CAPÍTULO II: ESTUDIO DE MERCADO
2.1. Análisis de la oferta
2.1.3. Perfil general del sector artesanal en Saraguro
O,er the )CilD, o number of �tudic� tm,e been conducted to U\�css nnd qunntif) lhc:
impact or ,nacsttng ancn1c-contam1nntcd ground"'111cr (Ahmad, Gold11r and Jow1) o.
2003) However a surpnsing lindlna of many or the studtc:s has been that 10 spuc of
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more lhan a decade of research, studies, and other interventions regarding arsenic 1n South and East Asia - no clear picture has yet emerged of lhe epidemiolog) of arsenic
in the region. Estimates of the (future) health impacts of arsenic ingestion ore mostly based on extrapolated data fron1 the United States of An1erica and Ta1,,an {China), and their validity for interpretation al a "ider scale is therefore frequently questioned
(World Bank, 2005).
Globally, the only large-scale screening. earned out in Bangladc,h through the l3angladcsh Arsenic Mitigation \Vater Suppl) ProJect (B,\J\-1\\'SP) and other Go'>cmmcnt of Bangladesh funding sources and donors, \\:hich included patient
idcntilication. indicated that for fe\\cr people sho,, signs of orscnicosis than could be expected fron1 extrapolation of the United States and T.ih,un epidemiological dnta
(t.laddison, Luque. und Pearce, 2004)
fhe ncg.ui,e health effects of arsenic inge.,tion ha, e been documented for the last 200 > c:ars In spite of the uncennint) rc:gard1ng e:-.uct 11un1bcrs, 11 is clc.ir that there
ill'\! maJOr cllccts, but 1t 1s not yet clear ho,, \\1de ptclld or �crious these ure or ,.,.hot the
relationship of di�eJSe to e:-.po�ure is in diITcrent selling..-,. It 1s. ho,,evcr, ob'>1ous that millions of people are at risk from nrscnic-induced disease, (Smedley, and Kinniburgh,
2002). \\'hat is not clear i1Ccord1ng to \Vorld Bank (2005) .ire
(11) ho\\ n1an) people in these n�I.: nn:as \\ ill be atTccted by arsen1c-related disease and \\'llhin \\hich timefran1e (cspcci,111) compared \\ith other ,vatcrbome diseases ,vherc clTect� ma) be more immcdintc:, such ns diarrhoea 111 undcr-li,e-ycnr•olds, \\l11ch 1s ofien fatal), and
(b) ,, hat c:-.actl} the he.11th cfh:cts 1uc going to be; 1hcre 1s still unccrto1nt)
,\hcthcr skin lcs1ons, t)p1eull) the most visible expression of nrscnicosis, nrc the lir.,t symptom or if internal c,1nccrs and other aihncnts cnn also be prcsc:nt in the ob cnce of skin lesions,
2.10.1. Signs and S)'mpto,ns of t\s
Acute ingcsuon of As 1s charucten,eJ b) the uppcamnlc of cl1111c.1l S) n1pton1s
wilh,n 30 minutes of 1nges11on. Inc oppcurnnce ol these could be dchi)cd 1f 11 15 ingested with food (Graeme: and Pollock, 1998) from the litc:rutun: 11 1s c:, 1dcnt that clinical marufcstAUons n:suh1ng from ancntc po110n1ng nn: sys1c:ms,spec11ic (Peterson
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cl al, 1977; Dahigcn ct al, 1978, Goldsmith 1980. \\ 1nship. 1984; l-lindcmash and McCurdy, 1986, Aschangrau. Zieler and Cohen, 1989; r-..torton and Caron, 1989,
Malachowski, I 990, Jolliffe, ct al, 199 l: ,\xclson. BorLon ) i. Bcneczh) ct al, 1992.
Wade cl al. I 993: Clarkson. I 99S, Abcmoth ) . Calderon and Chappel. 1997: l·run1k1n ct al 2001: Ng, \Vang and Shra,m. 2003: fsuji. Benson. Schoof and Hook 200-t).
According to the obse�ations of Grocn1c et al { 1998), and Ocnrnn1danc ct al ( 1999) gastrointestinal distress (characterized b) nausea. \Omiting, abdon1inal cmn1ps nnd diarrhoea that mil) be blood ,ta,ned) is usually the presenting S) mptom of acute nr-s.cnic poisoning ,vhile h ) potcnsion, tnch)cardia, neuropalh) and , nscular lc:.1ons gl\ en rise to gangrene of the extremities are also comn1on earl� signs. The poo;sibilit ) of n1ulti
organ liiilun: has also been postulated (Schoolmccstcr ct al, 1980. Gorb), 1990, }.lalacho,,ski, 1990: Subra111aniu w1d Koscncll. I 99R) Chronic exposure nta) prc:.cnt inform of abdominal pain. vomiting. diarrhoea, muscular \\cakncs� nnd cramping. pain to the cxtn:mitics, Cl')thcn1otous skin eruptions and s\\clhng of the C)clids, feet and hands, ,\ progrcssh c deterioration in the n1otor and sensor') rcspon)e:. ,na} also result ,vhich 1nny finally lead to shock nnd de.1th (\lead. 200S). The lethal dose 1s probnbl>
bet\\een I 00-200mg of arscnious ncu.l for nn odult indi\ ,dual although pcopll! have suf\ i vcd larger doses.
I he chnicul fc:a1ures of bo1h ocu1c :ind chronic ,\s poisoning/exposure h:i,c been suflicicnll ) docun1cntcd in th.: li1cralurc 1 he) include both cancer und non-c:incer
ctlccts ,,..hich often results from both ncu1c nnd chronic .:xposurcs (:\lead, 2005)
2.10.2. Acute exposure
,\cute expo urc 10 an..:nu: po1son1ng hos been found lo present in , nrious forms \\llh d 1 lfcrcn1 chruc:il m:in1fc�1u11on�. Thc�c 1111.:ludc·
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2.10.3. Dermal exposure
Severe foot burns occurred in a patient exposed to concentrated arsenic ncid
saturatcd clothing for eight hours (l'vlc\Villia.ms, 1990). Soft tissue deposits believed to be metallic arc;cnic ,.,ere noted on X-ray. ll1e patient ,vas transient\) encephalopathic nnd de,elopcd n chronic painful foot motor neuropath ) . T\\cnty four hour urine arsenic elimination rW1gcd Crom 2500 mg fnlhng 10 160 mg during on eight \\eek course of
pcnicillan1ine.
Garb and I line ( 1977) reported:
"o ,,orkcr splashed do\\n the left side of his bod) \\ith arsenic ncid in on industrial 11ccident I le immediate I) rcmo, ed 11 conta.m1na1cd glo, e and \\nshcd his hands but did not notice arsenic ncid 1n his left shoe for some ten 1n1nutcs
After "ashing the a!Tcctcd leg und rcn1ov1ng a soiled sock he continued to \\Ork for o further four hours b) ,vhich 11111e he had sustained second degree bums in the ocid-cxposcc.l areas. Eleven hours after the incident he developed pain and s,,elling at the contact sites plus nausea. ,omiting. diarrhea and 11bdon1inol pain necessitating hospital admi:.sion During the next three da)S his , ision become
··fol,!gy" ond he con1plnincd of o sore tongue and "aching teeth". 1\fh:r seven dn)·:. he developed a burning ,cnsation in the unexposed foot acco111p,111ied b) paro,esthesioe in all cxtrc111111es I le become proi;ressivel ) \\eokcr and ,,.,s confined to a , .. hcclchnir. 1 ,.,o years ofter the accident, diminished touch sensation and tendon rcOcxcs persisted and he could ,valk only ,,.ith o left leg brace and crutches. Chelating thcr,,p) \\tis not emplO)ed 01 uny tin11!" (pp 568).
2.10.4. I ngc,tion
The orJI 1oxic1t) of .ir�cnic acid is dependent on the amount ingested and the concentration of the prc�ration Tollis ( 1989) noted that ors.:nnte salts can react \\ilh
h ) drochloric ocid in thi: stomoch to liberate ar..c111c ncid nnd the corrc ponding mctol chloride. In this \\
11) poorly soluble snits such .,� h:ad arsenate cnn be II source of
nrscnic ucid ,..,hich is soluble nnd \\CII absorbed ,\lthough pent.l\,1lcnt ursenic 1s reduced in vi,o to the gcncrall ) more toxic 1r1,oh:nt nrsen1c 1nges11on of dilute orsen,c ocid salt solutions (less thnn three per cent) usually iltc \\ llhout scnous adverse eff ec ts
(1'1c\\'illioms., 1990), In 149 such coses 1n,ol\·ing sodiu,n orscnntc (2 28 per cent ont killer), 97 per cent of patients \\Crc DS)mptomotic ond onl ) one required ho�p11ul admwion (McWilliams, 1990)
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2.10.5. Gastrointestinal toxicit y
Of 57 cases of ant killer ingestion involving arsenic acid salts (maximum arsenate concentration of 3%) only seven patients ,.,ere S) mptomatic. All these vomited,
\\1th abdominal pain. diarrhea and nausea ,.,,ere also reported ( Kersjes et al. 1987).
Annstrong ct al ( 1984) reported eight family members (1,vo of ,-.hom died) poisoned b) well-,vater ,vhich contuined I 08 mg/L arsenic (form unkno,,11). It ,vas also reported thnt they all had gastrointestinal symptoms including di') mouth. vomiting, dysphasia and/or diarrhea. Urine arsenic concenlrotions ,,;ere direct\) related to the amount of
\\'Iller consumed. The estimated daily dosc of arsenic ingested b) thc survh ing fnmil) members ranged from 26-127 mg. An 11 )Car-old girl and a 27 year-old man died after
ingesting approxin,ately 77 mg and 166 mg arsenic daily rcspectivel) (duration unkno,vn). Autops)· of tht: n1os1 sc\'crel) poisoned patient sho\\cJ difi'usc
gastrointestinal tract inflnmmntion (,\rm strong et al, I 984 ).
t\ 32 year-old mnn ingested 900 mg of un nri.cnic uc1d suit. vomited \\ 1thin one hour and developed dinrrhocn three hour.. Inter. I (is elinicnl cour:;c \\lls con1plicnted b)
hypotcnsion und n:nnl failure but ofter 82 da)s chelation themp) ,,ith N-acct)lcysteine he fully recovered (Armstrong ct al, 1984). r\nothcr patient sun ived the deliberate ingestion of IO g of on urscnit ncid salt (t-.lathicu ct al. I Q92). Severe nausea, von1iting nnd abdominal tenderness dc,;eloped ,vithin 11ln:e hours ,vilh cardiovascular collapse nnd sub�quent ucule renal failure requirin1,1 haemodtnl)'sis. The patient made o full recover)· over three months.
Other gastrointestinal features of ar..cnu; poisoning include burning or the mouth ,ind throat ,-.1th dysphasia nnd h)'pcrsah,ution (I leyman cl al. 1956)
2.10.6. I lcpa10-101icit)
,\rrnstron1,1 ct ul ( 1984) namucd the ca�c of o 27 ) cnr-old n1un poisoned b)
\\ell \\Utcr containing I 08 rnl!ll u�en1c. lie presented ofter feeling un\\el\ lor sh. dn)., and on examination w115 joundicc:d with u bilirubrn conccntrauon of 120 11mol I lie collapsed and died later thol day nnd oulops) sho\\cd o li\cr 11rscn1c conccntmuon of 86 mp/kg. lte hod ingested an cstim111cd 166 mg nncn1c doily (duration unkno\\11) nnd had a urine ancnic concentmt1on of 1.6 mg/L ot po51 mortem Sc,en other membe rs of h i s
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ramily with lov;er arsenic exposure: sho,ved Lransiently elevated serum hepatic transan11nase nctivities nnd total bilirub 1 n conccntrollons.
Schoolmecstcr and \.\'hitc ( 1980) reported n 16 year-old ren,alc ,vho ingested 300 mg sodium arsenate in a suicide attempt. She developed se\'ere abdominal pain and vomillng ,vilhin 30 minutes. A 24 hour urine collecuon hod an arsenic conccntmlion of
14 .2 mg/L (time or collection not stated). Forty-eight hours Inter scrum hver transnn,innse nnd nlknlinc phosphnLnsc nc1iv111es ,verc elevated these nbnonnnlities resolved '"ithin six monU 1S . (values not gh en) but
2.10.7. Ncphrotoxicity
I lypo1ension or rhnbdomyolys1s follo,ving substantial arsenic acid ingestion may prec1p11ntc renal failure (wlnlli1cu ct nl, 1992: !Ian, Jeng ond Chen ct al, 1998).
Rcnnl conical necrosis hos also been dcscribed (Gerhardt ct al, 1978). l lncn1a1urio ,,ns reported in one patient in o series of 57 cases of sodiun, arsenate ingestion ("-crs1es ct nl, 1987). Pyurin. prote1nuria and clcvu1cd serum creatininc concentrations ,vcre reponcd in mtn1bers of a fant1ly poisoned \\"ilh nrscnic-contamin:ued \\cll-,vnter (Annstrong et al, 1984). TI,e n1ost severely poisoned pa11cn1, \\ ho died oOcr a six day illness. developed gross hucmoturin, a scrum cre.itininc: conccn1ro1ion of 390 µmol/L and heavy protc1nurio He had consumed an estimated 166 mg arsenic dnil> (dura11on unkno,,·n) and hud a urine arsenic concentration at post n1onc111 of chelation themp) \\as given. The other fnn11ly membe rs ,vcre treated \\'tili dimcrcuptol 1.6 mgtL No and f)l:nic1llnmine. Six e\'cntuolly recovered.
2.10.8. Cartliov:1scular toxicit)
Tachyeardin 1� reported lrcquentl) fol10,v1ng ingestion of uncn1c acid �Its and is contributed to by anxiety, 1ntraviuoular fluid depiction und possibly direct nrscnic•inducctl c11rdio-1oxici1y (Le Cullen and Reiner, 199-1, C. ullcn ct nl, J 1)95 ).
Vcntncul::u orrh)·th111i,", (Beel.man ct nl, I 91)J J hn\c hccn ohscr\'cd Other ECG abnonruui11L-s include prolungauun of the QI 1ntcn nl (Gol l l�ntith, 19110. Schoolntcc. tcr und \\'hite, 1980), idio-, cntriculnr rhythm and non-specific J. \\J\·c chJngcs
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(Annstrong ct al, 1984). Sudden onset bradycardia then nsystole has been rcponcd follo\,1ng massive acute arsenic ingestion despite vigorous resuscitation and no earlier
arrhythmia (Cullen et al, 1995).
Annstrong et al ( 1984) reponed a 27 year-old man ,, ho had consumed on unstated quantity of \\Cl1-,vo1er containing 108 mg/L arsenic. After a six day illness ( diagnosed as on upper respiratory tract infection) he collapsed and sustained a respiratory nrrcst and sc1turcs. An idio-vcntricular rhythm ,vns noted I le \\'llS
resuscitated but ren1nincd con101osc and died tarnponndc nrscnie-contaminnted \\'Iller; tht! outcome 1984). ,,as reported in another member of the same family \',ho had also drunk tn tlus case ,vas not stoled (t\rmstrong et al, a fe,, hours later Pcricnrdiol eftusion ,v1th
2.10.9. Ncuro-toxicity
In 57 sodium arsenate 1ngcs11ons involving solutions contninin!! I 5-3,0 per cent n�enntc, hcndnche, dizziness, lethargy and son1nolenec "ere each rcponed in 2 per cent of c.s�cs, 88 per cent of pattcnts ,,cl\! ilS) mptomatic (KcrsJe:; ct al. 1987). �lore
substantial arsenic ingestions have caused muscle cramps, o sensorincurnl hearing deficit (Goldsm11h, 1980); encephalopathy and sc12.urcs (Goebel et nl, 1990)
A pcnphcrul �cnsory und/or n1otor ncuropnthy has been described in sun·1vors of seven: acute arsenic poisoning although tlu:; is more typical follo,\'ing chronic exposure Am1strong et al (1984) rcponcd eight f.1mily members poi�oncd ,,·11h \\cll
\\Utc:r con1a1n1ng I 08 mg.IL ru.cn1c All developed snstro1ntcst1nul syn1ptorns ,vith
"altered mental stntus" and scizure:t noted in four Como developed in th re e pa11c1ns und
;1 peripheral nc:uropnth) in l\\ o. Goebel et nl ( 1990) dcn1onstrntcd ilcutc \\'Ullcriun dcgenen11ion or mychnotcd nerve libn:s in u pallcnt \\lho de, eloped n symmetrical rolyncuropathy ofter attempting �uicidc h) ingc�ting nrscn1c Chn1cnl 1n1provemcn1 \\as 3$M)Cintcd wi1h microscopic evidence of ncuruloHi c.t l regcnerot1on
,\ 46 )c.ir-old man developed feet nu111hncss ten da)s alicr drinl.:1111:1 o solution of sodiu1n ,ir-.cn.111: (conccn1rn11on unkno,,n) In 111tc1np1cJ suicide. l\,11 1nonths nflcr 1nscstion ncurol,111ic11l c:xu111in:11ion l.lcmonMmtc,l d1s1ul 1nusclc \\c,11.:ncs, hilatcnill),
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absent knee and ankle reflexes and reduced position and vibration scnse \Vith a high
stepping gait Sixteen months Inter there \Vas improvement in both sensory and motor deficits although residual disability ,,,as e, tdcnt at eight year follo\v-up (Le ct al, 1994 ).
2.10.10. Dcrn1:1l toxicit)
Le ct al ( 1994) described a patient \\ho developed a papular t!r)'thcmatous rash and gcnerohlcd epidermal dcsquamation one ,vcck uner drinking IO ml of on arsenate
solution (concentrotion unkno,\11). Striate leukonychio (�lees' lines} and h)perkcmtotic or hyperpigmented skin lesions are characteristic of chronic arsenic intoxicntion but hove been described nlso follo,ving substantial acute ingestion (Kyle and Pease, I 965, Shannon & Strnycr. rollo,ving urst:ntc ingestion (K 1989). Facial and pcnphera) oedema has illso been reported } lc und Pease. 1965).
2.10.11. llncrnoto,icity
In moderate or severe arsenic po 1 son1ng investigations typically sho\v unnem,a, lcucopcnia or pancy1open 1 a (Kyle nnd Pc.isc. 1965, ·\rmstrong ct ul. 1984) There may be evidence of 1 ntrav115cular hacn,ol}sis and the bl oo d film ofien shows basophilic sllppltng (Kyle nnd Pease, 1965), 1\-lathieu cl al ( 1992) th:soribcd n 30-ycar
old n,ale ,,ho ingested 10g sodiun, arsenate \\ilh suicidal intent lie developed severe gastro 1 ntesunnl features of ur..cnic poisoning ,vithin hours and requi re d hoen1odinly�is for management of ucutc n:nal futlure. Five dnys nficr ingestion he dcvcloped thrombocytopcrun nnd anacmi11. Bone marro\, cxnn,ination sho\\cd n1oturution arrest but n:covcr)' ensued o, er IO days.
2.10.12. lVlulti-orgnn to�icity
Sc:vcn: acute arsenic poisoning mny re sult in dc.ith from eurd 10 -respiratorv or •
hcpato rcnnl liiilun: (Am1strong ct ul 1984· Campbell 'Ind Alvurcz 1989, I.cc: ct ::ii, 2008;), Acute Rcspiralol') Distrc: , S}ndrome (ARDS) ho\ hccn Jcsenbcd b) Dolligcr ct ul ( l CJ92) ns possible c!Tccls of or .cn 1 c po 1 son 1 ng 1 nvolv 1 11r sub ! ,l,mtinl dnningc: lo
bod)' organs, In addition 10 this, inhalation of ,1rscn 1 c. compou111l� cnuscs rhi11 1 tis, pharyngitis, l11ryngltis and trachc:obro11cl111b (llollinjlcr. Zigl und l.ou,,·, I ()1)2), ,\rscnic
..
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is an eye irritant nnd ma) cause bums. �1ost inJuries result from e,po:;ure to dusts.
e,1using eon1un1:1ivitis, lnerimation, photophobia nnd chcmosis (�lc\\'illiam 1990).
2.10.13. Chronic c,posurc
Chronic C\!Hhurc to nrscn1c may result due to occupational nnd'or other anthropogenic source� i.lnd n,ay results to , arious degree of urscnical toxic II). Contac t
dcnnatitis has been rcponcd in ,vorkers exposed to urscnie aeid salts used in Cl)'!>tal manufncturc (Yeh, 1973 13urbaud ct al, 1995; \\'110. 2006). Ingestion of nrscnic
contn1ninatcd drinking \Vutllr, illic11 \\hisky (�loonshinc) tt t on1cs" or tr.1ditionnl rcnicdics have also been n.:portcd to ha,c caused chronic nrscnical poisoning (l·'cinglass,
1973; Chiou ct nl, 1995). In addition to these, p,1tien1s \\ith ch ro nic acid poisoning nla) present gcncrul toxic cficcts includine general debility, progrcsshe \\caknc:.s fever und S\\l!ats (Fcinglnss, 1973). Specific IO'<ic cflccts ha, c nlso been docun1cntcd literature including: in the
2.10.14. l)cr11111I to,icit) •
Arsenic hns been ,veil docu1ncn1cd ns one of the major risk factors for black foot disease (BfD), a peripheral ancrinl disease chur.ictcn1cd b) systemic atherosclerosis ns ,,ell ns di) g1u1grcne mid spontaneous on1put,Hions of afii:ctcd e11.trcn1itics.( 1 sen�.
1968. y ch, 1973 Chen \\ u • Lee, \Vong . Cheng and \Vu. 1988; usr P \, 1988:). OFD pat 11 :nts hnvc n high prc\'alcncc or arsenic-induced skin lesion� 1nc.lud1ng hyper pil'Olcntation. h)porl..cm t osis, and skin cancers (Tseng.. 1968). TI,cy also ha,c u high ri�k oft.lying from cancers of the lung. liver bladt.lcr kidney and prostate ns well ns ischcmic hcan t.lise� (Chen ct al 1988) Peripheral , asculur disease has also bc,:n l\'.poncd omons vintners ,vho hod consum1.-d nrscnic-contnm1notcd ,,·inc in Germon) and inhab11Jnts C\poscd to high•:ir..cn1c drinking \\'illcr in Chile and Mc11.ico
The chruuc1crstic dcllllnl manilcstcuions ore h ) ·pcrk c:ru tosis und "mindrop"
pi�rncntullon of the skin (Kyle and Pc,t\C, 1965: Shunnon und Strayer, J 989) I lypcrkt:ratosis :1ppcar u� multiple sm:ill nodules ,,hich may conlc�cc to form pluquc�
nnd nrc found rnost common!) on the paln1s nnd :,<1lc�. By con 1s more pro111i11ent in t he ll'<1llo1, groin, nnd areola as \\ell as nround the ,,.,is1, typically t rast. h ) p,:r pigmcnllltion
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