Incinerator toxic emissions: a brief summary of human health effects with a note on regulatory control

Medical Hypotheses (1999) 52(5), 389–396 © 1999 Harcourt Brace & Co. Ltd Article No. mehy.1994.0675

Incinerator toxic emissions: a brief summary of human health effects with a note on regulatory control S. C. Rowat Thought Transfer Research, North Augusta, Ontario, Canada

Summary Toxic emissions from municipal solid waste (MSW) and hazardous waste incineration are discussed, with reference to recent reviews and to government standards and controls. Studies of known effects of aromatic hydrocarbons, other organics, dioxins, metals, and gases, on fish, soils, plants, and particularly humans are briefly reviewed. A summary of potential problems with existing and proposed incineration is developed, including: (1) lack of toxicity data on unidentified organic emissions; (2) unavoidability of hazardous metal emissions as particles and volatiles; (3) inefficient stack operation resulting in unknown amounts of increased emissions; (4) formation in the stack of highly toxic dioxins and furans, especially under inefficient conditions, and their build-up in the environment and in human tissue; (5) the lack of adequate disposal techniques for incinerator fly ash and wash-water; (6) the contribution of emitted gases such as NO2, SO2 and HCL to smog, acid rain, and the formation of ozone, and the deleterious effects of these on human respiratory systems; (7) the effects and build-up in human tissue of other emitted organics such as benzene, toluene, polychlorinated biphenyls (PCBs), alkanes, alcohols, and phenols; (8) lack of pollution-control and real-time efficiency-monitoring equipment in existing installations. The inability of regulatory bodies historically to ensure compliance with emission standards is discussed, and a concluding opinion is offered that it is inadvisable to engage in new incinerator construction with present knowledge and conditions.

INTRODUCTION A number of government bodies have placed moratoriums on new incinerator construction and more stringent controls on existing units (1,2), presumably reflecting a growth of public opinion against waste incineration. Alternatives are being actively explored, including recycling, waste-reduction, and re-use of materials (1–4). Nonetheless, many municipalities continue to consider large scale waste incineration as an option, impelled by the growth of population (and hence a growing garbage problem) and the reduction in available land-fill area. Sufficient definitive studies on the effects of some of the substances emitted, as well as amounts emitted, are reported to be lacking in the relevant scientific literature (1,2,5), and proponents of incinerators are able to use the common law argument that the burden of proof lies Received 11 May 1994 Accepted 24 August 1994 Correspondence to: Steve C. Rowat, Thought Transfer Research, Bert Earl Road RR#3, North Augusta, Ontario, Canada K0G 1R0

with those who claim they would be harmed (6), and continue to press for what appears to be an easy and obvious solution to a persistent problem; while opponents can cite the same lack of data as reason for a moratorium. By a recent report, the latter will soon include the Clinton administration (7). The Province of Ontario feels that the sum of existing and unknown scientific data on the toxic effects of incinerator emissions already supports a ban. The Ontario Ministry of Environment and Energy has recently published a booklet, The Case Against Municipal Solid Waste Incineration (2), outlining reasoning that supports the Ontario ban on apartment building incineration since 1989 and general ban on the construction of solid waste incinerators in Ontario as of September 11, 1992 (8). The booklet lists known incinerator emissions such as carbon dioxide, carbon monoxide, heavy metals (lead, mercury, arsenic, cadmium), other metals (copper, nickel, selenium, vanadium, zinc), nitrogen oxides, and a multitude of organic compounds (such as benzene, dioxins, PCBs, and phenols) (1,2,5). Also stated as disturbing is that at 389

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the high temperatures reached inside an incinerator, new substances are formed, some of which we know the toxic properties of (such as dioxins, which are among the most toxic substances yet studied) (9–12), and some of which are completely new to us (1). The Ontario booklet sums up these considerations: There is great uncertainty about how these contaminants move through the environment, how quickly they break down, how they combine with other pollutants, or how they can build up in the food chain. Researchers have only begun to investigate the toxic effects of these pollutants on the most susceptible members of society. We know that many toxic chemicals can be more dangerous to developing embryos and young children, workers exposed to chemicals on the job, and people who have become hypersensitive to even very low levels of hazardous contaminants (2).

Oppelt, in a review of hazardous waste incineration studies (1990), expresses a similar point: ‘…what appears outwardly to be a straightforward, simple process is actually an extremely complex one involving thousands of physical and chemical reactions, reaction kinetics, catalysis, combustion acrodynamics, and heat transfer. This complexity is further aggravated by the complex and fluctuating nature of the waste fuel to the process. …[O]nly a relatively small percentage of the total hydrocarbon emissions have been identified.’ (1). And comparisons of hazardous waste incinerator emissions with municipal solid waste (MSW) incinerators have not revealed any significant differences (1). HUMAN STATISTICAL STUDIES Perhaps most important is the overall effect; these studies are rare because expensive and difficult to perform, but may have the most validity since the synergistic effect of all the pollutants together is the actual situation. Lisk reports that Zmirou, in a rare and ingenious study focused directly on an existing facility, showed that there was a significant increase in the consumption of medicines for respiratory problems among residents in a French village at distances of 2, 1, and 0.2 km from a municipal incinerator. In other words, that bronchodilators, expectorants, and cough medicines were purchased significantly more often, the closer to the incinerator (5). Ito et al. recently showed that daily winter deaths in London, UK varied significantly with the measurements of air pollution levels (13). Total particulate matter, sulfur dioxide, and acidic aerosol were measured. The authors make it clear that the complexity of the analysis made it impossible for them to know what portion of the increase was attributable to each pollutant, although it was demonstrable that each made some contribution to the effect. They give also an example of how the interaction between two of the components – acid aerosol and partiMedical Hypotheses (1999) 52(5), 389–396

culate matter – could produce a stronger effect than either alone. Sulfur dioxide and particulate matter are common incinerator emissions (1,5). Pearlman (14) showed a significant increase in bronchitis among children exposed for 2 and 3 years to elevated levels of nitrogen dioxide emitted from an industrial facility. Illness varied significantly with distance from the plant (14). (This was not an incinerator, but nitrogen dioxide is also found in incinerator flue gases, and is a major problem worldwide due to its automobile and industrial emissions) (14–19). It has been reported recently that there has been a four-fold increase in lung ailments in Canada since 1970 (20); and that childhood asthma rates near the Toronto Western Hospital, which imports hazardous waste from other hospitals to burn, ‘are among the highest in the world at up to 25% of the population’ (8).

SPECIFIC AIRBORNE INCINERATOR POLLUTANTS Dioxins and furans These are among the most heavily studied, and yet elusive, toxic compounds found in, and formed by, incineration. The problem has three main aspects: (1) dioxins are toxic in extremely tiny quantities; (2) they bioaccumulate in humans; and (3) incinerators manufacture them. (1) Dioxins are toxic in such tiny quantities – parts per billion or trillion, as opposed to parts per million (p.p.m.) for most other toxins studied – that it has been necessary to devise new (and expensive) analytical methods just to detect them at the levels they do damage (9). ‘A desirable detection limit of one part per trillion…is being reached with current methodology.’ (Huff 1980). Neal reports on various animal studies showing that the single lethal oral dose (LD50) ranges more than 3 orders of magnitude in different species, from 2 parts per billion/kg for Guinea pigs to 5000 for hamsters (i.e. 5 p.p.m./kg). Monkeys, rats, rabbits, and mice fall in between (11). This is for the 2,3,7,8-TCDD (2,3,7,8-tetrachloro dibenzo-p-dioxin) isomer, so far the most toxic found. But dioxins are formed as contaminants, rather than purposely, so they routinely exist as a complex mix of the different isomers – and we do not know for certain which will be the most dangerous to a given species. There are 75 possible isomers of polychlorinated dibenzo-p-dioxins (PCDDs), ranging from one to eight chlorine atoms in various geometric positions (9,10,21). There are also 135 different possible isomers of a variant with only one oxygen molecule (dioxins have two), which are called -dibezofurans, or furans (PCDDs). Some furan isomers have also been found to be extremely © 1999 Harcourt Brace & Co. Ltd

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toxic, although generally at a higher concentration than PCDDs; but this is greatly dependent on the isomer being studied (10). According to the review by Huff (9), toxic effects of TCDD found to recur in four or more human studies each are: chlorachne; liver damage; elevated liver enzymes; disorders of carbohydrate metabolism; cardiovascular disorders; neurological damage, including peripheral neuritis and lower extremity weakness; sensory impairments (sight, hearing, taste, smell); and depressive (psychological) syndromes. Other disorders, including fat metabolism, urinary tract, and pancreatic disorders, were reported in three or less studies each. Huff notes ‘an important and unique episode’ in which three scientists were self-exposed to TCDD while preparing it synthetically; two developed chlorachne within 8 weeks; one of those and the third developed delayed changes two years later, including ‘personality changes…; impairment of vision, taste, and muscular coordination; sleep disturbances; gastrointestinal symptoms; and hirsutism’ (9). (2) Dioxins bioaccumulate in humans. It is now wellknown that the plant–animal–human food chain concentrates many toxic substances, often storing them in fat tissue (22). Dioxins follow this pattern, and virtually all humans are now carrying a load of TCDD (the most widely studied form), generally at more than 3 parts per trillion (p.p.t.); in the USA the range is from 1.4 to 20.2 p.p.t. for non-occupationally exposed individuals (23). Pirkle et al. are reported as giving the half-life of TCDD in the human body as 7 years (23). Thus even marginal increases in the current intake will lead to yearslong increases in the storage levels. (3) Incinerators manufacture dioxins. PCDDs (and PCDFs, which can be assumed) can be formed by burning PCBs (polychlorinated biphenyls); it is a two-step process, the first being the production of PCBZs (polychlorinated benzenes) from PVC (polyvinyl chloride) (10). Buser (1985) states that strict controls have to be implemented for the burning of hazardous wastes in order to ensure safe disposal and to prevent environmental contaminations (10). Dioxins are believed to be formed in incinerators at a temperature of ~500°C and destroyed at a temperature of at least 900°C (1,5). But the incinerator must be running at maximum efficiency; dioxin survival, Lisk reports, ‘is favoured by low combustion temperature, wet refuse, insufficient or excess oxygen and inadequate residence time’ (5). And PVC in the waste being burned is reported as not necessary for dioxin formation; chlorine released from wood is apparently sufficient (5). Thus, not only hazardous waste, but general MSW incineration, will support dioxin production. In fact, MSW incinerators have been measured as consistently producing far more © 1999 Harcourt Brace & Co. Ltd

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dioxin and furans than hazardous waste incinerators; almost 1000 times as much (1). Although Travis and Hattemer-Frey (1991) calculate, using a theoretical dispersion model, that only 4% of the total all-source emissions of TCDD into the US environment comes from MSW incinerators (23), they admit puzzlement that their model-calculated sum of TCDD emitted from known sources accounts for only 11% of their estimated all-source emissions total – a major discrepancy (23). As a result, in the data they present, MSW incinerators can equally well be said to account for 36% of the (calculated) known sources of TCDD; or 45% if hospital incinerators are included. Automobiles are calculated to emit about as much. The remainder is made up of pulp-and-paper mill residue and residential wood burning. In addition, they state that with expected increases in incinerators, the ‘4%’ will rise to ‘8%’ (or 72% of known sources) by the year 2000. The main mode of human intake of dioxin is by food (23,24) with the great bulk of this reaching plants as particulate matter and being ingested by animals, which are later eaten by humans. Over 50% of the daily intake in the USA is estimated to come from beef alone, with only 3.4% from produce (23). Such estimates are difficult to make due to lack of data (23,24). Polycyclic aromatics Multiple investigators are reported to have found PCAs such as naphthalene, benzo(a)pyrene, anthracene, flouranthene, pyrene, phenanthrene and others in incinerator emissions and fly ash (5). Lisk cites reports that some of these, such as benzo(a)pyrene, are known carcinogens (5). Autrup et al. cite 16 separate studies that have been done on the toxic mechanisms of benzo(a)pyrene, showing that ‘Polynuclear aromatic hydrocarbons [PCAs], such as benzo(a)pyrene (BaP), are widespread environmental pollutants and likely human health hazards… The main emphasis of these studies has been to determine the pathways of activation into the ultimate carcinogenic forms and their reaction with DNA.’ (25). They go on in their study to show that carcinogenic metabolites of BaP bind preferentially in the human bronchial tube and esophagus, and to a lesser extent in the colon (25). Other researchers have shown that bromobenzene, thought representative of aromatic (polycyclic) hyrdrocarbons, binds in the lung and metabolizes to cause both bronchial and liver damage (26). Since Lisk reports on a study that found ‘the concentration of PCA in stack gases of an MSW incinerator increased more than 1000-fold during cold start-up of the plant,’ and another study finding ‘the highest concentrations of PCA on the smallest atmospheric particulates... and therefore in the respirable range,’ (5), a wide range Medical Hypotheses (1999) 52(5), 389–396

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of carcinogenic materials are possibly being emitted in a form ripe for absorption by the human breathing system. As noted in the Ontario booklet, performance data on incinerator efficiency are ‘usually conducted at new facilities operating at peak performance,’ and ‘…a large load of plastics or solvents…could result in a huge surge of toxic emissions.’ (2). Exactly what these emissions consist of is unknown. The US Environmental Protection Agency (EPA) has reportedly done field tests of eight incinerators, nine industrial boilers, and six industrial kilns, and showed measurable amounts of 55 hazardous chemicals from their list (called ‘Appendix VIII’) of approximately 400 known hazardous compounds (1). The most common were benzene, toluene, carbon tetrachloride, chloroform, methylene chloride, trichloroethylene, naphthalene, phenol, and bis(2-ethylhexy)phthalate; the range in concentrations between chemicals and also between different measurements at the same facility was very great, spanning 5 orders of magnitude (1). Thus, predictions of average or total output over time are difficult to make. More important, perhaps, is the knowledge that the EPA testing ‘has focused largely on identification of Appendix VIII compounds only.’ (1). Since a relatively small percentage of the total hydrocarbon emissions have been identified (1), this leaves a great deal unknown about PCA emission effects. Other organics Many studies reviewed by Lisk report an almost bewildering array of compounds in ash and emissions from MSW incinerators; these include PCBs, polychlorinated PCAs; chlorobenzenes and chlorophenols; halogenated organic acids, phthalates; aldehydes; ketones; organic acids; alkanes, and alkenes. Lisk comments: ‘…the presence of these compounds intact would indicate the incinerators were operated under conditions inadequate for their complete combustion.’ (5). Unfortunately, because of ‘what has been termed the most costly and disastrous accidental contamination ever to occur in US agriculture,’ (27), in which a significant portion of the food supply of the state of Michigan was accidentally poisoned, we know that PBBs, and by implication PCBs, which have a homologous molecular structure, achieve a steady state in the body. The results from a study of 1738 patients showed that PBBs are stored in the fat; and very little is excreted (22,27). A supporting animal study is reported by Wolff et al. (1979) stating that, in rodents, ‘PBB concentration of adipose [fat] tissue would not be expected to show an appreciable decline during the lifetime of the animal.’ (22). Another study was cited showing that DDT residues reach equilibrium in 1–3 years in humans (22). Wolff concludes: ‘It is not now Medical Hypotheses (1999) 52(5), 389–396

known what the health effects may be of such continued body burdens.’ (22). PCBs are reported by Kimbrough, in a review of the toxicity of polychlorinated polycyclic compounds, to be implicated in immunosuppression and liver damage, among other effects, and states that ‘long-term effects are...more critical for compounds such as PCBs… It would be erroneous to make predictions on long-term effects from results obtained in acute toxicity studies.’ (28). Metals and heavy metals At least 35 different metals are reported from MSW incineration, and most of these are found in all of the bottom ash, the fly ash, and the suspended particulate measurements, as well as undergoing enrichment in the fine ash (1,5). Several are indicated as possible carcinogens or causing adverse effects in humans, including cadmium, chromium, nickel, lead, mercury, arsenic, barium, and beryllium. Lisk states that ‘Aluminum, Copper, Iron, Lead, Titanium and Zinc are found largely in the slag, while more volatile elements such as Cadmium, Lead, Antimony, Selenium and Tin are vaporized in the combustion zone and condense on fine particulates which are either trapped or escape to the atmosphere as suspended particulates.’ (5). According to Oppelt, ‘the processes involved in the formation of particles are very complex and are only partially understood.’ (1). Polyvinyl chloride (PVC) in waste (plastic containers, bottles and plastic wraps) is reported to be a major source of chlorine in the incineration, so that ‘volatile chlorides of a number of elements such as Arsenic, Cadmium, Nickel, Lead, Antimony, and Zinc may be formed during incineration which may greatly increase their presence in fly ash and suspended particulates.’ (5). Mercury from mercury batteries is stated as ‘one of the most volatile and toxic elements in MSW.’ (5). Studies are cited showing that over 80% of the mercury is estimated to be released into the gas phase as halides. Other metals are also used in batteries and ‘deserve attention’ (5). Small boilers employing hazardous waste as a fuel, including waste oil, is a serious concern since 50–60% of the lead input is emitted from the stack (1). Data for metal emissions are ‘limited and incomplete… Data on air pollution control device effectiveness for metals are even more scarce.’ (1). And more than half of the 221 hazardous waste incinerators in the USA are reported as employing no pollution control equipment at all (1). Gases Among others (HCL, CO, HF, bromine), sulfur dioxide and nitrogen oxides are reported released from incinerators (1,5). Both SO2 and NO2 have been studied extensively © 1999 Harcourt Brace & Co. Ltd

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due to their release from other sources and their toxic effects on the human respiration system; both are now known to reduce the body’s ability to fight lung infection (14–16,29). Ozone, also toxic to the human lung antibacterial system, is not reported to be released from incinerators per se but is formed in the presence of sunlight on oxides of nitrogen (16), which do originate from incinerators as noted. Ozone can reach high concentrations, such as the 0.7 p.p.m. measured in the suburbs of Los Angeles (16); mouse studies at this concentration show impairment of bacterial killing in the lung in only 3–4 hours’ exposure (30). Oppelt reports that no real-time monitors exist for measuring destruction and removal efficiency of these or other stack emissions (1). Incinerator bottom ash and washwater pollutants The reader is referred to the Lisk and Oppelt reviews for a more thorough listing of which of the above pollutants also appear in wastewater and bottom ash from incinerators (1,5). Studies reported there note in particular cadmium, lead, and manganese among 20-odd metals, and a variety of organics including chlorinated benzenes, alcohols, phenols, aldehydes, ketones, esters, amines, amides, hydrocarbons, and dioxins and furans. Wastewater (5), and to an increasing extent under new EPA regulations, ash (1), must themselves be considered hazardous waste. Storage in ordinary land-fills carries an undetermined level of threat of leaching into the water table (1). Kamiya and Ose (1987) are reported as showing that the ability of the wastewater extracts to cause genetic mutation was ten times as great in an incinerator capable of only incomplete combustion; 10% of these mutagens were reportedly disposed in the wastewater (the rest as airborne emissions) (5).

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incinerator metal emissions on fish bioaccumulation, but the abstract of a recent study correlating human blood, erythrocyte and plasma levels of mercury and selenium with fish consumption (31) may indicate that such studies are warranted, since both mercury and selenium are incinerator emissions (1). Effects on soils and plants Multiple studies are reported about incinerator and other acid gas contributions to acid rain and acid rain’s ‘untoward effects on forests, aquatic systems and buildings.’ (5). Since a great deal of information has emerged about this in the scientific literature and popular press, this subject will not be covered in great detail here; but the reader is reminded that acid rain is a major environmentally damaging effect of incinerator and other acid gas source emissions. A 1984 Finnish study reportedly found that 11 elements on birch leaf samples, including iron, nickel, lead, zinc, titanium, chlorine, and cadmium, showed a strong correlation between concentration and closeness to an incinerator (5). Experiments using incinerator fly ash as a partial soil additive report increased uptake of a number of heavy metals, including cadmium and lead (5). Cabbage grown on 20% ash-amended soil contained 146 times the concentration of cadmium of controls (5). The concentration of TCDD on fruits and vegetables consumed by humans has been estimated to be 60% from air-to-leaf transfer, 33% deposition, and 8% root uptake (23). The authors refer to studies showing that air-to-leaf transfer components can volatize from the soil and be adsorbed on the leaf (23).

DISCUSSION Effects on fish

Toxic effects

Specifically incinerator-linked data are scarce. Travis and Hattemer-Frey, studying only the TCDD isomer of dioxin, state that ‘TCDD is bioaccumulating in fish’ and that ‘low-level contamination of fish is widespread,’ citing a US EPA study as source data (23). Wenning studied the 1,2,8,9-TCDD isomer specifically, and found it ‘as a contaminant in fly ash, river water, and sediments surrounding several MSW and industrial incinerators…’ (21). Lisk reports several studies establishing that fish retain the most toxic dioxins and furans (2,3,7,8-TCDD and 2,3,7,8-TCDF) preferentially when exposed to them from fly ash. Effect levels were observed as low as 38 p.p.t. (rainbow trout) for TCDD, with a bioconcentration factor ranging from 26 707 to 39 000 (5). Few data appear to have been collected specifically studying the effects of

Given the complexity of the pollutants identified as released in gases, particulates, and bottom ash or washwater from incinerators, the lack of definitive data on the effects of the incinerator-release of these compounds on human health is disconcerting, but understandable. For instance, researchers studying the overall human exposure (from all sources) to the TCDD dioxin stated: ‘There is a general perception that TCDD contamination is a localized problem and that control of a few, specific sources (such as MSW incinerators) will reduce human exposure to tolerable levels. The reality is that PCDDs and PCDFs are everywhere and virtually every man, woman, and child in the world is exposed to these compounds daily.’ (23). To conclude, however, that, because MSW is only one

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source of toxic contamination, that it is not necessary to control, or even eliminate, that source, is insufficient reasoning. A study of 35 individuals aged 20–90 in St Louis, USA, is reported as having their fat concentration of the most toxic isomer of TCDD increase directly proportionally with their age; the average level is 10 p.p.t. (5). And another reported study showed that levels of dioxins and furans were higher in cow’s milk sampled near an incinerator than elsewhere (5). Thus, we have at least suggestive evidence that: (a) human burdens of TCDD are increasing; and (b) incinerators are a source for human intake of TCDD. If this same pattern of long-term burden increase holds true for even a fraction of the other organic contaminants from incinerators – polychlorinated PCAs; chlorobenzenes and chlorophenols; halogenated organic acids, phthalates; aldehydes; ketones; organic acids – and for the metals, then the net detrimental effect of the incinerator on human health may significantly outweigh its benefits in energy retrieval and waste-stream reduction. In addition the noted effects of the gases and particulate matter on smog have both an acute and chronic component. Kamiya and Ose, cited in Lisk, ‘concluded that urban waste incinerators are the main source of that portion of environmental pollution due to incomplete combustion.’ (5). Regulatory control The recurrent question of whether an incinerator is efficient or not, with proponents of incineration pointing out that a properly designed and completely combusting unit will destroy even dioxins, misses an important point. Even if the technology can be shown to exist that can account for all avenues of toxic effluent from incinerators – gas, particulate, water and ash (and this does not appear proved) – are there sufficient political and regulatory safeguards in place to assure that such an incinerator will operate at this level on a daily basis? In answering this question, consideration might be given to the following: In recent confidential EPA tests, conducted for a report to Congress, ‘the first of their kind, involv[ing] samples from 15 of the 114 cement kilns in the United States – eight that burn hazardous waste and seven that do not.…[T]he EPA expressed greatest concern over the levels of arsenic, chromium, lead, dioxins and furans – as well as a variety of radioactive compounds – it found in the waste dust.’ (7). Both concrete products and kiln emissions were affected, and ‘EPA and state sources also said the Clinton administration will consider a moratorium on new hazardous waste incineration until more is learned about its impact on the environment and human health.’ (7). St Lawrence Cement, in densely populated Mississauga Medical Hypotheses (1999) 52(5), 389–396

near Toronto, disposes of ‘about 3.5 million litres a year of highly chlorinated waste solvents and plastic residues drawn from industries in Ontario and the United States… The plant has never been required to test for toxic residues, a policy the provincial Environment Ministry hopes to change…’ (7). Similar ‘hopes’ by that Environment Ministry received harsh criticism following the many-year-long struggle of a group of concerned Toronto citizens to ask, then force, the Ministry to take action concerning lead emissions from Toronto smelters. Lax, a lawyer involved who later wrote a comprehensive description of the social and legal battles (6), (the reader is referred to that instructive article), observed that: ‘The common law has traditionally favoured after-the-fact compensation of victims and has never developed adequate concern for prevention of harm… This legacy of the common law ought not to be applicable to matters of environmental health… The burden of proof must therefore be removed from the shoulders of the potential victim and placed upon the alleged polluter.’ (6). And further: There has been considerable reluctance on the part of government officials to act effectively to prevent environmental degradation or to protect public health from dangers caused by harmful substances secreted into the natural environment. Perhaps they appreciate and fear the inevitable questioning of our social and political systems that must form a part of the solution (6).

Thus, although the US EPA now has standards in place for some emissions, and has done some testing to see if those standards are met (1), no satisfactory explanation has been demonstrated for the effects of the unknown products of incineration, nor for the rationale behind a particular level being set as a standard. Risk assessment studies have been performed, but the EPA Science Advisory Board (SAB) has criticized their data base and

Fig. 1 Multiple allergy cycle #1: ‘zinc deficiency cycle’.

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recommended a more complete assessment be done (1). Meanwhile, according to Oppelt, ‘waste generators, faced with the specter of complying with the Hazardous and Solid Waste Amendments Act land restrictions or faced with the prospect of future multi-million dollar environmental damage settlements over contaminated groundwater, are looking to ultimate destruction techniques such as incineration as their only viable alternative.’ (1). And, in 1981 figures, industrial boilers and furnaces disposed of twice as much hazardous waste as incinerators did, and Oppelt’s first-listed ‘principal attraction to this approach’ is ‘exemption from incineration emissions performance standards.’ In the opinion of this writer, incinerators take waste that is concentrated and partly toxic, destroy some of it, produce new waste that is partly toxic, and spread the product extremely thinly throughout the environment. That the effects are hard to measure is understandable; perhaps that is one reason, even in some cases the most important reason, why incineration is done.

SUMMARY Any decision about incineration construction, moratorium, or closure should take into account at least the following: 1. Incinerator chemical reactions are extremely complex, and many of the resultant organic chemicals have not been identified and therefore have not been measured or tested for toxic effects. 2. Regardless of how well an incinerator operates, metals will still be emitted, often in combination with chlorine (or other halogens such as fluorine and bromine). Insufficient data exists on the amounts and hazards of these metals. 3. Some studies have demonstrated that incinerators often operate at less than peak efficiency, and polycyclic organics emissions can be increased 1000fold during a cold start-up. 4. Some of the emissions are almost invariably dioxins and furans, which are formed in the incinerator stack. These are highly toxic and are apparently building up in the fat tissues of all humans, world-wide, with an estimated 7-year half-life in the human body. 5. Incinerator fly ash and wash-water must at present be regarded as hazardous waste themselves, and no universally adequate solution has been found for their disposal. 6. Emitted gases such as NO2 and SO2 contribute heavily to acid rain and smog, and to the formation of ozone in smog in sunlight. NO2, SO2 and ozone have been proved to cause respiratory illnesses, and smog has been shown to cause increased death-rate. © 1999 Harcourt Brace & Co. Ltd

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7. Toxic effects and build-up in human tissue of other incinerator-emitted organics such as benzene, toluene, PCBs, alkanes, alcohols, and phenols are well documented. 8. As of 1990 reports, more than half of existing incinerators had no pollution control equipment, and no real-time monitor existed for measuring destruction and removal efficiency. In sum, although an efficiently operating, technologically advanced incinerator is theoretically capable of destroying complex hydrocarbons, it would still produce metals, sometimes conjugated with other elements, in ash and gas. And to what degree such an incinerator has been successfully built or is operating is an open question, due to our poor regulatory policies. In the opinion of this writer, until a major change in the political organization of incinerator control is clearly established, the building of any further incinerators would seem unwise. A more appropriate course is to begin careful monitoring of the existing units, combining this with continued exploration of other options of waste disposal, such as reduction of waste generation at source and re-use of materials.

ACKNOWLEDGMENTS This paper was prepared with partial support from the Internatural Canada Corporation, Wakefield, Quebec, Canada.

REFERENCES 1. Oppelt E. T. Air emissions from the incineration of hazardous waste. Toxicol Ind Health 1990; 6(5): 23–51 2. Ministry of the Environment and Energy. The Case Against Municipal Solid Waste Incineration. Government of Ontario, 1992 (Booklet). 3. Riha C. A. Energy efficient home made of recycled items. The Citizen, Ottawa, August 21, 1993. 4. Elliott J. The Last Straw in alternative housing. The Citizen, Ottawa, September 4, 1993: E1. 5. Lisk D. J. Environmental implications of incineration of municipal solid waste and ash disposal. Sci Total Environ 1988; 74: 39–66. 6. Lax C. C. The Toronto lead-smelter controversy. In: Leiss W., ed. Ecology versus Politics in Canada. Toronto: University of Toronto Press, 1979: 57–71. 7. Ferguson J. Toxins Linked To Waste Burning. The Globe and Mail, Toronto, 1993 (As reprinted in The AEHA Quarterly 15(2):16). 8. The Case Against Municipal Solid Waste Incineration. The Allergy And Environmental Health Association Quarterly 1992; 14(3/4): 25–27. 9. Huff J. E., Moore J. A., Saracci R., Tomatis L. Long-term hazards of polychlorinated dibensodioxins and polychlorinated dibenzofurans. Environ Health Perspect 1980; 36: 221–240. 10. Buser H. Formation, occurrence and analysis of polychlorinated dibenzofurans, dioxins and related compounds. Environ Health Perspect 1985; 60: 259–267. 11. Neal R. A. Mechanisms of the biological effects of PCBs,

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