon, but there was no change in alpha(7) subunit mRNA content. Diazoxon exposure also significantly reduced the protein levels of both alpha(4) and beta(2) nAChR subunits. Treatment with nicotine (10 mu M) or with the nicotinic receptor antagonists, mecamylamine (10 mu M) or dihydro-beta-erythroidine (DH beta E) (5 mu M) efficiently prevented the diazoxon-induced reduction in alpha(4) and beta(2) nAChR mRNA and protein in PC12 cells, but carbamaylcholine, a weak nAChR agonist, was ineffective. These data suggest that alpha(4)beta(2) nAChRs are involved in diazoxon-related toxicity and that nicotinic receptor antagonists could play a protective role against organophosphate-related damage. (C) 2008 Elsevier Ltd. All rights reserved.
Keywords: diazoxon, nicotinic acetylcholine receptor, mecamylamine,
ISI Document Delivery No.: 326GC

882. ---. Evaluation of nicotinic receptors agonists and antagonists against paraoxon exposed PC12 cells. 2008; 26, (1): 22-29.

Rec #: 65109
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: Chronic and acute exposure to organophosphate pesticides may lead to persistent neurological and neurobehavioral effects, which cannot be explained by acetylcholinesterase (AChE) inhibition alone. In an attempt to elucidate the mechanism by which paraoxon affects the nicotinic receptors gene expression, the effects of exposure of PC12 cells to 100 mu M concentrations of paraoxon for 48 h in the presence and the absence of nicotinic acetylcholine receptors (nAChRs) agonists and antagonists were characterized. Paraoxon at 100 mu M significantly inhibited AChE activity. On the mRNA level, the alpha(4) and beta(2) subunits of nAChR mRNA were significantly decreased in the cells exposed to paraoxon. On the protein level, alpha(4) and beta(2) subunits of nAChR protein were also significantly reduced. Mecamylamine (10 mu M), dihydro-beta-erythroidine (DH beta E) (5 mu M) and nicotine (10 mu M) efficiently prevented the decrease alpha(4) and beta(2) nAChR mRNA and protein in PC12 cells, but carbamaylcholine a weak agonist of nAChR was not efficient. These observations suggest that alpha(4)beta(2) nAChRs are involved in paraoxon related toxicity and nicotinic receptors antagonists could play some protective role against organophosphate related damages. (C) 2008 Elsevier B.V. All rights reserved.
Keywords: paraoxon, nicotinic acetylcholine receptor, mRNA, mecamylamine, AChE,
ISI Document Delivery No.: 300VY

883. Meinke, G.; Phelan, P. J.; Fradet-Turcotte, A.; Bohm, A.; Archambault, J., and Bullock, P. A. Structure-Based Analysis of the Interaction Between the Simian Virus 40 T-Antigen Origin Binding Domain and Single-Stranded Dna.

Rec #: 50339
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Crit Rev Biochem Mol Biol. 1997;32(6):503-68 (medline /9444478)
COMMENTS: Cites: J Virol. 1990 May;64(5):1973-83 (medline /2157865)
COMMENTS: Cites: Nature. 1997 Jan 9;385(6612):176-81 (medline /8990123)
COMMENTS: Cites: J Virol. 1989 Oct;63(10):4181-8 (medline /2550664)
COMMENTS: Cites: Mol Cell Biol. 1989 Sep;9(9):3839-49 (medline /2550804)
COMMENTS: Cites: J Biol Chem. 1988 Dec 25;263(36):19723-33 (medline /2848839)
COMMENTS: Cites: Mol Cell Biol. 2000 Jan;20(1):34-41 (medline /10594006)
COMMENTS: Cites: Adv Virus Res. 2000;55:75-134 (medline /11050941)
COMMENTS: Cites: J Virol. 2001 Mar;75(6):2839-47 (medline /11222709)
COMMENTS: Cites: EMBO J. 2001 Jan 15;20(1-2):295-304 (medline /11226179)
COMMENTS: Cites: Annu Rev Biochem. 2002;71:333-74 (medline /12045100)
COMMENTS: Cites: J Virol. 2003 May;77(9):5512-8 (medline /12692254)
COMMENTS: Cites: Nature. 2003 May 29;423(6939):512-8 (medline /12774115)
COMMENTS: Cites: Annu Rev Biochem. 1992;61:55-85 (medline /1323237)
COMMENTS: Cites: EMBO J. 2003 Dec 1;22(23):6205-13 (medline /14633980)
COMMENTS: Cites: J Virol. 2004 Mar;78(6):2921-34 (medline /14990710)
COMMENTS: Cites: J Biol Chem. 2004 Sep 10;279(37):38952-9 (medline /15247252)
COMMENTS: Cites: Acta Crystallogr D Biol Crystallogr. 1994 Sep 1;50(Pt 5):760-3 (medline /15299374)
COMMENTS: Cites: J Virol. 1990 Oct;64(10):4858-65 (medline /2168972)
COMMENTS: Cites: Nature. 1989 Apr 20;338(6217):658-62 (medline /2539565)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1989 Dec;86(24):9742-6 (medline /2574863)
COMMENTS: Cites: J Mol Biol. 1989 May 5;207(1):269-88 (medline /2661833)
COMMENTS: Cites: J Virol. 1993 Dec;67(12):7608-11 (medline /8230479)
COMMENTS: Cites: Nat Struct Biol. 1996 Dec;3(12):1034-9 (medline /8946857)
COMMENTS: Cites: J Virol. 1997 May;71(5):3972-85 (medline /9094674)
COMMENTS: Cites: Genes Dev. 1997 May 1;11(9):1098-110 (medline /9159391)
COMMENTS: Cites: Annu Rev Biochem. 1997;66:61-92 (medline /9242902)
COMMENTS: Cites: Acta Crystallogr D Biol Crystallogr. 1997 May 1;53(Pt 3):240-55 (medline /15299926)
COMMENTS: Cites: Acta Crystallogr D Biol Crystallogr. 2005 Apr;61(Pt 4):458-64 (medline /15805601)
COMMENTS: Cites: Annu Rev Biochem. 2005;74:283-315 (medline /15952889)
COMMENTS: Cites: J Mol Biol. 2006 Apr 7;357(4):1295-305 (medline /16481006)
COMMENTS: Cites: J Virol. 2006 May;80(9):4304-12 (medline /16611889)
COMMENTS: Cites: Nucleic Acids Res. 2006;34(14):3878-86 (medline /16899446)
COMMENTS: Cites: Nucleic Acids Res. 2006;34(15):4126-37 (medline /16935876)
COMMENTS: Cites: J Virol. 2006 Dec;80(24):12248-59 (medline /17005644)
COMMENTS: Cites: EMBO J. 2006 Nov 29;25(23):5516-26 (medline /17110927)
COMMENTS: Cites: EMBO J. 2006 Dec 13;25(24):5961-9 (medline /17139255)
COMMENTS: Cites: PLoS Biol. 2007 Feb;5(2):e23 (medline /17253903)
COMMENTS: Cites: J Virol. 2007 May;81(9):4808-18 (medline /17287270)
COMMENTS: Cites: J Virol. 2007 Sep;81(17):9162-74 (medline /17596312)
COMMENTS: Cites: Bioinformatics. 2007 Nov 1;23(21):2947-8 (medline /17846036)
COMMENTS: Cites: Bioinformatics. 2009 May 1;25(9):1189-91 (medline /19151095)
COMMENTS: Cites: Virology. 2010 Mar 30;399(1):65-76 (medline /20079917)
COMMENTS: Cites: Biochemistry. 2010 Mar 16;49(10):2087-96 (medline /20108984)
COMMENTS: Cites: Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 (medline /20124702)
COMMENTS: Cites: J Mol Biol. 2010 Apr 16;397(5):1276-86 (medline /20219473)
COMMENTS: Cites: Annu Rev Biochem. 2010;79:89-130 (medline /20373915)
COMMENTS: Cites: Acta Crystallogr D Biol Crystallogr. 2010 Apr;66(Pt 4):486-501 (medline /20383002)
COMMENTS: Cites: Cell. 1990 Jan 26;60(2):181-4 (medline /2153460)
COMMENTS: Cites: J Virol. 1998 Dec;72(12):9771-81 (medline /9811712)
ABSTRACT: The origin-binding domain (OBD) of simian virus 40 (SV40) large T-antigen (T-Ag) is essential for many of T-Ag's interactions with DNA. Nevertheless, many important issues related to DNA binding, for example, how single-stranded DNA (ssDNA) transits along the T-Ag OBD, have yet to be established. Therefore, X-ray crystallography was used to determine the costructure of the T-Ag OBD bound to DNA substrates such as the single-stranded region of a forked oligonucleotide. A second structure of the T-Ag OBD crystallized in the presence of poly(dT)(12) is also reported. To test the conclusions derived from these structures, residues identified as being involved in binding to ssDNA by crystallography or by an earlier nuclear magnetic resonance study were mutated, and their binding to DNA was characterized via fluorescence anisotropy. In addition, these mutations were introduced into full-length T-Ag, and these mutants were tested for their ability to support replication. When considered in terms of additional homology-based sequence alignments, our studies refine our understanding of how the T-Ag OBDs encoded by the polyomavirus family interact with ssDNA, a critical step during the initiation of DNA replication.
MESH HEADINGS: Amino Acid Sequence
MESH HEADINGS: Antigens, Viral, Tumor/*chemistry/genetics/*metabolism
MESH HEADINGS: Crystallography, X-Ray
MESH HEADINGS: DNA, Single-Stranded/*chemistry/*metabolism
MESH HEADINGS: Fluorescence Polarization
MESH HEADINGS: Magnetic Resonance Spectroscopy
MESH HEADINGS: Models, Molecular
MESH HEADINGS: Molecular Sequence Data
MESH HEADINGS: Mutagenesis, Site-Directed
MESH HEADINGS: Mutant Proteins/genetics/metabolism
MESH HEADINGS: Protein Binding
MESH HEADINGS: Protein Structure, Tertiary
MESH HEADINGS: Sequence Alignment
MESH HEADINGS: Simian virus 40/*physiology eng

884. Meire, Rodrigo Ornellas; Lee, Sum Chi; Yao, Yuan; Targino, Admir C; Torres, Joao Paulo M; Harner, Tom, and Meire, Rodrigo Ornellas. Seasonal and Altitudinal Variations of Legacy and Current-Use Pesticides in the Brazilian Tropical and Subtropical Mountains. 2012 Nov; 59, 108-116.

Rec #: 42429
Keywords: FATE
Notes: Chemical of Concern: CPY
Abstract: Abstract: Polyurethane foam (PUF) disk passive air samplers were deployed over summer (December-March) and winter (June-August) periods in 2007-2008 along altitudinal gradients in Brazilian southeastern and southern mountain regions. As part of the Global Atmospheric Passive Sampling (GAPS) Network, this work was initiated to address the lack of knowledge on the fate of legacy and current-use pesticides in South America, particularly in mountainous regions. Of the pesticides measured, concentrations in air were dominated by the current-use pesticides (CUPs) endosulfan (and its metabolite, endosulfan sulphate (EndoSO4)) and chlorpyrifos. Other pesticides that were regularly detected included alpha - and gamma -hexachlorocyclohexanes (HCHs), dieldrin, heptachlor epoxide and p,p'-DDE. Highest air concentrations were observed for total endosulfan (Endo I + Endo II + EndoSO4) (100s-1000s pg m-3), followed by chlorpyrifos, capital sigma DDT (mainly o,p'-DDT + p,p'-DDE), capital sigma HCH ( alpha -HCH + gamma -HCH), dieldrin and heptachlor epoxide. Seasonal variations did not show any clear trends for pesticides, except for endosulfan which reached concentration values one order of magnitude higher during summer at all sites compared to levels during winter. Along the altitudinal gradients, some pesticides showed higher atmospheric concentrations at sites above 1500 m which may indicate efficient high-altitude transport from regional sources. Northerly and southerly air back trajectories appeared to be the main continental influences at the two highest-altitude sites in both mountain regions. These trajectories travelled over extended crop areas from central Brazil to Argentina. A strong, positive correlation between air concentration and altitude was observed (Spearman's correlation, p < 0.05) for endosulfan, consistent with previous studies of endosulfan in mountainous regions in South America.
Keywords: Meteorological & Geoastrophysical Abstracts; Environment Abstracts
Keywords: Correlations
Keywords: Summer
Keywords: Environmental Studies
Keywords: Endosulfan
Keywords: Winter
Keywords: Chlorpyrifos
Keywords: Mountains
Keywords: Argentina
Keywords: Heptachlor
Keywords: Foam
Keywords: Pesticides
Keywords: Air sampling
Keywords: M2 551.5:General (551.5)
Keywords: Mountain regions
Keywords: Seasonal variations
Keywords: ENA 01:Air Pollution
Date revised - 2012-11-01
Language of summary - English
Location - Argentina
Pages - 108-116
ProQuest ID - 1222700911
SubjectsTermNotLitGenreText - Foam; Correlations; Mountain regions; Seasonal variations; Mountains; Chlorpyrifos; Heptachlor; Pesticides; Air sampling; Summer; Winter; Endosulfan; Argentina
Last updated - 2012-12-06
Corporate institution author - Meire, Rodrigo Ornellas; Lee, Sum Chi; Yao, Yuan; Targino, Admir C; Torres, Joao Paulo M; Harner, Tom
DOI - OB-b1fdbd11-8ec5-492f-8240csamfg201; 17270556; 1352-2310 English

885. Melnick, R. L.; Thayer, K. A., and Bucher, J. R. Conflicting Views on Chemical Carcinogenesis Arising From the Design and Evaluation of Rodent Carcinogenicity Studies.

Rec #: 51359
Keywords: REVIEW
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: J Occup Health. 2007 May;49(3):172-82 (medline /17575397)
COMMENTS: Cites: J Cancer Res Clin Oncol. 2000 Apr;126(4):246 (medline /10782899)
COMMENTS: Cites: Occup Environ Med. 1999 Mar;56(3):181-90 (medline /10448327)
COMMENTS: Cites: J Cancer Res Clin Oncol. 1999;125(3-4):219-25 (medline /10235477)
COMMENTS: Cites: Med Hypotheses. 1998 Jun;50(6):525-9 (medline /9710329)
COMMENTS: Cites: IARC Monogr Eval Carcinog Risks Hum. 1997;69:33-343 (medline /9336729)
COMMENTS: Cites: J Appl Toxicol. 1997 May;17 Suppl 1:S45-55 (medline /9179727)
COMMENTS: Cites: Fundam Appl Toxicol. 1996 May;31(1):1-8 (medline /8998945)
COMMENTS: Cites: Ann N Y Acad Sci. 1996 Dec 27;804:252-65 (medline /8993548)
COMMENTS: Cites: Biochim Biophys Acta. 1996 Jul 26;1302(2):93-109 (medline /8695669)
COMMENTS: Cites: Fundam Appl Toxicol. 1995 Aug;27(1):95-105 (medline /7589934)
COMMENTS: Cites: Toxicol Lett. 1995 Sep;79(1-3):107-14 (medline /7570646)
COMMENTS: Cites: Toxicol Pathol. 1994 Sep-Oct;22(5):457-72 (medline /7899775)
COMMENTS: Cites: IARC Monogr Eval Carcinog Risks Hum. 1994;60:73-159 (medline /7869582)
COMMENTS: Cites: Biochemistry. 1993 Jun 1;32(21):5598-604 (medline /7684926)
COMMENTS: Cites: Chem Res Toxicol. 1991 Mar-Apr;4(2):168-79 (medline /1664256)
COMMENTS: Cites: Rev Environ Contam Toxicol. 1992;124:111-44 (medline /1732994)
COMMENTS: Cites: Cancer Res. 1990 Oct 15;50(20):6592-9 (medline /2208121)
COMMENTS: Cites: Fundam Appl Toxicol. 1988 Apr;10(3):385-94 (medline /3286346)
COMMENTS: Cites: IARC Sci Publ. 1989;(96):17-34 (medline /2553598)
COMMENTS: Cites: Environ Health Perspect. 1989 Jul;82:125-63 (medline /2676495)
COMMENTS: Cites: Environ Health Perspect. 1989 Jul;82:109-24 (medline /2792037)
COMMENTS: Cites: Cancer Res. 1988 Dec 1;48(23):6739-44 (medline /3180084)
COMMENTS: Cites: Environ Health Perspect. 1984 Dec;58:385-92 (medline /6525993)
COMMENTS: Cites: Arch Toxicol. 1984 Oct;55(4):213-8 (medline /6517696)
COMMENTS: Cites: J Natl Cancer Inst. 1986 Feb;76(2):283-9 (medline /3456066)
COMMENTS: Cites: Toxicol Pathol. 1983;11(1):77-82 (medline /6681400)
COMMENTS: Cites: Am Ind Hyg Assoc J. 1987 May;48(5):407-13 (medline /3591659)
COMMENTS: Cites: Food Chem Toxicol. 1983 Dec;21(6):825-32 (medline /6363233)
COMMENTS: Cites: Arch Toxicol. 1977 Jul 19;37(3):233-6 (medline /332116)
COMMENTS: Cites: Natl Cancer Inst Monogr. 1979 May;(51):25-35 (medline /481577)
COMMENTS: Cites: Environ Health Perspect. 2004 Sep;112(13):1269-74 (medline /15345338)
COMMENTS: Cites: Crit Rev Toxicol. 2003;33(6):655-780 (medline /14727734)
COMMENTS: Cites: Toxicol Sci. 2003 Sep;75(1):7-15 (medline /12805639)
COMMENTS: Cites: Natl Cancer Inst Carcinog Tech Rep Ser. 1976 Feb;2:1-215 (medline /12844147)
COMMENTS: Cites: Ann N Y Acad Sci. 2002 Dec;982:177-89 (medline /12562636)
COMMENTS: Cites: Br J Cancer. 2003 Jan 13;88(1):84-9 (medline /12556964)
COMMENTS: Cites: Int J Occup Environ Health. 2002 Apr-Jun;8(2):144-52 (medline /12019681)
COMMENTS: Cites: Toxicol Pathol. 1984;12(2):126-35 (medline /11478313)
COMMENTS: Cites: Food Chem Toxicol. 2001 Jul;39(7):739-44 (medline /11397520)
COMMENTS: Cites: Environ Health Perspect. 2001 May;109(5):437-42 (medline /11401753)
COMMENTS: Cites: IARC Monogr Eval Carcinog Risks Hum. 2000;77:41-148 (medline /11100399)
COMMENTS: Cites: FASEB J. 2001 Jan;15(1):195-203 (medline /11149907)
COMMENTS: Cites: Environ Health Perspect. 2000 May;108 Suppl 2:283-305 (medline /10807559)
COMMENTS: Cites: Environ Health Perspect. 2000 May;108 Suppl 2:265-73 (medline /10807557)
COMMENTS: Cites: Toxicol Sci. 2000 Jun;55(2):433-43 (medline /10828276)
COMMENTS: Cites: Carcinogenesis. 2000 Apr;21(4):823-6 (medline /10753222)
COMMENTS: Cites: N Engl J Med. 2005 Jul 14;353(2):116-8 (medline /16014880)
ABSTRACT: Conflicting views have been expressed frequently on assessments of human cancer risk of environmental agents based on animal carcinogenicity data; this is primarily because of uncertainties associated with extrapolations of toxicologic findings from studies in experimental animals to human circumstances. Underlying these uncertainties are issues related to how experiments are designed, how rigorously hypotheses are tested, and to what extent assertions extend beyond actual findings. National and international health agencies regard carcinogenicity findings in well-conducted experimental animal studies as evidence of potential carcinogenic risk to humans. Controversies arise when both positive and negative carcinogenicity data exist for a specific agent or when incomplete mechanistic data suggest a possible species difference in response. Issues of experimental design and evaluation that might contribute to disparate results are addressed in this article. To serve as reliable sources of data for the evaluation of the carcinogenic potential of environmental agents, experimental studies must include a) animal models that are sensitive to the end points under investigation; b) detailed characterization of the agent and the administered doses; c) challenging doses and durations of exposure (at least 2 years for rats and mice); d) sufficient numbers of animals per dose group to be capable of detecting a true effect; e) multiple dose groups to allow characterization of dose-response relationships, f) complete and peer-reviewed histopathologic evaluations; and g) pairwise comparisons and analyses of trends based on survival-adjusted tumor incidence. Pharmacokinetic models and mechanistic hypotheses may provide insights into the biological behavior of the agent; however, they must be adequately tested before being used to evaluate human cancer risk.
MESH HEADINGS: Carcinogenicity Tests/methods
MESH HEADINGS: Carcinogens/*toxicity
MESH HEADINGS: Dose-Response Relationship, Drug
MESH HEADINGS: Public Health
MESH HEADINGS: Research Design
MESH HEADINGS: Risk Assessment eng

886. Melnyk, L. J.; Byron, M. Z.; Brown, G. G.; Clayton, C. A., and Michael, L. C. Pesticides on Household Surfaces May Influence Dietary Intake of Children. 2011; 45, (10): 4594-4601.

Rec #: 65159
Notes: Chemical of Concern: CPY
Abstract: Abstract: The physical and chemical environment influences children's exposures to pesticides in and around the home. Children's activities,. which increase their potential for exposure especially during eating, have been captured in the Children's Dietary Intake Model (CDIM). In addition to the chemical exposure associated with the food itself, this model incorporates excess dietary exposures due to handling of food during consumption. To stochastically evaluate CDIM, distributions of measured, and in some cases estimated, model factors were determined from measurements of permethrin, chlorpyrifos, and diazinon derived from assembled databases and laboratory experiments. Using the distributions of these factors, Monte Carlo simulations were performed to obtain distributions of total dietary intake of pesticides. To target the sources of pesticide contamination that were influencing total dietary intake, each factor was evaluated. We found pesticide surface concentration to be highly influential. By excluding surface concentration, we were also able to determine the influence of the other factors based on the F-statistic. Transfer efficiencies, followed by pesticide residue in consumed foods and amount of food consumed, were the next most influential factors within the model. With these distributions for model inputs, CDIM has the potential to more accurately predict total dietary intake of a contaminant by a child.
ISI Document Delivery No.: 761UQ

887. Mendes, M. C.; Lima, C. K. P.; Nogueira, A. H. C.; Yoshihara, E.; Chiebao, D. P.; Gabriel, F. H. L.; Ueno, T. E. H.; Namindome, A., and Klafke, G. M. Resistance to cypermethrin, deltamethrin and chlorpyriphos in populations of Rhipicephalus (Boophilus) microplus (Acari: Ixodidae) from small farms of the State of Sao Paulo, Brazil. 2011; 178, (3-4): 383-388.

Rec #: 65169
Keywords: SURVEY
Notes: Chemical of Concern: CPY
Abstract: Abstract:
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