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Science
This report provides a summary of new scientific research on the toxic effects caused by or associated with exposure to dioxin. The information in this report is drawn from a comprehensive assessment of the sources, fate, and health effects of dioxin contained in the Technical Support Document (TSD) to this report. The key points and conclusions of the TSD provide the basis for this report. Most of the research and studies discussed in this report have been published since a well publicized draft report on dioxin was released by the U.S. Environmental Protection Agency (EPA) in 1994. The American People's Dioxin Report is intended to inform the public and their representatives in government so appropriate action can be taken to safeguard the health of the American people. The scientific findings of this report make it clear that there is an extensive body of high quality scientific information describing the toxic effects of dioxin in people. This data indicates that dioxin is a potent chemical that produces a wide variety of toxic effects in animals and that some of these effects are occurring in people.
The report's most striking finding is the impact of dioxin on the growth and development of children. Most of the new studies on dioxin address its effects on children, notably the effects on the development of the immune, reproductive, and nervous systems, in particular cognitive and learning abilities. While exposure of the general population occurs through ingestion of many common foods, children exposed in utero (in the womb) during critical periods of development appear to be the most sensitive and vulnerable to the toxic effects of dioxin.
In particular, dioxin has been associated with IQ deficits and increased susceptibility to infections in Dutch children exposed to "background" levels of dioxins. (These "background" levels are essentially the average daily intake of dioxin from food.) Studies in Finland have shownthat dioxin interferes with normal tooth development in infants exposed to "background" levels. The Dutch studies have also shown an association between dioxin and a higher prevalence of withdrawn/depressed behavior in children. An association between PCBs and adverse effects on attentional processes and an increase in hyperactive behavior in children has also been reported in these studies.
This new evidence from human studies provides strong confirmation of the toxicity of dioxin and its impact on the general American public. With this in mind, Americans have a choice: take action to protect public health by eliminating dioxin creation or continue to allow dioxin to be created and not burden industry with the short term transition costs of elimination. Prudent public health policy would make every effort to eliminate environmental releases of dioxin and related compounds.
Description of Dioxin
Dioxin belongs to a family of chemicals with related properties and toxicity. There are 75 different dioxins, or polychlorinated dibenzodioxins (PCDDs), 135 different furans, or polychlorinated dibenzofurans (PCDFs), and 209 different polychlorinated biphenyls (PCBs). Each different form is called a "congener."
Not all of the "dioxin-like" chemicals have dioxin-like toxicity, and the toxic ones are not equally toxic. Only 7 of the 75 dioxins, 10 of the 135 furans, and 12 of the 209 PCBs have dioxin-like toxicity. These 29 different dioxins, furans, and PCBs all exhibit similar toxic effects caused by a common mechanism: binding to a particular molecule known as the aryl hydrocarbon or "Ah" receptor (see Chapter 5 of the TSD).
It is believed that the tighter the binding to the Ah receptor, the more toxic the chemical. The most potent member of this family is 2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD, which also has the greatest affinity for the Ah receptor.
The word "dioxin" is often used imprecisely. Some people restrict its use only to 2,3,7,8-TCDD, the most toxic and most studied dioxin. Others extend its use to the whole class of chemicals with similar toxicity and whose effects are controlled or triggered by the Ah receptor. In this report, the terms "dioxin" and "dioxins" are used to refer to any of the dioxin family members that bind to the Ah receptor and elicit dioxin like effects.
Toxic Equivalents
Although all dioxin-like compounds are thought to act in the same way, they are not all equally toxic. Their different toxicities may be due to their unique properties of absorption, distribution, metabolism, and elimination in a body and/or strengths of binding to the Ah receptor. Therefore, the health risk of each congener is assessed by rating their toxicities relative to TCDD, the most potent of the dioxins. TCDD is assigned a value of "1" and each of the 17 toxic dioxins/furans and 12 PCBs is assigned a "toxicity factor" that estimates its toxicity relative to TCDD. The resulting estimates are called toxic equivalency factors (TEFs), which have been recently updated by the World Health Organization.1 The toxic equivalency (TEQ) is determined by multiplying the concentration of a dioxin congener by its toxicity factor. The total TEQ in a sample is then derived by adding all of the TEQ values for each congener. While TCDD is the most toxic form of dioxin, 90% of the total TEQ value results from dioxin-like compounds other than TCDD.
The TEQ system is not perfect, but it is a reasonable way of estimating the toxicity of a mixture of dioxin-like compounds. There is good experimental support for the assumptions that underlie the TEQ system.1,2 TEQs make it possible to take toxicity data on TCDD, a compound about which our knowledge is vast, and estimate toxicity for other compounds about which much less is known.
Sources of Dioxins
Dioxin is found everywhere in the world - in water, air, soil, and sediment - even in places where dioxin or dioxin-containing products have never been used. This broad distribution is evidence that the sources are multiple and that dioxins can travel long distances. Unlike most chemicals, dioxins have no intended use or value. Dioxins are unintended by-products of many chemical and combustion processes which involve chlorine. They get into the environment from industrial air emissions, wastewater discharges, disposal activities, and from burning material that contains chlorine. The EPA estimates that 2,745 grams (gm) TEQ released into the air each year.3 Municipal solid waste incinerators, secondary copper smelting, and medical waste incinerators are identified as the top three sources of dioxin released into the air. Combustion sources account for nearly 80% of air sources. Dioxins are also released to water, soil and into consumer products, but these sources are poorly defined and only a few estimates have been made. A list of EPA's dioxin sources is shown in Table 1.
In developing a "national inventory" of dioxin sources, EPA only made estimates for 20 of 54 identified air source categories, due to their lack of confidence in the available data.3 Preliminary estimates are made for 12 of the 34 poorly defined source categories, but these estimates are not included in the national inventory. EPA assigned "negligible" emissions to another 11 of these source categories and made no estimates for another 8 source categories even though there is some evidence of emissions. Overall, EPA's confidence in the data used to define dioxin releases to air, water, land, and products is weak and underestimates dioxin releases.
Source categories that are left out of EPA's dioxin inventory include iron ore sintering, polyvinyl chloride (PVC) production, accidental/structural fires, landfill fires, backyard burning, releases from petroleum refineries, asphalt mixing plants, and contaminated sites and other "reservoirs" of dioxin. Regrettably, there are apparently no efforts to collect such data from these and other sources. Some of these source categories, if included, would contribute substantially to the national inventory and significantly increase the amount of dioxins estimated to be released into the environment.
Environmental Fate
Dioxins enter the atmosphere either directly from air emissions or
indirectly from volatilization from land or water, or from resuspension of
particles. Depending on temperature and each congener's vapor pressure,
dioxins are present in air as particulates or vapor. The more chlorinated
compounds tend to bind to particulates and are protected from chemical and
sunlight degradation. This protection may account for their relative
abundance in the environment.
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| Table
1
Inventory of Sources of Dioxin in the United States |
|
| Reference Year 1995 | Central
estimate
(gm TEQ/year) |
| Air: | |
| Municipal waste incineration | 1,100 |
| Secondary copper smelting | 541 |
| Medical waste incineration | 477 |
| Forest, brush and straw fires | 208 |
| Cement kilns (hazardous waste burning) | 153 |
| Coal combustion | 72.8 |
| Wood combustion - residential | 62.8 |
| Wood combustion - industrial | 29.1 |
| Vehicle fuel combustion - diesel | 33.5 |
| Cement kilns (non-hazardous waste burning) | 17.8 |
| Secondary aluminum smelting | 17 |
| Oil combustion - industrial/utility | 9.3 |
| Sewage sludge incineration | 6 |
| Hazardous waste incineration | 5.7 |
| Vehicle fuel combustion - unleaded | 6.3 |
| Kraft recovery boilers | 2.3 |
| Secondary lead smelters | 1.63 |
| Cigarette combustion | 0.81 |
| Boilers/industrial furnaces | 0.38 |
| Crematoria | 0.24 |
| Total | 2,745 |
| Products: | |
| Pentachlorophenol-treated wood | 25,000 |
| Bleached chemical wood pulp and paper mills | 24.1 |
| Dioxazine dyes and pigments | 0.36 |
| 2,4-Dichlorophenoxy acetic acid | 18.4 |
| Non-incinerated municipal sludge | 7 |
| Total | 25,050 |
| Land: | |
| Non-incinerated municipal sludge | 207 |
| Bleached chemical wood pulp and paper mills | 1.4 |
| Total | 208 |
| Water: | |
| Bleached chemical wood pulp and paper mills | 19.5 |
| Source: USEPA 3 | |
Airborne dioxins can be carried large distances downwind from
their sources as well as contribute significantly to local deposition.4,5
Eventually, airborne dioxins settle onto soil, plants, and water where they
enter the food chain. Dioxin will fall out onto crops that are fed to dairy
cows and beef cattle where it accumulates in the milk and meat of these
animals. Dioxin is attracted to and accumulates in fat. People who consume
the contaminated meat and dairy products ingest substantial amounts of
dioxin. When dioxin falls out onto waterways, it settles in sediments or
remains suspended in the water for long periods of time because dioxins
generally do not dissolve in water. Here too, the dioxins move up the
aquatic food chain to fish and then into people.
Dioxin in Food
Americans accumulate harmful levels of dioxins in their bodies mostly through the ingestion of food. Some segments of the population, such as nursing babies and people who eat a diet high in animal fat or foods contaminated because of their proximity to dioxin release sites, are exposed to higher than average levels of dioxin.6 Others, such as Vietnam veterans and some chemical plant workers, have accumulated additional dioxins because of their exposure to Agent Orange or other dioxin-contaminated chemicals in the workplace.7
Approximately 90%,6,7 and perhaps as much as 98%, 8
of the dioxin that average Americans are exposed to comes from the foods
they regularly eat. Because dioxins accumulate in fatty tissue, they are
found mostly in meat, fish, and dairy products. Consequently, when people
consume these foods, they also consume dioxins. As Table 2 shows, ground
beef has the highest dioxin content, with 1.5 picograms per gram (pg/gram)
which is equivalent to 1.5 parts per trillion (ppt), of all meats consumed
by Americans. Depending on what and how much people eat, the average daily
intake of dioxins for Americans is approximately 2.2 pg TEQ/kg body weight
(bw),9 ranging from 1 to 3 pg TEQ/kg bw.10 Daily
intake increases to 3 to 6 pg TEQ/kg bw if dioxin-like PCBs are included.
The ingestion of dioxin in common foods has resulted in widespread
low-level exposure of the general population.
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| Table 2 - Dioxin Levels in U.S. Foods | |
| Food Type | Total TEQ (pg/gram food) (ppt) |
| Ground beef | 1.5 |
| Soft blue cheese | 0.7 |
| Beef rib steak | 0.65 |
| Lamb sirloin | 0.4 |
| Heavy cream | 0.4 |
| Soft cream cheese | 0.3 |
| American cheese sticks | 0.3 |
| Pork chops | 0.3 |
| Bologna | 0.12 |
| Cottage cheese | 0.04 |
| Beef rib/sirloin tip | 0.04 |
| Chicken drumstick | 0.03 |
| Haddock | 0.03 |
| Cooked ham | 0.03 |
| Perch | 0.023 |
| Cod | 0.023 |
| Source: Schecter 26 | |
Dioxin Body Burden Levels
The average daily intake of dioxin results in an average dioxin tissue concentration in Americans that ranges from 28 to 41 nanograms (ng) TEQ/kg lipids (fat) and from 36 to 58 ng TEQ/kg lipids if dioxin-like PCBs are included.11,12 A single national average of 28 ng TEQ/kg or 28 ppt was estimated as part of the most extensive survey of dioxin in humans, the National Human Adipose Tissue Survey (NHATS). This survey was first conducted by the EPA in 1982.13 In 1987, the survey was repeated, and the results suggest some decreases in average dioxin body burdens, but the decreases may be due to improved analytical methods or to other issues involving methods of study. For most congeners, including TCDD, the differences between 1982 and 1987 tissue levels are not statistically significant.14
In addition to measuring exposure to dioxin by its daily intake, exposure can also be estimated by measuring how much of it builds up in the body. This is referred to as the "body burden" and is defined as the total accumulation of dioxin at any one time per kilogram of body weight.11 For a person this would be how much they have accumulated up to the time of the testing. Using the average tissue concentrations from the studies above, estimated average dioxin body burdens range from 6 to 9 ng TEQ/kg body weight. If dioxin-like PCBs are included, the average dioxin body burden ranges from 8 to 13 ng TEQ/kg body weight.11 In these estimates, TCDD contributes approximately 15% of the total TEQ.
These estimates represent average body burdens for a middle-aged person. Approximately 10% of the population can be expected to have at least three times this level and others as much as seven times these levels. These high exposure groups include nursing infants, children, some workers and farmers, people who rely on fish as a main staple of their diet such as some indigenous peoples and some fishermen, and people who live near dioxin-contaminated sites or dioxin-producing facilities. These groups have suffered a disproportionate share of dioxin exposure and many have already suffered the adverse health effects caused by these exposures.
Indigenous peoples, for instance, who eat fish and sea mammals from the
Arctic regions are exposed to dioxin at higher than average levels because
dioxin and PCB levels are particularly high in these foods.15
Dairy cows, meat cattle, or other animals fed crops grown on soil
contaminated with dioxin in the low part per trillion (ppt) levels
accumulate significant amounts of dioxins.16 An incinerator in
the Netherlands that emitted large amounts of dioxins contaminated milk
from cows grazing nearby. This milk was so contaminated that it was
declared to be hazardous waste by the Dutch government.17 On the
other hand, vegetarians, who consume less meat and dairy products, have
below-average body burden levels of dioxin.18
Dioxin in Breast Milk
Dioxin accumulates in breast milk because it readily dissolves in the
milk's rich fat content. During nursing, dioxin is transferred from mother
to baby 19, 20, 21, 22, 23, 24 who may absorb as much as 95% of
the dioxin in the milk.19, 20 Several studies reporting dioxin
in human breast milk indicate that levels range from 20 to 30 ng TEQ /kg
lipids in industrial countries and from 3 to 13 ng TEQ/kg lipids in less
industrialized countries (Table 3).6, 7 The World Health
Organization (WHO) reports a worldwide mean of 20 ng TEQ/kg lipids, with
values ranging from a low of 3.1 ng TEQ/kg lipids to a high of 110 ng TEQ/kg
lipids.25
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| Table 3 - Dioxin Levels in Pooled Breast Milk Samples from Various Countries | |
| Country | Total TEQ (ng/kg, lipid) |
| Vietnam - Da Nang | 34 |
| Japan | 27 |
| Germany | 27 |
| Canada | 26 |
| USA | 20 |
| Vietnam - Ho Chi Minh City | 19 |
| South Africa - White | 13 |
| Pakistan | 13 |
| Russia | 12 |
| South Africa - Black | 9 |
| Vietnam - Hanoi | 9 |
| Thailand | 3 |
| Cambodia | 3 |
| Source: Schecter, 1994 7 | |
Nursing infants ingest considerably more dioxins each day than
adults. Studies in the U.S. and in the Netherlands have estimated daily
intake of dioxins according to infant age. The U.S. study found that
nursing infants typically consume between 35 and 53 pg TEQ/kg body weight (bw)
per day in breast milk.26 The more current Dutch study found
that nursing infants typically consume about 112-118 pg TEQ/kg bw/day.27
If the Dutch study is correct and infants consume dioxin at the rate of
about 112-118 pg TEQ/kg bw/day, and adults typically ingest between 3 and 6
pg TEQ/kg bw/day,10 then nursing infants consume about 50 times
more dioxin per day than adults, confirming results from other studies.15,
26 It is estimated that approximately 10-14% of total lifetime
exposure can occur via nursing.27, 28Breast-fed babies
accumulate far more dioxins than do formula-fed babies. In one study,
dioxin intake was 50 times greater in breast-fed infants than it was in
formula-fed infants.23 In this same study, TEQ concentrations in
blood from 11 month old formula-fed infants were less than one fourth the
concentrations of the mother's blood and about 10 times less than the
concentrations in infants that are breast-fed for six to seven months.
Although nursing infants are at increased risk because of their higher intake of dioxins, extensive studies in the Netherlands indicate that the benefits of nursing outweigh the risks. Breast milk contains all the nutrients in ideal proportion for optimum growth and development; the psychological benefits of nursing are invaluable; 29 and breast-fed babies have fewer respiratory illnesses, fewer skin problems, cry less, have fewer allergies, and are less constipated than other babies. For these and other reasons, despite the dioxin levels found in breast milk today, the World Health Organization (WHO) and the federal Agency for Toxic Substances and Disease Registry (ATSDR) both promote and support breast feeding.6, 10
A "Safe" Level of Dioxin
Three separate government agencies have established a "safe"
or tolerable daily dose of dioxins. These guideline values are shown in Table
4. The table also
shows how much dioxin exposure is "allowed" according to the
guideline. This value is determined by multiplying the guideline value, in
picograms per kilogram (pg/kg) of body weight, by the body weight of an
average person, which is typically 70 kilograms or about 150 pounds. For
example, to convert ATSDR's Minimum Risk Level, multiply 1 pg/kg by 70 kg
which results in 70 pg. This means that any daily intake greater than 70 pg
would exceed the lowest measure of safety set by ATSDR. As the table shows,
the average daily dioxin intake of the American people exceeds the two
federal government guidelines and is within the range of the international
guideline. This average daily intake is more than 200 times higher than
EPA's guideline, over twice ATSDR's guideline, and in the middle of the
range of the WHO guideline.
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| Table 4 - Daily Intake of Dioxin (TEQ) Compared to Established Guidelines | ||
| Guideline | (pg/kg bw/day) | Equivalent
Intake for 70 kg adult (pg/day) |
| USEPA Risk Specific Dose 30 | 0.01 | 0.70 |
| ATSDR Minimal Risk Level 6 | 1.0 | 70.0 |
| WHO Tolerable Daily Intake 10 | 1-4 | 70-280 |
| Average Daily Intake of Dioxin in Food in the U.S. | 2.2 | 154 |
| Range
of Daily Intake of Dioxin
in Food in the U.S. |
1-3 | 70-210 |
| Range of Daily Intake of Dioxin and Dioxin-Like PCBs in Food in the U.S. | 3-6 | 210-420 |
According to the EPA, the American people's lifetime risk of getting
cancer from exposure to dioxin is 1 in 10,000.30 The risk
attributable to dioxin for highly exposed members of the population is 1 in
1,000. These risk estimates are based on ingesting a "risk specific
dose" of 0.01 pg TEQ/kg bw/day over a 70-year lifetime. At this dose,
there will be one additional cancer for every one million exposed people.
One cancer per million is often considered an "acceptable risk"
value.31 Since the average daily intake of dioxin ranges from 1
to 3 pg/kg bw/day (3-6 pg/kg bw/day if dioxin-like PCBs are included),
everyday the general American public is exposed to a cancer risk that is
100 to 300 times higher than the one-in-a-million "acceptable"
cancer risk. Table 4 shows that the American people are already well above
several federal and international guidelines for dioxin exposure as well as
the typical "acceptable" cancer risk value.
"Safe" Body Burdens
The biological effects of a toxin depend on the concentrations of that substance in a target organ over a critical period of time. These concentrations in turn depend on three important factors: the absorption, distribution and persistence of the toxin throughout the body. These factors help determine a person's lifetime accumulation, or body burden, of dioxin. As discussed earlier, body burden is the concentration of a substance in tissue or blood per kilogram of body weight. Because body burden measurements account for differences in absorption, distribution and persistence across species and between individuals, 32 they can be used to compare the doses needed to produce similar adverse effects in different species.
Such a comparison was made by the World Health Organization which made a list of the most sensitive adverse health effects associated with exposure to dioxin in animals. These health effects, which are shown in Table 5, are primarily effects on the reproductive and immune systems. The WHO found that the lowest observed adverse effect levels (LOAELs), which ranged from 10 to 73 ng/kg, are all within a factor of 10 of the average body burden of 10 ng/kg in the human population. The USEPA made a similar comparison in their draft reassessment report in 1994.30 The EPA included sensitive adverse effects in people, which are included at the bottom of Table 5. This table shows that adverse effects are occurring in some people with body burden levels similar to those that produce adverse effects in animals. The table also shows that the average body burden levels in the general American population is just below the levels that are causing adverse effects in animals.
Comparisons have also been made between the body burden levels of dioxin
in animals and people that result in cancer. The body burden levels of
dioxin at which exposed workers and experimental animals have higher
numbers of cancers are similar. For both the workers and experimental
animals, these body burden levels are also substantially higher than the
body burden levels of dioxin in the general human population.12, 25
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| Table 5 - Animal Body Burden Levels Associated with Sensitive Adverse Effects | ||
| Body Burden (ng/kg) | Species | Health effect (reference) |
| 10 | Mice | Adult immune suppression 33 |
| 28 | Rats | Decrease in sperm count 34 |
| 42 | Monkeys | Endometriosis 35 |
| 42 | Monkeys | Object learning 36 |
| 50 | Rats | Immune suppression 37,38 |
| 73 | Rats | Genital malformations (females) 39 |
| 14 | Humans | Altered glucose tolerance 40 |
| 14 | Humans | Decreased testis size 41 |
| 83 | Humans | Decreased testosterone 42 |
| 10 | Current average body burden in the general U.S. population | |
| Source: WHO, 1998; 10 USEPA, 1994 30 | ||
Sensitive Non-Cancer Effects Observed in the General Population
The Dutch Studies - Neurodevelopmental and Immune Effects
Main findings: Four point deficit in IQ and increased susceptibility to infections in 42 month old children exposed to typical daily intake levels of dioxins/PCBs.
Effects of dioxins and PCBs on neurodevelopment, the immune system and
thyroid hormones were observed in children from the general population of
the Netherlands.43, 44 These studies found that prenatal (before
birth) exposure to typical daily intake levels of dioxins/PCBs are
associated with:
-
Reduced birth weight and reduced growth from birth through 3 months of age; 45
-
Delays in psychomotor development at 3 months; 46
-
Neurodevelopmental delays at two weeks 47 and 18 months; 48
-
Alterations in thyroid hormones at birth and at 3 months; 49 and
-
Alterations in immune status from birth to 42 months.50, 51
The adverse neurological effects found at birth and at 18 months could not be detected at 42 months.52 However, a decrease in cognitive function as measured by a 4 point deficit in IQ was measured for the first time at 42 months.53 This difference may be explained by the different testing procedures used. Prenatal exposure to dioxins/PCBs were also found to be associated with other neurodevelopmental and behavioral effects at 42 months including a decrease in high level play, 54 an increase in non play activity, 54 and an increased prevalence of being withdrawn and depressed.55 These Dutch studies also found that postnatal (after birth) exposure to typical daily levels of dioxins/PCBs was associated with:
-
Delays in psychomotor development at 7 months; 46
-
Alterations in thyroid hormones at 3 months; 49
-
Alterations in immune status as indicated by an increased prevalence of recurrent middle ear infections and decreased prevalence of allergic reactions to food, pollen, dust and pets at 42 months; 51 and
-
An increase in mean reaction times, a decrease in sustained attention, and an increase in hyperactive behavior at 42 months.54
The Finnish Study - Developmental Effects
Main findings: An association between dioxin exposure and hypo-mineralization defects of permanent teeth.
A study of breast-fed Finnish children found an association between dioxin exposure and hypo-mineralization defects of permanent teeth.56, 57, 58 These findings suggest that the observed effects are primarily due to lactational exposures. In contrast, the effects observed in the Dutch children were associated primarily with in utero exposure and not in children who were breast-fed. Teeth defects are also observed in the rice oil poisonings in both Japan 59 and Taiwan.60 There are some toxicological data in animals to support effects of dioxin on tooth development. Dioxin causes defects of dental hard tissues in rats, 61 perhaps by altering the action of epidermal growth factor receptor.62 Dental defects and changes in ameloblasts (enamel-forming cells) in rhesus monkeys exposed to PCBs have been reported.63
Miscellaneous Studies - Neurodevelopmental and Reproductive Effects
Two studies of children in the U.S. found similar neurodevelopmental effects associated with exposure to typical daily exposure levels of PCBs.64, 65 An ongoing German study also found neurodevelopmental effects associated with low-level PCB exposure.66 Some of the results differ among these studies. In a study of children from the general Japanese population, exposure to dioxin-like compounds are associated with adverse effects on thyroid hormones and the immune system.67, 68
Children of women exposed in utero to a complex mixture of PCDFs, PCBs and other compounds in the Taiwan rice oil poisoning incident of "Yu-cheng"(which translates to oil poisoning), suffered a number of effects including damage to the nervous and respiratory system;69 higher than normal incidence of middle ear infections; 70 and reduced penis size at adolescence.71
In Seveso, Italy, the site of a major plant explosion that sent a cloud of dioxin into the community, children who developed chloracne experienced transient changes in immune parameters, but no adverse immunological effects.72 Also, the sex ratio of children born (48 females to 26 males) in Seveso was not normal for several years following dioxin exposure, 73 but the same effect is not seen after dioxin exposure in the Yu-cheng children.74 Though a major study of women exposed to dioxin at Seveso is underway, the existing epidemiological evidence showing the effect of dioxin exposure on endometriosis is limited and mixed.
One study in Israel found higher levels of dioxin in the blood of women with endometriosis than in controls.75 Workers with chloracne who worked at the Nitro, West Virginia trichlorophenol plant reported higher than expected sexual dysfunction and lower than normal libido.76
In summary, some evidence indicates that dioxin exposure interferes with
normal growth and development in children from the general population.
Developmental neurotoxicity associated with dioxin exposure includes
cognitive deficits, behavioral alterations such as increased
withdrawal/depression, hyperactive behavior, and attentional difficulties.
Other effects that are transient are decreased neuro-optimality (nerve
function) and decreased psychomotor ability. Developmental effects on the
immune system include increased susceptibility to infections, altered
lymphocyte subsets, and increased respiratory disease and otitis
(inflammation of the ear) in highly exposed infants. Developmental and
reproductive effects include altered sex ratio (more females born than
males), small penis and endometriosis. Many of the effects on the
development of the nervous system are more associated with in utero
exposure than with breast-feeding. The dental effects observed in the
Finnish children are more strongly associated with dioxin exposure from
breast milk, a finding consistent with the timing of tooth mineralization
in humans.
Hormonal Effects
Major findings: Decrease in testosterone in workers and an increased risk of diabetes associated with exposure to dioxin.
Exposure to dioxin has a variety of effects on hormone function in animals and in people. In a group of U.S chemical plant workers (the NIOSH cohort), dioxin-exposed workers have lower than normal testosterone levels and higher than normal follicle-stimulating and luteinizing hormone levels, both of which can reduce sperm counts.42
Dioxin interferes with the hormone insulin and alters glucose tolerance which leads to diabetes. In one study of 55 exposed workers evaluated 10 years after exposure, 50% of the workers were diabetic or have abnormal glucose tolerance, an early indicator of diabetes.77 Since this striking finding, there have been mixed findings of diabetes or glucose tolerance in several studies. In the NIOSH workers, the risk of diabetes increased 12% for every 100 ppt dioxin in blood lipid.78
In a study of the Ranch Hand veterans, the soldiers who had the highest exposures to Agent Orange, those with blood dioxin greater than 33.3 pg/gm (ppt) have a relative risk of 2.5 for diabetes.41 A relative risk of 1.0 means that an exposed person is no more likely to develop the disease than an unexposed person. In a follow-up study, the veterans exposed to dioxin had a relative risk of 1.4 for glucose abnormalities, 1.5 for diabetes, and 2.3 for the use of oral medications to control diabetes.79
This study also found that Ranch Hand veterans exposed to dioxin develop diabetes at an earlier age than other veterans and that non-diabetic Ranch Hands exposed to dioxin have a relative risk of 3.4 for serum insulin abnormalities.
In the ongoing study of the residents of Seveso, Italy, there is an
increase in deaths from diabetes in females in the second highest exposure
area and a slightly elevated increase (not statistically significant) in
males.72 Deaths from diabetes in the highest exposed area showed
a suggestive but not statistically significant increase, though the number
of deaths are too few to draw any conclusions.
Cancer Effects
Epidemiological data from high exposure situations suggest that a number of the effects of dioxin exposure seen in animals also occur in humans . However, because studies in humans cannot be done under the same controlled conditions as studies in experimental animals, dioxin's effects on humans are not as clear cut as they are in animal models. Nevertheless, similarities between humans and experimental animals allow reasonable comparisons and projections from dioxin's effects in animals to its effects on humans: they both have the Ah receptor and associated factors; a number of biochemical responses are similar; and, on a body burden basis, many human responses to dioxin are reasonably comparable to the responses in animals.11, 12
Updates of ongoing studies indicate that dioxin exposure causes cancer in humans in a dose-dependent fashion. The most important of these studies are the series of studies by Flesch-Janys and colleagues in Germany and by Bertazzi and colleagues in Italy. The studies of the German chemical plant workers attempt to quantify the dose-response relationship between estimated TCDD exposure and total mortality.80,81 The Italian studies of mortality among those exposed to the Seveso plant accident also focus on cancer mortality in populations grouped by exposure level.82 Both research groups recognize limitations and uncertainties in their studies including estimating exposure and defining specific causes of death, among other limitations of epidemiologic studies. However, both series of studies strengthen the conclusion that dioxin exposure is related to cancer mortality in humans in a dose-related fashion.
Two additional important studies are the update of the NIOSH chemical workers in the U.S.83 and analysis of a group of Dutch workers 84 that is part of a larger international group of workers.85 The NIOSH update also shows a dose-response relation between dioxin exposure and cancer mortality.
These studies together provide strong support for the decision by the World Health Organization's International Agency for Research on Cancer (IARC) to define TCDD as "carcinogenic to humans."25 In making an overall judgement of dioxin's carcinogenicity in humans, IARC now includes mechanistic information as well as human and animal data. For example, the importance of the Ah receptor in mediating dioxin's toxic effects and its presence in both humans and experimental animals is acknowledged. This decision is further supported by strong evidence in animal studies that show dioxin causes cancer in all studies that have been conducted. The U.S. National Toxicology Program (NTP) had upgraded dioxin from its status as "reasonably anticipated to be a human carcinogen" to "known to cause cancer in humans" in 1997,86 but reconsidered their decision based on procedural errors pointed out by industry. NTP has not decided whether they will upgrade dioxin or leave it as "reasonably anticipated to be a human carcinogen."
As discussed earlier, the lifetime risk of getting cancer from exposure
to dioxin is 1 in 10,000 for the general American population and 1 in 1,000
for highly exposed members of the population.30 These risk
estimates are based on ingesting a "risk specific dose" of 0.01
pg TEQ/kg bw/day over a 70-year lifetime. If these estimates are taken
seriously, then the average exposure of the American people to dioxin poses
an uncertain but potentially substantial risk, a point made at least a
decade ago.87
Sensitive Non-Cancer Effects Observed in Animal Studies
Studies of dioxin's effects in experimental animals indicate that it causes a host of toxic effects including cancer; reproductive and developmental toxicity; damage to the immune system; neurotoxicity; endocrine disruption; liver and skin toxicity. Among the sensitive effects observed in animals are a number of biochemical and cellular effects that occur at body burden levels of about 10 ng/kg or less, levels comparable to those found in the average person.88 These effects include production of the liver enzymes CYP1A1 and CYP1A2; alterations in hormones, such as epidermal growth factor (EGF), that affect growth and development; oxidative damage; and alterations in lymphocyte subsets,12 a measure of immune function. These observations suggest that dioxins cause biological effects at levels comparable to those found in the average American. At present, it is unclear if these effects are adverse or not.
Developmental neurotoxicity: Subtle deficits in object learning are observed in the offspring of rhesus monkeys chronically exposed to dioxin in utero and from breast milk.36 Similar exposure to dioxin also adversely affects long-lasting learning and memory in rats.89 In this study, deficits in exposed animals of both sexes for different learning tasks were observed. Some of these tasks may represent a response strategy rather than improvement in learning or memory.
Endometriosis: The incidence and severity of endometriosis in rhesus monkeys chronically exposed to dioxin rises as the dose increases.35 Surgically-induced endometriosis has been enhanced in dioxin-exposed monkeys 90 and in rats and mice.91 In human endometrial tissue, the Ah receptor is expressed, suggesting that it is involved during the reproductive phase of this tissue.92
Effects on the Developing Reproductive System: Pregnant rats exposed to a single dose of dioxin during the development of fetus' organs give birth to both male and female offspring with permanent damage to their reproductive systems.34, 39
Immunotoxicity: Pregnant female rats exposed to dioxin give birth
to offspring with an immune system problem called "delayed type
hypersensitivity" 37, 38 which renders the animals more
susceptible to viral infections. Captive harbor seals fed Baltic fish with
210 ng TEQ/kg lipid in their blubber develop delayed type hypersensitivity
relative to controls which were fed cleaner Atlantic fish with only 62 ng
TEQ/kg lipid in their blubber.93 The seals fed the contaminated
fish were less able to mount a normal immune response. Eight week old mice
treated with 10 ng/kg of dioxin die more frequently than controls when
exposed to influenza virus.33 This viral susceptibility occurs
at the lowest level of any effect observed in animals. This represents the
most sensitive adverse effect of dioxin exposure on record.
Conclusion: The American People are at Serious Risk from their Daily Intake of Dioxin in Food
This report integrates all the information including the newest studies
on dioxins' effects on human health and comes to the following conclusions:
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All American children are born with dioxin in their bodies. The greatest impact appears to be on the growth and development of children. Disrupted sexual development, birth defects and damage to the immune system may result.
-
Dioxin exposure has been associated with IQ deficits, increased prevalence of withdrawn/depressed behavior, adverse effects on attentional processes, and an increase in hyperactive behavior in children. These effects have been reported in 42-month old Dutch children whose exposure to dioxins/PCBs came primarily before birth.
-
Dioxin exposure has been associated with alterations in immune function including increased susceptibility to infections and changes in T-cell lymphocyte populations. These effects have been reported in 42-month old Dutch children whose exposure to dioxins/PCBs came primarily before birth. Altered immune function, reported at birth, 3, and 18 months of age, persists to 42 months of age in these children. Reported immune effects include an increase in middle ear infections and chicken pox, and a decrease in allergic reactions.
-
There is evidence of both developmental and reproductive effects in children exposed to dioxin. These effects include defects in permanent teeth, adverse effects on thyroid hormones, altered sex ratio (more females than males), and increased respiratory disease.
-
The average daily intake of dioxin in food poses a substantial cancer risk to the general American population. The lifetime risk of getting cancer from exposure to dioxin is 1 in 10,000 for the general American population and 1 in 1,000 for highly exposed members of the population. These risks are 100 and 1,000 times higher, respectively, than the one-in-a-million "acceptable" cancer risk.
-
Nearly all Americans are exposed to dioxin through ingestion of common food, mostly meat and dairy products. Dairy cows and beef cattle absorb dioxin by eating dioxin contaminated feed crops. The crops become contaminated by airborne dioxins that settle onto soil and plants. Dioxins enter the air from thousands of sources including incinerators that burn medical, municipal, and hazardous waste.
-
The average daily intake of the American people is already well above several federal guidelines and at mid-range of international guidelines for dioxin exposure. The average daily intake of the American people is more than 200 times higher than EPA's cancer risk guideline, over twice ATSDR's lowest adverse effect level, and in the middle of the range of the World Health Organizations's tolerable food intake.
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At higher risk of exposure to dioxin are children, nursing infants, some workers and farmers, people who eat fish as a main staple of their diet such as some indigenous peoples and fishermen, and people who live near dioxin release sites. These groups of people are likely exposed to at least 10 times as much dioxin as the general population.
Dioxin is an ubiquitous poison that is in our food and that causes many toxic effects in people and animals. The neurodevelopmental and reproductive effects observed in children may be the most disturbing new evidence. The small shifts in cognitive ability or thyroid levels may be the tip of the iceberg of the impact of dioxin on the general American public.
We know that the daily dioxin intake of Americans is already too high,
and exceeds several federal risk guidelines. We also know that some members
of the general population are particularly sensitive to exposure to dioxin
and others are exposed to higher than average daily levels. These are
infants and children, people who live near contaminated sites, fishermen
and indigenous people who rely on fish as a main staple of their diet,
workers, and others with high exposures. These groups have suffered a
disproportionate share of dioxin exposure and many have already suffered
the adverse health effects caused by these exposures. Every effort should
be made to eliminate environmental releases of dioxin and related
compounds. Americans have a choice: take action to protect public health by
eliminating dioxin creation or continue to allow dioxin to be created and
not burden industry with the short term transition costs of elimination and
related compounds.
References
-
Van den Berg, M., Birnbaum, L., Bosveld, A.T.C., Brunstrom, B., Cook, P., Feeley, M., Giesy, J.P., Hanberg, A., Hasegawa, R., Kennedy, S., Kubiak, T., Larsen, J.C., van Leeuwen, R., et al. (1998) "Toxic equivalent factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife." Environmental Health Perspectives 106 (12): 775-792.
-
Birnbaum, L.S. (1999) "TEFs: A practical approach to a real-world problem." Human and Ecological Risk Assessment 5:13-24.
-
USEPA (1998) The Inventory off Sources of Dioxin in the United States, USEPA, Office of Research and Development, EPA/600/P-98/002Aa, External Review Draft, April.
-
Cohen, M., Commoner, B., Richardson, J., Flack, S., Bartlett, P.W., Cooney, P., Couchot, K., Eisl, H., and Hill, C. (1998) Dioxin Sources, Air Transport and Contamination in Dairy Feed Crops and Milk. Center for Biology of Natural Systems, Queens College, Flushing NY.
-
Cohen, M., Commoner, B., Eisl, H., Bartlett, P., Dickar, A., Hill, C., Quigley, J., and Rosenthal, J. (1995) Quantitative Estimation of the Entry of Dioxins, Furans and Hexachlorobenzene into the Great Lakes from Airborne and Waterborne Sources. Center for Biology of Natural Systems, Queens College, Flushing, NY.
-
Agency for Toxic Substances and Disease Registry (ATSDR) (1998) Toxicity Profile for Chlorinated Dibenzo-p-Dioxins (update), U.S. Department of Health and Humans Services, Public Health Service, December.
-
Schecter, A. (1994) "Exposure assessment: Measurement of dioxins and related compounds in human tissues." in Dioxins and Health, Arnold Schecter, editor, pp. 449-486. New York: Plenum Press.
-
Hattemer-Frey, H.A., and Travis, C.C. (1989)"Comparison of human exposure to dioxin from municipal waste incineration and background environmental contamination." Chemosphere 18: 643-649.
-
Schecter, A. (1999) Personal communication.
-
World Health Organization (1998) Assessment of the health risks of dioxins: re-evaluation of the Tolerable Daily Intake (TDI). Executive Summary. Final Draft. WHO Consultation of May 25-29, 1998, Geneva, WHO European Centre for Environment and Health, International Programme on Chemical Safety, December.
-
DeVito, M.J., Birnbaum, L.S., Farland, W.H., and Gasiewicz, T.A. (1995) "Comparisons of estimated human body burdens of dioxin-like chemicals and TCDD body burdens in experimentally exposed animals." Environmental Health Perspectives 103: 820-831.
-
Grassman, J.A., Masten, S.A., Walker N.J., and Lucier, G.W. (1998) "Animal models of human response to dioxins." Environmental Health Perspectives 106 (Supplement 2): 761-775.
-
USEPA (1991) Chlorinated dioxins and furans in the general U.S. population: NHATS FY 87 results, USEPA Office of Toxic Substances, EPA-560/5-91-003.
-
USEPA (1994) Estimating Exposure to Dioxin-Like Compounds, Volume II: Properties, Sources, Occurrence and Background Exposures, USEPA, Office of Research and Development, EPA/600/6-88/005Cb, External Review Draft, June.
-
Papke, O. (1998) "PCDD/PCDF: Human Background Data for Germany, a 10-year experience." Environmental Health Perspectives 106 (S2): 723-731.
-
Stephens, R.D., Petreas, M.X., and Hayward, D.G. (1995) "Biotransfer and bioaccumulation of dioxins and furans from soil: chickens as a model for foraging animals." Science of the Total Environment 175: 253-273.
-
Air Pollution Aspects of Incineration Facilities for Household Waste and Comparable Commercial Waste, Ministry of Public Housing, Urban Planning and Environmental Management of the Kingdom of the Netherlands, July 14, 1989.
-
Schecter, A. and Papke, O. (1998) "Comparison of blood dioxin, dibenzofuran and coplanar PCB levels in strict vegetarians (vegans) and the general United States population." Organohalogen Compounds 38: 179-182.
-
McLachlan, M.S. (1993) "Digestive tract absorption of polychlorinated dibenzo-p-dioxins, dibenzofurans and biphenyls in a nursing infant." Toxicology and Applied Pharmacology 123: 68-72.
-
Pluim, H.J., Wever, J., Koppe, J.G., van der Slikke, J.W., and Olie, K. (1993) "Intake and fecal excretion of chlorinated dioxins and dibenzofurans in breast-fed infants at different ages." Chemosphere 26: 1947-1952.
-
Dahl, P., Linsdstrom, G., Wiberg, K., and Rappe, C. (1995) "Absorption of polychlorinated biphenyls, dibenzo-p-dioxins and dibenzofurans by breast-fed infants." Chemosphere 30 (12): 2297-2306.
-
Abraham, K., Hille, A., Ende, M., Helge, H. (1994) "Intake and fecal excretion of PCDDs, PCDFs, HCB, and PCBs (138, 153, 180) in a breast-fed and formula-fed infant." Chemosphere 29: 2279-2286.
-
Abraham, K., Knoll, A., Ende, M., Papke, O., and Helge, H. (1996) "Intake, fecal excretion, and body burden of polychlorinated dibenzo-p-dioxins and dibenzofurans in breast-fed and formula-fed infants." Pediatric Research 40: 671-679.
-
Schecter, A., Papke, O., and Ball, M. (1990) "Evidence for transplacental transfer of dioxins from mothers to fetus: Chlorinated dibenzodioxin and dibenzo furan levels in the livers of stillborn infants." Chemosphere 21: 1017-1022.
-
IARC (1997) IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 69, Polychlorinated Dibenzo-para-Dioxins and polychlorinated Dibenzofurans, Lyon, France.
-
Schecter, A., Startin, J., Wright, C., Kelly, M., Papke, O., Lis, A., Ball, M., and Olson, J.R. (1994) "Congener-specific levels of dioxins and dibenzofurans in U.S. food and estimated daily dioxin toxic equivalent intake." Environmental Health Perspectives 102: 962-966.
-
Patandin, S., Dagnelie, P.C., Mulder, P.G.H., Op de Coul, E., van der Veen, J.E., Weisglas-Kuperus, N., and Sauer, P.J.J. (1999) "Dietary exposure to polychlorinated biphenyls and dioxins from infancy until adulthood: A comparison between breast-feeding, toddler and long-term exposure." Environmental Health Perspectives 107 (1): 45-51.
-
Schecter, A., Papke. O., Lis, A., Ball, M., Ryan, J.J., Olson, J.R., Li, L., and Kessler, H. (1996) "Decrease in milk and blood dioxin levels over two years in a mother nursing twins: Estimates of decreased maternal and increased infant dioxin body burden from nursing." Chemosphere 32 (3): 543-549.
-
LeLeche League International (1994) Board Report, Leaven, May-June.
-
USEPA (1994) Health Assessment Document for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) and Related Compounds, Volume III of III, USEPA, Office of Research and Development, EPA/600/BP-92/001c, External Review Draft, June.
-
National Resource Council (1994) Science and Judgement in Risk Assessment, NRC Committee on Risk Assessment of Hazardous Air Pollutants, Board on Environmental Studies and Toxicology, Washington, DC: National Academy Press.
-
Birnbaum, L.S. (1999) "Risk Characterization of Dioxins." Presentation at USEPA National Health and Environmental Effects Research Laboratory, February 17.
-
Burleson, G.R., Lebrec, H., Tang, Y.G., Ibanes, J.D., Pennington, K.N., and Birnbaum, L.S. (1996) "Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on influenza virus host resistance in mice." Fundamentals of Applied Toxicology 29: 40-47.
-
Gray, L.E., Jr., Ostby, J.S., and Kelce, W.R. (1997) "A dose response analysis of reproductive effects of a single gestational dose of of 2,3,7,8-tetrachlorodibenzo-p-dioxin in male Long Evans hooded rat offspring." Toxicology and Applied Pharmacology 146: 11-20.
-
Rier, S.E., Martin, D.C., Bowman, R.E., Dmowski, W.P., and Becker, J.L. (1993) "Endometriosis in rhesus monkeys (Macaca mulatta) following exposure to 2,3,7,8-tetrachloro- dibenzo-p-dioxin (TCDD)." Fundamentals of Applied Toxicology 21: 433-441.
-
Schantz, S.L. and Bowman, R.E. (1989) "Learning in monkeys exposed perinatally to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)." Neurotoxicology and Teratology 11: 13-19.
-
Gehrs, B.C., Riddle, M.M., Williams, W.C., and Smialowicz, R.J. (1997) "Alterations in the developing immune system of the F344 rat after perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. II. Effects on the pup and the adult." Toxicology 122: 229-240.
-
Gehrs, B.C. and Smialowicz, R.J. (1998) "Persistent suppression of delayed-type hypersensitivity (DTH) in rats perinatally exposed to TCDD." Toxicologist 42: 1501.
-
Gray, L.E., Jr., Wolf, C., and Ostby, J.S. (1997) "In utero exposure to low doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin alters reproductive development of female Long Evans hooded rat offspring." Toxicology and Applied Pharmacology 146: 235-237.
-
Wolfe, W.H., Michalek, J.E., Miner, J.C., and Rahe, A.J. (1992) Air Force Health Study. An epidemiologic investigation of health effects in Air Force personnel following exposure to herbicides. Reproductive outcomes. Brooks Air Force Base, TX: Epidemiology Research Division, Armstrong Laboratory, Human Systems Division (AFSC).
-
Roegner, R.H., Grubbs, W.D., Lustik, M.B., Brockman, A.S., Henderson, S.C., Williams, D.E., Wolfe, W.H., Michalek, J.E., and Miner, J.C., (1991) "Air Force Health Study: An Epidemiological Investigation of Health Effects in Air Force Personnel Following Exposure to Herbicides. Serum Dioxin Analysis of 1987 Examination Results." NTIS# AD A-237-516 through AD A-237-524.
-
Egeland, G.M., Sweeney, M.H., Fingerhut, M.A., Willie, K.K., Schnorr, T.M., and Halperin, W.E. (1994) "Total serum testosterone and gonadotropins in workers exposed to dioxin." American Journal of Epidemiology 13: 272-281.
-
Lanting, C.I. (1998) Effects of perinatal PCB and dioxin exposure and early feeding mode on child development. Thesis, Erasmus University, Rotterdam.
-
Patandin, S. (1999) Effects of environmental exposure to polychlorinated biphenyls and dioxins on growth and development in young children, A prospective follow-up study of breast-fed and formula-fed infants from birth until 42 months of age. Thesis, Erasmus University, Rotterdam.
-
Patandin, S., Koopman-Esseboom, C., de Ridder, M.A.J., Weisglas-Kuperus, N., and Sauer, P.J.J. (1998) "Effects of environmental exposure to polychlorinated biphenyls and dioxins on birth size and growth in Dutch children." Pediatric Research 44: 538-545.
-
Koopman-Esseboom, C., Weisglas-Kuperus, N., de Ridder, M.A., Van der Paauw, C.G., Tuinstra, L. G., and Sauer, P.J. (1996) "Effects of polychlorinated biphenyl/dioxin exposure and feeding type on infants' mental and psychomotor development." Pediatrics 97 (5): 700-706.
-
Huisman, M., Koopman-Esseboom, C., Lanting, C. I., Van der Paauw, C.G., Tuinstra, L.G.M., Fidler, V., Weisglas-Kuperus, N., Sauer, P.J.J., Boersma, E.R., and Touwen, B.C.L. (1995) "Perinatal exposure to polychlorinated biphenyls and dioxins and its effects in neonatal neurological development." Early Human Development 41: 111-127.
-
Huisman, M., Koopman-Esseboom, C., Lanting, C.I., Van der Paauw, C.G., Tuinstra, L.G, Fidler, V., Weisglas-Kuperus, N., Sauer, P.J., Boersma, E.R., and Touwen, B.C.(1995) "Neurological condition in 18-month-old children perinatally exposed to polychlorinated biphenyls and dioxins." Early Human Development 43: 165-176.
-
Koopman-Esseboom, C., Morse, D.C., Weisglas-Kuperus, N., LutkeSchipholt, I.J., van der Paauw, C.G., Tuinstra, L.G., Brouwer, A., and Sauer, P.J.J. (1994) "Effects of dioxins and polychlorinated biphenyls on thyroid hormone status of pregnant women and infants." Pediatric Research 36: 468-473.
-
Weisglas-Kuperus, N., Sas, T.C.J., Koopman-Esseboom, C., Zwan, C.W., van der Ridder, M.A.J., Beishuizen, A., Hooijkaas, H., and Sauer, P.J.J. (1995) "Immunological effects of background prenatal and postnatal exposure to dioxins and polychlorinated biphenyls in Dutch infants." Pediatric Research 38: 404-410.
-
Weisglas-Kuperus, N., Patandin, S., Berbers, G.A.M., Sas., T.C.J., Mulder, P.G.H., Sauer, P.J.J., and Hooijkaas, H. (1999) "Immunological effects of background exposure to polychlorinated biphenyls and dioxins in Dutch toddlers," in Effects of Exposure to Polychlorinated Biphenyls and Dioxins on Growth and Development in Young Children, Patandin, S. Thesis, Erasmus University, Rotterdam. Chapter 9, pp. 157-168, submitted for publication.
-
Lanting, C.I., Patandin, S., Fidler, V., Weisglas-Kuperus, N., Sauer, P.J.J., Boersma, E.R; and Touwen, B.C.L. (1998) "Neurological condition in 42-month-old children in relation to pre-and postnatal exposure to polychlorinated biphenyls and dioxins." Early Human Development 50 (3): 283-292.
-
Patandin, S., Lanting, C.I., Mulder, P.G.H., Boersma, E.R; Sauer, P.J.J., and Weisglas-Kuperus, N. (1999) "Effects of environmental exposure to polychlorinated biphenyls and dioxins on cognitive abilities in Dutch children at 42 months of age." Journal of Pediatrics 134: 33-41.
-
Patandin, S., Veenstra, J., Mulder, P.G.H., Sewnaik, A., Sauer, P.J.J., and Weisglas-Kuperus, N. (1999) "Attention and activity in 42-month-old Dutch children with environmental exposure to polychlorinated biphenyls and dioxins." In Effects of Exposure to Polychlorinated Biphenyls and Dioxins on Growth and Development in Young Children, Patandin, S. Thesis, Erasmus University, Rotterdam. Chapter 7, pp. 123-142, submitted for publication.
-
Patandin, S., Koot, H.M., Sauer, P.J.J., and Weisglas-Kuperus, N. (1999) "Problem behavior in Dutch preschool children in relation to background Polychlorinated Biphenyl and Dioxin exposure." In Effects of Exposure to Polychlorinated Biphenyls and Dioxins on Growth and Development in Young Children, Patandin, S. Thesis, Erasmus University, Rotterdam. Chapter 8, pp. 143-156, submitted for publication.
-
Alaluusua, S., Lukinmaa, P-L., Vartiainen, T., Partanen, M., Torppa, J., Tuomisto, J. (1996) "Polychlorinated dibenzo-p-dioxins and dibenzofurans via mother's milk may cause developmental defects in children's teeth." Environmental Toxicology and Pharmacology 1: 193-197.
-
Alaluusua, S., Lukinmaa, P-L., Koskimies, M., Pirinen, S., Holtta, P., Kallio, M., Holttinen, T., and Salmenpera, J. (1996) "Developmental dental defects associated with long breast feeding." European Journal of Oral Science 104: 493-497.
-
Alaluusua, S., Lukinmaa, P-L., Torppa, J., Tuomisto, J., and Vertiainen, T. (1999) "Developing teeth as biomarker of dioxin exposure." Lancet 353: 206-207.
-
Kuratsune, M. (1989) "Yusho, with reference to Yu-Cheng." In: Kimbrough, RD., Jensen, AA., eds. Halogenated Biophenyls, Terphenyls, Naphthalenes, Dibenzodioxins and Related Products. 2nd ed. New York: Elsevier Science Publishers; pp. 381-400.
-
Rogan, W.J., Gladen, B.C., Hung, K-L., Koong, S-L., Shih, L-Y., Taylor, J.S., Wu, Y-C., Yang, D., Ragan, B., and Hsu, C-C. (1992) "Congenital poisoning by polychlorinated biphenyls and their contaminants in Taiwan." Science 241: 334-336, July, 15.
-
Alaluusua, S., Lukinmaa, P-L., Pohjanvirta, R., Unkila, M., and Tuomisto, J. (1993) "Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin leads to defective dentin formation and pulpal perforations in rat incisor tooth." Toxicology 81: 1-13.
-
Partanen, A-M., Alaluusua, S., Miettinen, P.J., Thesleff, I., Tuomisto, J., Pohjanvirta, R., and Lukinmaa, P-L. (1998) "Epidermal growth factor receptor as a mediator of developmental toxicity of dioxin in mouse embryonic teeth." Laboratory Investigation 78: 1473-1481.
-
McNulty, W.P. (1985) "Toxicity and fetotoxicity of TCDD, TCDF and PCB isomers in rhesus macaques (Macaca mulatta)." Environmental Health Perspectives 60: 77-88.
-
Rogan, W.J. and Gladen, B.C. (1991) "PCBs, DDE, and child development at 18 and 24 months." Annals of Epidemiology 1: 407-413.
-
Jacobson, J.L. and Jacobson, S.W. (1996) "Intellectual impairment in children exposed to polychlorinated biphenyls in utero." New England Journal of Medicine 335 (11): 783-789.
-
Winneke, G., Bucholski, A., Heinzow, B., Kramer, V., Schmidt, E., Walkowiak, J., Wiener, J.A., and Steingruber, H. J. (1998) "Developmental neurotoxicity of polychlorinated biphenyls (PCBs): cognitive and psychomotor functions in 7-month old children." Toxicology Letters 102-103: 423-428.
-
Nagayama, J., Okamura, K., Iida, T., Hirakawa, H., Matsueda, T., Tsuji, H., Hasegawa, M., Sato, K., Ma, H.Y., Yanagawa, T., Igarashi, H., Fukushige, J., and Watanabe, T. (1998) "Postnatal exposure to chlorinated dioxins and related chemicals on thyroid hormone status in Japanese breast-fed infants." Chemosphere 37: 1789-1793.
-
Nagayama, J., Tsuji, H., Iida, T., Hirakawa, H., Matsueda, T., Okamura, K., Hasegawa, M., Sato, K., Ma, H.Y., Yanagawa, T., Igarashi, H., Fukushige, J., and Watanabe, T. (1998) "Postnatal exposure to chlorinated dioxins and related chemicals on lymphocyte subsets in Japanese breast-fed infants." Chemosphere 37: 1781-7.
-
Hsu, C-C., Yu, M-L.M., Chen, Y-C.J., Guo, Y-L.L., and Rogan, W.J. (1994) "The Yu-cheng Rice Oil Poisoning Incident." In Dioxins and Health, ed. Arnold Schecter, New York: Plenum Press, pp. 661-684.
-
Chao, W-Y., Hsu, C-C., and Guo, Y-L. (1997) "Middle-ear disease in children exposed prenatally to polychlorinated biphenyls and polychlorinated dibenzofurans." Archives of Environmental Health 52: 257-262.
-
Guo, Y-L., Lai, T.J., Ju, S.H., Chen, Y-C., and Hsu, C-C. (1993) "Sexual developments and biological findings in Yu-cheng children." Organohalogen Compounds 14: 235-237.
-
Pesatori, A.C., Zocchetti, C., Guercilena, S., Consonni, D., Turrini, D., and Bertazzi, P.A. (1998) "Dioxin exposure and non-malignant health effects. A mortality study." Journal of Occupational and Environmental Medicine 55: 126-131.
-
Mocarelli, P., Brambilla, P., Gerthoux, P.M., Patterson, D.G. Jr., and Needham, L.L. (1996) "Change in sex ratio with exposure to dioxin." Lancet 348: 409.
-
Rogan, W.J., Gladen, B.C., Guo, Y-L., and Hsu, C-C. (1999) "Sex ratio after exposure to dioxin-like compounds in Taiwan." Lancet 353: 206-207.
-
Mayani, A., Barel, S., Soback, S., and Almagor, M. (1997) "Dioxin concentrations in women with endometriosis." Human Reproduction 12 (2): 373-375.
-
Moses, M., Lilis, R., Crow, K.D., Thornton, J., Fischbein, A., Anderson, H., and Selikoff, I. (1984) "Health status of workers with past exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in the manufacture of 2,4,5-trichlorophenoxyacetic acid: Comparison of findings with and without chloracne." American Journal of Industrial Medicine 5: 161-182.
-
Pazderova-Vejlupkova, J., Nemcova, M., Pickova, J., Jirasek, L., and Lukas, E. (1981) "The development and prognosis of chronic intoxication by tetrachlorodibenzo-p-dioxin in men." Archives of Environmental Health 36 (1): 5-11.
-
Sweeney, M.H., Hornung, R,W., Wall, D.K., Fingerhut, M.A., and Halperin, W.E. (1992) "Prevalence of diabetes and elevated serum glucose levels in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)." Presented at 12th International Symposium on Dioxins and Related Compounds: August 24-28, Tampere, Finland.
-
Henriksen, G.L., Ketchum, N.S., Michalek, J.E, and Swaby, J.A. (1997) "Serum Dioxin and Diabetes Mellitis in Veterans of Operation Ranch Hand." Epidemiology 8 (3): 252-258.
-
Flesch-Janys, D., Berger, J., Gurn, P., Manz, A., Nagel, S., Waltsgott, H., and Dwyer, J.H. (1995) "Exposure to polychlorinated dioxins and furans (PCDD/F) and mortality in a cohort of workers from a herbicide-producing plant in Hamburg, Federal Republic of Germany." American Journal of Epidemiology 142: 1165-1175.
-
Flesch-Janys, D., Steindorf, K., Gurn, P., and Becher, H. (1998) "Estimation of the cumulated exposure to polychlorinated dibenzo-p-dioxins/furans and standardized mortality ratio analysis of cancer mortality by dose in an occupationally exposed cohort." Environmental Health Perspectives 106 (Suppl 2): 655-662.
-
Bertazzi, P.A., Zocchetti, C., Guercilena, S., Consonni, D., Tironi, A., Landi, M.T., and Pesatori, A.C. (1997) "Dioxin exposure and cancer risk. A 15-year mortality study after the Seveso accident." Epidemiology 8: 646-652.
-
Steenland, K., Piacitelli, L., Deddens, J., Fingerhut, M., and Chang L.I. (1999) "Cancer, heart disease and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin." Journal f the National Cancer Institute 91: 779-785.
-
Hooieveld, M., Heederik, D.J.J., Kogevinas., M, et al. (1998) "Second follow-up of a Dutch cohort occupationally exposed to phenoxy herbicides, chlorophenols, and contaminants." American Journal of Epidemiology 147: 891-901.
-
Kogevinas, M., Becher, H., Benn, T., Bertazzi, P.A., Boffetta, P., Bueno-de-Mesquita, H.B., Coggon, D., Colin, D., Flesch-Janys, D., Fingerhut, M., et al. (1997) "Cancer mortality in workers exposed to phenoxy herbicides, chlorophenols, and dioxins. An expanded and updated international cohort study." American Journal of Epidemiology 145 (12): 1061-1975.
-
National Toxicology Program (1997) RC Draft Background Document for TCDD, September 30.
-
Commoner, B., Webster, T., and Shapiro, K. (1985) "Environmental levels and health effects of PCDDs and PCDFs." Presented at Dioxin '85, Bayreuth.
-
Birnbaum, L.S. (1998) "Sensitive non-carcinogenic effects of TCDD in animals." Organohalogen Compounds 38: 291-294.
-
Seo, B-W., Sparks, A.J., Medora, K., Amin, S., and Schantz, S.L. (1999) "Learning and memory in rats gestationally and lactationally exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)." Neurotoxicology and Teratology 21: 231-239.
-
Yang, J.Z., Foster, W.G. (1998) "Chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin modulates the growth of endometriosis in the cynomolgus monkey." Organohalogen Compounds 37:75. Additional data was presented at Dioxin '98.
-
Cummings, A.M., Metcalf, J.L., and Birnbaum, L.S. (1996) "Promotion of endometriosis by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rats and mice: time-dose dependence and species comparison." Toxicology and Applied Pharmacology 138: 131-139.
-
Kuchenhoff, A., Seliger, G., Klonisch, T., Tscheudschil-Suren, G., Kaltwaszer, P., Seliger, E., Buchmann, J., and Fischer, B. (1999) "Aryl hydrocarbon receptor expression in the human endometrium." Fertility and Sterility 71 (2): 354-360, February.
-
Ross, P.S., De Swart, R.L., Reijnders, P.J., Van Loveren, H., Vos, J.G., and Osterhaus, A.D. (1995) "Contaminant-related suppression of delayed-type hypersensitivity and antibody responses in harbor seals fed herring from the Baltic Sea." Environmental Health Perspectives 103: 162-167.
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Since 1995, the EPA has made and then broken numerous promises about the
release of a final version of the dioxin reassessment. Now, four years
later it has yet to be released and federal, state, and even local
governments have written rules for dioxin sources without the benefit of
the final reassessment's information about dioxin's toxicity.
In 1997, EPA said it would hold public hearings around the country to
discuss the policy implications of the reassessment. These hearings, like
the release of the final reassessment, have yet to happen.
Communities burdened by dioxin exposure are tired of waiting for EPA to
act. People at the grassroots know that truly protective public policy will
eliminate dioxin exposure. They know that the EPA has failed to protect
them with the measures it has taken so far. So the following policy
recommendations reflect communities' experience and knowledge about how to
stop dioxin exposure, and outline what protective public policy for dioxin
should include.
This section of the report recommends protective policies and is the
result of the collaboration of more than 50 activists from grassroots,
regional and national environmental groups who came together, in person and
through email and fax. This work built on previous activism on dioxin which
has been taking place for years in communities and through a national
network of grassroots dioxin activists. These activists have experienced
firsthand the results of EPA's lack of action on dioxin. While EPA has
delayed, made excuses, and broken promises, their communities continue to
be exposed to dioxin. They can recommend with considerable authority what
policies are needed to stop dioxin exposure.
This document is a starting point for stopping dioxin exposure. It
includes policy recommendations for twelve dioxin sources which are among
the largest. These twelve are addressed in this document because they are
logical places to begin talking about what truly protective policies must
include. Addressing these twelve sources won't take care of the whole
problem, but it will be a good beginning.
In most of the recommendations we have cited EPA's estimates of how much
dioxin was released into the air from different sources in 1995. These
estimates were published in 1998 as part of EPA's Inventory of Sources of
Dioxin. As discussed in Chapter Three of the Technical Support Document,
these estimates have many limitations and are often based on very little
data, the quality of which is often unknown. These estimates are presented
only to provide a way to compare, on a relative basis, the different
sources of dioxin.
The recommendations in this report are specific to each source and
include steps such as eliminating chlorine from a process or closing a
regulatory loophole. But all of these policy recommendations have some core
principles in common. These principles act as the foundation of any
recommendations the grassroots dioxin movement can make about any dioxin
source. These principles, which must be at the heart of any dioxin policy,
are described below.
Prevention Not Control
For any dioxin policy to have a chance of meaningful impact, it must
have at its core a commitment to the elimination of dioxin. This means that
policies must require that no dioxin be created in the first place, instead
of current practice which generally requires better control of the dioxin
at the end of the pipe. Prevention of dioxin involves several key
components.
First is the recognition that dioxin comes from processes which involve
chlorine or the combustion of substances containing chlorine. Addressing
chlorine is the only way to eliminate dioxin. EPA must reorient its dioxin
research and policy towards a materials focus, including a commitment to
identify processes and products whose production, use, or disposal create
dioxin and begin phasing out these processes and materials over time.
Fundamentally, EPA dioxin policy should require zero creation and
discharge of dioxin from all sources. This should include a position that
there is no safe or "acceptable" level of dioxin in food,
processed or raw, since food is the largest source of human exposure to
dioxin.
Precautionary Principle
The Precautionary Principle states, "When an activity raises
threats of harm to the environment or human health, precautionary measures
should be taken even if some cause and effect relationships are not
established scientifically." Growing evidence on the hazards of dioxin
demands precautionary action to prevent further exposure, even though
absolute proof of harm has not been established.
This should be the guiding philosophy behind all public policies,
including those on dioxin. Scientific uncertainty can no longer be an
excuse to avoid or continue the delay in establishing and implementing
effective policies to stop dioxin exposure. We know enough to act now.
The precautionary principle should replace the flawed technique of risk
assessment in the regulation of dioxin. Instead of using value-laden
estimates of risk to determine how much dioxin exposure is
"acceptable," the precautionary principle guides us in drawing
that line at zero. No more dioxin exposure is "acceptable"
because any additional exposure is too much.
Additionally, any policy based on the precautionary principle will shift
the burden of proof from communities, which currently have to convince
regulators that a facility is unsafe, to the industry or regulators
themselves. Instead of the community being forced to show that something is
unsafe in order to stop it, supporters of the proposal would have to prove
that a project is safe in order to proceed.
Consideration of All Pathways of Dioxin Exposure
Current policy relies on risk assessment which looks at each source of
exposure and each chemical independently, and only worries about how much
harm that one source will do for a defined exposure. This is an unrealistic
view because communities are often burdened with multiple polluting
facilities releasing many chemicals. Communities have also had past
exposures which must be considered. The use of risk assessment is also
inadequate because it only looks at cancer and completely ignores past
exposures, cumulative or synergistic (when chemicals combine to have a new
or greater effect) impacts, or multiple sources of exposure. Dioxin policy
must require consideration of cumulative and synergistic impacts from all
sources in an area.
Environmental Justice
For many years, incinerators, paper mills, cement kilns and other
dioxin-producing facilities have been disproportionately located in
low-income, tribal, people of color, or other disenfranchised communities.
This disparate treatment of people of color and low-income people has led
to disproportionate and adverse health impacts in these communities.
Any policy on dioxin must include a commitment to environmental justice.
As the principles of environmental justice state, "public policy
should be based on mutual respect and justice for all peoples, free from
any form of discrimination or bias... Environmental justice demands the
cessation of the production of all toxins and hazardous wastes, and that
all past and current producers be held strictly accountable to the people
for detoxification and the containment at the point of production...
Environmental justice also protects the right of victims of environmental
injustice to receive full compensation and reparations for damages as well
as quality health care." The full list of Principles can be found in
Appendix A.
Fish and land-based subsistence cultures are at higher health risk from
persistent bioaccumulative toxics in the food web and ecosystem. Base-line
sampling should be done in communities of color and low-income communities
to establish the levels of dioxin found in impacted communities and to
determine disparate toxic burdens. Currently, standards for chemical
exposure are written for white, middle-aged adults. Risk assessments do not
take into account the sensitive populations, such as elders, children, and
those already suffering from environmentally induced disease.
Just Transition
Phasing out dioxin will require substantial technological and economic
transformation, as numerous products and processes are removed from
production or converted to chlorine-free alternatives. This transformation
may be difficult to implement and it is essential that workers and
communities should not bear the economic burden of these changes. The
phase-out of dioxins should therefore be guided by a transition program to
protect, compensate and provide future opportunities for workers and
communities affected by the conversion.
A "just transition" (see the Principles for a Just Transition
in Appendix B) includes a commitment to income and benefit protection for
affected workers and their families, a commitment to involving unions and
protecting workers' right to organize through transition, and a commitment
to economic development in communities affected by transition.
Policy to eliminate dioxin must include a commitment to just transition.
It should also include a commitment to preserving jobs by supporting
industries which make the switch to technology needed to eliminate dioxin.
No Transfer of Dioxin from One Media to Another
Prevention, rather than control, of dioxin requires a commitment to
making sure that everything leaving a facility remains free of dioxin. This
includes byproducts such as ash and sludge, and products such as paper,
chemicals, and plastics. It is unacceptable to use pollution control
technology to simply transfer dioxin from air and water discharges into
sludge or ash which are widely dispersed in the environment. Dioxin must be
eliminated at the source, not just moved around by control technology.
Also unacceptable is the practice of "beneficial use" of
dioxin-contaminated sludge or ash. "Beneficial use" is a
euphemistic term describing the use of dioxin-contaminated wastes as
products. These wastes should be managed in a manner that prevents their
contamination from being dispersed into the environment. Instead,
"beneficial use" of wastes includes using incinerator ash and
other manufacturing wastes as ingredients in fertilizer, construction
material, or as landfill cover and spreading sewage sludge on land as
fertilizer and material for mine reclamation. "Beneficial use" of
dioxin contaminated materials such as sludge and ash is only beneficial to
the waste producers who avoid the expense of properly managing their waste.
The irresponsible policy of allowing these dioxin-contaminated substances
to be widely dispersed into the environment must stop immediately.
The Right to Know the Extent of Dioxin Contamination
In many of the recommendations in this report there are calls for
testing of agricultural products, fish, and soil near dioxin-producing
facilities. We have the right to know how much dioxin is in our food and
the environment. And while testing might at first provide more questions
than answers, it is a starting point for understanding the extent of the
dioxin problem. For too long the absence of data has been an excuse for not
taking action. While we take measures to prevent new dioxin exposure, we
must continue to try to document the extent of existing dioxin
contamination.
The progress made so far in stopping dioxin exposure has not been the
result of government policy. It has come from activism in communities
across the country, where incinerators have been shut down, paper mills
have agreed to clean up their processes, and local governments have passed
dioxin resolutions and agreed to buy chlorine free products. This report is
not meant to discourage this kind of grassroots activism. It is meant to
gather the lessons learned from these efforts and combine them into a
blueprint for government and industry action to stop dioxin exposure.
Continued local activism is what will convince all levels of government to
follow this blueprint and dioxin-producing industries to change their ways.
This report on dioxin policy recommendations can serve as a map for
government as it catches up with the people it is supposed to lead.
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Problem
Municipal solid waste (MSW) incinerators have many undesirable
environmental and economic impacts. Essentially, incinerators transform
household garbage, consisting primarily of recyclable, reusable, and
compostable materials, into dioxin, metals, and other toxic gases and large
amounts of toxic ash. The EPA has estimated that in 1995, MSW incineration
released from 492 to 2460 grams TEQ of dioxin, with a central estimate of
1100 grams TEQ. MSW incineration is the largest source on EPA's list of
dioxin emissions to air in 1995. Incinerator ash, which is highly
contaminated with dioxin and metals, is being increasingly dispersed
through the environment as many states allow it to be "recycled"
and used as landfill cover or in road and construction projects.
Incinerators are expensive and need constant feeding to generate enough
revenue to pay off the debt communities take on to build them. This leaves
little incentive for communities to recycle and reduce the amount of waste
they create.
No regulations can make incineration a rational or safe means for
managing MSW. Moreover, EPA has demonstrated neither the will nor the means
for adequately protecting public health and the environment from the
impacts of MSW incineration. This is illustrated by current federal
policies, which focus on trying to capture emissions from incinerator
stacks and are full of loopholes. One such loophole in the Clean Air Act
allows for a three-hour exemption from air emission permit standards during
start-up, shut-down, and malfunction, leading to regular prolonged
exposures to dioxin and other pollutants with no regulatory consequences
for the facilities. Other loopholes allow facilities other than
incinerators to burn municipal waste without the regulations and pollution
controls found at incinerators. These other burners include cement and
aggregate kilns, backyard burning, "small" (under 40 tons per
day) incinerators, and co-generation power plants.
Current federal policies, where they do apply, are not protective of the
environment and public health. They focus on better pollution control
technologies rather than preventing pollution by reducing toxics in the
waste stream. Better control technologies may reduce the amount of toxic
chemicals emitted from the smoke stack, but control technology simply
transfers contaminants from the air to the ash. EPA does not have a policy
that will adequately quantify the amount of pollutants in incinerator ash,
nor do they require its safe handling and disposal. EPA's choice of the
Toxic Characteristic Leaching Procedure (TCLP) to determine whether
incinerator ash is toxic has served to protect the incinerator industry
from the financial burdens associated with the handling and disposal of ash
as hazardous waste. The test does not require a determination of absolute
levels of toxic metals or dioxins, it just measures what leaches out when
acid is passed through the ash. The lime used in incinerator scrubbing
systems often neutralizes the acid, reducing the amount of leaching.
Because there is never a determination of what is really in the ash, the
use of the TCLP is grossly unprotective of wildlife, drinking water
supplies, and people exposed to the ash. This includes workers at
incinerator facilities and landfill sites, citizens in incinerator
communities and near landfills which use ash as daily cover, and citizens
exposed to ash reutilization schemes. Viable alternatives to incineration
exist. For example, recycling facilities create more jobs than an
incinerator and are less capital intensive to implement.
Recommendations
-
Eliminate Municipal Solid Waste Incineration
-
Close Loopholes on Non-Incineration Combustion
-
Categorize Incinerator Ash as Hazardous Waste
-
Implement Responsible, Long-Term, Non-Incineration Solutions for Municipal Waste Disposal
Eliminate Municipal Solid Waste Incineration
A. There should be an immediate shut down of all MSW incinerators not
defined as "waste-to-energy" facilities.
B. No permits for new "waste-to-energy" projects, with a five
year phase out of existing facilities.
Close Loopholes on Non-Incinerator Combustion
Municipal solid waste should not be disposed of by any thermal destruction processes. The following options for burning household waste, either as raw garbage or as refuse derived fuel (RDF), should be banned:
-
backyard trash burning
-
cement and/or aggregate kilns
-
co-generators (including, but not limited to, coal power plants)
-
commercial hazardous waste or industrial on-site incinerators
-
open burning at landfill sites
-
industrial, municipal, and school furnaces and/or other boilers
-
pyrolysis
Categorize Incinerator Ash as Hazardous Waste
A. An immediate ban on the utilization of MSW ash for any purpose (such
as use in cement or construction aggregate or
as landfill cover) due to its gross contamination
by heavy metals, dioxins, furans, and other toxic chemicals.
B. All MSW incinerator ash must be classified and disposed of as
hazardous waste.
Implement Responsible, Long-Term, Non-Incineration Solutions for
Municipal Waste Disposal
A. Waste management policies should lead to source reduction measures and intensive reuse, recycling and composting programs. In addition, incinerator workers should be given the opportunity to work in the alternative facilities or given appropriate compensation for job loss.
B. Non-incineration solutions should include, but are not limited to:
-
Clean production of consumer goods, which would exclude toxic ingredients such as heavy metals.
-
Intensive waste reduction measures for all waste generators.
-
Intensive recycling programs for, but not limited to, compostables, paper, metal, and glass for all waste generators. Recycling projects should ensure a safe workplace.
-
Federal mandates on packaging materials that prioritize reusable materials, such as glass, paper, and metal.
-
Taxes on all "use once, then throw away" packaging materials.
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Problem
Many hospitals, particularly those with on-site incinerators, routinely
burn some or all of their waste. But the majority of this waste is similar
to that found in the average household: cardboard, paper, cans, plastic
bottles, etc. Incineration is not mandated for any waste at the national
level. The Centers for Disease Control and Prevention states that
"hospital wastes for which special precautions appear prudent are
microbiology laboratory waste, pathology waste, bulk blood or blood
products, and sharp items such as used needles or scalpel blades. In
general, these items should either be incinerated or DECONTAMINATED
(emphasis added) prior to disposal in a sanitary landfill." Hospitals
do not need to burn all of their waste because viable alternatives exist. A
variety of non-incineration technologies are available for medical waste,
including autoclaves (steam sterilization), microwaves, and other
treatment. While more research needs to be done on emissions from these
types of facilities, current data indicate that dioxin is not likely to be
formed during these treatment processes.
The EPA has estimated that in 1995 medical waste incineration released
from 151 to 1510 grams TEQ of dioxin, with a central estimate of 477 grams
TEQ. Medical waste incineration is the third largest source on EPA's list
of dioxin emissions to air in 1995. Current EPA regulations focus on
controlling air pollution rather than actually reducing the toxicity of all
emissions. Such "end-of the pipeline" approaches are more
expensive and less protective than an approach which focuses on reducing
the toxicity of the waste stream through product changes and purchasing
decisions.
The agency has said that the Maximum Achievable Control Technology (MACT)
Rule for incinerators greatly reduces dioxin air emissions. But any amount
of dioxin released is dangerous. The rule does not address the formation of
dioxin in the incinerator, it requires technology which merely moves it
from the stack to the ash, which is often released into the environment.
Medical waste contains a higher percentage of plastic than municipal
solid waste. Polyvinyl chloride (PVC) plastic, in particular, is a large
part of the medical waste stream. In fact, 25 percent of plastic medical
products are made of PVC. But PVC is the least recycled type of plastic, so
PVC is a large part of the waste stream in medical waste incinerators. In
incinerators, PVC is a large contributor to the chlorine available for
dioxin formation. But many PVC medical devices can be replaced with non PVC
alternatives, including intravenous (IV) bags and fluid collection devices.
Some European countries have acted more aggressively to limit the use of
PVC, and in response there are US-based companies providing non-PVC IV bags
to Europe, which are not yet available in the US.
Recommendations
-
Eliminate Medical Waste Incineration
-
In the Interim, Strengthen Performance Standards for Incinerators
-
Phase-Out the Use of PVC In Medical Products
-
Develop Alternative Technologies for Medical Waste Treatment
-
Require Waste Reduction/Segregation Policies for Health Care Facilities
Eliminate Medical Waste Incineration
A. No new medical waste incinerators should be built.
B. Existing medical waste incinerators, both on-site and commercial,
should be phased out over the next five years.
In the Interim, Strengthen Performance Standards for Incinerators
A. The EPA must stop using the Maximum Achievable Control Technology (MACT) rule as justification that they have done enough to control dioxin, and instead move to a strategy to prevent dioxin generation and exposure.
B. Medical waste incinerator ash and scrubber effluent must be
designated as "hazardous" waste, rather than "special"
or solid waste. Policies should ensure that this ash is isolated from the
environment and that scrubber effluent is treated to remove contaminants
prior to release into sewage treatment systems.
Phase-Out the Use of PVC in Medical Products
PVC is a primary source of dioxin emitted from medical waste
incinerators. PVC products are rarely recycled, and they should not be
burned. The manufacturers of medical devices need to move away from making
products with PVC and begin using viable alternatives.
Develop Alternative Technologies for Treating Medical Waste
The EPA also needs to look at emissions from non-incineration treatment
technologies. There is currently a lack of information about what comes out
of autoclaves, microwaves, and other alternative disposal technologies.
While early indications are that these technologies do not produce dioxin,
we can't be sure without further investigation.
Require Waste Reduction/Segregation Policies for Health Care
Facilities
A. All levels of government need to address the waste stream that goes
into medical waste incinerators, not just regulate what gets emitted from
them. Specifically they should mandate that health care facilities recycle
or minimize as much of their waste as possible and where possible,
eliminate chlorine-containing products they purchase. These would include,
but not be limited to, all PVC products (IV bags, patient ID bracelets,
vinyl covers for patient records, shower curtains, etc.), and
chlorine-bleached paper and packaging. This would remove the majority of
the dioxin-creating products from the medical waste stream.
B. The health care industry needs to have a policy of ownership and
responsibility for their wastes, rather than the current practice of trying
to shift liability and responsibility to outside vendors, the government,
etc. Taking responsibility for their waste stream would mean implementing
strict waste minimization, recycling and toxicity reduction. This would
include asking vendors to minimize packaging, using chlorine-free products
and educating employees about the health and environmental impacts of their
product choices.
C. The health care industry needs to move toward sustainable materials use, and end its use of PVC and other plastics that are not recyclable.
|
Problem
The EPA has estimated that in 1995, hazardous waste incineration
released from 2.6 to 12.8 grams TEQ, with a central estimate of 5.7 grams
TEQ. Hazardous waste incineration is the fifteenth largest source on EPA's
list of dioxin emissions to air in 1995. Hazardous waste incineration is
one of the dioxin sources most contradictory to the precautionary
principle. By allowing incineration as a disposal method for waste that is
already toxic, EPA is encouraging the distribution and production of more
of these toxic materials. In addition, existing policies don't address the
cumulative impacts of the facilities and their emissions. The EPA prefers
to operate as if the absence of evidence is evidence of absence of harm.
Currently the burden of proving that hazardous waste incineration is unsafe
rests on the community while the polluters and the government can't prove
that these facilities are safe.
In addition, the siting of hazardous waste incinerators has become an
environmental justice issue. Time and time again, the government and
industry have tried to site these facilities on Indian Tribal reservations
or in low income, people of color communities. Again, it is up to the tribe
or community to prove that these facilities will have long-term health and
environmental effects. The permitting process does not provide for a
transparent, community-based decision-making process. Often, low-income,
people of color, and Indian tribal communities are the last to know about
the siting of toxic waste facilities in their community.
If all hazardous waste incinerators were shut down today, there would
still be hazardous waste to deal with. Therefore, effective, economically
viable, low-impact, non-combustion alternatives for hazardous waste
disposal are needed. But hazardous waste generators must also reduce the
amount of hazardous waste they create. Preventing the creation of new waste
will reduce the need to continue dangerous practices such as burning
hazardous waste. Toxics use reduction, the practice of changing the amount
and toxicity of waste by reducing or eliminating the use of toxic chemical
inputs, is a much more precautionary approach than trying to control the
emissions which come out of incinerator stacks.
Recommendations
-
Eliminate Hazardous Waste Incineration
-
In the Interim, Strengthen Policies To Protect Impacted Communities
-
Reduce the Creation of Hazardous Waste
-
Identify Alternatives to Hazardous Waste Incineration.
Eliminate Hazardous Waste Incineration
A. No permits for new hazardous waste incinerators.
B. A five year phase-out of all existing hazardous waste incinerators.
C. An immediate ban on the disposal of hazardous waste in other
industrial combustion facilities, including, but not limited to,
co-generation plants, cement and aggregate kilns, boilers, and incinerators
burning chemical weapons or other munitions. Hazardous waste should not be
burned as fuel.
In the Interim, Strengthen Policies to Protect Impacted Communities.
A. Provide full and easy public access (e.g. internet access to real
time data) to all monitoring data for all emissions and operational data
(unusual occurrences, shutdowns, etc.) for existing incinerators.
B. Appropriate agencies should investigate the health effects of
exposure to emissions on communities surrounding hazardous waste
incinerators.
C. Appropriate agencies should investigate the effects of hazardous
waste incineration on agriculture and livestock, including analysis of hay
and grasses near the facilities to monitor how dioxin and other pollutants
travel up the food chain.
Reduce the Creation of Hazardous Waste
A. Require hazardous waste generators to focus on the materials they
use, through a toxics use reduction program. Such programs should require
audits of toxic chemicals used in all production processes, planning to
reduce the amount of toxics used, and public reporting of toxics use, and
provide technical assistance for companies to meet these requirements.
B. Create capital investment initiatives for hazardous waste producers
to invest in pollution prevention and minimize the amount of hazardous
waste they create.
Identify Alternatives to Hazardous Waste Incineration
New disposal methods for hazardous waste must be non-combustion,
environmentally sound and preferably closed-loop. Before alternative
disposal methods are approved for widespread use, they must be carefully
evaluated.
A. A coordinated and integrated effort between private industry, EPA,
the Department of Defense, the Department of Energy, and all government
innovative technology projects to accelerate the identification and
deployment of non-incineration technologies for hazardous waste disposal.
B. Develop a set of criteria by which to measure the economic and
technical viability, appropriateness, and acceptability of alternative
disposal methods, which emphasize community health and ecological concerns.
The community should be an equal partner in this process.
|
Problem
Some cement and aggregate kilns burn hazardous and municipal solid waste
for fuel. Because of a loophole in federal law, wastes which are burned as
fuel are considered exempt from being regulated as hazardous waste. This
means that kilns which burn hazardous waste as fuel (they call it
"recycling") are not held to the same standards as commercial
hazardous waste incinerators, weak as those may be. This loophole provides
economic gains both for the hazardous waste generators, who avoid the
higher costs of hazardous waste treatment, and the cement and aggregate
producers, who get paid to take the waste they use as fuel and don't have
to buy as much traditional fuel. There should be a ban on using solid or
hazardous waste as fuel. Industry should instead convert to unadulterated
fuels such as natural gas which would have less impact on the environment.
According to EPA's dioxin sources inventory, making cement or aggregate
with hazardous waste fuel creates more dioxin than using conventional
fuels. The EPA has estimated that in 1995, cement and aggregate kilns
burning hazardous waste for fuel released from 48.4 to 484 grams TEQ of
dioxin, with a central estimate of 153 grams TEQ. Waste burning kilns are
the fifth largest source on EPA's list of dioxin emissions to air in 1995.
Kilns which do not burn waste for fuel were estimated to release from 5.6
to 56.3 grams of TEQ of dioxin in 1995, with a central estimate of 17.8
grams TEQ, the tenth largest source on EPA's list of dioxin emissions to
air.
The process of making cement also produces fine particles, or cement
kiln dust. This dust is captured by pollution control equipment, and in
other settings is typically described as "fly ash." EPA testing
has found cement kiln dust to contain dioxin, with dioxin content being
higher in dust from kilns which burn hazardous waste as fuel. The dust is
exempt from being regulated as hazardous waste, and can be disposed of in
landfills. But due to regulatory loopholes, dust from cement and aggregate
kilns is also mixed with clinker to make cement, distributed to unknowing
customers as soil amendment or stabilizing material for other waste, or
dispersed directly into the environment as it is spread on land. At the
kilns, the dust is often stored outside in piles. But cement kiln dust was
not included by EPA in their source inventory, because the agency considers
its disposal in landfills an assurance that the dust will not make it's way
back into the environment.
The cement industry began without the use of toxic fuel and for decades
it prospered without the economic crutch of providing hazardous waste
incineration. And many will argue that the market for cement will remain if
the kilns can no longer use waste for fuel. But if jobs are lost due to the
end of waste fuel, a just transition must be part of any policy for the
cement and aggregate industry.
Recommendations
-
Eliminate the Use of Hazardous Waste or Other Wastes as Fuel
-
Prohibit Land Application or Secondary Use of Cement Kiln Dust
-
During the Phase-Out of Hazardous Waste Fuels, Strengthen Policies to Protect Workers and Communities
Eliminate the Use of Hazardous Waste or Other
Wastes as Fuel
A. Government should encourage a voluntary immediate end to the use of
burning waste for fuel. If this doesn't happen, federal law should
institute a mandatory time line for the end of this practice.
B. No permits should be granted for facilities to switch to burning
waste for fuel, or for new facilities which would burn waste for fuel.
Prohibit Land Application or Secondary Use of Cement Kiln Dust
A. Legislation or policy must eliminate the loophole which allows
toxic wastes, such as cement kiln dust, to be "recycled" or used
as ingredients to avoid classification as hazardous waste.
B. Legislation or policy must prohibit the mixing of dust back into the
cement product.
C. In the interim, cement or aggregate which is made this way must be
labeled as such.
During the Phase-Out of Hazardous Waste Fuels, Strengthen Policies
for Workers and Communities.
A. EPA must identify and track the inter-media transfers (that is, from
fuel to product, from fuel to dust, from fuel to the air, etc.) of
chlorinated compounds in kilns burning hazardous waste.
B. EPA should collect and evaluate data on emissions and releases from
kilns burning hazardous wastes to determine what has been released into
surrounding communities.
C. Appropriate agencies should investigate the health effects of
exposure to these emissions on communities surrounding cement and aggregate
kilns burning hazardous waste.
D. Appropriate agencies should investigate the effects of kilns on
agriculture and livestock, including analysis of hay and grasses near the
facility to monitor how dioxin and other pollutants travel up the food
chain.
E. Policy should require public access to information on what fuels
kilns are burning and how wastes are being handled.
|
Problem
Dioxins are found in the water, air and solid wastes created at pulp and
paper mills. The largest cause of dioxins in the industry is the use of
elemental chlorine and other chlorinated compounds in the bleaching
process. In addition, salt-laden wood, chlorinated plastics, and sludges
are burned in on-site incinerators which produce energy for the operation
of the mill. These incinerators (called "hog fuel boilers")
generate dioxin, but are totally unregulated for dioxin. Dioxins have also
been found in bleached paper food containers and other products. The
EPA has estimated that in 1995, pulp and paper mill effluent contained from
13.8 to 27.6 grams TEQ of dioxin, with a central estimate of 19.5 grams TEQ;
that pulp and paper mill sludge contained from 20 to 40 grams TEQ, with a
central estimate of 28.4 grams TEQ; and that pulp contained from 17 to 34
grams TEQ, with a central estimate of 24.1 grams TEQ.
Current policies for the pulp and paper industry are not protective of
the environment and public health. The latest federal policy for the
industry, the "Cluster Rule," is a technology based standard
which mandates the "best available technology" for pulp and paper
mills. The cluster rule designates chlorine dioxide as the best available
technology for bleaching, a choice based more on economics than health
considerations. Chlorine dioxide was the industry's preference for
bleaching technology because it requires the least change from current
practice. But while chlorine dioxide bleaching produces less dioxin than
elemental chlorine bleaching, it does not eliminate dioxin releases. The
designation of chlorine dioxide as the best technology doesn't adequately
protect worker safety because chlorine dioxide poses significant accident
risks. Also, mills using chlorine dioxide cannot convert to "closed
loop" or zero discharge systems, which should be a goal for the
industry. And the rule has no requirements for testing air discharges of
dioxins. The cluster rule takes a back-ended approach, rather than looking
at the industry's impact on health and the environment. A protective policy
would acknowledge that the best technology for bleaching paper is one that
minimizes threats to worker and community health. The best technology is
chlorine-free, not chlorine dioxide.
Many U.S.-based companies are making short-sighted investments in
chlorine dioxide bleaching technology and virtually ignoring non-wood
fibers, which need little or no bleaching. The technical and economical
feasibility of processes that are free of dioxins, furans, organochlorines
and their precursors has been proven in the industry's more advanced mills
around the world. Worldwide, the industry is already moving gradually
towards the use of oxygen, ozone, peroxide and other non-chlorine bleaching
methods.
Recommendations
-
Adopt Totally Chlorine-Free (TCF) Processes and Technologies
-
In the Interim, Develop Strong Protective Policies and Eliminate Loopholes
-
Ensure Worker Health & Safety
-
Require Product Testing
Adopt Totally Chlorine Free (TCF) Processes and
Technologies
A. EPA policy should move toward the complete elimination of chlorinated
chemical feedstocks over the next five years. This timed phase-out will
allow the industry a gradual transition to Totally Chlorine-Free (TCF)
processing without undue economic burdens.
B. In its policy, EPA must set a ten-year time line for mills to achieve
the zero discharge goal of the Clean Water Act. Requiring mills to adopt
TCF technologies is the first step to achieving the goal of zero discharge
called for in the Clean Water Act.
In the Interim, Develop Strong Protective Policies and Eliminate
Loopholes
A. Rectify the Cluster Rule
EPA's decision to base the "best available technology"
standard for bleaching on the use of chlorine dioxide was irresponsible. To
rectify this part of the rules, the EPA policy should include the
following:
-
Time lines that require advanced technologies such as oxygen delignification, extended cooking, and ultimately, TCF bleaching as the best available technology for the industry. These Time lines could coincide with requirements for zero discharge of dioxins, furans, and other chlorinated compounds.
-
Testing of effluents and affected water bodies with high volume dioxin monitoring devices to record levels of dioxins currently considered "undetectable."
-
Regular testing of fish, aquatic plants and animals, and sediments in these areas. Zero tolerance for dioxin buildup in these organisms should be established.
-
Encouragement for the development and implementation of processes to eliminate chlorine donors, such as chlorinated process water.
B. Strengthen the Maximum Achievable Control
Technology (MACT) Rule
The EPA needs to take the potential for the pulp and paper industry to
emit dioxin and precursors to air more seriously. The new MACT I rule is a
step in the right direction, but assumes without adequate proof that levels
of chlorine compounds released to air will be reduced with a reduction in
methane emissions. The proposed MACT II rules need serious revision if they
are to protect public health. The EPA must:
-
Study, control, and eventually require elimination of air discharges of chlorine, chlorine dioxide, chloroform, hydrochloric acid and other chlorinated compounds.
-
Study whether dioxins and furans or their precursors are created by ambient air discharges and if there are other health effects from these discharges.
C. Combustion Processes and Waste Treatment
-
Chlorinated feedstocks, excluding untreated wood, but including sludges, salt-laden wood, and plastic waste from recycling operations, must be eliminated from incinerators (hog fuel boilers) and other combustion "process equipment."
-
Industry must further research how much dioxin is transferred from air and water discharges into solid waste and paper products, to better understand where the chlorine from bleaching processes ends up. Simply transferring dioxin through pollution control equipment is not acceptable.
D. Sludge
-
Chlorinated sludge should be considered and managed as hazardous waste. The sludge from processes using chlorinated compounds for bleaching must be tested on a regular basis. Strict standards must be set for the dioxin levels allowed in these sludges.
-
The EPA should prohibit the incineration or land spreading of chlorinated pulp sludge.
Ensure Worker Health & Safety
A. Appropriate government agencies, including the Occupational Safety
and Health Administration and the National Institute for Occupational
Safety and Health, must better evaluate the health of pulp mill workers and
communities who have been exposed to decades of chlorine use at mills. The
studies must look beyond cancer and include effects on the immune, hormone,
and reproductive systems, as well as developmental damage and chronic
respiratory diseases.
B. These government agencies must also better evaluate the worker and
community safety aspects of chlorine dioxide use at pulp mills. Chlorine
dioxide threats are greater than that of elemental chlorine, and its
chronic effects are largely unstudied.
C. The government and industry must find a consistent source of revenue
for Just Transition for mill workers and communities affected by these
changes.
Require Product Testing
A. Products bleached with chlorinated compounds must be tested for
dioxin on a regular basis.
B. Products must be labeled with the amount of dioxin they contain.
C. Strict standards calling for zero dioxin should be set for products.
D. Government and industry should explore the issue of potential health
impacts of dioxin in products which come in contact with food or sensitive
skin on a regular basis, such as napkins, bathroom tissues, sanitary
napkins, tampons, and the like.
In a broader context, the paper industry and government should be taking
positive steps to promote healthier processes and products. They should
encourage all levels of government to purchase totally chlorine-free or
processed chlorine-free paper products and sponsor public education
campaigns about the problems with dioxin and the role of chlorine-free
processes in reducing health risks.
|
Problem
Polyvinyl chloride (PVC) plastic's entire life cycle, from production
through use and disposal, has negative environmental impacts. PVC is made
from two carcinogens, ethylene dichloride (EDC) and vinyl chloride monomer
(VCM). The production of PVC creates large amounts of toxic chemicals,
including dioxins, furans, PCBs, and hexachlorobenzene. A 1993 Greenpeace
estimate of dioxin emissions would place PVC production among the largest
sources of dioxin in the U.S.
EPA used a combination of Greenpeace and industry data to come up with a
much lower estimate, but didn't include it in its 1998 sources inventory
because they felt that there was insufficient information to make a
"definitive release" estimate.
The PVC industry has been plagued by worker health and safety issues for
decades. The industry was aware of health problems among PVC plant workers,
including high rates of cancer, for decades before that information was
shared with regulators or workers. The industry spent years using public
relations and manipulating science in order to avoid disclosure and
liability for worker illnesses and deaths. A Federal Court has noted that
"the record shows what can only be described as a course of continued
procrastination on the part of the industry to protect the lives of its
employees."
PVC is widely used to make building materials, pipes, furniture, and
components of automobiles. Although not especially flammable, when PVC is
involved in a fire it gives off toxic hydrogen chloride gas which turns
into hydrochloric acid on contact with moisture in the lungs. PVC is
involved in a large portion of the approximately one million building and
automobile fires in the U.S. each year. Combustion of PVC in accidental
fires may be another significant source of dioxin in the environment.
When PVC is burned in medical waste and garbage incinerators, it is
among the largest single sources of dioxin in those burners. Extremely
toxic heavy metals in PVC, such as lead, cadmium and chromium, are also
released from the stacks and end up in the ash of these incinerators.
Pollution associated with the life cycle of PVC has a disproportionate
effect on low-income, people of color, and Indian Tribal communities. PVC
ingredients and their toxic by-products have contaminated the air, water
and soil of communities on the Gulf Coast of Louisiana and Texas where the
industry is concentrated. These communities have significantly higher
percentages of non-white residents than state and national averages. In
addition, incinerators which burn municipal, medical, and hazardous wastes
rich in PVC and its by-products tend to be located more predominantly in
African-American, Latino, and Indian Tribal communities.
Virtually all of the products made of PVC have safer substitutes
available, making the risks posed by PVC completely unnecessary and
unacceptable.
Recommendations
-
Phase-Out PVC
-
Ensure a Just Transition For Workers
-
During Phase-Out, Address Environmental Justice Concerns
Phase-Out PVC
EPA should announce a PVC "sunset" program, the intent of
which is to progressively reduce the production and use of PVC in the U.S.
to zero. Priority should be given to those uses that cause the most dioxin
formation during their life cycle (e.g., those most likely to be
incinerated or involved in fires) and are most easily replaced with safer,
chlorine-free substitutes.
A. Phase-out existing PVC production plants over five years, and permit
no new facilities. During these five years, begin the process of providing
for a just transition for workers, as described below.
B. Over five years, phase-out burning PVC waste in commercial burners
and incinerators.
C. More rapid phase-outs of:
-
All short-life PVC uses (packaging, toys, IV-bags, etc.).
-
PVC products in areas susceptible to fire (construction materials, PVC coated cables, appliances, and vehicles)
-
Combustion-based processes to recycle metals containing PVC residues (electrical cables, automobile components).
D. Promote alternative products. EPA should encourage
the government to purchase alternatives to PVC to help develop markets for
these products.
Ensure a Just Transition For Workers
Any plan to protect health and the environment from dioxin sources --
including a PVC sunset program -- must prevent or compensate for job loss
and economic disruption for communities and workers.
-
A tax during phase-out on the production of EDC and VCM would help to drive the transition away from PVC and finance the costs associated with it. The revenues from such a tax could be used for transitional measures to ensure that a PVC phase-out is just, equitable, and orderly for workers and affected communities. In particular, a transition fund could be used to assist affected workers and communities by providing funding for educational opportunities, income protection, health insurance, and research and development of safer PVC alternatives.
During Phase-Out, Address Environmental Justice
Concerns
-
EPA should apply its environmental justice policy and investigate and initiate action to prevent dioxin formation during the life cycle of PVC plastic. President Clinton's Executive Order 12898 on Environmental Justice requires that the agency improve "research relating to the health and environment of minority populations" and reduce pollution in these communities.
|
Problem
In these recommendations, the term "pesticides" refers to
pesticides, insecticides, herbicides, fungicides, rodenticides, and wood
preservatives. Some pesticides are contaminated with dioxin as a result of
manufacturing processes which use chlorine. Some of the better known
dioxin-contaminated pesticides include Agent Orange, 2,4,5-T, Silvex,
2,4-D, and pentachlorophenol. This dioxin contamination is not disclosed on
pesticide product labels. Other chlorinated pesticides are suspected to be
contaminated with dioxin because they contain chlorine. And as discussed in
the policy recommendations for other sources, burning chlorinated wastes
such as pesticides can create dioxins. Chlorinated pesticides should not be
burned for disposal or as fuel. There is no EPA estimate of the amount of
dioxin released during the production of pesticides because the manufacture
of some dioxin-contaminated pesticides is banned or strictly regulated, and
because the contents of pesticide formulations are considered confidential
business information. However some dioxin-contaminated pesticides, such as
2,4-D and pentachlorophenol are still used widely today and past releases
of banned substances can continue to be a source of exposure.
All pesticides, including those contaminated with dioxin, invade all
organisms (humans, pets, and wildlife) through the food we eat, the water
we drink, and air we breathe in our homes, schools, workplaces, and
habitat. Exposure is primarily involuntary, with people and wildlife being
exposed to hazards unknowingly. Workers and communities are exposed during
manufacture, transportation, application, and disposal. Farmers and farm
workers are exposed in all phases of pesticide mixing, loading, use, and
disposal, as well as in the harvesting of crops. In addition, people are
exposed as a result of off-target drift and contamination of groundwater
and surface water. Pets and wildlife are exposed to pesticides throughout
the environment: lawns, forests, crop lands, rangelands, soil, air, and
lakes, streams, and oceans.
Many pesticides which are now banned or highly restricted in the U.S.
are still produced domestically and exported to developing countries.
Communities in these countries are subject to the same public health and
environmental risks from these products which were deemed unacceptable
here. In an ironic "circle of poison" these banned and highly
restricted pesticides are used to produce food with hazardous residues and
sent back to the U.S. to find their way to our dinner tables.
Recommendations
-
Eliminate Dioxin-Contaminated Pesticides
-
In the Interim, Develop More Protective Pesticide Policies
Eliminate Dioxin-Contaminated Pesticides
A. The EPA should ban dioxin-contaminated pesticides. This could be done
under existing federal laws, including the "reasonable certainty of no
harm" standard of Food Quality Protection Act.
B. In the interim, establish an Elimination Task Force. The Task Force
will consist of practitioners and advocates of alternatives to the use of
such pesticides, and will investigate options for local, state, and
national plans for the elimination of production, use, and incineration of
dioxin-contaminated pesticides.
C. Support environmentally sound alternatives to dioxin-contaminated
pesticides. (For instance, phosphate pesticides cause chemical sensitivity,
so they are not a viable alternative.)
D. The plan to eliminate dioxin-contaminated pesticides must include a
commitment to a just transition and plans to prevent or compensate for the
economic and social dislocation that results from elimination.
E. In the interim, the export of banned dioxin-contaminated pesticides
must be prohibited.
F. Appropriate government agencies should establish a testing program
for pesticides suspected to be contaminated with dioxin. If they are found
to be contaminated, the pesticides should be included in the process for
elimination detailed above.
In the Interim, Develop More Protective Pesticide Policies.
A. Prohibit lending policies that require farmers to have a pesticide
use plan in order to get a loan.
B. Identify, through mandatory testing, pesticide manufacturing
processes and pesticide manufacturer locations that result in dioxin
formation.
C. Establish protective health-based standards for cleanup methods for
closed pesticide manufacturing and disposal facilities and provide
resources for strong enforcement.
D. Develop protective exposure standards and an education campaign for
workers involved in the manufacture, application, and disposal of
pesticides.
E. Forbid the preemption by state or federal law of local requirements
for posting of the use and/or presence of dioxin-contaminated pesticides.
F. Identify and label pesticides contaminated with dioxin.
G. Identify and publish lists of dioxin-contaminated pesticide
ingredients by trade name, common chemical name, and chemical name/CAS
number.
|
Problem
Petroleum manufacturing (oil and gas refining) uses and mobilizes
chlorine in multifaceted process systems that combine it with
petrochemicals, catalysts and heat. Of the industries known to generate
dioxin, oil and gas refining is the largest, by mass of material produced.
All refinery processes tested to date (reforming, cracking and oil-fired
boilers/furnaces) test positive for dioxin. Evidence also suggests the
production of dioxin-like PCBs by the industry.
Dioxin has been found in stack, wastewater, and runoff releases and
refined products. (Diesel and motor oil tested straight from the refinery
contain dioxin, chlorine, and dioxin precursors, and vast amounts of
petroleum coke are sold to be burned in other industries that are confirmed
dioxin sources.) The amount of dioxin released has not been estimated due
to lack of testing by government agencies and failure to test and report
the industry's dioxin releases via refined products distributed (and often
burned) just about everywhere. However, data from the San Francisco Bay
Area show a clear gradient of increasing environmental dioxin levels as one
moves from 100 miles away, to miles away, to the location of the refinery
and suggests that the industry is one cause of cumulative dioxin pollution.
The petroleum manufacturing industry is involved in creating conditions
of environmental injustice. Low income communities of color are on the
refinery fence lines and eat fish from the harbors where refineries dump.
Workers face severe health and safety threats and threatened and actual job
loss, while the industry consolidates and downsizes. Oil firms have an
unfair share of the power in decisions about what happens in communities.
Recommendations
-
Eliminate Chlorine from the Process
-
Ensure a Just Transition and Worker Health & Safety
-
Ensure a Transparent, Equitable and Verifiable Process
Eliminate Chlorine from the Process
The use of chlorinated solvents to recondition certain catalysts means
that chlorine is present in amounts which could form dioxin at many steps
in the refining process.
A. Identify all the preventable uses of chlorine in dioxin-producing
refinery processes, since dioxin cannot be produced without chlorine.
B. Eliminate the chlorine source in every dioxin-producing reaction in
the plants since oil can be refined without chlorine. Find alternatives
which prevent the addition of chlorine and chlorinated compounds throughout
the processing systems and related activities. For example, remove the
carbon buildup from metal catalysts without burning chlorinated solvents
and redesign or replace existing chlorine and chloride removal systems,
since the original 'desalters' were designed before it was recognized that
there is an urgent need to prevent the formation of dioxin from traces of
chlorine.
Ensure A Just Transition and Worker Health & Safety
Take all necessary steps to include community members and plant workers
and give them an equal voice in decision-making about how quickly the oil
company will zero out dioxin and how it will retain jobs and improve worker
health and safety while it does so.
-
Immediate up-front investment by the oil company operating the plant into funds which will pay not only capital costs for the switch to zero chlorine/zero dioxin solutions, but also pay for community members' and workers' work on the projects, for independent technical consultants hired and directed by the community and workers, for any costs of finding and verifying zero dioxin solutions, and for job retraining or transition.
Ensure a Transparent, Equitable and Verifiable
Process
Precautionary policy for oil and gas refining would base priorities for
action on what can be done and verified now to eliminate dioxin.
-
Ensure that the absolute need for a publicly verifiable dioxin elimination process is honored. The presence or absence of dioxin and chlorine at a root source is verifiable, and public information and verification is fundamental to community power, democracy, and the scientific process.
-
In addition, we need to stop oil and gas manufacturers from contributing to other polluting practices when they can no longer sell ethylene to PVC manufacturers; petroleum coke to power plants, foundries and cement kilns; low grade diesel and motor oil that spreads dioxin pollution; etc. Policy should take a preventive, zero-dioxin approach in the petroleum life cycle, which would include its use as a fuel in polluting practices such as those listed above.
|
Problem
Metallurgical processes are accompanied by the generation of numerous
pollutants, including dust, soot, solid waste and a variety of toxic
compounds. Historically, the industry has been under constant pressure to
reduce the resultant impact on the environment and the hazards to which its
workers are exposed.
In recent years, the thermal processes used in several metallurgical
operations in iron and steel-producing sectors as well as the copper,
aluminum, magnesium, nickel and other metal industries were identified as
potential dioxin sources. Research in some European countries, particularly
in Germany, Netherlands, Sweden, and Norway have shown that these
metallurgical processes, particularly iron sintering, are significant
contributors to national dioxin inventories. The United States and Canada
are aware of these sources, but so far only very few measurements have been
performed. Preliminary results from the small number of dioxin stack tests
on iron sintering plants indicate, however, that the measured dioxin
emissions are comparable to what has been found at European facilities of
the same type. Thus, the design and implementation of a comprehensive
dioxin testing program for metallurgical facilities in North America is
essential to assess the true magnitude of these emissions.
Based on the evidence from European studies of different metallurgical
processes, it is possible to identify ways to virtually eliminate the
dioxin emissions from these types of facilities. The studies indicate that
the emissions are chiefly due to the presence of input materials that are
contaminated with chlorinated organic compounds. Hence, one way to
virtually eliminate dioxin emissions is simply to avoid the introduction of
these compounds into metallurgical processes. One specific source of
chlorine is polyvinyl chloride (PVC) plastic, a ubiquitous material in
metal recycling facilities such as secondary copper smelting (PVC coated
wiring) and possibly steel recycling (PVC components in cars and
refrigerators.) PVC which goes through the combustion or heating processes
at these plants leads to dioxin creation. Despite the uncertainty of
estimating dioxin releases from metal production, EPA estimated that in
1995, secondary copper smelting released from 171 to 1710 grams TEQ of
dioxin, with a central estimate of 541 grams TEQ. Secondary copper smelting
is the second largest source on EPA's list of dioxin emissions to air in
1995.
However, reducing other chlorine inputs may be more difficult and bear
economic consequences for both the owner/operators of these facilities and
the employed labor force. In addition, while evidence from European studies
of metallurgical processes suggests that there are ways to reduce dioxin
emissions, so little is yet known about U.S. and Canadian plants that
remedial measures and the economic consequences of implementing them remain
poorly defined. In these circumstances the most important recommendation is
to establish a comprehensive survey of the impact of the present operating
practices in the different metallurgical operations on their dioxin
emissions. On that basis it would be possible to devise facility
type-specific remedial measures for preventing dioxin emissions at the
source - the entry points of chlorine - and to evaluate their economic
feasibility.
Recommendations
-
Determine the Causes and Amounts of Dioxin Production in U.S. Metals Facilities
-
Eliminate Chlorine Inputs in Metallurgical Processes
Determine the Causes and Amounts of Dioxin
Production in U.S. Metals Facilities
-
Government agencies should establish a comprehensive and updated dioxin stack test program for all source classes, including metallurgical facilities.
-
EPA should develop an audit program for different metallurgical facility types (integrated iron and steel plants, mini mills, grey iron foundries, secondary copper smelters, secondary aluminum smelters, and magnesium, nickel, and other metal production facilities) to identify points of entry for chlorinated compounds.
Eliminate Chlorine Inputs in Metallurgical
Processes
-
Establish requirements for facilities involved in the manufacture of ferrous and non-ferrous metal products to prevent wherever possible the contamination of their input materials with chlorinated compounds, including PVC plastic, a key pre-requisite to eliminating the possibility of dioxin formation during the thermal processes as part of their production sequence.
|
Problem
Dioxin and PCBs, a similarly toxic and persistent group of chemicals,
are often found together in contaminated sites and present similar
challenges to communities seeking safe, thorough cleanup. Currently, the
most common remedies are to incinerate or landfill contaminated soil. These
are not acceptable options to concerned communities, nor are they
protective of human health and the environment. Landfilling without
treatment simply moves the contamination to another community, which will
eventually be impacted when that landfill leaks. Containment on-site
without treatment just leaves the contamination for future generations. And
incineration creates emissions of dioxin and other toxic air pollutants,
and does not completely destroy the dioxin and PCBs in the material being
burned. Incineration is not an acceptable "treatment."
Communities need safe destruction of these contaminants which can be done
on-site, and with no adverse impacts on human health and the environment.
The use of incineration as a remedy is perpetuated by an industry and
government bias against innovative non-incineration technologies. This bias
can be seen in engineering curricula, regulatory training, and research
which focus on building better burners and landfills. Communities are often
frustrated by the lack of alternatives to incineration. As it now stands,
companies have no incentive to develop non-incineration technologies and
EPA has no mandate to certify alternatives for use in the field. Another
disturbing trend is leaving the contamination in place and relying on
"natural attenuation" to take care of the problem. Natural
attenuation essentially means performing no further treatment and waiting
for dilution, dispersion, evaporation, and eventually degradation to deal
with the contamination.
Current requirements for community participation in the choice and
oversight of cleanup methods are inadequate. Public participation practices
are often treated by government agencies as mere formalities, even though
it is the community which must live with the consequences of the cleanup.
For example, public notification about hearings often consists only of an
ad buried in the
back of the newspaper or in government bulletins citizens don't see. And
while Superfund's Technical Assistance Grant (TAG) program is a valuable
start towards improving public participation, it could be strengthened. One
improvement would be to allow TAG groups to fund independent testing of the
cleanup site. Citizens need data which is not generated by the parties
responsible for paying for the cleanup. But most importantly, citizens need
an equal voice in the decision-making process. If citizens express an
opinion or oppose a cleanup decision, current laws do not give this
viewpoint the same weight as those of government agencies or companies
paying for the cleanup.
Recommendations
-
Require Selection of Community-Accepted Cleanup Technologies
-
Develop Non-Incineration Destruction Technologies which are Effective, Feasible, and Portable
Require Selection of Community-Accepted Cleanup
Technologies
A. Communities affected by any cleanup decisions must have participation
and input equal to that of agencies and responsible parties in all
negotiations. The burden of proving a technology is harmful should not fall
to the community. Rather, the responsible parties and government agencies
should have to prove to the community's satisfaction that the proposed
technology is safe. Communities must have final veto power over any
decisions made which affect their well-being, including property values and
health risks.
B. In order to remedy the problem of inadequate community involvement in
the cleanup process, the following elements must be added to the public
participation process:
-
Meaningful notification and pre-hearing for any cleanup project, including written notices to community and environmental groups.
-
Funding for technical assistance, including the generation of independent test data, to community and public interest participants.
-
Capacity for effective and genuine community oversight must exist prior to the choice of a technology. This capacity should include timely sharing of relevant information about the project with a TAG group and the community.
-
Communities must be meaningfully involved from the beginning of the process. This includes giving equal weight and consideration to the input of the community, data generated by the community, and the information and conclusions of the community's TAG advisors. Decisions about cleanup should be made by a team which includes citizens. The team should receive adequate information and technical assistance to make an informed choice of an appropriate cleanup technology.
C. Existing cleanup standards should be enforced
uniformly. Responsible parties' influence should not result in a less
thorough cleanup.
D. Site-specific cleanup standards should be reviewed yearly with
respect to new information about health impacts and cleanup technology, and
adjusted to reflect new information.
E. Uniform, protective, health-based cleanup standards for all sites
should be established.
F. "Averaging" of contaminant levels to meet cleanup standards
must stop. This practice leaves large amounts of contamination behind
because highly contaminated areas are averaged with clean areas. Averaging
is currently allowed on residential property.
G. EPA's policy of off-site landfilling of contaminated soil with no
treatment must be discontinued.
H. Capping of contamination without treatment should be eliminated
instead of being a preferred method of site remediation. Capping is just
leaving the contamination for future generations.
I. On-site containment of contamination must be thorough, but should
only be used as an interim measure, until a destruction technology which is
acceptable to the community can be used at the site.
Develop Non-Incineration Destruction Technologies Which Are
Effective, Feasible, and Portable
A. The current regulatory system is not adequate to encourage
alternative (non-incineration) destruction technologies. We need a
regulatory process that is more responsive to the development of new
technologies and that facilitates such development, rather than impeding
it. Government support for such research and development should require
consideration of the technology's appropriateness to a broad range of
environments and social settings, including applications in developing
countries with relatively low technological capacity. Beyond government
support for development, EPA must commit to utilizing and testing new
technologies in the field and certifying them for use at cleanup sites.
B. To help communities deal with the inevitable trade-offs faced when
deciding between technologies, information on the performance of full-scale
conventional and alternative facilities should be made available. The
following technical criteria need to be considered when exploring
alternative methods of clean up:
-
Destruction efficiency
-
Potential for the production of dangerous compounds or by-products
-
Safety
-
Potential for uncontrolled/fugitive releases (from handling, storage, transportation, or processing)
-
Potential for vessel containment failure (leaks or other releases)
-
Potential for catastrophic release (such as an explosion)
-
What chemicals remain after treatment
-
Potential for the leftovers to be re-processed
-
Capability for and commitment to community/external monitoring throughout the life of the project
-
Complete access to information about the technology
-
Public acceptance
-
Need for any specialized resources, including trained personnel, water, electricity, etc.
-
Track record and reliability of the company/contractor and the technology (down time and maintenance issues)
-
Amount of time for project completion
-
Business factors (cost, management, insurance, regulation and oversight)
-
Portability (potential for on-site treatment)
-
Ability to dismantle and remove when cleanup is complete
-
Effectiveness of treatment process when it changes scale (capability to go from small experimental size to larger field unit or change scale for different project)
-
Potential for local labor and materials to be used
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Problem
Dioxin can be formed when coal is burned, because most coal contains
some chlorine. There are numerous environmental threats posed by coal
combustion, among them emissions of mercury, nitrogen oxides, sulfur
oxides, carbon dioxide and dioxin. The EPA has estimated that in 1995,
utility and industrial burning of coal released from 32.6 to 163 grams TEQ
of dioxin, with a central estimate of 72.8 grams TEQ. Utility and
industrial burning of coal is the sixth largest source on EPA's list of
dioxin emissions to air in 1995. A long term strategy to phase out the use
of coal will reduce all of the threats mentioned above.
Addressing the environmental impacts of coal burning requires measures
which will have an enormous impact on workers and some regions' economies.
Any policy on coal must acknowledge these impacts and include provisions to
minimize worker dislocation and community disruption through a program for
just transition.
As with most combustion processes, the ash from burning coal is highly
contaminated with dioxin, mercury, and metals. Coal ash from power plants
has been exempted from the Resource Recovery and Conservation Act (RCRA)'s
standards for hazardous waste. Some states are allowing the reuse of coal
ash as an aggregate material for construction, as a fill material to
reclaim strip mines, as landfill cover, or as an ingredient in fertilizer.
Such wide distribution of contaminated ash throughout the environment is a
dangerous policy. Just like incinerator ash, coal ash must be classified
and treated as hazardous waste, and not "recycled" or reused.
Recommendations
-
Eventual Phase-Out of Coal-Burning
-
Categorize Ash as Hazardous Waste
-
Ensure Just Transition for Workers
Eventual Phase-Out of Coal Burning
It is recognized that solar, wind, biomass, geothermal, and fuel cell
technologies are readily available, and can produce power with little or no
pollution. The cost of using renewable sources of energy is falling
dramatically, and should continue to do so as demand for renewable
technologies increases. Incentives for investment in energy efficiency and
renewable energy are critical to making them available to consumers in the
market place.
Due to the complex social, environmental, and economic issues
surrounding coal mining and the use of coal as a fuel, the implementation
of policies for coal should be worked out in detail by key stakeholders.
Advocates for the rights of coal miners and coal-fired utility workers, the
prevention of global warming, and alternative energy have been meeting to
define how a phase-out of coal burning could occur without lost wages for
workers or energy shortages and economic burdens for consumers. This
discussion process, called the "Blue-Green Dialogue," is not yet
complete. Out of respect to the amount of time, effort, and expertise these
stakeholders continue to dedicate to this process, we have not elaborated
implementation steps for the goal of phasing out coal burning. These
details should come from this stakeholder discussion. However, any
phase-out of coal should include, at a minimum, the following:
A. Increased federal procurement of renewable energy technologies.
B. Increased federal funding for research and development on energy
efficiency and renewable energy.
C. Requirements for utilities to produce at least a set percentage of
their electricity using renewable energy, such as solar, wind, and
geothermal. This percentage should increase on a regular basis.
Categorize Ash as Hazardous Waste.
A. An immediate ban on the utilization of ash from coal plants for any
purpose, due to its gross contamination from dioxin, mercury and other
pollutants of concern.
B. End the exemption for coal ash from classification as hazardous
waste. All ash must be managed as hazardous waste.
Ensure Just Transition for Workers
The coal industry has a dedicated labor movement and the phase-out of
coal is a serious transition for workers. There have already been a number
of jobs lost. It is critical that a phase-out of coal minimize worker and
community impacts, by including provisions for income and benefit
protection, a commitment to assisting workers in finding comparable
replacement work, and measures to ensure economic vitality for impacted
communities.
|
Problem
The EPA has estimated that in 1995, wood burning in industrial
facilities released from 13 to 65 grams TEQ of dioxin, with a central
estimate of 29.1 grams TEQ. Industrial wood burning is the ninth largest
source on EPA's list of dioxin emissions to air in 1995. Wood is burned
primarily as fuel, either to generate electricity or for heat. The
industrial sector accounts for over 70% of wood burned as fuel for
electricity in the U.S. About 25% is burned in residential homes and about
1% is burned by utilities to generate electricity. About half of the wood
consumed by the industrial sector is burned as wood waste such as wood
chips, bark, sawdust, or "hogged" fuel by the paper or lumber and
wood products industries. The rest of the wood consumed as fuel by industry
is burned in industrial furnaces.
In their 1998 dioxin sources inventory, EPA reported that dioxin was
found in all the industrial facilities burning wood which were tested.
However, much higher levels of dioxin were estimated to come from
facilities that burned wood containing higher levels of chlorine than
normal. For example, chipboard can contain high levels of chlorine because
of the binding agents it contains. Also, wood treated with
pentachlorophenol (penta) contains higher levels of chlorine than untreated
wood because penta is a chlorinated wood preservative which is often
directly contaminated with dioxin. When burned, pent-treated wood will
generate even more dioxins. Although EPA made no such estimate, other
studies have shown that about three times as much dioxin is generated at
facilities that burn penta-treated wood compared to non-treated wood.
Burning wood containing more chlorine would result in higher dioxin
emissions than those estimated above by EPA for burning untreated wood.
A number of incinerators that generate electricity have turned to
burning wood in recent years. Loopholes in federal regulations allow
companies that burn wood waste as fuel to generate electricity to bypass
stringent solid waste burning regulations and at the same time allow the
companies to charge more for the electricity they generate. The wood burned
in these incinerators includes virgin wood, wood waste, and construction
waste. Construction waste might include painted wood, treated railroad ties
and utility poles, and wood contaminated with chemicals spilled or released
during demolition.
The most common chemicals used to treat wood are pentachlorophenol
(penta), copper chromium arsenate (CCA), and creosote. Penta is banned in
26 countries. In the U.S., its use is restricted to treating utility poles.
There are an estimated 135 million utility poles in the U.S. and almost
half have been treated with penta. Approximately three million poles are
taken out of service each year. These discarded poles are not classified as
hazardous waste, so they can be disposed of in municipal waste landfills or
burned as fuel to generate electricity. The burning of penta-treated wood
generates a significant portion of the dioxin released from wood burning
and is a source which can be easily eliminated.
There are a number of loopholes in existing utility regulations that
encourage the burning of wood for generating electricity. One major
loophole is in the Public Utilities Regulatory Policies Act of 1978
(PURPA). One function of PURPA is to define from which sources, besides
their own, utility companies are required to buy electricity. Such
"Qualifying Facilities" include "small power production
facilities" and "co-generation" plants. (Co-generation
plants capture more energy than traditional electricity generators by
capturing the steam or heat which is generated in addition to the
electricity produced. The captured heat or steam is then used for
commercial, industrial, or heating purposes.) PURPA allows co-generation
plants to be fueled by waste such as tires, plastics, and wood, and
requires the electricity generated by Qualifying Facilities to be purchased
by utilities at rates that are often greater than what it costs the utility
to generate electricity at its own facility. Essentially, this acts as a
subsidy for waste burners because it guarantees a rate for the electricity
they generate.
Recommendations
-
Eliminate Industrial Burning of Treated Wood
-
Eliminate Chlorinated Wood Treatments
-
Close Loopholes that Encourage Burning Wood Waste
Eliminate Industrial Burning of Treated Wood
A. Prohibit the burning of penta-treated wood and other wood treated
with chlorinated compounds, whether in co-generation facilities, hazardous
waste incinerators, or other industrial boilers and burners.
B. Classify and manage penta-treated utility poles as hazardous waste.
C. Support development and implementation of methods to decontaminate or
destroy penta-treated wood without dioxin formation.
Eliminate Chlorinated Wood Treatments
A. Ban the use of pentachlorophenol and any other chlorinated compounds
for treating utility poles.
B. Establish a Task Force on alternatives to penta-treated utility poles, consisting of producers of alternative pole materials, knowledgeable community activists, and appropriate government
representatives. The Task Force will investigate national, state, and
local options for alternatives to penta-treated poles, and develop plans
for the eventual removal of penta-treated poles from the environment.
C. Until a ban goes into effect, develop protective exposure standards
and an education campaign for utility and construction workers exposed to
chlorinated wood preservatives.
D. Identify and promote environmentally sound non-pesticide alternatives for wood preservation treatments, including those used in other parts of the world.
E. Establish strong regulations requiring non-chlorinated treatment for
wood.
Close Loopholes that Encourage the Burning of Wood Waste
Eliminate subsidies for burning wood to generate electricity. Eliminate
the loopholes in the Public Utility Regulatory Policies Act (PURPA) which
allow the burning of chlorine-treated wood, plastics and other dirty fuels
such as tires in co-generation plants and burners from which utilities are
required to purchase power. Amend PURPA to allow only the use of clean
alternative energy sources in Qualifying Facilities.
Back to Table of Contents
Appendix A
Principles of Environmental Justice
WE, THE PEOPLE OF COLOR, gathered together at this multinational People of
Color Environmental Leadership Summit, to begin to build a national and
international movement of all peoples of color to fight the destruction and
taking of our lands and communities, do hereby re-establish our spiritual
interdependence to the sacredness of our Mother Earth; to respect and
celebrate each of our cultures, languages and beliefs about the natural
world and our roles in healing ourselves; to insure environmental justice;
to promote economic alternatives which would contribute to the development
of environmentally safe livelihoods; and, to secure our political, economic
and cultural liberation that has been denied for over 500 years of
colonization and oppression, resulting in the poisoning of our communities
and land and the genocide of our peoples, do affirm and adopt these
Principles of Environmental Justice:
- Environmental justice affirms the sacredness of Mother Earth,
ecological unity and the interdependence of all species, and the
right to be free from ecological destruction.
- Environmental justice demands that public policy be based on
mutual respect and justice for all peoples, free from any form of
discrimination or bias.
- Environmental justice mandates the right to ethical, balanced, and
responsible uses of land and renewable resources in the interest
of a sustainable planet for humans and other living things.
- Environmental justice calls for universal protection from nuclear
testing, extraction, production and disposal of toxic/hazardous
wastes and poisons and nuclear testing that threaten the
fundamental right to clean air, land, water, and food.
- Environmental justice affirms the fundamental right to political,
economic, cultural and environmental self-determination of all
peoples.
- Environmental justice demands the cessation of the production of
all toxins, hazardous wastes, and radioactive materials, and that
all past and current producers be held strictly accountable to
the people for detoxification and the containment at the point of
production.
- Environmental justice demands the right to participate as equal
partners at every level of decision-making including needs
assessment, planning, implementation, enforcement and evaluation.
- Environmental justice affirms the right of all workers to a safe
and healthy work environment, without being forced to choose
between an unsafe livelihood and unemployment. It also affirms
the right of those who work at home to be free from environmental
hazards.
- Environmental justice protects the right of victims of
environmental injustice to receive full compensation and
reparations for damages as well as quality health care.
- Environmental justice considers governmental acts of environmental
injustice a violation of international law, the Universal
Declaration On Human Rights, and the United Nations Convention on
Genocide.
- Environmental justice must recognize a special legal and natural
relationship of Native Peoples to the U.S. government through
treaties, agreements, compacts, and covenants affirming
sovereignty and self-determination.
- Environmental justice affirms the need for urban and rural
ecological policies to clean up and rebuild our cities and rural
areas in balance with nature, honoring the cultural integrity of
all our communities, and providing fair access for all to the
full range of resources.
- Environmental justice calls for the strict enforcement of
principles of informed consent, and a halt to the testing of
experimental reproductive and medical procedures and vaccinations
on people of color.
- Environmental justice opposes destructive operations of
multi-national corporations.
- Environmental justice opposes military occupation, repression and
exploitation of lands, people and cultures, and other life forms.
- Environmental justice calls for the education of present and
future generations which emphasizes social and environmental
issues, based on our experience and an appreciation of our
diverse cultural perspectives.
- Environmental justice requires that we, as individuals, make
personal and consumer choices to consume as little of Mother
Earth's resources and to produce as little waste as possible; and
make the conscious decision to challenge and re-prioritize our
lifestyles to insure the health of the natural world for present
and future generations.
Adopted, October 27, 1991
The First National People of Color Environmental Leadership Summit
Washington, D.C.
Appendix B
Principles of Just Transition
Notwithstanding the current economic expansion, job insecurity abounds.
Globalization, downsizing, automation and technology, and the use and abuse
of temporary workers are destroying millions of decent paying jobs. Adding
to the insecurity are environmental pressures that threaten to rapidly
change what is produced, and how and where production occurs.
These forces inevitably are used to divide us -- workers here versus workers in other nations, health and safety versus job security, and jobs versus the environment. We reject these no-win choices.
Just Transition offers an alternative path. It recognizes the ongoing nature of change in our economy, and the need to solve the social, economic, and ecological problems confronting us. Just Transition requires that any path to address such problems must minimize worker and community impacts. The chosen path will in turn determine the kinds and extent of assistance needed to help workers and communities hurt by these actions.
Fundamentally, Just Transition demands that workers and communities
economically harmed by policies for the public good be made whole. It also
requires that the right of workers to form unions and collectively bargain
throughout a transition process be maintained and strengthened.
The following outlines some of the key principles of Just Transition:
- National Commitment
Just Transition requires an overarching national commitment to a just society and full-employment economy that provides family-supporting jobs to American workers now and in the future. It fundamentally recognizes that workers and their families together make up the communities that are the foundation of our nation. For an economy to be sustainable, workers must be organized into unions and communities must provide citizens with quality jobs, housing, health care, education, transportation, public services, leisure activities and a healthful environment.
- Making Workers Whole
If public policies designed to protect the public good dislocate working people, then it is the obligation of public policy to make workers whole. We need to set a very high standard for what workers and communities receive due to dislocations caused in order to protect the public good. Making whole means maintaining full income and benefits for as long as it takes to get comparable work.
- Broad Eligibility
There must be a presumption that all dislocated workers in specific industries and regions affected by public policies are eligible for targeted transition assistance. Workers in many industrial sectors and regions are often threatened by multiple factors operating at the same time, often mutually reinforcing and not always easily distinguishable. Public policies frequently serve to exacerbate the impacts and hardships of dislocations due to technological and market forces. In these circumstances, Just Transition should apply to all affected workers regardless of the cause.
- Fairness
The real costs of public policies that protect the public good must not be shouldered disproportionately by any one group of people. We recognize that the public as a whole may benefit from policies that protect the environment. For example, while all of us gained from the ban on tetra-ethyl lead in gasoline, the thousands of workers who subsequently lost their jobs shouldered the real cost of that transition. Such an outcome violates our sense of fairness in society. In addition, these workers represent a significant resource lost to the economy if we do not re-employ their skills and experience.
- Labor's Role and Worker Rights
Workers and their representatives must be fully involved in the design, planning and implementation of Just Transition policies and programs from the national to the plant levels.
Just Transition must also maintain and strengthen the right of workers to form unions and collectively bargain throughout a transition process. Worker involvement and labor rights are intrinsically linked. Unions fear that the dislocations will thin their ranks making it more difficult to protect remaining members, and to protect and improve the living and working standards of unorganized workers in new and existing industries. Union membership should be integral to all Just Transition programs.
- Comparable Work
Just Transition must help working people subject to economic dislocations find comparable productive work. Most workers who become dislocated want to continue their work. If that work is eliminated due to public policy shifts, income and benefits must be maintained for as long as it takes to find productive alternative work. Workers must be provided sufficient forms and levels of assistance to help them find and qualify for new family wage jobs. Dislocated workers should be given preference to receive training and be hired for new jobs created by emerging industries within an affected region. For those who want to immediately take available jobs, even at lower wages, Just Transition must provide a wage subsidy to make them whole. However, we cannot let Corporate America provide the only definition of what productive work is. A broad range of work opportunities become possible if we as labor develop our own definition of what is productive.
- Full Social Accounting
Just Transition must be based on a full accounting of the social impacts of change. While companies measure costs in ways that fail to account for the full impact of their decisions on workers and the environment, our government must assure that accounting for potential impacts of policies carried out in the public interest wholly captures the effects on workers and their communities, as well as the costs of making them whole.
- Full Funding
Just Transition requires a separate, dedicated, reliable, and sufficient national source of funds.
To prevent the financial starvation of Just Transition, a sufficiently large dedicated fund is needed to protect dislocated workers affected by public policies. Ultimately, all domestic economic dislocations, such as those caused by environmental regulations, utility deregulation, trade agreements, and military base closures, should be covered by these funds.
- Advance Planning
Just Transition requires advance planning to ensure that adequate worker assistance mechanisms are in place before the hardships of dislocation are felt. Advance warning and preparations cut down the hardship and costs of transition after dislocation occurs. As former International Association of Machinists president William Winpisinger said regarding defense conversion, "When a gun is at your head, it's already too late." It is necessary to establish an early warning notification process for workers, unions and service providers, to ensure sufficient time to plan and implement the transition mechanisms prior to dislocation.
- Older Worker Protections
Special attention must be paid to the needs of older, high seniority workers during Just Transition. High seniority workers, especially those over 50 years old, are likely to have the hardest time with transition. Many may not be able to find alternative work or participate in redefined work/school options. Those workers should be given first choice at whatever options are available including full income and benefits until retirement, and pension and health care benefits should be guaranteed after they reach retirement age.
- Making Communities Whole
Financial and technical assistance and other policies will be needed to make communities whole. In several parts of the country, especially rural areas, some public policies can devastate a community or even an entire region. Even if workers are made whole, many may be unable to stay in their communities and support the local economy. At a minimum, an impacted community should receive funds that compensate them dollar for dollar for any loss of tax revenues to maintain the sustainability of the community. Just Transition aims to sustain economic development in such areas leading to a full economic recovery.
April 13, 1999
Draft produced by the Labor Working Group on Just Transition
This report
is by:
Center for Health Environment and Justice (CEHJ)
(It is strongly suggested that a visit be paid to the CEHJ website)
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