Toxicological profile for arsenic

https://www.ircwash.org/sites/default/files/Ng-2003-Global.pdf

A global health problem caused by arsenic from natural sources

pReVIously ClAssIfIed by IARC As “CARCInogenIC to humAns (gRoup 1)” And wAs deVeloped by sIx sepARAte woRkIng gRoups: phARmACeutICAls; bIologICAl Agents; ARsenIC, metAls, fIbRes, And dusts; RAdIAtIon; peRsonAl hAbIts And IndooR CombustIons; ChemICAl Agents And RelAted oCCupAtIons. thIs Volume 100f CoVeRs ChemICAl Agents And RelAted oCCupAtIons, speCIfICAlly 4-AmInobIphenyl, benzIdIne, dyes metAbolIzed to benzIdIne, 4,4’-methylenebIs(2-ChloRoAnIlIne), 2-nAphthylAmIne, oRtho-toluIdIne, AuRAmIne And AuRAmIne pRoduCtIon, mAgentA And mAgentA pRoduCtIon, benzo[A]pyRene, CoAl gAsIfICAtIon, oCCupAtIonAl exposuRes duRIng CoAl-tAR dIstIllAtIon, CoAl-tAR pItCh, Coke pRoduCtIon, untReAted oR mIldly tReAted mIneRAl oIls, shAle oIls, soot, As found In oCCupAtIonAl exposuRe of ChImney-sweeps, oCCupAtIonAl exposuRes duRIng AlumInIum pRoduCtIon, AflAtoxIns, benzene, bIs(ChloRomethyl)etheR And ChloRomethyl methyl etheR, 1,3-butAdIene, 2,3,7,8-tetRAChloRodIbenzo-pARA-dIoxIn, 2,3,4,7,8-pentAChloRodIbenzofuRAn, And 3,3’,4,4’,5-pentAChloRobIphenyl, ethylene oxIde, foRmAldehyde, sulfuR mustARd, VInyl ChloRIde, IsopRopyl AlCohol mAnufACtuRe by the stRong-ACId pRoCess, mIsts fRom stRong InoRgAnIC ACIds, oCCupAtIonAl exposuRes duRIng IRon And steel foundIng, oCCupAtIonAl exposuRe As A pAInteR, oCCupAtIonAl exposuRes In the RubbeR mAnufACtuRIng IndustRy. beCAuse the sCope of Volume 100 Is so bRoAd, Its monogRAphs ARe foCused on key InfoRmAtIon. eACh monogRAph pResents A desCRIptIon of A CARCInogenIC Agent And how people ARe exposed, CRItICAl oVeRVIews of the epIdemIologICAl studIes And AnImAl CAnCeR bIoAssAys, And A ConCIse ReVIew of the Agent’s toxICokInetICs, plAusIble meChAnIsms of CARCInogenesIs, And potentIAlly susCeptIble populAtIons, And lIfe-stAges. detAIls of the desIgn And Results of IndIVIduAl epIdemIologICAl studIes And AnImAl CAnCeR bIoAssAys ARe summARIzed In tAbles. shoRt tAbles thAt hIghlIght key Results ARe pRInted In Volume 100, And moRe extensIVe tAbles thAt InClude All studIes AppeAR on the monogRAphs pRogRAmme websIte (http://monogRAphs.IARC.fR). It Is hoped thAt thIs Volume, by CompIlIng the knowledge ACCumulAted thRough seVeRAl deCAdes of CAnCeR ReseARCh, wIll stImulAte CAnCeR pReVentIon ACtIVItIes woRldwIde, And wIll be A VAlued ResouRCe foR futuRe ReseARCh to IdentIfy otheR Agents suspeCted of CAusIng CAnCeR In humAns. D es ig n by A ude la d es m ot s

iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns

Arsenic poisoning in groundwater: health risk and geochemical sources in Bangladesh.

Chronic arsenic toxicity (arsenicosis) due to drinking of arsenic contaminated ground water is a major environmental health hazard throughout the world including India. A lot of new information is emerging from extensive research on health effects of chronic arsenic toxicity (CAT) in humans during the last two decades. Available literature has been reviewed to highlight the problem including its malignancies. Pigmentation and keratosis are the specific skin lesions characteristics of CAT. CAT also produces various systemic manifestations over and above skin lesions, important ones being chronic lung disease like chronic bronchitis, chronic obstructive pulmonary disease and bronchiectasis, liver disease like non-cirrhotic portal fibrosis and other diseases like polyneuropathy, peripheral vascular disease, hypertension and ischeamic heart disease, diabetes mellitus, non-pitting oedema of feet/hands, weakness and anaemia. Cancer of skin, lung and urinary bladder are important cancers associated with chronic arsenic toxicity. Stoppage of drinking of arsenic contaminated water is the main stay in the management of arsenicosis as specific chelation therapy has limited value. Early skin cancer, detectable by regular active surveillance, is curable. In addition to dermatological features, CAT produces protean clinical manifestations. Treatment of arsenicosis is unsatisfactory and is mostly symtomatic.

/pdf/chronic-arsenic-toxicity-human-health-28bgvysqkv.pdf

Chronic arsenic toxicity & human health.

In this study of 92 people using wells with arsenic concentrations of >0.05 ppm (and with 21 control subjects), 27 of them had clinical features possibly attributable to chronic arsenic poisoning. There was a positive relationship between frequency of clinical features, and well and hair arsenic concentrations. Although the relationship between toxicity and hair arsenic concentration was rather varied, 1 ppm appears to be satisfactory upper limit of acceptability. For drinking water, an acceptable limit of 0.01 ppm and a maximum permissible limit of 0.05 ppm of arsenic appear satisfactory, but leave little safety margin.

Electromyographic Abnormalities in Chronic Environmental Arsenicalism

Laetrile preparations obtained from a cyanide intoxicated patient were analyzed for their cyanide content by a microdiffusion colorimetric procedure. Cyanide was also determined in apricot, peach and apple seeds. The results were compared to those reported in the literature for cyanogenic glycoside containing seeds.

The cyanide content of laetrile preparations, apricot, peach and apple seeds.

Data are presented to Indicate the recovery one can expect with different diffusion times in the microdiffusion procedure for the determination of cyanide using Conway cells. Using a predetermined recovery factor, a diffusion time of 10 min is recommended for emergency situations. In the use of the pyrtdine-barbituric acid reagent for color development, It was found that the reagents could be added as rapidly as is manually possible and that while the color complex begins to fade as soon as developed, the error after 4 to 10 min ranges from 3 to 9%. 20 min estimated by authors (9), 30 min (10), and 45 min (11). Others may be cited. Setting up the aeration apparatus takes some time and keeping it available creates a storage problem. Microdiffusion techniques using the Conway cell generally specify 1 to 4 hr of diffusion time (12,13). Since microdiffusion with this cell provides a readily available, economical, and easily set up procedure, the authors decided to investigate ways of shortening the procedure to obtain meaningful results for emergency situations.

An evaluation and modification of a microdiffusion method for the emergency determination of blood cyanide.

A 34-year-old mother habituated to the excessive use of salicylates gave birth to a still born infant with a salicylate level of 25 mg/dL in the whole blood and 12 mg% in the liver. The analytical methodology for the determination of salicylates is described. Pathological findings included an acute chorioamnionitis and the widespread presence of congestion of the viscera with petechial hemorrhages-changes which are not uncommonly seen in infants suffering from intrauterine anoxia. The published findings on the effects of salicylates on the human fetus and on reported fetal blood levels have been reviewed.

Salicylate levels in a stillborn infant born to a drug-addicted mother, with comments on pathology and analytical methodology.

Simultaneous determination of diphenhydramine, methaqualone, diazepam and chlorpromazine by gas chromatography in extracts of liver tissue after enzymic digestion is described. The effectiveness of several digestion procedures is compared. Ketodase is shown to be the most efficient tissue digestion agent for the drugs investigated.

Simultaneous determination of diphenhydramine, methaqualone, diazepam and chlorpromazine in liver by use of enzyme digestion: a comparison of digestion procedures.

Herman A. Ellenberger

Papers

Electromyographic Abnormalities in Chronic Environmental Arsenicalism

The cyanide content of laetrile preparations, apricot, peach and apple seeds.

An evaluation and modification of a microdiffusion method for the emergency determination of blood cyanide.

Salicylate levels in a stillborn infant born to a drug-addicted mother, with comments on pathology and analytical methodology.

Simultaneous determination of diphenhydramine, methaqualone, diazepam and chlorpromazine in liver by use of enzyme digestion: a comparison of digestion procedures.