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Dioxin Risk: Are We Sure Yet?As EPA's dioxin assessment undergoes public scrutiny, it isrenewing debate on health risks and regulatory strategies.

O n January 13, EPA wi l l begin to sif tthrough and assess hundreds of com-ments, studies, and opinions on one ofthe thorniest environmental science andhealth policy issues facing the UnitedStates: the risk dioxin and related com-

pounds pose to humans. When the pub l ic com-ment period closes on that date. EPA's 2000-page draftdioxin risk assessment and risk characterizationmoves one step closer to becoming final, which is ex-pected this September. More than three years in prep-aration, the reassessment provides the most com-prehensive examination of dioxin-l ike compoundsundertaken by (he Agency. This Environmental Sci-ence & Teclinology Special Report presents an in -depth look at the report's major findings, the spec-trum of opinion on the validity of EP.\> assessment.and wavs to control sources of dioxin.

The latest assessment. Dioxin, one of the "mosttoxic chemicals regulated by HPA." according to HPAAssistant Administraio.' Lynn Goldman. has been thesubject of a series of Agency assessments dat ing backto the early 1980s. This most recent evaluat ion be-gan in 1991 because of several new studies as wellas controversy about the health threat from dioxin-

like compounds. One key piece of new informat ionemerged from a 1990 meeting of scientists at the Ban-bury Center in New York, where a consensus wasreached that dioxin-like compounds gain entry tocells by binding to a particular protein, the Ah re-ceptor. Agreement on this mechanism and the re-sults of studies of exposed workers led EPA to lakeanother look at (he compound.

Also d r iv ing the EPA reassessment were con-cerns bv industry and others that the human healththreat from dioxin had been overstated in risk as-sessments done in 1985 and 1988. This view, how-ever, is refuted bv the new assessment. EPA not onlyreaffirms the earlier view that dioxin is a probablehuman carcinogen, but also finds tha t noncancerhealth effects are greater than was previously thought.The report describes a complex and only partially un-derstood interplay among dioxin-like compounds.hormones, and other modulators of cell growth anddifferentiat ion. In shoring up past scientific news oncancer r isk from dioxin, the assessment also foundthat the upper bound risk estimates for cancer in thegeneral population exposed to dioxin may be as highas one in ten thousand to one in a thousand.

\ V h e n t h e r i s k r ea s se s smen t was f i r s t a n -

Milestones in EPA'sAssessment of Dioxin

EPA issues first dioxin risk assessment, |focused primarily on cancer and based |largely on animal studies. Dioxin |classified as a probable, highly potent)

| human carcinogen. |

OCTOBER: Scientific meeting at BanburyCenter, Cold Springs Harbor Laooratory, ;where experts agree that human effects f ron-!dioxin can be predicted from ef fects in |animals and the development of risk \assessment model based on dioxin binding ;to specific cellular receptor is needea. :

j EPA issues draft revised assessment, suggesting dioxin less potentGeneral agreement that current procedures inadequate to assessdioxin s human health risks Later in year, EPA Science Advisory Boardfinds no scientific basis for revising dioxin potency estimates butrecommends new model be developed for assessing risk.

I APRIL: EPA administrator directsAgency to beg ' maior| reassessment of risks from dioxin. Tasks include developmentof biologically based dose-response model, lab research tosupport study, update of health and exposure assessment,and research to characterize risk in aquatic ecosystems.

NOVEMBER: First of two public meetings convened by EPA; to receive comments and report progress

24 A • VOL 29 NO 1 1995 ENVIROMMENrAL SCIENCE & TECHNOLOGY

nounced by then-EPA Administrator William Reillyin 1991. it was expected to be completed in less thantwo years. However, the process took considerablylonger at least in part because EPA brought in out-side scientists to review each risk assessment chap-ter as it was being developed. Some 100 scientists in-side and outside EPA were involved in the review. Thisunprecedented action has been widely praised.

Noncancer effects. Most significant in this anal-ysis is the heightened concern about noncancer ef-fects in humans, including disruption of tfae endo-crine, reproductive, and immune systems, as weii asdioxin's impact on the developing fetus, which mavoccur in some cases at or near background levels fhedraft points to studies showing decreased spermcount in men, higher probability of endometnosisin women, weakened immune systems, and otherhealth problems. Certain highly exposed subpopu-lations may already be experiencing some of theseeffects, according to the new assessment.

The risk assessment document presents new in-formation on exposure as well as health effects (seep. 26A). The volume on estimating exposure to dioxm-like compounds in the United States represents themost comprehensive effort undertaken to identifysources and the major routes of exposure. Airbornedeposition appears to be the most prevalent meansof transport. The compound then makes its way intothe human food chain through mgestion of contam-inated plants by animals and bioaccumulanon o fd i -oxin in fattv tissue Human exposure through con-sumption of beef. dairy pr )ducis. tish, and other foodproducts can result in dose rates that are se\eral or-ders of magnitude greater than exposure through in-halation, which had been considered the primaryroute of genera] exposure in previous assessments.

Four primary sources are identified: combus-tion and incineration, chemical manufacturing, in-dustrial municipal processes, and reservoir sourcesin which dioxin may be recirculated throughout theenvironment once it is generated. Although incin-erators appear to be the greatest dioxin contribu-tor, the report notes that several sectors, such as thechemical manufacturing industry, may be large gen-erators but have not been characterized because ofinsufficient data.

Ql8 far —i—. Environmental groups generallysupport EWs •MMinciit but caH for immediate reg-ulatory action to limit sources of dioxin (see p. 29A)Agency officials, however, say they will not proposeregulatory changes based on the results of the riskassessment until after the report is finalized this fall.Still. EPA is proposing new regulations to limit di-oxin emissions from incinerators (see p. 33A).

Industry groups have voiced criticism of the draftreport as well as the proposed incinerator regula-tions (see p. 31A). Dioxin is created inadvertently bva host of industrial activities in which chlorine-based compounds are exposed to high heat in thepresence of organic material. Industrial processesidentified in the report include waste incineration.chemical manufacturing, chlorine bleaching of pulpand paper, and smelting.

As pan of the final draft review, EPA has asked sci-entists, industries, state and local governments, and oth-ers to provide new data on dioxin. Over the next fewmonths EPA will assess these comments, prepare a fi-nal version ot the risk document, and forward it to theEPA Science Advi- or.' Board for review. When the as-sessment is finalized, it will be the first EPA dioxinrisk assessment that has advanced beyond the draftstage in a decade —IEFF 10HNSON

SEPTEMBER: Exposure and healthassessment draft documents examined atEPA peer review workshops Most work oneight-chapter health assessment complete,But Agency delays final action on key human-Oldemiology chapter Complete risk-- sessment expected by year s end

SEPTEMBER: FinalI draft of exposure and'. r isk assessment' released Dioxin

reaffirmed as probablehuman carcinogen,new noncancer healtheffects found

Assessment of dioxin risk to aquaticlife to be released, but risk researchlimited to aquatic life Report toprovide literature review only forwildlife sections

APRIL: Interim report on dioxin risk to aquaticlife and wildlife released

SEPTEMBER: Epidemology peer review panelmeets and reviews long-delayed finalepidemology draft chapter

, JANUARY 13. Public comment period oni exposure, heath risk assessment, and| character izat ion closes

| SEPTEMBER' Following review by SAB.I risk assessment and risk characterizationj to be finalized EPA begins process of

•leveloping dioxin control strategy

D I 0 X I N R I S K

EPA's Dioxin ReassessmentHighlights from EPA's three-year effort to document

sources, exposures, and impact on health

Following are excerpts from EPA's health assessment(1) and exposure estimates (2, 3) ofdioxin (TCDD) andrelated compounds, which include chlorinated dihen-zodioxins (CDDs), chlorinated dibenzofurans (CDFs).and polychlonnated biphenyls (PCBs) thought to havedioxin-like toxicity. These draft documents do not rep-resent Agency policy. EPA's reference citations are notincluded: see documents listed in References for thisinformation. —Editor

Based on all of the data reviewed in thisreassessment and scientific inference, apicture emerges of TCDD and relatedcompounds as potent toxicants in ani-mals with the potential to produce aspectrum of effects. Some of these ef-

fects may be occurring in humans at very low lev-els and some may be resulting in adverse impactson human health.

The potency and fundamental level at which thesecompounds act on biological systems are analo-gous to several well-studied hormones. Dioxin andrelated compounds have the abili ty to alter the pat-tern of growth ariZTdifferentiation ot a number ot cel-lular targets bv initiating a series ot biochemical andbiological events resulting in the potential for a spec-trum of responses in animals and humans. Despitethis potential, there is current ly no clear Lnd^icati^nof increased disease in the geneTaTponiilatiOJ.i. at-trib^'te6Te~uTth8'dn"like compounds. The lack of aclear indicat ion of disease in the general popula-tion should not be considered strong evidence for noeffect of exposure to dioxin-like compounds Hither.lack ot a clear indication of disease may be a resultof the inabi l i ty ot our current data and scientific toolsto directly detect effects at these levels of human ex-posure ( / , pp. 9-87, 9-88)

The presence of dioxin-like compounds in the en-vironment has occurred primarily as a result of an-thropogenic practices.

Ancient human tissue sampling shows much lower

C D D / F levels than found today. Studies of sedi-ment cores in lakes near industrial centers of theUnited States have shown that dioxins and furanswere quite low until about 1920. These studies showincreases in CDD/F concentrations beginning in the1920s and continuing until about 1970. Decliningconcentrations have been measured since this time.These trends cannot be explained by changes in nat-ural processes and have been shown to correspondto chlorophenol production trends. On this basis, itappears tha t (he presence of dioxin-like com-pounds in the environment occurs primarily as a re-sult of anthropogenic practices (2, p. 12).

The ma)or identified sources of environmental re-lease have been grouped into four major types forthe purposes of this report: industrial/ municipal pro-cesses, chemical manufacturing/processing sources,combustion and incinerat ion sources, and reser-voir sources \3, pp 3-2, 3-3).

This assessment proposes the hypothesis that theprimary mechanism by which dioxin-like com-pounds enter the terrestrial food chain is via at-mospheric deposition.

Deposition can occur directly onto plant sur-faces or onto soil Soil deposits can enter the foodchain via direct ingestion (i.e., earthworms, fur preen-ing by burrowing animals, incidental ingestion bygrazing animals , etc ) . CCD/F in soil can becomeavailable to plants by volatilization and vapor ab-sorption or part icle resuspension and adherence toplant surfaces In addition, CDD/F in soil can ad-sorb directly to underground portions of plants, butuptake from soil na the roots into above ground por-tions of plants is thought to be insignificant 1.2. p. 31) .

The major route of human exposure is through in-gestion of foods containing minute quantities of di-oxin-like compounds ( / , p. 9-14).

Dietary intake is generally recognized as the pr i -mary source of human exposure to CDD/Fs. Sev-eral s tudies lia\e estimated that over 90 percent of

(he average daily expfluueJo CUD/ Fs are derivedfrom foods. CDD/Fs in fatty foods snrh-as-TIairv, tisH.and meat products are believed to be (he ma)or con-tr ibutors to dietary' exposures (3, pp. 4-22, 4-23).

Thi- published data on measured levels ofCDDs.CDFs, and dioxin-like compounds in U.S. food prod-ucts have generally come from studies of a specificfood product(s) in a specific location(s) rather thanfrom large survey studies designed to allow estima-tion of daily intake of the chemicals for a popula-tion [3. p. 4-25).

The scientific community has identified and de-scribed a series of common biological steps that arenecessary for most if not all of the observed ef-fects of dioxin and rotated compounds in verte-brates, including humans.

Binding of dioxin-like compounds to a cellularprotein called the "Ah receptor" represents the firststep in a series of events attributable to exposure todioxin-like compounds, including biochemical, cel-lular , and tissue-level changes in normal biologicalprocesses. Binding to the Ah receptor appears to benecessary for all well-studied effects ofdioxin but isnot sufficient, in and of itself, to elicit these re-sponses. This reassessment concludes that the ef-fects elicited by exposure to 2,3,7,8-TCDD are sharedbv other chemicals that have a similar structure andAh receptor-binding characteristics. Consequently, thebiological system responds to the cumulative expo-sure of Ah receptor-mediated chemicals rather thanto the exposure to any single dioxin- l ike com-pound (; . p.9-78)

I'he reliability of using animal data to estimate hu-man hazard and risk has often been questioned forth is class of compounds. Although human data arelimited, evidence suggests that animal models are ap-propriate for estimating human risk if all availabledata are considered. Humans have a fu l ly func-tional Ah receptor and both in vivo and in vitro stud-ies demonstrate comparabi l i ty of biochemical re-sponses in humans and animals ( 7 , p. 9-36)

There is adequate evidence based on all availableinformation to support the inference that hu-mans are likely to respond with a broad spectrumof effects from exposure to dioxin and related com-pounds if exposures are high enough [ I , 9-79).

The p o t e n t i a l for d ioxins and related com-pounds (0 cause reproductive and developmental tox-icitv m animals has been recognized for many yearsRecent laboratory studies have suggested that al-tered dgyelnprnpr^ may be among the mosl_sensi-tive TCDD encLpqmts in laboratory animal systemsal though the likelihood and level of response in hu-mans-are much less clear. . .

Of par t icular interest to the risk assessment pro-cess is the fact thai a wide van iv ofde\e lopmemalevents, crossing three \er tebrate classes and sev-eral species wi th in each class, can he perturbed, sug-gesting that dioxin has the potential to disrupt a largenumber of critical developmental events at specificdevelopmental stages ( / , pp. 9-44. 4-45)

With respect to male and female reproductive endpoints , there are clear effects to l lnwing dioxin expo-sure ot the adul t animal. Such reproductive effects

t <"c—<

U.S. sources of diaxin-like compounds o0,0EPA's draft reassessment presents the first compilation of nationwide

CDD/CDF emission estimates It shows that emissions from incinerators to _^^the atmosphere are the dominant dioxin source in the United States. (—'These "best guess" values are, according to EPA, "quite uncertain since thenationwide approximations were derived by extrapolating only a fewfacility tests" (2) No estimates were made of some potential sources, suchas chemical manufacturing, because of the lack of test data

Air- Medical wasteincinerators

Air Municipal wasteincinerators

generally occur at TCDD body burdens that are higherthan those required to cause the more sensitive de-velopmental end points ( 1 , p. 9-47).

Observations described in this assessment sug-gest a continuum of response to exposure to dioxin-like chemicals Bv a cont inuum of response we sug-ges. t h a t as dose inc reases , the p r o b a b i l i t y ofoccurrence of individual effects increases and the se-verity of collective effects increases. This con t in -uurn provides a basis for inferring a relationship be-tween some early events that are not necessarilyconsidered to be adverse effects with later events thaiare adverse effects.. . This inference mav be the mostcontentious 01 all ;;, pp. 9-73. 9-74).

Average background exposure leads to bodv bur-dens in the human population that average 40-60pgTEQ (TCDD equivalents]/g lipid (40-60 ppt) whenall dioxins, furans, and PCBs are included.

The term "background" exposure has been usedthroughout th is reassessment to describe exposureof the general popula t ion that is not exposed toreadilv identifiable point sources of d iox in- l ike com-pounds. Data on human tissue levels suggest tha tbody burden le\els among industr ia l ized nations arereasonably s imi la r These data can also be used toestimate background exposure through the use otpharmacokine^c models.

Using th i s approach. e\posure levels lo 2,3.7.8-TCDDjn^ndusinali/.ed na t ions are (.-itimated to beabout 0 3-0 6 p g ' l C D D / k g body we igh t /day Fs-Iimates based on (he contribution ofdioxinl ike PCBsraise the total to 3-6 pgTKQ/kg bodv weight/day. I'hisrange is used throughout th i s characten/at inn as anestimate of average background exposure to dioxin-l ike CDDs. CnFs, and PCBs.

High-end es t imates of body burden ot i nd iv idu -als in the general popula t ion (appro \ imi i te lv the top

AT Othersourcf

Heihk effects in humus and •HimilsThe exposure levels at which health effects from dioxin-likecompounds are observed vary widely among species. A sampling ofthe studies presented in the EPA dioxin health assessment indicatesthat some health effects are observed at estimated body burdenlevels close to the average human "background" body burden level.

Etimfd bodyburdmof

Effect_____ Speci— dioxin {ngflty}

"Background" level Human 9"Cm—Hy ——octotod" with (Hoxin •xpOMir*Chloracne

Cancer

HumanMonkeyRabbitMouse

Decreased testosteroneDecreased testis size

Altered glucose tolerance'Low-do— •ffwcts" in iEndometriosisDecreased sperm countDecreased offspring viability

Enhanced viral susceptibilityS«wrc«: RefBfence 1 , pp 9-55-9-65

HumanHamsterMouseHumanHumanRatHuman

in animateMonkeyRatRhesus

monkeyMouse

4&-30001000220

14,000

109-7000500

10008314

10,20014-110

5464

270

10% of the general population] may be greater thanthree times higher ( J . pp. 9-77, 9-78).

The margin of exposure between background lev-els and levels where effects are detectable in hu-mans in terms ofTEQs is considerably smaller thanpreviously estimated [ I , 9-81).

[n TCDD-exposed men, subtle changes in bio-chemistry- and physiology, such as enzyme induc-tion. altered levels of c i rculat ing reproductive hor-mones, or reduced glucose tolerance, have been fdetected in a l imited number ot available studiesThese findings, coupled with knowledge derived fromanimal experiments, suggest the potential for ad-a-verse impacts on human metabolism and develop-mental and/or reproductive biology. . .

Subtle changes in biochemistry and physiology areseen with TCDD exposures at or jus t se\eral toldabove average [bodv burden] TEQ levels. Since ex-posures within the general population are thoughtto be log-normallv distributed, individuals at the highend of the genera] population range (with body bur-dens estimated to be three, and perhaps as high asseven, times higher than the average) mav be expe-riencing some of these etfects.

The likelihood that noncancer eflects mav be oc-curring in the human population at environmental ex-posure levels is often evaluated using a margin of ex-posure (MOE| approach. A MOE is calculated bvdividing the human-equivalent an imal lowest ob-served adverse effect level with the human e\posure

level MOEs in the range ot ]()() to 1,()()() are gener-ally considered adequate to ru le out the likelilicuAdof significant effects occurring in humans baseJ^nsensitive animal responses. The average leve ls oJT[j-take of dioxin-like compounds in terms of TEC^Qnhumans described above would be well within aafc-tor of 100 of levels representing lowest observedran-verse effect levels in laboratory animals exposewroTCDD or TCDD equivalents. For several of the et-fects noted in animals, a MOE of less than a factorof 10, based on intake levels or body burdens, is likelyto exist.

. . . [It is) highly unlikely that a margin of expo-sure of 100 or more currently exists for these effectsat background intake levels, at least for some mem-bers of the human population ( 2 , pp. 9-81-9-83).

Dioxin and related compounds are likely to presenta cancer hazard to humans ( / , p. 9-85).

Since the last EPA review of the human data baserelating to the carcinogeniciry of TCDD and relatedcompounds in 1988, several new follow-up mortal-ity studies have been completed. . . . Although un-certainty remains in interpreting these studies be-cause not all potential confounders have been ruledout and coincident exposures to other carcinogensis likely, all provide support for an association be-tween exposure to dioxin and related compounds andincreased cancer mortality i ; , p. 9-39).

While ma)or uncertainties remain, efforts of thisreassessment to bring more data into the valuationof cancer potency have resulted in a risk-specific doseestimate (1 x 10"*' risk or one additional cancer in onemillion exposed) of approximately 0.01 pgTEQ/kgbody weight/day. This risk-specific dose estimate rep-resents a plausible upper bound on risk based on theevaluation of animal and human data. . .

With regard to average intake, humans are cur-rently exposed to background levels of dioxin-likecompounds on the order of 3-6 pg TEQ/kg bod\weight/day, including dioxin-like PCBs I his is moret h a n 500-fold higher t h a n the EPA's 1983 r i s k -specific dose associated w i t h a plausible uppe r -bound, one in a million risk of 0.006 pg TEQ / kg bodyweight /day . Plausible upper-bound n^k esti-mates for general population exposures to diovin andrelated compounds, therefore, mav be as high as 10 'to 10'1 (one in ten thousand to one in a thousand( ; , pp. 9-85, 9-86).

Referencesl i U S Envi ronmenta l Pro tec t ion Agencv Hemili i^i '^-

iTienr I^ocumenf for ^,3.7,8-Te[rnchSoro(iihen^o-p-! ' m ^ n ird)D: and Related Compounds. Vol i l l f \ i e r n . i l rr

v i e w draf t . Office of Health and E n v i r o n m e n t a l \ s^c^s-ment Otfice ot Research and Development 1 ) ^ ( . ( n r r i irnent Pr int ing Office Washington, DC. August l4" i4 I l ' \h()0 'BP-92'()01C

.>! I] "i Environmental Protection -\genc\ t-^niiianii^ I .;;o^ure to r)loxin-l,lke Compounds. l» / / £ \ t ' r « f ; i r • ' i / n ' -niiirv. eMernal review draf t . Office of Hea l th Jrul [ n \ i -r o n m e n t a l Assessment Office of Rrs tMi \ l i J n JDevelopment U S Government P r i n t i n g O l l i ( c '•.',, i -h -ington. DC, lune 1994. bPVfiOO/G-iiB/OO^Ca

!3l >J S Environmental Protection Agency Estimating I \ J K , -^ire to I'lioxiti-Like Compounds. Vol I I Properties s«i/i,-i..,()ccnrrpiu~e and Background F-rposiirvs: external re\ie\\ ilr.irOffice of Health and Environmental Assessment ( ) t l n r ,i|Research and Development U S Government 1'nnniii; ( i ft".i-e Washington, DC, lune 149.1, EPA/bUO/b-MM i|i i- , i i ,

D I 0 X I N R I S K

EPA on the Right TrackR I C H A R D C L A P P

P E T E R d e F U R

E L L E N S I L B E R G E L D

P E T E R W A S H B U R N

The public finally has access to the full of-ficial text of the current dioxin reassess-ment. In announcing the release, EPA de-clared that the present assessment differsfrom other assessments for procedural aswell as substantive reasons. The docu-

ment produced by EPA and independent scientistsis not, however, what industry expected when itpushed the Agency to undertake the reassessment.Instead of declaring the risks lower, the draft reportfinds the risks are greater than previously thoughtI'he environmental community is satisfied that EPAis at last on the right (rack.

EPA recognizes that the policy implications of thisreassessment may require new implementation strat-egies. We believe EPA is obligated to set a nationalpolicy consistent with the threat—one that identi-ties and eliminates all sources of or exposures to di-')\in-like compounds.

The process EPA used for this reassessment was.', iselv, akin to scientific peer review. From the out-

let, EPA announced that outside scientists would beintegrally involved in writing the documents to sum-marize the current knowledge of the dioxin-relatedcompounds. In the past, the perception had been thatEPA completed such assessments behind closeddoors, i'his process, albeit slow. was substantially en-hanced over past ones. and the results are corre-spondingly improved, despite missed deadlines.

A comprehensive analysisThe scope of the EPA dioxm reassessment includesnot )us t 2 ,3 ,7 ,8-TCDD but a l l d i o x i n - l i k e com-pounds. This approach is the only one consistent withresearch showing that a number of congeners actthrough the same receptor mechanism within cellsi 7 . . ? ) . The subsequent quantitative ranking of chem-icals according to their ability to act via the same re-ceptor mechanism yields a more complete analysisof the total load of dioxin-like compounds in (he en-

vironment and living systems.EPA also expanded the end points to include wild-

life and aquatic life. Past assessments ofdioxin werenever intended as more than human health assess-ments. Although the current effort produced an im-portant summary of wildlife and aquatic life ef-fects, that part was never completed as originallyenvisioned. Still, the limited report on wildlife andaquatic life (3) clearly indicates that these animalsare as sensitive as any oth-ers to the dioxin-like com-pounds.

The draftreport findsthe mk««r6greater thanpreviouslythought.

-Although EPA had pre-viously addressed some ofthz noncancer health ef-fects of dioxin, these ef-fects had not been giventhe same level of scrutinyas cancer. But the Ban-bun,- conference pointed tothe effectiveness of lowdoses in provoking developmental changes that havedramatic consequences. Now, the reassessment ac-knowledges that these noncancer end points are cuedvia endocrine systems altered by dioxin-like com-pounds, and the most sensitive biological system maybe the developing fetus.

Exposures and sources. I he question of howmuch dioxin is released into the environment nowand how much remains from past releases was orig-inally considered fairly straightforward. But when thereassessment was first publicly reviewed in Septem-ber 1992, comments indicated that a more com-plete source inventory was needed. Consequently, thecur ren t version contains a more complete sum-mary of sources, exposure pathways, and concen-trat ions in various media. According to the report,the greatest sources are incinerators. Also, aquatic dis-charges may result in important exposures throughthe food chain. But a large fraction is unassigned to

specific sounes, lec i rc i i l a i ion ot exis t ing ( .o i i ian i i -nation may be substantial .

The information is not complete, par t icular ly re-garding concentrations in all animal tissues How-ever, ihe report shows that the level and extent of con-tamination are greater than previously supposed.Dioxin-like compounds are widespread in soils, sed-iments, and animal tissues. In tood. fish has the high-est level of dioxin-like compounds (average 0 6-1.0pg/gj; beef is nearly half that; pork. chicken, and dairyproducts have onlv slightly lower concentrations thanbeef. For comparison, health advisories issued bystate agencies frequently caution against the con-sumption offish with 1-2 pg/g or more total dioxin-like compounds, based on toxic equivalents.

Human health. Earlier EPA health assessments ofdioxin, using the one compound, were based on two-year cancer bioassays. The seminal piece of work wasthe research by Kociba {4} on rat liver cancer thatyielded an estimated cancer potency of dioxin(2,3,7,8-TCDD specifically) higher than ever deter-mined for any compound. EPA used the standard as-sumptions of lineanry of the dose-response func-tion and lack of an effects threshold at low doses. Buteven at the outset of the current reassessment, it wasclear that both of these assumptions were beingtested. These assumptions, after all, drove the cal-culation of the cancer potency and subsequent dose-specific risk estimates.

No response thresholdThe acceptance of the Ah receptor mechanism ledto the suggestion that the response was not linear atlow doses and that a response threshold occurred atlow levels But d tocused examinat ion of the low-dose-response function refuted both notions (5i Thisc o n f i r m a t i o n of t h e n o n t h r e s h o l d and dose-response linearity assumptions reinforced EPAs ear-lier health assessments Consequently, EPA had to ac-cept that dio\m is t u l l \ as carcinogenic as originallyconsidered. The recent publ ica t ion of human epi-demiologicdl da ta t rom acc iden ta l and occupa-t ional exposures to diovin pro\ ided f u r t h e r e v i -dence of the carcmogemcitv Li t t l e doubt can nowexist that dioxin is a human carcinogen.

Even betore the reassessment began, researchpointed to the importance of noncancer effects ot thedioxm-like compounds A wealth of data existed, infact, on noncancer etfects, but these were consid-ered secondary to cancer But the elegant work car-ried out in the lab ot Peterson (6) changed that as-s u m p t i o n f o r e v e r M a b l y et al showed t h a tadministrat ion ot a single dose ot dioxin to a preg-nant rat can at tect the development of reproduc-tive (unction in male of f spr ing .

Mechanism of action. 1 he central point ot theBanbury conference was the molecular l e > e l of ac-t ion tor dio\in and related compornds Research-ers recognized tha t dioxin func t ions at the molecu-l a r level in much the same m a n n e r as s t e ro idhormones, via b inding to an intracellular protein re-ceptor 1'his reali/.aiion led to the recognition that anentire group of compounds capable ot binding to thissame receptor was competent to provoke the samesum' ol responses as 2.3.7,8- [CDU

I h e recep tor -based i n e t h a n i s i n nl i t cnon a t -tecled the S L i e n t i t i c reassessment mure t h a n an\other single aspect ol the larger issue 1 lie rei-eptoimechanism prompted EPA to undertake the ettort inthe belief that a better model would emerge trom un-derstanding the molecular basis. 1 he molecular path-way of receptor binding led to the inclusion ot ad-ditional chemicals that follow this path and theinference that these dioxin-like compounds can bequantitatively compared with 2,3.7,8-T(::L)D (the toxicequivalency, or rEQ, concept). And the tact that thereceptor mechanism is found in humans, experi-mental laboratory animals, and wildlife provides con-clusive support for the use of animal data.

Ekmmate s—rces Md ex—mresProblems with the use of science in environmentalregulation and policy making often revolve arounddetermining when the Agency has enough data tostop studying and start fixing the problem. EPA hasfaced that question for the past 10 years, and untilnow has determined that the evidence supported ac-tion to protect against cancer in humans. Now EPAfaces increasing data on low-dose effects of. and wide-spread exposures to, all dioxin-like compounds.

It is clear EPA must adopt a management ap-proach similar to that for lead and at least attemptto identify and eliminate all the sources. The leadmodel will serve EPA well in initiating a control strat-egy. With lead, EPA recognized that the entire pop-ulation was exposed through multiple sources, withhealth consequences at low-dose exposures. Thesource-by-source control strategy failed to protect hu-man health or the environment. Instead, all expo-sures had to be controlled or eliminated and sourcestreated similarly. The success of that approach hasbeen the decline in blood lead levels reported in 1994.

We believe there is no alternative but to take a sim-i l a r approach and e l iminate sources and expo-sures. In the case of the dioxin-like compounds, how-ever, the le^ u model must serve as onlv the start EPAmust rigorously el iminate sources as well as expo-sures, recognizing (hat each exposure threatens hu-man health and the environment.

ReferencesI ; Biological Basis lor Risk Assessment ol Dioxins and Kr -

laied Compounds' . Uallo, M A , Scheuplein, R ) ' . dnderHeijden K \ . h d s . Banbup, Kepon J.'i; Cold ^ p r i n ^ Har -bor Laburatorv Press New'lork. 1991

i - 2 i \hlbor^. LI (i e; al Hiir I Pliarinacol Environ luiico!Pliarrndcoi 1992,-"8. 179-99

J ' I n t e r im Hepon on Data and Methods tor Assessment otJ.3 7.H- Ielrachlnrodlbenzo-;.i-d]oi]n Risks to Aqual ic I i t rand Associated V \ i l d l i f e " , U S Lnvironmental Proteinon\gen<-\ Uash inRton . DC, 1993. LP\ /&()0/R-9J/0-)1

•l i Kouba, R ] >.'( al !i>xnoi \{)pl Plinrniaiol 1978 411 J7':'-iti.l

'ii P o r t i e r C f t al Inn/him -\pp! RiMCol 1993. .'U. W-'-ihb; M,ihl \ . I \ , Moore, K \\ . I'eierson. H I' Itixii.nl \iiin

I ' l l i l i n i i n . - n l 1992 ;;-). IHH-^26

Kn liuni CAupp i\ (in epidemiologist and professor i l l H n ' ' -{(in Unn'ersitv I ' e t e r deh'iir is d senior scientist fm i l i el-nrironmenltil Defence i-'nnd hllen Silber^i'ld is a se-nior scientist for [ l i e Environmental Defense Fund unitn member ot the Execiilire Committee of EISA's ^>cienreAdn.wn' Board. Peter Washburn is a staff scientist n ' l t l i[ l i e \fniiml Hesonrces Cotincii of Maine.

D I 0 X I N R I S K

EPA Assessment Not JustifiedE N V I R O N D I O X I N R I S K

C H A R A C T E R I Z A T I O N E X P E R T P A N E L

E PA has concluded that adverse impacts onhuman health may occur from exposure todioxin-like compounds at or within an or-der of magnitude of current backgroundbody burdens. We do not believe there issufficient scientific evidence to support this

alarming conclusion. Dioxin exposure clearly causesa variety of toxicologic effects in laboratory ani-mals, and scientists generally agree that most of theseeffects are mediated through the Ah recer^r. How-ever, the exposures estimated to give rise to humanbackground body burdens are far smaller than thoseknown to cause toxicity. The pivotal issue is thuswhether adverse human health effects can reason-ably be expected to occur at or near current back-ground body burdens.

EPA has equated acute and chronic exposure pat-terns on the basis of projected body burdens eventhough the corresponding daily doses can be or-ders of magnitude apart. Because adipose tissue, themajor storage site for dioxm, equilibrates slowly, acutedioxm administration will produce higher peak con-centrations in serum and target organs than will ad-ministration of the same total dose in small dailv in-crements. Use of body burden as a measure ofexposure is thus misleading.

Additmty questionedCompounds that bind to the Ah receptor include di-oxin-like polychlorinated dibenzoturans (PCDFs) andpoiychlonnaied biphenvis (PCBs) that are present invastly greater concentrations than 2,3,7.8-teirachlo-rodibenzo-p-dioxm (TCDD) itself. In fact, most of thebackground body burden in humans is caused bvthese other chemicals. Use ot'toxic equivalency fac-tors (TEFs) implies that all of these compounds actin an additive manner. However, this hypothesis iscontradicted by evidence of antagonism among di-oxm-like PCBs (Harper. N. et al.. manuscript); thatis. the net effect of mixtures of these congeners is less

than a simple summation ot 1 EF concentration prod-ucts. Moreover, even if TEFs tor some congeners areadditive for some particular endpoint, there is in-sufficient data to support the extrapolation to equiv-alent TEFs and their additivity for other endpoints.We urge caution regarding the use of TEFs, and rec-ommend more clarity regarding the mixed nature ofexposures, particularly in human populations.

Limited in.,plications of receptor theory. Recep-tor theory predicts thatbin - ..ig of dioxins to theAh receptor mav be lin-ear at very low expo-sures, so some bindingmay occur even at near-\an i shmg-poin t doses.However, t h i s t h e o r ydoes not p red ic t theshape of the dose-re-sponse c u r v e tor anvbiochemical or toxic re-sponse. In particular, itdoes not predict that re-sponses will result when-ever b i n d i n g occu r sThus, responses may ex-hibit thresholds.

There isinsufficientSC——ttfftC

evidenceto supportEPA'salarmingconclusion.

Cancer. Although dioxm has been shown to causecancer in laboratory' animals, the epidemiologic linkbetween exposure and increased human cancer riskis inconclusive at present Where positive associa-tions have been observed ( I , 2}, they are weak, evenamong persons with presumed heavy exposure aris-ing from chemical manufacturing processes or in-dustr ial accidents. A t t r i b u t i n g cancer excesses ob-served among workers to their presumed dioxinexposures is questionable given the workers' knownexposures to carcinogens such as asbestos and 4-ammobiphenyl. Furthermore, control for the influ-ences ot cigarette smoking and other cancer risk fac-

tors lias been inadequate. A l though t P\ f i i iphas i / c sthe positive associations tha t h a v e been u 'p i ined ,conflicting evidence cannot be dismissed and i i i i e r -native explanations cannot be ruled out

Developmental, reproductive, and endocrine ef-fects. When considered carefully, the reports ot ad-verse developmental effects in rodents and h u -mans show fundamental inconsistencies Becausehigh-dose in utero exposures result in the teminiza-tion of imprinted male rat mating behavior i J ) , i:PA

argues tha t s i m i l a r ef-fects can be expected inhumans. However, sex-ual behavior pat terningin rodents is fundamen-tally different from that inhumans; this endpoint istherefore of ques t ion-able relevance for poten-tial human risks. Otherdeve lopmenta l effectshave been noted in hu-mans and other primates,but onlv at doses so highas to cause maternal tox-icity.

There is noevidencethat dioxinexposurecompromisesimmunefunction inhumans.

I n c l u s i o n of e n d o -metriosis as a potential adverse effect is premature.The association ofendometriosis with dioxin expo-sure has been reported in one study of monkeys (••?) ,but only a posteriori, and alternative causes [i.e.. pre-vious exposures to other substances and surgicaltreatments) cannot be ruled out. Furthermore, a con-tradictory report (Arnold, D L e( al., manuscr ip t )showing no association between exposure to dio\m-like PCBs and die incidence ut endometnosis in mon-kevs is not considered in the current draf t ^uch se-lective emphasis does not accurately reflect the f u l lweight of the scientific evidence.

Evidence not conclusiveEndocrine disrupt ion lias been cued ;is another ad-\erse outcome ofdioxm exposure, but the evidenceis for high doses and even (hen is very weak 1-or f \ -ample. one study reported a s igni f icant increase inthe prevalence ot low total serum testosterone in thethird exposure quartile. but this f inding was not con-firmed in (he highest quartile. and the test tor trendwas not s igni f icant \3} A n o t h e r repor t L i t i n g de-creased glucose tolerance (6') has been nei ther peer-reviewed nor confirmed

These limited observations may be suggestive, butthey are not sufficient to conclude that people areat risk of reproductive, endocrine, or deve lopmen-tal effects at or near current body burdens

Immunological effects. I here is n') evidence thatdioxin exposure compromises immune f u n c t i o n inhumans In animals, effects have been noted omv athigh doses or with protocols that do not evalua te nor-mal immune funct ion ie g., in|ection challenges \ \ i t hsheep red blood or tumor cells) i-ltfects on i m m u -nological surrogate markers i,e g . d i s t r i b u t i o n ot r-cetl subsets and surface marker expression I have beenreported in some an imal exper iments , bu t thesemarkers have no known s ign i f i c ance to r (he i m -mune competence of the an imals . In exposed hu-

mans. such ettei.ts h a v e noi l i fcn tomidBiochemical changes. I t , .is I l ' \ suggf-'is, ii-.c > ] v

i'rage" human body burden is L u n e n t i v \ v n l u n an ' n -der ot magni tude of the level required to e l i i i t , i d -vcrse ettect.s. then s e n s i t i v e b iochemica l m a r k e r sshould already be elevated in the genera] popula -tion. A sensitive marker that lias been detected inmost tissues, including human placenta, is the in -duction ofcvrochrome P4501A1 Induction ol'thi!> en-zyme was markedly evident in placentas from thehighly exposed (Vusho and Yu-Cheng cohorts,, orsmoking mothers (7-9), but i t lias not been de-tected in the general nonsmoking popula t ion I tseems implausible that adverse health effects wouldoccur at background bodv burdens if these subtle bio-chemical changes have not been observed.

Conclusion. In summary, we do not believe tha tthere is sufficient scientific evidence to conclude thatadverse human health effects should be expected ator near current background body burdens. \\e urgethe scientific community to examine the issues care-fully. A credible and scientifically defensible est i-mate of potential human health risks from expo-sure to dioxin-like compounds will emerge onl\ artera thorough and critical peer review.

References; l i Fingernui, M A et al -V Engi I Med 1991, 324. 2 1 2 - I H2) Bertazzi. P A. et al Epidemiol 1993. •;i5], 398-40631 M a b l v . T A et al Toxicoi AppI Pliarmacol 1992, !1-1.^~-

107-tl Reier. S E e; al Fund Appt Toxicoi 1993, 21 433-415i Egeland.G M et al Am I Epidemic! 1994. !39. 272-81

i,bl Siveenv, M H et al "Prevalence of Diabetes and He-\ aled Serum Glucose Levels in Workers Exposed to 2.3 7 y-I e ( r a c h l o r o d i b e n z o - P - D i o \ i n i r C D U l ' , 12th I m e r n a -l i o n a l S \n ipoa iu tn on O|O\I[T) and Rela ted Lornpuuna- irainpere, [- inland. ^u^uit 1992

7 i l u c i e r . l i \\ b.ni'iroii To\icol Chem 1991 10 727- ' iH i \ \ o n p I k . sloop, I . l.ucier. G \V lexical -\ppi Phii'in

1986. H5. hO-68^ , l u n n o r ei ;il (:a ncer Res 1984 -f •I W}if

^HS ENVIRON Expert Panel on Dioxin Risk Character-iznTinn is a ^rotip of scientists assembled hv the E\'\ !-K().\ (.orpoiation on behalfofthe Ameru an barest andPaper Association iM-'&PA! to conduct ci rigorous tivelr t . ' i ' n ' t i ' of l:P.\s risk characterisation of dio\in t - ' i r r i -ons e.\perr panels hare commented on the draft ' ' u t t ' -nf-ihe-science chapters i\sued I ' v iPA and the eir.de-unolo^ic literature on dioxin ^support for these panelshas heeii prorided liv At'&PA iritliour regard to [ l i r r u i ! -i nine at the pcinet deliberations Panel members are Rciv-mond S (iieeiiberg. Emon,' l,lnirersit\', School of i ' n l ' -/IC l l e a l t l l . ! l ) S t ' p l l Morgolick. Johns Hopkins Unire'-'iiv.S( liool ot Hv^iene and Public Health. Donald R '•!cn-tison. Unnvrsm' ot Pittsburgh. School of Public Health.Peter Mnnson. Silrer ,S/?r;«^. MD. .\llan B Okev. ! . J ' n -I ' i ' l s l t v o l loioiilo. Department of Pharmacolog\', LiovidI O i l i ' e . } ( i ! e Unirersirv Scliool of ^fedicine. Depart-ment of Obstetrics and C,\'necolovr\-. Man Poland. i J i n -r < ' i s i [ y 0] \\'i>coiiMn-\ladison. l)i .fartinent ofOn^ol-o^v timi l n \ e p l s \ l i o d r i c k ^ . l.arisa Rtidenko n i i i iIhomas \ttiir. I..\\ IHO\'f,orpoia!!on. Arlington. . •

D I 0 X I N R I S K

Incinerators Targeted by EPANew limits proposed for biggest dioxin generators

I E F F J O H N S O N

i hen EPA officials announced the re-sults of the dioxin draft reassess-ment last September, they homed inon one particular industry for regu-latory action—waste incinerators—and laid out plans to cut dioxin emis-

sions drastically over several years. The proposedlimits, together with the heightened concern abouthealth effects from dioxin revealed by the reassess-ment, have breathed new life into an old debate overincinerator emissions and how to control them.

Environmental groups have long called for cut-ting what goes into an incinerator, be it paper, leadbatteries, or chlorine-based products that producedioxin when burned. The Agency, however, decidedto come out with limits based on what can beachieved by emissions controls, rather than relv onwaste stream limits or similar "pollution preven-tion" approaches. That choice is sure to be dis-cussed as EPA considers a final technological solu-tion to cut dioxin emissions.

"Waste combustion accounts for about 95% of allthe known dioxin emissions," Lynn Goldman. EPA as-sistant administrator for prevenuon, pesucides. and tox-ics. said in September when releasing the draft reas-sessment. "Medical and municipal waste combustiondominates combustion sources." she added How-ever, she said that any overhaul of environmental reg-ulations based on the draft reassessment must \vait un-til the draft is finalized in September 1995. Meanwhile,EPA will continue to "move forward in implementingits dioxin control programs," and at the top of EPA's list,according to Goldman, are incinerators.

Demonstrating Agency action, Goldman pointed toproposed air pollution control regulations for some 171municipal solid waste (MSW) incinerators issued un-der a court order Sept. 1, 1994 {[-"ederal Register, 1994,59. 48198, Federal Register, 1994, 59, 48228), and an up-coming proposal for 6700 burners of medical waste,which EPA is under court order to issue by February.

The MSW and hospital waste proposals are ex-

Keeping chlorinated products out of the incinerator wastestream is the strategy environmental groups are advocatingto reduce dioxin emissions

peered to be s i m i l a r and based on the same tech-nology GoldiTicin said tha t once implemented, theregulations 'vould rut emissions b\ 99°ii for the \\orstp o l l u t e r s I he \1S\\ proposal wou ld cover manysmaller un i t s tor (he l i r s t t ime and would bring allincinera tors up t i ) ne\v stand; Is. 1-or medical wasteinc ' inera iDrs . the proposal w i l l set the t i r s t federal lyrequired con t ro l s

Ihese two incinerator types contribute 20-50"o ofall dioxins (hat drift to 1'arth through air deposition, ac-cording to l.PA's (.\pusure estimate. Some 8100 got di-o\in p -r year come tnun these incinerators out of a to-tal ot 9 i(H) g emitleil in the atmospheie by all incinerator

What HaiHwed to Palp and Paper?Notably missing from this latest dioxm debate is the pulp and paperindustry. Once the proverbial bad guy in the dioxm controversy be-cause of its toxic emissions to lakes, streams, and oceans from thepulp-bleaching process, the nation's paper industry appears to beslipping off EPA's radar screen as it implements measures to cutchlorine use and reduce dioxins.

Cleanup in this industry, characterized by EPA as the nation'sthird largest polluter, is being driven by a proposed air-water "clus-ter" regulation that would cut annual dioxin emissions from 300 g to30 g. The proposed rule does not call for compliance until 1998, butthe industry is shifting from elemental chlorine pulp-bleaching pro-cesses to more benign ones and plans to cut dioxin emissions towater to "non(i—cf tevets by 1996, says Barry Polsky, of theAmerican Forest and Paper Association. But Polsky says the indus-try must continue to use some chlorine for pulp bleaching.

Hov.dver, 50 environmental groups want the industry to move tototalry chlorine free (TCP) pulp bleaching, eliminating all dioxm emis-sions, according to Jessica Landman, an attorney with the NaturalResources Defense Council. "Smart companies," Landman says,"should get out of the chlorine-using regulatory universe."

Ita—lf «• U.S. industry's professed reluctance to endorse TCPpulp, sections of the paper and pulp industry are quietly consideringthe advantages, several Industry sources say. But so far, most largecompanies sae TCP putp and paper only as a "niche" market thatdoes not merit the costs of n«w equipment and processes.

Several industry officials say this may change, and if it does, theindustry will follow the lead of Louisiana Pacific's Somoa, CA, pulpmill as weU as that of four or five smaller U.S. TCF mills.

Archie Beaton, director of the Chlorine Free Products Associa-tion, a trade group of paper companies, pnnters, and others in thepaper industry, says there are 68 TCF mills in the worid, hut fewerthan a dozen are in North America. He predicts that number willgrow as pulp mitts find it difficult to comply with cluster regulationemissions limits without dumping chlorine and as paper makersdiscover that customers want to buy paper made with TCF pulp.The industry, Beaton says, has even come up with a new logo forcrriorine-froe products: three dolphins chasing each others' tails.

—JEFF JOHNSON

sources, EPA says These figures are mid-point aver-ages with huge variances, however. The Agency be-lieves 2900-22.700 grams per \ear may come from allknown anthropogenic air sources. Bu t when un-kJ-iown sources and recirculanng dioxin are counted,EPA says as much as 50,000 g ma\ be raining down eachvear on the United States. These figures are in "toxicequivalents" (TEQ) for all dioxins and furans. based onthe toxicity of2,3,7,8-TCDD

No cause for panicNoting the variance in estimates and unmeasured andunknown sources, sc ient is ts point to the uncer-tainty of the figures, and crit ics—particularly thosein the regulated community—charge that incinera-tor operators are unfai r ly singled out. However, EPA

' officials note that air deposition of dioxin affects themost people and is the pathway with (he greatest im-pact on human health through bioaccumulation inthe food chain. Although there was "no cause for fearand panic," Goldman noted, "there was cause for gov-ernment to move forward on controlling risks."

The proposed MSW incinerator regulations would

reduce emissions to a level now achieved bv 'he top12"o of U.S. incinerators, EPA says. using a combi-nation of air scrubbers and baghouses coupled withinjection of activated carbon to capture dioxins and"good operating procedures" to limn their forma-tion. The proposal is scheduled to become final inSeptember 1995, and operators will have up to threeyears to comply. The dioxin requirements are part ofa general regulatory package to limit all emissionsfrom these burners. EPA says compliance with therule will cost the industry $450 million and force 60%of incinerator operators to install new scrubbers.

The-proposed medical waste incinerator stan-dards are expected to shut down many small, on-site operations, a boon for commercial incineratorcompanies that hope to step into the void.

The regulations, EPA says, will cut annual MSW di-oxin emissions to 30 g from 3000 g, and similar reduc-tions are expected from medical waste burners that pro-duce some 5100 g per year. But the technology-basedemissions controls upon which the emissions limits arebased are primarily "end-of-pipe" techniques, some-thing EPA has pledged to avoid. And although less di-oxm will go out the smokestack, it is unclear how muchless will actually be generated or how much will be cap-tured and shifted from air to ash to landfill.

The Agency's decision to rely on controls ran-kles environmentalists. "EPA is relying on the dis-credited strategy of sticking a control on a source ofpollution," says Barry Commoner, director of the Cen-ter for Biology of Natural Systems, Queens College,City University of New York. "Instead of attemptingto recapture the dioxin in a stack-gas scrubber—which is never perfect and only shifts the problemfrom stack emissions to fly ash precipitated in thescrubber—dioxin production can be prevented by us-ing intensive recycling programs."

Chlorine criticsCommoner targets chlorinated products, especiallythose made from polyvinyl chloride (PVC) that arehigh in chlorine. He urges that these products be keptout of the waste stream or that fewer be produced."In the long run, as long as chlorine is used, therewill be dioxin," he savs.

Environmentalists also say the proposed stan-dards are too weak and not reflective of reductionsachievable by top-performing MSW incinerators. Theyadvocate immediate implementation of toughenedemissions limits. But the overall focus of Green-peace, the Natural Resources Defense Council, theSierra Club, and others is on a general reduction inchlorine use in plastic and paper products and, at am i n i m u m , a mandatory nat ional recycling pro-gram for plastics to keep most chlorinated prod-ucts out of incinerator feedstock.

"It is not just recycling but redesigning the makeupof toxic sources," Marjone Clarke, a solid waste con-sultant w i th INFORM (New York City), says. "Weshould be substituting less toxic sources—in partic-ular. phas ing out polyvinyl chloride and paperbleached with chlorine. Add scrubbers and do therest, but we've got to do more than that."

Environmentalists have been joined by a heter-ogeneous chorus of dioxin and chlorine critics fromthe Great Lakes International Joint Commission to

health groups such as the American Public Health\ssociation, the Michigan State MeJical Society, andthe Genesee County (Flint, Ml) Medical Society

But William Carroll, a staff scientist with the Chlo-rine Chemistry Council of the Chemical Manufac-ture: J Association, disagrees: "Removing plastics fromthe waste stream may be a good thing to do but itwon't make much difference in dioxin emissions."

Further complicating an assessment of the role ofchlorinated products in dioxin generation and thebenefits of removing them from the waste stream areconflicting studies cited by both sides {1-4).

Emission controlsMeanwhile, EPA is moving ahead on incinerator emis-sions controls and has developed dioxin limits basedon what its engineers think a state-of-the-art MSWincinerator can achieve. In explaining current MSWincineration theory, David Cleverly, an EPA environ-mental scientist, and John Schaum, chief of EPA's ex-posure anicimrnt methods branch, emphasize thatdioxin formation depends in large part on what hap-pens in the seconds after trash is burned in the pri-mary combustion chamber. Although some dioxin isfound in municipal waste and not destroyed dur-ing the bum, this is probably not a major source, theysay. More frequently, dioxins are formed during ther-mal breakdown and molecular rearrangement ofchlorinated compounds, organic materials, and tracemetals during and after incineration.

Dioxin formation requires chlorine to be avail-able in some form in the MSW feedstock, but the ac-tual formation of dioxin takes place away from thecombustion chamber after gases, fly ash, and mis-cellaneous combustion products have began to cooland condense. For instance, when a material high inchlorine, like PVC, is burned, hydrogen chloride gas,chlorinated benzene, or other compounds that mayhelp form dioxin are created. Dioxin itself is formedas the flue gas moves away from the combustion zoneand into flue gas cleaning equipment.

Dioxin forms best at about 300 °C after combus-tion gases leave the 1000 °C combustion zone. Cur-rently, the best pollution control technologies rely onsystems to block dioxin formation by rapidly cool-;ng postmcineration gases with a spray dryer and col-lecting dioxin that does form with a scrubber afterit is bound to fly ash or activated carbon. Cleverlynotes that "in an ideal system, you would prevent di-

' oxm from being formed. That would be pollution pre-vent ion." Good combustion practices and use of aspray dryer to cool gases would fall into the cate-gory of pollution prevention, according to Cleverly.Among other systems in the pollution preventionrealm. Cleverly savs, are technologies to collect hy-drogen chloride gas before it leaves the combus-tion zone and systems for adding sulfur-based com-pounds that could stop the dioxin formation process.

These technologies and others that cut the amountot dioxin generated are being evaluated by EPA andindustry scientists, savs lames Kil^rnp. manager ofEPA's municipal waste combustion program.

EPA is building a pilot-scale incinerator at Re-search Triangle Park to learn more about the forma-tion of dioxin and to test dioxin inhibitors and the ef-lecl of temperature. A major objective of the research

incinerator. Kilgroe savs, will be to determine the ef-fect of waste composition on the formation of dioxin.

When asked whether data support removing PVCsand plastics, Kilgroe says, "There is no conclusive ev-idence that removing certain components will havea major effect on emissions. There '.s still enoughchlorine available in the waste to form dioxins, andremoving plastics will probably not reduce emis-sions to levels required by EPA's proposal."

RecycHMf ontionSchaum and Cleverly emphasize, however, that the reg-ulations do not prevent a community from trying to re-duce diorin emissions by limiting plastics, PVCs, orother chlorine sources in the waste stream. But it is upto the community or incinerator company to put sucha program together, although the proposed regula-tion does require communities to investigate recy-cling plans that could include the removal of chlori-nated wastes when new incinerators are sited.

One problem with removing chlorinated wastes,according to industry and EPA sources, is that plas-tics bum well. Along with paper, they conmbute mostof the heat content in municipal solid waste refuse,and their removal would result in a verv low Btu andinefficient operations, especially for waste-to-energy incinerations.

"What would you have left to bum?" an EPA sourceasks. "When you reduce the heat content of fuel, it willbe more difficult for incinerators to run economicallyand to generate sufficient energy through the wastes."

Less waste to burn and the loss of an efficient fuel,along with new emissions standards, is a scenario theincinerator industry does not want to see, espe-cially as the costs of its chief competitor, landfills,ketp looking cheaper to city officials.

A recent case the industry hopes to avoid repeat-ing is that of an 11-vear-old incinerator in Colum-bus, OH. Last year, EPA found that the Columbus in-cinerator was one of the nation's largest dioxinemitters, pumping some 900 g of dioxin TEQ into theair each year, about 30 times more than the Agencyhopes all 171 MSW incinerators will emit once thenew regulations are in place. The cost to comply withthe proposed regulations was said to be S65 mil-lion Meanwnile Ohio landfills were charging $32 aton to take in trash; the incinerator needed $49 a tonto break even—without the new equipment.

"When we first built the plant we assumed thatlandfill acreage would shrink, the price of electric-ity would increase, and recycling would not cut oursource of waste," savs Kirk McCov, public affairs of-ficial at the plant. "None of that happened. Now wecan't pay off the incinerator." In November the fa-cility's directors voted to shut the plant down

References[ 1 ) Boerekamps-Kaniers . I . l.ouw. R F i n a l Report R U l -

\'ROM Pro|ect, Department ot Cliemistrv, University of Lei-den, Fhe Netherlands, IW.i

[ 2 1 lohnke, B . iiteizner E l\iisle Manage Res 1992. 10. 345Mark. F Association of Pln'itics Manufacturers in EuropeTechnical Paper 1994Theisen. I el al. Chemosphere 1989, ;9, 423

Jeff lohnson is an associate editor on the WashingtonftaffofES&iT