TL: THE MANAGEMENT OF HAZARDOUS WASTES DISPOSAL A Review of Government Systems SO: Greenpeace New Zealand (GP) DT: May 1992 Keywords: toxics hazardous waste disposal new zealand gp reports legislation australasia / Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND Contributed by: GREENPEACE NEW ZEALAND Date: May 1992 Note: Study of Dow Elanco pesticide plant, New Plymouth, NZ Keywords: toxics hazardous waste New Zealand Research Jennifer Boshier B.E.(Chem) Consultant Ian McDonald OBE MSC(NZ) FNZIC Editor Jeanne Boland BA Hons, MA Typing Nicola Kerslake Diana Clark Acknowledgements The Commissioner wishes to thank all those individuals, groups and organisations who assisted by providing information and comment, in particular the reviewers of early drafts of the report, including Dr Wayne Temple PhD, CChem, FRSC, FNZIC. This document may be copied provided the source is acknowledged. ISBN 0-908804-35-0 [] PREFACE Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND New Zealand does not have a good record in establishing controls for managing hazardous substances. Since the Parnell Commission of Inquiry in 1973, and the ICI fire in 1984, there has been a series of government committees and task forces. These have consistently called for legislation and clear guidelines for managing hazardous materials. The appointment of the promised Hazards Control Commission is long overdue. I hope the information contained in this report will assist Government to develop appropriate legislation without further delay. This report has identified new and improved information on the nature and incidence of hazardous substances, such as dioxin. This does not mean we can afford to relax moves to put in place hazards control legislation. What it does mean is that standards can be set with greater precision and the public can be more confident that controls put in place in future will protect public health. My investigation into New Zealand's management of hazardous substances, such as dioxin, has obtained the most up-to-date information possible from some of the world's recognised experts. Personal communication was established with two of he main specialists. It is with some relief that I have found that management over the past 20 years, in the case study I reviewed, has been satisfactory to safeguard public health from perceived carcinogenic effects. However, the information obtained has also identified that ill health could result from dioxin exposure some 20 to 30 years later. The investigation has clearly demonstrated that when information on toxicity or other adverse effects is uncertain or insufficient, prudent and conservative environmental management should always be undertaken. It has also demonstrated that strict controls will be essential for all hazardous waste disposal. Helen R Hughes Parliamentary Commissioner for the Environment TABLE OF CONTENTS EXECUTIVE SUMMARY 1. INTRODUCTION 1.1 Background to investigation 1.2 Terms of reference 1.3 Authority for investigation 1.4 Public concerns 1.5 Public perception of risk 1.6 Disposal of pesticide wastes 2. CASE STUDY - COMPANY 2.1 History of 2,4,5-T manufacture 2.2 Manufacturing process 2.3 Analysis of 2,3,7,8-TCDD in product 2.4 Incineration of residues 2.5 Monitoring of emissions 2.6 Disposal of ash 3. CASE STUDY - ROLE OF DEPARTMENT OF HEALTH 3.1 Technical information 3.2 Overseas literature 3.3 Clean Air Act licences 3.4 Compliance and monitoring 3.5 Information made public by the Department 4.CASE STUDY - ASSESSMENT OF ACTIONS 4.1 Disclosure of information 4.2 Accuracy of emissions analyses 4.3 Clean Air Act licence conditions 4.4 Compliance 5.CASE STUDY - LOCAL AUTHORITY RESPONSIBILITIES 5.1 Development of Paritutu Road 5.2 Provisions in the District Scheme 5.3 Effects on residential development of the adjacent industry 5.4 Summary 6. INFORMATION ON 2,3,7,8-TCDD 6.1 Background 6.2 Sources of 2,3,7,8-TCDD in the environment 6.3 Hazard assessment 6.4 Kemner et al v Monsanto 6.5 Animal toxicity experiments 6.6 Mode of action of 2,3,7,8-TCDD 6.7 Epidemiological research 6.8 Exposure assessment 7. CHANGES IN REGULATORY REGIMES 7.1 Tolerable daily intakes 7.2 Europe 7.3 United States 7.4 OECD Guiding Principles 8. REQUIREMENTS FOR FUTURE CONTROL IN NEW ZEALAND APPENDICES I Conditions for the liquid waste and solid waste incinerators II Analysis of materials for 2,3,7,8-TCDD III Mass and concentrations GLOSSARY REFERENCES [] EXECUTIVE SUMMARY Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND Introduction This investigation into the disposal of hazardous wastes was initiated by a complaint of inadequate performance of public authorities and inadequate processes in place to fully assess the environmental impacts of the destruction of these hazardous wastes. This has not been the only expression of public concern on this subject directed to my office over recent years. The Planning and Development Select Committee has also asked me to report on a petition regarding the safe disposal of waste chemicals currently stored near Nelson. Regional Councils have informed me that they are refining their knowledge on the nature and quantity of hazardous wastes generated in their region but in many cases are unable to advise or act to dispose of these wastes because of the lack of suitable facilities in their region and the lack of strategic guidance from central government. Method of investigation This investigation has focused on dioxin and has obtained recent information on: epidemiological studies concerning people in the United States who worked in chemical manufacturing plants producing chemicals contaminated with dioxin 20 to 37 years ago; reviews of regulatory approaches to dioxin exposure; sources of dioxin in the environment. The term dioxin is used in this summary to refer to 2,3,7,8-tetrachlorodibenzo-p-dioxin which is the most toxic of the 75 similar chlorodibenzo-p-dioxins. The term dioxins refers to all the chlorodibenzo-p-dioxins. A case study was undertaken of a New Zealand industry which manufactured the agrochemical 2,4,5-T between 1964 and 1987. This chemical contained a contaminant dioxin which tests showed to be extremely toxic to animals, birds and fish. Under very high exposure conditions there is support for the hypothesis that dioxin is a human carcinogen. At environmental exposure levels the evidence for adverse human effects is at best inconclusive. The case study examined the role of public authorities in controlling the disposal of hazardous waste residues by incineration, the monitoring of the incineration process and whether separation of residents and hazardous industrial activities had been achieved. Sources of dioxin in the environment As analytical techniques have improved, dioxins and furans (similar chemicals to dioxins) have been found in a wide variety of compounds and processes. Identifiable sources include: municipal waste incinerators motor vehicles using leaded petrol pulp and paper manufacturing plants using chlorine-based bleaching processes pentachlorophenol used as a timber treatment compound flame retardants the metal industry sewage sludge Because of the ubiquitous nature of dioxins and furans in the environment, it is now postulated that any source of carbon and halogen which is incinerated in equipment with catalytic surfaces will generate dioxins and furans in the effluent gases. How dioxin works in cells Biochemical studies in the 1960's discovered that the mode of action of some carcinogenic compounds (the polyaromatic hydrocarbons) involved a receptor labelled the Ah or aryl hydrocarbon receptor. It has recently been agreed by researchers in the United States that before dioxin can cause any of the ill effects that it has been linked to, one event must occur. The compound must bind to and activate the Ah receptor. After that, the dioxin-receptor complex is transported to the cell nucleus where it interacts with DNA causing cell proliferation in certain organs. The researchers believe that dioxin has to occupy a certain number of Ah receptors in a cell before any biological response can ensue. The implication of this is that there could be a practical threshold for dioxin exposure, below which no toxic effects occur. Researchers have also found that there are a number of naturally occurring substances that also bind to the Ah receptor and that mimic the action of dioxin in cells. One such substance is present in large amounts in broccoli, cabbage and cauliflower. Epidemiological research The relationship between human health problems and dioxin exposure has been difficult to study. In one accident situation, residents of a small community successfully sued the Monsanto Company following a spill of a tank car of crude orthochlorphenol containing some dioxins. Eventually their case was rejected by an appeal court because damages had not been sustained. Further, dioxin was not proved to be present in the spilt material. Four major studies have been published in the last year which do shed light on the issue of whether exposure to dioxin causes health problems in people. The United States Air Force Ranch Hand study began in 1978 and involved about 1242 Forces personnel who actually handled and sprayed Agent Orange in Vietnam. The study has so far shown no significant illness, such as cancer or birth defects, compared to other veterans who did not handle Agent Orange. However, in March 1991 a report from the Ranch Hand study showed a significant increase in body fat and diabetes that correlated with dioxin concentration. The study is now to extend the physical examination tests to look more critically at the diabetics. Another study has been that of the United States Department of Veterans Affairs which studied 85,000 self-selected veterans in the 1980s. The Department concluded that Agent Orange caused no health problems that were significantly different from those of the general population. The largest of the four intensive studies is that of Fingerhut and her colleagues at the National Institute for Occupational Safety and Health in the United States, published in 1991. This was a retrospective cohort study of mortality among 5172 workers at 12 plants in the United States that produced chemicals contaminated with dioxin. Occupational exposure was documented by reviewing job descriptions and by measuring dioxin in serum from a sample of 253 workers. Of the 5172 workers, 1052 had died and the overall mortality for all causes of death was found to be similar to national rates in the United States. The 265 cancer deaths were studied in great detail as was a subcohort of 114 deaths where exposure had been for greater than one year and where the latency period had been greater than 20 years. The conclusion of the paper is as follows. "This study of mortality among workers with occupational exposure to dioxin (TCDD) does not confirm the high relative risks reported for many cancers in previous studies. Conclusions about an increase in the risk of soft tissue sarcoma are limited by small numbers and misclassification on death certificates. Excess mortality from all cancers combined, cancers of the respiratory tract, and soft-tissue sarcoma may result from exposure to dioxin (TCDD), although we cannot exclude the possible contribution of factors such as smoking and occupational exposure to other chemicals." An investigation into cancer mortality among workers at a German factory which had been highly contaminated with 2,3,7,8-TCDD found results that are consistent with the Fingerhut study. The Director of the Center for Environmental Health and Injury Control at the Centers for Disease Control, Atlanta, Georgia, commented on the Fingerhut study thus: "if dioxin is a human carcinogen, which I am assuming it is, it is a relatively weak one and is a carcinogen only at extraordinary doses". Exposure assessment in people These and other studies have indicated levels of dioxin that people have been exposed to in work, military and accident situations. Very little research has been done on the effects of dioxin exposure to residents of communities where point sources of emissions are situated. There is, however, a study under way in the United States to assess the exposure of residents of Jacksonville, Arkansas, since incineration of production wastes containing dioxin has recently begun. The most recent information is that of Dr Fingerhut who indicated that if the general population's exposure results in less than 20 parts per trillion (ppt) of dioxin in blood serum, then the health effects should be minimal. The link between the point source emission of potentially toxic compounds like dioxin and the body burden of people living around such a point source cannot yet be made with certainty. Because there are many other sources of dioxin in the environment this link may be difficult to establish. This means that prudent management of hazardous substances will continue to be required. An interesting point to emerge from the United States Department of Veterans Affairs's 1991 report is that the body burden of dioxin in the population in the United States appears to be falling from 12 parts per trillion in samples collected in the 1970s to 5-7 parts per trillion in 1990. Although no reasons have been ascribed for this decrease, one possibility is that the decrease in the lead content of petrol may have contributed to the change as well as more prudent management of chemicals containing dioxin. Changes in regulations overseas A major meeting of the World Health Organisation in 1990 on dioxins in the environment concluded that the main exposure. route for people was from food. The meeting assessed the available toxicological information and set a Tolerable Daily Intake (TDI) level for people at 10 picograms/kg body weight/day. The British Government subsequently raised the TDI in Britain from 1 to 10 picograms/kg body weight/day. The United States Environmental Protection Agency (EPA) is also assessing its way of regulating dioxins in the environment. The EPA method depends on a model which assumes that even one molecule of dioxin can cause a risk to health. The EPA Tolerable Daily Intake (TDI) of 0.006 picograms/kg body weight/day is intended to limit excess cancers to a one in a million chance. This model is being reassessed in light of the research information which implies that there is a threshold level below which cancer would not occur. This re-evaluation is due to take place in 1992. New Zealand case study The industry which is the subject of this case study had taken responsibility for on-site disposal of the hazardous wastes generated as part of its manufacturing process. The Company thus had information on the nature and quantity of wastes requiring disposal and as well had researched methods of disposal. The case study has shown that the Company's environmental management in carrying out the disposal of hazardous wastes was appropriate at that time given the known information. The regulatory agency's monitoring of the operation was adequate to assess that the company was complying with the regulatory controls. Company self-regulation of the incineration process with occasional audits by the regulatory agency was a valid means of monitoring the waste incineration. However, there was a public perception of risk which led to distrust of both the Company and the regulatory agency. A clear flow of reliable information from a credible institution on the environmental and public health implications of waste disposal programmes including incineration is essential now and in the future. Government system for control The case study has illustrated limitations in the Government system for the control of hazardous waste disposal. These limitations primarily relate to legislation that was previously in place and the lack of monitoring of the effects of the emissions in the environment. Since the 1980s, when the incineration of these hazardous waste residues was a matter of public concern, the system for control of hazardous substances has changed with the enactment of the Resource Management Act 1991. The present system is still fragmented and is not delivering a coordinated response to the control of hazardous waste disposal. The Resource Management Act 1991 has placed responsibilities on regional and local government to control the effects of activities which involve hazardous substances including the prevention or mitigation of any adverse effects of the storage, use, disposal and transportation of hazardous substances. These responsibilities are potentially overlapping and are not sufficiently clarified to allow each agency to contribute to an overall system. The control of discharges of contaminants to the air is now regulated under the Resource Management Act 1991 rather than the Clean Air Act 1972. This change has brought both benefits and disadvantages. The benefits include a more public system of assessing any application for the discharge of contaminants into the environment. The disadvantages include the loss of a central body of expertise on industrial processes built up over time by the Department of Health technical air pollution staff whose group was disestablished at the time of the enactment of the Resource Management Act 1991. This expertise is now dispersed between the public and private sector with no one central agency retaining any "corporate memory". The regulation of agricultural compounds is presently carried out under four separate Acts although a discussion document by the Ministry of Agriculture and Fisheries in 1989 proposed consolidation into an Agricultural Compounds Act. The links with a Hazards Control Commission would be in the areas of (agricultural) chemical usage, manufacturing of chemicals, transport of chemicals and downstream consequences such as clean up operations. There is insufficient information on the nature and quantities of hazardous materials generated or disposed of in New Zealand. There is no nationally accepted characterisation of hazardous wastes which allows comparisons among industries or regions to be made (although the Chemical Industry Council's Guideline for Waste Management published in 1991 is generally accepted). The Department of Health funded waste surveys did not provide a national system of identifying wastes so this information is of limited value in establishing policies for waste minimisation which is the first step in a hierarchy of waste management. Future New Zealand control One of the most important pieces of information to be recently established was of the ubiquitous nature of dioxin in the environment. This has altered the perception that any one source of dioxin should be controlled more than other potential sources. The risk of adverse human health or environmental effects upon exposure to dioxin does not appear to be as significant as was indicated by early animal toxicity experiments in the 1970s. However, under high exposure conditions elevated blood serum levels have been correlated to an increase in body fat and diabetes, after 20-30 years latency period. These and other findings have led the World Health Organisation to consider that "the introduction of dioxins and furans into the environment should be reduced to the extent possible that was consistent with sound engineering practices judged to be reasonable". The information obtained in this review indicates that incineration of chlorinated pesticide wastes is an appropriate means of disposal, provided the design of the facility and its operation are appropriate to the wastes requiring disposal. The regulatory controls on the environmental effects of the facility need to be technically adequate. Monitoring of the effects is essential. Disposal of waste pesticides from farms by high temperature incineration is a valid way of reducing the residual problem in this country. It is evident that very little pesticide waste is now being generated in the regions that have been surveyed. I have concluded that to achieve good environmental management of hazardous substances, the proposed hazards control legislation is urgently required. This legislation should integrate present controls in the Resource Management Act 1991 and the proposed Agricultural Compounds Act. The legislation would be implemented by agencies such as the proposed Hazards Control Commission and local government. Recommendations to the Minister for the Environment 1. A national policy on waste minimisation for hazardous wastes should be developed by and coordinated with any policy on waste minimisation being developed by the Ministry for the Environment. 2. A nationally accepted characterisation of hazardous wastes within a broader system of waste classification is required. 3. Clarification of the roles and responsibilities of regional and local authorities and industry for the management of hazardous wastes, including the control of hazardous waste treatment and disposal should be undertaken. 4. The development of risk assessment tools in order to assess appropriate treatment and disposal means for hazardous wastes and residues is required. 5. Access to technical information and research, both New Zealand and overseas, to base appropriate standards for environmental control is required. The Hazards Control Commission should identify the research needs to ensure that management of hazardous substances is not compromised through lack of appropriate information. 6. Standards for emission control for incinerators, for disposal of residues to landfill and other disposal methods and for the receiving environment should be researched and made available to the regulatory agencies. 7. The provision of information to the public on the risks and benefits of different options for hazardous waste management is required. 8. The Hazards Control Commission should encourage the development of emergency response plans by the facility management and the local authority. In developing such plans, the OECD's Guiding Principles for Chemical Accident Prevention, Preparedness and Response should be used. The Hazards Control Commission should explore the option of making the preparation of such plans mandatory. 9. The Hazards Control Commission should arrange for proper investigation into the human and environmental effects including long term research in the event of a major accident or spill of hazardous chemicals that affects a number of people. Recommendations to Local Government 1. Accurate and consistent information on the nature and quantity of hazardous wastes requiring disposal should be supplied by regional councils and unitary authorities to the Hazards Control Commission. 2. Monitoring of the environmental effects of effluents and emissions from any hazardous waste management facility will be an essential part of the control of hazardous waste facilities. 3. The provision of a clear, continuous flow of information to the public on the control of hazardous waste management facilities will be required. This will include information on effluent and gaseous emission concentrations as well as ambient levels in the receiving environment. [] INTRODUCTION Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND 1.1 Background to investigation In 1991 the Ombudsman received correspondence expressing concern about the methods used for the disposal of unwanted agricultural chemicals, the disposal of residues from the manufacture of agricultural chemicals and the public authority control of the disposal operation. The Ombudsman determined that the issues were ones of environmental management. Since the Parliamentary Commissioner for the Environment has specific statutory authority to investigate the environmental planning and management carried out by public authorities, the decision to undertake an investigation rested with the Commissioner. The complaint of inadequate performance of public authorities and inadequate processes in place to assess fully the environmental impacts of the destruction of these hazardous wastes was therefore passed to me. I began by establishing what the public authorities had done to monitor the incineration of residues and ascertaining what measures the public authority had taken to protect residents near a chemical industry. In researching these topics, recent information on the sources of dioxins in the environment, epidemiological studies and the review of regulatory approaches by the United Kingdom government and the United States Environmental Protection Agency (EPA) in respect to the compound (2,3,7,8-TCDD) was obtained. My investigation analysed the appropriateness of past legislation to control the disposal of chemical residues from one chemical plant and the actions of the public authorities and the company in carrying out their hazardous waste management. The information in this report should assist the Planning and Development Select Committee in their deliberations on a petition by Janine Mitchell and 4694 others regarding the safe disposal of waste chemicals currently stored near Nelson. The Resource Management Act 1991 provides for the establishment of a Hazards Control Commission having functions concerned with hazardous substances management. This gives New Zealand an opportunity to identify from past experience and from an increased awareness of the properties of particular chemicals and chemical processes what provisions will be needed in future legislation. 1.2 Terms of reference To analyse an agricultural chemical industry's disposal of hazardous wastes by incineration in order to: (a) assess the capability of the Government system to deliver sound environmental management decisions in respect to disposal of hazardous wastes; (b) assess the performance of the public authorities in controlling the effects of this hazardous Waste disposal. 2. To provide recent information on the sources and fate of dioxins in the environment. 3. To provide remedial advice, as appropriate, for future management of hazardous wastes. 1.3 Authority for investigation The role of the Parliamentary Commissioner for the Environment is to act as an independent auditor of the system for environmental management in New Zealand. Section 16(1)(a) of the Environment Act 1986 mandates the Commissioner to review the system of agencies and processes established by the Government for environmental management. Section 16(1)(b) of the Environment Act 1986 provides for the Commissioner to investigate the effectiveness of environmental planning and management carried out by public authorities. Section 16(1)(f) of the Environment Act 1986 provides for the Commissioner to undertake and encourage the collection and dissemination of information relating to the environment. 1.4 Public concerns The chemical 2,4,5-T has been one of the most widely applied herbicides in New Zealand, having been used in agriculture and forestry over the last 30 years. Throughout the period of its use in New Zealand, a number of concerns were raised by the public about its safety. One concern was that 2,4,5-T may have played a part in three "clusters" of human birth defects observed in South Taranaki, Northland and Waikato. Each of these was investigated by medical officers of the Department of Health but no evidence was found to implicate 2,4,5-T in any of the cases (McQueen et al 1977). In a further study of human birth malformations in Northland (Hanify et al 1981) no evidence was found to associate spraying of 2,4,5-T with the occurrence of any malformation of the central nervous system, including spina bifida. However, a statistically significant association between spray and malformation was found in the case of talipes (club- foot). The authors commented that whether this association indicates a causal relation remains to be established. A preliminary report of reproductive outcomes among pesticide applicators using 2,4,5-T in New Zealand (Smith et al 1981) found no significant differences in the rate of congenital defects for chemical applicators and agricultural contractors. Public concern has also been expressed that run-off from areas sprayed with 2,4,5-T might carry the herbicide onto properties in adjacent areas. This subject was reviewed by Norris (1981) who found that the amount of 2,4,5-T measurable in water courses fell rapidly after spraying had taken place and no residues higher than 0.01 ppm were recorded after 1 day. Monitoring in Southland following aerial spraying of cleared floodways found only trace amounts of 2,4,5-T in water samples collected downstream during or shortly after spraying (McKenzie and McMillan 1980). Much of the debate surrounding 2,4,5-T concerns the presence of a contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) which is present as an unavoidable trace byproduct during the formation of sodium trichlorophenate, a necessary intermediate in 2,4,5-T manufacture. Tests have shown 2,3,7,8-TCDD to be extremely toxic to animals, birds and fish. The effects on human health of exposure to low levels of 2,3,7,8-TCDD containing materials has been an ongoing concern. The manufacture of 2,4,5-T at a plant in New Zealand has, over the years, generated concerns from nearby residents as to the safety of the plant and the manner in which disposal of residues from the 2,4,5-T manufacture occurred (Brennan 1985). There have been at least eleven studies in New Zealand on either 2,4,5-T use or manufacture, many in response to public concerns. They are: 1. the 1972 report on 2,4,5-T by a subcommittee of the Agricultural Chemicals Board; 2. the 1977 report by the Department of Health on 2,4,5-T and Human Birth Defects; 3. the 1980 Report to the Minister of Health on an investigation into Allegations of an Association Between Human Congenital Defects and 2,4,5-T Spraying in and around Te Kuiti; 4. the 1980 Report of an Agricultural Chemicals Board Advisory Committee on Pesticide Hazards; 5. the 1980 Royal Society of New Zealand report on the Assessment of the Toxic Hazards of the Herbicide 2,4,5-T in New Zealand; 6. the 1986 report by the DSIR of an investigation of Bursting Disc Failure: Ivon Watkins-Dow TCP Process; 7. the 1986 report to the Director-General of Health of a Task Force on Chronic Agricultural Chemical Poisoning Notifications; 8. the 1986 report of the Ministerial Committee of Inquiry to the Minister of Health on the Possible Health Effects of Manufacture of 2,4,5-T in New Plymouth; 9. the 1987 Ministerial Committee of Inquiry. Supplementary Report to the Minister of.Health. Possible Health Effects of Manufacture of 2,4,5-T in New Plymouth; 10. the 1986 Environmental Council report on the Use of 2,4,5-T in New Zealand; 11. the 1989 Ministry for the Environment Technical Report of an Investigation into Residues of the Herbicide (2,4,5-T) and its Dioxin Component in Sheepmeats; A more recent concern has been about methods for destroying unwanted or unused pesticides from farms throughout the country. 1.5 Public perception of risk from pesticides There are several factors that influence the public perception of risk arising from pesticide manufacture and use. If an accident occurred at a manufacturing plant, then people who live adjacent could be exposed to unknown levels of toxic emissions. This exposure to an involuntary risk did occur at Seveso in Italy on 10 July 1976. No official emergency measures were taken until five days after the explosion and the probable presence of 2,3,7,8-TCDD was not disclosed to the local population until eight days after the accident at Seveso. The slow response of the company to admitting the problem at Seveso enhanced a perception that industry in general cannot be trusted to give timely information in the event of an emergency. Misinformation can also add to people's fears. For example, after the Seveso accident, there were photographs of people with burns from caustic soda and concentrated phenol being passed off as photographs of victims of 2,3,7,8-TCDD. In fact 447 people were treated for burns of whom only 34 subsequently had to be treated for chloracne (Marshall 1983). In 1979 there were reports of a high incidence of spontaneous abortions in a group of women living in Oregon, USA, and who were potentially exposed to 2,4,5-T from aerial spraying (Hayes and Laws 1991). The EPA study (EPA 1979) reported a link between the 2,4,5-T spraying and spontaneous abortion among pregnant women in Alsea, Oregon and 2,4,5-T was prohibited for sale or distribution in the United States. The perception that there was a link between 2,4,5-T spraying and reproductive effects was firmly established in the public mind even though this link was later criticised by scientists who concluded that the basic design of the initial studies was inadequate to demonstrate any positive or negative effect of 2,4,5-T. Another factor that has influenced public perception was the extensive and somewhat indiscriminate use of Agent Orange and other herbicides in the unpopular Vietnam War. The discovery that Agent Orange contained concentrations of 2,3,7,8-TCDD varying between 0.02 and 54 parts per million (ppm), coupled with research on animals indicating the toxic nature of the material, caused widespread anxiety in the United States. This use of pesticides was perceived as leading to unnecessary contamination of the environment and possible adverse health effects. The actions of the chemical companies in the United States in paying damages to United States Vietnam veterans over alleged health effects arising from using Agent Orange in Vietnam has led to the perception that the payments meant the companies were guilty of misconduct. Causality between contact with 2,3,7,8-TCDD and health effects was not established during the court case to elicit damages from the chemical companies. (Assumption of guilt if American companies pay damages cannot be necessarily made, as companies would rather avoid much more costly legal actions.) Another factor influencing public perception was instances of uncontrolled disposal of wastes from a few chemical plants in the United States in the late 1970s and early 1980s. The discovery that 2,3,7,8-TCDD contaminated waste oil had been used for dust control on the streets of Times Beach, Missouri, years before the streets were paved led to the evacuation of the town in 1983. The evacuation was ordered because the EPA assumed a worst case scenario based on the theory that even a single molecule of 2,3,7,8-TCDD could be enough to cause cancer or birth defects. This theory is now being re-evaluated (section 7.1). There was also great concern following the discovery. that a chemical dump within Hamburg city was contaminated with dioxins and with 2,3,7,8-TCDD (New Scientist 1984). Because 2,4,5-T has been used widely in New Zealand, primarily for gorse control, there has been a transference of the perception that widespread use per se is undesirable and a risk to health. Following the United States Vietnam experience, the public is concerned that exposure to dioxins even at very low exposure levels will cause adverse health effects. The early industrial experience, including accidents, with chlorophenols and associated chemicals showed that people were affected by exposure to these, chemicals. These incidents were perceived as exposing people to unknown risks. The toxicological experiments on animals carried out in the early 1970s showed severe toxic effects of 2,3,7,8-TCDD on several animal species. The relationship between animal toxicity data and the levels of 3,7,8-TCDD that could cause adverse effects for human exposure is a very difficult one. This problem of translating animal data to human exposure affects both the public and the regulators who must make decisions in the light of these uncertainties and unknowns. 1.6 Disposal of pesticide wastes There are pesticide wastes from manufacturing and from farming that require disposal. Several options could be appropriate for the disposal of either category of pesticide wastes, depending on the nature and quantity of the wastes. These are: recycling/reusing of wastes on-farm disposal landfill incineration followed by disposal of the ash to landfill. A recent publication (Department of Health 1991) outlines a guide to the handling and disposal of waste pesticides. The guide covers three main types of pesticide waste: contaminated containers and packaging, spillage and pesticide chemicals, residues and wastewater. The two main options are landfill and incineration. Guidelines as to the standards of landfill design and operation are given, as is general guidance on incinerator requirements. The quantities of waste pesticides requiring disposal in New Zealand are unknown. Not all the waste surveys funded by the Department of Health, undertaken by regions in 1989 and 1990, identified waste agricultural chemicals. Surveys of waste pesticides held on a sample of farms in the Waikato, Canterbury and Hawkes Bay regions have been carried out by the Agricultural Chemical & Animal Remedies Manufacturers' Association of New Zealand (AGCARM 1991). These surveys estimated the amount of wastes present on farms which were unwanted and either useable or obsolete rather than the amount of waste pesticides being generated annually. Even if figures could be collated for the whole country, they would not necessarily give an accurate picture of the annual generation of waste pesticides. A large proportion of waste pesticide is accumulated stock rather than new waste. Small amounts of waste pesticides could be disposed of by burning, evaporation, dilute spraying, neutralisation or landfilling (Ministry for the Environment, 1989). The problem arises when larger quantities of waste pesticides or factory wastes require disposal. Long term storage of hazardous wastes is a means of delaying a solution and can put an unnecessary burden on future generations to solve this generation's problems. While it has an initial attraction in that hazardous wastes are stored in a known locality with some degree of physical security, problems of keeping the wastes intact would loom over time. Incineration has been used to dispose of chemical wastes arising from the manufacture of pesticides and, more recently, to dispose of some unused chemicals collected from farms. The case study outlined in this report is concerned with the incineration aspect of hazardous wastes disposal rather than disposal by other methods. 2. CASE STUDY - COMPANY Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND The case study concerns the manufacture of the herbicide 2.4,5-T by the Company and the manner in which the Company has dealt with the wastes arising from this one product. The Company stored the wastes arising from the manufacture of this herbicide on site and from 1974 incinerated these and other wastes rather than dispose of them off-site. A brief history of 2,4,5-T production is given in Table 1 as a summary of actions taken by the Company from 1961 to 1992. 2.1 History of 2,4,5-T manufacture Table 1 2,4,5-T Manufacture at IWD 1961 Company moved to present site. Formulation of agricultural chemicals undertaken. Esterification plant installed to convert imported 2,4,5-T acid to product esters(1). 1964 Imported trichlorophenate used to prepare 2,4,5-T acid for esterification plant(2). 1970 Company imports tetrachlorobenzene and manufactures sodium trichlorophenate(3) at site using essentially the Boehringer process. Plant then incorporates all processes, 1,2,3 above, to convert tetrachlorobenzene to 2,4,5-T esters. 1974/75 Liquid waste incinerator installed and licensed under Clean Air Act 1972. Nov. 1975/ May 1979 182 batches of liquid wastes incinerated. Aug. 1976 Department of Health initiates an intensive review of the Company's process following the Seveso accident. 1978-79 Company modifies the trichlorophenate manufacturing process to reduce the amount of 2,3,7,8-TCDD produced. 1980 Solid waste incinerator installed. 1986 Accidental discharge of between 70 and 730 milligrams of 2,3,7,8-TCDD from a reactor producing sodium trichlorophenate due to a mechanical failure at the plant. 1987 Manufacture of 2,4,5-T ceases. May 1988/ Sept 1988 Incineration of chlorinated liquid wastes during this period. 1989-1990 Incineration of residual materials from 2,4,5-T manufacture. 199O- 1992 Incineration of wastes from the plant. When considering the manufacture of any product, it is important to note that chemical reactions rarely yield a single compound. However, for a chemical reaction to be useful industrially, the product mixture should contain mainly one compound. There are often purification steps required in order for an industrial product to meet end user requirements. Regulation of the incineration of the wastes was carried out between 1974 and mid 1991 by the Department of Health under the Clean Air Act 1972. Information on the incineration of residues and monitoring of the stack emissions is contained in Pilgrim's report (1986) together with subsequent correspondence. 2.2 Manufacturing Process 2,4,5-T is manufactured from trichlorophenol as is hexachlorophene which is used as an antibacterial agent in soaps and solutions. Chlorophenols, in general, have been used industrially since the 1930s in a great variety of products including pentachlorophenol for timber treatment and in wood sapstain products and in herbicide manufacture. 2,4,5-trichlorophenol is made by the dechlorination of 1,2,4,5-tetrachlorobenzene by alkaline hydrolysis. There are two possible methods for carrying out the alkaline hydrolysis of tetrachlorobenzene - an "atmospheric" method and a high pressure method. The "atmospheric" method (at a pressure of 1.5 atmospheres and 180C) uses ethylene glycol as the solvent and the high pressure (147C) method uses methanol as the solvent. The Company used the methanol hydrolysis process; and the technology was purchased from Boehringer in Germany. Note: this method is different to that used by Monsanto or Dow Chemical Co in the United States. Evidence that the methanol pressure hydrolysis process was used by the Company is provided by the presence of chlorinated anisoles as impurities. In the Company's process, the 1,2,4,5-tetrachlorobenzene was heated under pressure with sodium hydroxide in methanol. The intermediate sodium 2,4,5 trichlorophenate was separated then treated with chloroacetic acid and with suitable alcohols to yield the 2,4,5T esters. The temperature of the first reaction must be carefully controlled to limit the condensation of two molecules of sodium 2,4,5 trichlorophenate to form 2,3,7,8-TCDD which contaminates the phenate and thus the 2,4,5-T product (Hughes 1984). The presence of, and the significance of, concentrations of 2,3,7,8-TCDD at the parts per million level may not have been appreciated by any company when production of 2,4,5-T was first undertaken in the 1960s. Prior to 1970, 2,4,5-T was made in New Zealand from 2,4,5 trichlorophenol imported from a German source. The production of trichlorophenol from tetrachlorobenzene occurred in New Zealand only after 1970. In 1970 there was a world trend to reduce the 2,3,7,8-TCDD levels permitted in 2,4,5-T to 0.1 parts per million (ppm). At this time the Company, in New Zealand, incorporated an organic solvent extraction step which removed an unwanted reactant with some 2,3,7,8-TCDD. The changes in the 2,3,7,8-TCDD content of 2,4,5-T manufactured in New Zealand are outlined in Table 2. The total production of 2,4,5-T over this time period is approximately 9133 tonnes . The estimated quantities of 2,3,7,8- TCDD in the product decreased over this time, as shown by the decrease in concentration in Table 2. Quantities of 2,3,7,8-TCDD in the product decreased from a cumulative total of 1.87 kilograins (kg) up to 1972, 6 kg up to 1981 and 18 grams up to 1985 (Coster et al 1986). Table 2. Concentration of 2,3,7,8.TCDD in 2,4,5-T manufactured in New Zealand in parts per billion (ppb) 1960s Unknown, may have been up to 100,000 1969 Up to 1000 (average 800) 1972 100 1974 33 1978 22 1979 13 1984 5 (1982 maximum permitted in commercial product by the Pesticide Regulations 10 ppb) The reduction in the 2,3,7,8-TCDD content of the commercial product being produced between 1970 and 1979 created a substantial volume of xylene-trichloroanisole solvent mixture containing some 5.7 kilograms of "apparent" 2,3,7,8-TCDD. As shown in Table 2, the concentration of 2,3,7,8-TCDD in 2,4,5-T dropped because of this extraction step. In 1979 further modifications to the manufacturing process were made. The reactant and organic solvent were recycled within the process. The resulting chemical reactions reached an equilibrium with a lower ultimate 2,3,7,8-TCDD content in the trichlorophenol. The value of these improvements can be seen with reference to Table 2 where the 2,3,7,8-TCDD concentration in 2,4,5-T decreased between 1979 and 1984. Production of 2,4,5- T ceased in 1987. Because the reactant and organic solvent were being recycled, there was no accumulation of a solvent stream requiring disposal as had occurred between 1970 and 1979. There was, however, a waste stream associated with the phenoxy plant where the trichlorophenate is converted to 2,4,5 trichlorophenoxyacetic acid and esters. There was a water washing process which itself contained small concentrations of 2,3,7,8-TCDD. This was removed by organic solvent stripping creating a waste stream for disposal. There was a much smaller volume of this waste stream than had been the case between 1970 and 1979 (quantities of liquid wastes incinerated are given in Section 2.4 as an indication of the decrease in quantities of wastes generated). As part of the 1979 upgrade, the Company installed a blow down tank to prevent accidental emissions from entering the atmosphere. An accident in 1986 resulted in the release of some material to the atmosphere. This occurred because a segment of the bursting disc on the piping from the reactor to the blow tank was ejected through the flange system holding it in place. The reactor contents were thus not fully retained within the system; some were discharged through the flange. The reactor was pressurised under normal temperature control at the time, so no overheating occurred. There was no explosion as had occurred at Seveso and earlier incidents. Unlike Seveso, the Company's plant was enclosed and an effective deluge and containment system minimised the extent of environmental release. Public concern over the manufacture of 2,4,5-T by the Company was partly due to the explosions that happened at overseas plants in which there were reported factory releases of 2,3,7,8- TCDD. In at least two, Seveso (New Scientist 1983) and the Coalite (Milnes 1971) accident, the alkaline ethylene glycol process was used. The Company in New Zealand did not use this process. There are two main risks with the ethylene glycol process. One is the need for accurate temperature control in order to keep the concentration of 2,3,7,8-TCDD to a minimum. At a reaction temperature of 180C it is reported that the trichlorophenate contains less than 1 ppm 2,3,7,8-TCDD. Heating the phenate to 230-260C for two hours has produced 1600 ppm of 2,3,7,8-TCDD (Milnes 1971). If temperature control is not accurate when the sodium-2 hydroxy ethoxide, which is a reaction product of alkali and ethylene glycol, starts decomposing, there can be a rapid rise in temperature leading to an explosion. There can be little doubt that such uncontrolled decomposition, which was an operator error resulting in inadequate cooling, caused the Seveso accident (New Scientist 1983). During the hydrolysis process used at Seveso, all reactants were loaded together prior to the reaction. An additional and important difference between the process used by the Company and other processes was that the Company added the sodium hydroxide solution in a controlled manner during the hydrolysis process to limit reaction rates. 2.3 Analysis of 2,3,7,8-TCDD in 2,4,5-T As of 1971 every batch of 2,4,5-T produced by the Company was analysed for the 2,3,7,8TCDD content. Before 1985 the gas chromatographic separation was not isomer specific (refer section 2.5) and, as a result, the values found should be regarded as a maximum 2,3,7,8-TCDD content. After 1985 the analytical technique gave results for 2,3,7,8-TCDD content rather than a mixture of isomers. Table 2 shows the decreasing 2,3,7,8-TCDD content over time. From 1972 random samples were taken on behalf of the Agricultural Chemicals Board and analysed by DSIR. The analysis of 2,3,7,8-TCDD in 2,4,5-T product over time by the Company does show that the limits of detection that both the Company and DSIR achieved were in line with international trends. For example, in 1979 it was reported (USEPA 1979) that a United States Environmental Protection Agency (USEPA) contract laboratory limit of detection for 2,3,7,8-TCDD was 0.01 ppm. In 1980 the DSIR was reporting 0.024 +/- 0.004 ppm of 2,3,7,8-TCDD in 2,4,5T. By 1983 the DSIR found 0.007 +/- 0.004 ppm and the Company 0.005 ppm. This indicates that both laboratories were achieving similar results at that time though using different equipment and methods. For 2,4,5-T analysis purposes the New Zealand methods prior to 1985 were effective or at least consistent. In 1985 both the Company's laboratory and the DSIR installed more sophisticated equipment. A comparison between DSIR analyses (Hughes 1984) and Company (pers comm) analyses of 2,3,7,8-TCDD found in samples of 2,4,5-T esters 1980-83 follows: Table, 3. 2,3,7,8-TCDD results in ppm of 214,5-T Acid Equivalents DSIR COMPANY Mean & Standard Deviation of 12 samples each 1980 0.024 +/- 0.012 0.014 1981 0.009 +/- 0.003 0.007 1982 0.013 +/- 0.005 0.008 1983 0.007 +/- 0.00.4 0.005 2.4 Incineration of residues The destruction of the 2,3,7,8-TCDD- containing residues was an important feature of the Company's operation. In producing commercial products in which contaminant concentrations are carefully controlled, adequate attention must be paid to the treatment of residues which would probably contain much higher concentrations of contaminants. During December 1972 the Company sought approval from the Department of Health for a Clean Air Act 1972 licence to install a liquid waste incinerator to destroy chemical wastes and the licence was granted in May 1974. A Hygrotherm-Hirt liquid waste incinerator was installed and commenced operation in 1975. In the period November 1975 to May 1979 the xylene- trichloroanisole waste stream that had accumulated since 1970 was incinerated. During this period the incinerator operated for 17,200 hours and the feed stock had an "apparent" 2,3,7,8-TCDD level of 0.57 - 27.2 parts per million (ppm). There was off-line monitoring of the stack emissions carried out by the company with occasional Department of Health audits which involved separate sampling and analysis. A total of 566,080 litres of liquid wastes were incinerated, containing an estimated 5.7 kilograms of "apparent" 2,3,7,8-TCDD. The emission analysis indicated that less than 1.6 grams of "apparent" 2,3,7,8-TCDD was emitted from the stack. (The "apparent" 2,3,7,8-TCDD quantities arise from the inability of the testing equipment of that time to separate the dioxins and furans). Operation of the liquid waste incinerator ceased in May 1979 when most of the accumulated waste stream had been incinerated and the trichlorophenate process was modified to eliminate that waste stream (DowElanco 1991). A further quantity of liquid waste was destroyed from April to August 1985. Two-thirds of this waste was generated prior to 1978/79, and the remainder comprised pilot plant esters, xylene distillation residues and some other residues. On this occasion 57,546 litres were incinerated, containing 71.6 grams of "apparent" 2,3,7,8-TCDD with 17.6 milligrams of "apparent" 2,3,7,8-TCDD emitted from the stack. Clearly this quantity of waste was much smaller than the previous waste incineration programme. The Company maintained off-line stack emission monitoring which was audited by the Department of Health. A new liquid waste destruction programme commenced in May 1988 with wastes which had accumulated from the end of 1985. A total of 113,800 litres of liquid wastes containing an estimated 60 grams of 2;3,7,8-TCDD was incinerated. Most of these wastes resulted from the nominal operation of the phenoxy plant together with wastes from the decommissioning of the Trichlorophenol (TCP) process. The incinerator was not run on a continuous basis. It was estimated that the quantity of 2,3,7,8- TCDD emitted was 0.03 grams. (Dow Elanco 1991). The public were advised of this intended programme in a press release by the Department of Health. In July 1980 the Company was granted approval to install a Sunbeam-Comtro Model A35 solid waste incinerator suitable for the destruction of chemical wastes such as sludges, off-specification chemicals, spent activated carbon and contaminated steel drums. The incinerator was operated between July 1983 and March 1986 to destroy these chemical wastes, which may or may not have contained 2,3,7,8-TCDD. During this time the Company monitored stack emissions with occasional Department of Health audits. The mean 2,3,7,8-TCDD stack emission concentration was less than 2.5 nanograms(ng)/m3 and the mass emission to atmosphere was 8.24 milligrams for the 1887 hours of operation. Although the 2,3,7,8-TCDD content of the solid wastes was not routinely determined, a trial in July 1983, when 82.6 milligrams of 2,3,7,8-TCDD was incinerated, measured the mean concentration in the stack emission as less than 5ng/m3 (i.e. the detection limit). During December 1988 (Pilgrim 1990) two significant trials were conducted with the solid waste incinerator. In the first, 63.6 kilograms of 2,4,5-T butyl ester containing negligible 2,3,718-TCDD was incinerated at a rate of 12.5 kg/hour. This was followed by 39.75 kilograms of 2,4,5-T butyl ester containing 119.25 milligrams of 2,3,7,8-TCDD (i.e. 3.0 ppm) at a rate of 9.5 kg/hour. The incinerator operating parameters appeared identical for both trials and in each case emissions were monitored by the company and by the Department of Health. The results are expressed in toxicity equivalents (TEs) which have been developed to compare the presumed toxic effects of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF) isomers to the toxicity of 2,3,7,8-TCDD. These results seem to relate to the efficiency of combustion rather than to the 2,3,7,8-TCDD content of the feedstock. Results of further testing of emissions by DSIR and the Company during 1990/91 have confirmed these results (Dow Elanco 1992). They also demonstrate the important point that 2,3,7,8-TCDD can be formed under combustion conditions, as can other PCDDs (dioxins) and PCDFs (furans). Further, these results suggest that emission control requirements as concentrations or mass emissions are more appropriate than a minimum Destruction and Removal Efficiency (DRE) for known contaminants. 2.5 Monitoring of emissions When the liquid wastes incinerator was burning 2,3,7,8-TCDD-containing liquids, batch or off-line emission monitoring from the stack sampling point was undertaken. Prior to 1985 flue gas was sampled for 4-6 hours over a 24 hour period into dimethyl formamide/triethanolamine (DMF) in three collectors. Probes, inlet lines and collecting systems were covered to exclude ultraviolet light, although the system is opaque to ultraviolet light. After May 1985, the Department of Health system consisted of water scrubbing and resin adsorbers. During a complete period of incineration an integrated sample was taken by bleeding 1-2 litres/minute from the exhaust gases. Trials suggested that about 70% of the 2,3,7,8-TCDD recovered collects in the probe, the teflon line, and first drop out bottle, with the remainder in the three DMF collectors (or the resin columns). The flue gas samples were analysed, prior to mid 1985, with a gas chromatograph (GC) fitted with an electron capture detector (ECD). The system did not separate the individual dioxins and furans. The limit of detection for the stack emissions was 10 mg/m3 (ambient temperature). Results were expressed as "apparent" 2,3,7,8-TCDD but it was recognised by the Company (and by the Department of Health) that the method of analysis was not isomer specific and the results did include certain other organically soluble neutral compounds such as dioxin isomers. In 1984 the Company (IWD 1984) confirmed that it did not specifically identify the 2,3,7,8-TCDD isomer and that it did not check for other chlorinated dioxins. This was a consequence of the separation techniques and because the requirement was to measure 2,3,7,8-TCDD. Other constituents were simply substances interfering with the 2,3,7,8-TCDD measurement. Thus the "apparent" 2,3,7,8-TCDD results should be regarded as maximum 2,3,7,8-TCDD content. While off-line emission sampling was undertaken at all times during incineration operation, there were times when the recording gas meter malfunctioned. Since chimney gas flows were not continuously determined, the conservative design gas flow was used to calculate 2,3,7,8-TCDD destruction efficiencies. Actual volumes ranged from 4000-6800 M3/hr (320 to 390C) while the design flow is 9200 m3/hr at 320C. Prior to 1985 the Company used a Pye 104 gas chromatograph equipped with a Nickel 63 detector (the ECD) to analyse for 2,3,7,8-TCDD. These instruments and techniques were satisfactory for the purpose; due to improvements in chemical clean-up and the gas chromatographic systems, analysis detection levels were reduced from parts per million to parts per billion i.e. a thousand fold improvement. In August 1985 the Company installed more sophisticated equipment for 2,3,7,8-TCDD analysis. This was a standard Hewlett Packard Quadrupole Mass Spectrometer (MS) capable of measurements in the picogram range (i.e. 10[-12] grams). The columns used with the mass spectrometer could separate 2,3,7,8-TCDD and other contaminants, something which had not been possible using the previous equipment. The Company continued with the GC-ECD method of analysis until August 1986 when samples were also analyzed by GC-MS. Such advances led to a lowering of the limits of detection for the stack emission samples from the liquid or solid incinerators and enabled flue gas analyses to be quoted in terms of 2,3,7,8-TCDD rather than "apparent" 2,3,7,8-TCDD. 2.6 Disposal of ash Monitoring of 2,3,7,8-TCDD levels in ash resulting from the solid waste incineration process was also undertaken by the Company and the Department of Health. For example, the Department of Health monitored the incinerator on a continuous basis from 27 August to 19 September 1985 and 28 November to 20 December 1985. The ash from drum burn 31 (of a total of 39 drum burns) contained less than 200 ng 2,3,7,8-TCDD/kg. Composite ash from a further 11 drum burns contained less than 150 ng 2,3,7,8- TCDD/kg. The criterion adopted by the Company for off-site transportation of ash is that the concentration of 2,3,7,8-TCDD present in a batch is less than 1000 nanograms/kg ash. This is the level established by the Centres for Disease Control, Atlanta, Georgia. Once the ash satisfies this criterion it is disposed of at the Coulson Road landfill where it is mixed with volumes of domestic waste. Although there have been no independent analyses of ash leaving the Company premises, the Coulson Road landfill is comprehensively monitored by the Regional Council (Taranaki Regional Council 1991). The Puremu Stream downstream of the landfill showed only constituents of elevated ammonia and suspended iron matter, typical of a well-run municipal landfill. Leachate from the landfill is now pumped to the New Plymouth District Council Wastewater Treatment Plant. Effluent from the Treatment Plant was analysed by DSIR in March 1991 for organochlorine pesticides, polychlorinated biphenyls, organophosphorus pesticides and organonitrogen pesticides. In all cases these chemicals were not detected in the effluent. [3] CASE STUDY - ROLE OF DEPARTMENT OF HEALTH Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND From 1972 to mid-1991 the Department of Health had statutory responsibility for controlling emissions of air pollutants under the Clean Air Act 1972. The Department also had (and still has) responsibility for protection of public health under the Health Act 1956. 3.1 Technical information In order for an authority to control discharges of contaminants to the environment, it must first know what compounds are likely to be discharged. There are various sources of information which can be used. The major source of information is from the Company which is subject to regulation. Commercially sensitive information on a company's manufacturing processes or products is protected by secrecy provisions. Information on manufacturing processes was made available by the Company to the Department of Health at the time that a Clean Air Act licence was being issued. There were also regular meetings of Department of Health staff and the Company, particularly after the 1976 Seveso incident when an intensive review of manufacturing processes was undertaken by the Department of Health. Modifications to manufacturing processes were notified to the Department of Health in 1978/79 and 1981/82 in relation to the trichlorophenol plant and in 1986 following the "bursting disc" accident. Complaints from adjacent residents about objectionable odours in early 1985 resulted in improvements to ventilation air control to the phenoxy herbicide manufacturing area as a whole. These changes were also notified to the Department of Health. 3.2 Overseas literature and standards Generally, the approach of the Department of Health has been to rely on overseas publications for setting standards. The principal source of established and acceptable standards in the view of the Department is the World Health Organisation (WHO). However, when standards are not available from WHO, guidance may be taken from published standards from the United Kingdom, the United States of America, Australia, Germany or the Netherlands. Most of these standards refer to air pollutants commonly experienced from for example combustion sources, traditional industry or motor vehicles. Very few standards promulgated by recognised control agencies are applicable to emissions from the agricultural chemical industry. Operational criteria have been specified in both the United States of America and the United Kingdom for pesticide waste incineration (Graham 1988). A temperature of 1000C, 2 seconds residence time and the presence of free oxygen are recommended as being adequate for complete combustion of 2,3,7,8-TCDD and most other chlorinated organic compounds (Esposito 1980). In addition, for hazardous waste incineration generally, the US EPA requires a Destruction and Removal Efficiency (DRE) of at least 99.99%, along with limitations on the production of hydrogen chloride and particulate matter. There has been some concern expressed that 2,3,7,8-TCDD would not be destroyed by incineration since it is a compound very resistant to thermal decomposition. There are, however, numerous references to thermal destruction of 2,3,7,8-TCDD above 800C in the presence of free oxygen (Mercier et al 1976, Chemical Review: Dioxin 1988, Stehl et al 1973). Emission limits and ambient air standards were used by the Department of Health as a guide to adopting the best practicable means of control as required by the Clean Air Act 1972 and were reflected in the licence conditions. 3.3 Clean Air Act licences Regulation of the incineration of residues at the Company's plant was carried out pursuant to the Clean Air Act 1972. This Act placed an obligation on the occupier of any premises to adopt the best practicable means: (a) to collect and contain any air pollutant and to minimise by the selection of the most appropriate process equipment ... the emission of air pollutants from those premises; and (b) to render any air pollutant emitted-from those premises harmless and inoffensive. The definition of practicable took into account local conditions and circumstances, financial implications and the current state of technical knowledge. The Act did not require the adoption of best available technology although in some cases that technology is the best practicable means. Approval to install the liquid waste incinerator was given to the Company in May 1974 subject to the following conditions: (a) the height of the incinerator stack to be no less than 15 metres (b) the emission of hydrogen chloride gas to atmosphere shall not exceed 2.3 kg/hour (c) light smoke as defined in the Act shall not be emitted for more than 4 minutes in any period of 60 minutes (d) the process shall be designed and operated in such a manner so as to ensure that combustion is complete This first licence was issued on 12 July 1974 and was renewed on an annual basis until 1984. The 1982 amendment to the Act permitted licences to be issued for a stated period. In 1984 a licence was issued for a five year period and was reissued in 1990 to expire in 1995. The Department used guidelines to assess the incinerator performance for the 1975-1979 incineration programme. These were: 2,3,7,8-TCDD destruction efficiency not less than 99.9%; combustion chamber back end temperature not less than 1000C; free oxygen present in the flue gas prior to quench air addition. Changes to conditions on the licence were made on a number of occasions. In April 1977 the hydrogen chloride (HCI) emission rate was changed from not to exceed 2.3 kg/hr to not exceed 3.4 kg/hour.The stack was designed to disperse 4.5 kg/hr of combined HCI and sulpbur dioxide (SO2 in medium fuel oil diluent). The use of a lower sulphur content in fuel oil made some "dispersion capacity available. The original 2.3 kg/hour requirement was conservative and did not permit sufficiently rapid destruction of stockpiled 2,3,7,8-TCDD- containing liquid wastes. There had been no problems with raising the rate to 3.4 kg/hour, according to the Department of Health. In 1982 Condition (d) on the licence was changed. The requirement for "complete combustion" was suitable when the limit of detection of 2,3,7,8-TCDD in flue gas was appreciably higher than the actual incinerator performance. However, rapid improvements in limits of detection meant that the flue gas samples could be measured about the level of detection. As a practical guide to "complete combustion" the guidelines used during the 1975-1979 incineration programme were adopted as conditions on the Clean Air Act licence. A new Clean Air Act licence was issued in July 1985 with special conditions for the liquid and solid waste incinerators. This licence expired in March 1989. Conditions for the liquid waste incinerator included: (a) The capacity of the gases discharged (excluding steam)shall not exceed 20% when operating for the destruction of toxic material (b) HCI not to exceed 4.5 kg/hr (c) TCDD not less than 99.9% destruction of TCDD. Conditions for the solid wastes incinerator were: (a) the opacity of the gases discharged (excluding steam) shall not exceed 20% when operating for the destruction of toxic materials (b) HCI-not to exceed 1.5 kg/hr (c) TCDD not less than 99.9% destruction. In addition there were the following requirements: (d) the liquid waste incinerator shall be operated with a combustion chamber temperature not less than 1000C and free oxygen be present (e) the solid wastes incinerator shall be operated with a secondary combustion chamber temperature of not less than 1000C and free oxygen be present. A subsequent licence was issued in August 1990 with expiry on 31 March 1995. The conditions on this licence for the liquid and solid incinerators are more detailed and include a condition relating to contaminant concentration rather than percentage destruction efficiency. The full conditions for the incinerators are listed in Appendix I. As a result of evolving analytical techniques, changes in conditions on the licence were made. The results of the December 1988 solid waste incinerator trials and overseas' recognition that in burning chlorinated wastes both PCDDs and PCDFs were produced and therefore should be regulated also contributed to these changes. 3.4 Compliance and monitoring Compliance with conditions of a licence was ascertained by the Department of Health through regular process inspections, examination of process records with particular reference to process operating parameters, control equipment operating parameters including emission testing and other evaluations, maintenance records, evaluation of industry testing and analytical methods and by periodic testing of emissions of significance. The frequency of process inspections and emission testing varied with the perception of the significance of the process concerned. It also varied according to the resources of people who were available. Restraints on staff numbers within the Central Region Air Pollution Control Group, and on the analytical facilities available, meant that the Group had to adopt an auditing role in regard to actual emission testing. Following the United States practice, the policy of "self monitoring" by industry was encouraged. Process reviews of the Company have been summarised in Section 2.2. The detailed information was, in general, not made public because of the commercial and proprietary nature of some of the processes. The Company not only monitored the emission gases for 2,3,7,8-TCDD content but also monitored and recorded the level of carbon monoxide, oxygen, temperature and feed rate of the incineration process. During the 1975-1979 period when 2,3,7,8-TCDD-containing liquid wastes were being incinerated, the Department of Health undertook occasional auditing checks of the 2,3,7,8-TCDD content of the flue gases and also took samples of the liquid wastes. The samples were analysed by the DSIR. Destruction and removal efficiencies were calculated and incinerator performance assessed in terms of residence times and flue gas volumes by the Department of Health. During the April to August 1985 period the stack emissions were monitored by the Company and audited by the Department of Health. Samples taken by the Department of Health were analysed by DSIR. Incineration trials were undertaken in July 1988 to determine the percentage destruction of a chlorinated feedstock containing a known and consistent 2,3,7,8-TCDD concentration incinerated in the solid waste incinerator. In April 1985 soils inside and outside the Company's boundary were sampled jointly by the Company and Department of Health staff. The DSIR analysed the Department of Health samples, particularly samples from wind directions that would carry process gases or incinerator emissions towards industrial and residential areas. The highest results were from sample sets northwest B (0.14 ppb) and from East A (0.17ppb), followed by East B (0.11 ppb). These results can be compared with the United States Centers for Disease Control standard not exceeding 1 ppb for residential soils. There are various possible sources of 2,3,7,8-TCDD in the soils, including the Company process, distillation vents and the liquid waste incinerator. However, it is considered that the most likely source was the historical manufacture of 2,4,5-T from 1964 to 1969 when the imported trichlorophenol may have contained high concentrations of 2,3,7,8-TCDD. 3.5 Information made public by the Department The Department of Health submitted information (including results of testing programmes) to the Ministerial Committee of Enquiry reviewing possible health effects of manufacture of 2,4,5-T in July 1986 and to Professor Rappe in March 1987. The following information was also released to the public: the conclusions of the 1975-1979 liquid waste incinerator programme as summaries and also in the 1984/5 Biennial report dated July 1986 and in the 21st Report of the Principal Air Pollution Control Officer, 31 March 1987 individual test results for the April to August 1985 liquid waste incinerator programme, as individual press releases and as a summary (given to the Ministerial Committee of Enquiry on request) answers to questions from the Residents Against Dioxin (RAD) at meeting in May 1985 [] 4. CASE STUDY - ASSESSMENT OF ACTIONS BY COMPANY AND REGULATORY AGENCY Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND At various times during the period the Company was manufacturing 2,4,5-T, there was heightened public interest in the Company's operation. The actions of both the Company and the Department of Health have been the subject of public scrutiny over a number of years. 4.1 Disclosure of information A number of formal requests under the Official Information Act 1982 were made at various times to the Department of Health to obtain information relating to the Company's operations. Information which was not of a proprietary nature was provided, but details relating particularly to the chemistry and engineering of the trichlorophenol process modification of 1979 were not released. These modifications were explained to the public in a Dominion article of 25/3/85 as "The company had a secret 2,4,5-T-making process which did not generate dioxin in the waste stream." Subsequently the existence of (other) liquid wastes containing small amounts of 2,3,7,8-TCDD was made known. During the early 1980s there was confusion in the public mind about the nature of this "secret process" partly because of conflicting statements as to whether or not 2,3,7,8- TCDD-containing liquid wastes were being produced. Commercial confidentiality requirements meant that the Company's information given to the public was accurate (IWD undated) but did not spell out the significance of the process modification in terms of the decrease in 2,3,7,8-TCDD-containing liquid wastes requiring destruction. A Company is quite entitled to keep details of a process modification confidential and in this case, the modification was simple and apparently very successful. Any detailed description of such a process modification would benefit competitors. The regulatory agency had access to this commercial information but was required to maintain confidentiality. I believe that public understanding of the process modification would have been assisted if, in early 1985 before the April-August period of incineration, the Department of Health had explained the decrease in the 2,3,7,8-TCDD-containing wastes in relation to the 1975 to 1979 incineration. Public concern may not have then been so intense. The Clean Air Act 1972 was not a public process piece of legislation; therefore, the regulatory agency can be constrained in the release of information. The Act did not provide a specified path for disseminating information to the public. Information about technical air pollution control processes tended to be given at technical conferences. It is understandable that Department of Health staff had a cautious attitude to the release of information concerning any one company, as the staff were, to a large extent, dependent on the cooperation of company personnel to do their work. The Department of Health did make considerable efforts to provide information to the public. However, the public perception of risk was not alleviated by these efforts. I have previously commented on the fact that where there is a risk perception, the public are likely to distrust both the Company and the regulator. A clear continuous flow of reliable information from a credible institution is essential. 4.2 Accuracy of emissions analyses Public concern during the 1980s also focused on the adequacy of monitoring of the liquid waste incinerator when 2,3,7,8-TCDD-containing wastes were being burnt. The Company operated an off-line monitoring system to sample the flue gas. These samples were subsequently analysed for "apparent" 2,3,7,8- TCDD (prior to 1985) and 2,3,7,8-TCDD from 1986 onward. The Department of Health carried out occasional audits which involved separate sampling and analysis. The samples taken by the Department of Health were analysed under contract by DSIR Chemistry Division. The only source of publically available information on the emissions from the incinerators is published papers by Department of Health staff. The regulatory system in place at that time allowed for no independent checking of the work being undertaken. 4.3 Clean Air Act licence conditions As has been shown in section 3.3 the licence condition to ensure "complete combustion" has been modified from the time of the first licence in 1974 to the current licence issued in 1990. The changes have occurred as instrumentation to measure 2,3,7,8-TCDD in the flue gases improved to the point where the level of detection fell below the concentration of 2,3,7,8-TCDD in the flue gas. In 1982 changes to the Clean Air Act licence conditions were made, together with a new licence issued in 1985, to give a practical guide to what "complete combustion" was. The incinerator destruction and removal efficiency is not less than 99.9% 2,3,7,8-TCDD destruction. Standards in the USA vary from 99.9% to 99.9999% for "dioxins". The variation in standards is probably related to the capacity of an incinerator, its throughput, the 2,3,7,8-TCDD content of the wastes, its location and dispersion factors. It is difficult, and possibly unrealistic, to compare New Zealand standards to overseas standards when information on all these factors for individual incinerators is not readily available and the scale of incineration being undertaken is so different to the overseas incinerators. It should be recognised that both the Company's liquid waste and the solid waste incinerators are small when compared with many overseas incinerators which burn 2,3,7,8- TCDD-containing wastes. One problem with using percentage destruction and removal efficiencies is that it is dependent on the accuracy of 2,3,7,8- TCDD measurement methods and on having a homogenous feedstock to the incinerator. A more fundamental problem is that it does not necessarily control the mass of 2,3,7,8-TCDD discharge from the stack. At the time when guidelines were being set for the 1975-1979 incineration programme, a flue gas concentration/mass emissions limit for 2,3,7,8-TCDD was not considered a suitable guide. The reason given was that the flue gas concentration and mass emission of 2,3,7,8-TCDD could be proportionally reduced by reducing the 2,3,7,8-TCDD concentration of feedstock. However, the US EPA had adopted the concept of setting a standard based on the percentage of material destroyed. It is arguable that a mass emission limit on 2,3,7,8-TCDD or on PCDD/PCDFs could have been included in the Clean Air Act licence conditions earlier than 1990. In 1990 a new licence was issued which included a condition related to the emission of PCDD/PCDF compounds in terms of a concentration averaged over the duration of the test and a mass emission rate not to be exceeded. This licence also used the toxicity equivalent factor to measure the PCDDs and PCDFs present in the stack emissions. Some of the reasons for a change to the licence conditions have been referred to in Section 3.3. There was also a recognition on the part of the regulatory agency that when chlorinated wastes were burnt, the important factors were the mass emission/dispersion characteristics and the sensitivity of locality rather than the percentage destruction and removal efficiency. The analytical precision with which measurements of 2,3,7,8-TCDD could be made had also improved to the point where it was feasible to use a toxicity equivalent factor to assess incinerator performance. The other important factor was that the 2,3,7,8-TCDD content of the wastes requiring incineration had markedly decreased from the time of the first licence in 1974. In the late 1980s a measurement regime was introduced in which a toxic equivalent factor (TEF) (Safe 1990) was calculated relating known biological toxicity testing of PCDDs and PCDFs to 2,3,7,8-TCDD. In these systems 2,3,7,8-TCDD is given a value of 1. All other PCDDs and PCDFs are related to 2,3,7,8-TCDD and a factor is established which, multiplied by the concentration of that component enables a total to be reached which is defined as the toxic equivalent total. This recognises the fact that, while 2,3,7,8-TCDD is by far the most toxic of the PCDDs and PCDFs, the total pattern which depends on the particular concentrations of individual elements is what should be legislated against and not simply the 2,3,7,8-TCDD concentration. The World Health Organisation (WHO) December 1990 Consultation was cautious about the use of toxicity equivalent factor which has been developed to compare the presumed toxic effects of PCDD and PCDF isomers to the toxicity of 2,3,7,8-TCDD. In making these comparisons, it is assumed that all PCDD and PCDF isomers present in a mixture are equally well absorbed, and that the toxic effects of the components in the mixture would be additive. Such assumptions were regarded by the Consultation as simplistic and do not take into account toxicokinetic principles. Until adequate data are available, the Consultation recommends the toxicity equivalent scheme be used only as an interim approach for risk management purposes. I believe the licence conditions were adequate and that appropriate changes were made to reflect the knowledge gained as instrumentation improved, the changes brought about by the decrease in the 2,3,7,8-TCDD concentration of wastes requiring incineration after 1985 and the recognition that combustion per se produces PCDDs and PCDFS. The emphasis in thermal destruction of 2,3,7,8-TCDD- containing materials should be to use emission gas analyses to modify combustion conditions in order to comply with emission control regulation- In this respect, experiments at the Energy Laboratory, Massachusetts Institute of Technology (Stauffer 1991) using laser induced fluorescence (LIF) are pertinent. These have shown that in a combustion flame, very low concentrations (ppb) of polyaromatic compounds (PACs) can be measured in milliseconds. It is suggested that the detection of PACs may even signal the potential formation of dioxins and furans that may form catalytically on particle surfaces. The researchers conclude that using the LIF based detection/control devices to destroy all the PACs in a hazardous waste incinerator should make the formation of dioxins and furans highly unlikely. 4.4 Compliance It is clear that the Department of Health did keep in regular contact with the Company and did request and receive process and equipment upgrading information (Department of Health 1977) from time to time. Monitoring of the stack emissions was carried out by the Company as specified by the Clean Air Act licence. The ability of the Department of Health to undertake monitoring of the stack emissions and to get the samples analysed was constrained by resource limitations. The Department of Health encouraged a policy of self regulation with occasional audits to fulfil the regulatory responsibilities. Audits were carried out at suitable intervals and the regulator had full access to Company records. The policy of self regulation was acceptable. [] 5. CASE STUDY - LOCAL AUTHORITY RESPONSIBILITIES Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND Local authorities have responsibility for public well-being through the District Scheme provisions of the then Town and Country Planning Act 1977 together with public health responsibilities under the Health Act 1956. 5.1 Development of the Paritutu Road area Industrial subdivisions near the port area were carried out by the Taranaki Harbours Board in 1959, 1962 and 1967. Residential subdivision in Paritutu and Ngamotu Roads had preceded the establishment of this industrial zone. When the Company moved to its site in 1961/62 there were already some adjacent houses on Paritutu Road. The industrial zone (on the land used by the Company) provided for any type of industry. A small buffer area of Industrial B land provided for lighter industry immediately adjoining the residential area to the south. The manufacturing plant is located on a site approximately 200 metres from the nearest neighbour's boundary. In 1967 the New Plymouth City Council granted a specified departure to the Harbours Board to rezone an Industrial B. area to industrial D (for the Company's expansion) and to rezone a small residential zone immediately adjacent to Industrial B for warehousing. This zoning change meant the Industrial zones were brought closer to existing developed residential areas; with the area of undeveloped buffer residential land owned by the Harbours Board being converted to industrial uses. Table 5 outlines the history of subdivision in the area. 5.2 Provisions in the District Scheme The first District Scheme, covering both New Plymouth City and Taranaki County became operative in March 1962 and provided for 276 acres of industrial zone classified as Industrial A, B and D. Chemicals manufacture was listed as a predominant use of Industrial D zoned land. Bulk and location requirements for this zone were set out in Ordinance 15. No performance standards were included. In 1979 the District Scheme was reviewed and the industrial zones were increased from three (in the 1962 Scheme) to six. The three new zones were introduced to provide for better segregation of industry in the suburban areas. An Industrial 1.5 zone was developed from the former Industrial D zones which originally allowed any industry regardless of how noxious such an industry may be. (New Plymouth City Council 1979). However, the local authority considered that recent trends in regard to the dangers of allowing such freedom to establish noxious and dangerous industries within the built up confines of the City led to changes to the District Scheme to place some limitations in hazardous processes or storage of Dangerous Goods. Table 5. History of Land Development in Paritutu Road area 1948) 1951) Residential subdivision in Paritutu and Ngamotu Road areas are carried out under the Counties Act. Land within Taranaki County. 1955) 1956) 1959 Taranaki Harbours Board resolves to develop their land on Paritutu Road for future use by industry. 1960 In February 1960 the land for industrial development and the surrounding area is transferred from Taranaki County to the New Plymouth City. 1962 Further land in Paritutu Road is developed by the Harbours Board for industrial purposes (zoned Industrial D in the first District scheme). 1962 Watkins-Dow Ltd leases of some of this land. 1965 Harbours Board develops land for residential purposes between Paritutu Road, Port View Crescent and Findlay Street. 1965-1966 Housing south of company site is built by Ministry of Works and Development. 1967 Harbours Board is granted a Specified Departure to change zoning of land adjacent to the 1962 industrial development: Five acres of rural and five acres of Industrial B to Industrial D, four acres of residential to Industrial B as a buffer to Industrial D. 1969 Land immediately adjacent to the Industrial B zone is developed for residential purposes. 1972-1976 Housing is built by the Electricity Department due south of the site and subsequently transferred to the Housing Corporation. 1980-84 Housing to the south of Company site is built by Housing Corporation. The District Scheme statement indicates a need for further research on many other aspects of industries still permitted as predominant uses in this zone and possible development of further restraints. The main purpose of retaining the zone at all is to provide for the existing New Plymouth power station and the Company's chemical manufacturing plant. The Ordinances associated with the Industrial 1.5 zone are more detailed than the 1962 Ordinances in respect of bulk and location requirements. A Performance Standard for noise levels was also included in the 1979 Ordinances. The 1990 District Scheme provides an indication of further development of the assessment of effects of industry. The description of the Industrial 1.5 zone includes the following: "Little land is now zoned Industrial 1.5 within the old city area as such uses are more appropriately located well away from other types of urban uses. Any new areas of Industrial 1.5 land would need to be significantly separated from residential land and other sensitive uses by distance, landscaping, topography or other physical or visual separations." Conditional uses in any industrial zone would generally require a separation distance of 20-50 metres between any use and any residentially zoned property, depending on the nature of the industry. The 1990 District Scheme also requires that, prior to the establishment of any industry listed in appendix D-3, an environmental impact study that identifies all objectionable elements and shows how these can be alleviated to a satisfactory standard shall be carried out. Part of the environmental assessment for a noxious or hazardous industry would include a detailed consideration of the separation distance between the proposed use and other uses. If the environmental impact study indicates that unacceptable environmental problems remain, the use shall not proceed under the listing. 5.3 Effects on residential development of the adjacent industry At the time of the hearing for the Specified Departure application in 1979, some residents objected to the rezoning because of odour problems from the Company's plant. The then Plant Manager acknowledged that there was a problem relating to smell emanating from the works (New Plymouth City Council 1967). The smell was caused by the presence of chlorophenols. Prevailing winds in New Plymouth are from the westerly and southeasterly quarters so, a prevailing wind carries fumes from the plant towards the City approximately 23% of the time. In the 1980s residents living near the Company's plant were actively campaigning for a ban on the manufacture of 2,4,5-T because they believed the pesticide was a serious threat to their own health and to that of the New Zealand public generally. A Committee of Inquiry was set up by the Minister of Health to investigate the issue (Brinkman et al 1986). The Committee could find no substantial evidence that the manufacture of these pesticides has had any ill effects on the health of the residents of New Plymouth. However, the Committee was concerned over the blood tests of some Company employees, and some members of farming families. 5.4 Summary Because the Company's use of the industrial zoned land was a Predominant Use, no notification of changed production was required by the local authority. Council considered that the central government controls, administered through the Dangerous Goods Act 1974 and the Clean Air Act 1972, were sufficient (New Plymouth District Council 1992). I believe that the local authority has recognised the value of providing separation between new industries with the potential for noxious emissions and other uses. The problem of adequate separation of existing use industries and residential areas remains; in the past this requirement was not included in the District Scheme. [6.] INFORMATION ON 2,3,7,8-TCDD Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND 6.1 Background The chemical structure of 2,3,7,8-TCDD, or more correctly 2,3,7,8 tetrachlorodiberizo-p-dioxin was first established in 1956. 2,3,7,8-TCDD is one of a total of 75 structurally different chlorodibenzo-p-dioxins (PCDDs). There are 22 isomeric tetrachloro-dibenzo-p-dioxins or TCDDs of which the 2,3,7,8-TCDD has been identified as the most toxic. Closely associated with this group of compounds are those derived from furan. The dibenzo furan molecule has eight positions where chlorine may be substituted and because the molecule is unsymmetrical, there are a possible 135 polychlorodibenzofurans, or PCDFs, containing between one and eight chlorine atoms. Since these compounds are halogenated (chlorine or bromine), they and associated impurities are persistent in the environment and in the human body. 2,3,7,8-TCDD is said to have a half life of about 7 years in humans and about 10 years in soils, depending on their organic content (Science 1983). Although 2,3,7,8-TCDD was recognised in 1957 as a contaminant in 2,4,5-T (Tschirley 1986), real concern about the chemical was not raised until 1971 When researchers found that the 2,3,7,8-TCDD present in 2,4,5-T at 30ppm concentration caused teratogenic effects in mice and rats (Courtenay and Moore 1971), When the dangers of 2,3,7,8TCDD contamination were recognised, manufacturers reduced the 2,3,7,8-TCDD concentration in 2,4,5-T to less than 0.1 ppm. Analysing samples to measure 2,3,7,8-TCDD content is a complicated and expensive process. Details of the procedure are outlined in Appendix II. Detection methods have evolved since the 1960s when packed column gas-liquid chromatography systems were used. These systems were ineffective compared to modem equipment. As chemical methods were relatively insensitive and unreliable, a rabbit ear test was also used. For example, in 1965 a 10% concentration of some commercial 2,4,5-T in ethanol gave moderate to severe responses (Kociba et al 1978). The rabbit ear test was deemed positive if lesions similar to chloracne developed. The advent of gas chromatographs equipped with electron capture detectors (ECD) markedly improved the limits of detection. Under ideal conditions, the ECD would give a measurable peak for 0.01 nanograms of 2,3,7,8-TCDD. This method is outlined in American Organisation of Agricultural Chemists Methods (AOAC 1980). However, it would be unlikely that laboratories would have been able to distinguish many of the 22 tetrachlorodibenzo-p-dioxins or separate other dioxins during the later 1970s and early 1980s. Detection levels using this equipment did decrease from parts per million to parts per billion. Levels of 2,3,7,8-TCDD from that time should be quoted as "apparent" 2,3,7,8-TCDD because of the inability to distinguish the isomers. They should be regarded as a maximum 2,3,7,8-TCDD content for the same reason. The advances in detection limits that have been achieved are illustrated by the limits of detection assessed for samples from the Company's stack emissions as follows: Table 6. Detection limits in ng/m3 1975-79 10 1983-86 5 1988 <0.013 6.1.2 Toxicity The compound 2,3,7,8-TCDD has been identified as the most toxic of all the PCDDs and PCDFs and much of present knowledge is derived from studies of that substance. It was for many years referred to as "dioxin" before it was understood that 2,3,7,8-TCDD is one of many structurally similar compounds. There are great differences in toxicity among PCDDs and PCDFs. Toxicity requires there to be chlorine substitution on, inter alia, the 1 2 3 7 and 8 positions of both rings. Of the 210 PCDD's and PCDFs only 17 are regarded as toxic and have Toxicity Equivalent Factors (TEF) assigned to them. Within this group of 17 there are differences in toxicity of a thousand-fold (Safe 1990). Knowledge of the toxic properties of polychlorinated dioxins (PCDDs) dates from the late 1950s and early 1960s when millions of chickens died in broiler hatcheries in America (Vos et al 1974). Their deaths were ascribed to toxic fat mistakenly added to the feedstuffs. The source of the contamination was eventually tracked to the treatment of animal hides with pentachlorophenol and use of some 2,4,5 trichlorophenol to deflesh the hides to produce tallows or fleshing-greases (Hughes 1984). In 1971 the first report appeared in the literature regarding the extreme animal toxicity of 2,3,7,8-TCDD (Courtney and Moore 1971). As more work on animal toxicity was carried out in the 1970s, a considerable variation between animals in their sensitivity to 2,3,7,8-TCDD was found with LD50's for a guinea pig of 0.6 micrograms/kg body weight and for a hamster 3000 micrograms/kg body weight (Tschirley 1986). However, if other criteria are used, e.g. developmental toxicity, species sensitivity clusters within a ten-fold range (Chemical and Engineering News 1991). A recent review (Hayes and Laws 1991) summarises the extensive scientific literature on toxicity to livestock and laboratory animals. The identification of chemicals that are potential human carcinogens or teratogens relies largely on extrapolation from animal toxicity work. The tests are usually conducted at the maximum tolerated (toxic) dose which is factorially higher than pollution levels of the compound. 6.1.3 Effects on humans The literature repeatedly states that the primary effect on humans due to accidental exposure to 2,3,7,8-TCDD is the occurrence of chloracne. To date, chloracne is the most sensitive and specific indicator of overexposure to 2,3,7,8-TCDD that is available to humans (Hayes and Laws 1991). This was well-recorded at Seveso (Health Authority, region of Lombardy) and at other incidents such as in the Missouri horse arenas (Mercier et al 1976). In one case the horse arena soil was found to contain between 31.8 to 33,000 parts per billion of 2,3,7,8-TCDD. Over several weeks hundreds of birds, several cats and dogs and numerous rodents died after being exposed to the area. It is known that children played in the arena. At least two bad lesions described as consistent with chloracne, and one small six year old who frequently played in the arena soil had a case of haemorrhagic cystitis. Soil analyses showed the presence of 2,3,7,8-TCDD and additional tri- and tetra-CCDs (Buser & Rappe 1980). There were also significant quantities of 1,2,4,6,8,9-hexachloroxantbene, a by-product of hexachlorophene producing plant. Apparently, in 1957 the chemist who first established the structure of 2,3,7,8-TCDD applied 10 micrograms twice to his skin to demonstrate the effect of the compound (ILO 1983). In 1970 it was reported that in man the application of 70 micrograms per kilogram produced definite chloracne. Known amounts of 2,3,7,8-TCDD were applied to the skins of 60 volunteer prisoners (Tschirley 1986) at concentrations from 0.2. to 8 micrograms (i.e. 3 to 114 ng/kg for a 70 kg person). The dosages were repeated two weeks later and were chosen because these concentrations had caused chloracne in the rabbit ear test. None of the volunteers developed chloracne and no other symptoms were observed. A second experiment involved 10 volunteer prisoners who were treated with 107 micrograms of 2,3,7,8-TCDD per kilogram. Of these 10, eight developed chloracne but no other symptoms were noted. From these experiments one can only conclude that 2,3,7,8-TCDD does cause chloracne in humans when the dose is sufficiently high and that people are less sensitive than rabbits. The tests did not identify a threshold for the development of chloracne in humans. However, not every person exposed to high levels of 2,3,7,8-TCDD develops chloracne although they may have high levels of 2,3,7,8-TCDD in their blood serum (Zober et al 1990). People were also exposed to 2,3,7,8-TCDD-containing compounds through industrial accidents. The first reported industrial explosion involving 2,3,7,8-TCDD occurred in 1949 at a Monsanto plant in West Virginia. Reports in 1979 by a Dr Suskind concerning the health of the 121 workers who were exposed in 1949 and who developed chloracne have been criticised in a court case (Kemner et al v Monsanto Co & Ryder discussed in section 6.4) However, it must be pointed out that the first examination of the workers by Dr Suskind was made in 1953, at least four years before 2,3,7,8-TCDD was identified as a causative agent for chloracne. The structure of 2,3,7,8-TCDD was also not determined until 1957. Although the papers by Dr Suskind have been criticised in this court case, his work is fully supported by reports (Banks & Birnbaum 1991) which have appeared regarding the health of workers who were exposed at the Coalite explosion in 1968 (Chemical Safety Summary 1982). His work is also supported by a study covering 2,192 employees of the Dow Michigan Division (Chemical Safety Summary 1986) who may have been exposed to dioxins by working with chlorinated phenols and derived products between 1937 and 1980 and by a 34 year mortality follow-up of BASF employees after the 1953 accident (Zober et al 1990). Mortality rates through 1982 in the Dow study have been evaluated and show no increased death rates. Thus the findings regarding the Monsanto workers (Chemical and Engineering News 1979) are supported by studies of Dow Chemical Company employees and employees of the subsidiary of the Coalite Group in England. The understanding of the toxicity of 2,3,7,8-TCDD gained in the 1970S is now being re-evaluated in the light of further research results, a legal case and current or proposed changes to regulatory regimes. 6.2 Sources of 2,3,7,8-TCDD in the environment As analytical techniques improved, studies confirmed that 2,3,7,8-TCDD was the major isomer in 2,4,5-T formulations (Courtney & Moore 1971) and not present in samples of 2,4,D esters and amino salts from Canada. However, some of the esters and salts were contaminated with 1,3,6,8 TCDD isomer. It was soon apparent that many of the commercial chlorophenols contained a variety of PCDDs (dioxins) and PCDFs (furans). Pentachlorophenol (PCP) was of particular concern because, as a timber treating compound, it had been widely used in America for fencing and barn construction. In 1989 annual production world- wide was 45,000 tons (Nature 1980). In New Zealand PCP has been used for timber preservation with a maximum use of about 100 tonnes/annum and for the control of algae and moss. Sodium pentachlorophenate was used, prior to 1986, for anti-sapstain control (Bingham 1992). PCP use was limited compared to the use of copper chrome arsenate and boric acid preparations for timber preservation. Results published in 1984 (Rappe 1984) indicated the presence of 5 PCDDs and 5 PCDFs in commercial PCP with the most common contaminant, Octa-CDD, at a concentration of 500 ppm. Clearly these compounds were much more prevalent than bad been expected. 2,4,6-trichlorophenol and 2,3,4,6-tetrachlorophenol also had PCDD and PCDF constituents at the parts per million level. Thus instead of a problem with 2,3,7,8-TCDD, a whole range of PCDDs and PCDFs were found in traditional commercial products that had been available and used for some 50 years. The emission of PCDDs and PCDFs from municipal incinerators in the United States was the subject of EPA attention in 1980. The question of the temperature at which dioxin is destroyed is only one of the issues because, while dioxin can be destroyed by incineration, it can also be formed by de novo synthesis on fly ash following incineration. Any system where chlorine and carbon compounds are burnt together can yield dioxins and fnrans in the effluent gases. Mechanisms for the formation of PCDDs and PCDFs are still being proposed. It is likely that any source of carbon and of halogen incinerated in equipment with catalytic surfaces will generate PCDDs and PCDFs in the effluent gases. This could occur by the decomposition of the material to be incinerated and the formation of PCDDs and PCDFs by catalysis on hot metal and ash surfaces such as found in motor car exhausts and incinerator stacks. The consensus appears to be that the formation of PCDDs and PCDFs is principally generated at relatively low temperatures (about 200 - 400C) and that the rate of generation is likely to be very low above 800C, provided mixing of fuel and air is optimised. At a WHO Consultation in 1985 it was assumed that municipal solid waste (MSW) incinerators constituted the major source of environmental contamination by PCDDs and PCDFs (Rappe 1987). Subsequently, similar dioxin and furan patterns have been found in human milk samples from countries with few incinerators. There are also similar isomeric distributions for the PCDFs found in MSW incinerator emissions, in car exhaust gases and in dust from a baghouse at a steel mill. While there is a poor correlation between the isomeric distributions in environmental or human samples, one PCDD (1,2,3,7,8 PeCDD) is found in all biological samples and in all samples from incinerators and car exhausts. It was also found at a low level in a few technical PCP formulations. A recent 1990 WHO Consultation (WHO Europe 1990) concludes that for the general population food represents the main route of exposure to PCDDs and PCDFs. The Consultation recommended that all kinds of incinerators, including MSW incinerators, should reduce emissions to levels as low as technically achievable (e.g. 0.1 nanogram TEQ/M3). Special attention should be paid to fly ash which is the surface for de novo synthesis post combustion. Motor vehicles using leaded petrol are another source of PCDDs and PCDFs in the environment (Rappe et al 1987). The use of scavengers for leaded petrol results in the formation of a wide range of halogenated dioxins and furans. The 1990 WHO Consultation recommended that the use of leaded petrol he phased out as soon as possible. A limited study has been conducted in New Zealand on the analysis of PCDD and PCDF emissions from car exhausts for cars run on leaded and unleaded petrol (Bingham 1989). The study demonstrated that a range of PCDD and PCDF emissions can be detected from cars but that this may not be a major source in New Zealand. Pulp and paper manufacturing plants using chlorine-based bleaching processes have been found to produce PCDDs and PCDFs (Buckland et al 1990). Other bleaching processes can be adopted in order to minimise the presence of these contaminants in pulp and paper products, effluents and wastes. Other sources of PCDDs and PCDFs are the metal industry, sewage sludge and flame retardants. However, the origin of a large fraction of PCDDs and PCDFs is not known. Even though there are a number of sources of 2,3,7,8-TCDD in the environment, there is evidence from the United States that the body burden of 2,3,7,8-TCDD in the population appears to be falling. Samples collected in the early 1970s by the National Human Adipose Tissue Monitoring Program were reported to have mean background levels of about 12 parts per trillion (ppt). More recent work, such as that of the Centers for Disease Control, found background levels of 2,3,7,8-TCDD of 5-7ppt in 1990 (Chemical & Engineering News 1991). 6.3 Hazard assessment Concern has been expressed as to the appropriateness of ambient air quality standards both in New Zealand and overseas for 2,3,7,8-TCDD emissions. The focus has been on the potential hazards posed by PCDDs and PCDFs, 2,3,7,8-TCDD in particular. The 1990 WHO Consultation considered that "the introduction of PCDDs and PCDFs into the environment should be reduced to the extent possible consistent with sound engineering practices judged to be reasonable". Once a chemical has been identified as a potential human carcinogen or teratogen, further testing relies on rodent bioassays. About one half of all chemicals examined for carcinogenicity, whether natural or man-made, induce tumours in rodents, and over one third of all chemicals tested for teratogenicity induce birth defects. The tests are conducted at the maximum tolerated (toxic) dose; few of these chemicals have been tested below 10% of the toxic dose and scarcely any below 1% of the toxic dose (Ames 1987). Thus, a chemical may not be said to be "known" to cause cancer except at doses close to the toxic dose, yet pollution levels are rarely above 0.001% of the toxic dose. Neither scientific theory nor technique is capable at present of resolving the question of whether hazards exist for human exposure to chemicals at levels far below the toxic dose: expert opinion of the risk ranges from small (proportional to exposure dose) to zero. A high percentage of the natural chemicals ingested by humans are likely to be rodent carcinogens or teratogens at near-toxic doses. For example, natural carcinogens are present in mushrooms, celery, parsley, basil, mustard, peanut butter, fruit juices, coffee, tea, cooked food, bread, cola drinks, and alcoholic beverages. In addition, the vast bulk (at least 99.9%) of the chemicals we are exposed to in our food and drink are natural substances, and only a tiny proportion have been examined for carcinogenicity or teratogenicity. This is especially important as scientists are now capable of detecting chemicals at a level of one part per billion (one person in all of China) or one part per trillion (1/16 of an inch of the distance from here to the moon). Since scientists do not know enough to calculate risk for humans for low exposures to chemicals in the view of the above points, a relative rule is the best guide to follow. Ames (1987) suggests that the natural carcinogens in our daily food and drink rank enormously higher as possible hazards than common pollutants. Yet it is not at all clear that even these represent significant risks, as normally the levels are far below the toxic level. 6.4 Kemner et al v Monsanto Co. This court case involved residents of Sturgeon, Missouri, USA and the Monsanto Chemical Company. It arose out of a train derailment and subsequent chemical spill that occurred at Sturgeon on January 10, 1979. The evidence revealed that the defendant sent from its plant in Sauget, Illinois, a shipment by tank car of orthochlorphenol crude which may have contained small quantities of dioxins formed during the manufacturing process (the possibility of cross contamination in the manufacturing plant cannot be totally ruled out). The train derailed, and a gash on the bottom of the tank car caused some 19,000 gallons of orthochlorphenol crude to spill onto the tracks where the train-came to rest. There seems to be no question that there was some quantity of dioxins in the orthochlorphenol crude and that Monsanto either knew or should have known, but it was some days later before the clean-up crews were notified of the possibility of dioxins in the spill. The plaintiffs in this case were 65 individuals who were residents of Sturgeon at the time of the spill or who spent variable periods of time in Sturgeon after the spill. The plaintiffs alleged that they suffered personal injuries as a result of exposure to the dioxins, particularly 2,3,7,8-TCDD, which they alleged were contained in the spilled chemicals and that Monsanto was liable for such injuries under theories of strict products liability and wilful and wanton conduct. The jury returned its verdict after hearing evidence for 3 1/2 years and deliberating for eight weeks. The transcript of the proceedings totalled 91,555 pages with 6,333 exhibits.Punitive damages of $16.25 million were awarded against the company. Monsanto appealed the punitive damages verdict and in June 1991 the judges of the Illinois Appellate Court delivered their verdict. The Court overturned the $16.25 million punitive damage verdict against Monsanto. The jurors in the trial had found no injuries among people claiming to have been injured by exposure to dioxins but had decided to punish Monsanto for wrongful acts occurring from 1949 through to several years after the incident in Sturgeon, Missouri. The Appeals Court judges (Kemner et al v Monsanto Co & Ryder 1991) ruled that if there are no injuries, punitive damages cannot be exacted. No evidence was put forward that indicated 2,3,7,8-TCDD was present in the spilled orthochlorphenol. A request to have the appeal reheard was rejected. 6.5 Animal toxicity experiments Much of 2,3,7,8-TCDD's dreadful image stems from its label as one of the most toxic chemicals known (Vos 1974). It was widely thought that this label is attributable to research, between 1973 and 1978, in which the LD50 (the dose that kills half of a test population) was determined for eight species. The guinea pig was by far the most sensitive species tested; its LD50 for an oral dose was 0.6 micrograms/kg of body weight (Tschirley 1986). The hamster was the least sensitive animal tested with an LD50 about 1900 times higher than the guinea pig's. However, if other criteria are used, e.g. developmental toxicity, species sensitivity clusters within a ten-fold range (Chemical and Engineering News 1991). Research by Kociba and others in 1978, 1979 and 1980 (Kociba and Schwetz 1982) found that 2,3,7,8-TCDD was also a carcinogen in rats when daily doses above 0.001 microgram/kg/day were administered. In 1979 an expert Committee (FAO/WHO 1979) decided from the pharmacokinetic and pharmacodynamic data to accept that the rat was an appropriate species for toxicological extrapolation to man. However, Kociba (Kociba et al 1978) reporting on the chronic toxicity of 2,3,7,8-TCDD to rats, pointed out that rats fed one nanogram per kilogram per day for two years (i.e. -22ppt in the diet) suffered no effect considered to be of any toxicological significance. The FAO/WHO Committee stated "that in a rat a no effect level for 2,4,5-T is three milligrams per kilogram body weight per day and that a temporary acceptable daily intake for man was 0-0.003 mg/kg body weight or 3 nanograms/kg body weight when the 2,3,7,8-TCDD content of the 2,4,5-T was 0.05 mg/kg or 0.05 ppm. This implies a no effect level at a daily intake of 0.15 picograms per kilogram body weight. 6.6 Mode of action of 2,3,7,8-TCDD The biochemical knowledge necessary to understand how 2,3,7,8-TCDD works in the body has been developed since 1976, principally by Dr Poland (Kociba and Schwetz 1982). Researchers have found that 2,3,7,8-TCDD exerts many or all of its harmful effects in mammalian cells through binding to the Ah (aryl hydrocarbon) receptor (Safe 1990, Ames 1989). This means that no effect can occur until the receptor-dioxin complex is activated and transported to the cell nucleus where it interacts with DNA, setting off a series of events. This mode of action depends on the dose of 2,3,7,8-TCDD. Researchers also noted that other planar chlorinated dioxins, dibenzofurans and polychlorinated biphenyls (PCBs) could elicit a similar response although not as strong as 2,3,7,8-TCDD. There appears to be only one receptor for 2,3,7,8-TCDD that begins all 2,3,7,8-TCDD cellular activity. The receptor was recognised as a soluble intracellular protein (Kociba and Schwetz 1982), but its structure has not been identified. Subsequent research has identified that 2,3,7,8-TCDD has to occupy a certain number of Ah receptors on a cell before any biological response can ensue (Science 1991). The implication of this is a practical "threshold" for 2,3,7,8-TCDD exposure, below which no toxic effects occur. Ames (1989, 1990) believes that 2,3,7,8-TCDD is active as a promoter through its interaction with the Ah-receptor. Promotion, which is an essential step in carcinogenesis, is thought to involve a clonal selection of a mutant cell. Promotion is generally thought to be a threshold process. It can be caused by a variety of means, including 2,3,7,8-TCDD or other agents bound to the Ah receptor, which cause cell proliferation in certain organs (these vary in animals from species to species). Ames now believes that promotion itself is sufficient for carcinogenesis. This is supported by recent literature. (Iversen ed 1987). There are, however, a wide variety of natural substances (Ames 1987) which bind to the Ah-receptor. As far as examined, they all have the properties of 2,3,7,8-TCDD and seem to be more of a possible hazard than the levels of 2,3,7,8-TCDD ingested by people (typically 1-3 picograms/kg body weight/day in the USA). One such substance is indole carbinol (IC) which is present in large amounts in broccoli, cabbage and cauliflower and which binds to the Ah receptor. Just how many "natural dioxins" there are which mimic the action of 2,3,7,8-TCDD in cells is not known. 6.7 Epidemiological research Despite 2,3,7,8-TCDD's obvious toxicity to animals, the relationship between human health problems and 2,3,7,8-TCDD exposure has been difficult to study, even though a number of human exposure incidents are known. Most of these incidents exposed people to an unknown quantity of 2,3,7,8-TCDD-containing material. Many epidemiological studies undertaken to identify any major health problems always had so many shortcomings that researchers could not say whether 2,3,7,8-TCDD had a statistically significant effect or not. Another problem has been that long latency periods, (of the order of 20-30 years), are needed before the effects of some chemicals can be assessed. In order to find statistically significant differences in human health data, researchers must be able to collect and analyse very large data bases. This was difficult to do before the advent of computers. Four major epidemiological studies that have recently been published have attempted to assess 2,3,7,8-TCDD toxicity to humans. The first is the US Air Force Ranch Hand study begun in 1978. This is the oldest study of people exposed to 2,3,7,8-TCDD through 2,4,5-T and other herbicides and is the most controversial study. The participants were the US Forces personnel who actually handled and sprayed Agent Orange in Vietnam from 1962 to 1971. The original study involved 1242 Ranch Hand personnel although the actual number of participants did vary from examination to examination. The reports have found no statistically significant increase in illnesses such as cancer or reproductive effects compared to comparison veterans not exposed to Agent Orange. Some of the criticisms of the Ranch Hand study are valid. The small sample size is a problem for identifying increases in diseases like rare cancers. The study has had a 90% chance of detecting a 50% increase in all cancers. No-one has, however, doubted that those in the Ranch Hand study were exposed to 2,3,7,8-TCDD. The latest Ranch Hand report in March 1991 (Chemical & Engineering News 1991) lists blood levels of 2,3,7,8-TCDD in 866 Ranch Hand veterans and 804 comparison veterans. Values for 2,3,7,8-TCDD in blood serum ranged from 0 to 618 ppt in Ranch Hand personnel with a median value of 12.8 ppt. The median value of the comparison group was 4.2 Ppt. Aside from some other very minor correlations the report found a significant increase in body fat and diabetes that correlated with 2,3,7,8-TCDD concentration. The Ranch Hand study is now to extend the physical examination tests to look more critically at the diabetics. One of the issues arising from the Ranch Hand study was whether other service personnel in Vietnam suffered from exposure to Agent Orange and 2,3,7,8-TCDD. The Centers for Disease Control tried more than once to find a correlation between Vietnam service and health problems or blood serum dioxin concentrations and could not find one. The Department of Veterans Affairs in the United States also studied 85,000 self-selected veterans in the 1980s. The Department concluded that Agent Orange caused no health problems that were significantly different from those of the general population. The National Institute for Occupational Safety and Health (NIOSH) in the United States of America is conducting a medical study to evaluate the current health status of chemical workers who made products contaminated with 2,3,7,8-TCDD between 1951 and 1972. This major epidemiology study (Fingerhut 1991) was a retrospective cohort study of mortality among 5172 workers at 12 plants in the United States that produced chemicals contaminated with 2,3,7,8-TCDD. Occupational exposure was documented by reviewing job descriptions and by measuring 2,3,7,8-TCDD in serum from a sample of 253 workers. Causes of death were taken from death certificates. Of these workers, 1052 had died and the overall mortality for all causes, of death was found to be similar to national rates in the United States. The 265 cancer deaths were studied in great detail as was a sub cohort of 114 deaths where exposure had been for greater than 1 year (mean 6.8 years) and where the latency period had been greater than 20 years. No firm evidence linking 2,3,7,8-TCDD to increased cancer mortality could be found. The conclusion of the paper is as follows: "This study of mortality among workers with occupational exposure to 2,3,7,8-TCDD does not confirm the high relative risks reported for many cancers in previous studies. Conclusions about an increase in the risk of soft tissue sarcoma are limited by small numbers and misclassification on death certificates. Excess mortality from all cancers combined, cancers of the respiratory tract, and soft-tissue sarcoma may result from exposure to 2,3,7,8-TCDD, although we cannot exclude the possible contribution of factors such as smoking and occupational exposure to other chemicals." The conclusions of this study are similar to a much earlier study (Ott et al 1976) which had examined causes of death for all workers in a large manufacturing plant. Just how potent a carcinogen 2,3,7,8-TCDD is, is now the question. Fingerhut's study found that for several types of cancer previously associated with 2,3,7,8-TCDD no increases above expected levels were found. This finding has led the Director of the Centre for Environmental Health and Injury at the Centres for Disease Control to conclude (Chemical & Engineering News 1991): "I believe that a conservative interpretation of the Fingerhut study is that if 2,3,7,8-TCDD is a human carcinogen, which I am assuming it is, it is a relatively weak one and is a carcinogen only at extraordinary doses". Support for this view is provided by a study of cancer mortality among 1583 German workers in a chemical plant which had been highly contaminated with dioxin (Manz et al 1991). The results are consistent with the Fingerhut study and conclude with the hypothesis that 2,3,7,8-TCDD is a human carcinogen. The continuing study of the 253 workers by Fingerhut and her colleagues has shown a significant correlation between serum levels of 2,3,7,8-TCDD and duration of exposure to 2,3,7,8-TCDD (Fingerhut 1989). Consequently, it will allow follow up studies to assume that workers of longer duration will have higher levels of 2,3,7,8-TCDD in their blood. 6.8 Exposure assessment Estimates of exposure to 2,3,7,8-TCDD are needed in order to develop a sound regulatory framework. There have been many studies carried out in measuring 2,3,7,8-TCDD levels in blood serum, body fat and breast milk over the years. These studies have involved workers in factories, people applying herbicides and affected citizens in many countries. In one instance samples taken within one year after the Seveso incident were analysed and the results published in 1988 (Sweeney et al 1990). The range of results for these 10 samples was 1,772- 27,821 ppt. The extreme end of the range corresponds to some of the "last major exposure" calculations for workers exposed following the 1953 BASF plant explosion (Zober et al 1990) and also for a process engineer from a New Jersey Plant. In the former case the 2,3,7,8-TCDD level in blood measured 35.2 years after exposure was 553 ppt while in the latter the 2,3,7,8-TCDD level was 994 ppt measured some 35 years after exposure (Sweeney et al 1990). It is reasonable to assume that, immediately after a plant explosion involving 2,3,7,8-TCDD, levels in excess of 20,000 ppt in workers' blood could be expected during the plant clean-up phase. A level of 20,000 ppt suggests a body burden of some 2.2 ng/kg (assuming a 70 kg person) and exposure to contaminant levels well above 100 ppm. In a preliminary report of the NIOSH study, Fingerhut (Fingerhut 1989) presented the results of the analyses for 2,3,7,8-TCDD found in the blood serum of 46 study participants. In general, the mean of 8.2 ppt 2,3,7,8-TCDD found in the unexposed group is comparable to levels found in unexposed persons in industrialised nations. The mean serum 2,3,7,8-TCDD level of 208.2 ppt found in the workers greatly exceeds background levels. The current levels for workers are related to the duration of employment in the production of 2,3,7,8-TCDD contaminated materials. Since all workers were last exposed prior to 1973, serum levels of 2,3,7,8-TCDD at termination of employment were estimated by assuming a 7 year half-life. An update of Fingerhut's 1989 study of chemical workers (Sweeney 1990) provides more results. The serum 2,3,7,8-TCDD levels for 143 workers who were employed at either of two plants and 54 unexposed referents were measured. The mean serum 2,3,7,8-TCDD levels for all workers was 251.7 ppt and for all referents combined, the mean serum level was 7.8 ppt. The mean level of 2,3,7,8-TCDD present in the serum of workers at the date of termination of exposure (half-life extrapolated) was 2600ppt and 870ppt for the New Jersey and Missouri workers, respectively. Overall, the researchers found the levels in the workers significantly correlated with duration of exposure in 2,3,7,8- TCDD-contaminated processes. More results were reported in 1991 (Fingerhut 1991). Measurement of 2,3,7,8-TCDD in blood serum, as adjusted for lipids, in the sample of 253 workers from two plants was 233 picograms per gram of lipid with a range of 2 to 3400. A mean level of 7 picogram/gram was found in the comparison group of 79 unexposed persons, all of whose levels were under 20, a range found in other unexposed populations (Patterson et al 1989). The mean for 119 workers with one year or more of exposure was 418 picogram/gram. All the workers had received their last occupational exposures 15 to 37 years earlier. Another group of people who were affected by widespread use of 2,4,5-T as a herbicide in New Zealand were people living in rural communities. Comparisons between the toxic equivalents (TEs) calculated for PCDDs and PCDFs in the fat content of New Zealand breast milk samples (Bates et al 1990) with those from samples from Canada, Finland, Germany, the Netherlands, Sweden, United States and United Kingdom (Safe 1990) suggest that New Zealand samples were in the low to mid-range (16.47-18.06 ppt). With respect to 2,3,7,8-TCDD, the 17 rural and the 20 urban New Zealand women had average values of 5.13 ppt and 5.11 ppt. The New Zealand breast milk samples were also analysed for DDE, a breakdown product of DDT, and PCBs (Bates et al 1990). The DDE level was much greater than that in Europe, particularly in the area around Christchurch where grass grub was a problem and was treated with DDT. The PCB level is very much lower than in Europe. In general, the evidence suggests that the concentration of persistent chlorinated compounds in New Zealand does not differ greatly from those concentrations in other developed countries, apart from DDE. A study of the serum 2,3,7,8-TCDD levels in New Zealand pesticide applicators (Smith 1992) has documented substantial exposure to 2,3,7,8-TCDD from use of 2,4,5-T over many years in a group of nine workers. The study has found that serum levels of 2,3,7,8-TCDD increase only after several years of 2,4,5-T use. The study could not determine whether 2,3,7,8-TCDD exposure from prolonged use of 2,4,5-T poses significant health risks but Smith does conclude that previous reports in other countries of increased cancer risks from brief exposure to phenoxyherbicides are probably not attributable to the 2,3,7,8-TCDD that contaminates 2,4,5-T. The assessment of people's exposure to dioxins from other sources, such as fish, has been researched in Sweden (Svensson et al 1991) and in the United States (NCASI 1991). The serum levels of 2,3,7,8-TCDD in fish eaters in Sweden were not changed much despite the heavy intake of 2,3,7,8-TCDD-contaminated fish. The NCASI study has developed estimates for human exposure to 2,3,7,8-TCDD-contaminated fish and has shown that current USEPA risk estimates are conservative. A study currently under way in the United States by Dr Wendy Kaye (Fingerhut 1992) is assessing the exposure of residents of Jacksonville, Arkansas, since incineration of production wastes containing 2,3,7,8-TCDD has recently begun. Dr Fingerhut indicated that if the general population's exposure results in less than 20 ppt of 2,3,7,8-TCDD in blood serum, then the health effects should be minimal. The bactericide hexachlorophene is also prepared from trichlorophenol and so would be expected to contain 2,3,7,8-TCDD. There are few analyses published but levels of 0.2-0.5 nanograms/gm (pbb) have been recorded (Courtney and Moore 1971). The bactericide has been widely used in soaps and other compounds for skin contact. A recent research paper (Banks & Birnbaum 1991) suggests that skin absorption by 2,3,7,8-TCDD is extremely slow and that intervention (such as washing) could well be effective in preventing absorption. [] 7. REGULATORY REGIMES Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND 7.1 Tolerable daily intakes Previous research has been used by the regulatory agencies to set tolerable daily intakes of 2,3,7,8-TCDD. The assessments of exposure to 2,3,7,8-TCDD are used to evaluate the response of humans to varying doses. Thus the epidemiological research of Dr Fingerhut on the United States production workers may give the upper bounds of exposure limits for risk assessment purposes. The exposure of people other than chemical plant workers has been studied in examples like the Seveso accident, the Missouri horse arena situation, breast milk surveys, fish eaters in Sweden and the current research of Dr Kaye. Despite 2,3,7,8-TCDD's obvious toxicity to animals, no clear cut human health problems have so far been associated with 2,3,7,8-TCDD at environmental exposure levels. The presence of chloracne is still the most sensitive and specific indicator of overexposure to 2,3,7,8,-TCDD available for humans. Dr Fingerhut's work has shown that although body burdens of 2,3,7,8-TCDD were very high in some workers, these people were still alive 35 years later. However, public concern is not always with questions of lethality or mortality but with more subtle effects. Fingerhut and her colleagues have examined some health effects, such as whether bronchial conditions are more prevalent (Calvert et al 1989). However, what the data does not yet reveal is the general medical health of the workers over the 35 years since exposure to high levels of 2,3,7,8-TCDD. The finding of the latest Ranch Hand study (section 6.7) showed a significant increase in body fat and diabetes that correlated with dioxin concentration. This is being investigated further. The regulatory approaches of countries has been quite varied as Table 7 shows. This may have been brought about because a scientific consensus evolved in the 1970s that carcinogens should be treated differently and that the assumption should be made that even low doses could possibly cause some harm, even though at that time scientists lacked the methods of measuring effects at the low doses. This was a conservative approach to risk assessment in the absence of statistically significant effects at low levels and could explain the 1978 Canadian National Research Council and American approach. Different risk assessment models used in different countries-account for the considerable variations in Tolerable Daily Intakes (TDI). However, not all regulatory agencies have been so conservative. For example, the Ontario Ministry of the Environment supports the use of a threshold model for evaluating the carcinogenic risk of 2,3,7,8-TCDD (Washburn 1989). A major meeting of scientists involved in 2,3,7,8-TCDD toxicological work was convened by the WHO Europe office in December 1990 (WHO EURO 1990). The purpose of the Consultation was to review the scientific evidence and, based on a comprehensive toxicological evaluation, to develop guidelines for tolerable daily intake of PCDDs and PCDFs. The Consultative Group concluded that for the general population, food represents the main route of exposure to PCDDs and PCDFs. The total average daily intake, according to the Consultative Group, is approximately 03 pg 2,3,7,8-TCDD/kg body weight/day. (This figure is the same as the estimated ingestion in New Zealand.) The Group used a new approach to the risk assessment of 2,3,7,8- TCDD. It compared 2,3,7,8-TCDD tissue levels and health effects in laboratory animals and humans. It was concluded that 2,3,7,8- TCDD is carcinogenic in animals but that the evidence in humans is inconclusive. Since the compound is considered to be non- genotoxic and acts as a promoter-carcinogen, the Group decided to establish a Tolerable Daily Intake based on general toxicological effects. For pro-carcinogenic liver toxicity, reproductive effects and immunotoxicity tested in the various laboratory animal species, a no-effect level of 1000 picograms/kg can be identified. By using kinetic data this can be shown to be equivalent to a dose of 100 picograms/kg body weight/day in humans. An uncertainty factor of 10 was employed. Thus a Tolerable Daily Intake of 10 pg TCDD/kg body weight/day was recommended. Table 7. Tolerable Daily Intakes picograms of 2,3,7,8-TCDD/kg body weight/day 0 National Research Council of Canada (1978) 0.006 US EPA (as at 1991) 0.15 FAO/WHO (1979) 0.64 Centers for Disease Control, Atlanta, Georgia, US 1.0 Germany (1990) 0.3 Estimated ingestion in New Zealand 1 - 3 Estimated ingestion in Europe (WHO 1990) 4 Netherlands (1990) 10.0 Canada, VTHO, United Kingdom (1991) 7.2 Europe Following the WHO findings, the British Government in 1991, revised the level of 2,3,7,8-TCDD exposure which would prompt official action. The level has been revised upwards from 1 picogram/kg bodyweight/day to 10 pg/kg body weight (New Scientist 1991). It would appear that revised levels were considered, inter alia, because routine monitoring of foodstuffs by the Ministry of Agriculture, Fisheries and Food (MAFF) had found high levels of 2,3,7,8-TCDD in milk supplies from two farms. The Dutch government has also faced problems over milk with high levels of 2,3,7,8-TCDD. 7.3 The United States The USEPA has responded to new scientific information which has cast doubts on the model which is used for 2,3,7,8-TCDD risk assessment. The present model is a linear multi-stage model which assumes that risk rises in proportion to dose and does not allow for a threshold below which cancer would not occur. EPA had calculated that the tolerable daily intake of 2,3,7,8-TCDD for humans is 6 chemograms/kg body weight/day. This level would supposedly result in a one in one million chance of excess cancer from 2,3,7,8-TCDD. The new information included Fingerhut's epidemiology study and the results of a meeting at the Banbury Centre at Cold Spring Harbour Laboratory in November 1990. At that meeting a group of dioxin experts agreed that before 2,3,7,8-TCDD can cause any of the ill effects it has been linked to, one "necessary but not sufficient" event must occur; the compound must bind to and activate a receptor, known as the aryl hydrocarbon or Ah receptor. The group also agreed that 2,3,7,8-TCDD has to occupy a certain number of Ah receptors on a cell before any biological response can ensue. The result is a practical "threshold" for 2,3,7,8-TCDD exposure below which no toxic effects occur. This conclusion is clearly at odds with a linear model's underlying assumption that the risk of harmful effects begins with exposure to a single molecule. Not only are EPA scientists to come up with a new "biologically based" model but they have also been asked to find out background levels of 2,3,7,8-TCDD exposure for the general population. Other researchers will be studying the sources and routes of 2,3,7,8-TCDD exposure, most of which are dietary, and how it is passed up the food chain. This work is expected to be completed about May 1992 and will go to EPA's Scientific Advisory Board (SAIB) for peer review. The EPA review will merge the human epidemiology data, the animal toxicity information and the molecular biology to provide a firmer basis for regulation of this compound. Whether the EPA limit of 0.006 picograms/kg body weight/day changes or not, in view of the estimated ingestion of 2,3,7,8-TCDD as 0.3 picogram/kg body weight/day, remains to be seen but regulation may be based on a more realistic risk assessment model than is currently being used. 7.4. OECD Guiding Principles The OECD Environment Committee established an expert group in 1989 to develop guiding principles on the prevention of, preparedness for, and response to accidents involving hazardous substances. The objective of the Guiding Principles is to set out the general guidance for the safe planning, construction, management, operation and safety monitoring of hazardous installations in order to prevent accidents involving hazardous substances. Recognising that such accidents may nonetheless occur, the Guidelines seek to address mitigation of adverse effects through effective land use planning and emergency preparedness and response. The Principles summarise the roles and responsibilities of public authorities, industry, employees and their representatives, as well as other interested parties such as members of the public potentially affected in the event of an accident and non-governmental organisations. Safety in the Principles is considered to cover health, safety and environmental protection including protection of property. The OECD Council endorsed the Guidelines in 1991 and member countries (including New Zealand) are being encouraged to implement them, bearing in mind the different legal and institutional frameworks of member countries. [8]. REQUIREMENTS FOR FUTURE CONTROL IN NEW ZEALAND Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND This case study has examined the disposal of some manufacturing wastes contaminated with 2,3,7,8-TCDD which required treatment and disposal over a 10 year period. The public concern over this method of treatment and disposal centred on whether there were any adverse health or environmental effects arising from the disposal of these hazardous wastes. From the information that has been outlined in this review, in the absence of any cases of chloracne, it is unlikely that the community living adjacent to the plant was affected to the same degree as workers in American factories who were exposed to 2,3,7,8-TCDD at plants manufacturing chlorophenolic compounds over a lengthy time period. Similarly. the company workers seemed to have had limited exposure and to have been unaffected. However, there are no definitive answers to be given because the focus of the system for control of hazardous substances in New Zealand at that time rested on the control of gaseous emissions from the plant with little monitoring of the possible effects in the environment. I believe that this case study has shown that the Company's environmental management in carrying out the disposal of hazardous wastes by incineration was appropriate at that time, given the known information on incineration processes and the effects of 2,3,7,8-TCDD in the environment. The regulatory agency's monitoring of the operation was adequate to assess that the Company was complying with the regulatory controls. Company self-regulation of the incineration process with occasional audits by the regulatory agency was a valid means of monitoring the waste incineration. The ubiquitous nature of 2,3,7,8-TCDD in the environment has altered the perception that any one source of dioxin should be controlled more than any other potential source. The risk of adverse human health effects upon exposure to dioxin does not appear to be as significant as was indicated by early animal toxicity experiments in the 1970s. However, exposure to dioxin has been linked to ill effects, such as increased risk of diabetes, after some 20 to 30 years latency period. These and other findings have led the World Health Organisation to consider that: "the introduction of dioxins and furans into the environment should be reduced to the extent possible that was consistent with sound engineering practices judged to be reasonable". The information obtained in this review indicates that incineration of chlorinated pesticide wastes is an appropriate means of disposal provided the design of the facility and its operation are appropriate to the wastes requiring disposal. The regulatory controls on the environmental effects of the facility need to be technically adequate. Monitoring of the effects is essential. The argument that storage of hazardous wastes until such time as a "safe" method of disposal is developed needs to be re-evaluated given the risk management information about 2,3,7,8-TCDD. Disposal of waste pesticides from farms by high temperature incineration is a valid way of reducing the residual problem in this country. It is evident that very little pesticide waste is now being generated in the regions that have been surveyed. I have concluded that to achieve good environmental management of hazardous substances, the proposed hazards control legislation is urgently required. This legislation would be implemented by agencies such as the proposed Hazards Control Commission and local government. The present system is fragmented and lacks coordination. The Resource Management Act 1991 has placed responsibilities on regional and local government to control effects of activities which involve hazardous substances, including the prevention or mitigation of any adverse effects of the storage, use, disposal and transportation of hazardous substances. The control of discharges of contaminants to the air is now regulated under the Resource Management Act 1991. The Clean Air Act 1972 is still relevant in the transitional phase for licences existing before 1 October 1991. This change has brought both benefits and disadvantages. The benefits include a more public system of assessing any application for the discharge of contaminants into the environment. The disadvantages include the loss of a central body of expertise on industrial processes built up over time by the Department of Health technical air pollution staff whose group was disestablished at the time of the enactment of the Resource Management Act 1991. This expertise is now dispersed between the public and private sector with no one central agency retaining any "corporate memory". The regulation of agricultural compounds is presently carried out under four separate Acts viz the Pesticides Act 1979, Animal Remedies Act 1967, Stock Foods Act 1946 and Fertilisers Act 1960. A discussion document (Ministry of Agriculture and Fisheries 1989) proposed consolidation into an Agricultural Compounds Act. The links with a Hazards Control Commission would be in the areas of (agricultural) chemical usage, manufacturing of chemicals, transport of chemicals and downstream consequences such as clean up -operations. There is insufficient information on the nature and quantities of hazardous materials generated or disposed of in New Zealand. There is no nationally accepted characterisation of hazardous wastes which allows comparisons among industries or regions to be made (although the Chemical Industry Council's Guideline for Waste Management published in 1991 is generally accepted). The Department of Health funded waste surveys did not provide a national system of identifying wastes, so this information is of limited value in establishing policies for activities such as waste minimisation. This information is also needed in order to develop risk assessment tools for assessing appropriate treatment and disposal technologies in the future. Information on the fate of hazardous substances in the environment will also be necessary, as will data on dose-response relationships. Much of this information would arise from research of the environmental effects of different chemicals. Because the structural basis for "public good" science in New Zealand is being radically changed at present, it is unclear to which Crown Research Institute this research should be directed and even if more than one Institute should be involved. Where such science needs input from more than one Research Institute, it is expected that a mechanism for coordinating the research should be put in place. Information on new and emerging technology to treat hazardous wastes will be required by the proposed Hazards Control Commission, as will information on the new and improved control technologies for various possible facilities. It would be more efficient for one agency to collect such information rather than expect each regional or local authority to do so. This requirement means that establishing access to technical information in overseas regulatory agencies and research establishments will be an.) essential part of the proposed Hazards Control Commission's functions. Controls on the mass of hazardous materials emitted from an incinerator, for example, can only be achieved by measuring the emission gas analyses of particular compounds of known toxicity, such as the Massachusetts Institute of Technology research outlined in Section 4.3. Because of the difficulties in accurately measuring the hazardous substances in the feed to incinerators, even in a situation with a reasonably homogeneous feed stock, reliance on per cent Destruction and Removal Efficiencies for control purposes may not be as useful in the future. Just because another country adopts a particular control philosophy should not mean that New Zealand automatically follows suit. The provision of information to the public has been one of the features of this case study. There have been many studies conducted at the request of government on the subjects of 2,4,5- T use and manufacture as well as many requests for information on the environmental effects of living near a particular manufacturing plant. There is always a need for the public to understand any environmental and public health implications of waste disposal programmes including incineration. This information needs to be provided by a credible agency and provided on a continual basis. There is a difficulty in assessing scientific information on risks and benefits of different courses of action because of the uncertainties inherent in trying to establish cause and effect relationships. The long latency periods required to assess the effects of exposure to a chemical, compounded with the difficulty of separating out any effects from other chemicals, means that often the experts sound unsure or cautious about conclusions that can be drawn. The epidemiological studies for workers exposed to industrial chemicals contaminated with 2,3,7,8-TCDD 20 to 37 years ago are only now giving an indication that 2,3,7,8-TCDD is not as toxic to humans as had been assumed 10 to 15 years ago. The local community also needs timely and accurate information when emergency situations regarding chemical manufacture arise. The tragedy of the Seveso accident was that the breakdown in communication between the company, local authority officials and the community caused lasting mistrust of experts who came and went but never explained to the community what was known or not known about the long term effects of the accident. Partly, this was due to the real scientific uncertainties about the effects of 2,3,7,8-TCDD on people but nobody explained this to the Seveso community. New Zealand's own experience with respect to the ICI fire suggests that long term information programmes for affected communities should always be developed. The Resource Management Act 1991 provides for the establishment of a Hazards Control Commission but at the present time that part of the Act has not come into force. The way in which the Hazards Control Commission will work remains unknown. One of the purposes of this review is to identify aspects of hazardous waste management requiring action by Government and the Hazards Control Commission. To effect good environmental management of hazardous substances a national policy which includes the following matters is necessary. 1. A national policy on waste minimisation for hazardous wastes should be developed by and coordinated with any policy on waste minimisation being developed by the Ministry for the Environment. 2. A nationally accepted system for characterisation of hazardous wastes should be adopted. 3. Clarification of the roles and responsibilities of regional and local authorities and industry for the management of hazardous wastes, including the control of hazardous waste treatment and disposal should be undertaken. 4. Risk assessment tools to assess appropriate treatment and disposal means for hazardous wastes and residues should be developed. 5. Access to technical information and research, both New Zealand and overseas, to base appropriate standards for environmental control is required. The Hazards Control Commission should identify the research needs to ensure that management of hazardous chemicals is not compromised through lack of appropriate information. 6. Standards for emission control for incinerators, for disposal of residues to landfill and other disposal methods and for the receiving environment should be researched and made available to the regulatory agencies. 7. The provision of information to the public on the risks and benefits of different options for hazardous waste management is required. 8. The development of emergency response plans by the facility management and the local authority should be encouraged. In developing such plans, the OECD's Guiding Principles for Chemical Accident Prevention, Preparedness and Response should be used. The option of making the preparation of such plans mandatory should be explored. 9. In the event of a major accident or spill of hazardous chemicals that affects a number of people, proper investigation into the human and environmental effects including long-term research should be required. 10. Accurate and consistent information on the nature and quantity of hazardous wastes requiring disposal should be supplied by regional councils and unitary authorities to the Hazards Control Commission. 11. Monitoring of the environmental effects of any hazardous waste management facility by local government will be an essential part of the control of hazardous waste facilities. 12. The provision of a clear continuous flow of information to the public on the control of hazardous waste management facilities will be required. This will include information on effluent and gaseous emission concentrations as well as ambient levels in the receiving environment. [] APPENDIX I Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND Condition for the Liquid Waste and Solid Waste Incinerator Emission Concentration or Performance Criteria Visible emissions at The opacity of gases chimney exit discharged from either chimney shall not exceed 20% obscuration Hydrogen chloride Not to exceed 1.5 kg/hour as Hcl Poly-chlorinated The emission of PCDDs and/or diberizodioxins and PCDFs from either chimney shall polychlorinated not when averaged over the dibenzodioxins (PCDD/PCDF's) duration of the test exceed a concentration of 5 ng/m3 )ambient temperature) nor a mass emission of 5 ug/hour as 2,3,7,8-TCDD toxic equivalents NATO basis when burning wastes containing halogenated compounds or materials Combustion chamber Liquid waste incinerator - A minimum temperature of 1000C at the chamber backend and free oxygen present when incinerating halogenated organic wastes. Solid waste incinerator - Secondary combustion chamber temperature not less than 1100C and oxygen concentration preferably in the range 8-10% but not less than 6%. Monitoring of Incinerator Operating Parameters Liquid Waste Incinerator: Chimney effluent opacity, or combustion chamber carbon monoxide, continuously indicated and recorded. Combustion chamber backend temperature continuously indicated and recorded. Log sheet information: Feedstock type and destruction rate; operating times and variations; maintenance factors; and weather conditions. Solid Waste Incinerator: Primary chamber temperature indicated, and secondary chamber temperature indicated and recorded. Secondary chamber oxygen indicated and recorded. Log sheet information: Waste type and destruction rates; operating times, maintenance factors; and weather conditions. All monitoring information for both incinerators must be retained for at least 12 months and be made available to the licensing authority on request. [] APPENDIX II Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND Analysis of materials for 2,3,7,8-TCDD. The early overseas work in the 1960s on the toxic effects of 2,3,7,8-TCDD was done with separation techniques using packed column gas-liquid chromatography (GLC) which were ineffective by modern standards. This early work also predated the introduction of gas chromatographs equipped with electron capture detectors (ECDs). Levels of one part per million or even 10 ppm were probably very difficult to determine. The 1970s method involved first decomposing the samples with alkali then subjecting them to a series of extraction steps to concentrate the 2,3,7,8-TCDD. The fractions that are collected and concentrated are then separated by gas chromatography. The gas chromatograms are evaluated and the height of peaks compared to peaks obtained using standard solutions of known 2,3,7,8-TCDD concentrations. The method also has to be validated to ensure that "false positives" are not obtained through interference by other species which may be present if the extraction and clean up steps are not carefully carried out. Even if a peak was seen on the chromatograms at the parts per million level, the certainty that it was 2,3,7,8-TCDD would have been almost impossible to confirm. In the mid-1960s, for example, the contaminated fat fed to chickens was shown to contain toxic factors which were later identified as polychlorinated dioxins (PCDDs). Even by 1980 the official American Organisation of Agricultural Chemists method (AOAC 1980) for dioxins did not identify individual dioxins. PCDDs and PCDFs are frequently found in environmental samples at the parts per trillion and parts per quadrillion level. In order to measure these trace amounts, the analytical procedure must include a several thousand-fold concentration step. A typical effluent analysis may begin with a sample of 1 litre and end up with a final volume of 10 microlitres for the mass spectrometer analysis (Buckland 1990). GLOSSARY 2,3.7,8-tetrachlorodibenzo-p-dioxin: The most toxic of the polychlorinated dibenzo-p-dioxins. 2,4,5-T: trichlorophenoxyacetic acid, widely used as a herbicide in New Zealand prior to 1987. adipose tissue: A body tissue containing fat and oil. It is found chiefly below the skin and around the major organs acting as an energy reserve and also providing insulation and protection. AGCARM: Agricultural Chemical and Animal Remedies Manufacturers' Association of New Zealand Inc. Ah: ary] hydrocarbon. bioassay: A controlled experiment for the quantitative estimation of a substance by measuring its effect on a living organism. blood serum: Blood plasma from which the fibrin arid clotting factors have been removed by centrifugation or vigorous stirring so it cannot clot. carcinogenesis: The process of carcinogenesis is typically thought to involve a number of stages including initiation and promotion. Chemicals capable of initiating cancer by altering the genetic material of a cell are referred to as initiators. Substances that increase the incidence of tumours only when exposure occurs after initiation are called promotors. carcinogenicity: Tendency to cause cancer. carcinogens : Chemicals which induce the formation of tumours either benign or malignant. catalysis: The process of changing the rate of a chemical reaction by use of a catalyst. chlorophenol: Industrial chemicals used to make a wide variety of industrial compounds. cohort: A grouping of people with similar exposure history. congenital: Existing or as such from birth. DDT: dichlorodiphenyltrichloroethane - the best known of a number of chlorine-containing pesticides used extensively in the 1940s and 5Os. diluent: Diluting agent. DSIR: Department of Scientific and Industrial Research. EPA: The Environmental Protection Agency in the United States of America epidemiology: The branch of medical science concerned with the incidence of diseases in the community. ester: An organic compound formed by reaction between alcohols and acids. esterification: A reaction of an alcohol with an acid to produce an ester and water. gas liquid chromatography: The sample to be analysed is vaporised and swept through a column by a carrier gas. The various components of the sample separate while passing, through the column and are detected as they sequentially leave the column. The detectors used for chlorinated compounds were originally flame ionisation detectors and latterly electron capture detectors (ECDS) (see Appendix II). half-life: The time required for half the original material to degrade or decay. HCC: Hazards Control Commission. hydrolysis: A chemical reaction introducing an hydroxyl radical. isomer: Chemical compounds that have the same molecular formulae but different molecular structures of different arrangements of atoms in space. In structural isomerism the molecules have different molecular structures i.e they may be different types of compound or they may simply differ in the position of the functional group in the molecule. kinetic effect: A chemical effect that depends on reaction rates rather than on thermodynamics. LD50: The lowest amount of a pharmacological or toxic substance that causes death in 50% of a group of experimental animals. For each LD50 the species and weight of the animal and the route of administration of the substance is specified. lipid: Any of a diverse group of organic compounds occurring in living organisms that are insoluble in water but are soluble in organic solvents. median: The middle number or value in a series of numbers or values. MFE: Ministry for the Environment. MSW: Municipal solid waste. mutagenicity: Tendency to cause genetic changes. NATO basis: one of the recognised schemes for comparing the toxicity of 2,3,7,8-TCDD to other PCDDS. OECD: Organisation for Economic Cooperation and Development. PCBs: polychlorinated biphenyls - compounds which are very persistent in the environment. PCDDs: Polychlorinated dibenzo-p-dioxins (refer Section 6.1). Also called dioxins. PCDFs: Polychlorinated dibenzofurans (refer Section 6.1). Also called fnrans. soft tissue sarcoma: A rare form of cancer. solvent: A liquid that dissolves another substance or substances to form a solution. TCP: Trichlorophenol. teratogenicity: Tendency to cause foetal malformation. toxic substance: includes any poison or harmful substance that when absorbed into the human body is likely to destroy life or to be injurious to health. Toxic Equivalent (TE): The amount of 2,3,7,8-TCDD equivalents. For example 1,2,3,7,8-PeCDD at a 5 ppt level and a TEF of 0.5 has a TE of 2.5 ppt. The total TE of a mixture of compounds is the sum of the individual TEs. Toxicity Equivalent Factors (TEFs): The factor that relates the level of the PCDD or PCDF to the toxicity equivalent of 2,3,7,8- TCDD (which has a TEF of 1). For example 2.3,7,8-TCDF has a TEF of 0.1 and 1,2,3,7,8 PECDD has a TEF of 0.1. WHO: World Health Organisation. [] REFERENCES Source: Office of the PARLIAMENTARY COMMISSIONER FOR THE ENVIRONMENT Te Kaitiaki Taiao a Te Whare Paremata PO Box 10-241, Wellington, NEW ZEALAND AGCARM 1990. Survey of Properties for Unwanted Agrichemicals. Waikato. October 1990. AGCARM 1991. Survey of Orchard and Process Crop Properties for Unwanted Agrichemicals. Hastings May 1991. American Organisation of Agricultural Chemists 1980. AOAC Methods. 28.128, 28.129, 28.130. p.459 1980. Ames B. N. 1987. Letter to Commissioner, Connecticut Department of Environmental Protection. 22 October 1987. Ames B.N. 1989. Mutagenesis and Carcinogenesis: Endogenous and Exogenous Factors. Environ. Molecular Mutagenesis Vol. 14 Suppl 16 p.66 1989. Ames B.N. et al 1990. Nature's Chemicals and Synthetic Chemicals: Comparative Toxicology. Proc. Natl. Acad. Sci. USA Vol. 87 p.7782 1990. Banks Y. B. and Birnbaum L. S. 1991. Absorption of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) after Low Dose Dermal Exposure. Toxicol. Appl. Pharmacol. Vol. 107. p.302 1991. Bates M. et al 1990. Levels of PCDD's and PCDF's in the Breast Milk of New Zealand Mothers. 10th Intl Sym. on Chlorinated Dioxins and Related Compounds Bayreuth 1990. Bingham A.G. et al 1989. PCDD and PCDF Emissions in Car Exhaust and their Impact on the Environment. DSIR Chemistry Division Report No CD2397. June 1989. Bingham A.G. 1992. Background paper on Pentachlorophenol, Fungicides, Dioxins and Organochlorines. Prepared by DSIR Chemistry, NECAL Laboratory for the National Task Group on Site Contamination from the Use of Timber Treatment Chemicals. Report in prep. 1992. Brennan G. 1985. 2,4,5-T and Dioxin. Use and Manufacture in New Zealand, August 1985. Brinkman G.L et al 1986. Possible Health Effects of Manufacture of 2,4,5-T in New Plymouth. Report of Ministerial Committee of Inquiry to the Minister of Health. Wellington. October 1986. Buckland S.J. et al 1990. The Sources, Emission Profiles and Analysis of PCDDs and PCDFs. International Symposium on Halogenated Organics and the Environment. Adelaide 1990. Buser H.R. and Rappe C. 1980. High Resolution Gas Chromatography of the 22 Tetrachlorodibenzo-p-dioxin Isomers. Anal. Chem. Vol. 52, p.225 1980. Calvert G.M. et al 1989. Evaluation of Chronic Bronchitis, chronic obstructive pulmonary disease (COPD) and Ventilatory function among workers exposed to 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD). Presented at the 9th Intl. Syp. on Chlorinated Dioxins and Related Compounds. Dioxin 89. Toronto, Canada. Sept 17-22, 1989. Chemical Safety Summary 1982. Tetrachlorodibenzodioxin: A Survey of Subjects Ten Years after Exposure. Vol. 53, p.329. 1982. Chemical Safety Summary 1986. Dioxin Effects. Vol. 57, p.186. 1986. Chemical and Engineering News 1979. Study shows few health effects from dioxin. p.7, 1-4 October 1979. Chemical and Engineering News 1991. Dioxin Toxicity: New Studies Prompt Debate, Regulatory Action. p7. August 12, 1991. Coster A.P et al 1986. A Report by a Working Party to the Environmental Council. The Use of 2,4,5-T in New Zealand. Environmental Council August 1986. Courtney, K.D.and Moore J.A. 1971. Teratology Studies with 2,4,5-Trichlorophenoxyacetic acid and 2,3,7,8-Tetrachloro-dibenzo-p-dioxin. Toxicol. Appl. Pharmacol. 20, p.396.1971. Chemical Review: Dioxin. In Dangerous Properties of Industrial Materials Report. p.2 Sept/Oct 1988. Department or Health 1977. Internal Memo Discussion. IWD/Dept Health. 7th February 1977. Department of Health 1991. Waste Management Guide 06. Pesticide Wastes. February 1991. Dow Elanco (NZ) Ltd 1991. Notes of a meeting at Dow Elanco 27 June 1991. Parliamentary Commissioner for the Environment. Dow Elanco (NZ) Ltd 1992. Letter to the Commissioner for the Environment April 2, 1992. Esposito M.P. et al 1980. Dioxins. US Environmental Protection Agency Publication E PA-600-197, Nov 1980. EPA Cincinatti, Ohio, USA FAO/WHO Joint Report 1979. 4.39 p.58 Geneva 1979. Fingerhut M.A. et al 1989. Levels of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in the serum of United States chemical workers exposed to dioxin contaminated products: Interim Results. Chemosphere Vol. 19, p.835. 1989. Fingerhut M.A. et al 1991. Cancer mortality in workers exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin. The New England Journal of Medicine p.212, Jan 24, 1991. Graham B.W.L. 1988. The Management and Disposal of Pesticide Wastes. NECAL Department of Health. October 1988. Hanify J. A et, al 1981. Aerial Spraying of 2,4,5-T and Human Birth Malformations: An Epidemiological Investigation. Science Vol. 212, p.349 17 April 1981. Hayes W.J. Jr and Laws E.R. 1991. Handbook of Pesticide Toxicology. Vol. 3 Classes of Pesticides pp.1217 -1269 Academic Press Inc. 1991. Health Authority, Region of Lombardy, Regional Council 1976. Updating of the Information Relative to the Health Activities for the Population of the Area Polluted by Dioxin, 8 November 1976. Hughes J.T. 1984. Chemistry Division report 2345. Dioxins. International Labour Organisation. 1983. Encyclopedia of Occupational Safety and Health. p.638. 1983. Iversen O.H. 1987. Ed 'Theories of Carcinogenesis' 1987. Ivon Watkins Dow. undated. 'Clean Air and Incineration'. Ivon Watkins Dow 1984. Letter to Professor Wasserman, Dunedin. 26 November 1984. Kemner F.E. et al v Monsanto Co & Ryder. Appellate Court of Illinois Fifth District. 1991. Appeal from the Circuit Court of St Clair County No 80-L-970 Kemner F.E. v. Monsanto Co No 5-88-0420. Kociba R.J. et al 1978. Results of a Two-Year Chronic Toxicity and Oncogenicity Study of 2,3,7,8-Tetrachlorodibenzo-p-dioxin in Rats. Toxicol. Appl. Pharmacol. 46, p.279. 1978. Kociba R.J. and Schwetz B.A. 1982. A Review of the Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) with a Comparison to the Toxicity of other chlorinated dioxin isomers. Assoc. of Food and Drug Officials Vol. 46, pp.168-188. 1982 Manz A. et al 1991. Cancer mortality among workers in chemical plant contaminated with dioxin. Lancet Vol. 338 No. 8773 pp.959-64, 19 October 1991. Marshall V.C 1983. Letter to the Editor. Chemistry in Britain. August 1983. McKenzie L.R. and McMillan N.A. 1980. Monitoring of herbicide residues in the Oreti and Aparima Rivers following aerial spraying of cleared floodways. Report to Southland Catchment Board, 22 May 1980. McQueen, E.G. et al, 1977. '2,4,5-T and human birth defects'. Department of Health, Wellington, June 1977. Mercier M. J. et al 1976. Commission of the European Communities, Health and Safety Directorate. 2,3,7,8-Tetra Chloro Di Benzo-p-Dioxin. Document V/F/3499/76. 1976. Milnes M.H. 1971. Formation of 2,3,7,8-Tetrachlorodibenzodioxin by thermal decomposition of sodium 2,4,5-Trichlorophenate. Nature Vol. 232 p.395, 6 August 1971. Ministry for the Environment 1989. Pesticides: Issues and Options for New Zealand. Nature 1980. PCP dioxins found to pose health risks. Vol. 283, p.418 1980. National Council for Air and Stream Improvement Inc. 1991. An Assessment of Exposure to Dioxin from consumption of fish caught in Freshwaters of the United States impacted by bleached chemical pulp mills. Tech Bull No 620 Dec 1991. New Scientist 1983. Seveso's designer claims modification caused explosion. p.200, 28 April 1983. New Scientist 1984. Hamburg faces dioxin in the wind. 26 July 1984. New Scientist 1991. Britain raises the threshold for action on dioxins. p.7 20 July 1991. New Plymouth City Council 1967. Report of the Town Planning Committee to the New Plymouth City Council, 10 March 1967. New Plymouth City Council 1979. District Scheme Section 4.3 p.27 1979. New Plymouth District Council 1992. Letter to Commissioner for the Environment, 24 February 1992. Norris. L.A. 1981. The movement, persistence and fate of the phenoxyherbicides and TCDD in the forest. Residue Reviews 80, pp.65-135. 1981. Ott M.G. et al 1976. Determinants of Mortality in an Industrial Population. J. Occ. Medicine p.171, March 1976. OECD 1991. Environment Committee ENV/EC (91) 15, 16, and 17. October 1991. Patterson D.G. Jr et al 1989. Levels of polychlorinated dibenzo- p-dioxins and dibenzofurans in workers exposed to 2,3,7,8- tetrachlorodibenzo-p-dioxin. Am. J. Ind. ed. Vol. 16. pp.135-146. 1989. Pilgrim R.C. 1986. Submission to the Committee of Enquiry into Possible Health Effects of Manufacture of Agricultural Chemicals in New Plymouth, July 1986 Pilgrim R.C. et al 1990. Incineration of Hazardous Wastes in New Zealand. Proc. Intl. Clean Air Conf. Auckland, NZ. March 1990. Clean Air Society of Australia and New Zealand (NZ Branch). Rappe C. 1984. Analysis of polychlorinated dioxins and furans. Environ. Sci. and Technol. Vol. 18, No.3, p.78A 1984. Rappe C. et al 1987. Overview on Environmental Fate of Chlorinated Dioxins an Dibenzofurans. Sources, Levels and Isomeric Pattern in Various Matrices Cbemospbere Vol. 16, p.1603 1987. Safe S 1990. Critical Reviews in Toxicology. Polychlorinated Biphenyls (PCBs) Dibenzo-p-dioxins (PCDDs) Dibenzofurans (PCDFs) and Related Compounds. Vol. 21 p.51.1990. Science 1983. Missouri's Costly Dioxin Lesson. Vol. 219. p.367 28 January 1983. Science 1991. EPA Moves to Reassess the Risk of Dioxin. 17 May 1991. Smith A.H. et al. 1981. Preliminary report of reproductive outcomes among pesticider applicators using 2,4,5-T. New Zealand Medical Journal Vol. 93 pl77-179. 1981. Smith A.H. et al. 1992. Serum 2,3,7,8-Tetrachlorodibenzo-p-dioxin levels of New Zealand pesticide applicators and their implication for cancer hypotheses. Journal of the National Cancer Institute. Vol. 84 No 2 pp.104-8. January 1992. Stauffer N Ed. 1991. Cleaning up waste incinerators. E-Lab, MIT, July-Sept 1991. Stehl R.R. et al. 1973. The Stability of Pentachlorophenol and Chlorinated Dioxins to Sunlight, Heat and Combustion. From 'Chlorodioxins - Origin and Fate' ed Blair E.A. pp.119-125. Advances in Chemistry Series 120, American Chemical Society USA 1973. Svensson M.D. et al 1991. Exposure to Dioxins and Dibenzofurans through the consumption of fish. New Engl. J. of Medicine p.8. Jan 3, 1991. Sweeney M.H. et al 1990. Comparison of Serum Levels of 2,3,7,8-TCDD in TC production workers and in an unexposed comparison group. Chemosphere Vol. 20 Nos, 7-9 pp.993-1000. 1990. Taranaki Regional Council 1991. Internal Memo, February 1991. The New Zealand Ministry of Agriculture and Fisheries 1989. Regulation of Agricultural Compounds. Discussion Document. March 1989. Tschirley F.H. 1986. Dioxin. Scientific American Vol. 254, p.21 1986 United States Environmental Protection Agency, 1979. Notice of Intent to Cancel the Forestry, Rights-of-Way and Pasture Registration of Pesticide Products containing 2,4,5-T, 28 February 1979. Vos J.G. et al 1974. Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) in C57B1/6 Mice. Toxicol and Appl. Pharmacol Vol. 29 pp.229-241 1974. Washburn S.T. et al 1989. Human Health Risks of Municipal Solid Waste Incineration. Environ. Impact Assess. Rev. Vol. 9 No 3 pp.181-198. September 1989. WHO (EURO) 1990. Summary report of the Consultation on Tolerable Daily Intake from Food of PCDDs and PCDFs. 4-7 December 1990. EUR/IPC/PCS/ 030(s) 0369N. Zober A. et al 1990. Thirty-four-year mortality follow-up of BASF employees exposed to 2,3,7,8-TCDD after the 1953 accident. Intl Arch Occup. Environ. Health Vol. 62, pp. 139-157. 1990.