Summary
Dioxins are a class of chemical compounds which are extremely toxic to
animals and humans, and have been characterized as being some of the most
potent "man made" toxic chemicals ever studied. Consequently, in recent
years, there has been much public concern and intense scientific interest
about these chemicals.
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.
Risk Assessment
In December 1990, the World Health Organisation (WHO) produced a document
on human health and dioxin. In this document, a -- tolerable daily intake
-- for dioxin of 10pg/kg body weight/day (pg/kg/d) was proposed. Tolerable
daily intake (TDI) is used to define the maximum dose levels for lifelong
exposure that may be regarded as not detrimental to human health. The TDI
proposed by WHO has been adopted by many European governments. The Canadian
government has also legislated a TDI of 10pg/kg/d based on research by
Health and Welfare Canada. However, using a different method of risk assessment
for dioxin, the US EPA had set a value for the -- acceptable daily intake
-- (ADI) of dioxin of 6 fg/kg/d. This is 1670 times lower than the WHO
and Canadian TDI.
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:
-
Firstly, a National Institute of Occupational Safety and Health (NIOSH)
cancer mortality study in US workers, published by Fingerhut et al.(1991),
showed that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic
dioxin chemical known, appeared to cause cancer in humans.
-
Secondly, the Banbury Conference on dioxin toxicity held in October 1990
in Cold Spring Harbour, New York, produced evidence of several other important
findings on dioxin toxicity, including the fact that humans and experimental
animals respond to dioxin similarly, and effects in humans could be anticipated
by certain effects in animals.
In view of these two events, US EPA publically announced plans for the
reassessment of dioxin on November 15, 1991 (Federal Register 1991). Aims
of the reassessment included the development of a new model for estimating
human health risk from dioxin, updating research on health assessment and
exposure to dioxin and supporting research to characterise ecological risks
in aquatic ecosystems.
Dioxin-a by-product of chlorine chemistry
Dioxins are produced as unintentional by-products from the many processes
in which chlorine and chlorine-derived chemicals are produced, used and
disposed of. Industrial emissions of dioxins into the environment can be
transported long distances on atmospheric currents and to a lesser extent
in rivers and oceanic currents. Consequently, dioxins are now globally
ubiquitous. It is estimated that even if production ceases, levels in the
environment will take years to decrease. This is because dioxins are persistent,
taking decades or centuries to degrade, and can undergo continual recycling
throughout the environment.
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.
International Regulations
The phase out of persistent, toxic and bioaccumulative pollutants in the
environment has already been addressed at several international conventions
including: the Third International Conference on the North Sea (1990) in
which it was agreed that dioxin and other named substances should be reduced
of the order of 70% or more; the Paris Convention (1992) in which it was
agreed that toxic, persistent substances that are liable to bioaccumulate
arising from land-based sources should be phased out; the Barcelona Convention
(1993) in which it was agreed to phase out inputs from land based sources
to the Mediterranean of organohalogen compounds with these characteristics;
the International Joint Commission of the Great Lakes (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).programme.
An emergency strategy
Because there is already a large burden of dioxins in the global environment
which will persist for many years, aggressive measures must be implemented
if the exposure of the human population is to be significantly decreased.
Since all uses of chlorine and chlorinated organic chemicals are suspected
of dioxin formation at one or more points in their lifecycle, the phase-out
of dioxins necessitates the phase-out of all chlorine chemistry. Implementating
a programme to phase-out dioxin releases from industry should be based
on the following principles: Zero means zero. Dioxin releases from industry
must be eliminated, not simply reduced. The current environmental burden
will take years to decrease because of the persistence of these chemicals
and their continual recycling throughout the environment. Given the current
health threat it would be wholly inappropriate for environmental regulatory
bodies and governments to permit the release of any additional dioxin into
the environment.
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.
Dioxins in the environment and in humans
Chemical characteristics of dioxins
The term dioxin represents a class of chlorinated tricyclic, almost planar,
aromatic ethers that exhibit similar chemical and physical characteristics.
The number of chlorine atoms in these compounds varies between 1 and 8
resulting in a possible 75 polychlorinated dibenzo-p-dioxins (PCDDs) and
135 polychlorinated dibenzofurans (PCDFs). The most toxic congeners (members
of this group of chemicals) have chlorine atoms in positions 2,3,7 and
8. Due to the stability and persistence of these congeners, they are ubiquitous
in the environment and in humans.
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.
Levels of dioxin in the environment
Dioxins are very chemically stable. Some degradation occurs in the atmosphere,
but in other media, particularly in soils and sediments half lives are
measured in decades or centuries. Global distribution of dioxins occurs
largely by atmospheric transport and to a lesser extent in oceanic currents.
Due to poor solubility in water and comparatively low volatility (Friesen
et al. 1990), these compounds become attracted to fine particles and are
predominantly transported in suspension in air or water associated with
this particulate matter, rather than being in gaseous or dissolved states
(Nakano et al. 1990). For this reason dioxins are often found in high concentrations
in sediments, sludges and dusts. The spreading of dioxins from industrial
sources by atmospheric transport was demonstrated in a study by Kjeller
et al. (1991), in which agricultural soils, stored at intervals since the
1840s were analyzed. These archived samples were collected at an agricultural
research
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) |
| 1846 |
61(29) |
| 1846 |
54(29) |
| 1856 |
31 |
| 1893 |
31 |
| 1914 |
42 |
| 1944 |
62 |
| 1944 |
57 |
| 1956 |
74 |
| 1966 |
89 |
| 1980 |
81 |
| 1986 |
95 |
| 1986 |
88 |
| 1986 |
92 |
Long-range atmospheric transport of PCDD/Fs from industrial sources is
widespread, even in remote areas, but localised contamination around industrialised
areas is also evident. For example, in the UK average soil levels in urban
areas of total PCDD/Fs (1436 ng/kg) were reported to be four times higher
than in rural locations (335ng/kg) (Creaser et al. 1989). Spraying of land
with pesticides notably the chlorophenoxyacetic acid products 2,4-D, 2,4,5-T
and agent orange has been reported to lead to significant local contamination
increases (Hutzinger et al. 1982). The manufacture and disposal of chlorophenol
derivatives and associated process wastes are responsible for some of the
highest recorded PCDD/F pollution levels.
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).
Effects on fish and wildlife
Data from both laboratory and field studies on fish and birds have shown
that dioxins and furans cause detrimental effects to both adults and young
but particularly embryo mortality (Gilbertson 1989, Cook and Kuehl 1991).
In fish, dioxin exposure of eggs effects embryo development causing reduced
hatchability and increased mortality during the -- sac fry -- stage. Laboratory
experiments have shown high levels of PCDD/Fs in inland waters would cause
early life stage mortality in feral fish, thereby reducing fish populations
(Cook and Kuehl 1991). Similarly, in birds the embryo is more sensitive
to dioxins than adults. For example, since the 1960s there have been several
reported declines in populations of colonial fish-eating birds in the Great
Lakes in which dioxins have been associated with increased embryo mortality
(Fox and Weseloh 1987).
Human exposure
Human exposure to dioxins can occur through ingestion, inhalation and skin
absorption (Kutz and Young, 1976). Inhalation and dermal contact may be
important in individuals exposed to highly contaminated materials. However,
the major source of exposure to the general population is through ingestion
of food. It has been estimated that food intake represents 98% of exposure
to PCDD/Fs in humans with the remaining 2% coming from direct uptake of
air and soil (Travis and Hattemer-Frey 1987, Theelen, 1991).
Food
According to studies in Canada (Birmingham et al, 1989 a and b), Germany
(Furst et al, 1990), Norway (Faeden, 1991), Holland (Theelen, 1991) and
the UK (MAFF, 1992a), milk and milk products represent one third of the
total intake of PCDD/Fs from food. Animal fat in meat, poultry and fish
also contribute a large fraction of PCDD/Fs in diet. In a recent Dutch
study (Theelen et al 1993) these products represented one third of the
total intake and the final third came from various types of oil and fat
added to processed food items. Fish oil only represented 15% of the oils
which were used for this purpose but contributed to 90-95% of PCDD/Fs in
the products. Unusually high concentrations of PCDD/Fs in milk/animal fats
has been reported to occur near to sources of dioxin emission from industrial
processes (MAFF 1992b, Rappe & Kjeller, 1987, Liem et al. 1990). High
concentrations of particle-bound PCDD/Fs tend to be deposited close to
emission sources resulting in contamination of herbage. Ingestion of both
soil and plants by cattle in such areas can then lead to elevated levels
of PCDD/Fs in milk/animal fat. For example, a study of dioxin contamination
in cow-s milk from dairy farms located in the vicinity of municipal waste
incinerators in the Netherlands, revealed increased levels of PCDD/Fs of
up to 13.5pg TEQ/g of milk fat from areas near Rotterdam ( -- Lickbaert
area -- )and Zaandam (Liem et al. 1990). A potential health risk to humans
from consumption of milk and milk products from these areas could not be
ruled out. The Dutch government proclaimed an upper limit for dioxin in
milk and milk products of 6pg TEQ/g of fat and provisionally restricted
the consumption of these products in the affected areas. In a recent report
on dioxins in food in the Netherlands, it was concluded that reduction
of local emissions from industries are necessary if any substantial reduction
of human exposure is to be achieved (Theelen, 1993).
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.
Soil and sediments
The occurrence of elevated levels of TCDD in soil has been considered to
be a potentially significant public health concern since 1980 (Gough, 1991).
Exposure can occur through dermal contact and soil ingestion. (Paustenbach,
1992). Agricultural and building workers may have a higher exposure to
dioxin from these routes than the general population. Also, children are
likely to have more contact with soil both dermally and through ingestion
than adults. This is an important point for consideration when setting
levels for remediation of residential sites. Kimbrough et al. (1984) concluded
that 1 ppb of TCDD in soil was the level at which to begin consideration
of action to limit human exposure. In some instances, target levels of
less than 1 ppb or less have been set in the US (EPA 1987, 1990). In industrialised
areas, PCDD/Fs discharged into rivers become associated with particulate
matter in the water column and reach high levels in sediments, and hence
reach aquatic food chains (Evers et al 1988). Exposure to humans may therefore
increased in individuals who have a pronounced consumption of fish, especially
sporting fishermen (Potting 1989).
Levels in human blood, tissue and breast
milk
In general, levels of PCDD/Fs in blood, adipose tissue and milk are higher
in industrialised nations than in developing nations (WHO 1989, Schecter
et al. 1991b). Within a given country average dioxin tissue levels, which
reflect food intake, are usually similar in diverse geographical regions
and in industrialised/rural regions of a country (Furst et al. 1992). It
has been found dioxins can persist in human tissues for decades. For example,
individuals exposed occupationally to high levels of 2,3,7,8-TCDD and 2,3,7,8tetrabromodibenzo-p-dioxin
(TBDD) had elevated levels of these compounds in their tissues up to 34
years after exposure (Schecter and Ryan, 1988).
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.
Toxicity of dioxin
Public concern about effeccts of dioxin on human health was hightenend
in 1976 following an accident at Seveso in Italy, when an expolosion at
a chemical factory caused the release of high levels of TCDD. The most
commonly reported effects on humans following this accident and other incidents
of high dioxin exposure was a skin rash called chloracne. However, since
then numerous animal experiments and several epidemiological studies in
humans have shown that dioxin causes a wide range of health effects.
How dioxin exerts toxic effects
Research experiments over the last 15 years have established that most
toxic effects of PCDD/Fs and some PCBs are mediated by the Ah (aromatic
hydrocarbon) receptor (reviewed by Okey et al. 1994, Hanson 1991). If these
chemicals bind the Ah receptor, another protein called -- aryl hydrocarbon
receptor nuclear transferase -- also interacts with the receptor to form
a complex which can bind to DNA. This complex can activate the expression
of specific genes once bound to DNA (Swanson et al. 1993).
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.
Effects on reproduction and development
and the immune system
Evidence from animal experiments and from incidents of accidental or occupational
exposure to dioxin in humans, has shown that dioxins have detrimental effects
on development, reproduction and immune system function. More disturbingly,
recent experiments indicate that dioxins can have an effect on the levels
of certain hormones and enzymes, and cells of the immune system, at levels
(body burdens), which are at, or near to, levels currently found in the
human population in industrialised countries. For example, the level of
a male reproductive hormone called testosterone is affected by chronic
(long-term) exposure to dioxin at low levels in animals, and after occupational
exposure in humans. Another effect is the induction of some enzymes, such
as the liver enzyme (cytochrome p450), the function of which is to detoxify
chemicals in the body. Although the clinical significance of these effects
in humans is yet to be evaluated, it is possible they could cause changes
in metabolism which could lead to adverse health effects. Changes in levels
of certain cells of the immune system have been found to occur in animals
after chronic low dose exposure to dioxin. Members of the population who
are exposed to a higher levels of dioxin, for example, from a high fish
or sea mammal consumption, are more at risk of having adverse effects from
dioxin (EPA 1994).
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)
Developmental toxicity
In fish, birds and mammals, exposure to dioxins causes toxic effects to
the developmental stages of life. Recent laboratory studies suggest that
altered development may be among the most sensitive TCDD endpoints. Because
developmental toxicity following exposure to dioxins occurs across these
three vertebrate classes, it is likely to occur in man (Peterson 1993).
Dioxins have been reported to cause developmental toxicity in mammals including
decreased growth, structural malformations, functional alterations and
prenatal mortality. Functional alterations are the most sensitive including
effects to the male reproductive system and male reproductive behaviour
in rats, and neurobehavioural effects in monkeys (Peterson, 1993). Similar
toxic effects on development have been reported in humans exposed to high
levels of dioxins.
Effects of accidental/occupational
exposure
In humans, exposure to dioxins during gestation can result in toxicity
to the developing foetus with effects including foetal death, structural
malformations, organ dysfunction and growth retardation. In the Yusho and/or
Yu-Cheng incidents in Japan and Taiwan, in which people consumed rice oil
contaminated with PCDD/Fs and PCBs, all of these outcomes occurred (Kuratsune
1989, Rogan 1989, Yamashita and Hayashi 1985). Increased incidence of prenatal
mortality and low birth weight were observed suggesting foetal growth retardation
had occurred (Peterson 1993). Organ dysfunction involving the central nervous
system (CNS) characterised by developmental delay or psychomotor delay,
including impairment of intellectual development, was reported to occur
in children born to mothers exposed in the Yu-Cheng incident (Rogan Fet
al. 1988, Hsu et al.). Although it can be concluded from these studies
that transplacental exposure to PCDD/Fs and PCBs can affect CNS function
postnatally, it is difficult to delineate which congeners were responsible
(Peterson 1993). This is because some PCB congeners exert their effects
through the Ah receptor, but other non TCDD-like PCBs are thought to act
through a different mechanism. However, experiments in mice and monkeys
do suggest that TCDD-like PCB congeners and dioxins that exert their effects
through the Ah-receptor are probably involved in producing the observed
postnatal neurobehavioral effects in humans (Peterson 1993).
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).
Studies of effects on humans at current background
levels
In humans, of particular concern are studies which have recently been conducted
on current background exposure to dioxins and PCBs. Inuits from Arctic
Quebec have a relatively high body burden of PCDD/Fs and PCBs due to their
diet, largely from sea mammals and fish. A study was undertaken to test
whether in utero exposure to PCDD/Fs and PCBs effected the health status
of Inuit newborns. Results showed that newborn males were born smaller
than females. The height of the males correlated negatively with levels
of both PCDD/Fs and
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).
Reproductive Toxicity
In sexually mature laboratory mammals, effects of TCDD on the reproductive
system have only been observed at relatively high doses, which are usually
toxic to the animal. The most sensitive signs of reproductive toxicity
in male and female mammals is a decrease in spermatogenesis (sperm count)
and the ability to conceive and carry a pregnancy (Peterson, 1993). Other
effects include reduced testis and accessory sex organ weights, abnormal
testis structure, reduced fertility, decreased testicular testosterone
synthesis and other sex hormone effects. In females, reduced fertility,
reduced litter size and effects on female gonads and menstrual cycle have
been reported (Peterson 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 the immune system
Evidence from numerous animal studies and some epidemiological studies
in humans has shown that the immune system is a target for PCDD/Fs and
PCBs. This is of concern because the function of the immune system is to
maintain health, and if immune system functioning is impaired, this can
result in an increase in the incidence of infectious diseases and some
types of cancer. Evidence from animal studies suggests there are multiple
cellular targets within the immune system that are altered by TCDD. Also,
it appears that TCDD can indirectly effect the immune system, for example,
by altering the activity of certain hormones (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.
Carcinogenicity
TCDD has been reported to be the most potent rodent carcinogen yet tested
(Skene et al, 1989). Animal studies have provided conclusive evidence that
TCDD is a multistage carcinogen, increasing the incidence of tumours at
sites distant from the site of treatment (US EPA 1994). Although animal
studies provide substantial presumptive evidence of the human carcinogenicity
of TCDD, actual validation must include evidence from human studies (US
EPA 1991). Unfortunately, some epidemiological studies in humans have been
flawed by methodological limitations such as no direct measurements of
dioxins in blood or tissue to adequately characterise the dose, small sample
size, lack of a control group with a lower dioxin body burden, and an inadequate
latency period after exposure for the development of cancer (Schecter 1991).
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.
Risk Assessment
For the purposes of risk assessments from PCDD/Fs there is general agreement
that the international toxicity equivalence factor (I-TEF) which has been
established by NATO/CCMS should be used (Kutz et al, 1988, NATO/CCMS A6,
1989). Nevertheless, some national risk assessments and regulations still
use their own Toxicity Equivalency Factors. Tolerable Daily Intake (TDI),
is used in risk assessment to define maximum dose levels for lifelong daily
exposure that may be regarded as being not detrimental to human health.
The World Health Organisation (WHO) and Health and Welfare Canada have
set a tolerable daily intake for PCDD/Fs of 10 pg dioxin or equivalents
per kg body weight (pg/kg/d) (WHO/Euro 1991, Gilman et al. 1991, respectively).
US EPA employs a different method of risk assessment in which an Acceptable
Daily Intake (ADI) is calculated based on an increased lifetime cancer
risk of one in a million. The US ADI is 6fg/kg/d (Greenlee et al. 1991),
which is considerably lower (1670x) than the WHO and Canadian TDI. This
clearly demonstrates the large scientific uncertainty in risk assessment
methodology. The different methods adopted by US EPA, Health and Welfare
Canada and WHO are discussed below.
WHO and Health and Welfare Canada method of risk assessment
WHO and Health and Welfare Canada use the Safety Factor Model to calculate
risk assessment. This model assumes that there is a threshold or level
of dioxin, (known as a no adverse effect level),(NOAEL), below which no
deleterious effects on health occurs.
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]
US EPA method of risk assessment
US EPA uses the cancer statistical method of risk assessment, which calculates
an excess lifetime risk of cancer for a given exposure to dioxin. It has
been calculated that an exposure of 6 fg/kg/day 2,3,7,8-C4DD in humans
will be associated with an increased lifetime cancer risk of one in a million.
The mathematical model used by US EPA for calculating risk assessment is
the Linear Multistage Model. In this model, the dose-response curve for
excess carcinogenic risk, is assumed to be linear through to dose zero.
In other words, the model assumes that there is not a threshold (or level)
below which no deleterious effect on health occurs. Therefore, the model
does not predict a no adverse effect level (NOAEL) for dioxin.
WHO and Canadian assumptions
For the average North American exposure to dioxins is thought to be about
2-4 pgTEQ/kg/day. Since this is less than the TDI, the Canadian government
concludes that the average citizen is adequately protected (Gilman et al.
1991, Feeley and Grant 1993). WHO (1990) estimated exposure to dioxins
for the general population was approximately 1.9 pgTEQ/kg/ day and it would
therefore seem that the population was adequately protected by the TDI.
However, there is not general agreement about using the safety factor
model for risk assessment of dioxins, which is based on the following assumptions:
-
Dioxin has a threshold, a level below which no deleterious effect occurs.
-
Experiments used in risk assessment identified the most sensitive end-points.
-
Relative effects in animals and humans can be adequately compared based
on average daily dose, even for persistent compounds like dioxin which
accumulate in the body, rather than on body burden.
Recent research, mostly carried out by US EPA in the reassessment of dioxin,
indicates that these assumptions are not consistent with current data.
Therefore, the TDI proposed by WHO and Health and Welfare Canada may not
be valid. The three assumptions are discussed below.
1. Dioxin thresholds?
WHO and Health and Welfare Canada argue that dioxin has a threshold because
(a) no observed adverse effect levels have been identified in risk assessment
experiments (b) TCDD is a tumour promotor and does not damage DNA (c) effects
of TCDD are mediated by a receptor (WHO 1992, Feeley and Grant 1993).
(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 factor
(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."
It 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.
2. Most sensitive end-points in risk assessment
The WHO and Canadian TDI depends on the assumption that the experimental
effects they considered are the most sensitive endpoints. Recent research
on laboratory animals, however, shows that dioxin causes effects at lower
doses than previously thought. This is clearly illustrated by an experiment
which found that chronic low dose exposure to TCDD in rhesus monkeys caused
endometriosis (Rier et al. 1993). Endometriosis is a non-cancerous condition
which occurs in humans and nonhuman primates, characterised by growth and
proliferation of endometrial cells at sites outside the uterus, and is
associated with chronic pain and infertility. Although its cause is unknown,
endometriosis is thought to involve the immune system and regulation of
hormones, both effects consistent with the action of dioxin-like compounds.
A previous study has also described an association between exposure to
PCBs and endometriosis (Campbell et al 1985).
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.
3. Body burden
Risk assessment proposed by the WHO and Health and Welfare Canada assumes
that relative effects in rats and humans can be compared on average daily
dose. However, dioxins are persistent and accumulate in the body. It is
very probable that biological effects depend on concentrations present
in a target organ over a critical period of time rather than on dose.The
limited evidence regarding the relative response of human and animal cells
exposed to the same concentration of TCDD suggests that humans are no less
sensitive to certain biochemical effects than rats (Lucier et al. 1991).
This conclusion was also reached by Birnbaum et al. (1993) from the EPA's
research team:
"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.
4. Future Risk Assessment
US EPA is currently re-evaluating the risk of exposure to dioxin using
more mechanistically based models in a so called "biological basis for
risk assessment". Lucier et al (1993) have suggested that for all future
risk assessments, modelling biological phenomena should include risk assessment
at the organism level (eg) survival, the tissue level (eg) carcinogenicity
and at the cellular and biochemical level. At the biochemical level, because
TCDD appears to act like a potent and persistent hormone agonist, information
on receptor mediated events should be included in risk assessment. Additionally,
since PCDD/Fs cause reproductive/developmental effects and endocrine toxicity
it is suggested that non-cancer endpoints should be included for biological
based models of risk assessment.
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.
5. Formation and sources: dioxin and chlorine chemistry
Dioxin is not manufactured on purpose but it is formed as an
unintentional by-product in many processes in which chlorine and
chlorine-derived chemicals are produced, used, and disposed of.
The major primary sources of dioxins include combustion
processes, especially municipal waste incinerators, and
industrial processes such as the pulp and paper industry and the
manufacture of organic and inorganic chlorinated chemicals.
Table 3 lists known and suspected dioxin sources identified in
scientific literature and by government agencies.
Combustion sources
Incinerators
Incinerators of all kinds are known to emit dioxins. A number of
studies in Europe, USA, Canada and Asia have demonstrated the
presence of PCDD/Fs in fly ash and flue gas from municipal waste
incinerators (Rappe & Buser 1989). Studies by Vogg and Stieglitz
(1986) showed that particulate carbon can react with oxygen and
inorganic chlorines with copper (II) as a catalyst to form
organochlorine compounds including dioxins and furans, and
concluded that this de novo synthesis is the primary source of
dioxins/furans produced in municipal waste incineration. Studies
have shown that fly ash from refuse incinerators and elements
such as chlorine, zinc, potassium, copper and sodium may act as
catalytic agents for increased dioxin formation (Hinton & Lane
1991, reviewed by Fielder et al. 1990). controlled inputs of
these elements into incineration feedstock may therefore lead to
unpredictable levels of dioxins being formed.
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 chemicals
Production of
chlorine gas
| Chlorine electrolysis with graphite electrodes
Chlorine electrolysis with titanium electrodes |
Chemical industry
- use of chlorine gas
| Chlorinated aromatic chemicals -- manufacture (chlorobenzenes, chlorophenols, PCBs others)
Pesticides
Dyes
Speciality chemicals
Chlorinated solvents -- manufacture (trichloroethylene,
tetrachloroethylene, carbon tetrachloride)
PVC plastic -- manufacture of feedstocks (ethylene dichloride,
vinyl chloride)
Production wastes
Effluent
Sludge from effluent
treatment
Air emissions
PVC plastic products
Other aliphatic organochlorines -- manufacture (epichlorhydrin,
hexachlorobutadiene)
Some inorganic chlorides -- manufacture (ferric and copper
chlorides, sodium hypochlorite) |
Uses of chlorine gas
-- other industries
| * Pulp and paper -- chlorine bleaching
Mill effluent
Mill sludge
Pulp and paper products
Emissions from sludge incinerators
Water and wastewater disinfection
Refined metals -- manufacture with chlorine (Ni, Mg) |
| Use of organochlorines
|
Manufacture of chlorine-free chemicals with chlorinated
intermediates (nitrophenols, parathion, others)
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 |
Incineration, Recycling and Fires
(primary dioxin precursor in
parentheses)
|
* Medical waste incinerators (PVC) Air emissions
* 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)
|
Environmental
transformation
|
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.
Vehicle fuels
Cars are a significant source of dioxins in the urban
environment and near major roads (see eg Ballschmiter et al.
1986, Bingham et al. 1989). It has been estimated that in 1988
the emissions of PCDD/Fs from cars in the UK would have been in
the region of 700g/year. However, since the decline in use of
leaded petrol, the emissions could have declined to half that
amount. The dioxin produced by burning leaded petrol is due to
the addition of dichloroethane as a scavenger (Marklund et al.
1987). Where analysis of emissions from a variety of vehicles
has been carried out, leaded petrol was found to cause the
highest emissions, followed by unleaded petrol. Dioxins were not
detected from diesel vehicles (Markund et al. 1990). This was
thought to be largely due to the far lower content of chlorine
in diesel fuel (0.61ppm) compared with unleaded gasoline (14ppm)
and leaded gasoline (63ppm). However, another contributing
factor might be the chlorinated materials in engine lubricant
oils which contain high levels of chlorine (290-310ppm) and in
which PCDD/Fs are detectable (Marklund et al. 1990, Ballschmiter
et al. 1986). Rotard et al. (1987) also reported ppb levels of
PCDD/Fs in oils which are recycled and resold as lower priced
products. This is indicative of the hazards of recycling
hazardous wastes.
"Natural" Combustion Sources
Bumb et al. (1980) first reported that natural combustion
sources produce PCDD/Fs. Indeed, combustion is the most likely
source for preindustrial dioxin generation, which has been
widely reported (see eg Ligon et al. 1989, Hashimoto et al.
1990, Czuczwa & Hites 1984 and 1985). Subsequently it has been
claimed that sources such as domestic and industrial coal
burning contributes a large proportion of total emissions (eg
Harrad and Jones 1992b). However, studies of atmospheric
emissions from coal-burning power plants did not detect any
PCDD/Fs (US EPA 1987, Fiedler et al. 1990). Evidence from
sediment cores from the Great Lakes (Czuczwa & Hites 1985)
indicates that the increase in dioxin concentrations in the
environment correlate not with coal consumption but with
production of chlorinated aromatic compounds. This would argue
against coal combustion being as significant a source as some
researchers believe. Similarly, dioxin releases from forest
fires/wood burning are probably due to contamination of the wood
by phenoxyherbicides (Fiedler et al. 1990) or from resuspended
material from aerial deposits (Schaum 1993). A study by the
German EPA reported that ash from the combustion of
chlorine-free materials such as wood, paper, and chlorine-free
plastics contained undetectable or extremely low concentrations
of dioxin, but after combustion of chlorinated plastics,
chlorinated solvents and pesticides produced much higher
concentrations dioxin were detected, as shown in Table 4, (Pohle
1991). Also, Danish studies indicate that the high dioxin
emissions reported to occur from wood stoves were caused by the
burning of wood impregnated with the wood preservative
pentachlorophenol (Vikelsoe, 1993).
Industrial sources
Processes in the pulp and paper industry
Large amounts of chlorine or chlorine compounds are used in the
pulp and paper industry for bleaching the pulp. Fiedler et al.
(1990) have reviewed the pulping process and the stages at which
dioxins are released. Dioxins are present in the effluent,
sludge and the pulp itself with atmospheric emissions being less
significant. Increasing the amount of chlorine dioxide used
compared to chlorine gas does considerably reduce dioxin
emissions, but not eliminate them. WHO (1990) recommended that
other bleaching processes which do not use chlorine were
available and should be adopted. The aim of this would be to
reduce the levels in paper products to below 1ppt (ng/kg) TEQ to
minimise migration into food in contact with paper products.
Alternatives to chlorine are widely accepted (Harriman & Capps
1989) and totally chorine free (TCF) technologies are now
available (see eg Henricson, 1993, Kamyr 1993), which would
prevent any dioxin formation. Proponents of TCF technology point
out that not only will this technology virtually eliminate
organohaolgen emissions, but will allow closing of the bleach
plant~s water circulation, reducing the emissions of all kinds
to the aquatic environment (Kukkonen 1993).
Processes in the chemical industry
The following processes have been listed according to their
significance of potential sources of chlorinated and/or
brominated PCDD/Fs (Heindl and Hutzinger, 1986, Hutzinger et al.
1988):
- Processes to manufacture chlorophenols and their derivatives.
- Processes to manufacture chlorobenzenes and substituted chlor benzenes.
- Synthesis of aliphatic chlorine compounds.
- Methods involving chlorine-containing intermediates.
- Inorganic chlorochemical processes.
- Processes applying chlorinated catalysts and solvents.
- Processes to manufacture brominated flame-retardants (brominated biphenyls, diphenylethers, etc.)
Chlorinated aromatic chemicals
Chlorinated aromatics are used in the production of pesticides,
nylon, synthetic rubber, dyes, pharmaceuticals and speciality
chemicals for plastics. The processes of aromatic chlorination
and radical side chain chlorinations are associated with dioxin
production, eg. chlorophenols, chloronitrobenzenes and
2,3,6-trichlorophenoxyacetic acid (Hutzinger 1988). Extremely
high contamination levels are associated with chlorophenol
manufacturing facilities and associated waste disposal sites
worldwide, including the UK (Berryman et al. 1991),
Czechoslovakia (Zemek & Kocan 1991) and the USA (Cummings et al.
1987).
Synthesis of aliphatic compounds: PVC
PVC production
A series of European studies have clearly established that very
large quantities of dioxin are formed in the production of vinyl
chloride monomer, the building block for PVC. Studies found high
levels of dioxins in the environment associated with the
production of PVC (Evers et al. 1989 and 1993). The thermal
cracking of EDC can lead to substantial waste arisings of spent
copper catalyst (Norsk Hydro 1992) which is a known catalyst in
the production of dioxins.
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.
PVC incineration
PVC also contributes to dioxin formation during incineration and
has been reported as being the largest single source of chloride
in hospital waste incinerators (Marrack 1988). Several reports
have found a direct relationship between the amount of PVC in
waste fed into an incinerator and the amount of dioxin emitted
(Ozvacic 1990, Danish EPA 1993). In the Netherlands, separation
of refuse effectively removes most of the organic chlorides in
combustible materials such as food and wood wastes, leaving PVC
as the only major source of chlorine. Reducing PVC feed has been
found to result in significant decreases in dioxin emissions
(Boerekamps Kanter 1993). Based on these findings the Dutch
Environment Ministry concluded:
~These new experiments by the University of Leiden demonstrate
clearly a relation between the content of PVC in household waste
and dioxin formation in waste incinerators. On the basis of
these experiments there is no reason to reconsider present
policies regarding PVC applications: the main feature of this
policy is that PVC applications for which no feasible system of
recycling and reuse can be established the use of more
environmentally sound alternative materials is to be preferred~
(Netherlands Environment Ministry 1994).
Recycling of PVC-containing products
PVC has been identified as being responsible for dioxin
formation during the recycling of copper in copper cables
(Christman 1989), steel (Tysklind 1989, Aittola 1993) and
aluminium, lead, zinc and steel (Aittola 1993).
PVC in fires
Accidental fires at PVC factories and in offices and homes
result in high emissions of dioxins (Quebec Environment Ministry
1993, UBA 1992). In Germany, dioxin concentrations of up to
10,000 ng/m2 on surfaces from accidental fires with large
quantities of PVC have been found and concentrations of up to
200ng/m2 after normal fires in homes and offices (Fiedler 1993).
As a consequence of the release of dioxins from accidental
fires, the German EPA and Ministry of Health have proposed the
following:
"The use of plastics containing chlorine and bromine should be
completely excluded, as far as is possible. UBA and BGA propose
a ban on the use of plastics containing chlorine and bromine in
apparatus susceptible to fire, in the manufacture of chip-board,
as well as the labelling of plastics containing chlorine and if
necessary a ban of the use of PVC in packaging." (UBA 1992).
Synthesis of aliphatic compounds: chlorinated
solvents
Solvents account for approximately 10% of all chlorine
production, and are a correspondingly significant source of
dioxins. Dioxins occur in the manufacture, use and disposal of
chlorinated solvents. PCDD/Fs have been identified in the
manufacture of trichloroethylene, tetrachloroethylene and
1,2-dichloroethane in concentrations of up to 50ppt (sum
PCDD/Fs). Hexachlorobenzene has been identified in carbon
tetrachloride, trichloroethylene and tetrachloroethane (Rossberg
1986). Heindl et al. (1987) reported such results indicated
that the synthesis of short-chain chlorinated hydrocarbons can
lead to PCDD/F formation. The uses of chlorinated solvents in
metal finishing synthesis/extraction with chlorinated solvents
and dry cleaning produces dioxins (Drechler 1992). Dioxin
concentrations of 140ppt have been identified in the
distillation sludge from the use of perchloroethylene in dry
cleaning (Lexen 1992).
Inorganic chlorochemical processes
Dioxins are formed during the production of chlorine gas by the
chlor- alkali process. Older chlor-alkali facilities which use
graphite electrodes produce large quantities of dioxin.
Chlorine gas has been found to be contaminated with dioxin-like
compounds in concentrations ranging from 40 to 210 ppb
(Hutzinger 1988). High concentrations of dioxin of up to 650ppb
total PCDD/Fs have been found in the sludges from spent graphite
electrodes used in this process (Rappe 1991). It was thought
that replacement of graphite electrodes with titanium electrodes
would prevent dioxin formation during the chlor- alkali process,
but recent data from Sweden indicates that in modern
chlor-alkali plants, dioxins are still produced due to reaction
of chlorine with trace quantities of organic materials found
mainly in plastic pipes and valves (Andersson 1993). These
results are presented in Table 7
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).
Processes involving chlorinated
intermediates: pesticides
96% of all synthetic organic pesticides contain chlorine or are
manufactured using chlorinated intermediates (CRA 1993).
Consequently, dioxins would be expected to occur as by-products
in the manufacture of virtually all synthetic pesticides
including chlorophenols, chlorophenoxy acetic acids,
dichloropropene, lindane, atrazine and simazine. Dioxins and
furans have been detected in the widely used chlorophenoxy
herbicide 2,4-D in the US at a concentration of 160 ppt (TEQ)
(Schecter 1993). In the production of lindane from
hexachlorocyclohexane (HCH) PCDD has been found in the ppm
range, and Cl8DD up to 32mg/kg (reviewed by Fiedler et al.
1990). p-chloranil (tetrachlor-1,4- benzoquinone) is used as a
fungicide and seed disinfectant and has been found to be highly
contaminated with PCDD/Fs (Christman et al. 1989).
Metallurgical processes
Elemental chlorine gas used in the production of certain metals
combines with any organic material present to form
organochlorine by-products, including dioxins. High
concentrations of dioxins and related compounds have been
identified in the emissions from several types of metal
processing plants.
Dioxins may be formed when chlorine is used in the production of
refined nickel and magnesium. Annual emissions from one
magnesium plant in Norway 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.
Phasing out dioxins
Recent laboratory and epidemiological research, much of it carried out
under the auspices of the USEPA-s reassessment of the toxicity of dioxin,
indicates that environmental contamination with PCDD/Fs has reached a critical
level. It is becoming clear that the general human population and particularly
those with a higher than average exposure to dioxin, for example from diet,
are at risk from being affected by the dioxin contamination built up over
a lifetime of exposure. Unborn and young children are most at risk. The
size and longevity of the current global dioxin burden means that all sources
of dioxin contamination must ultimately be eliminated if any significant
lowering of human exposure levels is to be achieved. This will necessitate
the phase-out of all chlorine manufacture and uses.
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 between
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."
The 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:
"[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.
Immediate priorities: major dioxin sources
Since all uses of chlorine and chlorinated organic chemicals are suspected
of dioxin formation at one or more points in their life cycle, the phase-out
of dioxins necessitates phase-out of all chlorine chemistry.
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:
1. Incineration and other combustion
sources
Firstly, no permits for new combustion facilities that burn chlorinated
wastes and products should be issued. Secondly, existing permits should
include timetables for eliminating all dioxin releases. Finally, the addition
of chlorinated compounds to fuels, including gasoline and motor oils should
be immediately phased out.
2. Pulp and paper
Alternative technology is available in the pulp and paper industry for
bleaching (Harriman & Capps 1989). Presently, oxygen based and other
non-chlorine based bleaching methods are available and in increasing use
(see eg Henricson 1993, Kukkonen 1993). Chlorine use in this industry is
therefore possible to avoid and should be phased out.
3. PVC
A PVC phase-out programme should be established with progressive reductions
towards zero for the production and use of PVC. A ban on short life PVC
uses such as packaging, toys and non-essential medical supplies should
be implemented immediately. All uses of PVC in areas susceptible to fire
and products subject to combustion based recycling should be prioritised
in time lines for phase-out.
4. Chlorinated aromatic chemicals
A phase-out programme should be established, especially concentrating on
open uses (ie.) pesticides and substances such as 1,4-dichlorobenzene which
are in globally widespread domestic use.Products which are associated with
the production of highly dioxin- contaminated wastes, such as the chlorophenols,
should be prioritised.
Secondary actions
Phasing out all uses of chlorine and chlorinated organic chemicals involves
significant economic and technological change that will require phased
implementation. While immediate action should be given to priority sectors
listed above, the following dioxin producing sectors should be placed on
time lines for phase-out, with schedules based on magnitude of releases.
Those for which alternatives are available should be phased out rapidly
and research for alternatives in other applications must be given a high
priority.
1. Chlorinated solvents
A timetable for the phase-out of production and use of all chlorinated
solvents should be established. Alternatives for chlorinated chemicals
such as intermediates, catalysts and speciality chemicals should be developed.
Some chlorine-free alternatives to chlorohydrin and phosgene intermediates
have already been developed (Robert 1994).
2. Chlorine-related pesticides
A phase-out timetable should be initiated. The National Academy of Sciences
reported that farmers can adopt organic farming methods, reduce or eliminate
the use of synthetic pesticides and still enhance their profits and crop
yields (NAS 1989).
3. Metallurgy
The use of chlorine in high temperature metallurgy should be phased out.
4. Water and wastewater treatment
Alternatives to using chlorination in drinking water and sewage include
ultraviolet light, ozone, hydrogen peroxide, slow sand filtration and membrane
filtration. Time lines for the implementation of chlorine -free water treatment
methods should be set while insuring that adequate disinfection continues.
5. Remediation
A substantial quantity of dioxin and PCB contaminated materials are present
in landfills, sediments and stored industrial wastes. Closed-loop methods
for degradation of these materials are in many cases highly developed (eg
Jain 1993, review by Picardi et al. 1991) and could be implemented far
more widely.
Economic implications
Phasing-out dioxin sources will require substantial technological and economic
transformation, as numerous products and processes are removed from production
or converted to chlorine-free alternatives. Although this conversion will
require substantial investment in some sectors, most of the alternative
products and processes provide economic benefits in terms of increased
employment, improved efficiency, decreased expenses for chemical conversionprocurement,
waste disposal, liability and remediation, and the elimination of the 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.
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