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DiazepamBenzodiazepines are CNS depressants, anxiolytics and muscle relaxants. Their mainsite of action is at the gamma-aminobutyric acid (GABA) receptor. The GABAAreceptor is a ligand gated chloride ion channel and part of a superfamily of receptorswhich also includes the nicotinic acetylcholine receptor and the glycine receptor.GABA is the major inhibitory neurotransmitter in the mammalian central nervoussystem. Benzodiazepines, including diazepam, alter GABA binding at the GABAAreceptor in an allosteric fashion but these drugs do not directly activate the receptors(Sellström, 1992; Marrs, 2004).Currently, the most important anticonvulsant is diazepam. The combination ofatropine and diazepam is more effective in reducing mortality than atropine oroxime alone. It was also shown that diazepam enhanced the efficacy of low doses ofatropine. In the cholinergic nervous system, diazepam appears to decrease thesynaptic release of ACh. The main consequence of the action of benzodiazepines inCNS is hyperpolarization of neurons making them significantly less susceptible tocholinergically-induced depolarization. The ultimate result is cessation ofpropagation of convulsions (Sellström, 1992; Marrs, 2004).In patients poisoned with OP, benzodiazepines may have a beneficial effect inreducing anxiety and restlessness, reducing muscle fasciculation, arresting seizures,convulsions, controlling apprehension and agitation and possibly reducing morbidityand mortality when used in conjunction with atropine and an oxime. Diazepamshould be given to patients poisoned with OP whenever convulsions or pronouncedmuscle fasciculation are present. In severe poisoning, diazepam administrationshould be considered even before these complications develop. The recommendeddose of diazepam in cases of OP poisoning is 5-10 mg intravenously in the absenceof convulsions and 10-20 mg intravenously in cases with convulsions, which may berepeated as required (Johnson and Vale, 1992; Jokanović, 2009a). WHOrecommends the dose of diazepam of 5 to 10 mg intravenously slowly over threeminutes which may be repeated every 10 to 15 minutes (maximum 30 mg) in adultsand 0.2 to 0.3 mg/kg intravenously slowly over three minutes in children (maximum5 mg in children up to 5 years old, and 10 mg in children older than 5 years) (IPCS,1998).Pyridinium OximesExtensive studies over the past few decades have investigated the mechanism ofaction of pyridinium oximes. The rate of spontaneous reactivation of phosphorylatedAChE can be accelerated by pyridinium oximes that have a chemical structurewhich ‘fits’ the structure of the inhibited AChE. The oximes can only be of benefitas long as inhibited AChE is not completely converted to the aged form which isresistant to both spontaneous and oxime-induced reactivation. Oximes reactivatephosphorylated AChE by displacing the phosphoryl moiety from the enzyme byvirtue of their high affinity for the enzyme and their powerful nucleophilicity.Phosphorylated oximes are formed during reactivation reaction (Figure 2) and someof them appear to be potent inhibitors of AChE (Luo et al., 1999; Ashani et al.,2003; Worek et al., 2007). It was shown that phosphorylated oximes of 2-substitutedpyridinium compounds (e.g. PAM-2, HI-6) are rather unstable while those of 4-pyridinium aldoximes are markedly stable (Worek et al., 2000; Ashani et al., 2003;Kiderlen et al., 2005).AcademyPublish.org - The Impact of Pesticides48
Figure 2. Reactivation of phosphorylated acetylcholinesterase with PAM-2 andformation of reactivated enzyme and phosphorylated oxime.O ORAChE-P +OR N CH=NOH AChE+CH 3N CH=NOCH 3O ORPORPyridinium oximes are effective against OP-inhibited AChE in the peripheralnervous system, but have a limited penetration across the blood-brain barrier due totheir pharmacokinetic profile and the presence of quaternary nitrogen atom(s) intheir structure. However, it appears that oxime penetration through blood-brainbarrier is underestimated since soman can cause seizure-related opening of theblood-brain barrier (Carpenter et al., 1990; Grange-Messent et al., 1999) and enablepassage of higher oxime concentrations into the brain. It was shown that 0.5-1.0LD50 of sarin caused a dose-dependent increase in permeability of blood-brainbarrier in midbrain, brainstem, cerebrum and cerebellum in rats 24 hours afterpoisoning (Abdel-Rahman et al., 2002). Sakurada et al. (2003) have determined theamount of PAM-2 passing accross the blood-brain barrier at approximately 10% ofthe given dose which may be effective in reactivation of OP-inhibited AChE inbrain. Additional data indicate indicate that in OP poisoning, when given withatropine, PAM-2 can pass bloodbrain barrier at higher concentrations.In addition to performing AChE reactivation in OP poisoning, pyridinium oximesmight also show direct pharmacological effects. This issue is discussed in detail byJokanović and Stojiljković (2006) and Jokanović and Prostran (2009). In addition,the structure-activity relationships for pyridinium oximes developed as AChEreactivators were discussed by Jokanović and Prostran (2009) and Musilek andcoworkers (2011).Observational studies of pralidoxime and obidoxime suggest that the ability toreverse AChE inhibition with oximes varies with the pesticide ingested. AChEinhibited by diethyl OP pesticides, such as parathion and quinalphos, seems to beeffectively reactivated by oximes, but AChE inhibited by dimethyl OP, such asdimethoate, monocrotophos and oxydemeton-methyl, apparently responds poorly.AChE inhibited by S-alkyl-linked OP, such as profenofos, is not reactivated byoximes at all. This difference is probably caused by variations in the rate of aging oninhibited AChE induced by different OP pesticides.Figure 3. Chemical structure of pyridinium oximes used in the medical treatment ofhuman OP poisoning. X indicates an anion.AcademyPublish.org - The Impact of Pesticides49
Page 1 and 2: The Impactof PesticidesEdited by:Pr
Page 3 and 4: Other access free resources from Ac
Page 5 and 6: The Impact of PesticidesPrepared an
Page 7 and 8: Table of Contentsp.203-p.224 Behavi
Page 9 and 10: About authorspublished by Elsevier.
Page 11 and 12: About authorsof medical researchers
Page 13: About authorsdifferent spatial scal
Page 16 and 17: About authorsEducation:Bachelor’s
Page 18 and 19: About authorsSensors - A Nanotechno
Page 20 and 21: Section 1HUMAN EXPOSURE TO PESTICID
Page 22 and 23: ecently explored on preliminary stu
Page 24: individuals within 1 day (Jokanovic
Page 27 and 28: occupational environmental health r
Page 30 and 31: must be considered, since effective
Page 34 and 35: Jensen BH, Petersen A, and Christen
Page 36 and 37: Ragas AMJ, and Huijbregts MAJ (1998
Page 38 and 39: Weichenthal S, Moase C, and Chan P
Page 40 and 41: human poisoning, general acute symp
Page 42 and 43: Management of the cholinergic syndr
Page 44 and 45: 1982; Lotti, 1992; Jokanović et al
Page 46 and 47: exposed populations, revealed high
Page 50 and 51: Among the many classes of oximes in
Page 52 and 53: inhibited by dichlorvos (a dimethox
Page 54 and 55: Dawson, 1995). It appears that the
Page 56 and 57: Eddleston M, Eyer P, Worek F, Moham
Page 58 and 59: Jokanović M, Kosanović M (2010b).
Page 60 and 61: Ray DE (1998). Chronic effects of l
Page 62 and 63: Worek F, Eyer P, Kiderlen D, Thierm
Page 64 and 65: developing countries is due to suic
Page 66 and 67: count and morphology, as well as se
Page 68 and 69: PON1 modulation of genetic damageFe
Page 70 and 71: elationship between OP exposure and
Page 72 and 73: Blatter-Garin MC, James RW, Dussoix
Page 74 and 75: Hung RJ, Hall J, Brennan P, Boffett
Page 76 and 77: Rojas-García AE., Solís-Heredia M
Page 78 and 79: Occupational Exposure to Pesticides
Page 80 and 81: considered as conditions typical of
Page 82 and 83: observed adverse health outcome. Su
Page 84 and 85: within cells can oxidize biomolecul
Page 86 and 87: of the study. A face-to-face questi
Page 88 and 89: PesticidesFungicideInsecticide-Nema
Page 90 and 91: Table 4. Mixtures of pesticides use
Page 92 and 93: In pesticide applicators, Table 7 s
Page 94 and 95: DISCUSSIONThe agricultural workers
Page 96 and 97: changes in the antioxidant enzyme C
Page 98 and 99:
Bajpayee, M.; Pandey, A. K.; Parmar
Page 100 and 101:
Environmental health criteria 155.
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Palus, J.; Rydzynski, K.; Dziubalto
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Singh, N.P.; McCoy, M.T.; Tice, R.R
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INTRODUCTIONPopulations may be occu
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exposure scenarios on the basis of
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not present adverse health effects
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greenhouse workers exposed to malat
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Paraoxon is then either metabolized
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cyclohexene-1,2-dicarboximide, CAS
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metabolite of phthalates, such that
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scenarios were simulated, assuming
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Table 2. Biological reference value
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References N a urinarybiomarkeStudi
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Figure 2. Representation of a BRV d
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Figure 4. Conceptual representation
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Figure 6 Conceptual representation
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REFERENCESACGIH, 2011. Documentatio
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Bradway, D.E., Shafik, T.M., 1977.
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EPA, 1999b. Registration Eligibilit
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Hines, C.J., Deddens, J.A., Jaycox,
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McCollister, S.B., Kociba, R.J., Hu
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Verberk, M.M., Brouwer, D.H., Brouw
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important IGFBP for binding IGF-1 i
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secretion of IGF-1 (Tannheimer et a
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FIGURESFig. 1. An “hormetic” ef
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Landi F, Capoluongo E, Russo A, Ond
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Smith WJ, Underwood LE, Clemmons DR
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Section 2PESTICIDES IN THEENVIRONME
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vicinity of subsoil waters and ther
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Hieracium pilosella, southernwood -
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formed clusters (Figure 3). Ultrast
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Fig. 5. Fragment of hepatocyte of t
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Szarek, J, Skibniewska, K, Wojtacka
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negative effects (ZALUCKI et al., 2
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Figure 2. Appropriated sampling pro
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Figure 4. Illustration of the conse
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(HAILE et al., 1998). Earlier resul
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Table 1. Distribution of the applic
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Means followed by the same letter i
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(involving pests and natural enemie
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efore the pest emergence and their
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Table 3 (continuation)…AcademyPub
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Table 5. Effect of different fungic
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Table 6. Magament used including do
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adopted by Brazilian soybean grower
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Pickle, C.S.; Caviness, C.E. Yield
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This chapter reports on Dutch surfa
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several different occasions at any
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The greatest number of pesticides a
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Accumulated ExceedanceIt is useful
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For the years 2003-2009 the calcula
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Bonzini S, Verro R, Otto S, Lazzaro
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atios of the pesticide amounts in t
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Table 1. (Cont.) Runoff ratios of p
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mefenacet and simetrin were observe
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Table 2. (Cont.)Pesticide concentra
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Table 2. (Cont.)Pesticide concentra
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Fig. 3. Typical weekly variation of
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(BAM) in water (Pukkila et al. 2009
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Table 5. Concentrations of pesticid
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Table 6. Maximum concentrations of
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Iwafune, T, Inao, K, Horio, T, Iwas
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Suzuki, M, Takemine, S, Yoshida, M,
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factor, etc. Levels of pesticides i
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factor of 10 above ambient sea wate
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weight sample. Minimum were shown f
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Figure 3. DDTs in mussel samples fo
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Figure 5. HCB in mussel samples for
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Figure 8. Methoxychlor in mussel sa
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ACKNOWLEDGEMENTAuthors thank UNEP/M
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Pesticide Risk Index of Del Azul Wa
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on that presented in Swanson et al.
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eference value for that substance.
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predict the aquatic toxicity of a s
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Calculation Model of Aggravating Fa
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To estimate the values of Human Hea
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water in comparison with the durati
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Cypermethrin (95 th percentile (P 9
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Table 8 shows the results of the De
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are many ranking systems of dangero
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REFERENCESAres J. (2004). “Estima
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Mackay D. and Paterson S. (1991).
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Long-term Monitoring of Pesticides
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Sampling sites of the survey in 200
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than those in Lake Biwa and Seta Ri
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Fig. 7 Detection of fungicides in R
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Fig. 11 Detection of herbicides in
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Monitoring of pesticides in Yanamun
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A measured volume (1000 mL) of the
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SimetrynePretilachlorConcentration
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Fig. 18 Maximum concentrations of t
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Ecological risk assessmentFig. 20 Y
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REFERENCESAgradi E, Baga R, Cillo F
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Time Trend Variation of Selected Pe
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Table 1. Physical and chemical prop
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marketed under variety of trade nam
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Figure 3. Long-term trends of globa
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laboratory animals fed or injected
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fed for a lifespan at 5-1,600 mg/kg
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Soil samplingSoil sampling was foll
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Figure 5. Map showing sampling area
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concentration (MAC) in surface soil
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Table 7. Concentrations of HCH isom
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Shanghai and Guanting Reservoir (Ch
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Contrary to the results of ΣDDT, t
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DDT metabolites, the ratio of (p,p
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2001). Therefore, the predominance
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Mean concentration (ng g -1 dw)3002
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CONCLUSIONSAn evaluation of selecte
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Hung, D.Q., Thiemann, W., (2002),
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Viet, P.H., Hoai, P.M., Minh, N.H.,
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found in tissues or fluids samples
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Study area and SamplingThis study w
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the liver, mainly to p,p'-DDE and p
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33,370 ha, whilst that of woody cro
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Increase in crops area (x1000)Ha)25
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Table 1. Blood concentrations of or
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Council Directive 90/533/EEC of 15
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Konstantinou, IK, Goutner, V, Alban
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Smith, AG (2004). “Toxicology of
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Pesticides are used in order to pro
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EXPERIMENTALMaterialsIsoproturon wa
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RESULTS AND DISCUSIONEquilibrium is
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As seen in Table 4, as the concentr
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Fig.4. Breakthrough curves of isopr
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Fig.6. Breakthrough curves of isopr
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Fig.8. Experimental and theoretical
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Section 3PESTICIDE ANALYSISAcademyP
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scandal’ are familiar to the gene
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ecoveries (>70%) for certain pH-dep
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Due the versatility of the QuEChERS
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of application, with some still sca
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The main supercritical solvent used
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extracting the pesticides from the
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would be appropriate for the routin
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chromatography with negative-ion el
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GPC was applied as a nondestructive
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Charlton A.J.A., Stuckey, V. (2009)
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Lehotay, S.J., Mastvoska, K. & Yun,
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Rodrigues, F. M., Mesquita, P. R. R
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Analytical methods to assess the im
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acetylcholine, a neurotransmitter t
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1.3 to 22.3% for all pesticides. Li
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Malathion, parathion, fenitrothion,
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Fuller, BH and Berger, GMB (1990).
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Table 1. Largest exporters of coffe
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Fig. 1: Structures of (a) Phosphate
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ELECTROCHEMICAL BIOSENSORBiosensors
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inorganic and organic species a lar
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surface area and be easily modified
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Acetylcholine + H 2 O AChE Choline
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Wang, 2010) and tetracyanoquinodime
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PDDA/AChE/PDDA/CNT/GCAChE-Au-PPy/GC
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ng/mL and good precision (RSD ) 5.3
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FUTURE PERSPECTIVESThe detection of
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Du, D; Wang, M; Cai, J; Qin, Y; Zha
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Martorell, D; Cespedes, F; Fabreaga
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The Pesticide Action Network (PAN).
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About EditorMilan JokanovićProfess
Page 418:
THE IMPACT OF PESTICIDESPesticides
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