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Management of the cholinergic syndrome is described in the second part of thisreview.Intermediate syndromeThe term Intermediate Syndrome (IMS) was first described by Senanayake andKaralliedde (1987) because it appeared in the interval between the end of thecholinergic crisis and the onset of OPIDP. Following exposure to various OPpesticides, clinical manifestations of IMS typically occur within 24 to 96 hours, andaffect patients without fasciculation or other cholinergic signs. The reportedincidence of IMS ranges from 7.7% to as high as 84% (Shailesh et al., 1994).Although IMS is well recognized as a disorder of neuromuscular junctions, its exactetiology, incidence, and risk factors are not clearly understood. IMS generallyoccurred among patients with prolonged and severe inhibition of AChE, howevernot every patient with severe AChE inhibition developes IMS. Other risk factors ofIMS include delayed metabolism of OP pesticides due to toxicokinetic factors orimpaired organ function, severity of poisoning, elevated muscle enzymes, andinadequate or late oxime therapy. IMS has been linked with exposure to specific OPpesticides having dimethyl phosphate structure (e.g. fenthion, dimethoate,monocrotophos, dichlorvos, methylparathion) but also developed after exposure toparathion (ethyl phosphate) and methamidophos (phosphoramidate) (De Bleecker etal., 1993; Yang and Deng, 2007). Two typical cases of IMS caused by fenthion anddiazinon were recently described by Jokanović and coworkers (2010).Marked weakness of neck flexion and varying degree of proximal limb muscleweakness, manifesting as weakness of shoulder abduction and hip flexion, are theregular clinical features. Respiratory insufficiency is also common and frequentlydraws medical attention to the onset of the syndrome. Other possible manifestationsare involvement of muscles innervated by motor cranial nerves and decreased deeptendon reflexes. Studies conducted in nineties have shown that intermediatesyndrome goes along with excretion of cholinesterase inhibitor metabolites in theurine and by severe depression in cholinesterase levels. It was suggested that thecondition might reflect the recirculation of lipid soluble cholinesterase inhibitorsfrom body fat compartments or gastric fluids (De Bleecker, 2006).John and coworkers (2003) demonstrated an association between the developmentof IMS and increased activity of enzymes creatine phosphokinase and lactatedehydrogenase, the markers of muscle function, in 25 patients with acuteorganophosphate poisoning. Muscle injury was seen in all patients beginning atadmission, peaking over the first 5 days and then declining over the next 5 days.Temporal profiles of blood muscle isoenzymes showed significantly greater muscleinjury in those patients with greater severity of poisoning at admission, those whodeveloped intermediate syndrome and in patients with longer duration intermediatesyndrome. Khan et al. (2001) and Dhandapani et al. (2003) demonstrated thatoxidative cellular damage of muscle membranes could be associated with musclenecrosis. In a prospective study conducted by De Bleecker (1995) muscle biopsyperformed in 19 patients with OP poisoning showed only minimal number ofnecrotic fibers. IMS could be explained by the reduction in number of functioningcholinergic receptors at the postjunctional membrane, or a failure of acetylcholinerelease. All these abnormal findings on electromyography suggested a combinedpresynaptic and postsynaptic defect, without sensory impairment (Baker andSedgwick, 1996).With appropriate therapy, recovery from IMS occurs 5-18 days after the onset ofweakness. The recovery among patients who survived IMS follows a distinctAcademyPublish.org - The Impact of Pesticides42
pattern, starting first with muscle power recovery in cranial nerve-innervatedmuscles, followed by respiratory muscles, proximal muscles, and neck flexors.Since IMS carries a high risk of death among patients with respiratory failure,prompt recognition of the syndrome is the basis of IMS treatment. IMS managementis mainly supportive since there are no specific antidotes available for this lifethreatening syndrome. As IMS generally takes place at the same time with severeOP toxicity and persistent inhibition of AChE, early gastrointestinaldecontamination, followed by appropriate therapy involving atropine and oximes,and prompt institution of respiratory support, should be helpful in ameliorating themagnitude and/or the incidence of IMS. The prognosis of IMS appears to befavorable if respiratory failure can be promptly recognized and treated accordingly(De Bleecker et al., 1993; De Bleecker, 2006; Yang and Deng, 2007).Organophosphate Induced Delayed PolyneuropathyOrganophosphate induced delayed polyneuropathy (OPIDP) is unique toxicologicalphenomenon in that it is caused by a single exposure to certain OP with effectsusually appearing after 10 to 20 days or later. OPIDP is toxicologically differentfrom OP poisoning in that it is based on different mechanisms which do not involveAChE and appear a few weeks after OP poisoning has been medically solved withstandard therapeutic measures and patient dismissed from hospital. OPIDP is also adifferent syndrome from IMS.Table 2. Organophosphorus pesticides reported to cause OPIDP in man (Jokanović etal., 2002; Lotti and Moretto, 2005; Jokanović and Kosanović, 2010).OP insecticide No ofLocationYearcasesChlorpyrifos 2 Italy, India 1986Dichlorvos 5 Romania, Turkey, Brazil, 1980, 2002-2006Korea, IndiaEthyl parathion 1 Germany 1993Fenthion 3 USA 1985Isofenphos 1 Israel 1987Isofenphos/phoxim 1 Italy 1995Leptophos 80 USA 1974Malathion 2 Japan, Turkey 1991, 2009Merphos 1 USA 1977Methamidophos > 45 Sri Lanka, Italy, China, 1981, 1998Turkey, USAMevinphos 1 Serbia 2010Mipafox 3 UK 1952Omethoate 1 France 1972Phosphamidon/ 1 China 2002MevinphosTrichlorfon 22 Romania, Iran, Japan, 1983 -1986HungaryTrichloronat 1 Poland 1975The interest in OPIDP appeared after thousands cases of poisoning withtriorthocresyl phosphate (TOCP) that occurred mainly due to beverage and foodcontamination in USA in 1930 and Morocco in 1959 (Johnson, 1982; Morgan,AcademyPublish.org - The Impact of Pesticides43
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 44 and 45: 1982; Lotti, 1992; Jokanović et al
Page 46 and 47: exposed populations, revealed high
Page 48 and 49: DiazepamBenzodiazepines are CNS dep
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
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In pesticide applicators, Table 7 s
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DISCUSSIONThe agricultural workers
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changes in the antioxidant enzyme C
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Bajpayee, M.; Pandey, A. K.; Parmar
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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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