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SCIENTIFIC AMERICAN 783613 SCIENTIFIC Established 1845 A M f l f l T C A N FebrUary 1986 Volume 254 Number 2 Dioxin Concern that this material is harmful to health or the environment m ay be misplaced. Although it is toxic to certain animals, evidence is lacking that it has any serious long-term effect on human beings by Fred H. Tschirley Dioxin. The word evokes a variety \ of reactions; Much of the pub lic worries that the compound will cause poisoning even at minimal exposure. Toxicologists, knowing the seven toxic effects of dioxin in experi mental animals but being uncertain about comparable serious effects on people, call for more research. Regula tors, who must make decisions based on this conflicting evidence, a n left wondering what to do. As one who has spent many years studying thedioxin issue, I hope in this article to provide a useful r'Tspective for making judg ments about the potential hazard of the material. Dioxin is actually a name for a fami ly of chemical compounds. The name refers to their basic structure: two oxy gen atoms joining a pair of benzene rings. Substitution of chlorine atoms for hydrogen atoms on the rings pro duces a chlorinated dioxin, of which there are many. The chlorinated di oxin of interest here is 2J,7,8-tetrachlorodibenzo-p-dioxin, usually ab breviated to TCDD. It is a by-product of the manufacture of trichlorophenol, which serves in the manufacture of two herbicides (the best-known being 2,4,5-trichlorophenol, or 2,4,5-T, one of the ingredients'of Agent Orange) and the antibacterial agent hexachlorophene. TCDD is also produced in a variety of combustion processes. The legacy of Agent Orange, Times Beach, Seveso, several industrial acci dents and other instances of human exposure to significant amounts of TCDD is widespread concern about adverse health effects resulting from minimal exposure to the material. Yet none of the many studies directed at this question have demonstrated that TCDD causes severe chronic human effects. Moreover, not one human death has been attributed to TCDD, even though exposure has been high in a number of cases. The issue points up the broader problem of the difficulty faced by regulators who must make judgments on the basis of incomplete scientific knowledge on the one hand and public fear on the other. TCDD was first recognized in 1957 as a contaminant of 2,4,5-T, when 31 workers involved in the manufacture of the herbicide in West Germany de veloped the dermatologic affliction now called chloracne. It is a skin erup tion resembling acne and takes its name from, the fact that it is caused by exposure to various chlorinated organ ic chemicals. General awareness that TCDD is a potential hazard to health and the environment arose in 1970, when a House subcommittee held a hearing on "Effects of 2,4,5-T on Man and the Environment." The hearing dealt among other things with a study by the Bionetics Research Institute showing that 2,4,5-T caused birth defects in animals. Testimony suggested that the teratogenic component of 2,4,5-T may have been TCDD. In the sample of 2,4,5-T tested by Bionetics the di oxin occurred as a contaminant at an extremely high concentration: 27 8 parts per million. Since then there has been a steady accumulation of information about the sources of TCDD, its environ mental face and its toxic effects. One well-defined source is the formation of TCDD during the manufacture of 2,4,5-T. The amount of TCDD formed increases as the temperature of the re action and the pH (degree of alkalini ty) increase. In 1977 investigators in the Neth erlands reported that polychlorinat ed dibenzo-p-dioxins (PCDD's) were present in the fly ash from a munici pal incinerator. Typically such an in cinerator burns; among other things, organic wastes containing chlorine. Similar reports soon came from Switz erland, Canada and Japan. It was be lieved the compounds resulted from the condensation of chlorophenols. Later quantitative data demonstrated from a wide variety of combustion sources the presence of TCDD's that could not be explained on the basis of preexisting polychlorinated phenols. These findings led R. R. Bumb of the Dow Chemical Company and 12 of his co-workers to put forward in 1980 the hypothesis that PCDD's can result from trace chemical reactions in fire. The hypothesis has been challenged because the reactions have not been defined. Nevertheless, PCDD*s have now been found in the effluent and ash of so many combustion processes that there is no longer serious argument about their formation during combus tion, even though the precise nature of the process remains obscure. Moreover, TCDD has been specifi cally identified in soil and dust from numerous places, in soot from the chimneys of wood furnaces, as resi dues in river fishes (some from riv ers whose watersheds do not have in dustrial operations known to form 29 783614 f O R A T A TKT'nrc \ +,AOATA T kT n rn PLASTIC TARPAULINS cover much of tbs opa a rts of th Dtatowd Alkali Co. plant io Newark N J , because the Uad may be contaminated by a chlorinated dloxiai2J , 7,S>tctiachlorodttcQZispi dlorin, OKsally abbreviated as TCDD. From 1943 through 1948 the company m aeafactond chemicals a t the ptaat. Including the berW* d d a 2^ 5>T. TCDD it a by-prodaet of the manufacture of 2,4,5-T. Federal aad state officiate had the tarpaulin pot down as a precao don became TCDD is toxic, to a somber of animals to ted (a ex> periam ta. The material has not been shown to have severe chrouic effects on beings. It does produce some.sbovMcrm effects. 30 [. TCDD) as residues in the eggs of her ring gulls and recently in adipose tissue from more than 100 people in Canada, the U.S. and Vietnam. It appears that TCDD is a ubiquitous chemical, par ticularly in industrialized nations. One might then ask why it was not detected sooner. For one thing, no one looked for it seriously before the 1970's. At the time it would not have been found anyway, except in unusual circumstances, because analytic chem ists were only able to detect concentra tions of a few parts per million. Since then the detecting equipment has im proved at least a miltionfold, so that concentrations of a few parts per tril b lion are now detected routinely. In ad dition dilution and the destruction of TCDD by light may reduce concentra tions to undetectable levels. As analyt ic technology improves, one can ex pect that TCDD will be found in many more sites than are currently known. I a a* roalc fecfe In places where TCDD is protected from light it is an extremely per sistent material. In the early 1970's it was thought the half-life of TCDD (the time required for half of a given amount to be degraded) was about a year; later studies in the U.S.- suggest ed the half-life might be as long as three years. Recent reports from Italy raise the possibility that the half-life of TCDD in soil might be 10 years or even more. Although precise data are meager, TCDD is known to be strongly held by most soils. The strength of the binding is inferred from the fact that known concentrations of TCDD applied .to soil have remained near the surface. Even in the sandy soil examined in Florida the concentration- of TCDD in the upper 13 centimeters was as high as 1,300 nanograma per kilogram 10 to 12 years after application. In the most heavily contaminated zones near Scveso TCDD has been found at a depth of 136 centimeters. Moreover, the concentrations well be low the surface were slightly but sig nificantly higher in 1977 than they were in 1976, soon after the accident took place; The presence of soil fis sures does not adequately explain this unexpected vertical distribution. The processes that degrade TCDD in soil are poorly known. Microorgan isms .do degrade the substance, but at a low rate. S. D. Aust of Michigan State University found a wood-decay ing fungus (the white mold Phanerochactt chryosporium) that breaks down TCDD without observable mortality of the organism. The rate of degrada tion is low, but it 'is conceivable that contaminated sites could be inoculated CHEMICAL STRUCTURE of a dioxin and of TCDD b depicted. The dibeoxo-p-dloxia molecule (a) consbti of two benzene rings joined by two oxygen atoms (light color). From oae chlorine atom to right atoms cam satatttnte for hydrogen atoms (gray) attached to car bons (block) at the numbered poaittoas to form any of the 75 chlorinated dioxins. The chlo rinated dioxin kaown as TCOD (i) b shown with its four chlorine atoms (dark color). with the mold to speed up the degrada tion process. Sunlight degrades TCDD rapidly by splitting off the chlorine atoms. The reaction requires a hydrogen donor, which is usually available in water or in the wax on leaves. Experiments by Donald G. Crosby of the University of California at Davis showed that 40 percent of the TCDD layered on a glass plate remained after six hours in sunlight; the amount was from 23 per cent to negligible when the material was applied as drops on leaves of the rubber plant, but on a loam soil the figure was 83 percent. TCDD is a highly toxic chemical in experimental animals. The first ani mal-toxicity test performed is usually a determination of the LDufi the dose that kills half of a test population. Be tween 1973 and 1978 the LDu> of TCDD was determined for eight spe cies. The guinea pig was by far the most sensitive species tested: its LDso far an oral dose was .6 microgram per kilogram of body weight. The hamster was the least sensitive animal tested*, its oral-dose LDM was about 1,900 times as high as the guinea pig's. Its intraperitoneal level, 3,000 micrograms per kilogram, was about 3,000 times as high as the oral dose for the guinea pig. The reasons for the extreme range of acute (short-term) toxicity may re late to the relative speed of clearance from the body. In the hamster half of a dose is removed within 13 days, com pared* with 30 days for the other spe cies tested. Even though the hamster is much less sensitive than the guinea pig, an intraperitoneal LDso of only.3,000 micrograms per kilogram signifies an extremely toxic material: the toxicity is comparable to that of the insecti cide parathion. Many essentially acute symptoms have been observed in human beings. They include chloracne, digestive dis orders, effects on some essential en zyme systems, aches and pains of mus cles and joints, effects on the nervous system and psychiatric effects. These symptoms have been transitory except for a few severe cases of chloracne. Additional tests have measured the chronic, or long-term, effects of 31 783616 TCDD in rodents, rabbits and nonhu- man primates. Chloracne, the most sensitive indicator of human exposure to TCDD, has also appeared in rab bits, nonhuman primates and hairless mice. The skin and body can become dry and scaly. A few species lose hair. Some nonhuman primates lose finger nails and toenails without apparent ev idence of pain. TCDD also causes reproductive ef fects in experimental animals. Cleft palate and abnormalities of the kidney were caused in the offspring of ex posed mice at dosage levels of from one nanogram to three nanograms per kilogram of body weight per day. Sim ilar doses in rats caused the death of fetuses. In monkeys a dose of 1.7 nano- grams per kilogram per day for two years caused abortions in four out of seven pregnancies. TCDD is a proved carcinogen in rats and mice. Although the test results i vary somewhat, there is fairly good i1 agreement among tests by different in vestigators. The liver is the primary 1I target in both rats and mice, although 1 the brain, the respiratory system and the thyroid gland have also been in volved in a few studies. It is important to recognize that an oncogenic re III sponse was reported only after the ani mal had ingested high doses of TCDD over a long period of tune. Rats showed no oncogenic response ac dos age levels of from one nanogram to 1.4 nanograms per kilogram per day; mice showed none at dosage levels ranging from one nanogram to 30 nanograms. Moreover, a study by R. J. Kociba of Dow Chemical and his co-workers showed that rats tolerated a daily dose 1` t of one nanogram per kilogram per day for two years without showing toxico logic effects. v S I E N IN FORMATION oi TCDD darfag-th m b t t n r i o t 2^4-Mcblofopbcuol (TCF) aro tbow s. (TCP b a u d 'to taska tba boM ddea 1A 4-T and SQvex aad tka aatibectcrial ag ia t kaxaddocopkcs&) la tka precr o od maJdof TCP a molcula ot eklorobcaxaaa b hydrolyzed (i) la tha p ro caci of eauadc soda to fona 3A5*trichloropheaata Tara molacala od tba pianata (J) coatMaa to fona TCDD ( They loaa atoase a i aodiam (Atte) aad chiodai. Tha hlfher tka teta petaturo and tka alkaatty aro, tha (reat ar la tha am oaat a i TCDD that ia forroed. Wbca tba a sista n troperoturo b abova 180 dap a C drita, a kaat-formiaf n actlo a ocea n i tt haa baca tba cauca a i industriai accidenta. 32 N evertheless, the findings from the tests on animals intensified con cern about the effects of TCDD on people. On several occasions people have been exposed to "high" levels of TCDD. In this context "high" ts a rela tive term because with one exception-- a group of prisoners who volunteered for tests with TCDD--the amount of the material to which a person was ex posed is not accurately known. The criterion I employ here to distinguish high from low exposure is whether or not the exposure results in chloracne. The case of the prisoners is im portant because known amounts of TCDD were applied to their skin. In the first experiment 60 volunteers were treated with concentrations ranging from 200 to 8,000 nanograms (from three to 114 nanograms per kilogram for a 70-kilogram person), and the ' ^ JLV U U U lonhu: ijion piiaure n rabairless ecome e hair, finger:ntev- ive efCleft cidney if exfrom is per . Slmith of nano* r two >ut of nrats suits good at innary ough and n inrtant reani:DD Rats dos) 1.4 nice ging ims. a of <ers lose day ico- the onon pie of da red of ex ile ish or :e. nof In re ag m m he S^-* dose was repeated two weeks later. The dosages chosen were (hose that SPECIES ROUTE LDm (mtaoqntitv per WlogrxmJ had caused chloracne when they were GUINEA PIG (MALE) ORAL .8 applied to the ears of rabbits. None of the volunteers developed chloracne. and no other symptoms were ob served. The second experiment in volved 10 volunteer prisoners who GUINEA PIG (FEMALE) RABBIT (MALE.FEMALE) RABBIT (MALE,FEMALE) RABBIT (MAUE.FEMALE) ORAL ORAL DERMAL in traperito n eal 2.1 115 275 252-500 were treated with 107.000 nanograms MONKEY(FEMALE) ORAL <70 of TCDD per kilogram. Eight of them developed chloracne, but no other symptoms were noted. From these experiments one can RAT (MALE) RAT (FEMALE) MOUSE (MALE) ORAL ORAL ORAL 22 45-500 <150 conclude only that TCDO does cause MOUSE (MALE) INTRAPERITONEAL 120 * chloracne in humans when the dose is DOG (MALE) ORAL 30-300 sufficiently high but that people are less sensitive than rabbits. The tests did not identify a threshold for the development of chloracne in human OOG (FEMALE) FROG HAMSTER (MALE,FEMALE) ORAL ORAL ORAL >100 1,000 1,157 . beings--a piece of information that HAMSTER (MALE,FEMALE) INTRAPERITONEAL 3,000 would be of great value. The number of people who have ACUTE TOXICITY of TCDO In experimental animah is ascertained on tbe bash of the been exposed to high levels of TCDD LDsa*the dost (la mlcroimma per kilogram of body weight) that kills half of a test group. cannot be determined accurately, but it must be in the thousands. Alistair Hay of the University of Leeds has es acne (184 cases, 164 of them children tute of Occupational Safety and Health timated that in the chemical industry under the age of 15), headaches and reported that two of the seven people alone about 2,000 workers have had digestive upsets, but no long-term ef had in fact died of cancers other than high exposure. Low levels of exposure fects such as birth defects and chromo soft-tissue sarcoma. Moreover, the ex have undoubtedly been experienced somal damage have been identified. It posure of three others to TCDD could by people who handle the herbicides is too early to tell whether the inci not be documented. Such findings fall 2,4,5-T and Silvex, in which TCDD dence of cancer is abnormal. far short of being hard evidence for the was a contaminant; by Vietnam veter An accident in a Monsanto plant in proposition that TCDD causes soft- ans exposed to Agent Orange (SO per Nitro, W.Va., in 1949 exposed more tissue sarcoma. cent of which was 2,4,5-T); by resi than 200 workers to TCDD. Of 122 Other studies also fail to support dents of Tunes Beach, Mo., where who developed chloracne, 121 were Hardell's hypothesis. In the state of waste oil .that contained TCDD was monitored for the next 30 years. The Washington no consistent pattern of spread on the ground in several places; total number of deaths in that group death due to soft-tissue sarcoma was by chemical-industry workers making did not differ significantly from that found among occupations in which the products that include the material, expected in the population at large, workers would have been exposed to and by many thousands of people who and there were no excess deaths due TCDD. A study in Finland found no have eaten food (notably fish) contain to cancer or diseases of the circulato cases of the disease among 1,900 peo ing trace amounts of TCDD or have ry system. Similar findings have been ple who applied herbicides, nor was been exposed to fallout from combus made after other industrial accidents, their death rate from any natural cause tion processes that form TCDD. The except for two in which an excess of different from that of the total male total number of individuals with such deaths from cancer was found in small population in Finland. The U.S. Air low exposures probably runs well into 'groups of the people exposed. Force, in its Ranch Hand study of the millions. A particular type of cancer (soft-tis about 1,200 military personnel who sue sarcoma, a generic term for more sprayed Agent Orange in Vietnam, The possibility of chronic effects than 100 different types of rare cancer) found no cases of soft-tissue sarco from exposure to TCDD causes has become a focus of concern because ma. Finally, examinations by the Vet far greater public concern than that of of a survey of Swedish forestry work erans Administration of 85,000 self- acute effects. An aspect of this prob ers by Lennart Hardell of the Uni selected veterans showed fewer cases lem about which little is known is the versity of Umea. He concluded that of these cancers than the national av effect of protracted exposure to low their exposure to 2,4,5-T (and thus to erage would suggest levels of the material, as might occur TCDD) had caused six times the nor Reproductive effects are also a sub in an occupational setting or from inci mal incidence of soft-tissue sarcoma. ject of concern because of the animal dental exposures to, for example, the This study led to an investigation findings. The most celebrated case al- fallout of combustion effluents or to of chemical-plant workers in the U.S. leging'such effects in humans is com fish that contain low levels of TCDD. who had been exposed to 2,4,5-T and monly known as the Aisea II study, A look at .some of the major expo other chemicals. Seven apparent cases made by the U.S. Environmental Pro sures to TCDD, approximately in or of soft-tissue sarcoma were discov tection Agency.* The study reported a der of their severity, reveals few if any ered, raising the level of concern sub link between the spraying of 2.4,5-T unambiguous chronic effects. The in stantially. Subsequent events have em on foliage and spontaneous abortion dustrial accident at Seveso in 1976 ex phasized the difficulties in accurate di among pregnant women in Aisea, Ore. posed some 37,000 people of all ages agnosis of soft-tissue sarcoma and in This study has come in for much to considerable amounts of TCDD. accurate identification of exposed indi criticism, notably by an interdiscipli A relatively small number of them viduals. At a conference in 1983 Mari nary group at Oregon State Universi showed transient effects such as chlor- lyn A. Fingerhut of the National Insti ty. The group concluded that an assc- 33 /n Q O T n JKTHTO i  ciadon betweenherbicide spraying and samples of the liver and fat tissues mans. Yet health effects on humans are t spontaneous abortion could not be where TCDD resides.) Without such rarely proved in the case of environ shown from the data relied on by the information a dose-response relation mental chemicals to which the public ill-. agency. Other studies--in _Australia, cannot be established. is variably exposed at subacute levels Hungary, New Zealand and the U .S .- TCDD has been called the most tox that can only be estimated (and then failed to find a link between the use of ic synthetic chemical known to man. If only in the crudest approximation). A 2,4,5-T and birth defects. its acute toxicity to the guinea pig, case in point is aflatoxin, the product and even the rat and the mouse, is the of a mold that develops commonly in Because of the extreme acute toxicity criterion, the statement is probably stored oilseed crops such as peanuts. and the multiple chronic effects of correct. If its considerably lower toxic In animal tests aflatoxin is one of the TCDD in animals, regulatory agencies ity to the hamster is the criterion, how most potent carcinogens known, but it have had to consider what to do in or ever, the statement would surely not has not yet been proved to have this der to protect people from exposure to be true. Yet there is no need to quib effect in human beings. the material. Such agencies must ex ble: TCDD is unquestionably a chemi Diversity in reaction to stimuli is a trapolate animal data to human beings cal of supreme toxicity to experimen hallmark of biological organisms. Re in all but a few instances, in spite of tal animal*. Moreover, severe chronic actions to toxins are no exception to the fact that the validity of this type effects from low dosages have also the general rule. People may be more, of extrapolation has not been ascer been demonstrated in experimental less or equally sensitive to a given tox tained. Compounding the difficulty is anim al*. Therefore the concern about in than an experimental animal is. Ex the lack of a simple, accurate method its effects on human health and the en trapolation is neither art nor science; it for determining whether and at what vironment is understandable. Is simply the most rational way to as level TCDD occurs in the tissues of When toxic chemicals are at issue, a sess a hazard in the absence of defin exposed individuals. (The present test regulatory agency has few options be itive data. Hence regulatory actions requires a surgical procedure to obtain yond extrapolating animal data to hu continue to be based on the animal data even when the human data, al though they are not definitive, may WORKERS LOCATION DATE EXPOSED OP ACCIDENT REMARKS be sufficiently compelling to allow a scientific judgment that the hazard to 1948 250 Monsanto plant in 122 casts ot chloracne being studied; 32 people has been overestimated. Nido. W.Va. deaths v. 46.4 expected; na excess deaths That appears to be the case with \ I horn malignant neoplasms or circulatory disease TCDD. Investigators are in general agreement that TCDD is less toxic to I 1953 75 BASF plant in ludwigsftaien 55 cases ot chioncne, 42 severe; 17 deaths v. 11 to 25 expected (four gastrointestinal humans than it is to experimental ani mals, but the available information is cancers andtwooat-oed lung cancers); most not sufficiently compelling to stimu common injuries were impaired senses and late a change in regulatory posture Avar damage toward either more or less restriction of exposure to the material. I suspect 1950 ? Rhone Poutenc plant in Grenoble 17caa#3 ot cWongie, also elevated Epid and cholesterol levels in the blood that the direct evidence of TCDD's ef fects on humans will never be either more or less comp- ng than it now is. 1903 106 NV Philips plant in Amsterdam 44chloracne eases (42severe), of whom 21 also had Internaldamage or camral-nervoussystem disturbances; eight deaths (six possible myocardial infsicdons); soma symptoma ot ftdgue The public's perception of a toxin is an important determinant of the pos ture taken by a regulatory agency. The public has heard a great deal about both the acute and the chronic effects 1904 61 DowChemical plant in Midland, MldL 49 cuee ot chloracne; four v. 7.8 expected deaths; three cancer deaths v. 1.5 expect of TCDD on experimental animals but little about the substantial body ed, ones aoft-ttseue sarcoma of data showing that human beings are less sensitive. The initial reports 1966-69 78 Continua leaks in Spotena plait near Prague 78 cases of chloracne; live deaths; many of the 50 workats studied for more than 10 yean have hypertension, elevated blood levels of Opidand cholesterol, pndtebetae; dgnifleart amounts of severe liver and neurotogie damage of TCDD's acute toxicity, followed by reports of its carcogenicity and repro ductive effects, have instilled a public fear that probably cannot be dispelled even by adequate information about the countervailing experience with hu 1960 ? Rhone-Poutenc 21 chioncne casee plant in Qrenoble man beings. The regulatory agency is therefore left in the position of having 1960 90 Coalite & Chemical 79chloracnecaaee; onedeatfi fromcoronary plant In Derbyshire ' thrombosis to deal with not only the available evi dence but also the public's fear. 1978 150 ICMESA plant Worfcan are being studied dong with he U.S. Environmental Protection TI in Sevaao, Italy expoaed townspeople; more than 500 ` residents treated for presumed toxic symptoms;134 confirmed chloracne casee; Agency has responded to the pub lic's fear with a number of regulations overal mortality rata normal intended to control the formation and release of TCDD and to limit individ INDUSTRIAL ACCIDENTS have exposed more **800 workers to i l p U k u t i m o a t i ual exposure to i t Those regulations o t TCDD. The accident at S o re la 1976 alto expand soar 37,000 reikient* o t nearfay could be made stronger or weaker on rn a a m M a ii Tha data ara baaad oa a to d y made by tba Americas M ed ial Aseodetloa. the basis of new evidence. What the 34 t GENF 010808  ins are iv^onpublic levels d then on). A -oduct >nly in anuts. of the but it *e this li is.a s. Re* ion to more, n to*5. Ex ace; it to as* defin:tions aimai a. ai- may ow a rd to agency has not done--and might be said to have a responsibility to do--is to try to dispel the public's fear on the basis of the evidence that exposure to low concentrations of TCDD in the en vironment appears not to have serious chronic effects on human beings. The TCDD case is further exacer bated by its relation to the defoliation program in Vietnam, an unpopular program in an unpopular war. The many and diverse health effects al leged by Vietnam veterans to have been caused by exposure to Agent Or ange have been widely publicized. The public is generally aware that the com plaints were settled out of conn for $180 million, and many people believe the settlement was an admission of guilt by the chemical companies that manufactured Agent Orange. Appar ently few people know of Federal Judge Jack B. Weinstein's statement to the attorneys for the plaintiffs that "in no case have you shown causality for the health effects alleged." A troublesome mafter exemplified by the TCDD issue is the appropriate utilization of scientific resources. A. L. Young of the Office of Science and Technology Policy has calculated that more than a billion dollars will have been spent by the Federal Government for research and other dioxin-related matters before all the major studies now in progress have been completed. Additional expenditures of both time and money have been made by chemi cal companies, private organizations and government agencies. The total outlay is a tremendous amount for an issue of questionable importance. Two years ago a conference on di oxin at Michigan State concluded that the TCDD case is relatively less im portant than a number of other issues and that the nation's limited scientific resources should be devoted to the is sues posing a greater threat. On the basis of the evidence turned up so far, the conclusion is still valid. 14 with neral vie to l ani on is :imusture ction >pect 's efither w is; .inis posThe bout fects nais iody ings arts dby pro* tblic lied aot hu- -y /ing evi- ; I ti 608010 non ub* ons and 'id* ons on DECOMPOSITION OP TCDD takes placa whea the ultraviolet react!oa a n show n la soil, w hen sunlight cannot get at the mete* the la sunlight splits off the molecola* chiodo* atoms. SU steps la the al, TCDD tends to bo quite persistent, enduring as long as 10 yv 't 35 / 783620