Forensic Science International

164 Pages·2004·10.143 MB·English

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ForensicScienceInternational166(2007)85–90
www.elsevier.com/locate/forsciint
Lethal paradoxical cerebral vein thrombosis due to suspicious
anticoagulant rodenticide intoxication with chlorophacinone
F. Papina, F. Clarotb,*, C. Vicomteb, J.M. Gaulierc, C. Daubind,
F. Chapone, E. Vazb, B. Proustb
aForensicDepartment,CaenUniversityHospital,Caen,France
bMedicalForensicInstitute,RouenUniversityHospital,CharlesNicolle,Rouen,France
cPharmacokineticandToxicologyLaboratory,LimogesUniversityHospital,Limoges,France
dIntensiveCareUnit,CaenUniversityHospital,Caen,France
eNeuropathologyDepartment,CaenUniversityHospital,Caen,France
Received9February2006;receivedinrevisedform4April2006;accepted9April2006
Availableonline23May2006
Abstract
Superwarfarinexposureisagrowinghealthproblem,describedinmanycountries.Theauthorsreportacaseofsuspiciouschlorophacinone
poisoningwithaproblematicdiagnosis.Theyreviewtheliteratureanddiscussparticularitiesofanticoagulantrodenticideintoxication,aswellas
theapparent contradiction betweenanticoagulant intoxication and lethal thrombosis.
#2006Elsevier IrelandLtd.Allrights reserved.
Keywords: Rodenticide;Chlorophacinone;Poisoning;Anticoagulant;Cerebralveinthrombosis
1. Introduction an oral oestroprogestative contraception – presented in the
emergency department with a massive hematuria. On admis-
Rodenticide intoxication is rare, as these products are no sion, the patient was apyretic and physical examination
longer used as rodenticide due to its hazardous effects on confirmed macroscopic hematuria and had abdominal pain in
humans. Nevertheless, these products may still be found in therighthypochondralregion,whichinitiallyoccurred3days
certain garden sheds, and could have a ‘‘criminal’’ use. earlier. No particular violence related lesion was observed.
The authors report a case of suspicious chlorophacinone The patient was initially treated by analgesics and
poisoning with a problematic diagnosis. Particularities of intravenous NSAIDs.
anticoagulant rodenticide intoxication are discussed; useful- Bloodlaboratorytestsrevealedahyperleucocytosis(12,500/
nessofbloodanalysisinsuspectedpoisoningorintoxicationis 3mm) which resulted in antibiotic treatment and hospitaliza-
underlined. tion for suspected infected renal colitis.
The authors also discuss the physiopathological character- The following day, abdominal ultrasonography was per-
istics of their case, as well as the apparent contradiction formed and revealed pyelo-calicis hyperechogenicity with no
between anticoagulant intoxication and lethal thrombosis. dilatation. Moreover, a slight fluid collection was observed
medially to the right kidney, and a mobile echogenic residue
was also found in the bladder.
2. Case report
Thepatientcontinuedtohavepainandhematuria,andatday
4shesuddenlypresentedconvulsivelossofconsciousness.She
A 34-year old woman, farm worker, with no particular
was transferred to the intensive care unit in a comatose state
previousmedicalhistoryormedication–withtheexceptionof
(Glasgow scale 4) and was then sedated, intubated, and
ventilated.
* Correspondence to: Institut de Me´decine Le´gale, CHU Rouen, Charles
Initialneurologicalexaminationshowedhypotoniccoma,a
Nicolle,76031RouenCedex,France.Tel.:[phone];
non-reactive left mydriasis and rapidly bilateral areactive
fax:[phone].
E-mailaddress:[email protected](F.Clarot). mydriasis.Shewasadministered100mgofmannitolandaCT
0379-0738/$–seefrontmatter#2006ElsevierIrelandLtd.Allrightsreserved.
doi:10.1016/j.forsciint.2006.04.003
86 F.Papinetal./ForensicScienceInternational166(2007)85–90
Further subsequent toxicological analysis performed on a
serum sample collected during hospitalization, the 4th day
before the death, revealed a high level of chlorophacinone:
25.9mg/L.
Atautopsy,performed4daysafterdeath,wefoundaslight
nailandlipcyanosis,pulmonaryasphyxialesion,andatrachea
oedema. Moreover, autopsy revealed diffuse haemorrhagic
signs(i.e.multipleecchymosis,visceralhaemorrhages,pleural
andperitonealbloodcollection,diffusesubarachnoidhaemor-
rhage, and renal intracavity haemorrhage). The biological
samples collected were sent to the laboratory for forensic
toxicological analysis.
Macroscopic and histologic examination confirmed a
bilateral and diffuse alveolar pulmonary oedema, a multi-
visceralcongestion,anddemonstratedaconcentricmyocardial
hypertrophy.
NeuropathologicalexaminationconfirmedSLSthrombosis.
Italsoshowedaleftfrontalregionhaemorrhagicinfarctlesion,
a diffuse oedema, and herniation of the fifth temporal
circumvolution (Fig. 3).
Policeinvestigationwasnotabletoassesstheoriginofthe
Fig. 1. Initial CT scan show a large left hemisphere haemorrhagic cerebral
infarct,adiffuseoedema,asubarachnoidhaemorrhage,andarightshiftingof intoxication, which was not considered as criminal, but
themidlinestructurewithaleftventriculedisappearance. accidental or suicidal.
scanwasperformedwithnocontrastagent(Fig.1).Itrevealed 3. Materials and methods
an extended left hemisphere haemorrhagic cerebral infarct,
associatedwithdiffuseoedemaandmidlinestructureshiftedto Venous blood sample was collected during hospitaliza-
theright.Biologicalscreeningrevealedaslightanemia(10.3g/ tion, the fourth day before the death. Initially, blood was
dl), an increased hyperleucocytosis (19,490/3mm) and a taken to perform coagulation tests but extensive toxico-
normal platelet count. Coagulation study showed an unex- logical screening (including a chlorophacinone assay) was
plained verylowprothrombintime (10%)and especially very subsequently performed in a serum sample, due to the
lowlevelsofVitaminKdependantfactors(II,VII,IX,andX). diagnostic problems, using high-performance liquid chro-
However, antithrombin III and factor V were normal. matography coupled with diode-array detection (HPLC–
Cerebral angiography, performed to assess the brain DAD).
perfusion state, revealed a thrombosis of the superior Asecondtoxicologicalinvestigationssetwasperformedina
longitudinal sinus (SLS) (Fig. 2). forensic context 4 days after death, on autopsy biological
Despite intravenous Vitamin K injection and adapted samples (peripheric blood, urine, pleural effusion, and gastric
resuscitation, our patient died in an irreversible comatose contents). No visceral, particularly liver, analysis was
state, at day 4. performed.
Fig.2. Cerebralangiography(vialeftvertebralartery)showslackofflowofthesuperiorlongitudinalsinusandacapilar‘‘marshy’’stasis(leftimage).LackofSLS
opacificationisconfirmedbyleftlateralsinusvenography(rightimage).
F.Papinetal./ForensicScienceInternational166(2007)85–90 87
Fig. 3. Macroscopic brain examination confirmed a left frontal haemorrhagic infarct lesion, extended to the caudate nucleus head and the corpus callosum.
Examinationshowedaswellaherniationofthe5thtemporalcircumvolution.
Chlorophacinone assays in serum were performed using a 4. Results
previouslypublishedmethod[1].Thisanalyticalprocedurewas
also applied for chlorophacinone determinations in forensic Toxicologicalscreeningrevealedanteandpostmortemhigh
samples(i.e.blood,urine,andgastriccontents)accordingtothe blood concentration of chlorophacinone (ante mortem tox-
resultsofapreviousanalyticalvalidationstepinsuchbiological icological screening was performed on venous peripheral
matrix. blood;postmortembloodwasobtainfromsubclavianartery).
Briefly,thismethod,routinelyappliedforthesimultaneous Citalopramanddesmethyldiazepamwerealsodiscovered,but
identification and quantitation of 13 hydroxycoumarin and at therapeutic levels.
indandione anticoagulant drugs [2] and rodenticides, used a Postmortemtoxicologicalanalyseswerealsoperformedin
reversed-phase liquid chromatography with diode-array urine(15mL)andgastriccontents(40mL);resultsareshown
detection technique. Extraction step consisted of an acidic in Table 1.
andalkalineliquid–liquiddoubleextractionwithdiethylether–
ether acetate (50:50, v/v). High-performance liquid chroma- 5. Discussion
tography was performed using gradient elution with an
acetonitrile and phosphate buffer on a Nucleosil C18, 5mm Rodenticidesarethenamegiventoanyofthegroupoftoxic
particle size (150mm(cid:2)4.6mm i.d.) column. Detection and substances that are used to kill rodents. Rodenticides are a
quantitationlimitsforchlorophacinonewere20and50mg/L, group of compounds that exhibit markedly different toxicities
respectively.Thestandardcalibrationcurvewaslinearfrom50 tohumansandrodents.Thevarietiesofrodenticidesusedover
to 5000mg/L; within-run precision coefficient of variation theyearsarenumerous,leadingtothepopularexpression,‘‘to
(CV) was less than 10%, and between-run precision CV was buildabettermousetrap’’.Adultswhoingestthesesubstances
less than 20%. are most likely individuals attempting suicide; however,
poisoninghomicidesmay occurwiththese agents duetotheir
ready availability.
Table1 Superwarfarin exposure is a growing health problem [3],
Chlorophacinonelevels
described in many countries. In 2002, in U.S.A., according to
Blood Urine Urine Gastriccontents Gastriccontents the Toxic Exposure Surveillance System (TESS) of the
(mg/L) (mg/L) (mg) (mg/L) (mg) American Association of Poison Control Centers (AAPCC),
Antemortem 25.9 – – – – 19,674 human exposures to rodenticides have been reported.
samples According to the 2002 TESS data, anticoagulant rodenticides
Postmortem 9.4 6.8 0.102 4.8 0.192 wereassociatedwith16,822ofrodenticideexposures,butonly
samples
two lethal intoxications were observed [2]. These cases are
88 F.Papinetal./ForensicScienceInternational166(2007)85–90
always reported as accidental exposition, suicide attempts or reservesofprothrombinhavediminished[2,4,9,12–14,26–30].
Mu¨nchausen syndrome [4–8]. Table 2 showed 16 cases of chlorophacinone intoxication
At the turn of the century, rodenticides were composed described in the literature.
heavy metals such as arsenic, thallium and phosphorus along
with red squill and strychnine. This changed in the 1940s as 5.1. Our case raises multiple problems
investigatorsdiscoveredthatwarfarincouldbetransformedin
bishydroxycoumarinwhenfungiinmoldysweetcloveroxidize First, concerning the origin of the intoxication, which was
coumarin to 4-hydroxycoumarin. Warfarin was quickly not (and will probably never been) assessed. Because our
adopted as the major rodenticide and in 1940, bishydrox- patient,andherfamily,werefarmworkers,theyconsequently
ycoumarin was synthesized and used clinically 1 year later as had access to concentrated rodenticide for professional use.
an oral anticoagulant under the American trade name Regarding the elevated blood level of chlorophacinone, it is
dicumarol. uncertain that intoxication involved granules, because this
However,rodentsresistancetowarfarinbecameprevalentin volumewouldhavebeentoobulkytoingest.Onlytheoilform
the 1960s via autosomal dominant gene transmittance [9]. is known to be sufficiently concentrated to be hazardous, in
Novel compounds were synthesized to combat rodent smallquantities,abletobeingested‘‘accidentally’’.However,
resistance, thereby creating a new class of anticoagulants— anaccidentalingestionofoilychlorophacinonewouldsuppose
the superwarfarins [10]. package reconditioning, or a severe neurological state
The term superwarfarin refers to a group of compounds, impairment. Suicidal intoxication was considered but our
second-generation anticoagulants, which are extremely long- patient had no previous suicidal history, nor psychiatric
acting.Thesefat-solubleanticoagulantsarecolorless,tasteless, symptoms.Criminalpoisoningwasalsoconsidered,butpolice
and odorless compounds [11]. investigationsfoundnoargumentsinfavourofthishypothesis.
Superwarfarins,aswarfarin,inhibithepaticsynthesisofthe Second,thecoexistenceofahaemorrhagicsyndromeandan
VitaminK-dependentcoagulationfactorsII,VII,IX,andXand anticoagulant intoxication was initially disturbing. However,
theanticoagulantproteinsCandS.Chlorophacinonestopsthe the first hypothesis considered was that SLS thrombosis
synthesis of the active form of Vitamin K via inhibition of occurred initially and subsequently induced neuropsychiatric
1
Vitamin K epoxide reductase, which blocks coagulation impairment.Accidentalorsuicidalingestionwouldhavebeen
1–3
factor synthesis (II, VII, IX, and X) [2,9,12–16]. consequent to these alterations. Nevertheless, our patient’s
Superwarfarins are metabolized by hepatic cytochrome P- husband did not described major or sufficient behavioural
450isoenzymestohydroxylatedmetabolites.Itisuncertainthat abnormalities in favour of this hypothesis.
whole metabolites are inactive [9]. In fact, the review of the literature regarding warfarin has
Chlorphacinone is an indandione-derivative with a pro- explained this apparent contradiction [31–33]. Certain studies
longed effect of the superwarfarins family [11]. This antic- involved warfarin levels, monitored by measuring the
oagulantisapproximately100timesmorepotentthanwarfarin prothrombin time, which responds to reductions in levels of
onamolarbasis[9].Thehalf-lifeofsuperwarfarinvariesfrom threeVitaminK-dependentclottingfactors(factorsII,VII,and
16 to 69 days compared with 37h for warfarin [16,17]. The X). It has been demonstrated that during the first 48h of
mosthumantoxicformisanoilybase(concentrationof2.5g/ treatment,theanticoagulanteffectofwarfariniscausedmainly
L), which is found in numerous commercial products world- byareductionintheactivityoffactorVII,whichhasahalf-life
wide. However, this form is no longer sold in France (since of6h.Incontrast,theantithromboticeffectofwarfarin(which
2000) as it has been considered a health hazard. isthoughttobecausedprimarilybyareductionintheactivity
Each Vitamin K-dependent factor differs in its degradation offactorII)isdelayedforaslongas60h.Therefore,duringthe
half-life; factor II requires 60h, factor VII requires 4–6h, first 48h of therapy, the anticoagulant and antithrombotic
factor IX requires 24h, and factor X requires 48–72h. The effects of warfarin may be unrelated. In addition, because the
half-lives of proteins C and S are approximately 8 and 30h, half-life of the Vitamin K-dependent anticoagulant protein,
respectively.Asaresult,becauseantivitaminKreducesfirstthe proteinC,issimilartothatoffactorVII,theearlyanticoagulant
activity of anticoagulant proteins C and S, a hypercoagulable effect ofwarfarin(whichresults fromreduction offactorVII)
state may be initially induced. Rapid loss of protein C could be counteracted by a procoagulant effect (which results
temporarily shifts the balance in favour of clotting until from reduction of protein C). Moreover, it has been also
sufficient time has passed for antivitamin K to decrease the demonstratedthatgreaterdoseofwarfarinwasassociatedwith
activity of coagulant factors [18–21]. asignificantlymorerapiddecreaseinproteinCactivity(which
Chlorophacinonepoisoninginducesprolongedprothrombin decreased before levels of factors X and II were substantially
time (PT), elevated international normalized ratio (INR), reduced). Therefore, the combination of markedly reduced
extended activated prothromboplasmin time, and decreased proteinClevelsandnear-normallevelsoffactorsIIandXover
Vitamin K-dependent factors levels. Bleeding is the most the first 2 days of warfarin therapy could produce an initial
commonclinicalfeatureandmayoccurfromanymucosalsite hypercoagulable state.
ororgan[22–25].Thefirsthaemorrhagicsignsusuallyoccur3– Obviously,itisnotpossibletostudychlorophacinoneeffects
7 days after intake, depending on the dose ingested, and the on humans, but it is probably scientifically possible to
substance half-life (from 6 to 23 days), when the body’s extrapolate warfarin data to superwarfarins.
F.Papinetal./ForensicScienceInternational166(2007)85–90 89
Table2
Reviewoftheliterature(whenchlorophacinonebloodlevelorabsoptionisreported)
Reference #Case Sex Intoxication Death Absorption Symptoms Biologicaltests Chlorophacinone
(age reason (Yes/No) mode,dose (appearancedelay) (appearancedelay) bloodlevel,
(years)) ingested half-life(Hl)
Dusein 1 M(28) Suicide N Oral,Unknown Cutaneousmucous PT=0%, Unknown
etal.[26] haemorrhage(day10) APT=65/32(day10)
Murdoch 2 F(37) Suicide N Oral,625mg None INR=1.2(hour18) Unknown
etal.[30]
Chataigner 3 F(79) Suicide N Oral,375mg Haematomas, PT=92%(hour1.5) Unknown
etal.[4] ecchymosis(day37)
4 M(45) Suicide N Oral,500mg None PT=43%(hour18) Unknown
5 M(18) Suicide N Oral,625mg Multiplecutaneous PT=75%(hour1.5); Unknown
mucoushaemorrhage hypocoagulability
(day16) (day2)
6 M(21) Suicide N Oral,750mg Haematuria(day15) PT=53%(afew Unknown
hourslater)
7 M(54) Suicide N Oral,750a` 1500mg None PT=38%(day2) Unknown
8 M(27) Suicide N Oral,Unknown None PT=18%(day2) Unknown
9 M(72) Suicide N Oral,Unknown Microscopical PT=65%(day16) Unknown
haematuria(day2)
10 M(52) Suicide N Oral,500–1200mg Haematuria, PT=100%(afew Unknown
haematomas(day2) hourslater)
11 M(61) Suicide N Oral,500mg Haematuria(day19); PT<10%(day21) Unknown
gumsbleeding(day21)
Burucoa 12 F(20)ans Suicide N Oral,250mg Lumbarpain, Hypocoagulability Day12:2mg/L,
etal.[9] macroscopical (day7) Hl:6.5days
haematuria(day7)
13 F(60)ans Suspected N Unknown,unknown Macroscopical Hypocoagulability 12.9mg/L,
suicide haematuria, Hl:22.8days
vaginalbleeding,
gumbleeding,
thighecchymosis
14 M(23)ans Suspected N Unknown,unknown Abdominalpain, Hypocoagulability 1.2mg/L,
suicide macroscopical Hl:11days
haematuria,
gumbleeding
Arditti 15 F(27)ans Suicide N Oral,625mg Asthenia,inhalation PT<10%,APT= Hour80:43mg/L,
etal.[12] pneumopathy 44/32(hour80) Hl:7.6days
(hour80)
Lagrange 16 M(33)ans Suicide N Oral,1875mg Nausea(hour8) PTnormal(hour8) Hour8:27.6mg/L
etal.[14]
INR:internationalnormalizedratio;PT:prothrombintime;APT:anti-prothrombintime.
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ForensicScienceInternational166(2007)91–101
www.elsevier.com/locate/forsciint
Detection of gunpowder stabilizers with ion mobility spectrometry
C. West*, G. Baron, J.-J. Minet
De´partementdesExplosifsetIncendies,LaboratoireCentraldelaPre´fecturedePolice,39bisruedeDantzig,75015Paris,France
Received11November2005;receivedinrevisedform5April2006;accepted7April2006
Availableonline7July2006
Abstract
Thisstudyisthefirstreportedionmobilitydetectionofethylcentraliteanddiphenylamine(DPA)smokelessgunpowderstabilizers,together
withthenitrosoandnitroderivativesofdiphenylamine.First,theapplicabilityoftheionmobilityspectrometry(IMS)forthesubstancesofinterest
wasdetermined.Theexistenceofnumerouspeaks,bothinpositiveandnegativemodes,clearlydemonstratesthesuccessoftheseexperiments.All
mono and di-nitro derivatives of DPA tested were detected with this method. Unfortunately, many of the ions generated were not accurately
identified.However,reducedmobilityconstantsrepresentativeofeachiongeneratedunderdefinedoperatingconditionscouldbeusedforpurpose
ofcompound identification.
The methodwas thensuccessfully testedonrealgunpowder samples.
BytheuseofIMS,wemanagedtoestablisharapid,simpleandsensitivescreeningmethodforthedetectionandidentificationofsmokeless
gunpowder organiccomponents.
#2006Elsevier IrelandLtd.Allrights reserved.
Keywords: Diphenylamine;Ethylcentralite;Smokelessgunpowder;Ionmobilityspectrometry(IMS)
1. Introduction varnishes, celluloid films and pharmaceutical industry, while
NG also occurs in pharmaceutical preparations [2].
Smokeless powders are commonly used in modern Organicadditives,suchasdinitrotoluene(DNT)isomers—
ammunition. Additionally, they are frequently used in the used as a flash suppresser, dibutylphthalate—used as a
constructionofimprovisedexplosivedevices(IEDs)relatedto plasticizer,methylandethylcentralite(EC)anddiphenylamine
criminal and terrorist acts. Therefore, in the latter case and in (DPA)—used as stabilizers are also present in gunpowder
firearmdischargecases,theidentificationofsomecomponents composition.
that can associate residue samples with unfired gunpowder ECisregardedasacharacteristicmaterialingunpowderbut
provides valuable evidence to the forensic scientist. When it is not present in all compositions.
inorganic gunshot residues have not been recovered or their DPA is also commonly used in the perfumery, in the food
characteristicsarenon-specific,theanalysisoforganicresidues industryandasantioxidantintherubberandelastomerindustry
is required to provide complementary information. [3], thus, the single detection of DPA is not a diagnostic of
The main component of smokeless gunpowder is nitrocel- gunpowder presence.
lulose(NC).Insingle-basedpropellants,itistheonlyenergetic ItiswellknownthatDPAstabilizestheenergeticcomposition
material in the composition, while in double-based powders, by binding nitrous oxide gases originating from NC decom-
nitroglycerin(NG)isalsopresent.Intriple-basedgunpowders, position,andconvertingthemintostablecompounds.Themain
otherexplosivecomponentscanbefound,nitroguanidinebeing reactionproductsofnitrousoxidegasesandDPA(seeFig.1)are
themostfrequent.However,NCandNGhavebeenregardedas N-nitroso-diphenylamine (N-NODPA), 2-nitrodiphenylamine
beingalackofconclusiveevidence[1]asNCiswidelyusedin (2-NDPA) and 4-nitrodiphenylamine (4-NDPA). N-NODPA
is believed to be the primary intermediate before the nitro
derivatives are formed by a Fischer–Hepp rearrangement –
leading to 2-nitroso-diphenylamine (2-NODPA) and4-nitroso-
* Correspondingauthor.
diphenylamine(4-NODPA)–andanoxidationstep[4,5].These
E-mailaddresses:[email protected](C.West),
[email protected](J.J.Minet). nitroso and nitro derivatives also act as stabilizers [5,6], and
0379-0738/$–seefrontmatter#2006ElsevierIrelandLtd.Allrightsreserved.
doi:10.1016/j.forsciint.2006.04.004
92 C.Westetal./ForensicScienceInternational166(2007)91–101
Fig.1. DominatingreactionroutesoftheinitialDPAdegradationinanaginggunpowder[4–6].(1)DPA,(2)N-NODPA,(3)2-NDPA,(4)4-NODPA,(5)4-NDPA,(6)
2-NDPA,(7)2,4-NDPA,(8)2,40-NDPA.
further react with nitrous oxide gases to form highly nitrated NODPA is the primary intermediate formed and is therefore
derivativesofDPA,suchasN-nitroso-2-nitro-diphenylamine(N- present in high proportions.
NO-2-NDPA), 2,4-dinitrodiphenylamine (2,4-NDPA) and 2,40- Normal phase and reversed phase high-performance liquid
dinitrodiphenylamine (2,40-NDPA). The last compound to be chromatography (HPLC) [5,8] are both commonly applied,
formedwouldbethe2,20,4,40,6,60-hexanitrodiphenylamine,that with varied detectors: either with UV–vis spectrophotometry
wouldlaterfacedecompositionintopicricacid. [9],amperometricdetection[5,10],fluorimetricdetection[11]
The other origins of DPA, possibly causing environmental ormorerecently with mass spectrometry [12]. HPLCleadsto
contamination in casework samples, can be minimized if the satisfyingseparationsofthemajornitroandnitrosoderivatives.
nitratedderivativesofDPAcanalsobeidentifiedinthesample, Equallygoodseparationswerereportedwithsupercriticalfluid
as those are unique to smokeless gunpowder. chromatography [4,13] and micellar electrokinetic chromato-
Therefore,ifbothenergeticcompoundssuchasNCandNG, graphy [8]. A tandem MS method was recently reported [14].
and organic additives such as EC or DPA and some of its In the forensic laboratory, casework samples are often
nitrated derivatives can be identified simultaneously in case- complex mixtures issuedfromthe solvation ofacomplex and
work samples, the presence of gunpowder is ascertained. dirty matrix. In this case, thin layer chromatography (TLC) is
Because the amount of stabilizer initially introduced in the the most appropriate technique. In our laboratory, we
composition is very small (about 2%), a highly sensitive traditionally use TLC, followed by an oxidation step, for the
analytical method is required. detection of stabilizers. This method suffers from poor
Theuseofgaschromatography(GC)fortheanalysisofDPA sensitivity and is very time consuming, but it is the most
derivativesislimitedbythelowvolatilityofthehighlynitrated appropriate for the analysis of dirty samples.
derivatives. Indeed, tri- and tetra-nitrodiphenylamine analogs Additionally,incasestudies,methodsofidentificationbased
need very high operating temperatures (upto3208C)[4].GC onnoncorrelatedseparationmechanismsareneeded.Amethod
withthermalenergyanalysisdetection(GC–TEA)isgenerally that would provide orthogonal identifications to the classical
preferedtoGCcoupledtomassspectrometry(GC–MS)asthe chromatographicmethodsisrequired.Thus,thecombinationof
latterisreportednottobesensitiveenoughforreal-lifesamples twosuchmethodswouldenhancetheidentificationpowerand
[7]. Furthermore, N-NODPA and other nitroso derivatives of the analytical reliability.
DPA are generally reported to degrade in the injection port in Ion mobility spectrometry (IMS) is commonly used by
GC. The failure of GC to elute N-NODPA intact severely forensic scientists to identify the major explosives, narcotics
restrictsitsusefulnessintheanalysisofDPAderivatives,asN- and chemical warfare agents. Basically, IMS refers to the