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Selected Case Studies of Suspected Dioxin Poisoning 165
and Allen (132) published a note on herbicides and spina bifida. They examined all the children referred to in the television program and found one case o f an open neural tube defect (spina bifida cystica) w hile the other children were normal in every respect. It w as possible that these apparently " norm al" children had spina bifida occulta, how ever, in none o f them had radiography been done and it was probable that the children had nothing more than sacral dimples.
As a final note in relation to this episode, the follow ing brief article appeared in the N ew Z ealand M edical Journal (9):
Publicity on certain chemicals as causation of malformations of the human fetus has been widespread. Some of the publicity has been sensation mongering and not all the remarks from the profession have been in keeping with a balanced assessment of scientific evidence. It is proper that there should be intelligent public awareness of the various environmental hazards that may come from the use of chemicals. . .in farm ing. . .however, those who would write of their experiences in medical journals must remember that disasters are the staple of the sensation mongers in the news media industry. Until recent publicity there had been no suggestion that 2 ,4 ,5-T, which has been used for over 20 years in New Zealand, was responsible for congenital malfunctions either in man or in farm animals. It is the duty of the physicians (and scientists) who have any concern for science to attempt to make valid observations that can be repeated. In the problem at issue, fetal malformations are natures common mistakes which we have no desire to perpetrate or to increase, although they are the inevitable price that is paid for our place on the evolutionary scale. There are extensive gaps in our knowledge but they will be filled only by patient work. Unresolved problems of fetotoxicity can only be solved by accurate recordkeeping at all stages of pregnancy.
The Missouri Horse Arena Episode
M any o f the episodes discussed in this chapter involved " suspected" TCDD poisoning; how ever, the M issouri H orse A rena Episode is one in which TCDD was confirm ed to be the causative agent. ' In 1972, T he M issouri Division o f Health and The Center for Disease Control, A tlanta, G eorgia (13) reported an investigation o f a horse arena in eastern M issouri w here 54 o f 57 horses exposed to the arena had died o f an illness characterized by skin lesions, severe weight loss, and heptotoxicity. Birds, dogs, cals, insects, and rodents w ere also found dead in and around the arena, and one 6-year-old girl exposed developed hem orrhagic cystitis (characterized by blood in the urine). A nalysis o f urine cultures for bacterial and viral pathogens were negative. Im m ediately prior to the onset o f illness, the arena had been sprayed with salvage oil for dust control.
The report (13) also noted that sim ilar horse illnesses and deaths occurred in two other horse arenas in the eastern M issouri area sprayed by the sam e salvage oil
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166 Tlie Chlorinated Dibenzo-p-Dioxins
com pany. T he three arenas had been sprayed within I month o f each other. K J Subsequent to investigation, soil from all three arenas was' excavated and dis
posed. No further problem s occurred since the excavations. A s with earlier episodes, the report soon received national attention. Unfortu
nately, som e new spapers m isquoted the report by im plying that the cause o f the incident w as a result of spraying'contam m ated2,4,5-T herbicide (12).
C arteret al. (44) and Kim brough et al. (122) have published detailed chemical, ep idem iological, and pathological data o f the. episode. T he investigations con cluded that a hexachlorophene factory in southwestern M issouri had accumulated distillate residues containing 306 to 356 ppm T C D D . It was these distillate residues that w ere subsequently disposed of via a salvage oil com pany and sprayed on the horse arenas. Furtherm ore, as Kimbrough et al. (122) noted, the investigation dem onstrated that the im proper disposal.of toxic chemical wastes may have serious consequences. Com panies responsible for the disposal of such wastes . should be aw are o f the toxicity o f these chemical waste products and should practice proper m ethods o f disposal.
C om m oner and Scott (46) have review ed the M issouri Horse Arena Episode in an attem pt to provide consultative data to the Italian G overnm ent in the wake o f the Seveso, Italy episode. T heir review focused on the hum an reactions (symptoms) to accidental TCD D exposure and the problem of soil degradation of TCDD. They also provided an excellent chronological account o f the episode.
T h e response o f the horses to T C D D in the above episode is o f special interest. In 197.0, P insent*and L ane (160) reported on a illness in four horses, and the subsequent death o f one, following the spraying o f a brushwood killer (2,4-D and 2,4;5-T ) to destroy nettles around the m argin of a pasture containing the horses. T h e horse .that died had rem ained on the pasture fo r 12 days. T h e postm ortem exam ination revealed extensive lesions in the esophagus and stom ach with de generative changes involving the liver and kidney. T he authors concluded that neither the clinical picture nor the postm ortem Findings supported a plant poisoning syndrom e, and thus it was not possible for the possibility o f poisoning by the herbicides. In view o f the findings by K im brough et al. (112), it would
pear that the horses may have been exposed to T C D D . Beale et al. (24) have recently reexamined the young girl who had developed hem orrhagic cystitis follow ing repeated exposure to TCD D in one o f the horse arenas sprayed w ith waste oils (see Ref. 13). In the 5-year interval since exposure, the patient had grown norm ally, and both her height and weight were above the 75th percentiles. Detaijed physical, -chemical, and neurological examinations w ere also conducted and found to be norm al. The sam e studies were done on the p atien t's - s is te r and m other, exposed sim ultaneously, but less extensively to dioxin, and the results w ere also norm al. Beale et al. (24) concluded: " Our experience dem onstrates that people exposed to dioxin can recover com pletely w ith no apparent sequela from the toxin. It remains to be determined whether the
Selected Case Studies of Suspected Dioxin Poisoning 167
ex posure to dioxin in these children will result in abnorm al pregnancies or affect their offspring."
T h e Seveso, Italy Episode
P erhaps th e m ost publicized chem ical accident in m odem tim es is the TCD D episode in Seveso, Italy. This episode has attracted worldwide interest and concern. H undreds o f scientists, physicians, and veterinarians have participated in either on-site inspections, conferences, or consultations into the various facets o f this episode. In addition, the episode has now acquired such political significance that its outcom e could change the political structure of a nation.
A lthough the Seveso, Italy episode did not involve 2,4,5-T or other phenoxy herbicides, it did, how ever, involve the potential raw material required for their synthesis, that is, trichlorophenol. Thus, in relation to the phenoxy herbicides (and hexachlorophene), this episode represents to m any people an inherent danger associated with its industrial production. Hence, the question: can we do without trichlorophenol products and thus insure our safety from another such industrial accident?
A volum inous am ount o f literature has been written on this episode, although it has been only 2 years since it occurred. Much of this material has been either laym an oriented, factually confused, politically pointed, or lim ited primarily to hum anistic interest. Thus, we have seen in newspapers and magazines, articles titled " A .D e a d ly S a g a ," " The G raveyard on M ilan's D oorstep," "T o x ic Cloud over S ev eso ," and "T h e Poison That Fell From The S k y ." However, the human dram a o f this industrial accident cannot, and must not, be minimized.
Parks andSuIIam (158) have assem bled, translated, and reviewed an impressive collectio n o f selected articles from the Italian press for the period 10 July to Septem ber 1976. In-the introduction to this collection o f articles, Parks and Sullam stated:
The social, economic, moral, medical and administrative problems which fell on Italy out of that poisonous cloud are of vast extent and complexity. They cast a very long shadow on the future, involving the rebuilding of shattered lives, the care of burned and disfigured children, health care and the monitoring of health for thousands of people for many years to come, and the shaping of policy decisions regarding industrial regulations and the operations of. multinational enterprises to which this incident forces the attention of the Italian Government.
D ata on levels o f TCD D found, the m agnitude o f the contamination, or the extent o f hum an or animal illnesses or injuries, are still sketchy. Nevertheless, the follow ing inform ation on the episode is available from published documents.
T h e e p iso d e o f T C D D poisoning occurred on 10 July 1976 in Seveso, Italy, a sm all tow n 40 km north o f M ilan (95,174). The source o f the TCDD was a
192 The Chlorinated Dibenzo-p-Dioxins
T C D D is the dioxin o f m ost concern. It occurs prim arily in pesticide m ade from trichlorophenol, for exam ple, 2,4 ,5 -T and silv ex herbicides. Q uantitatively it is a very potent teratogen; how ever, qualitatively the nature of the teratogenic effect of T C D D is far less than m any other com pounds, such as thaiidam ide or V itam in A. T he one teratogenic response most com m only associated w ith .TCDD is cleft palate. TCDD tends to cause death o f the em bryo or fetus rather than a w ide range o f abnorm alities. Present data suggest that in m am m als. T C D D may be carcino genic. TCD D tends to accum ulate in the liver o f rodents, but in nonhuman prim ates it is associated w ith tissues having a high lip id content, particularly the skin, m uscle, and fat. In m an, exposure to T C D D is characterized b y 'th e appearance of chloracne and its absence m akes it unlikely that system ic disorders present are related to TCD D . Asthenic and vegetative sym ptom s are often present in overexposure, but are difficult to interpret. They w ould norm ally bdexpdctedlfo ? clear with tim e. There is no conclusive evidence a t this tim e that T C D D is m utagenic, teratogenic, or carcinogenic in m an.
M ost TCD D that is applied to the environm ent during pesticide applications, pro b ab ly photodegrades w ithin the first 24 h r. Ir is p ro b ab ly n o t translocated in plants with the soil then serving as the residual reservoir. T he half-life in soil varies from 200-340 days, depending upon soil type and clim ate. M icrobial degradation is probably responsible for the soil disappearance o f T C D D . A nim als that com e in contact w ith contam inated soil o r vegetation, will bioconcentrate TCDD in their liver; however, at present, there are no field data available that indicate that the levels o f TCD D found in these anim als have a biological effect.
W ith the current production technology, phenoxy herbicides may be produced containing less than 0.1 ppm TCD D , W hen these herbicides are properly applied to the environm ent, TCDD residues are nondetectable. W hether significant bioac cum ulation occurs in livestock feeding on herbicide-treated rangeland at sufficient levels to be present in m eat consum ed by m an rem ains to be determ ined. O n this determ ination will depend the future use o f trichlorophenol-based herbicides.
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201. Van Miller, J. P ., R. J. Marlar, and J. R. Allen. 1976. Tissues distribution and excretion of tridated tetrachlorodibenzo-p-dioxin in nonhuman primates and rats. Food Cosmet. Toxicol. 14(I):31-34.
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204. Vinopal, J. H ., I. Yamamoto, and J. E. Casida. 1971. Preparation of tritium-labeled 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and structure activity investigations of TCDD and other related dibenzo-p-dioxins. Am. Chem. Soc., Abstr. Pap., 162nd Nat. M eet., Pestic. Chem. Sec., Abstr. No. 79.
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206. Vos, J. G ., J. A. Moore, and J. G. Zintcl. 1974. Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in C57B1/6 mice. Toxicol. Appl. Pharmacol. 29(1):229241.
207. Waldbott, G. L. 1973. Mutagenic pollutants. In Health Effects o f Environmental Pollutants. C. V. Mosby Co.: St. Louis, pp. 207-216.
208. Walsh, J. 1977. Seveso: The questions persist where dioxin created a wasteland. Science 197(4308): 1064-1067.
209. Whiteside, T. 1977. A reporter at large: The pendulum and the toxic cloud. The New Yorker, 25 July 1977. p. 30-55.
210.- Williams, D. T ., H. M. Cunningham, and B. J. Blanchfield. 1972. Distribution and
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I
Ii i
excretion studies of ociachlorotl Toxicol. 7(l):57-62.
211. Woolson, E. A ., R. F. Thoma? dibenzo-p^dioxin contentin selei
212. Woolson, E. A. and P. D. J. Er. eagle samples. Adv. Chem. Ser.
213. Worden, A. N. 1973.Toxicolog
214. Wootton, J. C ., N. R. Altman hydropericardium-producing fa-, 45(3):739-746.
215. Yaitzoff, A ., D, Firestone, D. 1961. Studies o f the chick edem Chem. Soc. 38:60-62.
216. Young, A. L .T 974. Ecologies. C-52A),-Eglin AFB Reservati Environics and Flame MunitionAir Force Armament Laborator
217. Young, A. L ., J. A. Calcagn toxicology, environmental fate, dioxin. Technical Report OEHI Health Laboratory, Aerospace'
218. Young, A. L., C. E. Thalken,' consequences o f massive quant five-year field study. Paper p February 14, 1974; Las Vegas.
219. Young, A. L., C. E. Thalken, a o f repetitive aerial application Egltn AFB, Florida. TechnicaFactors Office, Air Force Ar* Department o f Chemistry anti 80840. 127 p.
220. Young, A. L ., P. J. Lehn, and aquatic ecosystem. Weed Sci. .
221. Young, A. L ., C. E. Thalken: 1976. Fate of 2,3,7,8-tetraci. Summary and decontamination Chemistry and Biological Sciet
222. Zitko, V. 1972. Absence of .aquatic animals. Bull. Environ.
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211. Woolson, E. A ., R. F. Thomas, and P. D. i. Ensor. 1972. Survey of polychlorodibenzo-p-dioxin content in selected pesticides. J. Agric. FoodChem. 20(2):351-354.
212. Woolson, E. A. and P. D. J. Ensor. 1973. Dioxin residues in lakeland sand and bald eagle samples. Adv. Chem. Ser. 120:112-118.
213. Worden, A. N. 1973. Toxicology and the environment. Toxicology l(l):3-27.
214. Wootton, J. C., N. R. Artman, and J. Craig Alexander. 1962. Isolation of three hydropericardium-producing factors from a toxic fat. J. Assoc. Off. Anal. Chem. 45{3):739-746.
215. Yartzoff, A ., D. Firestone, D. Banes, W. Horwitz, L. Friedman, and S. Nesheim. 1961. Studies of the chick edema factor. II. Isolation of a toxic substance. / . Am. Oil. Chem. Soc. 38:60-62.
216. Young, A. L. 1974! Ecological Studies on a Herbicide-Equipment Test Area (TA C-52A), Eglin AFB Reservation, Florida. Technical Report AFATL-TR-74-12. Environics and Flame Munitions Branch; Flame, Incendiary and Explosives Division, Air Force Armament Laboratory, Eglin Air Force Base, FL. 32540. 141 p.
217. Young, A. L., J. A. Calcagni, C. E* Thalken, and.J. W. Tremblay. 1978. The toxicology, environmental fate, and human risk of Herbicide Orange and its associated dioxin. Technical Report OEHL-TR-78-92. USAF Occupational and Environmental Health Laboratory, Aerospace Medical Division, Brooks Air Force Base, TX. 247 p.
218. Young, A, L ., C. E.Thalken, W. E. Ward, and W. J. Caimey. 1974, The ecological consequences of massive quantities of 2,4-D and 2,4,5-T herbicides. Summary of a five-year field study. Paper presented to the Weed Science Society of America; February 14,1974; Las-Vegas, NV. 6 p.
219. Young, A. L., C. E. Thalken, andW. E. Ward. 1975. Studies of the ecological impact o f repetitive aerial applications of herbicides on the ecosystem of test area C-52A, Eglin AFB, Florida. Technical Report AFATL-TR-75-142. Environics and Human Factors Office, Air Force Armament Laboratory, Eglin Air Force Base, FL and Department of Chemistry and Biological Sciences. U.S. Air Force Academy, CO 80840. 127 p.
220. Young, A. L., P. J. Lehn, and M. F. Mettee. 1976. Absence of TCDD toxicity in an aquatic ecosystem. Weed Sci. Soc. Am., Abstr. No. 107. p 46.
221. Young, A. L ., C. E. Thalken, E. L. Arnold, J. M. Cupello, and L. G. Cockerham. 1976. Fate o f 2,3,7,8-tetrachIorodibenzo-p-dioxin (TCDDJ in the environment: Summary and decontamination recommendations. USAFA-TR-76-18. Departmentof Chemistry and Biological Sciences, USAF Academy, CO 80840. 41 p.
222. Zitko, V. 1972. Absence of chlorinated dibenzodioxins and dibenzofurans from aquatic animals. Bull. Environ. Contam. Toxicol 7(2/3): 105-110.
223. Zitko, V ., O. Hutzinger, and P. M. K. Choi. 1972. Contamination of the Bay of Fundy-Gulf of Maine area with polychlorinated biphenyls, polychlorinated
~ terphenyls, chlorinated dibenzodioxins, and dibenzofurans. Environ. Health Perspect. 1:47-50.
204 The Chlorinated Dibenzo-p-Dioxins
dibenzo-p-dioxin. Infect. Immun. 12(6): 1319-1324.
196. Tomica, M ., S. Ueda, and M. Narisada. 1959. Studies on the dibenzo-p-dioxin derivatives. XXV11. Synthesis of polyhalodibenzo-p-dioxins. Yakugaku Zasshi 79:186-192.
197. Ton That, T ., A. Tran Thi, T. Nguyen Dang, P. Pham Hoang, B. Nguyen Nhu, B. Ton That, S. Hoang Van, and S. Do Kim. 1973. Le cancer primaire du foie au Vietnam. Chirurgie 99:427-436.
198.. Tschirley, F. H., Binns, W ., C. Cueto, B. C. Eliason; H- E. Heggestad, G. H. Hepting, P. F. Sand, and R,. F. Stephens. 1970. Investigations of spray project near Globe, Arizona. Investigation conducted February 1970. Mim., U .S. Dep. Agric., Office of Science and Education. 29 p.
199. Tung, T. T ., T . K. Anh, B. Q. Tuyen, D. X. Tra, andN . X. Huyen. 1971, Clinical effects of massive and continuous utilization of defoliants on civilians, preliminary . survey. Vietnamese Studies 29:53-81.
200. Van Miller, J. P., J. J. Lalich, and J. R. Alien. 1977. Increased incidence of neoplasms in rats exposed to low levels of 2,3,7,8-tetrachIorodibenzo-p-dioxm. Chemosphere 9:537-544.
201. Van Miller, J. P .( R. I. Marlar, and J. R. Allen. 1976. Tissues distribution and excretion of tritiated tetrachlorodibenzo-p-dioxm in nonhuman primates and rats. FoodCosmet. Toxicol. 14(I):31-34.
202. Villanueva, E. C., V. W. Burse, and R. W. Jennings. 1973. Chlorodibenzo-p-dioxin contamination of two commercially available pentachlorophenols. J. Agric. Food Chem. 21(4):739-740.
203. Villanueva, E. C .; R. W. Jennings, V. W. Burse, and R. D. Kimbrough. 1974. Evidence of chlorodibenzo-p-dioxin and chlorodibenzofuran in hexachlorobenzene. J. Agric. Food Chem. 22(5):916-917.
204. Vinopal, J. H ., I. Yamamoto, and J. E. Casida. 1971. Preparation of tridum-labeled 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and structure activity investigations of TCDD and other related dibenzo-p-dioxins. Am. Chem. Soc., Abstr. Pap., 162nd Nat. Meet., Pestic. Chem. Sec., Abstr. No. 79.
205. Vinopal, J. H. and J. E. Casida. 1973. Metabolic stability of 2 ,3 ,7 ,8-tetrachlorodibenzo-p-dioxin in mammalian liver microsomal systems and in living mice. Arch. Environ. Contam. Toxicol. 1(2): 122-133.
206. Vos, J. G., J. A. Moore, and J. G. Zinkl. 1974. Toxicity of 2,3,7,8-tetrachIorodibenzo-p-dioxin (TCDD) in C57B1/6 mice. Toxicol. Appl. Pharmacol. 29(I ):229241.
207. Waldbott, G. L. 1973. Mutagenic pollutants. In Health Effects o f Environmental Pollutants. C. V. Mosby Co.: St. Louis, pp. 207-216.
208. Walsh, J. 1977. Seveso: The questions persist where dioxin created a wasteland. Science 197(4308): 1064-1067.
209. Whiteside, T. 1977. A reporter at large: The pendulum and the toxic cloud. The New Yorker, 25 July 1977. p. 30-55.
210. Williams, D. T ., H. M. Cunningham, and B. J. Blanchfield. 1972. Distribution and
Vla!V ifs '.it
i .1
1 *i
excretion studies of octachlc Toxicol. :7( 1):57-62.
211. Woolson, E. A ., R. F. Tho dibenzo-p-dioxin content in s
212. Woolson, E; A. and P. D. J. eagle samples. Adv. Chem:i.
213. Worden, A. N. 1973. Toxic;
214. Wootton, J. C ., N. R. Are hydropericard ium-producing 45(3):739-746.
215. Yartzoff, A ., D. Firestone, 1961. Studies of the chicked Chem. Soc. 38:60-62.
216. Young, A. L. 1974. Ecolot C-52A), Eglin AFB Reser Environics and Flame Munit Air Force Armament Labors
217. Young, A. L ., J. A. Calc; toxicology, environmental fa dioxin. Technical Report OI Health Laboratory, Aerospa*
218. Young, A. L ., C. E. Thalke: consequences of massive qu five-year field study. Pape February 14, 1974; Las Veg
219. Young, A. L., C. E.Thalker of repetitive aerial applicati Eglin A FB, Florida. Techni Factors Office, Air Force . Department of Chemistry a 80840. 127 p.
220. Young, A. L ., P. J. Lehn, au aquatic ecosystem. Weed Sc
221. Young, A. L ., C. E. Thalke 1976. Fate of 2,3,7,8-tetr; Summary and decontaminati Chemistry and Biological Sc
222. Zitko, V. 1972. Absence < aquatic animals. Bull. Em in
223. Zitko, V ., O. Hutzinger, ai Fundy-Gulf of Maine ar terphenyls, chlorinated di Perspect. 1:47-50.
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excretion studies of octachlorodibenzo-p-dioxin in the rat. Bull. Environ. Contam. Toxicol. 7(l)i57-62.
2U . Woolson, E. A., R. F. Thomas, and P. D. J. Ensor. 1972. Survey of polychlorodibenzo-p-dioxin content in selected pesticides. J. Agric. FoodChem. 20(2):351-354.
212. Woolson, E, A. and P. D. J. Ensor. 1973. Dioxin residues in lakeland sand and bald eagle samples. Adv. Chem. Ser. 120:112-118.
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213. Worden, A. N. 1973. Toxicology and the environment. Toxicology l(l):3-27. 214. Woolton, J. C., N. R. Artman, and J. Craig Alexander. 1962. Isolation of three
hydropericardium-producing factors from a toxic fat. J. Assoc. Off. Anal. Chem.
45(3):739-746.
1 , 215. Yartzoff, A ., D. Firestone, D. Banes, W. Horwitz, L. Friedman, and S. Nesheim.
M 1961.,Studies of the chick edema factor. 11- Isolation of a toxic substance. J. Am. Oil.
Chem. Soc. 38:60-62.
216. Young, A. L. 1974. Ecological Studies on a Herbicide-EquipmenfTest Area (TA
C-52A), Eglin AFB Reservation, Florida. Technical Report AFATL-TR-74-12.
$k , Environics and Flame Munitions Branch; Flame, Incendiary and Explosives Division, Air Force Armament Laboratoiy, Eglin Air Force Base, FL. 32540. 141 p.
m 217. Young, A. L ., J. A. Calcagni, C. E. Thalken, and J. W. Tremblay, 1978. The
. toxicology, environmental fate, and human risk of Herbicide Orange and its associated
P
dioxin. Technical Report OEHL-TR-78-92. USAF Occupational and Environmental Health Laboratory, Aerospace Medical Division, Brooks Air Force Base, TX. 247 p.
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218. Young, A. L,, C. E. Thalken, W. E. Ward, and W. J. Caimey. 1974. The ecological consequences of massive*quantides of 2,4-D and 2,4,5-T herbicides. Summary of a
five-year field study. Paper presented to the Weed Science Society of America;
February 14, 1974; Las Vegas, NV. 6 p.
219. Young, A. L .,C . E. Thalken, and W. E. Ward. 1975. Studies of the ecological impact
of repetitive aerial applications of herbicides on the ecosystem of test area C-52A, ici Eglin AFB, Florida. Technical Report AFATL-TR-75-142. Environics and Human
Factors Office, Air Force Armament Laboratory, Eglin Air Force Base, FL and
Department of Chemistry and Biological Sciences. U.S. Air Force Academy, CO "i? 80840. 127 p.
f;*/>.
220. Young, A. L., P. J. Lehn, and M. F. Mettee. 1976. Absence ofTCDD toxicity in an aquatic ecosystem. Weed Sci. Soc. Am., Abstr. No. 107. p 46.
' ' i 221. Young, A. L., C. E. Thalken, E. L. Arnold, J. M. Cupello, and L. G. Cockerham. 1976. Fate of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the environment; Summary and decontamination recommendations. USAFA-TR-76-18. Department of Chemistry and Biological Sciences, USAF Academy, CO 80840. 41 p.
222. Zitko, V. 1972. Absence of chlorinated dibenzodioxins and dibenzofurans from aquatic animals. Bull. Environ. Contam. Toxicol. 7(2/3): 105-110.
223. Zitko, V., O. Hutzinger, and P. M. K. Choi. 1972. Contamination of the Bay of Fundy-Gulf of Maine area with polychlorinated biphenyls, polychlorinated terphenyls, chlorinated dibenzodioxins, and dibenzofurans. Environ. Health Perspect. 1:47-50.
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