|ACHIEVING ZERO DIOXIN
An emergency strategy for dioxin elimination
By Michelle Allsopp
Designed and distributed
tel: +44 71 833
During the week of September 12th 1994 the US Environmental Protection Agency (EPA) intends to release its reassessment of environmental and human health risks from exposure to dioxin. It is expected to conclude that exposure to dioxin poses a largescale, long term threat to public health and the environment-not only due to cancer risks but because of possible birth defects and damage to immune systems.
In the light of these findings Greenpeace has published this report-outlining how and why dioxin is affecting the environment and human health. It identifies the key sources from industrial uses of chlorine and highlights dioxin sources not adequately considered by the EPA. Finally this report suggests strategies for eliminating all these sources. However, it is thought that the EPA reassessment will widen and deepen the debate about exposure levels to dioxin and seriously challenge current assumptions.
Recent studies carried out under the auspices of US EPA reassessment of dioxin, indicate that assumptions made in the calculation of the WHO and Canadian TDI are not consistent with current research findings. This means that the TDI of 10pg/kg/d may be too high, and therefore may not be protective of public health. The main controversy surrounds the assumption made in the derivation of WHO and Canadian TDI, that a threshold or -- safe dose -- of dioxin exists, below which no adverse effects on health will occur.
Recent studies, however, do not support the idea that such a threshold exists for dioxin. Also, health effects caused by dioxin are now known to occur at lower doses than those that were assumed in the calculation of the TDI. Consequently, it is very probable that the TDI set by WHO and Health and Welfare Canada is incorrect and therefore is not protective of human health. However, no reassessment of the WHO TDI is planned for the future.
In 1985 and 1988 the United States Environmental Protection Agency (US EPA) prepared assessments on human health risks from exposure to dioxin. However, in April 1991 US EPA Administrator William Reilly announced that another reassessment of dioxin would be undertaken. The reasons for this reassessment were two-fold:
Human exposure to dioxins is almost exclusively from food intake, especially from meat, fish and dairy products. Unusually high exposure to dioxins in humans following for example accidental/occupational exposure, together with experiments in laboratory animals, have shown effects of dioxin on health include developmental and reproductive toxicity, effects on the immune system and carcinogenicity. Even more disturbing are findings from recent studies which show that concentrations of dioxins in human tissue in the general population (of industrialised countries) are already at -- or near-those levels where health effects may occur. Recent research on health effects from dioxin indicates the following important points:
1. In fish, birds, mammals and humans, evidence shows that the developing foetus/embryo appears to be very sensitive to toxic effects of dioxin. Developmental effects in humans, seen after high accidental/occupational exposure to dioxins include: pre-natal mortality; decreased growth; organ dysfunction, for example involving effects to the central nervous system such as impairment of intellectual development; functional alterations including effects to the male reproductive system.
2. Animal and/or human studies have shown that some effects, for example cellular changes in the immune system, changes in the levels of male sex hormone testosterone, and changes in other enzymes and hormones, may be occurring in humans at, or near to, current levels (body burdens) of dioxins found in the general population of industrialised countries. Such effects could lead to adverse effects on human health.
Members of the population who have higher than average exposure to dioxin, for example through having a high fish or sea mammal diet, are more at risk from such adverse effects including the possibility of reduced sperm count, impairment of the immune system and endometriosis in women.
3. Biological effects from dioxins appear to depend on the concentration present in a target organ over a critical time period rather than on dose. Animal experiments have shown that exposure to very low doses of dioxin during an extremely short critical period during gestation is sufficient to cause detrimental health effects on the foetus.
4. In industrialised countries, levels of dioxins in breast milk often result in nursing infants having dioxin intakes far in excess of the TDI proposed by WHO. This becomes of even greater concern when it is considered that health risk assessments of dioxins do not take other chemicals into account such as polychlorinated biphenyls (PCBs) which humans are exposed to. The effects these chemicals have on given health points may be additive to dioxin or synergistic, i.e. produce a larger than additive enhanced effect.
5. Evidence from studies of occupational/accidental exposure to dioxin in humans together with animal studies indicatesthat dioxin causes cancer in humans. US EPA estimated that current background exposure to the general population results in cancer risks ranging from 1 in 1000 to 1 in 10,000.
Pollution prevention, not control. The use of pollution control devices, filters, treatment systems and disposal methods such as burning or burying simply shifts chemicals from one environmental medium to another or delays their release until a later date. Therefore to achieve zero releases of dioxin from industry, attention should be focused preventing the release of dioxin by changing the industrial processes and feedstocks that result in its formation.
Address all dioxin sources. US EPA, WHO and other environmental regulatory bodies, must address all known industrial sources of dioxin in order to bring future releases of dioxin to zero. Research should be initiated to identify unknown and suspected sources.
Set priorities for dioxin elimination. Since dioxin is associated with the many uses of chlorine in industry, eliminating dioxins will require substantial technical and economic conversion. Timetables should be set which prioritise the largest dioxin producing sectors and for those sources for which alternatives are already available. A moratorium should be placed on new dioxin permits, so that no new permits are issued and existing ones are modified to include timetables for reduction and eventual elimination of dioxin releases.
Major sources of dioxins which should be urgently considered include incineration, pulp and paper production, use and production of PVC and uses and manufacturer of chlorinated aromatic chemicals.
Secondary actions to phase out other chlorine uses include phasing out Chlorinated solvents and chlorine related pesticides, chlorine use in metallurgy and inorganic processes utilising chlorine.
Although phasing out dioxin sources will require substantial investment in some sectors, most of the alternative products provide economic benefits in terms of increased employment, improved efficiency, decreased expenses for chemical procurement, waste disposal, liability and remediation, and the elimination of social costs associated with damage to health and the environment. Technological and economic transformation may be difficult to implement and it is essential that workers and communities should not bear the economic burden of these changes. The phasing out of dioxins should therefore be guided by a democratic transition programme to protect, compensate and provide future opportunities for workers and communities affected by the conversion.
2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD or TCDD, sometimes called dioxin) is the most potent of all congeners and has higher toxicity than any other synthetic molecule (Fiedler and Hutzinger 1990). The dioxins can be ranked against TCDD by a system known as Toxic Equivalents (TEQ). These factors have been internationally adopted for the PCDD/Fs as well as certain types of polychlorinated biphenyls (PCBs) (WHO 1994). Current practice adopts the international toxicity equivalence factor system although older data may be reported using 2,3,7,8-TCDD concentrations alone. Other toxicity equivalents factors are in use (see eg Maisel & Hunt 1990) and total PCDD/F concentrations may also be reported.
station in England from land which had never been treated with pesticides or any potential source of dioxins. The levels therefore represent background figures for an industrialised nation where input was exclusively via atmospheric deposition. The data is presented in Table 1, and clearly shows the increasing levels of dioxins over time with increasing industrialization.
Table 1: Increasing background contamination of agricultural soils since the start of the chlorine industry
|Date||Concentration (pg/g total PCDD/F)|
Similar problems are seen to be associated with trichlorophenols which as well as being precursors to the chlorophenoxy acids, have a variety of other industrial applications. The site of the Spolana Chemical Company in Czechoslovakia is one of the most highly contaminated in the world, despite the fact that production of chlorophenols only occurred for three years between 1965 and 1968. Concentrations of between 0.6 and 2000 ng/g (ppb) of 2,3,7,8-TCDD was detected in production wastes. Contamination of ground waters to 0.005ug/L has also occurred (Zemek and Kocan 1991).
Studies in the UK have estimated that virtually all environmental burden (99.9%) resides in soils and sediments, with soils alone representing 95% (Harrad and Jones 1992a and 1992b). It was estimated in these studies that the annual flux and contemporary UK environmental burden of PCDD/Fs correlate reasonably well. However, only 12% of the annual flux can be fully accounted for by estimated emissions from primary sources, (eg. combustion sources). This discrepancy between annual flux and emissions has also been recognised in studies in Sweden and USA (Rappe 1990, Travis et al. 1989). Although the existence of as yet unidentified sources or gross underestimates of known sources is a possible explanation of the shortfall, it is suggested that much of this disparity may be due to secondary releases from the use and disposal of chlorophenols and the recycling of existing loading through the environment. Because of the persistence of PCDD/Fs and their continual recycling through the environment it is probable that even if primary emissions of PCDD/Fs are reduced, a decrease in environmental burdens will take some time (Harrad and Jones 1992a and 1992b). PCDD/Fs tend to accumulate in the fatty tissues of animals because they are lipophilic (ie. soluble in fats and oils). This is particularly evident in aquatic environments in benthic organisms which are continually in contact with sediments, and in filterfeeders which can take up particulate matter suspended in the water column. As contaminated animals are eaten by others, the predator absorbs a large proportion of PCDD/Fs in its prey. Thus animals at the top of food chains can accrue heavy burdens, a process known as biomagnification. At the top of aquatic food chains the impact is most apparent in fish-eating colonial birds, marine mammals and polar bears (Norstrom et al. 1990, Oehme et al. 1988, Ono et al. 1989).
Sewage sludges are relatively enriched in PCDD/Fs and applications of sludges to agricultural land used for grazing can increase human exposure. Transfer of PCDD/Fs to livestock can occur by ingestion of sludge adhered to vegetation. The degree of human exposure from this is estimated to be very dependent on the amount of adherence of sludge to the vegetation (Wild et. al. 1994). It was proposed by WHO (1990) that sewage sludge application to agricultural land should be banned where there is potential for bioaccumulation in the food chain and human exposure. Given the tendency of dioxins to persist and become redistributed through the environment, spreading of dioxin contaminated sludge should not be permitted under any circumstances.
Human milk dioxin levels are of particular concern because newborns are believed to be highly sensitive to dioxins (Vos and Luster, 1989). In industrialised countries, nursing infants can ingest far more than the WHO TDI of dioxins. For example, studies undertaken by WHO (WHO 1988, WHO/EURO 1989), on levels of dioxins in human breast milk in Europe, Japan, Canada and selected areas of USA, indicate the average daily intake for breast-fed infants between 0 and 6 months of age is estimated to be 13pg 2,3,7,8TCDD/kg body weight (or 90pg TEQ/kg body weight). However, WHO (1992) stated that the TDI should not be applied to breast-fed infants since the TDI concept for these substances is based on lifetime intake. It was estimated (WHO 1990) that intake of dioxins during a 6 month nursing period would correspond to less than 5 % of the lifetime intake based on calculations of fat accumulation in the infant. It was still recommended however, that lactating mothers should not try to lose weight intentionally since dioxins could be mobilised from fat stores. Current levels of dioxins in human milk mean that the margin of safety for breast-fed babies calculated by risk assessments in Europe is very low (Theelen, 1991). Studies carried out by WHO (WHO/EURO 1989) regarding risk assessment in infants associated
with exposures through human milk concluded that -- a safety margin still exists, although rather small-(WHO 1992). This becomes of greater concern because health risk assessments of dioxins do not take other chemicals into account and the effects of such compounds could be additive or synergistic for given health endpoints (Schecter, 1991). Furthermore, dioxins are also transferred to the foetus via the placenta and health risks to humans appear to be particularly great in developmental stages (Mably et al. 1992, Peterson 1993, Pluim 1993). Therefore, the reduction of environmental contamination with dioxins is essential, not only for the present population but for future generations.
For example, it can activate a gene encoding cytochrome p450 enzymes (which are enzymes involved in the activation and detoxification of chemicals in the body), and there is also evidence that it may mediate expression of several other genes including those that regulate cell differentiation and growth. Therefore, dioxins can have a broad range of effects on organisms.
Different dioxin congeners bind the Ah receptor with different strengths giving rise to the variation in toxicities. Although there is evidence that the Ah receptor mechanism is involved in many different effects caused by dioxin (reviewed by Peterson 1993) there may be TCDD effects which are not Ah receptor mediated.
According to a draft of the EPA's reassessment:
Subtle changes in enzyme activity indicating liver changes, in levels of circulating reproductive hormones in males, in reduced glucose tolerance potentially indicative of risk of diabetes, and in cellular changes related to immune function suggest the potential for adverse impacts on human metabolism, reproductive biology, and immune competence at or within one order of magnitude of average background body burden levels...
Individuals at the high end of the general population range may be experiencing some of these effects. Some more highly exposed members of the population may be at risk for frankly adverse effects including developmental toxicity, reduced reproductive capacity based on decreased sperm counts and potential for increased fetal death, higher probability of experiencing endometriosis, reduced ability to withstand an immunological challenge and others. -- (EPA 1994)
Effects on CNS function have also been reported to occur in fourteen children (7 girls and 7 boys) born between 1977 and 1983 to mothers who resided in the TCDDcontaminated environment of Times Beach, Missouri, during and subsequent to pregnancy. (Cantor et al. 1993). Times Beach was contaminated with TCDD during the early 1970s when contaminated waste oil was sprayed on roads and at many horse arenas for dust control. Tests to evaluate brain function (neurophysiology) in these children relative to an age and sex matched population were carried out in 1992. Results showed that children exposed to TCDD in utero and post-natally exhibited abnormal brain measures (neurophysiological dysfunction), principally in the bilateral frontal lobe regions of the brain, relative to unexposed children, with females exhibiting more dysfunction than males. It is believed that abnormal frontal lobe region function can affect intellectual processes.
Effects on development occur at very low doses. In fish, birds, animal studies and in the Yusho/Yu-Cheng incidents, it is evident that the developing embryo/foetus is more sensitive to the dioxin-like chemicals than the adult mother. In animal experiments this foetal toxicity can occur at relatively high doses or chronic low dose exposure to dioxins. More disturbingly, animal experiments have shown that only transient exposure to relatively low levels of TCDD at critical times during gestation may be sufficient to cause irreversible disruptions in organ structure or function (Peterson 1993). An example of this is the developing male reproductive system in rats. Exposure to TCDD at a very low dose (64ng/kg) on day 15 of pregnancy has no detectable effect on the mother but decreased testosterone concentrations in male foetuses and neonates, and testes decent was delayed. The decreases in testosterone was partly responsible for effects from the exposure which extended into adulthood. These included a reduction in sex organ weights, a decrease in sperm count and effects on sexual behaviour. It was concluded that the male reproductive system in rats is highly sensitive to in utero and lactational TCDD exposure, and appears to be more sensitive to such exposure than any other organ or organ system in rats studied to date (Mably et al. 1991, 1992).
PCBs found in breast milk fat, and female height correlated positively (Dewailley et al. 1993a). Since this observation is consistent with studies on animals and with children born to exposed mothers in the Yu-Cheng incident (Rogan et al. 1988), it suggests that levels of PCDD/Fs and PCBs currently found in these people do effect newborns by exposure in utero.
In a separate study, Inuit neonates up to one year old were reported to have increased episodes of acute otitis media (infected inflammation of the middle ear) which correlated statistically with levels of PCDD/Fs and PCBs found in breast milk. The results implied that the increased acute otitis media episodes were possibly due to deficiencies in the immune system caused by exposure to PCDD/Fs and PCBs (Dewailly et al. 1993b). Dioxins influence thyroid hormone status in animals (Henry et al, 1987) which may influence the maturation of the CNS and have consequences for psychomotor development (Birrell et al, 1983). A recent study on healthy breast-fed babies has been conducted in the Netherlands. It revealed that dioxins transferred by the placenta and by breast milk caused changes in thyroid hormone concentrations and that this was most likely due to interference with the thyroid regulatory system (Pluim et al, 1993).
WHO reported that in chemical workers who were accidently exposed to dioxins -- there is no evidence that exposure to the male has resulted in abnormal reproductive effects -- (WHO 1992). However, since then, accidental exposure of chemical workers to dioxins was shown to decrease testosterone levels (Egeland et al. 1994). It has been reported that sperm counts have fallen and disorders of the male reproductive tract have increased since the 1950s (Sharpe & Skakkebaek 1993). It is possible that dioxins and other organochlorines play a part in this, with effects on individuals exposed in utero being greater than effects on exposed adults. In regard to in utero exposure of dioxin and human fertility, the study on in utero exposure in rats (Mably et al. 1991) discussed above, illustrated a worrying point. It was found that a single low dose exposure during day 15 of pregnancy caused a reduction in sperm count. Rats produce ten times as much sperm than required for fertilization, and consequently there was little effect on fertility. However, a reduction in sperm count in humans of a similar magnitude to that seen in the study on rats would be expected to decrease fertility in humans, because the number of sperm produced per ejaculation is close to that required for fertility. It is therefore possible that more highly exposed members of the human population may be at risk from decreased sperm count (EPA 1994).
Effects on immune system functioning have been found to occur in children born to mothers who resided in a TCDD contaminated area in Times Beach, Missouri, during and subsequent to pregnancy (Smoger et al. 1993). Tests were performed on these children at the ages of 9 to 14 years and revealed significant changes in the numbers of several types of cells involved in immune system function. The results were consistent with previous analyses of exposed human populations, and experiments on marmosets, and showed that immune deficiencies caused by in utero and post-natal exposure to TCDD may persist for 10 years or more.
Liver damage and effects on immune system functioning were also documented to occur in patients following the Yu-Cheng episode in 1979 in Taiwan (Chang et al, 1981, 1982 a, b). However, a recent report has demonstrated possible effects on the immune system in humans at current background levels. This study on subjects in Sweden who had a high fish consumption from the Baltic Sea, showed that organochlorines including dioxins from the diet appeared to have an effect on a subset of lymphocytes (white blood cells) called natural killer cells (Svensson et al, 1993). However, further studies are needed for conclusive evidence.
Epidemiological studies which have used relatively large sample sizes and some direct measurements of dioxin in blood or tissue to estimate exposure, monitored cancer incidence rates in cohorts of workers exposed to TCDD in the workplace (Manz et al. 1991, Zober et al. 1990, Fingerhut et al. 1991 a and b). All of these studies reported an overall increase in mortality for all cancers combined and for lung cancer. Data from several studies most notably Hardell et al.(1979) have also suggested that soft tissue sarcomas may be associated with exposure to PCDD/Fs.
In the studies by Fingerhut et al (1991 a & b) respiratory cancers were
significantly increased and did not appear to be attributable to smoking. There
was a significant overall increase in mortality (46%),(standardised mortality
ratio (SMR)115; 95% confidence interval,103 to 130) in all cancers combined
compared to the control group. If respiratory system cancers were not included
in this data, the overall increase was still significantly elevated (48%), (SMR
117; 95% confidence interval, 100 to 136). The study concluded that excess
mortality from all cancers combined, from respiratory cancer and soft tissue
sarcoma, was consistent with TCDD being a carcinogen. However, the study could
not completely exclude the possible contribution from exposure to other
occupational chemicals or smoking. Overall, data from epidemiological studies
appear to be consistent with animal studies on the carcinogenicity of dioxin,
and consequently US EPA concluded the following:
"With regard to carcinogenicity, a weight-of-the evidence evaluation suggests that dioxin and related compounds are likely to present a cancer hazard to humans -- While the epidemiological data alone are not yet deemed sufficient to characterize the cancer hazard of this class of compounds as being "known", the unequivocal evidence in animal studies, inferences drawn from mechanistic data, and the suggestive evidence of recent epidemiology studies support the characterization of dioxin and related compounds as likely cancer hazards." (US EPA 1994)With regard to risk assessment of cancer, US EPA estimates that current background exposures could cause up to 3% of all cancers in the US:
"Modelling estimates suggest that current background exposures may result in upper bound population cancer risk estimates in the range of one in ten thousand (104) to 1 in a thousand (103) attributable to exposure to dioxin and related compounds." (US EPA 1994)It is becoming evident that some of the biochemical responses produced by TCDD and PCDFs are similar in humans and experimental animals, and that receptor-mediated events are critical to carcinogenic action. Lucier et al. (1991) investigated the binding capacity of several receptors and the induction of the enzyme cytochrome P-450 to these compounds in both human and rat tissue. The study showed that humans were as or more sensitive than rats to dioxin-like chemicals with respect to their biochemical markers. Such evidence, together with animal and epidemiological studies, suggests that TCDD is a human carcinogen.
The risk assessments made by WHO were based on general toxicological effects in various laboratory animal species, and included pro-carcinogenic liver toxicity, reproductive effects and immunotoxicity (WHO 1990, WHO 1992). Health and Welfare Canada based risk assessments on the rate of cancer formation in rats (Kociba et al. 1978), and birth defects and certain reproductive effects in rats (Murray 1979). From the risk assessment experiments both WHO and Health and Welfare Canada identified that no observable adverse effect was observed at a dose of 1000pg/kg/day. Health and Welfare Canada applied a safety factor of 100 to the no observable adverse effect level (NOAEL) (Boddington et al. 1990, Feeley and Grant 1993), which resulted in a TDI of 10pg TEQ/kg body weight/day. The purpose of the safety factor is to protect against the possibility that humans may be more sensitive to dioxin than rats, as well as the likely differences in sensitivity between people. WHO derived a TDI by using kinetic data which showed that the no effect level of 1000pg/kg/d in animals was equivalent to a dose of 100pgTEQ/kg/day in humans. Because of insufficient data based on reproductive effects in humans a safety factor of 10 was employed giving a TDI of 10pgTEQ/ kg/day [WHO 1990, WHO 1992]. This TDI has been adopted by most European governments. However, different safety factors have been applied to the NOAEL in some countries, or different risk assessment methods have been employed, resulting in several different TDIs, as shown in Table 2.
[Table 2: Tolerable daily intakes of dioxin in different countries goes here]
However, there is not general agreement about using the safety factor model for risk assessment of dioxins, which is based on the following assumptions:
(a) A NOAEL of 1000pg/kg/d was identified in experiments by WHO and Health and Welfare Canada from risk assessment experiments. In such experiments, if a large dose of a chemical increases the rate of a toxic effect relative to unexposed control animals, but a small dose does not, it is possible that a threshold does exist for this outcome. However, it is also possible that the effect really does occur at lower levels but the experiment is not powerful enough to detect it. For example, if the true probability for developing cancer at a certain dose is 1 in 1000 and only 50 animals are tested, it is unlikely that an increased number of tumours will be observed. Thus a lack of an observed increase in an effect by itself, does not mean there is a threshold. Proper interpretation of NOEALs therefore requires an understanding of the underlying biology and the limitations of experimental protocols. Unfortunately, some regulatory agencies presume the existence of thresholds, even when biological knowledge is limited.
(b) Carcinogens that directly damage DNA in cells resulting in the formation of cancer are known as genotoxic agents. It was previously thought that if a genotoxic agent damaged the DNA in a single cell in such a way that the control mechanism for cell replication was changed, the cell could multiply unchecked and could eventually lead to the formation of cancer. Although in principle this appears to be true, it is not quite this simple because there is now evidence that cancer is a multi-stage process involving several mutations and multiple mechanisms governing selective growth of these genetically altered cells (Barret et al. 1992). Since very small doses of a DNA-damaging agent are potentially capable of causing mutations in cells which could lead to cancer, many regulatory bodies prudently assume that DNA-damaging carcinogens have no threshold.
Cancer can also be caused by agents that do not directly damage DNA,
(non-genotoxic agents), but instead increase the growth rate of normal and/or
abnormal (mutated) cells, thereby increasing the risk of tumour development.
Such agents are known as tumour promoters. Experimentally, a tumour promoter is
defined as something which does not cause cancers by itself but instead greatly
enhances the number of tumours initiated by another agent. Unlike DNA-damaging
carcinogens, promoters are often presumed to possess thresholds.
Dioxins are non-genotoxic and appear to act as tumour promoters. (reviewed by Shu et al. 1987). WHO and Health and Welfare Canada argue that because dioxin is a tumour promoter and is therefore not directly mutagenic, it will exhibit a threshold. However, this view is over-simplistic because it is thought there are multiple mechanisms responsible for tumour promotion (Barret et al. 1992). Although TCDD is not directly mutagenic, it may cause indirect damage to DNA because it can induce enzymes capable of converting certain other compounds into DNA-reactive forms. (Huss et al 1994, Webster 1994). Also, TCDD has been shown to transform certain human cells grown in cell culture into cancerous forms (Yang et al. 1992). Overall, the evidence indicates that it is not necessarily true that a threshold exists for dioxin just because it is classed as a tumour promoter. This argument is upheld by US EPA who therefore use the LMM model for risk assessment in which the dose-response curve for excess carcinogenic risk is assumed to be linear through to dose zero, and does not assume a that there is a threshold.
(c) It is generally accepted that effects of TCDD are mediated by a receptor,
(Ah-receptor). If dioxin binds to a receptor it can trigger different
biochemical responses, which can be monitored experimentally. It has been
suggested that dioxin must bind a minimum number of receptors for any effect to
occur, i.e. that doses below this threshold will have no biochemical
consequences. However, recent studies from the EPAs reassessment on the response
of certain biochemical endpoints in animals exposed to dioxin, showed no
indication of a threshold (Tritscher et al 1992, Portier et al 1993, Birnbaum
1993a). For example, "No evidence for low dose nonlinearity was observed for
sensitive biochemical responses -- . (Birnbaum 1993a)
This means that even at very low doses of dioxin, a level was not found where no biochemical response was detected.
In another study, Portier (1993) reported:
"[Our findings] are consistent with the knowledge that for some receptor-mediated responses, there is a proportional relationship between receptor occupancy and biological response, even at low ligand concentrations. The results presented here illustrate that a threshold for the biological effects of TCDD exposure cannot be assumed simply on the basis that dioxin response is receptor-mediated-If TCDD-mediated effects on cytochrome p-450 induction or epidermal growth factorIt is unclear precisely how these biochemical endpoints relate to cancer or other toxicological endpoints, since the mechanism by which TCDD causes diseases is poorly understood. Nevertheless, these findings argue against the idea that a threshold exists for receptor-mediated events.
(EGF) receptor binding are reliable surrogates for toxicity or toxicity is induced by similar mechanisms, the risks from exposure to TCDD are as high or possibly higher than were estimated by the EPA using a linear model. If this is the case, there should be considerable concern for the high levels of TCDD already present in human tissues."
In the experiment by Rier et al (1993), TCDD was administered in the animals feed (from 1977-1982) at doses of 5-25 parts per trillion (ppt). The frequency of endometriosis in unexposed animals would expected to be about 30%. However, endometriosis occurred in 3 out of seven (43%) animals at a dose of 5ppt and in five out of seven (71%) at 25ppt. The lowest dose administered corresponded to approximately 130 pg/kg/d (Peterson 1994a). This is 7 -- 8 times lower than the NOAEL of 1000 pg/kg/d proposed by WHO and Health and Welfare Canada. These preliminary results indicate that the WHO and Canadian dioxin guideline is not protective of human health because increased endometriosis was found at a dose an order of magnitude less than the assumed NOAEL. However, since the total number of animals in this study was small, further studies are in progress to confirm the findings.
"Results in enzyme induction from both rats and mice would suggest that at current environmental levels, (1-10 pg/kg/day) people may be experiencing small but significant increases in these markers of response. Highly exposed populations may be at special risk. Since animal studies suggest that changes in hepatic enzyme induction occur at body burdens similar to those at which immunotoxicity in mice and permanent effects on the reproductive system occur in rats, it is reasonable to hypothesize that subtle effects on these parameters may be occurring in the human population." [Birnbaum 1993]Chronic low dose exposure to dioxin in animal experiments have shown adverse effects to health, for example, an effect on immune system cells in marmoset monkeys (body burden 6 -- 8ng/kg, Neubert et al. 1992) occur at body burdens which are similar to, or within an order of magnitude of current human body burdens (estimated as 510ng/kg, EPA 1994). The body burden in monkeys which received a dose of 5ppt TCDD in diet, and appeared to cause endometriosis,(Rier et al. 1993) was 27ng/kg, and is therefore within an order of magnitude of current human body burdens (EPA 1994).
Such evidence, together with other animal experiments and limited human data, indicate that current body burdens in the general population in industrialised countries are already at, or within one order of magnitude, of levels where subtle changes in enzyme activity indicating liver changes, in levels of reproduc tive hormones in males, and in cellular changes related to immune function may occur. These effects suggest there is potential for adverse impacts on human metabolism, and reproductive and immune system function (EPA 1994). This is of particular concern for more highly exposed members of the population (eg. from higher than average levels of dioxins and PCBs in diet) who may be at risk of effects on development, reproduction, such as reduced sperm count, possibly endometriosis in women, and effects on the immune system, as discussed previously in this report. The critical period of time of exposure to give an effect may be relatively short as in in utero exposure, or could be relatively long as in the development of some cancers. It is very evident from recent studies that current body burdens in women which are passed through the placenta and through breast milk to the foetus/infant are of particular concern.
Recent studies have shown that assumptions made in the derivation of WHO and Health and Welfare Canada TDI may no be longer valid. Adverse effects have been observed at lower levels than the proposes NOAEL of 1000pg/kg/d and there is no evidence that for the existence of a threshold for dioxin effects. However, WHO have not planned reassessment of the TDI in the future.
2.5 million metric tons of hazardous waste were incinerated in the USA alone in 1987 (Dempsey and Oppelt 1993). Trial burns in 1993 at the Waste Technologies Industries hazardous waste incinerator in Ohio revealed mean dioxin emissions of 1.2 grams per year (TEQ), or 13.6 ug/ton of waste burned (ENSR 1993). If all waste were burned this efficiently, atmospheric emissions alone in the US would total 34g/year. However, real-world conditions will be far from this efficient and inclusion of emissions to liquid and solid wastes will raise this estimate far higher.According to the German EPA (UBA 1990), older municipal waste incinerators (MSWI) from about 10 years ago would have emitted between 20 and 50ng TE/ Nm3; current MSWI emit approximately 8ng TE/Nm3 and state of the art ones about 1ng TE/Nm3. Hospital waste incinerators in Germany have been reported to emit 15ng TEQ/ Nm3 to 18 ng TEQ/Nm3 (reviewed by Fiedler 1990). In the US 50ng TEQ/Nm3 was detected in the flue gas of hospital waste incinerators (Hauchmann et al. 1989).
Table 3: Known or suspected processes that form dioxin and related
|Chlorine electrolysis with graphite
Chlorine electrolysis with titanium electrodes
- use of chlorine gas
|Chlorinated aromatic chemicals --
manufacture (chlorobenzenes, chlorophenols, PCBs others) |
PVC plastic -- manufacture of feedstocks (ethylene dichloride, vinyl chloride)
Sludge from effluent treatment
PVC plastic products
Some inorganic chlorides -- manufacture (ferric and copper chlorides, sodium hypochlorite)
|Uses of chlorine
-- other industries
|* Pulp and paper -- chlorine bleaching
Pulp and paper products
Emissions from sludge incinerators
Refined metals -- manufacture with chlorine (Ni, Mg)
|Use of organochlorines||Manufacture of chlorine-free chemicals
with chlorinated intermediates (nitrophenols, parathion,
Degreasing/extraction with organochlorine solvents in alkaline or reactive environments
Oil refining with organochlorine catalysts
Use of pesticides with heat (wood treatment, etc)
Iron/steel sintering with organochlorine cutting oils, solvents or plastics
* Burning gasoline or diesel fuel with organochlorine additives
Use of chlorine-based bleaches and detergents in washing machines and dishwashers
Recycling and Fires
(primary dioxin precursor in parentheses)
|* Medical waste incinerators (PVC) Air
* Municipal waste incinerators (PVC) Air emissions Ash residues
* Hazardous waste incinerators (solvents, chemical manufacturing wastes) Air emissions Ash residues
Cement kilns burning hazardous waste (solvents, chemical manufacturing wastes) Air emissions Cement kiln dust
Accidental fires in homes and offices (PVC)
Fires at industrial factilites (PVC, PCBs, other chlorinated chemicals)
Aluminium recycling/smelting (PVC)
Steel and automobile recycling smelting (PVC)
* Copper cable recycling/smelting (PVC)
* Wood burning (pentachlorophenol wood preservatives, PVC)
|Transformation of chlorophenols to dioxins in the environment|
|* Addressed by the EPA in documents related to its dioxin reassessment. (Cleverly 1993, Schaum 1993). List includes sectors in which formation of dioxin or related compounds (PCBs, chlorinated dibenzofurans, and/or hexachlorobenzene) has been confirmed in chemical analyses, as well as sectors in which dioxin formation is "known or suspected" according to EPA (EPA 1985, PCTN 1985) or NATO (Hutzinger 1988).|
Sewage sludge incineration releases dioxin because of organohalogen contamination from a number of sources. Industrial tie-ins to the sewerage system can introduce a wide range of contaminants (see Johnston et al. 1993). Organochlorines such as chlorobenzenes can be introduced from domestic as well as industrial sources (Wang & Jones 1991). In the USA, the practice of chlorinating sewage may exacerbate the problem. Cement kilns have been used to incinerate hazardous wastes, but there are considerable problems with the use of this technology, most notably the lack of emissions control. Few cement kilns have the complex air pollution control devices required on hazardous waste incinerators. Handling of hazardous wastes by inexperienced personnel could also pose health and environmental threats. High levels of chlorine in the feedstock could also cause formation of alkali-halogen rings leading to clogging and poor emission control, and even under idealised test conditions, chlorinated emissions were detected (Lauber 1982). The primary motivation for the use of cement kilns to dispose of hazardous waste is economic and the imposition of stringent testing and emissions controls would probably preclude their use for this purpose.
The WHO have recommended a limit of 0.1ng TEQ/m3 for all incinerators, with particular attention being given to avoiding contamination of the environment with fly ash (WHO 1990). The EC draft proposal on the incineration of hazardous waste (CEC 1993) proposes a guideline of 0.1ng/m3 until 1st January 1997 when it will become a binding limit value. Although some researchers maintain that it is possible to reduce emissions to below 0.1ng/m3 (see eg Rappe 1993), the EC draft only proposes a guideline until 1997 because standardised methods of measurement are not available. The draft directive also omits to control emissions via liquid effluents or solid wastes generated by the incinerator.
In summary, it is apparent that both technical and legislative measures to prevent dioxin contamination of the environment by incineration are inadequate. Ultimately, waste minimisation and alternative destruction techniques must be implemented to replace incineration and eliminate this source of dioxin pollution.
In May 1994, the Swedish Environmental Protection Agency found that PVC itself contains measurable quantities of dioxins and furans (SEPA 1994). Pure PVC suspension from two Swedish PVC producers was found to contain a full range of congeners of dioxins, furans and PCBs, with total concentrations ranging from 0.86-8.69 ppt, as shown in Table 5.
Recent analyses commissioned by Greenpeace on effluents from a PVC plant and on residues from PVC manufacture have confirmed that this industrial sector may be an important contributor of certain dioxin congeners. In the first case, effluent from a SOLVAY plant was analyzed at the University of Amsterdam. In the second case, soils samples taken from the vicinity of the oxychlorination reactor at Norsk-Hydro in Sweden were analyzed by SAL Laboratories in the UK. The results are shown in Table 6.
In both cases, the target congeners were the seventeen chlorinated dibenzo-p-dioxins and dibenzofurans with chlorine substitution at the 2,3,7,8 positions. In the case of the waste the total nontargeted isomers comprised 5.02 ng/g PCDD and 165.8 ng/g PCDF. In both cases the samples reveal an unusually high preponderance of OCDF. The analytical report on the waste sample also observed that in addition to the target congeners, there were numerous other PCDDs and PCDFs present.
Norsk-Hydro, in a press release, have claimed that the sludge landfill at Rafnes contains 18 grammes of dioxin in total. An average loading of 0.095 grammes per kilogram is estimated, while 0.42 grammes enter the landfill each year. Assuming that this is expressed in EC/NATO TEQs, and that for convenience it is comprised of 100% OCDF then this translates to totals of 18kg at a sludge concentration of 95 grammes per kilo and an annual input of 420 grammes. These are significant amounts of persistent organochlorines. A need therefore exists for a full, reported, characterisation of the content of these sludges. A full evaluation of the behaviour of the various congeners in aquatic systems is required to justify the use of TEQ systems which have been developed solely on the basis of mammalian toxicity studies. Moreover, the dioxins serve as an index of the presence of other persistent chlorinated organics in the process wastes.
~These new experiments by the University of Leiden demonstrate clearly a relation between the content of PVC in household waste and dioxin formation in waste incinerators. On the basis of these experiments there is no reason to reconsider present policies regarding PVC applications: the main feature of this policy is that PVC applications for which no feasible system of recycling and reuse can be established the use of more environmentally sound alternative materials is to be preferred~ (Netherlands Environment Ministry 1994).
Experiments by (Rappe et al. 1989) identified PCDFs but not PCDDs in drinking water which was chlorinated using chlorine gas. Additionally, the regeneration of carbon filters used to remove contaminants from drinking water results in dioxin formation since the filters accumulate organic contaminants (Hutzinger 1988).
Dioxins may be formed when chlorine is used in the production of refined nickel and magnesium. Annual emissions from one magnesium plant in Norway are estimated to be several hundred grams of TEQ to water and 6 grams per year to air. Emissions from a nickel plant have been estimated at 1g/year (TEQ) to water alone. In addition high concentrations of PCDFs have accumulated in fish tissues near the nickel production facility (Oehme et al. 1989).
Recently, iron and steel plants have been found to be major sources of dioxin. German analyses show that such plants may emit dioxin in their stack gas in concentrations of 3-10 ng/M3 (TEQ) (Lahl 1993). Dioxins are produced in this process because of the introduction of chlorinated chemicals such as cutting oils and solvents. Air emmissions from these plants account for 300-1000g/year (TEQ) in Germany alone (Lahl 1993). Since U.S production of steel is approximately twice as great as that in Germany, dioxin emissions may therefore be in the range of 600-2000g/year making this one of the largest known dioxin sources (U.S DOC 1993). The WHO (1990) recommended that emissions from the metal industry should be minimised by optimising technical procedures and equipment.
A strategy to deal with toxic and persistent pollutants in the environment
which is being increasingly implemented at both the national and international
level is the precautionary approach (Stairs and Johnston 1991). This philosophy
does not advocate that discharge of a compound should be allowed in the
environment until damage to the environment has been proven, but rather it
requires that materials should not be discharged unless it can be established
that they will not be deleterious. It also avoids problems deriving from the
limitations of our understanding of toxicology by removing the assumption that a
safe level of a particular compound or compounds can be estimated. Thus industry
is often not just required to restrict emissions of environmental toxins, but to
reduce them to zero. The phasing out of toxic, persistent and bioaccumulative
pollutants in the environment has been addressed at several international
meetings. At the Third International Conference on the protection of the North
Sea (1990) it was agreed that:
"for substances that cause a major threat to the marine environment, and at least for dioxins, mercury, cadmium and lead, to achieve reductions betweenThe Paris Convention agreed in September 1992 to the following commitment under article 3 of Annex I on the Prevention and Elimination of Pollution from Landbased Sources:
1985 and 1995 of total inputs (via all pathways) of the order of 70% or more, provided that the use of Best Available Technology or other low waste technologies measures enables such reductions."
"[I]t shall, inter alia, be the duty of the (Paris) Commission to draw up: (a) plans for the reduction and phasing out of substances that are toxic, persistent and liable to bioaccumulate arising from land-based sources."Similarly, all contracting parties to the Barcelona Convention agreed in October 1993 to phase out inputs from land-based sources to the Mediterranean of categories of known and suspected pollutants. Specifically, the following recommendations were passed (UNEP 1993):
"...the Contracting Parties reduce and phase out by the years 2005 inputs to the marine environment of toxic, persistent and bioaccumulative substances listed in the LBS Protocol, in particular organohalogen compounds having those characteristics..."and:
"...to promote measures to reduce inputs into the marine environment and to facilitate the progressive elimination by the year 2005 of substances having proven carcinogenic, tetatogenic and/or mutagenic properties in or through the marine environment."Similarly, in the US, the American Public Health Association has made a recommendation specifically on the phase out of chlorine and related compounds. In 1993, the APHA found that:
"the only feasible and prudent approach to eliminating the release and discharge of chlorinated organic chemicals and consequent exposure is to avoid the use of chlorine and its compounds in manufacturing processes."On this basis the organisation resolved that chlorine and chlorinated organic compounds be treated as a class for phase out, with exceptions to be made only for uses that can be demonstrated to pose no significant hazard or for which no alternatives are available (APHA 1994).
The International Joint Commission on the Great Lakes (IJC) has recognised the fact that dioxin formation occurs throughout the field of chlorine chemistry and that the mix of by-products formed in the life cycle of chlorine and chlorinated organic chemicals cannot be prevented or controlled. Thus the IJC has called on the US and Canada to begin a phase-out of all chlorine and chlorinated organic chemicals as industrial feedstocks (IJC 1992, IJC 1994).
In the US the White House has also begun to move towards the comprehensive regulation of the field of chlorine chemistry. In its proposal for the Clean Water Act, President Clinton proposed to develop "a national strategy to reduce, substitute, or prohibit the use of chlorine and chlorinated compounds." Specifically this recommendation consisted of an 18-month and a 12-month period of policy formulation and review, with the focus on major chlorine uses, including pulp-bleaching, PVC and solvents.
In the largest dioxin producing sectors for which alternatives are available and feasible, action should be taken immediately. Those sectors that require longer implementation phases should be placed on time lines for dioxin elimination. Major sources of dioxins which need to be urgently considered include the following:
Technological and economic transformation may be difficult to implement and it is essential that workers and communities should not bear the economic burden of these changes. The phasing out of dioxins should therefore be guided by a democratic transition programme to protect, compensate and provide future opportunities for workers and communities affected by the conversion.
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