Document 6wJqwrrX4DKMBXQLyazXqzpxE

I* A. Mfi, It-Of AUG 181972 HUNS 0 8 6 2 6 8 10 -03 AUG ' f* 1972 MQNS 0 8 6 2 6 9 ENVIRONMENT REPORTER l 11. 1*72 THE BUREAU Of ISA IKJNAL Af FAIRS. ItyC- Vdusi 3. Number IS Alt POLLUTION lafwni Uk \idei unmitor dev duped ........................ 443 Uforautiua on awbrnc cmUmrm(s mwld for OSHA criteria. vljudjrd* ................................................................ 445 ATOMIC FNt'RGY MiimimIm rf udmtMda^ nyaod by AEC, TVA, CtHiuaouwcaltk ktlbtMi ...................................................... 437 HU MICALS EPA incMacali lo FIP1A ................................. 431 ik>v>c 'uKiMtirailKV ippiirn Ml ................................. 434 Rcw yiuup may be anlMwd by EPA ...........................434 COSTRACTS l-'SSO Rivard renns EPA coMixl ................................... 440 MICHIGAN ' Suifof diedde. fed daodmds now effect..................... MOTOR VEHICLES Export of uacerltffod ears allowed by F.PA ....................... Technical appendix available from EPA ............................. NEW JERSEY Grants meiiod for dsmoostmtioo racydmn pronrami .. NEW MEXICO Air pidfodon repabdonf astaMidied................... ........ Envuonmeatal agency pleas baarinp on mptoc tank nrfos NOISE InteraalioaeJ conference to be hdd .................................. OCEANOGRAPHY 447 443 EDUCATION Air piAium lummy courses kMM ............................... 443 CoHcpr envgameataldiwiHatmMlisiod .............................444 FLFCTRIC POWER Senate plant dune background report imood......................... 444 ENERGY Bureau f Mines mummiuci popca Prnblimi renewed before Home ' Impact of federal " ENTORCEMLNT EPA issues I SO-day nelktr .................................................... 433 New York City Orms to halt touic metal Skkqm............ 43B FEDERAL AID FPAtem;, HLTD basic water. FLORIDA ^ Heated water discharges fended..............................................445 GASOUNE Termination of lead discharges recamnwfrd .....................434 GENERAL POLICY CEO usuet Hurd Amuml Report ............................................437 Conferees approve bdl to dmfop water, pane mourret .. 435 NOAA swards 11A aidboo sea grant ................................ . 447 OHIO _Gomaoc appends dbacter of tnvneaaaatda^acy ___ 443 EPA ktEoleum Aapat charges at ledt on North Slope exntod for IS n CanonKtto twM eapforation efforts iaadcqnoit Interior Department sots hearten an p ` :> Witncams rapport proponed OB Petal POPULATION CUhcas Popnbi IEMENT EPAwakiMan SOUD WASTE NASMI ad urges urn of water t for market etpnamon Eadronmcotol statrmrett Bited ............................................441 EPA sppafots urban affairs direcior....................................... 444 Fourth eawcoaments! iimach Mf SwipMd ...............435 Howe approves cssferm report ao EPA aporoanatfom . 43B Pirn drat NiaonsshsCiapni load oapsadfagbiii........ 431 Senate approves funds for dilerr eamMctfon of control New bniA on Toxicity of Chlorinated Hydrocarbons and Related Compounds A Kovicw Inrluding Chlnrlnnttd Dibenzodioxins and Chlorinated Dibenzofarana D. Kimhrmifth, MD, Chambltt, Ga l VarltM chlorinated technical compound*. Mmdji, 3,4,B-IHeMoroph*n- Chloracne oxyaeetle aeld (2,4,S-T), and European chlori This disease ie described by the formation nated Mphenyle (Phenoolor DPd and Ctoph*n of comedones with or without cyata and AM), have been found to be contaminated wKh trace amaunla of eMerlnetad dlboniefurana or pustules. The follicular oriAccs are filled oMerfneted dtbentodknina. Toxic fat which pro* with sebaceous and keratinous material. t ducea hydroperloardlum In ohlefcene aiao contaku ohlorfnaled dlbentodloxlns. Thee* and other tech* nleal chlorinated compound* such a* the tech* Melanosis and a secondary inflammatory reaction may exist Chloracne was described for the first time by Herxheimer' in 1899 nleel penlaohlorophenol have been bnplloatod In who thought it was produced by free chlo oausfnfl ohforaone, liver dl*eo*e, leratopenlclty, rine. Wauer* in 1918 and Teteky1 in 1927 mNaaaae In cattle, and ehleft edema. The liter** suggested the term "pernakrankheit." They hire on the loalelty of the oMortnated technical felt that this skin disease was produced by compound* I* reviewed. It la mantlonad fiat certain chlorinated hydrocarbons. Jones and c 2,4,t-T and tha chlorinated Wphanyla alee Induce perphyrta. Whatbar dm various dlaaaaa antttlaa Alden4 were among the first to report a case am caused by the contaminants, combinations of chloracne in a 26-year-old male Negro of dm ohandoal and Ns contaminant* or by dm who worked for three years distilling chlori ob*mlB*l* themashrae need* further evahmtlen. nated biphenyls. This patient also com plained of lassitude, loss of appetite, and loss of libido. 1 RECENTLY several chlorinated com Chloracne is one of the most frequent pound*, such im the polychlorinated biphe forms of occupational dermatitis, and many nyl find 2,4,5-trichlorophcnoxyacotic acid cases have been reported in the United (2,4,B-T), have recoived a (treat deal of at States as well as in Europe, particularly tention. Polychlorinated biphenyls (PCB) Germany and England. are increasingly found in our environment Teleky* reported in 1949 that he personal F and 2,4,5,-T has been uned extensively as n herbicide. Occasionally these and other chlorinated technical compounds have caused dismass that boar similarity to each other. ly had seen at least "150 to 280 workers" in four different factories with chloracne. He stated that liver disease occurs independent ly from chloracne, and usually manifests Rome of thorn* chemicals have been found itself after an exposure time of four to six to bo contaminated with chlorinated dibeit- months, but may occur in as short a time as sofurans or chlorinated dibensodioxine. The seven weeks. Occasionally loss of appetite, various diseases produced by one or more of nausea, and edema of the face and hands the different technical compounds are dis are the first symptoms. Abdominal pain nnd closed in this paper. Attention is focund on vomiting follow, and then jaundice develops. the various contaminants and (heir possible At autopsy, acute yellow atrophy of the relationship to different diseases in a variety of species. Tha need for further welt-coordi nated epidemiological and experimental ani mal studies ia pointed out ftabmltted for publication Oct 8. 1971; accepted . March 9,1072. Prom tha Chambtaa Tmdraiotry Laboratory, Bnvi- liver is found. He cites Flinn and Jarvik* who reported cases of acute yellow atrophy with fatal outcome following exposure to Halowaxcs. Halowaxes, which are chlorinat ed naphthalenes, as well as the PCB (Aroclors) were increasingly used after 1930 to insulate cables. Teleky" cites many other rvwmantel Protection Agency, ChamWaa, Ga. Reprint mguaate to Qwmbtee Tmioology Labora tory, Bnvliouuwntel Protection Agency, 4770 Bu ford Hwy, Cbamblaa, Ga 80041 (Dr. Kimboush). case reports (Drinker et al,T Jones,9 Greenburg eft el,9 Cotter,10 McLechtdue end Robertson,11 and Collier19). Von Oettin- Arch Environ Health--Vol 35, Aug 1973 MGNS 066270 12K TOXWiTY OF nYnnOCAnnONft--KtMBROOGH ne cftlortnatwl (SbanxofurMt. dncribn the occurrence of chlorncno in workers exposed to these chem icals. He cites several references which indiente that dermatitis is the result of the local effect or direct contact with the chemical, while the toxic hepatitis results from absorp tion. Chlorncno has been reported in workers exposed to chloronnphthalenee, chlorobiptvnnyls, chktrodiphenyloxidss, certain petroioum products, and solid chlorophenols.14 More recently Meigs et al,f and Hofman and Mensghini1* reported 14 and 13 casea of chlorncne, respectively. Expoeure to dhkjrinoted biphenyls was established in mart of these casea. Birmingham17 observed chloracne in 15 employees who had painted flat sections of glass with enamel and then bekod it. The enamel had Aroclor (a PCB) Incorporated In it. Plewig1* produced chlor acne experimentally on the upper back of eight mole adults by applying Halowax 1014, pmtechloronaphthnlene, and hexachloronnphthnlene. Bauer et a)1* reported chloracne in work ers that handled technical 2,4,5-trichlorophenol. In some of these workers neuromus cular wonknma, psychopsthologicsl changes, blepharoconjunctivitis, and liver involve ment abo occurred. Kinwnig and 8chulw found that pure 2,4,5-trichlorophenol did not produce hyperkeratosis when applied to the rabbit ear. (The rabbit car test in used as a screening tent to determine whethor a compound is likely to produco chlorncne. The chemical, dissolved in propylene glycol, is painted on the rabbit ear. If the test is positive, erythema occurs within two days and in a few weeks hyperkeratosis de velops. ) The rabbit skin offers us an experi mental method that will indicate the ability of substances to produce acnciform derma titis in man.*1 Pure 2,4,5-trichlorophonol did not affect the rabbit ear, and neither did 1.2.4.5- totrachlorobenaene, the starting ma terial in the manufacture of 2,4,5-trichlorophenol. However, technical 2,4,5-trichloro* phenol which was used in the production of 2.4.5- T did produce hyperkeratosis of the rabbit ear. It was concluded that by-prod ucts which had resulted during alkaline hy drolysis of 1,2,4,5-tetrachlorobenzene were the causative agents. Kimmig and Schulz9* isolated several con taminants and found that some of them, namely tetrachlorodibensofuran (Figure) at a concentration of 0.05% as well as tetrachlorodibcnaodloxin (Figure) at a concentra tion of 0.0%%, produced hyperkeratosis in the rabbit ear. A hepatotoxic effect was also observed with these compounds. They also found that pure pentachlorophenol did not produce hyperkeratosis of the rabbit ear. Chloracne was observed in workers of a West German plant who produced tech nical pentachlorophenol from hexachlorobenzene.89 The technical material also in duced hyperkeratosis in the rabbit ear. It is possible that (ethnical pentachlorophenol contains toxic impurities, particularly since pentachlorophenol is produced by alkaline hydrolysis from hexachlorobenzene. Dibenzodtoxin and dibenzofuran themselves do not cause liver necrosis or hyperkeratosis when applied to the rabbit ear; however, they become highly toxic when they contain three or more chlorine atoms.90 Some of the work ers with chloracne also develop eye irrita tion, hepatotoxicity, intolerance to alcohol, neuromuscular symptoms, porphyria cuta nea tarda, and psychologic alterations.99 Ac cording to Braun,94 chloracne seems to re sult from direct contact with the chemicals producing it Crow,8* on the other hand, points out that chloracne can also be pro duced by systemic absorption. Arch Envimn ht*alth--Vol 25, Aug J972 X-t This disease in c Olnfson80 in 1047. . denro war publiHhn chlorinated naphtha case.97 CnUlc with . decline in vitomin / toms of poisoning im tion, diarrhea, poiyv and discharge from cough, poor oppetit maculae in the boect hyperkeratosis of Ut ecopic examination shows central lobula cells with bile duct tion of the glands ii bladder. Cystic dile tubulea of the renal t degree of Abrade end pancreas, wee also of crosis and cirrhosis i the nephrons, and the endometrium wer after ingestion of f chlorinated naphtit Link'1* fed hexaehhm swine and produced the liver and kidneys vaginal epithelium A depression of the * was also observed. Drinker and eo-w* liver of rets was a mots were fed high naphthalene, pmtor hexachloronaphthalei phenyls. When Scho chloronophthnlene to to moderate fatty de with ccntrilobular \ cells. Degenerative ch the kidneys and the tosie. it can be condud that highly chlorine dues liver changes cows, x-disease of tie drop in the vitamin A the leading manifesto is possible that the represents a menifee liver disease. Sikae et al*9 found produced in cattle MGNS 086271 X-dtw'nm* This dtaeane in cnttle was described by Olafaon" in 1047. A few years Inter evi* donee wnn pitblwhid showing that highly chlorinated naphthalenes award the dm* oaso.,T Cattle with x-dweam bIkjw a rapid dooiina in vitamin A plasma levels. Symp toms of poiaoning include excessive lamina tion, diarrhea, polyuria, marked salivation, and discharge from the nostrils. A chronic cough, poor appetite, and numerous red maculae in the buccal mucosa develop, and hyperkeratosis of the skin follows. Micro* aoopic examination of autopsy material hows central lobular degeneration of liver cells with bile duct proliferation and dila tion of the glands In the wall of the gall bladder. Cystic dilation of the collecting tubulsa of the renal cortex, with a moderate defies of fibrosis and degenerated cells in the pancreas, was also observed." In sheep, ne crosis and cirrhosis of the liver, damage to the nephrons, and squamous metaplasia of the endometrium were the principle findings after ingestion of feed containing highly chlorinated naphthalenes." Huber end Link'* fed hexachloronaphthalenes to young wino and produced degenerative lesions of the liver and kidneys and hyperplasia of the vaginal epithelium with keratin formation. A depression of the vitamin A plasma level was also observed. Drinker end oo-workers7 found that the liver of rata was affected when the ani mals were fed high doses of tetrachloro- naphthalene, pentachtoronaphthalene, and haaachloronaphthalene or chlorinated bi phenyls. When Sthoettle et alat fed hexa- chloronnphthalene to rata, they observed mild to moderate fatty degeneration of the liver with centrilobulor vacuolatkm of hepatic oslls. Degenerative changes were observed in the kidneys and the skin showed hyperkera tosis. It can be concluded from these reports that highly chlorinated naphthalenes pro duce liver changes in several species. In eowa, x-diaeaas of the akin, together with a drop in the vitamin A plasma level, is one of the leading manifestations of the disease. It ia possible that the vitamin A deficiency represents a manifestation of concomitant liver disease. . Siksa at al" found that x-diaeaaa oould be produced In cattle with highly chlorinated nnphlhnlcmti, hul also with jx'lrnlrtnn prod ucts such os crank coso oil. Tho toxic prod ucts were excreted in the milk and produced x-disease in the calves drinking the milk. They cited other authors who were able to produce tho disease with A complex wood preservative and a lubricant. Bell-1* tested the ability of various com pounds of the chlorinated naphthalene group to produce x-disease. He discovered that dtehlorinated and trichlorinated naph thalenes did not produce tho disease while tetrachloronaphthalene had an effect, and the higher chlorinated naphthalene, pentochloronaphthalene, hexochloronaphthalcne, heptachloronaphthalene, and octachknonaphthalens, caused severe disease. Octachtoronaphthalene was lew toxic than hexachloronaphthalene and heptachloronaphthalene. Chick Edema In 1967,1a disease occurred in a large number of chickens which, at first glance, neemad to represent an epidemic. It was soon discovered that the residues of certain distilled animal fate produced the condition when they were added to the chicken diet1*'17 The disease was called chick edema because it manifesto itself with hydroperi cardium and ascites in chickens. Ducks and turkeys experience a reduction in growth. Allen and Lalteh" produced hydroperi cardium and ascites in chickens when enough toxic fat was given to kill most of the birds in five weeks. (`"Toxic fat*' is a term used for fat found in chicken feed that induces chick edema.) When the concentra tion of toxic fat was reduced and fed to the chickens for 160 days, hydropercardium and ascites developed lees frequently, but testicu lar hypoplasia became apparent. Simpson el al" dweribed proliferation and hypertrophy of the vascular endothelium end possible necrosis of hepatic end bile duct tissue in chickens and turkeys. When monkeys (Ma caco mulatto) were fed toxic fat, alopecia, subcutaneous edema, decreased total serum protein (with a reversal in the albumin-glob ulin ratio), and reduced hematopoiesis and spermatogenesis developed. Gastric ulcers occurred in 66% of the animals. Focal areas of necrosis and degeneration were observed in the liver; and the bile duct epithelium was found to be affected when it was exam ined under the electron microecope. Dilato- Arch Environ Health--Vol 35, Aug 1973 1 y lunimrijwwi HONS 08627.! Table l.-4)lfMN Rmittint From Exposure CMtrtn* Carlain petroleum product* Cbtoronaphthetenre (mainly ponto, bon*, and bool*) Cbtoroblpbonyt* CMorodtphcnyfowldea Ohtorophcnola (technical 2,4,S.trtehtorephenot. ponloebloropbonol) Technical 2,*,5*T PotMtoflcot Finding* of the llm IHH OofocH ond tetnet Footer Chtertneled naphthalence Ctrtoln tochnleol 2.4,5-T Chlorinated Mphonyt* PurlNod material Technical 2.4.S-T ond from toxic fat* otbor chiorophonole Polychlorinated biphenyl* x*at*oo# ht Cottle Highly chlorinated nophtbotonoo Petroleum product* `'Text* lot" It itrm uaod lor lot found in chiehon rood that Indueaa ehleb adtma. Hon of the Imrt and hypertrophy of the cardiac muaclc wore alao present.40 Tonic fat ia not tho only product capable of producing the chick edema syndrome. Chlorinated biphenyl products, used aa a plastic!mr In a paint, have caused hydroper icardium and ascites in chickens,41 and two of seven Bengalese finches fed PCB de veloped hydropericardium.43 Tho seven finches of a total of 66 birds died during the ooume of the experiment A mixture of pentnchlnronnphthaime and hoxmMoionnphtha- k*m\ when fed to chickens, resulted in chick edema,41 He toxic fat which contained the chick edema factor was studied intensively. Flick ct nl44 separated a purified crystalline concentrate which produced chick edema and decreased the hatchabillty of injected eggs. Embryonic deformities were also produced. Flick ct al40 were not able to produce testic ular hypoplasia m cockerels when Urey fed low doses of toxic fat (0.6% and 1.0%) to the cockerels for 12 weeks, as had been re ported by Allen and Lnlich.** In 1067, Cantroll el al4* reported that ](23J>B>B*hexachlorodtbensop-dioxin was one of the toxic compounds producing chide edema, Tomita et al4T had shown earlier that the heating of pentachlorophenol pro duced octoddoraiibenso-p-dtoxin. Higgin botham et al4* showed that the chide edema factor represented chlorinated difaerao-p-dioxins. The taro principal compounds iso lated were 2^,7-trichiorodibenao-p-dioxin and 2^,7,6,-tetmchforodibenao-p-dloxin. The authors suggested, as a poesible source of contamination, fata and fatty adds contain ing commercial ehlorophenole. When crude fats and tallows are heated to produce fatty adds chlorophanol residues might be con verted to a chick edema factor. It was mentioned earlier In this article that the Aroclors can produce chick edema. The Aroclors (PCB) are used primarily as dielectric fluids for capacitors and trans formers, as industrial fluids for hydraulic, for gas turbine and for vacuum pumps, and aa heat transfer fluids. They are also used aa plastirizers and are widely distributed in the environment4* Aroclor is a trade name un der which theee compounds are marketed in the United States. They can be found in Synthetic resins, synthetic and natural rub bers, cellulose resins, paint varnish, wax, asphalt and In ally! starch. They have been employed for duet prevention, moisture proofing, sealing, impregnation, and vapor suppression to prolong the residual life of insectirides. They increase the toxidty of dieldrin and DDT in insects.** Depending on the amount of chlorine they contain they are assigned certain numbers. Aroclor 1260 for instance, contains 60% chlorine, while Aroclor 1242 has an approximate chlorine oontent of 42%. Miller,*1 in 1944, tested a commercial chlorinated biphenyl with 42% chlorine and observed liver damage In rab bits, guinea pigs and rata. Skin changes were observed in the animals who received subcutaneous injections and application of the material to the skin. The skin lesions produced by subcutaneous injection were histologically similar to those of chloracne in man. Direct application to the skin pro duced inconsistent lesions compatible with low-grade irritation. Von Oettuigenl#<w**-WT> discusses some of the earlier work on the toxicity of the Aroclors In his book The Halogenated Hydrocarbons, Toxicity and Potential Dangers. Nishizumi" observed changes in the liven of mice and monkeys after feeding them chlorinated biphenyls. The author undertook this work because of an outbreak of poisoning that involved at Arch Environ Health--Vol 35, Aug 1973 toTechnical CempeenUe CStaft Toxic fat* Cftlortnolod tlp*Owt Mfatwr* et pmmm--i least 600 people lit ingested rice bean at mated with ehlosc PCB (Kancchlor 46 leaked into the net holes in a pipe used manufacturing prow mentation and ah brown pigment dept Stillbirths were uarr of the mother. Adult orexln, fatigue, erim* like discharge from and dark-brownish p Vos and Koeman* several pelyehtoriww ens, quail and rata, the toxicity of two polychlorinated bfph and Clophen A6D) a which was produced The European comi toxicity and produca* crosis. Chick edams with European com Arodor 1260. AU duccd porphyria. Cht faensafuran, pentach hexachlorenaphthalet the European sample from the United Sta cardturn occurred ocr Arodor 1260, the aut indicative of small qi tor in this preparatie* Terete * Recently. Bionethe Betheada, Md (tanput m HONS OB6273 HTtetmted Compound } Cfttafc Mm To-- lit* MMute --fitscMsrsMphltnlM* md haiachtoronapMhalens Table 2.--Toxic ContentInent* Found in Seme Technical Compounds* 2,4,5>lrlehtoreptMnol /TotrocMorodlbantofuran ( ITetracMorodibeniodtoxin 2.4.ST TexfC tat Curoocan chlorinated biphonyla (Phonoetor OPS and Clophon A 60) Uatod in Tabto J. 1 ITatrachlorodibonrodtoxin C 1,2.3.7,S,9 haxacMorodlbancop-dtoxin < J.3.7 trlfhlnrodlb-ms p dloaln (2.3,7.S tatrachlorodlbanzo s-dtoxln [Tatrachtorodlbantohiran < Pantochtarodlboncoturan (Haxachloronaphthalana taunt 900 people in Western Japan who had indented rice bran oil that had been contain* insted with chlorobiphenyls, a Japanese PCD (Kanechlor 400). Hie chlorobiphenyta leaked into the rice bran oil through pin holes in a pipe used for heat exchange in the manufacturing process. An increase in pig mentation and abnormal grayish dark- brown pigment deposits in the skin of still born and newborn Infants was observed.*1 Stillbirths wars unreinted to PCD poisoning of the mother. Adults showed chtomcne, an orexia, fatigue, edema of the eyelids, cheese like discharge from the meibomian glands, and dark-brownish pigmented nails.14 Vos and KoemanM studied the toxicity of several polychlorinated biphenyls in chick en*, quail and rats. Hm authors compered the toxicity of two European commercial polychlorinated biphenyls (Phenoclor DPS end Clophen A0O) and one (Aroclor 1200) which was produced in the United States. The European compounds showed higher toxicity and produced centrilobular liver ne crosis Chick edema was a common finding with European compounds and rare with Aroclor 1260. All three compounds pro duced porphyria. Chemical analysis of these throe compounds revealed tetrachlorodibensofuran, ponlachkmxlibeiiaofuran, and hexachloronaphthatane as a contaminant in the European samples but not In the sample from the United States.11 Since hydvopericerdium occurred occasionally in chicks fed Aroclor 1200; the authors felt that this was indicative of small quantities of a toxic fac tor in this preparation. by Emerson et at" found a temtogenic effect of technical 2,4,5-T in rats. Apparently, the technical 2,4,5-T was contaminated with 27 ppm of 2,3,7,8-tetrechlorodibenzo-p*dioxin. In the study publtahed by Courtney et nl,M it was stated that the technical 2,4,5-T which was found to be teratogenic in two strains of mice and one strain of rats was con taminated with 30 ppm 2,3,7,8-tetrachlon>dibenaodfoxin. Emerson et el" tested 2,4,5T that only contained 1 ppm 2,3,7,8-trtrnchiorodibenxo-p-dioxin at comparable desago levels and did not elicit s teratogenic effect, this finding was substantiated by Sperschu et alM who studied teratogenic effect of 2,3,7,8-tetrach)orodibenzo-p-dioxin in the rat. A slight effect was observed at a doee of 0.125fig/kg/day when the materiel was giv en by gavage from day 6 through day 15 of gestation. At the level of 0.5jig/kg/day, the effect was quite pronounced. Courtney and Moore19 were able to produce cleft palates and kidney malformations in three strains of mice with high doses (100 mg/kg subcuta neously daily from day fi to 15 of preg nancy) of analytical grade 2,4,5,-T that contained less than 0.05 ppm 2^,7,8-tetrachlorodibenso-p-dioxin. Keplinger et el11 reported a decreased survival of pups in rat reproduction studies when fed 100 ppm of Aroclor 1242 end 1254, and poor hatehability of eggs from chickens fed 10 or 100 ppm of Aroclor 1242 or 100 ppm of Arochlor 1254. It has been said4" that a purified crystalline concentrate from toxic fat lad to the development of embryonic deformities in chickens. ^ Teratogen--is Comment Bsemtiy, Bfoneties Research Laboratory, In some instances, the same chemical ccmBath--da, Md (unpublished data), as died pounds are responsible for the occurrence of Arch Environ Health--Vol 35, Aug 1973 130 TOXICITY OF HYDROCARBONS--KIMBROUGH chlomcfto in people, liver dimiwe in Hcvernl contamination of tho technical chemicals species, x-dinrane in entile, chick edema, and with various highly toxic substances, woll teratologic or other effects on the fetun. Not coordinated epidemiological studios, and ad nil of the dineane entities have thus far been ditional experimental studies in animals are produced by all of the compounds (Table needed to clarify these problems. 1). Some of the compounds in question have Chloracne has been produced experiment been shown to bo contaminated with chlori ally in men by Shelley and Kligman (Arch nated dibenso-jMlioxins or chlorinated di- Derm 75:689, 1957). The authors cite addi bonsofurans (Table 2). The degree of con tional references on experimental dermal ex tamination seems to vary with different posure of animals and men to chlorinated compounds. Some companies manufacturing naphthalenes. these compounds have instituted clean-up procedures which remove the greatest port of the contaminants. Improved hygiene Rderenon among the workers and improved ventila tion of tho working ares have. In many instances, reduced the incidence of chlorecne. Whether all disease entities described 1. Herxbehner K: Ubtr Cfortikna. Munch Mtd Wtchr 48:278, ISPS. 2. Wauer H: OmiUidw Brkrankungen (torch gecMerte Xohkmnmnbii, Zbl Get* Hyg 6:100, ISIS. are caused by the chlorinated dibeneodfox(ns or the chlorinated dlbcnxofurons in not yet known. Some of theso chemicals aro highly toxic, ns illustrated by the fact that two applications of 10pg of 2,3,6,7,-tetrachlorodihorao-p-dtoxin applied to human skin** produced chtoracne-iike symptoms. Single oral donas of 2tytg to 50pg/kg/body weight resulted In fatal liver necrosis in rabbits."9 There is no readily available information on the metabolism of these compounds in animals and their breakdown in the environment.** It is probable that they are stable. Crosby at al* found that 2,3,7,8-tetrachlorodibcnzo-p-dtoxin and its hesnologuos decomposed rapidly in alcohol solu tion under artificial light and natural light However, photodecompoaition was negligi ble In aqueous suspensions and on wet or dry soil. It is unknown whether the disease entities discussed are the result of one or sev eral contaminants or the combined effect of 3. Tslsky L: Dla Peroahrankheit (Chlorakna). Klin Weehr 6:845-848; 007-001,1037. 4. Jcmea JW, Aldan HW: An nmoiform darmator- geato. Arch Derm ffyph .13:1022-1034, KRNV 5. Tetchy 1/ tJhw Neurero Forwrtwingemcthnrlen und Forarhungcn mif dam OaMat dor Gowarbokrankhaltan. KUn Weehr 27:249-267, 1040. 6. FIinn FB, Jarvik NE: Actions of cartain dtiorbiatad naphthalan** of tha lhrar. Proe 8oc Exp Biol Med 36:118-120,1996. 7. Drinker CK, Warren MF, Bennett GA: Tha problem of paaaibla ayatamhi effecte from eaHain chlorinated hydrocarbons. J Indaetr Hyg Toxic 19:282-311, 1987. S. Janes AT: The etiology of acne with special reference to acne of occupational origin. J Induatr Hyg Toxic 28:290-312, 1941. 9. Crcanburg L, Mayers MR, Roes Smith A: Tha ayetomic offset ramiting from nmm to certain chlorinetad hydrocarbon*. J Inauetr Hyg Toxic 21:29-38,1988 10. Gbttar LH: Pantachtorinaled naphthalanaa in industry. JAMA 125:273-274, 1944. 11. McLecMchto NGB, Roberta* D: Chlerinatad naphthalene polmilng, Brit Med J 1:691-692, 1942. 12. Oalliar B: Poisoning by chlorinated naphthatanas. Lmncei 244:72-74. 1943. 19. Van Oattingen WF: The Hahgenaled Hydrocarhont, Toxicity and Potential Danger, publication 414. Public Health Sandro, 1966. tho chemical compound and its contaminant Another unsolved problem is the observa tion that some of these compounds such as technical 2,4,5-T indues porphyria.** The chlorinated biphenyls also cause porphy ria.** Whether porphyria is the result Of the chemicals themselves or of the con taminants, or both, is not known. Crow41* suggests that the porphyria produced by technical 2,4,5-T may have been caused by contamination of the chemical with crude chtorobenxenM, which were used to produce the chlorophenols from which' the 2,4,5-T was made. Better awareness of the possible 14. Schwarts L, Itolipan L. 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