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J 3W front; Wiener TierMrztlxcha Monatsschrift, vol.42, 1955 Front the Madico-forensic and Ambulatory Clinic of the Veterinary College Hanover (Director: Pxof.Br.E.Hupka) CONCERNING FLUE DUST POISONING IN THE ENVIRONS OF METAL SMELTERS by E.Hupka with T Figures and 3 Tables The increasing advance of industries into agricultural areas has as one consequence that ever more frequent complaints are heard about poisoning of ani mals through waste gases and effluents. Proving such poisonings is very diffi cult because the clinical and pathological symptoms vary considerably, and the chemical proof of poison in the body encounters particular difficulty because the body harbours most of the allegedly toxic materials in varying quantities by nature. Of all industrial waste materials, lead is Considered particularly dan gerous to animals; without a doubt, lead-containing flue dust and water have a harmful effect on the organism whan it is compelled to ingest greater amounts of them over longer periods of time. But especially the incontestable proof of lead poisoning is extremely difficult, i.a. proof pf'damage to health actually trace able to the ingestion of lead; numerous issues concerning lead poisoning on range land in the vicinity of smelting works remain contested because of insuf ficient proof. Qften the definite establishment of a flue dust poisoning foun ders on the circumstance that the flue dust concerned does not contain one toxic dust but several, and the the question comes up:which poison is actually the one damaging to health? On the other hand, by addition and accumulation,other poiso nous effects are created and also new and changing illnesses. Two such cases of a new type of illness, likely produced through the simultaneous action of sever al toxic substances, shall now be reported on: In the years before the last war and in the years following it, there oc curred,in the vicinity of two smelting works situated far apart, sicknesses among colts and also among cattle that were identical in their course and their pathological-anatomical evidence. The works in question smelt lead and zinc orea, where, besides traces of other elements, substantial quantities of lead, zinc, and sulphurous acid escape with the smoke from the stacks and later settle on the soil as flue dust. Near one of tha metal works there is a superphosphate 754 N 27640 2* * factory, in whose flue gases there is also hydrofluoric acid. First, I want to describe the course of the sickness and the pathological changes, and then to discuss the causes, because I have succeeded,in two feeding tests,to produce the same symptoms of a sickness, I. Course of Sickness The sicknesses do not appear in animals kept in stables, but only in those on range land, and up to a distance of ,5 km radius from the smelter. In the one case it is fertile marshland where the works are situated, in the other case both smelter and grazing land are located in the German sub-alpine mountains. In the immediate vicinity of the smelter, the green expanse gave way to areas with no vegetation or those where only weeds grow. Sams 500 m distant, one can observe good grass growth again, but, seen from afar, the tips exhibit a slightly yellow ish to reddish discolouration. From about 3,000 m an, one does not note this change on the grasses any mors. The indications of health disorders,which make their appearance during the course of the grazing period, are of a peculiar kind and have not been described so far* The German literature, in any case, does not contain examples Of a re lated kind. Mainly horses are affected, and among those predominantly colts, presumab ly because they remain exposed to the waste gases continuously for several 765 months on the range, while the older horses are on pasture only at night as a rule. However, with cattle, too, the same changes can be observed, although not so often and not to that extent. Beside a decline in nutritional condition and in milk yield,and a rough coat at undiminished appetite, above all the tired, stiff gait stands out. Later, the joints show increases in circumference, and they accept finger impressions, but they are without pain or elevated tempera- 766 tore; finally, considerable thickening takes place in the immediate neighbour hood of the joints, namely at the epiphyses, In this stage, the joints assume an angular position, they can be bent and stretched only under great pain, and they fold over forward, so that the animals can walk almost only tip-toe style, as illustrated in the pictures below (Figs, 1 and 2). The changes mentioned are most obvious on the carpal joints and hocks, and to a lesser degree on the knee, shoulder, pastern, end crown- joints. When moving forward, the animals apparent- ly do not feel-eft^ great pain, but they do not like to move,and when they do. DUP040009021 there is a definite creaking sound at the joints of the limbs that can also be heard at the intervertebral joints when the head or neck is being moved. Accord ing to veterinarians practising in the area, with older horses whistling in the i reariwj ) larynx is observed strikingly often) after dissection, it became evident that in several cases there had been definite atrophy and a chicken meat-like discolour ation of the larynx muscles. Occasionally, animals on pasture are afflicted with / spitting and difficulty in swallowing, but these troubles disappear oh stabling. Frequently, the visible mucous membranes show a slightly yellowish discoloura tion* If the symptoms on the joints exist only in a small degree, then healing may Come about over winter. Mostly, however, horses as well as cattle have to be desttoyed because of progressive emaciation and difficulty in movement. Fig.1 (left) incipient stiffening of the joints. DUP04Q009022 -4 - I had the opportunity to Study the sickness on the pasture and in the stables and to observe a few diseased Colts in the clinic, too; I could confirm the evidence cited above in every respect, A few very sick animals were killed and subjected to a post-mortem examination in the Pathological Institute of the Veterinary College Hanover. The following,highly interesting evidence was taken from the joints, and I am obliged to Prof.Dr.Cohrs, director of the Pathologi cal-anatomical Institute, for allowing me to use it. The synovial fluid was in creased and slightly turbid in appearance, the capsular walls and surroundings were altered oedematicaily. At the joint surfaces, the articular .cartilage was often detached to a large extent from the underlying bone, so that a blister formed underneath. In some instances, some bits of cartilage had chipped off and were contained loosely in the joint; occasionally, the cartilage had dis solved and attrition was evident. Once in a while the lifted cartilage chip had fallen down again and covered loosely the worn spot. In the less severe cases, only thickening at the cartilage edges and incipient cartilage atrophy was noted. Changes similar to those at the joints of the limbs were also found at the intervertebral joints, especially at those of the neck. Here the interverte bral discs were at times completely detached and infiltrated with blood. The remaining evidence of the autopsy was negative. Since it was reasonable to as sume flue dust poisoning, it was seen to it that chemical analyses for lead and arsenic were carried oul^onaiA^ livers of horses killed in the region around the smelting works; these assays gave quite remarkable results (of. Table 1). One of the colts killed was afflicted with tape-worms which exhibited a brown to black discolouration. The chemical analysis showed a high lead content. Blood teats always gave contents of from 11,000 to 15,000 granulozytes. Table 1, Zinc, lead, and arsenic analyses on livers taken from animals from tha affected area. The liver contains, calculated in mg per 1 kg of fresh material: i (continued next page) DUP040009023 - 5- 1 . t ' .4 1 9 1 | V to, Zink me 183,6 165,0 822,0 338.0 37,5 23.1 145,8 w ; TO,5 . 615,0 Blci mu 1,2 .5,73 1,45 0,36'* *0 Arsen (AS,Q,). . ` " -- "! 0 --- 5,4 -r- |! 1,5 I | 1.8 S 767 " ,i is 1 ij r.. Zw Zink mg 113,1 13,8 |22,5 12 Pb Blci mg ' 1,95, 0,24 1 0,75 0 As Arsen . -i- -- Is l ts 6.9 16,5 12,9 15,9 1,8 0 0 0 * ** \ -- ' t? ' 20 n 33 21,9 49,8 0 0 0 0 'o *** - > 0 0 . "* *v : 25 ' *4 ! SB ' 20 | 30 | 31 33 3* ' '2in- Zink mg 9 Sp 217,5 234,4 22,2 0 | 0 278,4 490,8 81 Blci mg 33 Sp SP ,/^i At*e;n! ". 0 Sp *'* . 1,5 i 0,7 _1 - r,56 "/ 1,14 0 39 H * 110,4 11,7 10,2 0 1,05 0 mmm ` ' Table 1 {left) ^ (Caption on pre vious page) v " . 38 3 40 , 41 43 44 45 46 *1 50 ` ',*24 Zink mg 657 2920 1310 :39 289 80 484,8 219,0 93,7 46 690 200 37 ;.?!* Blei mg 6,0 26,6 5.3 j 3.5 7,9 1,6 11,4 2,0 0,63 0,8 3,6 3,6 2,9 /A* Arstn'x. 1 .. -- - --J 20 50 50 0 II. Feeding Test As the management of the smelting works were interested in a clarifica tion of the damages, we were asked to carry out a feeding experiment with flue duet from the two plants that were the possible causes of the harmful effects to health. The analysis of the flue dusts, performed by smelter staff, showed! Table 2s Flue dust No. I (right) i_ Pb 44,70%; . Zn \21 s ' 8,20'K As ; 0,22%; r ci., 5,60%; Fe Cd * 4 --* _ ji Pb : ` ' i 16,87% i;v- Zn. xj;23,i4%;^ S ; SO* v:j 8,33% j . As ' ;i 0,52% . Fe 5,805 " -% Cd. 2,22% F_ Table 3: Flue dust No. II (left) As test object served in each case a warm blooded colt, about one year old *h- and in moderately good nutritional Condition. Any hidden conditions of sick ness were excluded by a thorough general examination. < DUP040009024 -6- Colt Np,,1, fed with flue dust No.1 (Table 2): From March 22nd, 1951, on, this colt received hay from the pasture in the vicinity of the metal smelters, and a daily ration of about 1-fc kg oats. On April 30th, articular swelling could first be noted bn the right hock, and on May 23rd on the left one, too. Its gait became a little stiff. Since the evidence of ill ness did not change substantially afterwards, from June 5th on 5 g (i table spoon) of the above flue dust (of.Table 2) were mixed into the oats, in addition to each forage ration. The colt thus received each day 15 g of the flue dust, besides the dusted hay. On June 3th already, difficulty in swallowing appeared, along with some regurgitation, decreasing on June 11th. Yet again and again later on, some food particles could be found in the nose, and the horse ate more slowly, so that it had to be assumed that the act of swallowing caused difficul ty, if only at times. As the daily flue dust ration was increased to 20 g on July 27th, intensive swallowing difficulties occurred by August 1st; so much so that neither food nor water could be swallowed down. On August 3rd, ths colt showed symptoms of pneumonia, and it was killed gust before it would have died. DUP040009025 -7- Towards the end, the colt's gait had become more end more laborious and stiff. Apart from the hocks, the two elbow joints showed distinct Increases in cixcump ferenee in the last stage. An increase in the number of leucocytes was already evident in blood tests from May 2nd bn; there were between 11,000 and 14,500. Beside the hay affected with flue dust fall-out, the colt had ingested addition ally a total of 975 g flue duat over 56 days* After dissection, acute catarrhal pneumonia of both diaphragm lobes was determined, with food particles in the bronchi,rfurthermore oedema in the inter lobular septa, gelatinous impregnation of the trachea in the course of the lymph duct, and moderate general icterus; in other words, the symptoms of an aspiratory pneumonia. In the hocks and elbow joints there were the above described ul cers on the cartilages, distinctly formed (Fig.3). Deposits of gall pigment were found in the liver and in the kidneys. The chemical examination of 100 g liver for lead gave an assay result of 1.52 mg, and the analysis of 1000 g hay gave a lead content of 60 to 65 mg. Ac cording to information from that assay office, lead occurs in hay usually in so small traces that they cannot be measured macroscopicaliy; their determination is then only possible by delicate microanalytical methods. In accordance with the investiagtions by DANCKW0RTT,, the lead content in the liver must be consider ed as substantially elevated. DANCKWORTT reached the conclusion, on the basis of his investigations, that the normal lead content of a liver is approximately 0,1 to 1.0 mg. 769 Colt No,2, fed with flue dust No.II (Table 3); c In a second feeding experiment, we checked the toxipfity .of flue dust No,II which comes from a.:plant near the first smelter, located in the Same district but processing different raw materials (Table 3). The analysis of this flue dust was different from the first one mainly on account of the lead snd zinc content. Whereas flue dust No.I (Table 2) had a lead content of 44.79% and a zinc content of 5.21%, flue dust No.11 (Table 3) contained only 16.87% lead, but 23.14% zinc. The other values did not differ very much. A six months old warm blood colt of Hanoverian breed, taken into the cli nic on September 22nd, 1952, was used as test horse. The colt was well fed and exhibited no disorders in its general condition. Because a heavy infection with DUP04Q009026 ascaridas and strongylides was proven by examination of the faeces, treatment against the worms was administered before the feeding experiment started. After the horse had a bout with the glanders, the feeding test could not begin until November 25 st, 1952. At first, the colt was given 3 g of the five dust daily, mixed into its fodder. From November 29th on, the daily ration waa increased to 5 g, end from December 12th oh to 8 g, yet no changes in its nutritional or ga<neral condition wars noted. As 10 g of the flue dust were admixed to the fodder, beginning January 8th, 1953, the colt refused acceptance, so that from now on the dust had to be administered by a nose probang. Because the general condition did not change even now, the amounts given were stepped up further, namely on January 21st to daily 1:5 g, on January 26th to 20 g, and on February 4th even to 30 g daily. On March 25th acute symptoms of poisoning appeared, so that the flue dust doB.as were discontinued, only to be resumed on April 10th, after the symp toms had waned. Initially, 10 g daily were given, then from May 5th 20 g daily, and from Mby 12th to June 11th 30 g daily. From November 21st, 1952 until June 11th, 1953, the colt has thus ingested a total of 3,270 g flue dust. 770 Fig.4 s Swollen carpal joints Fig.5 s High degree of swelling of the hocks f DUP040009027 9 Clinical report: Temperature and pulse remained within normal limits dur ing the entire feeding experiment. Fodder acceptance was regular until January 5th, and varying from then on. At various meal times the ration was not eaten up. The colt yawned often and preferred to stand or lie in a dark corner of its stall, as if shying away from light# However, the eye test was negative. The gait became stiff, and the carpal joints, hocks, and pasterns exhibited a dis tinct increase in circumference, feeling moderately tough, warm, and painful to the tbuch{Figs.4 and 5), From April 23rd, 1953, on, swelling could be observed on the: knee and shoulder joints, too. Also from then oh, the colt had difficulty in getting up. Blood tests, which were carried out continually, showed modifications only in thp white blood portion, similar to the first colt tested. The number of white blood corpuscles always hovered around the upper limit, between 8,000 and SryHtto 12,000. barter-count and haemoglobin content showed a downward trend in the cour- eryftitpcyfc se of the illness. While the colt had an aster count of 8 million and a haemo globin content of 72.9 before the feeding experiment, towards the end of the ex periment these figures had dropped to 5 million erythrocytesjand 50 Hb. The basophilics^a^s on the erythrocytes, well knownin the medicine of humans, could never be observed by us. Nor did tha differention of the blood pictures allow us to recognize any deviations; likewise, calcium and phosphorus deter minations in the blood serum indicated no changes. The so-called lead fringe, purpdrted to be a diagnostic for lead poisoning, also failed to appear, in this or the first test colt. The Pathological-anatomical Institute (director: Prof.Dr.COHRS) issued the following autopsy report on the colt killed on June 11th, 1953; The big parenchyma showed no pathological-anatomical changes macroscopically. At the transi tions from bony to cartilaginous ribs there were chestnut-sized swellings. The tarsal and carpal joints and their bony bases had thickened considerably. Thera was a lentil-sized ulcer, in the process of healing, in the elbow joint at the ulna. The histological examination showed a fine-grained, interlobular pigment in the liver, and a low degree of nephrosis in the kidneys. Chemical examination: In the last weeks of the experiment, three lead determinations were done on the blood; in late March, when exhibiting distinct symptoms of poisoning, 0.466 mg lead were found, and after the symptoms had re- * UdUdf ^ ce^ded, 0,325 mg and 0.200 mg. After death, the plasma, the liver, and the 771 *J fwiuvuctUy (victi^-^ovw 'ftvt, fit * J**--j j I* of- -fUt C*mI kt -t o k. *<&* cowfsiw^ #. , - DUP040009028 - 10 - kidneys were tested for lead, and the following values wars determined; 0.055 mg in 100 ml liquor, 2,770 mg Art 1QQ g liver substance 0.670 mg in IDG g kidney substance. ,. The soil analyses for lead, zinc, and copper gave the following assays, in the direction of the wind towards Northeast; 0.4 km distant; 300.19 mg lead, 1.0 km distant: 53,0 mg lead, 3.0 km distant: 6.0 mg lead, 400.0 mg zinc, 162.0 mg zinc, 23.0 mg zinc, 40,0 mg copper (in 100 g); 10.Q mg copper (in 100 g); 0.9 mg copper (in 100 g). In the other wind direction, the contents were lower. At about the same time, we could observe two colts for several weeks, which had grazed in the vicinity of a metal smelting works in a central German mountain region. The clinical and pathological-anatomical evidence was the same. 772 Heres, too, swellings at the joints and the stiff gait were the most notable features. After killing, the previously described changes on the articular car tilage was observed in all pathologically altered joints, sometimes to a con siderable degree. In one case, the epiphysis suture was simply severed. The articular capsules were oedematically altered, the synovial fluid was much in creased. Unfortunately, we did not succeed in ascertaining the composition of flue dust concerned (cf. Fig,6). DUP040009029 * 11 - III:. Critical Consideration concerning the Aetiology and Symptomatology of these Poisonings Whan studying tha analyses of the flue dusts, the large quantities of lead and zinp stand out; but these are not the same in the two flue dust samples, for in flue dust I the lead predominates and in flue dust II the zinc {smelter I: Pb 44.79% .Zjfi 5.21% smelter II: Pb 16.87%, Zn 23.14%). That is to say smelter ' I lets more lead and less zinc escape, and smelter II mote zinc and leas lead. Of the other toxic components, there exist in substantial amounts: iron {smal- 773 ter II 6.8Q%|), sulphur {smelter I 8.20%, smelter II 12.53%), sulphurous acid {smslter II 8.33%), and chlorine {smelter I 5.60%). Besides, arsenic, cadmium, and selenium occur in traces. It is natural to see in lead and zinc the cause of the sidkness. However, experience gained up to now speaks against viewing ohe of the twd pois|pn$ as the sole causa..In the human and veterinary medicine, the following symptoms are cited as chronic consequences of lead poisoning: damages to the netVdus system, with preference to certain nerves, like the racuirens (roaring), vagus {chronic colics), glossopharyngeus {pharyngo-paralysis, regur- gitatipn), Radial'paralysis (inability to stretch the front limbs), and para lysis of thg optic nerve with partial blindness. With humans, the basophilic stifling is [considered a particularly important Symptom in the early stages; this stifpling of the ,ret$porpuscles is a consequence of damage to the blood- forming bonp marrow. Furthermore, chronic organ disorders, such as nephroses (leaded kidneys), diseased blood vessels, and damage to the heart muscles, are said to appear. The stomatitis ulcerosa with the lead fringe, mentioned many times in the literature, is missing with horses end cattle,probably because these animals do not exhale by mouth. For the lead fringe is supposed to form by the combination of the hydrogen sulphides in the air with the lead,giving lead sulphide; however, since the horses do not breathe with their mouths, a lead fringe cannot form, A comparison of the symptoms that appeared in practice and in our testf horses doubtlessly shows similarities: roaring, pharyngo-paralysis, spitting, probably caused by difficulties in swallowing, chronically diseased kidneys, emaciation. It is also interesting to note that these symptoms appeared more intensively and in a shorter time with flue dust I of the higher-lead con tent than with flue dust II with the lower lead content. n examining the results of the numerous lead assays on livers of animals DUP040009030 that took sick on the pasture, it is striking to note that the lead content was elevated in most cases, and mostly very much so, on the basis of the statements by BANCKWQRTT that a lead content in the liver of over 1,0 mg must be regarded as pathological (of.Table 1), In the two test colts, too, it was found after kil< ling them that the amount of lead in their livers was higher, In colt I the amount was 1,52 mg24 per 100 g liver, and in colt II 2,72 mg% per 100 g liver sub' stance. An institute of forensic medicine has termed the quantities of lead in the blood as considerable also. Moreover, the high values in the soil in the surroundings of the plant are striking. In second place, it is natural to allege that large amounts of zinc have a toxic effect. Indeed, zinc poisoning plays a big part in the veterinary liter ature, such poisonings are again and again suspected. However, despite numerous feeding experiments, bo one has succeeded in producing a chronic zinc poisoning yetj presumably, because zinc is a passing poison which is not reabsorbed or ac cumulated , leaving the intestines quickly. But in cases of acute poisoning be cause of ingestion of large amounts of zinc salts, heart paralysis and damages to the KcretivB organs are said to occur. Even in healthy animals' livers, the zinc content varies so much, and occasionally is so high, that no firm conclu sions can be drawn from it. The other components of the flue dust are present only in small amounts, so that it can scarcely be assumed that they exert a damaging effect on the or ganisms of the animals. Besides, of these poisons no symptoms of sickness are known that progress even remotely like the ones described above. Changes in the bone are known only in fluorosis, but they are of an entirely different kind. Thera, they are a matter of osteoporotic and osteosclerotic processes, especial ly at:the tubular bones and accompanied by a brown discolouration of the teeth. The bones do show knotty enlargements up to pigeon egg size at the tala asses, but no lifting of the epiphyses or ulceration at the articular cartilage (Fig,7). Therefore, it can be assumed that, although symptoms of chronic lead poisoning are predominant, a new type of sickness enters the picture, created through the synergic effects of other toxic substances (probably zinc) and characterized mainly by the localization in the joints. Or else, our knowledge of chronic lead poisoning is insufficient and doBS not correspond to the actual situation. Be cause of the frequency of the alleged damages from lead, and because of the long drawn-out litigation resulting from them, it would appear urgently 774 DUP040009031 - 13 advisable to clarify the correct course of the disease in lead poisoning by feeding pure lead compounds to horses and cattle. Fig.7 (right): Exostoses at the meta carpus of a horse af flicted with fluorosis Summary 'f- ... Summary , , 'i>; V';; Chronic articular swellings have been observed in tolls and cattle grazing in the'.. ; vicinity of two forges. At autopsy an increase of synovia is stated; further it is observed that (he articular, cartilage is detached to a varying extent from the underlying bone. `Xater on, roaring, due to paralysis1 of lfte recurrent nerves,, developed In several edits. ' Analysis of the forge dusts yielded following results; . `, ; i Forge 1: Pb 16,87%; Zn 23,41%; 5 12,53%; Fe5,80%; Cd2,22%; As 6,52%. . V , Forge 2: Pb 44,79%; Zn 5,28%; S 8,20%; Ck, 5,00%; As 0,22%, , ' Identical articular lesions could be reproduced-in two colts, each having been fed S for several weeks on rations containing forge dusts. Further, manifestations of pharyngo-. .7 paralysis appeared which in one case resulted in pneumonia due fo pharyngeal uys* . i i' plwgia. Tire author suggests that the condition is due to kadpoisoning being cdmpii-1,; catcd by other toxic eubstanccs. Analyses of several coll livers showed in all cases a lead content exceeding 0,2 mg per 100 g, , -a Literature References . .. '* Literatur: C o h r s, P.: Dtsch, ticrSrzH. Wschr, 53 : 22 (i946). -- D a n c k w o r t S, '(O.V.): Dtsch. iicrarrll..Wschr. 49 s 365 (1941). -- FrGhnerJVi ke r: Lehrbuch der.vy ' Toxikologic. Vcilag F. Enke, Stuttgart 1953. -- Q tint her, IS.: Vet. Diss., Hannpver ..'y* . 1954. r- iiupka. li.i Dtsch. iierSrztf. Wschr. 49.: 349 (1941).y-i* 0*H, W, v.l Veb.-av `` Diss., Hannover 1942, ' ' ' *: V-.' $;' Cohrs, P. Danekwcsrtt, FxSh ner-V 51k er GQnther, H. Hupka, E. Gasan, W.v. German Veterinary Weekly, 53: 22 (1946) German Veterinary Weekly, 49:365 (1941) ' Textbook pf Toxicology, published by F .Enke,...Stuttgart, 1953 Veterinary dissertation, Hanover, 1954 -German Veterinary Weekly, 49:349 (1941) Veterinary dissertation, Hanover, 1942, WPL11X169 DUP040009032