Document Z51o7yXbj9OgXO5v2bvgE3xd

A Divispnof The Society of The Plastics Industry, Inc. Robert H. Burnett Executive Director August 12, 1994 TO: VI Executive Board RE: Greenpeace Attack Enclosed for your reading pleasure is the latest assault by our friends at Greenpeace - "Achieving Zero Dioxin". By any measure, it is the slickest and most professional looking document they have produced, but as usual, riddled with inaccuracies and outright false statements. As a top priority, we have asked Edward Howard and Company along with several member company representatives to take this apart and highlight the PVC-specific areas that require refutation. The format and distribution of our rebuttal will be similar to that used for the "Truth About Vinyl" piece which is our response to the Greenpeace handout at NPE entitled "No Future for PVC". We anticipate having this for final review and distribution no later than Monday, August 22. RHB/pmb cc: Issues Management Committee J. Svalander, ECVM T. Matsui, JPA L. Freeman, SPI P. de la Cruz, K&H B. Lienhart, CCC CTL014381 65 Madison Avenue Morristown, NJ 07960 (201) 898-6699 Fax ft (201) 898-6633 Th$ onQWl cQ0y of 9** locum**pnmd on meydtdpap*. Achieving ZERO Dioxin An Emergency Strategy for Dioxin Elimination SfteeNneacr CTL014382 ACHIEVING ZERO DIOXIN An Emergency Strategy for Dioxin Elimination by Joe Thornton Greenpeace Chlorine-Free Campaign 1436 U Street NW Washington DC 20009 Thanks to Rick Hind, Lisa Finaldi, Jack Weinberg, Scott Brown, Lynn Thorp, and Tom Webster for their review and assistance in the preparation of this document, and to the . . 4 million Greenpeace supporters who made this report possible. Printed on totally chlorine-free paper. July 1994 CTL014383 -i - :rcoc TABLE OF CONTENTS Summary of findngs 4 EPA's Dioxin Reassessment: New Science on Dioxin Toxicity. Exposure to dioxin Trends in dioxin contamination Roots of the reassessment finding #1: "Background" dioxin pollution is a hazard to public health finding #2: Cancer hazard to humans finding #3: Severe effects on reproduction and development finding #4: No safe dose 11 Formation of Dioxin ...................................................................................................................................... Dioxin and Chlorine Chemistry Other sources: The Myth of "Natural Dioxin" 20 Priority Sectors: Major Dioxin Sources......................................................................................................... Incineration of chlorine-containing wastes Chlorine bleaching at pulp and paper mills PVC plastic 28 Secondary Sectors: Other Dioxin Sources ................................................................................................... Chlorine production / Chlor-alkali process Pesticides Chlorinated Solvents Water and wastewater chlorination Chlorinated aromatic chemicals Other chlorinated organic chemicals Inorganic chemicals: metal chlorides and bleaches Metallurgical processes Environmental transformation of other organochlorines 38 Recommendations: A National Strategy for Dioxin Bminartion.................................................................... 45 Need for Emergency Action Principles of the Zero Dioxin Strategy Step 1: General policy changes Step 2: Immediate action in priority dioxin sectors Step 3: Other dioxin sources: Begin phase-out of chlorine chemistry Political and economic implications References............................................................................................................................................. -..... 51 CTL014384 2- - Tables and Figures Table 1.1 Summary of Processes That Form Dioxin and Related Compounds ............................... 9 Figure 2.1 Dioxin Body Burdens in Selected Countries.............................................................. 11 Figure 2.2 Trends in Dioxin Contamination in Great Lakes Sediments .......................................... 13 Table 2.1 Health Effects Associated with Dioxin and Related Compounds ................................... 1-7 Table 3.1. Dioxins in Ash from Burning Organochlorines vs. Chloride Salts ................................... 23 Figure 3.1. Dioxin Concentrations in Ancient and Modem Humans .............................................. 24 Table 3.2 Pesticides with Dioxin Contamination Known or Suspected ........................................ 26 Table 3.3 Industrial Chemicals with Dioxin Contamination Known or Suspected ........................... 27 Table 3.4 Pesticides with Hexachlorobenzene Contamination Known or Suspected ......................... 27 Table 3.5 Industrial Chemicals with Hexachlorbenzene Contamination Known or Suspected.............. 27 Table 4.1 Dioxin Releases from Incinerators ............ 29 Table 4.2 Dioxin Releases from Pulp Mills ............................................................................. 30 Table 4.3 Dioxin Releases from PVC Lifecycle................................................................'...... 31 Table 4.4 Dioxin in PVC Plastic Products.............................................................................. 32 Table 4.5 Dioxin Releases from ICI's Modem EDC/VCM Facility in Wilhelmshaven, Germany............. 33 Table 4.6 Dioxins in Effluent and Soild from Two EDC/VCM Plants in Europe....... :....................... 34 Table 5.1. Dioxins in Waste From A Modem Chlor-Alkali Plant.................................................... 39 Table 5.2 Solvents and Other Apliphatic Organochlorines Contaminated with Dioxin-Like Compounds . 40 Table 5.3 Dioxin and Related Compounds in Inorganic Chlorides ..................................... 43 t CTL014385 3- xocc. SUMMARY OF FINDINGS EPA's scientific reassessment of dioxin indicates that dioxin pollution poses a large-scale, long-term threat to public health and the environment. Although the reassessment has not yet been released in final form, EPA documents associated with the project - published scientific papers, released draft chapters, public presentations, and research updates- make the following points dear: Dioxin concentrations in the food supply and the bodies of the general human population are now in the range at which effects on reproduction, development and the immune system are known to occur in laboratory animals. Health damage has been documented in humans at dioxin body burdens just slightly higher than those found in the general population. And a substantial body of evidence indicates that wildlife populations are experienring reproductive and developmental effects at background concentrations of dioxins and related compounds. The developing infant and fetus are at the greatest risk from dioxin exposure. At very low doses, dioxin can lead to permanent hormonal changes, birth defects, reduced sperm count infertility, endometriosis, and impaired ability to learn. Dioxin is also a very potent immune suppressor, leading to increased susceptibility to infectious disease. The weight of evidence indicates that dioxin causes cancer in humans. Cunent "background" dioxin contamination results in cancer risks to the general population ranging from 1 in 1,000 to 1 in 10,000. These risk estimates suggest that dioxin is responsible for 350 to 3500 cancers in the U.S. annually. There does not appear to be a threshold or "safe dose* below which effects do not occur. EPA's research has been unable to identify a level of exposure, no matter how low, at which dioxin does not bind to rts receptor, interact with DNA, and induce enzymes and growth factors that are involved in both cancer and non-cancer effects. This body of evidence suggests that dioxin exposure may be causing subtle effects now among large sectors of the general public, but the lack of an uncontaminated control group makes rt impossible to determine with certainty whether this is the case. The data dearly shows, however, that existing environmental concentrations of dioxin place the human population at risk, and any increase in these concentrations will increase that risk and/or the severity and number of persons affected. Because the potential health damage is severe - and because the entire public is exposed and potentially affected - this situation calls for immediate action to reduce human exposure to dioxin and prevent further dioxin releases. DIOXIN IS FORMED THROUGHOUT CHLORINE CHEMISTRY Dioxin is never manufactured on purpose. It is formed as an unintentional by-product in scores of processes in which chlorine and chlorine-derived chemicals are produced, used, and disposed. In fact, the evidence suggests that virtually or absolutely all chlorine-related products and processes are associated with dioxin formation at some point in their lifecyde. The many industrial processes in which the formation of dioxins and related compounds has been identified are shown in table 1.1. The formation of dioxin begins with the production of chlorine gas itself in the "chlor-alkali" process. It was formerly believed that only older facilities using graphite electrodes produced dioxin, but new Swedish data indicate that dioxins are formed in even the most modem chlor-alkali plants with titanium electrodes. Because the production of chlorine itself results in dioxin formation, all "downstream" processes in which chlorine is used are linked to dioxin, as well. :xxo: cTL014386 -4 - Dioxin appears to be formed whenever chlorine is used in industrial processes in the presence of organic (carbon-containing) substances. Thus, dioxin and related compounds have been identified from pulp mills that use chlorine or chlorine dioxide bleach; from chemical plants that use chlorine to produce other chemicals; from metallurgical plants that use chlorine to produce refined metals; and even from the use of chlorine to disinfect water and wastewater. Dioxin is formed as a by-product when chlorine is used to produce organochlorine chemicals, it has long been recognized that dioxins occur iri the production of aromatic (benzene-based) organochlorines, such as chlorobenzene, chlorophenols, PCBs, and many pesticides. But dioxin is also formed in the manufacture of the full range of organochlorines, from the simple to the complex, from cyclic to aliphatic compounds, including solvents, feedstocks for PVC plastic, and specialty chemicals and intermediates. In addition, dioxins have been identified in some inorganic chlorine compounds, such as feme and copper chlorides and hypochlorite bleach. Dioxins can also be formed when chlorinated organic chemicals are used - particularly in environments that are reactive, heated, or alkaline. Thus, dioxins are formed when chlorinated solvents are used as degreasing agents along with sodium hydroxide', when chlorinated chemicals are burned in vehicle fuels as scavengers or additives, when organochlorine catalysts are used in oil refining, and when organochlorine pesticides are heated in the pressure-treatment of lumber. In addition, dioxins can also be formed when organochlorines are used as intermediates in the production of other chemicals - even those in which chlorine does not appear in the final product such as the pesticide parathion or the chemical nitrophenol. Dioxins are even formed when some other organochlorines, such as chlorophenols, are released into the environment and are then subject to biological, physical, or chemical transformation. Finally, dioxins are formed whenever any organochlorine chemical - product or waste - is burned. Combustion is the largest sector of dioxin sources, and dioxins have been identified from all types of incinerators that bum organochlorines, including incinerators for hazardous waste, garbage, medical waste, sewage sludge, and so on. Dioxins are also formed when organochlorines are introduced Into combustion-based recycling processes - such as when PVC-coated copper cables or automobiles are recycled in secondary smelters. Very large quantities of dioxin are formed when chlorinated chemicals - particularly PVC plastic - bum in accidental fires at homes, offices, and industrial facilities. * RANKING DIOXIN SOURCES In Its reassessment documents, EPA makes a preliminary attempt to catalogue dioxin sources, identifying two of the largest known sources of dioxin: * Incinerators that bum chlorinated wastes, including garbage, hazardous waste, and hospital waste, along with other facility types in the combustion sectors; Pulp mills that use chlorine and chorine-dioxide bleaches. But EPA's list neglects dozens of other dioxin sources that have been identified in the scientific literature and government reports and underestimates actual emissions from incinerators. As a result, the agency's list accounts for only 10 to 50 percent of the 25,000 grams of dioxin that EPA estimates are deposited into the environment each year. Major sources neglected by EPA include the following; -5- * All references to EPA's dioxin source estimates are based on EPA reassessment documents prior to July 1994. Future EPA documents may revise these estimates. CTL014387 :rccc  Chemical industry. Diox'n is produced in the manufacture of chlorine and a full range of chlorinated organic chemicals, including PVC, pesticides, solvents, and other chemicals used in rubber, dyes, plastics, and other products. PVC plastic. Throughout its lifecycle, PVC appears to be responsible for more dioxin formation than any other product. When PVC feedstocks are manufactured, large quantities of dioxins are formed and are released in air emissions, water releases, solid and liquid wastes. Recent Swedish studies have found that the PVC plastic itself is contaminated with dioxin. PVC is also the largest source of chlorine - and thus the major dioxin precursor - in most of the largest combustion sources of dioxin, including hospital waste incinerators, trash incinerators, and copper and steel smelters. Finally, the accidental burning of PVC in home and building fires appears to be an extremely large dioxin source. Preliminary estimates suggest that PVC may account for up to one-third of all dioxin formation. Garbage incinerators. EPA's estimate of combined dioxin emissions from the nation's 120 garbage incinerators is 15 times lower than measured dioxin emissions from a single incinerator in Columbus, Ohio. Garbage burners appear to be the largest point sources of dioxin, with total nationwide emissions hundereds of times higher than EPA estimates. Cement kilns that bum hazardous waste. High dioxin emissions have been documented from these facilities, in which more hazardous waste is burned than in officially designated "incinerators." Hazardous waste incinerators. EPA underestimates actual emissions from these facilities by basing its estimate on a trial bum at a single facility. Data from real incinerators - which operate under non-optimal or upset conditions - indicate that EPA has underestimated actual dioxin releases by more than 20 times. Ash and dusts from all types of waste incinerators, which may carry up to 100 times more dioxin into the environment than air emissions. Metallurgical industries in which chlorine or organochlorines are present such as the steel, nickel, and magnesium industries. Environmental transformation - other organochlorines released into the environment can be transformed into dioxins by natural processes. EMERGENCY ACTION : A NATIONAL STRATEGY FOR DIOXIN ELIMINATION The emerging science makes dear that cunent dioxin contamination poses a serious threat to public health and the environment with future generations at the greatest risk if dioxin pollution continues. Because these compounds are so persistent in tire environment and the human body, dioxins that havi already accumulated will not disappear quickly. In response to its findings, EPA should initiate a comprehensive national dioxin elimination program, with the goal of redudng human exposure and preventing the formation and discharge of dioxin into the environment from all sources. The program should be based on these prindples: Zero means zero. Dioxin releases must be eliminated, not simply reduced. Because dioxin is so persistent, the ecosystem has no capacity to safely "assimilate" dioxin inputs. Even dilute discharges build up'm the environment over time, eventually reaching unacceptable concentrations. Thus, zero is the only acceptable discharge of dioxin, and the current crisis demonstrates the failure of the "acceptable discharge' approach to persistent toxic substances. Given the current health threat it would be wholly inappropriate for EPA to permit the continued release of any additional dioxin into the environment. Pollution prevention, not control. Once dioxin is produced, it is too late to prevent its discharge into the environment; pollution control devices, filters, treatment systems, and disposal methods such as burning and burying simply shift captured chemicals from one environmental medium to another or delay their release until a later date. Dioxin discharges can be eliminated only through primary prevention: industrial processes and feedstocks that result in dioxin formation must be changed so that no dioxin is formed. :xxxx CTL014388 6- - Because dioxin occurs throughout the field of chlorine chemistry, this goal appears to require the planned phase-out of chlorine and chlorinated organic feedstocks from industrial processes. Address ell dioxin sources. EPA must address all known and suspected sources of dioxin in order to bring future releases of dioxin to zero. All identified dioxin sources must be subject to action, and EPA should inmate research to identify all unknown or suspected sources. * Set priorities. Because dioxin is associated with the many uses of chlorine in our industrial economy, eliminating dioxin will require substantial technical and economic conversion. The largest dioxin-producing sectors for which the alternatives are available and feasible now should be subject to immediate action. Sectors that require longer implementation phases should be placed on timelines for dioxin elimination. STEP 1: GENERAL POLICY CHANGES 1. National poGcy. EPA should establish a national Zero Dioxin program with the goal of eliminating the formation and release of dioxin within 10 years, through the elimination of those products, feedstocks, and processes that lead to dioxin formation. 2. Moratorium on new dioxin permits. EPA should grant no new permits for facilities to release dioxin into any environmental medium. 3. Sunset existing dioxin permits. EPA should modify all existing dioxin release permits to include timetables for the reduction and eventual elimination of all dioxin releases. 4. Comprehensive approach to ell sources. For the many dioxin sources that are not currentiy permitted or regulated, EPA should begin a process to identify and prioritize all dioxin, sources and require their elimination within 10 years. All facilities that manufacture, use, or dispose of chlorine or chlorinated organic chemicals should be required to test for dioxin formation in their products, processes and wastes. Any identifiable release of dioxin and related compounds should be reported under federal Right-to-Know programs. STEP 2: IMMEDIATE PRIORITIES: PHASE-OUT MAJOR DIOXIN SOURCES EPA should take immediate action in the largest dioxin-produdng sectors. In these s^ptors, regulatory action can have the most significant impact on total dioxin pollution. 1. Indneration. Incinerators that bum chlorinated wastes are the largest known producers of dioxin. EPA should take the following actions: Race an immediate moratorium on permits for new combustion facilities that bum chlorinated wastes and on permits for expanded capacity at existing units. Modify immediately all permits for combustion devices to include sunset provisions to reduce and finally eliminate the input of chlorinated wastes and products. This policy should indude indnerators, boilers, kilns and furnaces that bum hazardous wastes; indnerators for trash, hospital waste, sewage sludge, tires, and soils; and metal smelters. Minimize the burning of chloride-containing wastes (i.e., food and yard wastes) through trash separation programs. In turn, focus waste reduction programs on eliminating the generation of chlorinated indnerable wastes, particularly solvents, PVC, and wastes from the production and use of chlorinated substances in the chemical industry. Immediately ban the' addition of chlorinated compounds to fuels, including gasoline, diesel, and others. -7 - :xxxx CTL014389 2. Pu(p and Paper. The use of chlorine, chlorine dioxide, and other chlorine-based bleaches in the paper industry is the largest source of dioxin discharges directly to waterways and one of the largest dioxin-producing sectors overall. In other parts of the world, totally chlorine-free pulp bleaching is rapidly becoming the industry standard. EPA should establish rapid timelines for the phase-out of all chlorine-based bleaches in the pulp and paper industry. 3. PVC plastic. Throughout its lifecycle, PVC results in more dioxin formation than any other single product. EPA should immediately establish a PVC phase-out program, with progressive reductions toward zero in the production and use of PVC. Particularly rapid phase-outs should be applied to short-life uses of PVC (packaging, toys, etc.), PVC in areas susceptible to fire (construction, appliances, and automobiles), and PVC in products that are recycled in combustion-based processes (i.e., cables and cars). EPA should also modify all discharge permits for chemical plants that produce PVC feedstocks to indude sunset provisions on dioxin discharges to all environmental media. STEP 3: SECONDARY ACTIONS: PHASE-OUT OTHER CHLORINE USES While immediate action occurs in the priority sectors discussed above, the following dioxin-producing sectors should be placed on timetables for phase-out. 1. Chlorinated solvents. In production, inrineration, and some uses, chlorinated solvents cause dioxin formation. EPA should establish a rapid timetables for phasing-out the production and use of these chemicals. 2. Chlorine-related pestiddes. Dioxins are formed in the production, some uses, and disposal of chlorine-containing pestiddes and in the production of non-chlorinated pestiddes made with chlorinated intermediates. EPA should establish a phase-out timetable for all chlorine-related pestiddes. 3. Other chlorinated organic chemicals. Dioxins are formed in the production, some uses, and disposal of other chlorinated organic chemicals, such as intermediates, catalysts, and spedalty chemicals. EPA should establish timelines for phasing-out the production and use of all other chlorinated organic chemicals. Any uses that serve a compelling sodal need (i.e.,pharmaceuticals) for which alternatives may not yet be available should receive temporary exemptions. * 4. Metallurgy and inorganic chemicals involving chlorine: Dioxins are formed when chlorine and chlorinated compounds are used in metallurgical processes and in the production of some inorganic chlorinated chemicals. EPA should establish phase-out timetables for the use of chlorine in high-temperature metallurgy, and for the manufacture of inorganic chlorinated chemicals associated with dioxin formation. 5. Wastewater treatment Dioxins and related compounds are formed in the chlorination of drinking water and sewage and in the incineration of sludge from wastewater treatment plants. EPA should establish timelines for the implementation of chlorine-free water treatment methods while insuring that adequate disinfection continues. In most cases, chlorine-free methods for water disinfection can be implemented more quickly than the use of chlorine as a residual can be eliminated. 6. Remediation. A substantial quantity of dioxin and PCB-contaminated materials are now present in landfills, sediments, and extant industrial wastes. EPA should intensify the development and application of non-combustion methods for degradation of these materials. :nxc CTL014390 -8- TABLE 1.1. SUMMARY Of PROCESS THAT FORM DfOXIN AND RELATED CHEMICALS Production of chfarino gas Cttaine etecirofysis with jpphite electrodes Chlorine electrolysis with titartum electrodes Chenical industry-use of chlorine gas Chlorinated aromatic chemicals - manufacture (chlorobenzenes, chlorophenols, PCBs, others} Pesticides Dyes Specialty chemicals Chlorinated solvents - manufacture {trichloroethylene, tetrachloroetfryfene, carbon tetrachloride} PVC plastic-manufactureof feedstocks (ethylenedichloride, viryt.cnkxide) . . Production wastes Effluent. .. Stedge from effluent treatment. 1: . Air emissions - PVC plastic products .. Other alphatic oraanochtorines - marufacture fepichJorhydrin, hexBchlorobutacSene} Some inorganic chlorides -manufacture (ferric and copper cttorides. sodium hypochlorite)' Uses of chlorine gas - other industries * Ptip and paper - chlorine bleaching Mill effluent .. NBI sixtae Pulp and paper products Emissions from sludge incinerators Water and wastewater dissection Refined metals - manufacure with chlorine (Ni, Mg) '- Uses of organochlorines Manufacture of chlorine-free chemicals with chlorinated intermediates (nrtrophenols, paratfton, others) Degreasing/extraction with organochlorine solvents in Saline or reactive environments Oil retiring with organochlorine catalysts . Use of pesticides with heat (wood treatment etc.) Ironfetee sintering with oraanocttorineTcuttteg oils, solvents, or plastics * Burning gasoline or cfiesel fuel with organochlorine additives. . Use of chlorine-based bleaches and detergents in washing machines and tfehwashers Incineration, Recycling, arid Fire* (primary dtori precursor in parentheses) 4 Medical waste incinerators (PVC): Air emissions . 4 MunidpaJ waste incinerators {PVQ \ ." \. Air emissions Ash residues 4 Hazardous waste incinerators (solvents, chemical manjfacturteg wastes) . Air emissions Ash residues Cement kites burning hazardous waste (solvents, chemical manufacttaing wastes) Air emissions . Cement kiln dust Accidental fires in homes and offices (PVQ ,v , . Fires at industrial faculties (PVC, PCBs, other chlorinated chemicals) Alumirun recycling/smelting (PVC) Steel and automobile recycling/smelting (PVQ 4 Copper cable recyding/smelting (PVQ Aksninum recycfing/smelting (PVQ 4 Wood burning (pentachlorophenol wood preservatives, PVQ Envaonroental transformation Transformation of chlorophenols to dioxins in the environment 4 Addressed by EPA in documents related to its dioxin reassessment. (Oeverty 1993, Schaum 1993) List indudes sectors in which formation of dioxin or related compands (PCBs, chlorinated dibenzofurans, and/or hexachlorobenzene) has been confirmed in chemical analyses, as well as sectors in which dioxin formation is 'known or suspected' according to EPA (EPA 1980, EPA 1985, PCTN 1985} or NATO (Hutzinger 1988). 9- - xccc CTL014391 political and economic implications Because dioxin can be formed at some point in the lifecyde of all or virtually all chlorine-related processes, the only feasible method for preventing dioxin releases is to target the critical step - the production of chlorine and related compounds. Controlling dioxin formation at later steps in the chlorine "use-tree" would require specific regulations on scores of processes and thousands of chemicals. Because dioxin is an inevitable by-product of the field of industrial chlorine chemistry, addressing dioxin pollution requires a comprehensive approach to the class of chlorine-based products and processes. Numerous srierrtific and political institutions have called for a phase-out of chlorine chemistry in order to eliminate the formation and release of persistent toxic substances. For instance, the International Joint Commission on the Great Lakes has called on the U.S. and Canadian governments to bring to zero all discharges of persistent toxic substances to all environmental media; particularly priority was placed on the dioxin family. In 1992 and 1994, the UC recognized that dioxin formation occurs throughout the field of chlorine chemistry and that the mix of by-products formed in the lifecycle of chlorine and related compounds cannot be prevented or controlled. Thus, the UC has called on the governments to phase-out all uses of chlorine and chlorinated organic chemicals as industrial feedstocks. In 1993, the American Public Health Association made a similar recommendation, finding that "the only feasible and prudent approach to eliminating the release and discharge of chlorinated organic chemicals and consequent exposure is to avoid the use of chlorine and its compounds in manufacturing processes." APHA resolved that chlorinated organic compounds should be treated as a class for phase-out, with exceptions only for uses that can be demonstrated to pose no significant hazard or for which no alternatives can be found. In 1992 and 1993, the 15-nation Paris Convention on the Northeast Atlantic and the 21-nation Barcelona Convention on the Mediterranean Sea agreed that the discharge of persistent bioaccumulative toxic substances - particularly organohalogens such as dioxins - must be brought to zero on rapid timelines. And in early 1994, the White House itself began to move towards the comprehensive approach to the field of chlorine chemistry in its proposal for the Clean Water Act proposing to develop "a national strategy to reduce, substitute, or prohibit the use of chlorine and chlorinated compounds" in several important use sectors. For all major dioxin sources, chlorine-free alternatives are available and feasible now. There are few or no technical barriers to the elimination of dioxin releases associated with paper bleaching, PVC, solvents, sewage and drinking water disinfection, pesticides and many chemical manufacturing processes. In many cases, these alternatives result in direct economic benefits as investments in process changes are paid off with reduced costs for chemical procurement, pollution control and disposal, liability, increased resource efficiency, and more reliance on skilled labor then chemicals. But phasing out all dioxin sources will require substantial conversion. In some industries - particularly the manufacture of chlorine-based chemicals - the transformation may be difficult. Workers and communities should not bear the economic burden of changes to protect public health and the environment. The Zero Dioxin Strategy should be guided by a transition planning process involving labor, communities, and all other stakeholders. Revenue from a tax on on chlorine and related chemicals should be distributed to ensure that investment in alternative products and processes takes place in the same locations where chlorine-based processes were formerly used; it should also be used to protect, compensate, and provide future opportunities for workers and communities that are affected by conversion. :rccc CTL014392 - 10- 2: NEW SCIENCE ON DIOXIN HAZARDS Exposures to dioxin According to EPA, an average person in the U.S. is exposed to 3 to 6 picograms* of dioxin (TEQ) * * per kilogram of body weight per day, including dioxin-like PCBs. [EPA 1994] An average adult has accumulated a body burden of 40 to 60 parts per trillion in his or her fat. About 90 percent of these exposures occur due to contamination of the food supply, particularly through fish and animal products. The remainder occur through inhalation of contaminated air and ingestion of contaminated water. In most industrialized nations of the world, dioxin body burdens and exposures are in the same range as in the U.S.; levels are somewhat lower in developing nations. [Schecter 1991] Concentrations of dioxins in breast milk from numerous countries are shown in figure 2.1. Infants receive even higher exposures. Because mothers' milk is highly contaminated, an average infant that nurses for one year receives 60 pg/kg/day of dioxin, not including dioxirHike PCBs - 10 to 20 times greater than an average adult dose. An average infant receives 4 to 12 percent of his or her entire lifetime exposure within the first year of life - a critical period of development and sensitivity to toxic chemicals. Figure 2.1. Dioxin in Human Milk from Selected Countries S. Vietnam (Da Nang) S. Vietnam (Saigon) Germany Japan Canada USA Pakistan S. Africa (white) S. Africa (Hack) USSR N. Vietnam (Hanoi) Thailand HlHH Cambodh Source: Scheditor 1991 0 10 20 30 ppt TEQ (lipid basis) 40 * A picogram is one one-trtfonth of a gram. ~ TEQ. or toxic equivalents, expresses the total quantity of diotin-Ske compounds relative to the toxicity of 2.3,7,Wetrachlorodibenzo-p-dioxin. Unless noted, al values given in this document are expressed as TEQ. -11 - CTL014393 Once emitted into the environment dioxins persist for decades or centuries. Moreover, dioxins are also highly bioaccumulative, so they multiply in concentration as they move up the food chain. Thus, even dilute discharges of dioxin accumulate in the environment over time. Dioxins can also be transported long distances on air and water currents; wildlife migration and food shipments result in further dispersion. As a result dioxins contaminate the environment wildlife, and humans in areas thousands of miles from any known sources, including the Arctic and the deep oceans. Persons living near or woricing in facilities that are dioxin sources and those who consume higher-than-normal quantities of dioxin-corrtaminated foods are subject to even greater exposures. Trends in Dioxin Contamination When persistent toxic substances are released into the environment they are degraded slowly - if at all. Over time, these substances accumulate in air water, soil and sediment and bioaccumulation results in even higher concentrations in the foodweb and the bodies of the general population. Trends in contamination by these substances tend to follow this general pattern: new or increased discharges of a chemical result in slowly increasing environmental concentrations; the increase levels off when a 'steady-state" is reached - the point at which the rate of 'removal"- either through degradation or accumulation in sediments, soils, and vegetation - matches the rate of release. Any given rate of release will correspond to a specific steady state. Thus, if discharges are reduced, levels will slowly decline and then plateau at a new steady state. For instance, PCB concentrations in water and the food chain increased steadily from the 1940s to the 1960s, after which they leveled off. After the production of PCBs was banned in the 1970s, levels decreased during the 1980s. The decline has now stopped, however, plateauing at a level still considered unsafe. [UC 1991) Data on trends in dioxin contamination suggest a similar pattern. Sediment cores show that levels rose consistently from 1940 to 1970 and then reached a relatively steady state. [Czuczwa 1987] Regulatory changes in the 1970s - increased controls on some incinerators, restrictions on leaded gasoline (which contains chlorinated additives) and bans on several highly dioxin-contaminated pesticides - resulted in reduced dioxin emissions, after which concentrations declined slowly in Great Lakes sediments and in some but not all species of wildlife over the perioed 1977-1987. (Allan 1991 ] Data on trends in dioxin contamination of human tissues are very sparse but seem to fit this pattern. One study (Stanley 1990] found that levels may have decreased slightly in the 1980s following consistent increases during the preceding decades; "however, it is not known whether these declines were due to improvements in the analytical methods or actual reduction in body burden levels," according to EPA. [EPA 1994] If these declines are real, they probably reflect the pattern described above. According to Swedish scientists; "Within the Swedish Dioxin Survey, levels and trends of PCDD/PCDF have been determined in various media. During the last twenty years an overall decrease in the levels is recorded. The major part of this decrease dates back to the late 1970s and the early 1980s. The situation of today seems to be quite constant and resembles what has been found for PCB. Analyses of human breast milk show a similar trend. " [Johansson 1993] This pattern suggests that reducing industrial releases of persistent toxic substances will result in decreased contamination of the environment and human tissues. If releases continue at a reduced rate, CTL014394 - 12- concentrations will decline only until a new steady state is reached. Further, the "removal" of these substances at steady-state into sediments, soil, and vegetation is actually a form of accumulation, and at least some of these sequestered stores will eventually be released again into the ambient environment, where they will be available for uptake by wildlife and humans. Thus exposure to highly persistent and toxic substances and the build-up of these compounds in human tissues - can be prevented only if releases of these compounds are brough to zero. Figure 2.2. Trends in dioxin contamination in Great Lakes sediments. -----!----------i----------i----------i----------1---------- I i --I---------1-----------1----------f-- 1870 1880 1890 1900 1910 1920 1930 1940 1950 1960 1970 1980 Source: Czuczwa and Hites 1986. Roots of the Reassessment In April 1991, under pressure from the chlorine and paper industries, EPA announced a multi-year reassessment of the toxicity of dioxin. The project was ostensibly intended to incorporate into EPA regulations new science that had been developed since the agency last formulated dioxin policy in 1985. (Another reassessment, also begun under pressure from dioxin-producing industries, proposed in 1987 to weaken dioxin standards by a factor of 16, but was rejected by EPA's Science Advisory Board. [EPA 1988)) EPA announced the dioxin reassessment at the height of a scientific and public relations campaign in which dioxin-produdng industries and their scientists argued that new data on the mechanisms of dioxin's toxicity implied that dioxin is less of a hazard to human health than previously thought. In particular, an understanding had emerged that dioxin's effects begin when a molecule of the chemical binds to a "receptor" protein within the cell, then enters the cell nucleus and interacts with DNA to trigger a cascade of biochemical reactions, including the synthesis and metabolism of hormones, their receptors, enzymes, growth factors, and other substances. Industry had argued that dioxin's interaction with the receptor meant that dioxin was less -13- CtL014395 :rcccc. toxic than previously thought and that there would be a threshold, or safe dose of dioxin, below which no adverse effects would occur. [Bailey 1992] Contrary to the industry's intent, however, EPA's reassessment has concluded that dioxin is more toxic than previously thought and poses a significant hazard to the health of the general population. Although the final draft for public review is slated for release in summer 1994, drafts of the reassessment, research updates, published scientific papers and presentations, all by EPA and the scientists woricing on the reassessment clearly indicate the direction of EPA's final report. Finding #1:"Background" dioxin pollution is a threat to the general population. EPA's reassessment indicates that dioxin pollution threatens the health of the general public. Several lines of evidence support this conclusion. First, EPA scientists have concluded that the general population's current body burdens and exposures are already in the range at which health effects occur in laboratory animals, including rodents and primates. Persons subject to higher-tharvaverage exposures - because they live near local dioxin sources or regularly consume highly-contaminated foodstuffs - are at even greater risk. According to a draft of EPA's reassessment: Subtle changes in enzyme activity indicating liver changes, in levels of circulating reproductive hormones in males, in reduced glucose tolerance potentially indicative of risk of diabetes, and in cellular changes related to immune function suggest the potential for adverse impacts on human metabolism, reproductive biology, and immune competence at or within one order of magnitude of average background body burden levels.... Individuals at the high end of the general population range may be experiencing some of these effects. Some more highly exposed members of the population, may be at risk for frankly adverse effects including developmental toxicity, reduced reproductive capacity based on decreased sperm counts and potential for increased fetal death, higher probability of experiencing endometriosis, reduced ability to withstand an immunological challenge and others. [EPA 1994] EPA's Assistant Administrator for Research and Development echoed this conclusion: "Certain non-cancer effects, including changes in endocrine function associated with reproductive function in animals and humans, behavioral effects in offspring of exposed animals, and changes in immune function in animals have been demonstrated. Some data suggest that these effects may be occurring in people at body burden levels that can result from exposures at or near current background.... Risks from ubiquitous background levels of dioxin in the general population need to be carefully considered. " [Bretthauer 1992] This conclusion was reinforced in a recent scientific publication by EPA's chief toxicologist on the dioxin reassessment: "Results in enzyme induction from both rats and mice would suggest that at current environmental levels, (1-10 pg/kg/day) people may be experiencing small but significant increases in these markers of response. Highly exposed populations may be at special risk. Since animal studies suggest that changes in hepatic enzyme induction occur at body burdens similar to those at which immunotoxicity in mice :rccc CTL014396 - 14- and permanent effects on the reproductive system occur in rats, it is reasonable to hypothesize that subtle effects on these parameters may be occurring in the human population. [Birnbaum 1993] And EPA's dioxin research team restated this conclusion in a presentation to an international scientific conference in late 1993: "[EPA's] documents reflect input from the expert panel that concluded that current body burdens of dioxin and related compounds (TEQJ are at or near the point where responses would be expected to occur.. As the panel recommended, additional emphasis was placed on non-cancer endpoints, since effects on the immune system and developmental reproductive effects appear to be occurring at extremely low levels". [Birnbaum 1993a] Second, there is substantial evidence to indicate that populations of wildlife species high, on the food chain are suffering health damage due to reproductive and developmental impairment due to "background" exposures to dioxin and related compounds. In the Great Lakes, for instance, exposure to dioxin-like compounds has been linked to large-scale hormonal, reproductive, and developmental impairment among numerous species of predator birds, fish and wildlife; these impacts are primarily transgenerational, affecting the offspring of the exposed organism. [Giesy 1994, UC 1991) Finally, according to EPA, effects on humans - including hormonal and metabolic changes - have been documented at dioxin body burdens and exposures that are only slightly higher than those to which the general population is subject. [EPA 1994] For instance, while the average American's dioxin body burden is estimated at 9 ng/kg, workers with dioxin body burdens of just 13 ng/kg have been found to have significantly decreased levels of serum testosterone. Further, laboratory experiments on primates have also documented health effects at dioxin exposures and body burdens at or near those of the general human population. For instance, at body burdens just 3 times greater than that of the average U.S. resident rhesus monkeys suffer significantly increased incidence of endometriosis, while marmosets experience altered immune system responses. [EPA 1994] These data indicate that if there is any "margin of safety" left between the current exposure of the average American and the level at which health damage begins, this margin is a small one. In summary, the evidence suggests that dioxin exposure may be causing effects now among large sectors of the general public, but the lack of an uncontaminated control group makes it impossible to determine with certainty whether this is the case. The evidence clearly shows, however, that existing environmental concentrations of dioxin place the human population at risk, and any increase in these concentrations will increase that risk and/or the severity and number of persons affected. Finding #2: Cancer hazard to humans In 1985, EPA found that dioxin was the most potent synthetic carcinogen yet tested. [EPA 1985] Since that time, industry representatives have attempted to argue that dioxin may be carcinogenic in laboratory animals but not in humans. EPA's reassessment reviewed the laboratory and epidemiological data, however, and concluded that dioxin poses a severe cancer hazard to both humans and animals. According to EPA's draft reassessment: -15- CTL014397 :rccc With regard to carcinogenicity, a weight-of-the evidence evaluation suggests that dioxin and related compounds are likely to present a cancer hazard to humans.... White the epidemiological data alone are not yet deemed sufficient to characterize the cancer hazard of this class of compounds as being "known," the unequivocal evidence in animal studies, inferences drawn from mechanistic data, and the suggestive evidence of recent epidemiology studies support the characterization of dioxin and related compounds as likely cancer hazards. [EPA 1994] According to a summary by EPA's dioxin research team: "Dioxin does cause cancer in humans." [EPA 1992] In fact, EPA estimates that 'background" dioxin exposures to dioxin-like compounds result in very high cancer risks throughout the general population. Modeling estimates suggest that current background exposures may result in upper bound population cancer risk estimates in the range of one in ten thousand (10-4) to 1 in a thousand (10-3) attributable to exposure to dioxin and related compounds. [EPA 1994] (emphasis added) Thus, dioxin exposure currently poses cancer hazards that are 100 to 1000 times greater than the standard "acceptable" risk of one cancer per million. According to EPA's risk estimates, dioxin would cause from 350 to 3500 cancers each year in the U.S. - up to 3 percent of all cancers. EPA's finding that dioxin can be considered a human carcinogen is reinforced by the recent conclusion of the U.S. National Institutes of Medicine, a division of the National Academy of Sciences. After reviewing several hundred epidemiological reports on dioxin and cancer, the panel concluded that there is "sufficient evidence" of an association between exposure to dioxin and dioxin-contaminated herbicides and soft-tissue sarcoma, non-Hodgkins' lymphoma and Hodgkin's disease in humans. The panel also found "limited/suggestive evidence" for an association between dioxin exposure and respiratory cancer, prostate cancer, and multiple myeloma. Umited/suggestive evidence refers to strong evidence that nevertheless cannot complete exclude a possible role for chance or confounding factors. [Fallon 1993) Finding #3: Severe effects on reproduction and development Recent research indicates that the effects of dioxin on the reproductive, developmental, and immune system effects are even more severe than cancer. EPA's reassessment has confirmed that dioxin interferes with a wide range of biochemical substances, including sex and thyroid hormones, insulin, growth factors, and enzymes. These changes can result in an array of effects on reproduction, development and immune system function, as shown in table 2.2. Many of the non-cancer effects found in dioxin-exposed rodents have already been documented in primates and human populations exposed to dioxin or dioxin-like compounds, including alterations in male sex hormones, altered thyroid function, immune suppression, impaired neurological function on development reduced penis size, behavioral changes, immune system effects, and birth defects. :rocc. CTL014398 - 16- --------------------------------- TABLE 2J2. 1 Health Effects Associated with Dioxin and Related Chemicals --------------- Metabolic changes; wer^tt loss, wasting syndrome, feta/ death, altered glucose and fat met^ofism * Hormonal changes [indudrtg alterations in sex, thyroid, and other hormones) Birth defects ' Impaired neurological development and subsequent cognitive deficits ' Male reproductive towaty: reduced sperm count . ' testicular atrophy abnormal testis structure : reduced size of genita/ organs feminization of hormonal aid behavioral responses \ . * Female reproductive toxicity. ' hormonal chaiges decreased fertility. inability to maintain pregnancy ovarian dysfunction endometriosis * Immune suppression and increased siisceptibilrty to infectious diseases * Effects on the fiver, thymus, spleen, bone rnarow, and skin Diabetes '.' Source; adapted from PA 1934. ' .' According to EPA, "In mammals, postnatal functional alterations involving learning behavior and the developing reproductive system appear to be the most sensitive to perinatal dioxin exposure." [EPA 1994] During key periods of development, the fetus or infant is exposed to large quantities of dioxin as the mother's body burden is partially liberated and transferred to the infant across the placenta and via breast milk. Doses low enough to cause no visible changes in an adult can produce serious and long-lasting effects on infant or fetal development. These impacts may be invisible at birth but appear later as functional deficits during childhood, puberty or adulthood, leading to reduced fertility, altered behavior, diminished intellectual capacity, and impaired immune defenses. According to EPA's draft reassessment; Recent laboratory studies have suggested that altered development may be among the most sensitive TCDD endpoints.... Developmental toxicity endpoints are observed at tower TCDD exposure levels than are endpoints of male and female reproductive toxicity.... Of particular interest to the risk assessment process is the fact that a wide variety of developmental events, crossing three vertebrate classes and several species within each class, can be perturbed, suggesting that dioxin has the potential to disrupt a large number of critical developmental events at specific developmental stages. Not only can these changes lead to increases in embryo/fetal -17 - V'fVV CTL014399 mortality, but they can disrupt organ system structure and irreversibly impair organ function, even after only transient perinatal TCDD exposure. [EPA 1994] Finding #4: No safe dose EPA's reassessment indicates that any dose of dioxin, no matter how small, can cause biochemical changes that may lead to a wide range of effects on the heaith and function of an organism. There does not appear to be any threshold or safe dose below which dioxin does not cause these biochemical changes. According to a recent reassessment update by EPA's research team: No evidence for low dose nonlinearity was observed for sensitive biochemical responses. [Birnbaum 1993a] EPA based this conclusion on research conducted by the National Institute for Environmental Health Sciences (NIEHS), which investigated the relationships between dioxin dose and certain effects, including receptor binding, enzyme and growth factor induction, and certain other key parameters. For none of the effects tested was a threshold evident. [Portier 1993] According to NIEHS: '[Our findings] are consistent with the knowledge that for some receptor-mediated responses, there is a proportional relationship between receptor occupancy and biological response, even at low ligand concentrations. The results presented here illustrate that a threshold for the biological effects of TCDD exposure cannot be assumed simply on the basis that dioxin response is receptor-mediated.... If TCDD-mediated effects on cytochrome p-450 induction or EOF receptor binding are reliable surrogates for toxicity or toxicity is induced by similar mechanisms, the risks from exposure to TCDD are as high or possibly higher than were estimated by the EPA using a linear model. If this is the case, there should be considerable concern for the high levels of TCDD already present in human tissues.' [Portier 1993} It is possible that certain effects that follow these biochemical disruptions will be related to dioxin exposure in a non-linear or threshold fashion. But according to EPA, "This point is somewhat moot however, given that background exposures to dioxin are ubiquitous and associations between dioxin exposure and certain types of cancer have been noted at body burdens within 1 -2 orders of magnitude of average background body burdens, obviating the need for large-scale low dose extrapolations." [EPA 19941 Even H there is a safe dioxin dose, we are already at near, or above that threshold. Additional exposures cannot be considered "safe." These findings have extraordinary implications for public heahh and regulatory policy. Since no dioxin exposure can be considered safe - and any additional exposure may result in incremental increases in the severity of toxic effects - there is no longer any such thing as an "acceptable" discharge that does not pose a hazard to public health. This fact implies that the regulatory policies and models used in the U.S. and Europe is no longer appropriate and have failed to protect public'health. These regulatory systems are based on permitting discharges within specified limits, so long as they are not predicted to result in exposures that exceed an individual's "acceptable daily intake." If any additional dioxin exposure poses a public health hazard, the basis for granting permits is no longer valid, and the regulatory framework must shift to the prevention of releases. EPA has admitted as much, although it has not even begun to establish a prevention-based policy. In particular, EPA admits that the use of a reference dose (RfD) - and its corollary, the "acceptable daily intake" - CTL014400 - 18- is not appropriate, since these standards are based on the assumption that there can be a safe level of exposure: In (he case of dioxin and related compounds, calculation of an RfD based on human and animal data and including standard uncertainty factors to account for species differences and sensitive subpopulations would result in reference intake levels on the order of 10-100 times below the current estimates of daily intake in the general population. For most compounds where RfDs are applied, background exposures are generally low, are not persistent and are not taken into account. Dioxin and related compounds present an excellent example of a case where background levels in the general population are likely to have significance for the evaluation of the relative impact of incremental exposures associated with a specific source. Since RfDs refer to the total chronic dose level, the use of the RfD in evaluating incremental exposure in the face of a background intake exceeding the RfD would be inappropriate [EPA 1994] (emphasis added) In light of the existing public health threat from dioxin, regulatory policy must shift from approving "acceptable" exposures and discharges to preventing dioxin formation and release. According to EPA, The weight of the evidence suggests concern for the impacts of these chemicals on humans at or near current background levels. Additional, incremental exposures occurring as a result of proximity to a point source of release or specific human activity patterns such as consumption of high levels of more highly contaminated foods, should be evaluated relative to background levels and the impact of the incremental exposure on both transient and steady-state body burdens. This situation is somewhat akin to the scientific approach taken for evaluating lead in children. This approach has been useful in providing public health-based advice to decisionmakers faced with difficult regulatory choices. [EPA 1994] EPA thus identifies the need for a wholesale shift in the regulatory approach to dioxin. EPA should immediately suspend its practice of approving additional discharges and exposures through permits, controls, acceptable discharges, and "reference doses." Instead, the agency should develop a coordinated national program to reduce human exposure to dioxin and prevent further release into the environment of dioxin and related compounds. -19- CTL0144Q1 3: FORMATION OF DIOXINS In its Reassessment, EPA makes a preliminary attempt to catalogue dioxin sources, and it correctly identifies incinerators that bum chlorinated waste and chlorine-bleaching pulp mills as primary sources. But EPA's list omits dozens of other dioxin sources* that have been identified in the scientific literature and government reports - including those prepared by researchers within EPA. As a result, EPA's list of dioxin sources accounts for only 10 to 50 percent of the 25,000 g/year of dioxin that the agency estimates are emitted into the environment each year Dioxin is never manufactured on purpose. Instead, it is formed as an unintentional by-product in scores of processes in which chlorine and chlorine-derived chemicals are produced, used, and disposed. In fact, the data suggest that all chlorine-based products may be associated with dioxin production at some point in their lifecycle. Dioxin and related compounds are produced in the following processes, implicating the entire field of chlorine chemistry: The chlor-alkali process in which elemental chlorine gas is produced from salt All uses of chlorine gas (and other chlorinated oxidizing and bleaching agents) in industrial processes, such as the pulp, metallurgical, and water treatment sectors; Use of chlorine in the chemical industry to produce chlorinated organic (and some inorganic) compounds with a wide range of structures; Some uses of chlorinated organic chemicals, particularly those in reactive, alkaline, or heated environments; Incineration, combustion-based recycling, or accidental burning of any chlorine-containing product or of any waste from any of the above processes. DIOXIN AND CHLORINE CHEMISTRY Elemental chlorine gas is a highly reactive substance; it combines almost immediately with organic (carbon-containing) materials to produce organochlorines. The formation of organochlorines takes place quickly and randomly; this process is impossible to prevent and difficult to control. Thus, complex mixtures of hundreds or thousands of organochlorines are formed whenever chlorine comes into contact with organic material. These complex organochlorine mixtures frequently - and possibly always -- contain dioxins and related compounds. Virtually all industrial chlorine chemistry is suspected of generating dioxin-like compounds at some point during manufacture, use, and disposal. A number of lines of evidence support this judgment. First, dioxins are produced when chlorine is manufactured from salt in the chlor-alkali process, as discussed in chapter 5. Dioxin is thus implicated in all "downstream" processes - the entire field of chlorine chemistry. * Throughout this document, processes are considered sources of dioxins or dioxin-like compounds if they involve the formation of any of the following: chlorinated dibenzo-p-dioxins, chlorinated dibenzofurans, hexachlorobenzene. or octachtorostyrene. Hexachlorobenzene itself contains dioxins rid furans at concentrations over 200 ppm. [Esposito 1980|. Given the structural similarity of HC8 to dioxin and the occunence of dioxin in HCB, the presence of HCB in any product or process points to the presence of dioxin. According to one study: 'Hexachlorobenzene. octachtorostyrene, and other highly chlorinated compounds are formed under similar conditions as PCDD/F, and their presence in the emissions of a technical process should therefore be a good indicator for reaction mechanisms which may also create PCDD/PCDF. [Oehme 19891 CTL014402 -20- Second, dioxins are formed as trace by-products in the synthesis of the full range of chlorinated organic chemicals. In its preliminary dioxin reassessment documents, EPA notes, "Dioxin-like compounds can also be formed during the manufacture of certain compounds such as chlorinated phenols, benzenes, and others. The releases associated with chemical manufacturing could not be quantified due to lack of test data. Potentially such releases could occur via the product itself or as emissions to the air, land or water." [Schaum 1993) But the problem is much broader than this language suggests. Dioxins are known to be formed in the production not just of a few aromatic (benzene-based) chemicals, as EPA implies, but in a wide range of organochlorines, including those that do not resemble dioxin in their chemical structures - from simple to complex molecules, from aliphatics to aromatics, including solvents, pesticides, feedstocks for plastics, chemical intermediates, dyes, and others. Tables 3.2, 3.3, 3.4 and 3.5 present industrial and agricultural chemicals that are known or suspected of dioxin formation during their manufactur. Many but not all are benzene-based; aliphatic organochlorines associated with formation of dioxin and related compounds include 1,2-dichloroethane, carbon tetrachloride, trichloroethylene, tetrachloroethylene, hexachlorobutadiene, and epichlorohydrin. [Heindl 1987, Hutzinger 1988, Rossberg 1986]. Although a large number of chlorinated chemicals have not yet been tested for dioxin formation, the wide variety of products known to be associated with dioxin formation supports the hypothesis that dioxins are formed throughout a full range of uses in the chemical industry. On the other hand, the data contradict the notion that dioxin is associated only with a handful of products. The formation of dioxin in these chemical manufacturing processes cannot be prevented. Although producers attempt to exercise control over production conditions - such as temperature, pressure, and material purity - transient variations always occur, resulting in the production of complex by-product mixtures, including dioxin. In 1987, EPA recognized this fact: The manufacture of ha/ogenated organic chemicals results in the formation of small amounts of undesired side reaction by-products. These contaminants may be contained in the product chemical, separated into a processing step residue, or lost to the air or wastewater as a pollutant.... PCDDs and PCDFs are formed from a wide variety of chemicals, involving complex reaction pathways.... The large number of isomers is one of the reasons for the complexity and difficulty in the analysis and determination of dioxins and furans [as impurities in other chemicals.) (Lee 1987) Dioxins can also be formed when organochlorines are used, particularly in reactive environments - i.e., at elevated temperature or in chemical reactions. Dioxin production has thus been identified from the burning of vehicle fuels with chlorinated additives, the use of organochlorine catalysts in the steel industry, treatment of wood with pentachlorophenol, synthesis of chemicals and pharmaceuticals using organochlorines as intermediates, extractants, or reaction media, degreasing and cleaning of equipment with chlorinated solvents in the presence of strong alkalis or at elevated temperature. Finally, dioxins are formed when any organochlorine is burned - in an incinerator, recycling facility, or in an accidental fire. According to EPA, 'The formation of dioxin is generally understood to occur as a result of burning organic material with chlorine-containing material." (EPA 1986) Thus dioxins have been identified in the emissions and residues of the all types of incinerators burning wastes containing any organochlorine -21 - CTL014403 contaminated wastes, including hazardous wastes, garbage, medical waste, and sewage sludge. Large quantities of dioxins are also formed when organochlorine substances - such as PVC - bum in accidental fires or are introduced into combustion-based industrial processes such as primary and secondary smelters for copper, steel, aluminum, and iron. Incineration is the dominant disposal method for spent organochlorine products (i.e., solvents, PVC, etc.) and for the chlorinated wastes that are produced whenever any organochlorine is manufactured. EPA has estimated that 37 percent of all wastes fed to incinerators are halogenated and that approximately 12.8 million metric tons of halogenated incinerable hazardous wastes are generated each year in the U.S. Of this quantity, 1.04 million metric tons are chlorinated solvents, 1.25 million metric tons are liquid chemical wastes, and 9.78 million metric tons are halogenated solids - primarily from the chemical manufacturing industry. [Oppelt 1987, Oppelt 1993] In theory, incinerators are designed to convert organochlorines into hydrochloride acid, carbon dioxide, and water; real-world incinerators, however, never take this reaction to completion. The problem is not limited to poorly operated or aging incinerators; dioxins are formed in even the most sophisticated "state-of-the-art" incinerators According to EPA: The complete combustion of all hydrocarbons to produce only water and carbon-dioxide is theoretical and could occur only under ideal conditions.... Real-world combustion systems virtually always produce PICs [products of incomplete combustion] some of which have been determined to be highly toxic. [EPA 1990] Dioxins are formed as products of the diverse and unpredictable reactions that take place in the furnace and the cooler zones of an incinerator. Localized and short-term variations from ideal combustion occur constantly in incinerators; when large-scale upsets (explosions, flame-outs, puffs, etc.) take place, even greater quantities of dioxin and other PICs are formed and released. OTHER SOURCES: THE MYTH OF "NATURAL" DIOXIN Industry advocates have argued that large amounts of dioxin are produced by "natural" sources, particularly forest fires, the domestic burning of wood, and the combustion of coal. This argument put forward by Dow scientists as the "Trace Chemistry of Fire" theory, is intended to refute the idea that public policy should focus on the elimination of industrial sources of dioxin, particularly those associated with chlorine chemistry. One aspen of the "Trace Chemistry of Fire" theory is correct, while the rest has been soundly disproven. It is possible for trace amounts of dioxin to be produced from salt, if enough energy is present to convert stable ionic chlorides into chlorine or organochlorines. Thus, dioxin can be formed in incinerators when salt is burned; according to one study, the quantity of dioxin formed per unit of chlorine is about half that when organochlorines are burned. [Danish EPA 19931 Other studies indicate that dioxin formation from salt combustion may be even lower; a German EPA study found high dioxin concentrations in the ash residue from the combustion of chlorinated plastics, chlorinated solvents, and pesticides, but concentrations were orders of magnitude lower or non-detectable when chlorine-free materials such as wood, paper, and chlorine-free plastics were burned, as shown in table 3.1. [Pohle 19911 :rcoc CTL014404 -22- Notwithstanding the fact that burning organochlorines produces more dioxin, rt is true that burning salt at high temperatures can produce dioxin. Thus, the introduction of salt to incinerators should be minimized. Since food and yard wastes - the major sources of salt in incinerators - are best composted and can be safely land disposed if necessay, there is no barrier to reducing the burning of salt-containing materials. The Netherlands, for instance, has a program to separate this "green waste" for compost from other types of municipal waste. TABLE 3.1. DIOXINS IN ASH FROM THE BURNING OF ORGANOCHLORINES AND CHLORIDE-CONTAINING MATERIALS --------------------------------------- -- -- Material (# of samples) Writingpaper;: : Wood,'Cotton; Wool' ` - ,V FWyethylere:, Ml-'-l Otoirie-freejxtfycfcforprene aftenatiye1 FV wood (w/tesidues?) ' "rZ. Coffee fitters (2) PVC plastic (10) PVDC plastic Chloro-polyethylene plastic Chloroparaffin Potychforoprene plastic PVC flooring production samples PVC window-frame production samples PVC cables (w/copper) PVC cables (w/o copper) Other PVC products * Dichloromethane 1,1,1 -trichloroethane Tetrachloroethane Trichloroethylene Perchloroethylene Chlorobenzene p-Chloronitroberaene o-Chloronitrobenzene p-Chlorotoluene Eplchlorohydrin 2.4-D Ururon (pesticide) 1. Acrylonitrile-butadiene rubber) 2. PVC gloves, hose, pipes, tape. etc. Total PCDD/F(ppt) Total 237S-PCDD/F ppt Total PCDO/F (TEG- ppt) :r' :ZZ0k>Z}2 21.4 6.3-7.7 244-2067 3,304 840 1,049 323-1096 352-1847 7.5-969 669-2970 416-843 158-954 26.302 21,746 9.072 120,915 212 16.135 190,096 32,293 1,033 1.532 178.016 3.110 o 0.61-0.76 7.5-122.1 20.5 27.6 14 2.2-14.0 25.7-38.4 22.3-52.1 26.2-129.4 20.7-46.6 7.2-492 975 831 37.9 18.5 1 0.7 29.7 1.331.9 NO 117 168 253 y-p - 'll:' ";^'<:0.1 >:V V:0.65 0.15-0.23 3.2-42.2 14.1 10 5.3 0.7-4.7 8.2-14.5 8.8-18.1 11.4-52.6 7.4-16.6 2.5-16.5 478 340 132 149.5 0.4 0.5 21.5 216 NO 36 361 32 Source: Pohle 1991 -23- CTL014405 :rccc But the most important part of the Trace Chemistry of fire theory - that much or most dioxin can be explained by "natural" combustion unrelated to chlorine chemistry - has been proven false. Several lines of evidence indicate that virtually all dioxn found in the environment is produced by industrial sources associated with the production, use, and combustion of chlorine and organochlorine chemicals - not salt combustion. Second, historical trends in dioxn levels in human tissues and sediment cores clearly show that dioxn pollution was not a problem before industrialization and the development of chlorine chemistry in particular. Studies of sediment and soil patterns in the Great Lakes show that dioxin pollution was negligible or non-existent before the rise of chlorine chemistry in the Twentieth Century, and that levels skyrocketed only when chlorine chemistry rapidly expanded after World War II, as shown in figure 2.2. [Czuczwa 19861 Further, two studies have found that diox'ns and furans are almost completely absent from the tissues of pre-industrial humans who habitually burned wood indoors and were thus highly exposed to wood smoke. Dioxn levels fTEQ) were less than 2 percent of the levels found in current human tissues, as shown in figure 3.1.. [Schechterl 9911 Based on these studies, EPA has concluded: "The theory that much of today's body burden could be due to natural sources (such as forest fires) has been largely discounted by testing of ancient tissues which show levels much lower than those found today." (Schaum 1993] Figure 3.1 Dioxin concentrations in ancient and modern humans. Source: Schechter 1991. :xrcc CTL014406 -24- Third, the data do not show that the burning of wood per se produces significant amounts of dioxin. Organochlorine pesticides, solvents and other chemicals have been distributed throughout the global environment, and they have been deposited on and absorbed into trees, their wood and foliage, and other forest materials. Thus, a forest fire or a domestic wood fire bums industrial chemicals in addition to natural wood, and dioxin emissions are most likely a reflection of these chlorine inputs. According to EPA, "Only one test has directly measured CDD/CDFs in the smoke from forest fires, and the authors cautioned that all or a portion of these emissions could represent resuspended material from aerial deposits rather than originally formed material." (Schaum 1993) Further, a recent industry study found that the burning of natural wood results in very low dioxin emissions, while the burning of waste wood chips and wood in the presence of household waste results in dioxin emissions that are higher by a factor of 100 to 1000. [Schatowitz 1993] Danish studies indicate that the high dioxin emissions documented in emissions from wood stoves were caused by the burning of wood impregnated with the wood preservative pentachlorophenol. [Vikelsoe 1993] For this reason, the German EPA has prohibited the burning of PVC-coated wood in home or industrial stoves and furnaces. EPA's estimates that forest fires emit 300 to 3000 grams/year of dioxin per year, industrial wood burners 70-1600 g/year, and domestic wood burners 40400 g/year. If these figures were accurate, these "natural" sources would account for only 1.6 to 20 percent of EPA's estimate of total U.S. dioxin releases. But EPA admits that these numbers are almost certainly significant overestimate. EPA derived its figures for both sources by combining total particulate generation rates with the levels of dioxin found in chimney soot, admitting that "dioxin levels in soot are likely to be much higher than what is actually emitted on particulates due to accumulation in chimneys." [Schaum 1993] For all the reasons discussed above, then, it appears that the contribution of salt combustion to total dioxin emissions is less than one percent while the vast majority is related to chlorine chemistry. The burning of chlorides in combustion facilities should be minimized through the removal of food and yard waste, but the focus of any dioxin reduction program must be on the products and processes associated with industrial chlorine chemistry. -25- CTL014407 - Table 3-2 Pesticides with Doan Formation Known orSuspected it Manufacture Dtodn contaminabon known Vf4<Norophac30xY>X3^msehyi-l-tt W-l.2.4 Zy-fnethyWne hirf< chfanaphwnnil Brianox MrthyW2.4-dirf>bco- pheooxy-2-nrtroberaooafe ... CNoranI It Z3.S^5'te*cNofo-2.5- : cydohexadiena-1,4 dVrwi . ^rwnt-T-t6-2-b<Xw Chioroooti.//' . t.44lchlam-2-dkned\oxybant6n& ' C*totohtoot O^orosurow f/ 344- (4-ddosophenorxyfr Monunx* trx*>ton>*cott If 3-jp-cMompheny<)- 1,1- dmethyteaa trich- feoMeate* Nobucxi 11 T-butyf3-|3,+-did>kxT>phonvil- l^matiiylurea CHorophenott'.."vatioua" : 2.4-D// (2.4HKchfatDphcnoyriaofcticodd2.4-DB satt//2,4-^diiorc>phnoxyiKityTTC jcid 2,4-DP//2-l 2^4-dkii^cphgCTcrryyropionic acid OicamOa, danathybmine salt // .phorryVl.l-dimed^Ylur** ; 40au--unu.u.*.n.u--a. Ctytoimet* H 4-t*rt-butyf-2^fitonJp6e<TY* . : -methyl TrMs2hy4phu*f>fio*eiadste DC^Aj/2,2^^t*tr*cNon>>X, < benzene dev* Oxaderoa7/ 2-tert-bucyM' VL*-&etiorn H impro poxy* phenyddeJea* f,3.4-oxad<aoArv$-oneJ o^enzyi^-chlorbpdenol- o-Dtchfaraberoene - . 3.S-dtcNofo- 2-roethoxvtienztm: add, boxyfc acid.-dimethyl eeser ' O-K*bromo-2,SdicWorcpharTyt O.O-denethyi' Dtcamba 1(3. frdichtoro- 2-mrtjejcyreeic iod DicapthorVi^hoaphorothioic add,. o-42-' . chtoro 4 rittupbonyJHfroO-iti^thyl sate* Dfchlofenthfon// Phoephorcthfoie add* EOT' . Oegechiore&ie (2.4-CftJapmMrimn- t-yfl . . DichtefeienJ ft Z^dkiJaiabomuiJtifte ' Cb^wittW^I2^kMMp>miY<K}.0- phoephorathbate PwdiMi // phoephoroihaotc add. o,o-<Sethy(^o>(4-r9ophenYl} ester . Pantsefaforobefizonitnfe o-2.4-cfichiOfophaoyt o.-o-diaftry* eater- . Died aodium Isosona) //2t4 dEchtofophoroxy ethyl suitale. sodom, safe . dtetrj< pho*ptxwrtfiiot. Oichfone \ Diehfane U Z3^chfc>ro-1.4-nepteheAi<vxlona Pet itecirfurodtroberaene PentadihKOphenyl laurate fipco<nop<opv4-3.4-defttoicben2oot DMPA Diefafep-tnethyf Ppererain // 3-42-methy4p<pendboi Erbon 2,4-dk4oeophenyl p-nttropheoyt other (TOO propyl-3.4-dichbrobonzota Erbon// 2^2-diehJoropropanoicaddi 2,4^dchlera-0>4o-ddDroanfinoH*tzunntt PUnavIn fl 4-medr^eulfonyO-Z6' dinrtro40^- 2-<2.4,5-trich4oropNenoxy) ethyl ester - Hxch(oroph*n U 2^'-m,tfyfano- ' bu{3.4,&`tnchJoropheno4 '2,&4fchtoro-4'nftn)anfine- dBubermron // N-IIH-elimptmrril . amino|cai6ony<)*Z.B-difluorDbanzen,de| dipropylaniino fto<eno<os ff 0-|4-ticornd2-htoropheny(h O- "ethyl S-pmpyt phbeyhoruthiosteS bobic 20 It 2,2**metfivWto btc DimethyltegechlorotaephthAtote . Prepanj//3,4-dbhloropropbnanAde (3.4.6-C3chkxophooiJ. monosodium salt DeWtrebuty^henoi. unmonfare nflt p^Odorophenyl-2,4,6-tnddoeopheeiyttt4fid Nitrofen// 2.4-diehbrophenvt-p-tKtJUphenyi . A-.G-dWtro-o-crosol p-Oichlorobenzene ether . Dixon/ 3d3.4-d*cWotophmf(f' Ration U 2-chbfO-l-rZ.4.-dicHdropheny4 w>yf Pentachtorophenol (PCP1 arid mails 1,1-dimcthyksea diethyl phosphate Ronnel //.phosphorcthioic add, o.o-denethyf- Eridoulfen, Ronton it 3H3.&<flehtofophenYfl-5- 0-12,4,5-trichioropheny9 otter Erbon " %; etheny4-S-methyl-2.4-osagolidine dipne Scone Fenvaiarst*// Saaone Savex/2-(2.4,S-trichlorophenoxylprop>ontcscirf.' . cyenc<3-phonagyphen>3aiethvl-4- cHom Sodium pentachbropherwto 2.4.5-T // (2.4,5-<richloropl>eroxYi Acetic odd-. '.-itpfMm-aathTMhvOboraamoootal* T,Z4.5-ttrachioro-3nfaoberuene 2.4, S-tricHorophenol ' Hwatinste// H-2-chtaro 4 OifluoromothytK ToOachtotoioophthoWalo 2.3.4,6-tstrechlarephenol phenyl-01.-veHnet:* t-cyeno- . Ttnehloiopri*n( Tetradifon nSchenoxypherrifl methyl rtf fi*W*or/l 7 -Or!2^4-dichio<ophey4f"2*t2pcopinyfaocYlthYt>1KHn<idio(* ' Tetrachfaeophenols 2.2*-thiobi t4-chforo-6-methylphenon 2.3.6-irichlo<cb*nzoic odd Dioxin cxmttiminetkxi 'pass&a" Qardona ft 2-cWofo-tH2.4,5-trkhkjroph*nyfl TncMorobersoyl chionde . vinyUmethyl pttnptwto . 2,3,-trieNo*ophervyiaoei*e aod or aodum aaft AWon (10-(2-cNoro-1-rZJ5-dicMo<ophen\41-" - very1b O.O-dethyl phosphorothoete-'. Afcyl dimethyl 3.4 djehtorobergyl i-nnenan . chloride fleeachtoratMrsene htvoo: ' bryni .. KoRhara U 'l.t-bi(cHofOphonv4- '' Sotscee: Espoaito IS60, PTCN 1S8S. Cubonphenothion II PhoeptocodhNde od. Z2.2-trtddoieduno4 . . ttotot origind fat lnc<ud*d compound* ikWy t-fH-ChlomijhsnYlfthiolmottiYU o,oderthyi . lindm i/'g-h*ncNoiocY^ah*un* ester MCPA U (4-chtero-o-toioTyO acetic add to produce any habpansted dtieruodicoons. indudnp brorvenarted, flpohnatad, end bdW Certoophenochion QtlorenJ MO'S II 4-12 wtfiyt 4 eMowptxnoicy} '.butyricodd nt*d comyxxwdi. Th*M compound, fwvm been onretted bom thi* fist. However, non- Chlorbromuron Maooprec If 214 eWom 2-wriiyiprianoxyt hstogenated products made from dibnneted 5-chloro-2-{2.4-dk^iorophenoTYl phenol propbrecadd intermedietes have been mae^ained. 2,2* -methylane-bie {3.4,6>triefeforo-phenoQ .xccx CTL014408 -26- Table 3.3. Commercial Chemicals with Dioxin Formation Known or Suspected During Manufacture HtGH PROBABttJTY Of DiOXiN FORMATION 4-bromo-2,5-dichlorcpbenol 2-cNoro-4-fluorophenol 2.4-cfibromophenol 2.3-cficNorophenol 2.4-dichlorophenol 2.5-dchlorophenol 2. S-<chlorophenoI 3.4-dichlorophenol 2.4.5-trichlorophenol 2-chloro-1,4-diethoxyt5-fftrobruteoe 5-cbloro-2,4-dimethaxy-eniHne chlorohydroquinone o-chlorophenol 2-cN<wo-4-phenvtpberaoJ 4-chlororesordnol ' 3.5- dichlorosalicylic acid POSSJ8SJTY OF CMXXJ FORMATION o-chlorofluorobenzene 3-chloro-4-f)uoro-nitrobenz8ne 3-chloro-4-fluorophenal ' . 4-chloro-2-nrtrophertol chloropantafluorobenzene 3.4-dichloroaniline o-dichlorobenzene 3.4-dichlorobenzaldehyde 3.4-tfichiofobniotrichlorid ' , 3.4-dichforobenzotrifluorida 1.2-dichloro-4-nitrobenzorM 3.4-GSchlorophenylisocyanata 1.2-dthydroxybenzane-3.5-disutfonic acid, disodium salt 2.5-dihydroxybenzenesuifonic acid 2.5-<hydroxYbenzenesi#fonic acid, potassium salt 2.4-diritrophenol 2.4-dMtrophenexyethanol 3.5-djrftrosaticytic add fumaricadd hexachiorobenzene maleic add maleic anhydride o-nctroarisole 2-nrtro-p-cread o-nitrophenol pantachloroanilina '' o-phanatidina phenol (from chlorobenzene) ' .1-phenol-2-*uffonic add, ' formaldehyde condensate ! phenyl ether phthalic anhydride picric add sodium picrata t ,2,4,5-tetrachlorobenzane letrachforophthalic arbydride 1,2,4-trichlorobenzeno 2,4,6-trinrtroresoranol Source: Esposito 1980. Original Sst included compounds likely to produce any haloge- nated dberuodioxins, induding brominated, fluorinatod, and iodinated compounds: These campounds are omitted '..from this fist. Non-halogensted products made from chlo rinated intermediates included. Table 3.4. , 20 Pesticides Known or Suspected to be Contaminated with Hexachiorobenzene * OCPA IDacthal) * Chiorothaionil COaconri 2787, Bravo, Terrrri) * Pentachtororstrobenzene (PCNB.Tarrachalort 5,5.7,8-Tetrachioroquinaxaline tChforpLinox) Pentachlorophenoi (CNorphen) Pentachlorophenol zinc salt Pentachlorophenoi sodium salt Pentachlorophenol potassium salt Dehydroabiatylamine pentachlorophenste 1,2.4,5-Tetrachloro-3-nhrobenz*ne (Polossn) 2.2.2-Triehloro-N-(pent*chloro- phenyUacetimidoyichlorida ' 2.3,S,6-tBtrachloro-fl-methoxY-N-methyl-tsraphthalamata 2.4.5 Trichlorophenoxyacetic add 12,4,5-T) 2.3,6-Trichlorobenzoicadd (2.3,6-TBA) Endrin * AHyl ehloridetfchloropropene 1,2,3-Trichioropropane Dahydroabaietyiamine pantachlorophenata * ffcoioram * Manufacturers have acknowledged the presence of hexachkxobenzene as an impurity in these products. Source: PCTN 1985. ., : Table 3.5. Chemicals Known to Generate Hexachiorobenzene in Manufacture Carbon tetrachloride Chlorinated benzenes Chlorine HexacNorocydopentadtene Pemachloronitrobenzene Pentachlorophenol Tetrachioroethylene Trichloroethylene Source: USEPA 1985b. -27- CTL014409 :xm: 4: PRIORITY SECTORS: MAJOR DIOXIN SOURCES EPA's investigation, along with other information, points to three major processes as the largest dioxin sources. These sectors - incinerators, chlorine-bleaching of pulp and paper, and PVC plastic - account for the majority of known dioxin emissions. 1. INCINERATION OF CHLORINE-CONTAINING WASTES The largest group of identified dioxin sources are waste incinerators. EPA estimates that total dioxin emissions from such plants total 565 to 5343-g/year. Because EPA omitted certain major dioxin sources in this category (cement kilns burning hazardous waste, contaminated ash residue from waste incinerators and other combustors, etc.) and underestimates emissions from others, actual emissions are even higher. EPA identifies the following incinerator types as major dioxin sources [Shaum 1993, Cleverly 1993]: * Hospital waste incinerators, which bum primarily packaging, containers and disposable implements such as gloves and tubing. Chlorine is present primarily from PVC. EPA estimates annual dioxin emissions at 500-5100 g/year. * Garbage incinerators. EPA estimates air emissions at 60-200 g/year, but 1992 tests on a single garbage incinerator in Columbus, Ohio, revealed average dioxin emissions of 984 g/year (TEQ). (OEPA 1994] In other words, a single incinerator was found to emit up to 16 times more than EPA's total estimate for all of the nation's 120 incinerators. Of these, 40 are like the Columbus facility in their use of electrostatic precipitators - pollution control devices that operate at temperatures in which dioxin formation is maximized. [Connett 1994] If the Columbus incinerator trial bum is representative, emissions from these 40 incinerators alone would total dose to 40,000 g/year of dioxin, and sa range of 4,0004,0,000 g/year can be assumed until more data are available. In additionto air emissions, much greater quantities are deposited in the ash residues from these farilities, which are typically disposed in landfills, where leaching occurs over time. Chlorine is present primarily from PVC, with additional amounts entering in bleached paper, other organochlorine chemicals (i.e., solvents, paint strippers, paints, and pestiddes) and chloride from vegetable materials. * Hazardous waste incinerators. EPA estimates air emissions from these facilities at only 2.5-8.4 g/year. This figure, however, significantly underestimate actual emissions, for a number of reasons, first it is derived from a single trial bum at one indnerator; it is widely recognized that trial bums underestimate actual emissions, because neither operating conditions nor the materials burned resemble those of daily operation. Further, EPA does not include dioxin in ash and liquid residues from hazardous waste inanerators; releases in these forms may be 100 times greater than those in air emissions - or even greater - if pollution control devices are at least 99 percent effective, as indnerator operators daim. Trial bums in 1993 at the Waste Technologies Industries "state-of-the-art' hazardous waste indnerator revealed mean dioxin emissions of 1.2 grams per year (TEQ), or 13.6 ug/ton of waste burned. (ENSR 1993] An estimated 2 million tons of hazardous waste are burned each year in inanerators, according to EPA. If all U.S. incinerators achieved the dioxin emissions found in an idealized trial bum at this "state-of-the-art," annual air emissions would total some 27.2 grams per year. Real-world operation and upset conditions may increase dioxin emissions by a factor of up to 10; emissions from this sector would thus total up to 272 grams per year. :mx CTL014410 -28- If pollution control devices are 90 to 99 percent effective, ash from these incinerators would carry an additional 270 to 27,000 grams of dioxin (TEQJ into the environment per year. * Sewage sludge incinerators. EPA estimates emissions from these facilities at 1 -26 g/year, based on tests at three facilities. Dioxin emissions are the result of organochlorines in the sludge, primarily due to the chlorination of sewage, with smaller amounts entering in industrial discharges into sewer systems. * Drum and band reclamation facffities that recycle used chemical containers. EPA estimates annual dioxin emissions at about 2 g/year. Chlorine enters these facilities as chemical residues in drums and banels. * Vehicle fuels. Chlorinated compounds, such as 1,2-dichloroethane, are added to leaded gasoline and some other fuels as scavengers and for other purposes. The combustion of these chemicals in engines results in dioxin formation. EPA estimates that vehicle emissions result in the release of 8 to 870 grams of dioxin per year (TEQ). Fuels that do not contain chlorinated additives do not produce dioxin emissions. [Maridund 1990] Germany has prohibited the use of chlorinated additives in vehicle fuels. Tabfe 4.1; C-V: .... Dioxin Formation from Incinerators ....... Dioxin Releases (g/yr - TEQ) - ' . EPA estimate : revised estimate Hospital waste incinerators =' Municipal waste incinerators.; .. .. .; 500-5100 A . ar emissions-. ' 3Sh :. .; v-: : Hazardous waste incinerators .60200. . '"V; . 4,00040,000 . . 600-20,000 atr emissions ash: .:>, . 2.5-8.4: " *.;/: ;; 27-270 / ' \: 270-27,000.:-. Cement kilns bixnihg hazardous waste '. airerhissioris . dust/;--^ . " . - 800. - ' * ... . 1 18:: V Other industrial furnaces burning hazardous waste. . - . ND ' - Seweage sludge incinerators - , ; Tire btaning (incinerators, kilns, etc:} Vehicle fuels .: v : : Drum and barrel reclaimers .v Carbon regeneration lacijities,* . ' . 1-26, -- 8-870; 1-3:. . ND . . . . Sources: Seriatim 1993, Cleverly 1993i: Revisions explained in this text Al estimates are pre&nharyand are subject to significant uncertainty, .. -'./A : -i. In addition to these combustion sources, there are several types of incinerators that are known dioxin sources from which EPA did not estimate dioxin emissions, including: * Cement kilns that bum hazardous waste. Although cement kilns bum more hazardous waste than officially designated commercial incinerators and are known to be important dioxin sources, EPA made no estimate of dioxin emissions from these facilities. Data indicate, however, that these are important dioxin -29- CTL014411 :;axc sources. A 1993 testing program for EPA examined dioxin emissions at 15 U.S. cement kilns that bum hazardous waste; mean dioxin emissions per kiln were estimated at 20 grams of dioxin (TEQ) per year. [Schreiber 19931 Based on this figure, total drawn emissions from the 34 waste-burning cement kilns and the 6 waste-burning aggregate kilns in the U.S. would total 800 g/year. These estimates do not indude emissions from the approw'mately 200 other boflers/industrial furnaces that bum approximately 500,000 tons of hazardous waste per year. Cement and aggregate kilns release even greater amounts of dioxin in their solid residues, induding kiln dust and the cement products themselves. In a 1994 Report to Congress, EPA found diow'ns and furans in dust from five of six waste-burning cement plants sampled, with average concentrations of 42.2 ppt TEQ. [EPA 1993] Waste-burning cement kilns generate about 2.78 million metric tons of dust per year. [EPA 1993) Based on these figures, dust from these kilns carries 118 grams of diow'n (TEQ) into the environment each year. EPA found that these dusts enter the environment during storage, transport, and disposal, and concluded that significant uptake into the foodchain and human exposures are possible. [EPA 1993] Dust from aggregate kilns adds an additional but unknown quantity of diow'n. Diow'ns are also deposited into cement and aggregate products, but no data are available to estimate annual quantities. * Tire incinerators. Only limited data are available on emissions from tire burners. One test at a "state-of-the-art" dedicated tire incinerator in Modesto, CA, found significant dioxin emissions from that facility. Burning 5800 pounds per hour of tires, the incinerator emitted diow'ns and furans at a rate of .0236 grams per year (TEQ). [CARB] Tires are burned in cement plants, pulp mill boilers, tire incinerators, and utility boilers. [Blumenthal 1992] Because no data are available on the total number of tires burned each year, total national annual emissions from such facilities cannot be estimated. Small quantities of chlorinated chemicals are added to tires as additives, stabilizers, plasticizers, etc. 2. CHLORINE BLEACHING AT PULP MILLS EPA identifies the use of chlorine and chlorine-based bleaches in the pulp and paper industry as the largest source of diow'n discharges directly into waterways. Large quantities of dioxin are also released into the air, into paper products, and into the land when contaminated sludge is disposed. Total diow'n emissions from pulp mills are estimated at 238-1166 grams/year (TEQ). [Schaum 1993, Cleverly 1993] EPA makes no estimate of dioxin releases from the incineration of pulp mill sludge, a process known to generate dioxins. i . DIOXIN RELEASES FROM PULP MILLS (g/yr -TEQ) Medium Water Land (sludge)? ; Products; I, Kraft fiquor boilers Sludge incineration TOTAL Low Hioh 56 360 . 84 :vV"v 300 , 97 : ,: 7 500/ 1.. V: *" ::6 :\ ND ND 238 1166 Sources: U.S. EPA (Schaum 1993, Cleverly 1993) ND=no data. :xxrc CTL014412 -30- ny cl'p mills ra\ a switched from chlorine gas :o cr.lcr dm'i(ia ir.'a.v Ivs, thus reducing draxn tr ns by 35 much as GO paiccnt. EPA's estimates of dioxin r isos reflect tins crcroe, wen the .'ewer end tmge representing estimates from a xfemizc-d" paper industry us.ng cl' s dioxide bleach. Accciding to EPA, the upper estimate '//as based on a 1938 survey, ami tire !cwcr estimate represents conditions believed to c-e mere representative of current release rates, though not yet Independently confirmed." Even under this scenario, dioxin rs'eases to a1! mc-cia sail total over 235 g/year. Jog even "modernized" elder,re bleach,ing pulp nulls one of the largest dioxin-producing sectors known. Significant cuanat js cf dioxin have also been identified in consumer products made from tine pulp m 'I sludges and wastes. Dioxin concentrations ranging from 9.5 to 200 ppt have been defected in tall oil acid, ta I c;l resins, and soaps and detergents made from tall oils frem chlorine-bleaching pulp mills. [Rappe 1990], Pacer products made from chlorine dioxide-bleached pulp also contain dioxin; concentrations range from 0.2 to 1.3 ppt. [Gruber 19931 3. PVC PLASTIC PVC plastic is the largest single use of chlorine, consuming almost 4 million tons of chlorine in the U.S. about 30 percent of all the chlorine produced. PVC is used in pipes, flooring, wail coverings, packaging, furniture, automobiles, office products, appliances, cables, and certain medical products. Since PVC is the largest single use of chlorine, rt is no surprise that it results in more dioxin production during its lifecycle than any other product. Dioxin is produced and released in the manufacture of PVC feedstocks, the burning of wastes from production of PVC and its feedstocks, die incineration cf FVC products n trash and hospital incinerators, the secondary smelting of moral products containing PVC (such as automobiles and PVC-coatod copper cables), and the accidental burning of PVC in flies. TABLE 4.3 Dioxin sources associated with PVC: preliminary estimates Process Wastes from EDC/VC synthesis PVC products Municipal Waste Incinerators Hospital Waste Indner^ors Copper reclamation plants Steel redamaljon plants BtdcSngfjes TOTAL Dioxin released (TEQgfyr) 500-1000 10-100 4,000* 500-5100 230-310 10-110 500-5,000 % caused byP'yC 100 100 50 75 75 50 75 Dhxn released due to PVC (TEQ g/yr) 500-1000 10-100 2,000 375-3825 1G6-23Q 5-55 375-3750 3,430 -10,950 * low end of revised naticnal estimate, based cn trial bum at Columbus, Cho, incinerator. (CEPA 1994) Dm? to limited database, all estimates are prelirrsnary and subject to significant impretisicn. Basis for estimates explained in text. -31 CTL014413 P/C f/^nufeciure A senes of European studies have clearly established that very large quartettes of aioxin are formed in the production of vinyl chloride monomer - the building-block for PVC. Dioxin formation Is particularly significant in the "oxychlenrarjon" stage, when the feedstock ethylene dichloride is combined with hydrochloric acid and oxygen - in the presence of a copper catalyst - to produce VCM. Dioxins have boon detected in the wastes (or "tars") from tills process, in air emissions, water discharges, and in sediments downstream near discharge pipes from these facilities. Dioxins are only one group in a complex cocktail of by-products farmed in VCM manufacture, including hexschlorobenzene, hexachlorobutadiene, hexachloroethane, carbon tetrachlonde, and other "heavy" and "light" organochlorines. In May 1994, the Swedish Environmental Protection Agency found that PVC plastic itself contains measurable quantities of dioxins and furans. [SEPA 1994] Pure PVC suspension from two Swedish PVC producers was found to contain a full range of congeners of dioxins, furans, and PCBs, shown in table 4.4. Total concentrations, including PCBs, ranged from 0.86 to 8.69 ppt (TEQ). Based on these figures and annual U S. production of 5.7 million tons, PVC products carry an estimated 4 to 40 grams of dioxin (TEQ) into the U.S. environment each year. Dioxin congoner 2378-TCDD 12378-PeCOD 123478-HxCDD 123678-HxCDD 123789-HxCDD 1234678-HpCDD 2378-TeCDF 12348(78)-Pc-CDF 23478-PeCDF 234678-HxCDF 1 23478(9}-HxCDF 123678-HxCDF 123789-HxCDF 1234789h'pCDF 1234678-HpCDF QCDF OCDD 3344-TeCB PeCB (118) 33445-PeCB PeCB (105) 334455-HxCB Tota( PCDD/F/B Total (TEQ) TABLE 4.4 DIOXIN IN PVC PLASTIC PRODUCTS Sampfa 1 - PVC piastre (ppt) Sampfa <0.1 <0.2 <0.4 0.4 <0.4 26. 0.6 0.2 0.2 <0.2 0.1 <0.1 <0.3 <0.4 1. <0.9 55. 7.80 450.00 1.20 58.00 <.70 0.1 0.6 0.3 1.5 1.1 5.4 2.7 8.2 6.2 8.2 4.9 4. 1.5 2.4 13. 7.4 6. 31.00 399.00 18.00 68.00 4.70 <604.2 0.86 594.3 8.69 Source: Swedish EPA 1 394. Two samples of puro PVC suspension from two Swedtsh PVC p'arus were analysed. :rm: CTL014414 - 32 - of EDC as a feedstock for PVC p'astic: A 1SS3 study by the University of Amsterdam estimated, based cn 3 laboratory simulation of the oxychlcrinaticn process for the production of EDC that 419 grams cf dioxin ffEG) are formed fer each 100,000 tons of EDC produced. [Evers 198S] * 'n early 1934, the German EPA found extraordinarily high dioxin concentrations in wastes and wastewater treatment sludge from ICI's VCM/PVC plant in Wilhelmshaven, Germany, as shown in table 4.5. This plant is considered a modem factor,'. [Lower Saxony 193d] * VCM plants appear to be the most important source of dioxins in the North Sea and the River Rhine, according to a 1393 study of the dioxin fingerprint in sediments conducted by the Dutch Government and the University of Amsterdam . [Evers 1993] In 1990, dioxins wore found in the wastewater discharges from Sofvay's VCM plant in Rheinberg, Germany; total discharges were estimated at up to 8 grams TEG/ytiar. [Adeft 1990] In 1992, Norsk Hydro analyzed wastes from rts VCM plant in Stenungsgund, Sweden; dioxins were found in four waste streams, and total dioxin discharges into wastes were estimated at 321 grams TEQ/year. [Hydro-Plast 1992] A 1993 study by the University of Umeaa confirmed the occurrence cf dioxins in wastes from this facility. [Andersson 1993] A 1988 study by the University of Amsterdam found that the fingerprint of dioxin congeners in sediments from the River Rhine suggested that HTA' VCM plant was a major source of dioxin into that river. [Evers 1988] * A 1988 study by the Stichting Rainwater, a Dutch environmental organization, found that concentrations of dioxins and furans in the Rhine were significantly higher downstream from Solvay's VCM plant in Rheinberg, Germany, than upstream. [Verhoog 1988] A 1992 study by several Swedish universities found high levels of hexachlorobenzene, pentachlorobenzene and several congeners of dioxins and furans in sediments near Norsk Hydro's plant in Stenungsund. [Cato 1392] In 1993, Greenpeace commissioned the University of Amsterdam and SAL laboratory in the UK to analyze samples of effluent from a Solvay VCM plant and soil samples from the vicinity of a Norsk-Hydro oxychlorination reactor in Sweden. Botin contained significant quantities of dioxins and furans, as shown in Table 4.6. [Johnston 1994] r 'Hals Troisdod Ag Table 4.5 Dioxin from ICI's VCM/PVC plant in Wilhelmshaven, Germany Metal sludge Metal sludge cake Wastewater treatment sludge Sediment near discharge pqne Mussels near discharge Dioxin concentration na/ka TEG 408,270 413,790 7,199 1.7-3.9 0.71 - 4.44 Source: Lower Saxony Ministry of Environmental Affairs, 1994. -33 - xxxx. CTL014415 Thus, this body cf evidence shows that dioxins can be produced at a rate cf up to <*-CO g TEQ per 100,000 tens cf EDC. Using a very conservative estimate of 5 to 10 crams dioxin (TEQ) per 100,000 tonnes cf EDC [Wang-Anderson 1S92], and assuming U.S. production cf 10.4 m:!'ion tonnes of EDC per year, dioxin formation Tern tin's sector is estimated at 500-1OCO grams (TEQ) per year. Table 4.6 Dioxins in Effluent and So3 from two EDC/VCiVi plants in Europe Congener Effluent pg/U pg/L (TEQ) Y/asie {dry \vt.) og/g ng/g (TEQ) 2373-TCDO 12378-PeCDD 123478-HxCOD 1234678-HpCDD OCDD Other isomers 2378-TCDf 12378-PeCDF 23478-PeCDF 123478-HxCDF 123670-HxCDF 234673-HxCDF 123789-HxCDF 1234678-)-!pCDF 1234789-HpCDF OCDF Other isomers nd nd od 21 125 12 7.3 7.3 12 18 rid nd 228 24 4621 - ixf - nd - nd 0.2 nd 0.1 1.7 5.02 1.2 nd 0.4 nd 3.7 nd 1.2 3.4 1.8 .65 - nd - 1.7 2.3 17 0.2 nd 4.6 6700 165.8 - .001 - 0.34 0.07 - 0.17 0.17 - 6.7 Total 5068.3 15.7 G8S5.2 7.5 Source: Johnston et al 1994.. TEQ based on NATO-ITEQ system. The Norwegian government has also estimated., based largely on industry-supplied data, annual dioxin emissions from its VC/EDC plants into various media: 25 to 250 mg to air, 6-1 (X) mg into wastewater, 420 mg into sludge, 7.3 grams into EDC tars, and 10 grams in internal process streams. (SFT 1994] Assuming that U.S. production of VC/EDC is 15 times larger than that in Norway [SRI 1993), annual dioxin releases from the U.S. industry can be estimated as follows: Air: Water Sludge T-rS Internal streams 0.38 to 3.8 g/year (TEQ) 0.09 to 1.52 6.384 110. 152 Total 268 - 272 g/year (TEQ) CTL014416 - 34 - EPA cid not acknowledge the body of evidence indicating that FVC manufacture is a major dioxin source, citing a "lack of data." According to the agency, Recent!'/, seme claims have been made that significant dioxin emissions may occur during the production of vinyl chloride monomer and associated products. However, insufficient emission data are currently available to evaluate these reports. [Schaurn 19931 indi'eration of PVC products PVC is the l-rgest waste source associated with dioxin emissions from garbage and hospital waste incinerators. In numerous studies of combustion processes, PVC lias been idestifled as a precursor for dioxin formation. [Christman 1989, Thiesen 1989] According to one scientific report, "Samples from real fire accidents as well as from laboratory combustion tests ... demonstrate that in case PVC-containing materials take part in combustion processes, PCDD/Fs can be found in the decomposition products in considerable concentrations. Therefore, these results confirm the classification of PVC-containing materials as PCOD/F precursors. [Thiesen 1989] The German EPA has estimated that rigid PVC - such as botties and pots - is responsible for approximately 50 percent of all chlorine fed to municipal waste incinerators, though it constitutes only 0.5 percent of the total mass of wastes. [Brahms 1989] The Dutch Environment Ministry has estimated that PVC constitutes 40 percent of all chlorine - in either organic or inorganic form - fed to garbage incinerators, and the majority of organic chlorine. Analytical studies by the Ministry demonstrated that reducing the fraction of PVC burned results in a corresponding reduction in the emissions of dioxin and chlorophenols. [Boerekamps-Kanters 1993] Several reports have found a direct relation between the amount of PVC in the waste fed into an incinerator and the amounts of dioxin emitted. [Ozvacic 1990; Danish EPA 1993]. In the Netherlands, where an effective garbage separation system removes most cf the organic chlorides in compostable materials such as food and wood wastes, PVC remains the only major source of chlorine and the major dioxin precurso; reducing PVC feed results in significant decreases in dioxin emissions. [Boerekamps Kanter 1993] Based on these findings, the Dutch Environment Ministry concluded: "These new experiments by the University of Leiden demonstrate clearly a relation between the content of PVC in household waste and dioxin formation in waste incinerators. On the basis of these experiments there is no reason to reconsider present policies regarding PVC applications: the main feature of this policy is that PVC applications for which no feasible system of recycling and reuse can be established the use of more environmentally sound alternative materials is to be preferred." [Netherlands Environment Ministry 1994] In 1993 the Danish EPA found that "during incineration chlorinated dioxins and dibenzofurans are formed, and although emissions are reduced significantly by flue gas cleaning and better operation conditions, these persistent substances can still be spread and accumulated through food chains. PVC is the most S'gprfiraot :nd'v:dusl source of chlorine in muric'pal wzzte." [Danish EPA 1593! PVC is also the largest single source of chlorine in hospital waste incinerators. Chlorinated plastics (PVC) account for 9.4 percent of the total weight of "red bag" infectious waste, according to one study. (Marrack 1988] PVC is used in hospitals for packaging, containers, bags, tubing, and other uses. -35 - :nxc CTL014417 Receding cf PVC-containing products EPA has identified secondary copper smelters as one of the largest known dioxin sources, releasing 220-310 g/year TEQ. (Schaum 13931 Dioxin is produced at these facilities when PVC-ccated copper wire and cables are heated at very high temperatures for recycling. PVC is the primary source of chlorine feed to these units. According to one Germany study, Considerable amounts of dioxins and furans have been found in the flue gas as well as in soil from the near vicinity of copper reclamation plants, in these facilities, scrap copper containing varying quantities of PVC-coated cables is precleaned by combustion or pyrolysis and then recycled in a copper smelter, in the ambient air near a copper smelter, we could find in emission measurements surprisingly high concentrations of dioxins and furans. [Christman 1989] Recycling of steel with PVC is another major dioxin source. The two major sources of chlorine inputs are vinyl residues - particularly from automobiles - and chlorinated cutting oils. According to the authors: This pilot study clearly shows that PCDDs and PCDFs are formed during scrap metal melting processes. Combustion of PVC has been reported as one source of PCDDs and PCDFs in different combustion and pyrolytic processes, in this study, PVC is also found to give the highest emissions. [Tysklind 1989] A 1993 study by Finnish researchers also found very high emissions of dioxin from a metal reclamation plant and concluded that PVC was the most important dioxin precursor. According to the authors: The measured emissions may indicate that a large part of the chlorinated organic compounds are formed due to the chlorine in PVC plastic (PVC plastic in cables and car components). [Aittoia 1993] According to one Swedish study of such facilities, secondary steel smelters discharge dioxins in quantities ranging from 200 to 2200 ng per ton of steel (TEQ). An estimated 50.1 million tons per year of steel are recycled in U.S. secondary smelters. [U.S. DOC 1993] Dioxin emissions from this sector can thus be estimated at 10-110 grams per year (TEQ). f In rts preliminary dioxin reassessment documents, EPA noted that 'The secondary smelters which recover metal from waste products such as scrap automobiles have the potential for dioxin formation due to the plastic and associated chlorine in the feed material. Other countries such as Germany have identified this industry as potentially important." [Schaum 1993] EPA did not estimate dioxin emissions from any metal-PVC recyclers, however, except copper smelters. PVC in Fres Almost half of all PVC is used in building, construction, and furniture, including pipes, flooring, wallpaper, siding, wastebaskets, molded furniture, and other products. PVC probably constitutes the single most abundant synthetic material in the home. Just as burning PVC in an incinerator or smelter results in dioxin formation, so does accidental burning cf PVC in home and burning fires. Because combustion conditions in these fires cannot be optimized, dioxin :mx CTL014418 - 36 - forma ton may be even greater than in incinerators. Numerous studies have associated the presence of FVC in "res with major dioxin emissions. Gorman scientists have identified dioxin concentrations cf up to 10,000 ng/m2 on surfaces from accidental fires with large quantities of PVC and concentration of up to 200 ng/m2 alter "normal" fires in homes and offices. Soot samples from a fire at a German kindergarten - where substantial quantities cf PVC construction material burned - have been found to contain dioxin concentrations as high as 45 ppb TEQ - equivalent to 15,000 ng/m2. [Redler 1993] On July 1, 1993 a fire destroyed a plastics plant near Montreal, consuming an estimated 1 5,000 kg cf PVC in the factory. Tests by the Quebec Environment Ministry showed that ash from the fire was contaminated dioxins and furans at concentrations of 18 ppb (TEQ). Soil near the plant contained dioxins and furans at 0.55 ppb. Dioxin production in the fire was estimated at 40 to 85 grams, although the basis for this estimate is unknown. [Quebec Environment Ministry 19931 According to that figure, this single fire would be one of the largest known dioxin sources in Canada. In October of 1992 Microplast, a PVC recycling company in Lengrich, Germany, caught fire. The German Environmental Protection Agency (UBA) found that residues in the warehouse contained dioxn concentrations of 13.7 ppb TEQ. Cabbages growing 600 meters away showed an 88-fold increase in dioxin concentration above background levels. Cabbages growing 2.4 km downwind still exceeded the maximum acceptable limit for food of 1 ng/kg and were banned for sale. [UBA 1992] On November 27, 1992, a fire completely destroyed Euromat, a PVC factory in Diest, Belgium, which produced PVC granules for cars, cable, shoes, and the medical industry. Approximately 100 tons of PVC burned, and dioxins were found in fire residues in concentrations up to 87 ppt. PVC is now ubiquitous in construction projects. Any fire in a modem building is an important dioxin source, and any modem building is a potential dioxin source. Because PVC fires have been linked to significant dioxin production, the German Environment Ministry has called for the use of substitutes for PVC in all areas susceptible to fires. With fires in which PVC products are involved, the- residues contain higher amounts of dioxin than is the case with fires without PVC materials. The gases from PVC fires a/so include hydrogen chloride. PVC materials should not be used where the ciean-up measures which may be necessary lead to significant disruption of the public infrastructure.... PVC products in the building industry should be substituted for in those areas of use in which considerable dangers to the environment and health occur, and extensive ciean-up measures become necessary, as a result of the possible formation of dioxin and hydrogen chloride in fires.[German Env. Ministers 1992] The German EPA and Ministry of Health have made a similar order: "The use of plastics containing chlorine and bromine should be completely excluded, as far as is possible. UBA and BGA propose a ban on the use of plastics containing chlorine and bromine in apparatus susceptible to fire, in the manufacture of chip-board, as well as the labelling of plastics containing chlorine and if necessary a ban on the use of PVC in packaging. " [UBA 1992] An estimated 500,000 fires occur each year in Germany. [Fielderl 993] Based on the production of 40-85 g of dioxin [TEQ) at a single fire in a PVC factory in Canada, and the findings of comparably high concentrations of dioxin in residues from fires in "normal" buildings, total U.S. dioxin emissions from accidental fires may range from 500 to 5000 grams per year. -37 CTL014419 5: SECONDARY PRIORITIES: OTHER DIOXIN SOURCES A number of other sectors and product groups have been identified as important sources of dioxin during their manufacture, use, and/or disposal. These sectors include solvents, pesticides, other chlorine-based chemicals, water and wastewater treatment, and metallurgical processes. 1. CHLORINE PRODUCTION Dioxin contamination begins at the very first stage of chlorine chemistry - the production of chlorine gas through the electrolysis of salt water. Carbon-containing compounds C3n be present as impurities, in plastic materials, or from the graphite electrodes in some electrolytic ceils. [Schmrttinger 1986] Once produced, chlorine immediately reacts with these organic compounds to form organochlorine by-products. Chlorine gas has been found to be contaminated with dioxin-like compounds in concentrations ranging from 40 to 210 ppb, including the PCBs decachlorobiphenol and nanochlorobiphenyl, octachlorostyrene, and tetrachlorobenzene. [Hutzinger 1988] Based on these estimates, the 13 million tons of chlorine produced in the U.S. each year would thus contain from 472,000 to 2,480,000 grams of these dioxin-like compounds each year (not TEQ). Very high concentrations of dioxin (up to 650 ppb total) have been found in the sludges from spent graphite electrodes used in this process. [Rappe 1991] The dioxin-like compounds octachlorostyrene, HCB, and hexachloroethane are also found in these sludges. Most chlorine plants have replaced graphite electrodes in recent years with titanium substitutes. For years it was assumed that the removal of graphite electrodes eliminated dioxin formation from chlorine production . But data recentiy released by chlorine manufacturers in Sweden indicate that even the most modem chlor-alkali plants produce substantial quantities of dioxin. It appears that trace quantities of organic materials - particularly from plastic pipes and valves - are reacting with chlorine to produce dioxins. According to studies by the University of Umeaa, dioxins have been detected in sludge and plastic piping from chlor-alklai plants in concentrations of 4.65 and 5.13 ppt (TEQ), respectively. (Umeaa 1994] These data are presented in table 5.1 Because production of chlorine itself results in dioxin formation, all "downstream" products that rely on chlorine are thus associated with dioxin formation. 2. PESTICIDES For several decades, dioxin has been identified as a contaminant of some pesticides, such as 2,4,5-T, one of the major components of Agent Orange. New information suggests, however, that the problem is not limited to a few chemicals but actually extends throughout the entire range of ciiionne-based synthetic pesticides. :rcoc CTL014420 - 38 Th3 chlorine industry has argued that SS percent of all synthetic organic pesticides contain chlorine cr are manufactured using chlorinated intermediates. (CRA 1993] As a consequence, d'oxins apcear to occur as by-products in the manufacture of virtually all synthetic pesticides. Dioxi'n-like compounds are known or Table 5.1 Dioxins in Waste from A Modern Chior-AJkafi Plant Congener 2378-TCOD Total TCDD 2378-TCDF Total TCDF 12378-PeCDD Total PeCDD 12378-PeCDF 23478-PeCDF Total PeCDF 123478-HxCDD' 123678-HxCDD 123789-HxCDD Total HxCDO 123478-HxCDF 123678-KxCDF 123789-HxCDF 234678-HxCOF Total HxCDF 1234678-HpCDD Total KpCDD 1234678-HpCDF 1234789-HpCDF Total HpCDF OCDD OCDF Total TEQ Sludge (ng/L) .021 .19 . -47 2.17 .037 - .37 1.94 .70 7.4-8 .16 .09 .11 1.62 20.5 3.79 7.26 .84 36.0 .72 1.48 58.2 19.4 101 5.45 63.4 4.65 Polymer waste (ng/L) .0025 .02 .69 2.91 .016 .06 2.74 .79 7.66 .039 .008 .011 .13 30.6 7.99 .77 .42 25.3 .13 .22 38.5 7.09 57.9 .69 87.1 5.13 Source: University of Umeaa 1993. Samples are sludge and plastic pipe from a Swedish chlor-alkaS plant usrig titanium eiectrodesTEQ values using NATO method. suspected contaminants of approximately 100 pesticides, ranging from chlorophenols and chlorophenoxy acetic acids to dichloropropene, lindane, atrazine, and simazine. (See tables 3.2 and 3.4.) For instance, dioxins and furans have been detected at 160 ppt (TEQ) in 2,4-D, one of the most widely used herbicides in the U.S. [Schecter 19931 U.S. production of 2,4-D is estimated at 65 million pounds per year (EPA 1991 ]; dioxin contamination of this pesticide alone would account for the release 4.7 g of dioxin per year, plus additional amounts from production emissions and wastes. Dioxin concentrations in pesticides can -39 - CTL014421 :rxxr: be very high: for in3r2r.ce, wastes from the production of lindane may contain cdxi'n concentrations as high as 50 ppm (TEC! [Schciz 1337]. Dioxins are also associated with pesticides that do not contain chlorine but are mace with chlorinated intermediates. For instance, dioxins are known or suspected contaminants in parathion and ammonium dhitrcbutylphenol. [Esposito 1980, PCTN 985] Dioxins are also produced when the chlorine-containing wastes from pesticide manufacture are incinerated. Because these products are usually produced in mufti-step, complex processes, waste generation at pesticide plants is typically quite high; further, virtually all such wastes contain chlorine, since chlorine is involved in the production of almost all pesticides. Most pesticide production wastes are incinerated, leading to additional dioxin formation and release in the combustion process. In some cases, dioxins can be produced when chlorine-containing pesticides are used. For instance, dioxins have been identified as by-products when pentachlorophenate wood preservatives are heated to the temperatures used in pressure-treatment of lumber. [Rappe 1978] Chlorinated pesticides and the wastes from their production also produce dioxins when incinerated. EPA has estimated that 13,200 tons of incinerable pesticides are generated each year, plus presumably much larger quantities of chlorinated production wastes. [Oppeft 1987] 3. CHLORINATED SOLVENTS Solvents account for close to 10 percent of all chlorine production, and they are a correspondingly significant source of dioxins. Dioxins occur in the manufacture, use, and disposal of chlorinated solvents. Dioxin-like compounds are formed when chlorinated solvents are manufactured. Dioxins and furans have been identified in tetrachloroethyler.e, and 1,2-dichloroethane in concentrations up to 50 ppt (sum PCDD/Fs). (Heindl 1987] In addition, hexachlorobenzene has been identified in carbon tetrachloride, trichloroethylene, and tetrachloroethane. [Rossberg 1986] According to a German research team that found dioxin in a number of solvents and other aliphatic organochlorines, "These results suggest that the synthesis of short-chain chlorinated hydrocarbons can lead to PCDD/PCDF formation." (Heindl 1987] Table 5.2 Solvents and other Aliphatic Organochlorines Contaminated with Dioxin and Related Compounds Compound Carbon tetrachloride 1,2-Dichloroe thane Epichlorchydrin Kexachlorobutadiene Tetrachioroethylene Trichloroothvfeno Trichloroethylene * Contaminants detected HCB OCOF HpCDD, HxCDO, OCDD, HpCDF,OCDF OCDF OCOD, HC8 HCB TCDF, PeCDF, HxCDD, HxCDF, HpCDO, HpCDF, OCDO, OCDF References Rossberg 1986 Heindl 1987 Heindl 1987 Heindl 1987 Heindl 1987, Rossberg 1986 j Rossberg 1986 Heindl 1987 Heindl 1987 * Used in the presence of NaOH nniHiiumwnnimffTiTii'wii w rurewu mwarm narr: :xxn: CTL014422 -40- U.S. production of chlorinated solvents totals approximately 3 million tons per year. If dioxin contamination averages only 1 ppt these products would cany an estimated 2 grams per year of dioxin into the environment. However, because most solvents aie quite volatile - and dioxin is not-- the presence of dioxin in these products suggests that significantly greater amounts may be present in the heavier wastes from chlcr'nated solvent production. Although large quantities of hexachlorobenzene have been identified in wastes from these processes, no data are available on dioxin levels in these residues. The use of chlorinated solvents can also result in dioxin formation. Dioxins can be formed when chlorinated solvents are used for degreasing in the presence of alkalis - a common circumstance in many industrial applications. For instance, combining trichloroethylene with sodium hydroxide results in the formation of dioxins, furans, hexachlorobenzene, and octachlorostyrene. "It should be pointed out that trichloroethylene in alkaline medium is used occasionally in industrial processes: for the degreasing of metals, a combination of trichloroethylene, alkaline cleaners and emulsifiers is used at elevated temperatures. (Heindl 1987] The German Environmental Agency has confirmed this conclusion, finding that dioxins are produced in the following processes: "synthesis/extraction with chlorinated solvents, metal finishing, and dry cleaning." [Drechler 1992] Dioxin concentrations of 140 ppt have been identified in the distillation sludge from the use of perchloroethylene in dry cleaning, [l^exen 1992] The source of these dioxins, however, has not been determined: they may be formed in the dry cleaning or distillation process, occur as contaminants in the "virgin" perchloroethylene, or are accumulated in dothes and then washed out in the deaning process. Chlorinated solvents are also a primary source of chlorine - and thus of dioxin emissions - in hazardous waste incinerators. Although seme portion of spent chlorinated solvents are recycled, the vast majority are burned in incinerators or cement kilns. In 1983, about 1.1 million metric tons of chlorinated solvents were available for incineration, according to EPA estimates. [Oppelt 1987] 4. WATER AND WASTEWATER TREATMENT The chlorination of sewage and drinking water results in the formation and release of dioxins in a number of ways. First, the process of chlorination itself appears to produce diox'n-like compounds. Swedish researchers have found that chlorinated dibenzofurans are formed when chlorine-free dibenzofurans naturally present in water are treated with chlorine. The authors wrote, . "The pattern identified in this report.... could be called the chlorine pattern. For the tetraPCDFs it consists of the same isomers as the pulp leaching pattern. However, the chlorine pattern also contains higher chlorinated PCDFs, but no PCDDs. (Rappe 1989] Other researchers have identified chlorinated phenoxyphenols, also called "pre-dioxins" as a by-product of the chlorination of water. [Ondeira 1989] The ircreration cf chlorinated residues from wastewater and drinkrig water treatment plants results in further dioxin emissions. EPA has identified sewage sludge incinerators as a source of dioxin, with total emissions estimated at 1 -26 grams (TEQ) per year. Further, carbon filters used to remove contaminants from drinking water accumulate chlorinated disinfection by-products; when these filters are "recharged" at high -41 - :xrcc CTL014423 temperature, dioxins are formed and released. German scientists have found that the regeneration cf carbon fibers, "heavily loaded with organic chlorine," results in dioxin formation; littJe or no dioxin is released when no chlorine is added. [Hutzinger 1988] EPA estimates dioxin releases from this sector at less than 1 g/year. 5. CHLORINATED AROMATIC CHEMICALS. As discussed above, dioxin has been identified as a by-product in the production, use and disposal of the fuil spectrum of organochlorine compounds. Dioxins are contaminants in a wide-range of chlorinated benzenes, chlorinated phenols, and other chlorinated chemicals with ring structures. According to NATO scientists: AH processes involving the manufacture of chlorophenol derivatives a/so are suspected of producing PCDD and PCDF. Most likely all technical ch/orophenols and chlorophenol derivatives contain small amounts of PCDD and PCDF. These values show that all aromatic chlorinations are suspect of causing PCDD/ formation. Moreover, radical-side-chain chlorinations such as the chlorination of toluene are also relevant, because a small degree of nuclear chlorination can also occur. The following products are manufactured by chlorination or radical chlorination: chtoronitrobenzenes, chloroani/ine, 2,3,6-trich/orophenoxyacetic acid. [Hutzinger 1988] These compounds are used in a wide variety of processes in the chemical industry. Many are used in the production of pesticides, and some chlorophenols are commercial pesticides themselves. Chlorinated aromatics are used in the manufacture of specialty chemicals and additives for plastics, nylon, synthetic rubber, dyes, and pharmaceuticals. Extremely high concentrations of dioxins have been identified in several types of synthetic dyes - including phthalocyanine, dioxazine, and other dyes - as well as candles and other products made with these dyes. [Hutzinger 1988] The Swedish Environmental Protection Agency has identified dioxins in wastes from the pharmaceutical industry, in concentrations of approximately 2.5 ppt. [Lexen 1992] 6. OTHER CHLORINATED ORGANICS Other chlorinated organic chemicals are associated with dioxin formation. The production and use of many of these compounds in the chemical industry have been identified as dioxin sources. In addition, whenever these products are used, wastes are produced containing a diverse cocktail of chlorinated wastes. The majority of these wastes are burned, leading to additional dioxin emissions. For instance, epichlorohydrin - an intermediate used in the production of epoxy resins - is itself contaminated with dioxin. Dioxins and related compounds have also been found in concetnrations as high as 425 ppt (total) in hexachlorobutadiene, a short-chain aliphatic organochlorine used in the production of rubber and plastics. (Hutzinger 1988) In addition, chlorinated intermediates are by definition used in highly reactive environments, and the formation of dioxin is a likely outcome. According to NATO scientists, "All industrial chemical processes hv which chlorine or hydrogen chloride is cleaved from intermediate products must be critically regarded with respect to PCDD/PCDF formation. Such chemicals and substance which contain no chlorine in the end product (in particular those resulting from eliminations, dehydrochlorination, and alkaline hydrolyses! should be especially considered. " [Hutzinger 1988] :rxxc CTL014424 -42- Air emissions and wastewater effluents from oil refineries that use crganochlorine compounds to regenerate spent catalysts. Concentrations of total dioxins and furans in in liquid effluent were found to bo as high as 100 ppq, while concentrations in air emissions wore over 200 ng/M3 - greater than that found in many incinerator stack gases. [Thompson 1990] Chlorinated 'wastes from the production and use of these other organochlorines also results in dioxin formation and release. Production of any organochlorine results in the generation of waste liquids, solids, and sludges, and incineration is the dominant disposal method for these wastes. EPA has estimated that a 9.78 million metric tons of halogenated solvents, 0.72 miilion metric tons of halogenated sludges, and 1.25 million metric tons of halogenated liquids (excluding solvents) were available for incineration in 1983. [Oppeft 1987] 7. INORGANIC CHLORINE CHEMICALS: CHLORIDES AND BLEACHES According to NATO, "The processes to manufacture metal chlorides, chlorine, NaOCI (sodium hypochlorite) and hydrochloric acid are suspected of causing PCDD/F formation. " [Hutzinger 1988] Of particular concern are inorganic chlorine compounds containing iron or copper, since these metals are catalysts that accelerate dioxin formation. Tests at the University of Bayreuth have found detectable quantities of dioxin in chlorides of iron, aluminum, and copper. [Hutzinger 1988] Swedish researchers have found that iron chloride used for water treatment contains significant quantities of dioxin and furans. [Rappe 1991] Sodium hypochlorite (common household bleach) has been found to contain hexachlorobenzene and tetrachlorobenzene - markers of possible dioxin contamination - in the low parts per trillion range. IHutzinger 19881 In addition, the use of chlorine-based bleaches and detergents in home dothes washing machines and dishwashers has been found to increase the concentration of dioxins in wastewater from these appliances. According to Swedish researchers, net production of dioxin is 8 pg TEQ per dishwashing cycle and 6 pg TEQ per dothes washing cycle. [Rappe 1992] * Table 5.3. Dioxins and Related Compounds, in Inorganic Chlorides Compound HpCDO Iron chloride (FeQ3l Aluminum chloride (AIQ3) Copper chloride (CuO) Copper chloride (CuQ2) Titanium tetrachloride Siicon tetrachloride Sodum hypochlorite (NaOG) - - 0.03 - - HpCDF 12 - 0.08 0.1 - - (ppb) OCDD QCDF - 48 0.1 34 0.2 0.08 0.6 0.5 ---- PCB-9 200 - 0.09 - - PCS-tO 830 - 0.08 0.02 0.02 - OCS 280 77 .3 0.04 - HCB TC8 4000 . 1100 - 1 0.2 4--.001 . 004 PCB-9 = nanochJorobipherryl, PCS-10 = decachlorobiphenyl, OCS = octachlorostyrene; TC8 = tetrachlorobenzene. Source: Hutzinger 1988 :xxxx-43- CTL014425 8. METALLURGICAL PROCESSES Eemental chlorine gas used in the production of certain metals combines with any organic material present to form organochlorine by-products, including dioxins. High concentrations of dioxins and related compounds have been identified n the emissions from several types of metal processing plants. Dioxins may be formed when chlorine is used in the production of refined nickel and magnesium. Annual emissions from one magnesium plant in Norway have been estimated at 500 g/year (TEC!) to air and water, while emissions from a nickel plant have been estimated at 1 g/year (TEQ) to water alone. Emissions of hexachlorobenzene from the magnesium factory were estimated at over 350,000 grams per year. In addition high concentrations of PCDFs have accumulated in fish tissues near the nickel production facility. [Oehme 1989] Recentiy, iron and steel plants have been found to be major sources of dioxin. German analyses show that such plants may emit dioxin in their stack gas in concentrations of 3 - 10 ng/M3 (TEQ). [Lahl 1993] The Swedish and Dutch governments have also identified iron sinter plants :s very large sources of these compounds. (Rappe 1992] Dioxins are produced in this process because of the introduction of chlorinated chemicals such as cutting oils and solvents. According to one analysis: "Sintering plants serve for recycling of dusts, scrap and abrasion from other . processes of the metallurgical plant to recover the iron for further use in the blast furnace. But this reasonable waste management method is accompanied by the problem of introducing traces of chlorine and organic compounds responsible for the generation of PCDD/F within these plants. [Lahl 1993] According to one analysis, air emissions of dioxins from these plants acount for 300-1000 g/year (TEQ) in Germany alone. [Lahl 1993] U.S. production of steel is approximately twice as great as that in Germany; dioxin emissions from this sector in the U.S. may thus range from 600 to 2000 grams per year, making this one of the largest of all known dioxin sources. [U.S. DOC 1993] 9. Environmental transformation of other organochlorines * Several studies have found that chlorophenols may be transformed under environmental conditions into dioxins and related compounds. These transformations may occur due to enzymatic or photolytic reactions. [Oberg 1990, Oberg 1992, Plimmer 1973] Several studies have found that the concentration of dioxins in sewage sludge and compost actually increases over time with no apparent input of dioxins, it appears that chlorophenols - and possibly other organochlorines - are being transformed into dioxin during the composting process. [Oberg 1992, Shafer 1992] Typically, the total TEQ in such a mixture may increase by 2- to 3-fold during composting. [Oberg 1992] If chlorophenols can be transformed into dioxin, it is plausible that some other organochlorines particularly other aromatics such as chlorobenzenes, PCRs, phenoxy hertticides, and others - could be changed into dioxins as well. The production of dioxin due to the environmental transformation of organochlorines released into the environment from industrial and agricultural sources may be a significant unquantified dioxin source. No data are available from which to estimate dioxin production due to this phenomenon. :rxxx CTL014426 -44 - 6: RECOMMENDATIONS: THE ZERO DIOXIN PROGRAM NEED FOR EMERGENCY ACTION EPA's reassessment indicates that dioxin contamination poses a serious threat to public health. Because dioxin is so persistent in the environment and in the human population, contamination that has already occurred will not disappear quickly. One analysis found that if all exposures to PCBs could be stopped immediately, It would take six generations before body burdens would return to non-detectable levels. [Swain 1988] The first principle of environmental and public health practice is prevention. It is not ethical or necessary to delay action until it has been conclusively proven that dioxin contamination has caused large-scale damage to health and the environment. By then, it will be too late. The evidence indicates that current dioxin contamination poses current or future threats to the general population, and It is possible that the damage may have begun already. This information provides more than adequate scientific support for a shift in regulatory policy, based on the principles of public health protection. Environmental policy on dioxin must shift to preventing further releases and exposures. EPA should initiate a comprehensive dioxin elimination program, including immediate action to eliminate the largest dioxin sources and medium-term measures to address additional dioxin-producing sectors. Based on the conclusion that the environment and the human population are already excessively loaded with these compounds, EPA must act now to bring all additional emissions of dioxins to zero. Policy changes on dioxin can be modeled, in part, on experience with another pollutant - lead. In the 1970s and 1980s, health scientists found that lead - a persistent metal emitted by a multiplicity of sources, including vehicles, chemical plants, and paints - - had accumulated in the environment and in the bodies of the human population to levels that threatened the health of a large fraction of the nation's children. Subsequently, EPA policy - once a source-by-source approach that sought to control and permit lead releases - was transformed into an overall strategy to prevent lead emissions from every identifiable source, with the goal of reducing lead exposure and body burden for every American. Although EPA has not strictly followed this policy, the result has been significant achievements, including the phase-out of leaded gasoline and paints - the largest single sources of lead emissions- and consequent reductions in environmental contamination and blood lead levels in young children. With the lead model in mind, EPA should immediately establish a national program that applies a prevention-based approach to all known sources of dioxin, while identifying and targeting additional, yet-to-be-identified sources. The goal of the program should be to eliminate all discharges of dioxin and achieve substantial reductions in environmental concentrations, human exposures, and human body burdens of dioxin and related compounds. The large number of dioxin-producing products and processes makes the implementation of a dioxin elimination program more difficult than a lead prevention policy. Installing dioxin-free alternatives in the full range of industrial sectors will require substantial technical and economic conversion. On the other hand, the health hazard posed by dioxin is compelling, and measures to protect public health and the environment should -45 CTL014427 not be delayed. In the largest dioxin-producing sectors for which the alternatives are available and feasible, act'on should be taken now; those sectors that require longer implementation phases should be placed on timelines for dioxin elimination. Thus, a dioxin elimination program should be divided into tiers for immediate and medium-term action. PRINCIPLES OF THE ZERO DIOXIN PROGRAM 1. ZERO MEANS ZERO. Sources of dioxin must be eliminated, not simply reduced. The ecosystem may have the capacity to "assimilate" limited quantities of chemicals for which there are substantial natural biogeochemical cycles (such as carbon or nitrogen compounds), but it has no ability to assimilate persistent synthetic toxic substances - such as dioxins. Even dilute releases of these chemicals build up in the environment over time, eventually reaching levels that threaten public health and the environment. Thus, the ecosystem's assimilable capacity for dioxin and related compounds is zero. The current crisis, in which dioxin levels have reached the range that threatens public health, demonstrates the failure of the "acceptable discharge" approach to dioxin. Given the current health threat, it would be wholly inappropriate for EPA to continue to permit the release of dioxin into the environment - even in reduced amounts. To protect public health, inputs of dioxin and related compounds into the environment must be eliminated. 2. POLLUTION PREVENTION, NOT CONTROL. Once dioxin is produced, it is too late to prevent its discharge into the environment; pollution control devices, filters, treatment systems, and disposal methods such as burning and burying simply shift captured chemicals from one environmental medium to another or delay their release until a later date. Pollution control is an inappropriate strategy for a class of persistent chemicals that resist treatment and disposal methods, for which the ecosystem has no assimilable capacity, and which have already accumulated to excessive levels in the environment. The goal of eliminating dioxin discharges can only be achieved if the Zero Dioxin Program focuses on prevention. The industrial processes and feedstocks that result in dioxin formation must be chapged so that no dioxin is formed. Products that involve the formation of dioxin at some point during their lifecycle manufacture, use, or disposal - must be altered rf possible or otherwise banned. Processes that result in dioxin formation, such as incineration or the pulp bleaching, must eliminate the feedstocks that lead to dioxin production or be shut down altogether. 3. ADDRESS ALL DIOXIN SOURCES. The program must address all known and suspected sources of dioxin in order to bring future releases of dioxin to zero. In its reassessment documents, EPA has focused on only a few of the many sources of dioxin; these account for only 10 to 50 percent of all dioxin releases. The Zero Dioxin Program must take a comprehensive approach to all dioxin sources, including those that are suspected. 4. SET PRIORITIES FOR DIOXIN ELIMINATION. Some products and processes are known to account for large quantities of dioxin during their lifetime. The Zero Discharge program should be implemented so that the largest sources - and those for which alternatives are most readily available - are phased-out on the shortest timelines. :nxc CTL014428 -46- STEP 1: ESTABLISH A NATIONAL ZERO DIOXIN PROGRAM 1. National goal. EPA should establish a national Zero Dioxin program with the stated goal that all releases of dioxin be brought to zero within 10 years through the elimination of those products, feedstocks, and processes that lead to dioxin formation. 2. Moratorium on new dioxin permits. EPA should grant no new permits to release dioxin into any environmental medium. 3. Sunset existing dioxin permits. EPA should modify all existing dioxin release permits to include timetables for the reduction and eventual elimination of all dioxin releases. 4. Comprehensive approach to all sources. For the many dioxin sources that are not currently permitted or regulated, EPA should begin a process to identify and prioritize all dioxin sources and require their elimination within 10 years. All facilities that manufacture, use, or dispose of chlorine or chlorinated organic chemicals should be required to test for dioxin formation in their products, processes and wastes. Any identifiable release of dioxin and related compounds should reported under federal Right-to-Know programs. STEP 2: IMMEDIATE PRIORITIES: MAJOR DIOXIN SOURCES In the largest dioxin-producing sectors, EPA should take immediate action to reduce and eliminate dioxin releases. 1. Incineration. Incinerators that bum chlorinated wastes are the largest known producers of dioxin. EPA should take the following actions: Race an immediate moratorium on permits for new combustion facilities that bum chlorinated wastes and on permits for expanded capacity at existing units. Modify immediately all combustion device permits to include sunset provisions to reduce and finally eliminate the input of chlorinated wastes and products. This policy should apply to all combustion devices, including but not limited to incinerators, boilers, kilns and furnaces that bum hazardous wastes; incinerators for trash, hospital waste, sewage sludge, and tires; and metal smelters and sintering plants. In turn, focus waste reduction programs on eliminating the generation of chlorinated incinerable wastes, particularly solvents, PVC, and wastes from the production and use of chlorinated substances in the chemical industry. Immediately ban the addition of chlorinated compounds to fuels, including gasoline, diesel, and jet fuel. Minimize the burning of chloride-containing wastes (i.e., food and yard wastes) in trash incinerators through garbage separation programs. 2. Pulp and Paper. The use of chlorine, chlorine dioxide, and other chlorine-based bleaches in the paper industry is the second largest dioxin-producing sector and the largest source of dioxin discharges directly to waterways. Oxygen-based and other alternative bleaching methods are available and in use in 55 pulp mills throughout the world to produce a range of high-quality, bright paper suitable for the most demanding uses.[Albert 1934] EPA should establish rapid timelines for the phase-out of all chlorinebased bleaches in the pulp and paper industry. -47 CTL014429 3. PVC. In manufacture, use, accidental combustion, recycling and disposal, PVC results in more dioxin formation than any other single product. Wood, metals, ceramics, glass, wood, paper, and chlorine-free plastics provide the necessary technical properties to replace PVC in virtually all uses; over 80 communities, along with numerous hospitals and manufacturers of automobiles, consumer products, flooring, furniture, e'ectronics equipment and office products in several European nations have virtually eliminated PVC in a full range of applications. EPA should take the following actions Establish a PVC phase-out program, with progressive reductions toward zero in the production and use of PVC. Immediately ban short-life PVC uses, such as packaging, toys, and non-essential medical supplies. Initiate a phase-out of all uses of PVC in areas susceptible to fire and in products subject to combustion-based recycling (i.e., construction, furniture, automobiles, and cable sheathing). Initiate a phase-out of PVC in all other uses. Exceptions can be made if there are minor PVC uses that serve compelling social needs for which alternatives are not yet available (i.e., certain medical uses). Modify all discharge permits for chemical plants that produce PVC feedstocks to include sunset provisions on dioxin discharges to all environmental media, including deposition of dioxin into wastes and residues for disposal or treatment. 4. Chlorinated aromatic chemicals. This class of chemicals, with their close structural relationship to dioxin and related chemicals, result in significant quantities of dioxin formation in manufacture, use and disposal. EPA should immediately ban all open uses of chlorinated aromatic compounds (i.e., pesticides) and establish a phase-out program for all other uses. STEP 3: SECONDARY ACTIONS: BEGIN CHLORINE PHASE-OUT As discussed in this report, all uses of chlorine and chlorinated organic chemicals are susepcted of dioxin formation at one or more points in their lifecycle - from the production of chlorine itself to the disposal and recycling of chlorinated products and wastes. Thus, a dioxin phase-out program is tantamount to a phase-out of chlorine chemistry, and all uses of chlorine must be critically regarded for dioxin formation. * Phasing-out all uses of chlorine and chlorinated organic chemicals, of course, involves significant economic and technological change that will require phased implementation. While immediate action takes place in the priority sectors discussed above, the following dioxin-producing sectors should be placed on timetables for phase-out, with schedules based on the magnitude of releases, the availability of alternatives, and the ease of their implementation. 1. Chlorinated solvents. During production, incineration, and some uses, chlorinated solvents result in dioxin formation. Viable water-based, mechanical, and chlorine-free chemical alternatives are available for cleaning, degreasing, and coating in a full range of industries. EPA should establish a rapid timetable for the phase-out of the production and use of all chlorinated solvents. 2. Chlorine-related pesticides. Dioxins are formed in the production, some uses, and disposal of chlorine-containing pesticides and in die production of non-chlonnated pesticides made w.th chlorinated intermediates. The National Academy of Sciences has found that farmers can adopt organic farming methods, reduce or eliminate the use of synthetic pesticides, and enhance their profits and crop yields. (NAS 1989] EPA should establish a phase-out timetable for all chlorine-related pesticides. :mx CTL014430 -48- 3. Other chlorinated organic chemicals. Dioxins are formed in the production, some uses, and disposal of all other chlorinated organic chemicals, such as intermediates, catalysts, and specialty chemicals. Alternatives are available now for most such uses (i.e., chlorine-free alternatives to chlorohydrin and phosgene intermediates have been developed by major chemical companies) [Robert 1994] and can be developed for others. EPA should establish timelines for phasing-out the production and use of all other chlorinated organic chemicals. Uses that serve a compelling social need (i.e., pharmaceuticals) for which no alternatives are available should be exempted from the program. 4. Metallurgy and inorganic chemicals involving chlorine. Dioxins are formed when chlorine and chlorinated compounds are used in metallurgical processes and in the production of some inorganic chlorinated chemicals (certain metal chlorides, hypochlorites, etc.). EPA should establish phase-out timetables for the use of chlorine in high-temperature metallurgy and for all inorganic chlorinated chemicals in which dioxin formation has been identified. 5. Wastewater treatment. Dioxins and related compounds are formed in the chlorination of drinking water and sewage and in the incineration of sludge from water treatment plants. Effective alternatives -- including ultraviolet light, ozone, hydrogen peroxide, slow sand filtration, and membrane filtration - are in use in water systems across the world. EPA should establish timelines for the implementation of chlorine-free water treatment methods while insuring that adequate disinfection continues. In most cases, chlorine-free methods for water disinfection can be implemented more quickly than the use of chlorine as a residual can be eliminated. 6. Remediation. A substantial quantity of dioxin and PCB-contaminated materials are now present in landfills, sediments, and stored industrial wastes. EPA should intensify the development and application of non-combustion methods for the degradation of these materials. Politics! and economic implications Faced with severe health hazards of environmental pollution, society has repeatedly taken large-scale action to prevent further harm. In addition to the lead example, the U.S. government has banned or restricted numerous individual toxic substances as well as the class of polychlorinated biphenyls. More/ecently, most of the world's governments have agreed to phase-out the production and use of the class of chlorofluorocarbons and other ozone-depleting substances. An even more ambitious approach is necessary and justified to address the severe hazards posed by the accumulation of dioxin in the environment. Calls for a phase-out chlorine chemistry to eliminate the production of persistent toxic pollution, however, have ample precedent: The International Joint Commission on the Great Lakes has recognized the fact that dioxin formation occurs throughout the field of chlorine chemistry and that the mix of by-products formed in the lifecycle of chlorine and chlorinated organic chemicals cannot be prevented or controlled. Thus the UC has called on the U.S. and Canada to begin a phase-out of all uses of chlorine and chlorinated organic chemicals as industrial feedstocks. [IJC 1992, IJC 1994] The American Public Health Association has made a similar recommendation. In 1993, the APHA found that "the only feasible and prudent approach to eliminating the release and discharge of chlorinated organic chemicals and consequent exposure is to avoid the use of chlorine and its compounds in manufacturing processes." On this basis, the organization resolved that chlorine and chlorinated organic -49- CTL014431 compounds be treated as a class for phase-out with exceptions to be made only for uses that can be demonstrated to pose no significant hazard or for which no alternatives are available. [APHA 1994] The 15-nation Paris Convention on the Northeast Atlantic and the 21-nation Barcelona Convention on the Mediterranean Sea have agreed that the discharge of persistent, bioaccumulative toxic substances particularly organohalogens such as dioxins - must be brought to zero on rapid timelines. The White House itseif has also begun to move towards the comprehensive regulation of the field of chlorine chemistry. In its proposal for the Clean Water Act, President Clinton proposed to develop "a national strategy to reduce, substitute, or prohibit the use of chlorine and chlorinated compounds." Specifically, this recommendation consisted of an 18-month study and a 12-month period of policy formulation and review, with the focus on major chlorine uses, including pulp bleaching, PVC plastic, solvents, and water treatment. Wrthout question, phasing-out dioxin sources will require substantial technological and economic transformation, as numerous products and processes are converted to chlorine-free alternatives. Although this conversion will require substantial investment in some sectors, most of the alternative products and processes provide economic benefits in terms of increased employment improved efficiency, decreased expenses for chemical procurement waste disposal, liability and remediation, and the elimination of the social costs associated with damage to health and the environment. The medium- and long-term economic benefits to industry and society have been dearly demonstrated for chlorine-free pulp bleaching, elimination of chlorinated solvent use in manufacturing and dry deaning industries, pestiride-free agriculture, and numerous chlorine-free methods of chemical manufacturing. [Thornton 1994] The transition is significant enough that there will be substantial costs and benefits and the possibility of economic dislocation in sectors that manufacture chlorine and chlorine-based chemicals. If it is guided by careful planning, the economic benefits of this conversion process can be maximized, the costs minimized, and both distributed equitably. Thus, the long-term aspects of the Zero Dioxin Program should be subject to a transition planning process, with the participation of all stakeholders - induding labor, communities, environmentalists, chemical users and chemical producers. The goal of this process should be to insure that the safest and most beneficial alternatives are used, to minimize economic dislocation by directing investment in dioxin-free alternatives to those communities where dioxin-produring processes have been phased out, and to protect workers and communities who do experience economic dislocation by providing income protection, health coverage, and the opportunity for substantial advanced education, retraining, and/or placement. The International Joint Commission, labor unions [OCAW 1993], the APHA, and environmental organizations have all called for such transition planning and/or worker protection as essential components of any chlorine phase-out program. CTLOI4432 -50- REFERENCES Adetr (1990). Untersuchung des abwasser auf Diowne und Furane, Deutsche Sofvay Werke Rheinberg. (letter to Dusseldorf Regierungspresident) Dusseldorf: Solvay, 23 August 1990. Afttola, J. et al (1993) Measurements of Organochloro Compounds at a Metal Reclamation Plant," Chemosphere, 27:65-72. Albert, R. (1994). "TCF Mills." Distributed at the Non-Chlorine Bleaching Conference, Amelia Island, Rorida, March 1994. See also, J. Pearson (1992). TCF: there's no holding back the tide. Pulp and Paper International, April 1992, p. 72. Allan, R., et al. (1991) Toxic Chemicals in the Great Lakes and Associated Effects: Volume I - Contaminant Levels and Trends. Ottawa: Government of Canada, 1991. Andersson, P,, et al. (1993). Analys av PolykJorerade Dibensofuraner och Polyklorerade Dibensodioxiner i Processprover fran Hydro Plast AB. Universityof Umea, Sweden. September 1993. (APHA) American Public Health Association! 1994). Resolution 9304: Recognizing and Addressing the Environmental and Occupational Health Problems Posed by Chlorinated Organic Chemicals. American Journal of Public Health 84(31:514-515. Bailey, J. (1992) Dueling studies: how two industries created a fresh spin on the dioxin debate. Wall Street Journal, February 20, 1992, p. 1. Bimbaum, L. (1993). The mechanisms of dioxin toxicity: relationship to risk assessment. Environmental Health Perspectives, in press. Bimbaum,L. et al. (1993a) The US EPA's scientific reassessment of the risks of exposure to dioxin. Organohalogens 14:1-4, 1993. Blumenthal and Serumgard, J. (1992). Scrap tires find future on the road and in the tank- World Wastes, August 1992, 42-49. (BLAU 1992) Bund/Lnder-Ausschuss feuer Umwehfragen zu PVC; (Federal/State Commission on Environmental Questions reg. PVC), Dusseldorf Septmber, 1992. * Boerekamps-Kanters, J., and R. Louw. (1993) Rnal report of the RUL-VROM project: GFT, PVC, Afvalverbranding en 'Dioxine' (Green Waste Fraction, PVC, Waste Incineration and 'Dioxins'), Centre for Chemistry and the Environment. Department of Chemistry of the University of Leiden, the Netherlands, report number CCESRS 93-09. Brahms, E. et al (1989). "Papier Kunststoff Verpackungen. Bne Mengen und Schadstoffbetrachtung." UBA Berichte, Berlin. Bretthauer, E. (1992). Update on Dioxin Reassessment Activities: Memo to the Administrator. Washington, D.C.: U.S. Environmental Protection Agency, Office of Research and Development October 9, 1992. Browner, C. (1993). Draft Strategy for Combustion of Hazardous Waste. U.S. Environmental Protection Agency, May 18, 1993. See also, U.S. EPA, Environmental Fact Sheet: Source reduction and combustion of hazardous waste. May 18, 1993. Cato, J. (1992). Investigation of sediments off the Bohus Coast 1990: Coastal Water Monitoring Program of the Goteborg and Bohus County. Sveriges Geologiska Undersokning. Rapporter och meddelanden nr 74. -51 - :xxxx CTL014433 (CARB 1990). Lew, G. Preliminary test data from the Modesto Energy Company Evaluation Test,. Sacramento: California Air eEsources Board. February 1990. (CRA) Charles River Associates (1993). Assessment of the Economic Benefits of Chlor-alkali chemicals to the United States and Canadian Economies. Prepared under contract to the Chlorine Institute, Washington D.C., Christmann, W., (1989) "Combustion of Polyvinylchloride-An Important Source for the Formation of PCDD/PCDF." Chemosphere 19:387-392. Cleverly, D. (1993). USEPA Exposure Assessment Group, Office of Health and Environmental Assessment, Office of Research and Development, "Dioxin Reassessment Update," for Presentation at the EPA Regional Waste Combustion Permit Writers Workgroup Meeting, December 15, 1993. Connett, P. (1994). The Columbus, Ohio, waste-to-dioxin trash incinerator. Waste Not 275:1-2, April 1994. Czcuzcwa, J., and R. Hites (1986). Airborne polychlorinated dibenzo-p-dioxins: sources and fate . Chemosphere 15:1417-1420. (Danish EPA 1993) Miljoministeriet Miljostyrelsen (Danish EPA), "PVC and Alternative Materials," (English translation) Copenhagen, 1993. Drechsler, W. (1992) The Formation of PCDDs and PCDFs from the industrial use of chlorinated compounds. 12th International Symposium on Dioxins and Related Compounds. Organohalogens 8:231. ENSR (1993). ENSR Consulting and Engineering. Trial Bum Results, Waste Technologies Industries, East Liverpool, Ohio. May 1993. Esposito, M., T. Tieman, and F. Dryden (1980). Dioxins. Washington, D.C.: U.S. EPA, EPA-600-2-80-197. Evers, E,, K. Ree, and K Olie (1988). Spatial variations and correlations in the distibutionof PCDDs PCDFs and related compounds in sediments from the river Rhine. Chemosphere 17:2271-2288. Evers, E. and K. Olie (1989)."De Vomning van PCDFs, PCDDs en gerelateerde Verbindingen bij de Osychlorering van Etheen," University of Amsterdam, MTC publication hr. MTC89EE, 1989. Evers, E., H. Klamer, R. Laane, and H. Govers (1993). Polychlorinated dibenzo-p-dioxin and dibfenzofuran residues in estuarine and coastal North Sea sediments: Sources and distruvtion. Environemntal Toxicology and Chemistry 12:1583-1598. Fiedler, H. (1993). Formation and sources of PCDD/PCDF. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 11:221-228. Fiedler, H,, 0. Hutzinger, and J. Hosseinpour. (1993) Analysis and remedial actions following an accidental fire in a kindergarten. Organohalogens 14:19-23. (GCE, 1990) Sondergutachten des Rates von Sachverstandigen fur Umweltfragen vom September 1990 "abfall wirtschaft" Stuttgart 1991, paragraph 770. (German EPA, 1991) J. Theisen et al., "Investigation in possible risk to the environment from burning plastics," commissioned by the German EPA, report no. UBA-FB 104 09 222. German Environment Ministers (1992). Impacts on the Environment From the Manufacture, Use and Disposal and Substitution of PVC. German Joint Federal-State Committee on Environmental Chemicals for the German Environmental Ministers, September 1992. .'rax CTL014434 -52- Giesy, J. Ludwig and D. Tillrtt (1994). Deformities in birds of the Great Lakes region: assigning causality. Environmental Science and Technology 23(3): 128-135A. Gruber, L.( E. Stohrer, and H. Santi (1993). PCDD/F in the paper industry: new results and mass balances. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 11:315-318. Harrad, S., A. Sewart, and K. Jones. (1992). PCDD/Fs in the Birtish environment: sinks, sources and temporal trends. 12th International Symposium on Dioxins and Related Compounds. Organohalogens 9::89-92. Heindl, A., and 0. Hutzinger (1987). Search for industrial sources of PCDD/PCDF - III. Short-chain chlorinated hydrocarbons. Chemosphere 16:1949-1957. Hutzinger, 0., and H. Fielder (1992). From source to exposure: some open questions. 12th International Symposium on Dioxins and Related Compounds. Organohalogens 9:1-5. Hutzinger, 0., and H. Fiedler (1988). Formation of dioxins and related compounds in industrial process. Pilot Study on International Information Exchange on Dioxins and Rlated Compounds #173. North Atlantic Treaty Organization Committee on the Challenges of Modem Society, August 1988. HydroPlast (1992). Erinringar med alniedning av Nya yttranden 1992-09-23 och 1992-10-02 fran Greenpeace i arende M92/610-8. (IJC 1991). International Joint Commission on the Great Lakes. 1991 Science Advisory Board Report. Windsor: International Joint Commission. (IJC 1992). International Joint Commission on the Great Lakes. Sixth Biennial Report. Windsor: International Joint Commission. (IJC 1994). International Joint Commission on the Great Lakes. Seventh Biennial Report. Windsor: International Joint Commission. Johansson, N. (1993) PCDD/PCDF and PCB, the Scandinavian Situation. Organohalogens 14:337-340. Johnston, P. S. Troendl, R. Clayton, R. Stringer, and K. Stairs (1994). PVC: The Need for an ndustrial sector approach to environmental regulations. Submission to the Sixth Meeting of the Working Group on Industrial Sectors. Amsterdam: Greenpeace International, January 1994. * Lahl, U. (1993). Sintering plants of steel industry: the most important thermal PCDD/F source in industrial regions? 13th International Symposium on Chlorinated Dioxins and Related Compounds Organohalogens 11:311-314. Lexen, K,, C. deWitt, et al. (1992). Polychlorinated dibenzo-p-dioxin and dibenzofuran levels and patterns in samples from different Swedish industries analyzed within the Swedish dioxin survey. 12th International Symposium on Dioxins and Related Compounds. Organohalogens 9:131-134. Lee, A., B. Campbell, and W. Kelly (1987). Dioxin and Furan Contamination in the Manufacture of Halogenated Organic Chemicals. Cincinnati): U.E. EPA Hazardous Waste Engineering Research Laboratory. EPA/600-S2-86/101. Lower Saxony Ministry of Environmental Affairs (1994). Data report and press release, dioxin data from ICI facility, Wilheimshaven, Germany. March 22, 1994. Marklund, S., et al. (1990). Emissions of PCDDs nd PCDFs in gasoline and diesel fueled cars. Chemosphere 20:553-561. -53- CTI.0l4435 :mx Mantykoski, K., J. Passivirta, and E. Manmla (1989). Combustion porudcts of biolsludge from pulp mill. Chemosphere 19:413-416. Marrack, D. (1988). Fort Bend Medical Clinic, Houston, Texas, "Hospital Red Bag Waste: An Assessment and Management Recommendations," JAPCA, Volume 38, No. 10, October 1988. (MrT, 1993) "The M.I.T./Norwegian Chlorine Policy Study," M.l.T. Program in Technology, Business and Environment, M.l.T. Center for Technology, Policy and Industrial Development, March, 1993. Malsch, R. (1993). Determination of dioxins and furans in coloured candle wax. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 11:321-324. (NAS 1989) Committee on the Role of Attemative Farming Methods in Modem Production Agriculture, Board on Agriculture, National Research Council, National Academy of of Sciences. Alternative Agriculture. Washington, D.C: National Academy Press. Netherlands Ministry of the Environment (1994). Letter to Austrian Ecology Institute, re: Advertising Code Commission (PVC). January 14, 1994. Nishikawa, H. et al. (1993) Emission of organic compounds by combustion of waste plastics involving vinyl chloride polymer. Chemosphere 25(12): 1954-1960; Oberg, T., and G. Allhammar (1989). Chlorinated aromatics from metallurgical industries: process factors influencing production and emissions. Chemosphere 19:711-716. Oberg, L., et al (1990). Peroxidase catalyzed oxidation of chlorophenols to polychlorinated dibenzo-p-dioxins and dibenzofurans. Arcivesof Environmental Contamination and Toxicology 19:930-938. . Oberg, L., et al (1993) De novo formation of PCDD/F in compost and sewage sludge - a status report. Organohalogens 11:297-302. (OCAW 1993) Miller, R., and Lewis, S. Submission to International Joint Commission, Seventh Biennial Meeting. Denver: Oil Chemical and Atomic Workers International Union, October 1993. Oehme, M., S. Mano, and B. Bjerke (1989). Formation of poly-chlorinated dibenzofurans and dibenzo-p-dioxins by production processes for magnesium and refined nickel." Chemosphere 18:1379-1389. * (OEPA 1994) Ohio Environmental Protection Agency. Risk Assessment of Potential Health Effects of Dioxins and Dibenzofurans Emitted from the Columbus Solid Waste Authority's Reduction Facility. February 28, 1994. (OME 1993) Ontario Ministry of the Environment. Guide to Eating Ontario Sport Fish, 1993-1994 (17th edition). Toronto: Ontario Ministry of the Environment. Oppeft, T. (1986). Incineration: a critical review. Journal of the Air Pollution Control Association 37(51:556-586. Oppelt, T,, and Dempsey, C. (1993). Incineration: A critical review update. Air and Waste 43:25-51. Ozvacic, V. et al. (1990) Biomedical Waste Incinerator Testing Program. Chemosphere 20:1801-1808. Pohle, H. (1991). Investigation of Possible Environmental Dangers Caused by Burning Plastics. Socetty for Workplace and Environmental Analysis, Ltd., for German EPA (104-07-222), July 1991. Portier, C., et al. (1993) Ligand/receptor binding for TCDD: implications for risk assessment. Fundamental and Applied Toxicology 20:48-56. :nxr. CTLO14436 - 54 - Plimmer, A., et al. (1973) Photochemistry of dioxins. Chlorodioxins: Origin and Fate, E. Blair, ed. Advances in Chemistry 120: 50ff. Washington, D.C.: American Chemical Society. (PTCN 1985). Pesticides possibly contaminated with dioxin list compiled in OFP. Pesticide and Toxic Chemical News 13(15):34-38, February 20, 1985. Quebec Environment Ministry (1993). Resultats d'analyse des sols avoisinants I'usine Plastibec Ltee. 29 June 1993. See also Francoeur Le Devoir, L. "Contamination a la dioxine a Sainte-Tberese.' Le Devon. 2 July 1993. See also, Picard. A. "Quebec fire site seriously contaminated." Toronto Globe and Mail, 3 July 1993 ,A4. Rappe, C., et. al. (1989). Formation of PCDDs and PCDFs by the chlorination of water. Chemosphere 19:1875-1880. Rappe, C., et al. (1990). Levels of polychlorinated dioxins and dibenzofurans in commercial detergents and related products. Chemosphere 21:43-50. Rappe, C., et al. (1991). Levels .profile and pattern of PCDDs and PCDFs in samples related to the production and use of chlorine. Chemosphere 23:1629-1636. Rappe, C., and R. Andersson (1992). Analysis of PCDDs and PCDFs in wastewater from dishwashers and washing machines. Organohalogens 9:191-194. Remmers, J., A. Dupuy, et al. (1991). Dioxin and furan contamination in chloranil and carbazole violet. 11th International Symposium on Chlorinated Dioxins and Related Compounds. Research Triangle Park: U.S. Environmental Protection Agency and others, September 1991, p. 317. Robert, G. (1994) Chlorine companies adopt defiant stand. European Chemical News, 14 Feb. 1994, 32-34. Rossberg, M., et al (1986). Chlorinated hydrocarbons. Ullman's Encydopediaof Industrial Chemistry. Fifth Edition, ed. W. . Gerhartz. New York: VCH Publishers, 233-398. Scholz, B., (1987). Determination of polychlorinated dibenzo-p-dioxins and dibenzofurans in wastes of technical hexachlorocyclohexane. Chemosphere 16:1829-1834. Schatowitz, B,, G. Brandt et al (1993). Dioxin emissions from wood combustion. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 11:307-311. Schaum, J., D. Cleverly, M. Lorber, L. Phillips, and G. Schwarz (1993). Sources of Dioxin-Like Compounds and Background expoure levels. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 14:319-326. Schechter, A., 0. Papke, A. Lis, and M. Ball (1993). Chlorinated dioxin and dibenzofuran content in 2,4-D amine salt from Ufa, Russia. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 11:325-328. Schecter, A. (1991) Dioxins in hmans and the evironment. Biological Basis for Risk Assessment of Dioxins and Related Compounds, Banbury Report 35:169-214. Schmittinger, P., et al. (1986). Chlorine, in W. Gerhartz ed., Ullman's Endydopedia of Industrial Chemistry, Frfth Edition. New York: VCH Publishers. A6:399-480. Schreiber, R. (1993). 2,3,7,8-TCDD equivalent emissions from long wet or long dry cement kilns burning hazardous waste in the U.S. during trial bums. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogens 11:229-232. -55 - :mx CTL014437 SFT 1993. Norwegian State Pollution Control Authority. Input of organohalogens to the convention area from the PVC industry. Submission to the Oslo and Paris Commissions. Oslo, November 1993. Shafer, K., et al (1993). An investigation of PCDD/F in a composting peration. Organohalogens 11:425^30. Stanley, J., et al. (1990) Polychlorinated dienzo-p-dioxin and dibenzofuran concentration levels in human adipose tissue samples from the continental United States collected from 1971 to 1987. Chemosphere 20:895-892. Swain, W. (1988). Human health conseuences of consumption of fish contaminated with organochlorine compounds. Aquatic Toxicology 11(3):357-377. Swedish Environmental Protection Agency (1994). Sample reports #610s09 and 061 OsOI 7: PVC suspension/PVC plastic and PVC suspension used to make PVC. May 5, 1994. Theisen, J., et al. (1989) Determination of PCDFs and PCDDs in Fire Accidents and Laboratory Combustion Tests Involving PVC-Corrtaining Materials. Chemosphere 19:423-428. Thompson, T., R. Clement N. Thornton, and J. Luyt (1990). Formation and emission of PCDDs/PCDFs in the petroleum refining industry. Chemosphere 10:1525-1532. Thornton, J., Weinberg, J., and Patter, J. (1994) Transition Planning for the Chlorine Phase-Out: Costs, Benefits, and Opportunities. Washington, D.C.: Greenpeace USA. Tysklind, M., et al. (1989) PCDO and PCDF Emissions From Scrap Metal Melting Processes at a Steel Mill. Chemosphere 19:705-710. (UBA) German Federal Office of the Environment (1992). Environmental Damage by PVC: An Overview. Berlin: Umweitbundesamt, June 1992. U.S. Department of Commerce (1993). Statistical Abstracts of the United States. Washington: U.S. Government Printing Office. U.S. EPA. (1985). Health Assessment Document for Polychlorinated Dibenzo-p-dioxins. EPA Office of Health and Environmental Assessment EPA/600-8-84/014f. U.S. EPA (1987). Naional Dioxiin Study Tier 4: Combustion Sources: Engineering Analysis Report. Washington: U.S. EPA Office of Air Quality Planning and Standards, EPA/450-84-014h. U.S. EPA (1990). Standardsfor owners and operators of hazardous waste incinerators and burning of hazardous wastes in boilers and industrial furnaces: proposed and supplemental proposed rule, technical corrections and requests for comments. Federal Register 55:82ff, April 27, 1990. U.S. EPA (1991). Pesticide Inudstry Sales and Usage: 1989 Market Estimates. Washington: EPA Office of Pesticides and Toxic Substances. U.S. EPA. (1993) Report to Congress on Cement Kiln Dust. Washington, D.C.: EPA Office of Solid Waste, EPA-530-S-94-001, December 1993. U.S. Environmental Protection Agency (1994). Risk characterization of dioxin and related compounds - draft. Washington, D.C.: Bureau of National Affairs. May 3, 1994. Verhoog, W., J. Duffe (1990). De Rijn: Dioxinen en andere Microverontreinigingen in Industriel Afvalwaterlozingen. Amsterdam: Stichting Reinwater. :xxxx. CTL014438 -56- Vike'soe, J., H. Madsen, and K. Hansen (1993). Emission of dioxins from Danish wood-stoves. 13th International Symposium on Chlorinated Dioxins and Related Compounds. Organohalogerts 11:405-408. Wagner, J.C. & Green, A.E.S. (1993) Correlation of chlorinated organic compound emissions from incineration with chlorinated organic input. Chemosphere 26(11): 2039-2054. Wiiken, M., B. Zescmer-Lahl, et al. (1991). PCDD/F contamination of different pesticides produced in former GDR. 11 th International Symposium on Chlorinated Dioxins and Related Compounds. Research Triangle Park: U.S. Environmental Protection Agency and others, September 1991, p. 318. Williams, D., G. LeBel, and F. Benoit (1992). Polychlorodibenzodioxins and pdychlorodibenzofurans in dioxazine dyes and pigments. Chemosphere 24:169-180. CTL014439 -57 - :rccc