Environmental Health PerspectivesVol. 19, pp. 183-189, 1977

Epidemiology and Toxicology ofArsenic Poisoning in Domestic Animalsby Lloyd A. Selby,* Arthur A. Case,*Gary D. Osweiler,* and Howard M. Hayes, Jr. t

Arsenic poisoning is one of the more important causes of heavy metal poisoning in domestic animals.Two speciedogs and cattle-are intoxicated more frequently than other animals; yet sporadic instancesof poisoning have been observed in cats, horses, and pigs. Cases observed by veterinary dinicians areeither peracute, acute, or chronic intoxications. Frequently the initial and only indication that a severeproblem exists with peracute poisoning in a cattle herd is dead animals. Chronic intoxications are alsoobserved in cattle. Acute intoxication is the most common form of arsenic poisoning observed anddocumented in the dog. Also intoxicated dogs were younger, i.e., 2-6 months of age. Arsenic is a severealimentary tract irritant in domestic animals, and treatment in most instances consists mainly of symp-tomatic and supportive treatment. The source of intoxication, when it can be determined, is usually dips,sprays, powders, or vegetation contaminated by pesticides containing arsenic.

IntroductionArsenic is second only to lead as a cause of heavy

metal intoxication in domestic animals. Clinically,arsenic intoxication occurs as an acute or peracuteintoxication, although chronic forms of the diseasehave been observed, especially in cattle. Intoxica-tion results from consumption of the trivalent inor-ganic or organic forms of arsenic. Trivalent arsenicis the more toxic form of the element for domesticanimals (1). Arsenic occurs in small amounts natur-ally in soil and native vegetation (2, 3). However,most instances of intoxication result from the con-sumption of soil, vegetation, or discarded materialsthat contain or are contaminated with high levels ofarsenic. When the source of the intoxication can befound, it is usually herbicides or insecticides con-taining arsenic. Described in this report is a review

*College of Veterinary Medicine, University of Missouri,Columbia, Mo. 65201.tEnvironmental Epidemiology Branch, National Cancer Insti-

tute, Bethesda, Md. 20014.tColorado State University, University of California, Univer-

sity of Georgia, University of Guelph (Ontario), University ofIllinois, Iowa State University, Kansas State University,Michigan State University, University of Minnesota, Universityof Missouri, Ohio State University, Purdue University(Lafayette, Indiana), and University of Saskatchewan.

of the basic toxicology of arsenic intoxication inanimals and an evaluation of the medical recordsfrom 13 North American veterinary coliegest forthe 11-year period of 1964-1974. We also reviewedcases from the Missouri State Diagnostic Labora-tory at Columbia, Missouri, as well as selected datacollected by the authors in their field investigationsof suspected intoxication outbreaks in cattle, laterdocumented as arsenic intoxication.

BackgroundMan and lower animals are highly susceptible to

inorganic arsenic. But in the diagnostic laboratory,arsenic poisoning is most frequently encountered inthe bovine and feline species resulting from con-tamination of their food supply. Occurrence of ar-senical poisoning in these two species is closely fol-lowed in other forage-eating animals, such as thesheep and horse. Arsenical poisoning in most ani-mals is usually manifested by an acute or subacutesyndrome. Chronic poisoning, although it has beenreported in animals, is seldom seen and has notbeen clearly documented. Experience with fieldcases of arsenic poisoning indicates that animalswhich are weak, debilitated and dehydrated aremuch more susceptible to arsenic poisoning thannormal animals. This may be because of reducedexcretion rate via the kidneys (4).

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Inorganic arsenic is found in nature and is syn-thesized in many complex and varied forms, havingmany uses from medicinal to forensic. In practice,the most dangerous arsenical preparations are dips,herbicides, and defoliants in which the arsenical isin a highly soluble trivalent form, usually trioxide orarsenite. Unfortunately, animals (such as dogs andcalves) will frequently seek out and eat materialssuch as insulation, rodent baits, dirt, and foliagethat have been contaminated with an inorganic ar-senical.

Soluble forms of arsenic, such as sodium arse-nite, are readily absorbed from all body surfaces.Arsenic trioxide and other less soluble arsenicalsare poorly absorbed from the digestive tract and arelargely excreted unchanged in the feces. Once ab-sorbed, pentavalent arsenic is readily excreted bythe kidneys, whereas trivalent arsenic is more read-ily excreted into the intestine via the bile. It is gen-erally considered that regardless of whether an ar-senical is introduced into the body as trivalent orpentavalent arsenic, all the major actions can beattributed to the trivalent form. Arsenicals are sus-pected of having a metabolic function (5) and ulti-mately, they exert their effects by reacting with sul-fhydryl groups in cells (6).While most textbooks report that arsenic is ac-

cumulated in the tissues and slowly excreted, thisphenomenon appears to be true only in rats. Mostspecies of livestock and pet animals apparentlyrapidly excrete arsenic (7). This phenomenon isvery important when one considers arsenic levels intissues as a means of confirming suspected poison-ing.

Peracute and acute episodes of poisoning by in-organic arsenic are usually explosive with highmorbidity and moderate mortality over a 2- to 3-dayperiod. Symptoms are manifested by intense ab-dominal pain, staggering gait, extreme weakness,trembling, salivation, vomiting (in dogs, cats, pigs,and perhaps even cattle), diarrhea, fast, feeblepulse, prostration, rumen atony, normal to subnor-mal temperature, collapse, and death.

In subacute arsenic poisoning, animals may livefor several days, exhibiting depression, anorexia,watery diarrhea, increased urination at first fol-lowed by anuria, dehydration, thirst, partialparalysis of the rear limbs, trembling, stupor, coldextremities, subnormal temperature, and death.The watery diarrhea may contain shreds of intesti-nal mucosa and blood. Convulsive seizures havebeen reported but are not an expected manifesta-tion. Poisoning from arsenical dips usually resultsin some of the signs noted previously, in addition toblistering and edema of the skin followed by crack-ing and bleeding with associated secondary infec-tion (4).

Characteristic gross lesions associated with inor-ganic arsenic poisoning include reddening of thegastric mucosa (abomasum in ruminants) whichmay be localized or general, reddening of the smallintestinal mucosa (often limited to the first few feetof the duodenum), fluid gastrointestinal contentswhich are sometimes foul smelling, soft yellow liverand red, edematous lungs. In peracute cases ofpoisoni.ng, occasionally no gross postmortemchanges are noted. The inflammation is usually fol-lowed by edema, rupture of the blood vessels andnecrosis of the mucosa and submucosa. Sometimesthe necrosis progresses to perforation of either thestomach or intestine. The fluid gastrointestinal con-tents may contain blood and shreds of mucosa.Hemorrhages on all surfaces of the heart and on theperitoneum may occasionally be observed (4, 8).

Histopathologic changes include gastric and in-testinal edema of the mucosa and submucosa, ne-crosis and sloughing of mucosal epithelium, renaltubular degeneration, hepatic fatty change and ne-crosis, and capillary degeneration in vascular bedsof the gastrointestinal tract, skin, and other organs.In cases involving cutaneous exposure, a dry,cracked, leathery, peeling skin may be a prominentfeature.The urine of poisoned animals may contain pro-

tein, red blood cells and casts. The arsenic level inthe urine varies with the form of arsenic, route ofexposure and species but usually ranges from 2-10ppm (4).

Materials and MethodsMedical records in the Veterinary Medical Data

Program (VMDP) for the years 1964-1974 were re-viewed for cases with a diagnosis of arsenic intoxi-cation. The VMDP is a data collection and storageregistry sponsored by the National Cancer Insti-tute, to which veterinary university hospitals/clinicssubmit standardized abstracts about each medicalepisode occurring at their facility. All diagnoses ofarsenic poisoning were considered regardless of thediagnostic techniques used to arrive at a diagnosis.In a majority of instances the diagnosis of arsenicintoxication was based only on clinical observa-tions. Also, because a majority of the intoxicationsoccurred in two species-dogs and cattle-majorconsiderations of the epidemiology and toxicologywere confined to these two species. Furthermore,comparison with controls, i.e., cases presented toone of the clinics without arsenic intoxication, willbe considered only for dogs as approximately 70%of the arsenic intoxicated animals observed in the13 veterinary hospitals/clinics occurred in thisspecies. The medical records in the VMDP registrywere either compiled directly from a disk file or

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they were abstracted onto computer cards andanalyzed using the Statistical Package for the SocialSciences (SPSS) or the Statistical Analysis System(SAS) computer programs (9, 10).The effects of the independent variables of age,

breed and sex upon a diagnosis of arsenic poisoningwere evaluated by estimating the relative risk ofoccurrence by Gart's method (11). Comparisonswere made with a reference population drawn fromthe same medical facilities and study period as thecase series. The reference population was tabulatedby the patient-years-at-risk method.

In addition to reviewing the veterinary clinic rec-ords, the records of one of the diagnostic clinics inMissouri was reviewed for possible instances of ar-senic intoxication. With these records, a majority ofthe instances of arsenic intoxication occurred incattle. In some of these outbreaks one of the au-thors conducted field investigations and/or hadanalyzed tissues or feed for arsenic. "Typical" ex-amples of these investigations will be presented tofacilitate our discussion of the toxicology andepidemiology of arsenic intoxication in domesticanimals.

Results

Between June 1964 and July 1974 a total of 93animals were diagnosed as having arsenic intoxica-tion in the VMDP registry. Of these 93 animalsshown in Table 1, 64 (69%) were dogs, 18 (l9o)cattle, 5 (5%) cats, 4 (4%) pigs, and 2 (2%) werehorses. Thirty-three (35%) of the cases were treatedas outpatients. Of those animals hospitalized themedian length of hospitalization was less than 2days. Sixty-eight (73%) of the animals survived theinitial intoxication experience. Approximately 10patients with arsenic intoxication were diagnosedannually from 1968 to 1974, except 1970, when 21animals were seen with arsenic intoxication. A ma-jority of these animals were intoxicated cattle. Thisrepresents 44% of the total of cattle diagnosed witharsenic intoxication during our survey period.

Table 1. Incidence of arsenic intoxication by species: VeterinaryMedical Data Program, 1964-1974.

Species Frequency PercentageDogs 64 68.7Cattle 18 19.4Cats 5 5.4Pigs 4 4.3Horses 2 2.2

Total 93 100.0

Table 2 presents a comparison of selected vari-ables for dogs (N = 64) and Cattle (N = 18). Ap-proximately twice as many dogs as cattle weretreated as outpatients, and for those animals hos-pitalized the median number of days that they werehospitalized was half as long for dogs as it was forcattle. Another contrasting variable was that 83% ofthe dogs were discharged alive, where only 50% ofthe cattle were discharged alive from the clinicS.Concerning clinical procedures, 53% of the dogswere diagnosed strictly on clinical findings,whereas only 22% of the cattle were diagnosed withthe same criteria. Figure 1 gives the percentage dis-tribution by month of arsenic poisoning diagnosedin dogs and cattle for the complete study period.The month which was the mode in most species wasJune. The fluctuation in this particular chart for cat-tle percentages may be due in part to the smallnumber of animals observed.

Table 2. Comparison between dog and cattle arsenic intoxica-tion for selected variables: Veterinary Medical Data Program

1964-1974.

Average value

Variable Dogs Cattle(N= 64) (N= 18)

Treated as outpatients, % 33 17Median time of hospitalization

for inpatients, days 1.3 3.5Female, % 56 56Discharge status 83% alive 50% aliveMedian age, months 9 12Clinical procedures

Clinical diagnosis only, % 53 22Gross pathology, % 14 33Histopathology, % 14 28

L4

3

-

C-

V

r2

1

AGE (YEARS)

FIGURE 1. Percent distribution, by month, of arsenic poisoningdiagnosed (e) in dogs (N = 64) and (x) in cattle (N = 18) byVeterinary Medical Data Program (VMDP) participantsthrough 1975 (FY).

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Taking the analysis a step further, Table 3 pre-sents the crude attack rate per 100,000 patient-years-at-risk for the 64 dogs observed with arsenicpoisoning. This distribution appears bimodal withtwo peaks, one in 1970, one in 1972 respectively.However, in pursuing this type of analysis further,

Table 3. Arsenic poisoning in 64 dogs seen by participants, Veteri-nary Medical Data Program.

Number Crude rate/100,000Year of cases patient years-at-risk

1964-1969 15 14.721970 10 24.561971 8 18.201972 12 24.101973 9 15.881974 10 16.60

Figure 2 presents the attack rate per 100,000patient-years-at-risk adjusted by age and sex, aswell as the relative risk, for dogs with arsenicpoisoning. This adjusted attack rate was againbimodal, with the highest peak in dogs 2-6 monthsof age and second highest peak occurring in dogs4-6 years of age. However, the age risk values indi-cate 2-6 months of age as the time of life of signifi-cant risk in dogs. Finally, the last comparison madewith the clinical data was a breed risk for dogs. Riskvalues calculated for breeds represented by six ormore cases among the series by sex are shown inTable 4. No significant associaticn was detected

Percent

If

20

10

Table 4. Estimated relative risk { of arsenic poisoning by breedand sex in dogs reported to the VMDP, 3/64-12/74.

95%confidence

Observed Ra intervalb

BreedDachshund 6 2.0 0.83-5.14German shepherd dog 6 1.3 0.54-2.%Poodle, miniature and toy 7 1.2 0.52-2.82All breeds combined 64 1Mix breed 14 0.9 0.43-1.53

SexFemale 36 1.3 0.75-2.12Male 28 1

aAdjustment made for sex in determiing breed risk; for breed in deter-mining sex risk.

bWhen confidence interval includes I, R is not significantly dfferentfrom that among the reference group at p <0.05.

ords at the University of Missouri-Columbia for theperiod January 1970-December 1975, i.e., theperiod during which records were available. A totalof 26 cases of arsenic toxicosis were diagnosed inlivestock at this diagnostic laboratory. A compari-son of the number of instances of intoxication byspecies by year is presented in Table 5. The major-

Table 5. Frequency of arsenic intoxication observed by species andyear at the Veterinary Diagnostic Laboratory, Columbia,

Missuri.

Year Cattle Swine Equine Cat Dog1970 41971 41972 3 1 11973 5 1 11974 21975 2 2

1976 (to July) 4 1 1Total 24 4 1 3

ity of those that were diagnosed in this laboratorywere cattle. Taking this analysis a step further, therecords that were available between 1970-1975were then examined to try to determine the numberof animals in the herd, number of animals affected,

-' / , _< _ > _ ,,i.e., primarily those that died from the intoxication,possible case fatality rate, as well as the source ofthe arsenic intoxication. These results for some 12outbreaks are summarized in Table 6. As shown inJAN FEB FR APR M/AY JUN JLY AUG SPT OCT NOV DEC Table 6, in 58% of the outbreaks the source of in-

IGURE 2. Rate/100,000 patient years-at-risk adjusted for sex by toxication was determined. To give a better appre-age and relative risk by age (the vertical lines represent 95% ciation of the difficulties involved in documentingconfidence intervals). The data represent 64 dogs with arse- field outbreaks of arsenic intoxication, the follow-nic poisoning. ing examples are presented.

(p - 0.05) between arsenic poisoning and these pa-tient characteristics.We then turned our attention to an evaluation of

the Veterinary Medical Diagnostic Laboratory rec-

Outbreak A. Weeds were sprayed with a her-bicide containing sodium arsenite as part of themaintenance program on a defense establishment inwest central Missouri. The person applying the

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Fi,

186

Table 6. Number in herd, mortality, case fatality ratio and possible source of intoxication for cattle with arsenic poisoning,University of Missouri Veterinary Clinic-Columbia.

Number Number Case/fatalityFarm ID in herd dead rate Source of arsenic

1 26 24 0.92 Herbicide2 79 8 0.10 Herbicide or grasshopper bait3 16 6 0.38 Cattle had access to an old

house; were found eating awhite powder in the house.

4 100 1 0.01 None determined5 95 1 0.01 None determined6 200 11 0.06 None determined7 10 5 0.50 Access to trash, refuse, etc.8 60 5 0.08 Road fence sprayed with brush

killer 55.8% sodium arsenite9 38 2 0.05 None determined10 30 3 0.10 Powder containing 18,750 ppm

arsenic

11 25 2 0.08 None determined12 30 2 0.07 None determined

(Liver 150 ppm arsenic)13 30 8 0.27 Fence row sprayed with brush

killer14 25 18 0.72 Mixed in feed from unmarked

container 40% sodium arsenite15 36 11 0.31 Herbicide 40% sodium arsenite

60% suggested source ofTotals 800 107 0.13 arsenic intoxication

weedkiller sprayed through the fence, coveringweeds for a yard or so outside the defense stationfence, and 24 of 26 young cattle in this adjacentpasture died of arsenic poisoning. Field observa-tions and a history suggested that the cattle ap-peared to be attracted to foliage which had beensprayed with arsenical herbicide.

Outbreak B. An owner uncovered a metal drumin a corner of a combination machinery shed andhay barn. The container was so old that any originallabels were lost or had become illegible. He thoughtthe drum contained a molasses supplement, so hemixed the contents with feed which was then fed tofeeder calves. The cattle became seriously ill withina few hours and many died. Necropsy of the deadcattle revealed evidence of arsenical poisoning.Tests for arsenic on tissue and contents of the di-gestive tract were positive for arsenic. The remainsof the material in the drum which the owner thoughtwas molasses proved to contain 40% sodium arse-nite, undoubtedly a weed killer and not a molassessupplement! The owner lost 18 of 25 calves.Outbreak C. A rancher stated that his cattle

were "eating dirt," and it was poisoning them. Hesubmitted a dead animal to necropsy after his localveterinarian had made a tentative diagnosis of arse-nic poisoning. The soil sample, as well as tissuesfrom the dead animal, contained high levels of arse-

nic. Search of the site where the cattle were seen tobe "eating dirt" revealed that the cattle had un-earthed an old metal drum, buried many years agoalong with other trash. Time and erosion had ex-posed the arsenic container, and the cattle finisheduncovering it. As in outbreak A, cattle seemed tobe attracted to discarded material or soil containingarsenical compounds.

DiscussionThe clinical and toxicological signs of arsenic in-

toxication in domestic animals have been the samesince the disease was first reported. Arsenic is nothighly corrosive; it does, nevertheless, cause se-vere inflammation, eventual edema, and subse-quent necrosis of the gastrointestinal mucosa andsubmucosa, if the animal survives the peracutephase. Thus, the major clinical sign seen is a severegastroenteritis, primarily a diarrhea.

If one counts specimens sent to the diagnosticlaboratory with a request that the specimen beanalyzed for arsenic, one would include a majorityof the diarrheas of unknown etiology. What is pre-sented herein are the confirmed cases of arsenicintoxication in domestic animals; as such, they rep-resent only a small portion of the true incidence.The incidence of arsenic intoxication reported toour diagnostic laboratory agrees with the observa-

August 1977

tions of Hatch and Funnell, who reported 21 posi-tive diagnoses of arsenic poisoning in cattle duringan 8-year period in Ontario, Canada (12).Common sources of arsenic, when the source

could be determined (Table 6), included sprays,dips, and powders used as insecticides or her-bicides. In a majority of the intoxicated cattle thismaterial was consumed voluntarily from suchsources as feed, contaminated soil, materials left ontrash piles, in vegetation along fence rows, oraround buildings that had been sprayed with a weedkiller. In approximately 80% of the dogs intoxicatedwith arsenic, the source was found to be ant orroach bait containing arsenic, e.g., a sodium-arsenate compound. In these instances, the dogswere presented to the clinic with a history of vomit-ing and some muscular weakness and musculartrembling. Subsequent interview with the ownersuggested that in a majority of cases an insecticidecontaining arsenic had been used in the area wherethe dog was housed or allowed to roam free. Manytimes owners of poisoned animals are not awarethat an arsenical compound was available; that is,they do not realize that ant bait may contain arse-nic.

In many cases of arsenic intoxication in largeanimals, no source of arsenic was detected. Oftenconsiderable effort is required on the part of theclinician or diagnostician to assist owners in findingthe source. It is characteristic that the owner will"look harder" when a positive diagnosis of arsenicintoxication has been confirmed or suggested. Apositive clinical diagnosis of arsenic intoxicationstimulates owners to help detect the source of thecompound. In the instance of intoxication in largeanimals, often a field trip is an invaluable aid to theclinician and toxicologist in defining the location ofthe source of the compound, since the owner maynot be aware of what to look for (e.g., signs of eat-ing treated foliage, remains of containers or pow-ders) as a source. Cattle owners used the compoundfrequently as a weed killer, and it was only on sub-sequent investigation that it was documented thatsuch compounds were the cause of the intoxication.One statement we have made to owners in the paston field investigations is: "You and I have beensearching this pasture for an hour looking for thesource of the intoxication. These calves have beenpresent in this pasture for approximately 3 to 10days, and they have been more successful in locat-ing the source for consumption and intoxication."It sometimes appears that animals, especially cat-tle, develop an increased desire to consume weedssprayed with an arsenic weed killer, not because ofa change in palatability of the plant but possiblybecause arsenic compounds tend to taste salty, andthus attractive, to the animals.188

In diagnosis of arsenic intoxication, wet chemis-try tests, such as the Reinsch test (13), are used as ascreening tool; and, if positive, then more definitivechemical analysis must be used to quantitate thelevels of arsenic; e.g., arsine evolution (14). A posi-tive test does not conclusively confirm arsenicintoxication, for this test is sensitive to as little as 2ppm of arsenic. In Missouri, for example, thegeometric mean of arsenic found in soil varied from13 ppm in the glaciated prairies portion of the stateto approximately 7 ppm in the oak-hickory-pinearea. In every sample of soil that was analyzed forarsenic, the inorganic form of the element was de-tected in all of the major vegetation-type areas (3).

If we contrast the epidemiology of arsenic in-toxication in the major species that were presentedto our diagnostic laboratory and 13 veterinaryclinics, we see quite a different view. A majority ofthe small animals, dogs and cats, are admitted to theveterinary clinic; whereas a greater majority of cat-tle cases are submitted to the diagnostic laboratoryor seen on ambulatory service. The picture of arse-nic intoxication by species is in part related to thetype of animal population that these two facilitiesobserve during the year. Dogs are more apt to betreated as outpatients than cattle. Also dogs werehospitalized a shorter period of time and more ofthem survive the intoxication, possibly not becauseof greater resistance to the arsenic, but rather be-cause of a lower degree of exposure. In addition,most intoxications in dogs were diagnosed solely ona clinical examination and history. Younger animalsare more likely to be intoxicated with arsenic. Forexample, in calculating the rate of arsenic poisoningfor 100,000 dog-years-at-risk, adjusting for sex andage (see Fig. 2), there was a threefold increase fordogs 2-6 months of age compared to dogs under 2months of age. Our initial impression before adjust-ing for age and sex was that possibly younger ani-mals were being exposed to arsenic in the dam'smilk; this is not the case. Further evaluation of theclinical records, however, did not support thishypothesis.

It has also been suggested that Thiacetarsamide,a trivalent organic arsenical and the only drug thathas consistently been found to kill adult canineheartworms that infect dogs (15), might cause arse-nic intoxication. Recent work by a number of clini-cians shows that an animal treated for heartwormswith the arsenical treatment schedule does have atemporary rise in some liver function tests and insome instances animals will die shortly after treat-ment, suggesting a reaction to the arsenical drug(16, 17). Yet, overt arsenic intoxication has notbeen confirmed as the cause of death.

Finally, in an earlier report we were concernedwith the potential public health aspects of arsenic

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intoxication, primarily in cattle and other food-producing animals (18). Depending on the form ofthe compound, arsenic may be excreted in the feceswithout absorption, with minimal absorption, or, ifabsorbed, it is primarily excreted through urine andthe half-life is found to be fairly rapid, being anumber of hours rather than days or weeks, com-pared to many other chemical compounds. The po-tential public health risks in cattle were felt to beminimal, if nonexistent. Preslaughter withdrawalafter a single, acute exposure was recommended at14 days; with multiple exposure 6 weeks with-drawal. In contrast, in the dog, the second speciesin which greater numbers of cases occurred, arsenicgenerally is consumed by a younger dog who is ac-tive, playful and inquisitive. The potential publichealth risk relative to dogs is not from a food-producing standpoint, but rather for children whoare exposed to the same area as the pet. There isalso a potential public health risk that has been as-sociated with another domestic animal; i.e., sheep.It has been recognized that arsenic can cause skinand lung cancer, especially in sheep dip workers(19). Monitoring domestic animals with a history ofarsenic intoxication may offer clues to environmen-tal hazards yet unknown to humans.

AddendumAccording to information received from Bencko

(20), excessive contamination of the environmentby arsenic has resulted in the extinction of bees'colonies up to 30 km in the direction of the prevail-ing winds from the Novaky power plant in Czecho-slovakia. Examination of soil and vegetation in theexposed area showed a relationship between arse-nic in the soil and vegetation. The quantity of ni-trogen in the soil was diminished with increasingquantity of arsenic. Also, soil samples containingapproximately 165 ppm of arsenic showed di-minished quantities of bacteria as well as protozoa,and no worms were found in samples containingarsenic in values about 150 ppm.

Influence of arsenic on the reproductive func-tions of domestic animals was encountered in thisarea. In a village near the power plant, there was apig-breeding farm specializing in large-scale pro-duction of piglets. After the power plant went intooperation, the incidence of abortions among sowsincreased with time to the point where it was neces-sary to close the farm and move it away from thepower plant. Arsenic is known to be a capillary-toxic poison. Due to environmental pollution, thepregnant sows received in their forage sufficientdoses of arsenic to damage the placental blood

capillaries to the extent that abortions began tooccur. Abortion rates also increased among cattlein this area but did not reach epidemic proportions.

REFERENCES

1. Clarke, E. G. C., and Clarke, M. L. Gamer's VeterinaryToxicology, 3rd ed., Williams and Wilkins, Baltimore, 1967,p. 441.

2. Vinogradov, A. P. The Geochemistry of Rare and Dis-persed Chemical Elements in Soils, 2nd ed., ConsultantsBureau, New York, 1959.

3. Erdman, J. A., Schaklette, H. T., and Keith, J. R. Geolog-ical Survey Professional Paper 954-C, U. S. GovernmentPrinting Office, Washington, D. C., 1976.

4. Buck, W. B., et al. Clinical Diagnostic Veterinary Toxicol-ogy, 2nd ed., Kendall-Hunt, Dubuque, 1976.

5. Lenihan, J. M. A. Technology and humanity. In: Pro-ceedings of Trace Substances in Environmental Health.D. D. Hemphill, Ed., University of Missouri, Columbia,1967, p. 141.

6. Goodman, L. S., and Gilman, A. The PharmacologicalBasis of Therapeutics, 3rd ed., MacMillan Company, NewYork, 1967, p. 944.

7. People, S. A. Arsenic toxicity in cattle. Ann. N. Y. Acad.Sci. 111: 644 (1964).

8. Buck, W. B., Ramsey, F. K., and Duncan, J. R. Diseasecaused by physical and chemical agents: chemical and plantpoisonings. In: Canine Medicine. E. J. Catcott, Ed. Ameri-can Veterinary Publications, Wheaton, 1968.

9. Nie, N. H., et al. SPSS-Statistical Package for the SocialSciences. McGraw-Hill, New York, 1976.

10. Barr, A. J. et al., A User's Guide to SAS76. SAS InstituteInc., Raleigh, 1976.

11. Gart, J. J. Point and interval estimation of the commonodds ratio in the combination of 2x2 tables with fixed mar-ginals. Biometrika 57: 471 (1970).

12. Hatch, R. C., and Funnell, H. S. Inorganic arsenic levels intissues and ingesta of poisoned cattle, Can. Vet. J. 10: 117(1969).

13. Martin, T. D., and Berrier, H. H. Detection and diagnosisof arsenic and mercury poisonings via the Reinsch test. Vet.Med. Small Anim. Clin. 71: 433 (1976).

14. Braman, R. S. Applications of the arsine evolution methodsto environmental analysis. Environ. Health Perspect., inpress (1976).

15. Committee Report. Procedures for the treatment and pre-vention of canine heartworm disease. J. Am. Vet. Med.Assoc. 162: 660 (1973).

16. Carlisle, C. H., et al. The toxic effects of Thiacetarsamidesodium in normal dogs and in dogs infested with Dirofilariaimmitis. Austral. Vet. J. 50: 204 (1974).

17. Rosenberg, M. A., et al. A mathematical formula as an aidin the treatment and prognosis of canine heartworm disease.Vet. Med. Small Anim. Clin. 71: 496 (1976).

18. Selby, L. A., et al. Public health hazards associated witharsenic poisoning in cattle. J. Am. Vet. Med. Assoc. 165:1010 (1974).

19. Hill, A. B., and Faning, E. L. Studies in the incidence ofcancer in a factory handling inorganic compounds of arse-nic. I. Mortality experience in the factory. Brit. J. Ind.Med. 5: 1 (1948).

20. Bencko, V., personal communication, 1976.

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