Impacts of
Polyvinyl Chloride
Building Materials

by Joe Thornton, Ph.D.
A Healthy Building Network Report
Impacts of
Polyvinyl Chloride
Building Materials

by Joe Thornton, Ph.D.
A Healthy Building Network Report
This report was prepared by the author and does not represent the opinions of The University of Oregon or any of its affiliates.
Healthy Buiding Network, 2002Washington, D.C.
The United States ISBN 0-9724632-0-8 Printed in the United States of America on acid-free, recycled paper, using soy-based ink.
p. 1 Greenpeace p. 41 Leuders/Greenpeace.
p. 53 Basel Action Network. PVC coated wire waste sorted and burned by villagers in Guiyu, China. Cancer causing polycyclic aro-matic hydrocarbons and dioxins will result from burning wires made from PVC and brominated flame retardants. p. 77 Bryce lankard/Greenpeace 1996. Cows graze outside PVC manufacturing facility in Giesmar, Louisiana. Dioxin emissions tothe environment move up the food chain. Fatty foods such as meat and dairy products are the primary source of dioxin exposure tomost humans.
p. 97 Stone/Greenpeace 200. Lake Charles, Louisiana area children suffer health impacts due to pollution from PVC manufacturingfacilities.
The Healthy Building acknowledges the following people and organiza-tions for their important contributions to this report.
Dr. Joe Thornton's willingness to accept this assignment on short noticeand under a short deadline is testament to his ongoing commitment tothe related goals of sound science and environmental justice.
Timely and helpful peer review were provided by the following experts: Barbra Batshalom, Founder & Executive Director, the Green Roundtable(www.greenroundtable.org) Mark Rossi, Health Care Without Harm (www.noharm.com) Ted Schettler, MD, MPH of the Science Environmental Health Network(www.sehn.org) Jan Stensland, Principal, Inside Matters (www.insidematters.com) Gail Vittori, Co-Director, Center for Maximum Potential BuildingSystems (www.cmpbs.org) HBN also appreciates the thoughtful review and contributions of PaulBogart, Charlotte Brody, RN, Health Care Without Harm(www.noharm.org); Gary Cohen, Environmental Health Fund; CharlieCray; Lisa Finaldi, Greenpeace (www.greenpeaceusa.org); Jamie Harvieof the Institute For A Sustainable Future (www.isfusa.org); JeannetteMcCulloch, Valerie Denney Communications (www.vdcom.com); AnnePlatt McGinn, Worldwatch Institute (www.worldwatch.org).
Tom Lent of the Healthy Building Network over saw final editing andproduction by Dragon Well Digital Media Group.
Funding for this project was provided by: Alida Messinger CharitableLead Trust; The John Merck Fund; the Mitchell Kapor Foundation; andthe New York Community Trust.
The Healthy Building Network is a project of the Institute for Local Self-Reliance (www.ilsr.org) which provides excellent institutional support forour work, especially Mr. Jonathan Burnworth.
Bill WalshNational CoordinatorHealthy Building NetworkNovember, 2002 Environmental Impacts of Polyvinyl Chloride Building Materials Joe Thornton, Ph.D., is Assistant Professor in the Center for Ecology andEvolutionary Biology at the University of Oregon. His research focuseson the health and policy implications of global chemical pollution and onthe molecular evolution of animal endocrine systems. He holds Ph.D.,M.A., and M.Phil. degrees in Biological Sciences from ColumbiaUniversity and a B.A. from Yale University. Dr. Thornton is the author of Pandora's Poison: Chlorine, Health, and aNew Environmental Strategy (MIT Press 2000), which the British scien-tific journal Nature has called "a landmark book which should be read byanyone wanting to understand the environmental and health dangers ofchlorine chemistry." From the late 1980s to the mid-1990s, Thorntonwas research analyst and then research coordinator for Greenpeace's U.S.
and international toxics campaigns. There, he authored seminal reportsand articles on organochlorines, dioxin, breast cancer, waste incineration,risk assessment, and the precautionary principle. In 1995, Dr. Thorntonjoined Columbia University's Earth Institute, where he wrote Pandora'sPoison and expanded his research into the basic science of the biologicalsystems that can be damaged by toxic chemicals. He also co-authored thearticle and American Public Health Association resolution that launchedthe campaign to eliminate polyvinyl chloride (PVC) products from med-ical uses due to their central role in dioxin formation in medical wasteincinerators. Dr. Thornton has spoken before the U.S. Congress, theEPA Science Advisory Board, the American Association for theAdvancement of Science, the American Public Health Association, theInternational Joint Commission, and a variety of other organizations andaudiences. His work has been published in numerous scientific journals,including Proceedings of the National Academy of Sciences, Annual Reviewof Genomics and Human Genetics, Public Health Reports, Bioessays,Systematic Biology, and International Journal of Occupational andEnvironmental Health. v About the Author
Summary of Findings
The lifecycle of PVC International action on PVC PVC and chlorine chemistry Production of chlorine Synthesis of EDC and VCM Polymerization, compounding, and molding Disposal of EDC/VCM wastes The Vinyl Institute's self-characterization of dioxin releases Use of PVC products
By-product formation Indoor air quality: release of toxicants Accidental combustion Disposal of PVC Products
Environmental Impacts of Polyvinyl Chloride Building Materials Background on Persistent Organic Pollutants (POPs)
Global distribution of POPs Endocrine disruption Dioxin and related compounds Trends in PVC markets 1. Persistent organic pollutants addressed by UNEP's International 2. Mercury releases from the world chlor-alkali industry, 1994 3. Releases of EDC and VCM in PVC production stages; Norwegian government estimates, 1993 4. Inventoried dioxin sources in North America, Europe, and the world 5. Dioxins in ash from burning organochlorines and chloride containing materials 1. The lifecycle of PVC 2. Effect of chlorine on oil solubility and bioaccumulation on organic chemicals 3. Dioxin deposition in European sediments 4. Dioxin deposition in European sediments vii Contents
Summary of Findings In the last 40 years, polyvinyl chloride plastic (PVC) has become a majorbuilding material. Global vinyl production now totals over 30 milliontons per year, the majority of which is directed to building applications,furnishings, and electronics. The manufacture, use, and disposal of PVC poses substantial and uniqueenvironmental and human health hazards. Across the world, govern-ments, companies, and scientific organizations have recognized the haz-ards of PVC. In virtually all European nations, certain uses of PVC havebeen eliminated for environmental reasons, and several countries haveambitious programs to reduce PVC use overall. Scores of communitieshave PVC avoidance policies, and dozens of green buildings have beenbuilt with little or no PVC. Firms in a variety of industries haveannounced measures to reduce PVC consumption and are using or pro-ducing alternative materials in a variety of product sectors, includingbuilding materials. This paper discusses the hazards of the PVC lifecyclethat have led to this large scale movement away from PVC products.
The major hazards of the PVC lifecycle discussed in this report are sum-marized below.
PVC production is the largest use of chlorine gas in the world. PVC
consumes about 40 percent of total chlorine production, or approxi-
mately 16 million tons of chlorine per year worldwide. PVC is the largest
production-volume organochlorine, a large class of chemicals that have
come under scientific and regulatory scrutiny in the last decade because
of their global distribution and the unusually severe hazards they tend to
pose. PVC (vinyl) is the only major building material that is an
organochlorine; alternative materials, including most other plastics, do
not contain chlorine and do not pose the hazards discussed in this report.
Environmental Impacts of Polyvinyl Chloride Building Materials Hazardous by-products are formed throughout the PVC lifecycle. At
numerous points in the vinyl lifecycle, very large quantities of hazardous
organochlorine by-products are formed accidentally and released
into the environment.
Production: Formation of hazardous organochlorine by-products begins
with the production of chlorine gas. Extremely large quantities—on the
order of one million tons per year—of chlorine-rich hazardous wastes
are generated in the synthesis of ethylene dichloride and vinyl chloride
monomer (EDC and VCM, the feedstocks for PVC).
Combustion: Still more by-products are created and released to the
environment during the incineration of hazardous wastes from EDC
and VCM production, the incineration of vinyl products in the waste
stream, the recycling of vinyl-containing metal products by combus-
tion, and the accidental burning of PVC in fires in buildings, ware-
houses, or landfills.
By-products of PVC production are highly persistent, bioaccumula-
tive, and toxic.
The chemical mixtures produced in the synthesis of
EDC and VCM include such extremely hazardous and long-lived pollu-
tants as the chlorinated dioxins (polychlorinated dibenzo-p-dioxins),
chlorinated furans (polychlorinated dibenzofurans), PCBs (polychlori-
nated biphenyls), hexachlorobenzene (HCB), and octachlorostyrene
(OCS). In addition, a very large portion of these mixtures consists of
chemicals that have not yet been identified or tested. Many of the by-
products of the vinyl lifecycle are of great concern, because of their per-
sistent bioaccumulative toxicity:
Persistence means that a substance resists natural degradation, builds up
over time in the environment, and can be distributed globally on cur-
rents of wind and water. Many of the by-products of the PVC lifecycle
are now ubiquitous global pollutants, which can be found not only in
industrialized regions but in the planet's most remote ecosystems.
Absolutely every person on earth is now exposed to these substances.
ix Summary of Findings
Bioaccumulation means that a substance is fat-soluble and therefore
builds up in the tissues of living things. Most bioaccumulative sub-
stances, including many formed during the PVC lifecycle, magnify as
they move up the food chain, reaching concentrations in species high on
the food chain that are millions of times greater than their levels in the
ambient environment. These substances also cross the placenta easily and
concentrate in the breast milk of human and other mammals.
Toxicity. The feedstocks, additives, and by-products produced and
released during the lifecycle of PVC have been shown to cause a range of
health hazards, in some cases at extremely low doses, including:
• Cancer
• Disruption of the endocrine system
• Reproductive impairment
• Impaired child development and birth defects
• Neurotoxicity (damage to the brain or its function), and
• Immune system suppression.
When its entire lifecycle is Dioxins. Among the most important by-products of the PVC lifecycle are
dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) and a large group of struc-
considered, vinyl appears turally and toxicologically related compounds, collectively called dioxins or to be associated with dioxin-like compounds. Dioxins are never manufactured intentionally butare formed accidentally whenever chlorine gas is used or chlorine-based more dioxin formation organic chemicals are burned or processed under reactive conditions. than any other single Dioxins are formed during numerous stages of the vinyl lifecycle.
Formation of dioxins has been documented in production of chlo-rine, synthesis of the feedstocks EDC and VCM, burning of vinylproducts in accidental fires, and incineration of vinyl products andthe hazardous wastes from PVC production.
Environmental Impacts of Polyvinyl Chloride Building Materials Vinyl is a major dioxin source. Vinyl is the predominant chlorine
donor and therefore a major and preventable cause of dioxin forma-
tion in most of the leading dioxin sources that have been identified.
When its entire lifecycle is considered, vinyl appears to be associated
with more dioxin formation than any other single product.
Dioxins are global pollutants. Dioxins are now found in the tissues
of whales in the deep oceans, polar bears in the high Arctic, and virtu-
ally every human being on earth. Human infants receive particularly
high doses (orders of magnitude greater than those of the average
adult), because dioxins cross the placenta easily and concentrate in
breast milk.
There is no known safe dose of dioxin. Dioxin causes damage to
development, reproduction, and the immune and endocrine systems
at infinitesimally low doses (in the low parts per trillion).
The dioxin exposure of the Toxicological studies have not been able to establish a "threshold"dose below which dioxin does not cause biological impacts.
average American already poses a calculated cancer Dioxin is a potent carcinogen. Dioxin is the most potent synthetic
carcinogen ever tested in laboratory animals and is a known
risk of one in 1,000 to one human carcinogen. in 100—thousands of Dioxin poses health risks to the general public that are already too
times greater than the high. The dioxin "body burden" of the general human population of
usual standard for an the United States is already in the range at which adverse healthimpacts occur in laboratory animals. The dioxin exposure of the aver- "acceptable risk." age American already poses a calculated cancer risk of one in 1,000 toone in 100—thousands of times greater than the usual standard for an"acceptable risk." Phthalate plasticizers. In its pure form, PVC is rigid and brittle. To make
flexible vinyl products, such as roofing materials, floor tiles and wall cover-
ings, plasticizers must be added to PVC in large quantities – up to 60 per-
cent of the final product by weight. The dominant group of plasticizers
used in vinyl are a class of compounds called phthalates, which pose consid-
erable health and environmental hazards. Vinyl is the only major building
Summary of Findings product in which phthalates are used extensively, and it accounts for about90 percent of total phthalate consumption. Over 5 million tons of phtha-lates are used in vinyl every year.
Phthalates have become global pollutants. Phthalates are moder-
ately bioaccumulative and moderately persistent under some condi-
tions. They can now be found in the water of the deep oceans, air in
remote regions, and the tissues and fluids of the general human popu-
lation. Infants and toddlers are subject to exposures several times
higher than those of the average adult.
Massive quantities of phthalates are released into the environ-
ment each year.
Millions of pounds of phthalates are released annu-
ally into the environment during the formulation and molding of
vinyl products. Phthalates are also released when vinyl is disposed of
in landfills or incinerators or when PVC products burn accidentally.
More than 80 million tons of phthalates are estimated to be con-
tained in the stock of PVC products now in use in buildings and
other applications.
Phthalates leach out of vinyl products. Phthalates are not chemi-
cally bonded to the plastic but are merely mixed with the polymer
during formulation. They therefore leach out of the plastic over time
into air, water, or other substances with which vinyl comes in contact.
Phthalates damage reproduction and development. Phthalates
have been found to damage the reproductive system, causing infertil-
ity, testicular damage, reduced sperm count, suppressed ovulation,
and abnormal development and function of the testes and male
reproductive tract in laboratory animals. They are known carcinogens
in laboratory animals.
DEHP exposure is already too high. An expert committee of the
National Toxicology Program recently reviewed the hazards of diethyl-
hexyl phthalate (DEHP, the most common vinyl plasticizer) and
expressed "concern that exposure [of infants and toddlers in the general
U.S. population] may adversely affect male reproductive tract develop-
Environmental Impacts of Polyvinyl Chloride Building Materials ment" and "concern that ambient oral DEHP exposures to pregnant orlactating women may adversely affect the development of their off-spring." The average American's dose of the plasticizer DEHP is nowapproximately equal to EPA's reference dose – the maximum "accept-able" exposure based on studies of health impacts in laboratory animals.
Lead and other heavy metal stabilizers. Because PVC catalyzes its own
decomposition, metal stabilizers are added to vinyl for construction and
other extended-life applications. Common PVC additives that are partic-
ularly hazardous are lead, cadmium, and organotins, with global con-
sumption of each by vinyl estimated in the thousands of tons per year.
Metals do not degrade in the environment. All three of the major
PVC stabilizers resist environmental breakdown and have become
global pollutants.
Metal stabilizers are highly toxic. Lead is an exquisitely potent
developmental toxicant, damaging brain development and reducing
the cognitive ability and IQ of children in infinitessimal doses.
Cadmium is a potent neurotoxin and carcinogen, and organotins can
suppress immunity and disrupt the endocrine system.
Metal stabilizers are released through out the vinyl product
Metal stabilizers are released from vinyl products when they
are formulated, used, and disposed. Releases of lead stabilizers from
interior vinyl building products have been documented. Metals can-
not be destroyed by incineration but are released entirely into the
environment, via air emissions or ash residues. Trash incinerators are
a dominant source of lead and cadmium pollution, and PVC con-
tributes a significant amount of these metals—an estimated 45,000
tons of lead each year—to incinerators.
Accidental fires in buildings and landfills are also potentially importantsources of lead, cadmium, and organotins. In a fire, metals in PVC willbe released to the environment; an astounding 3.2 million tons of lead arepresent in the current stock of PVC in use. Potential lead releases fromthis stored PVC must be viewed as a major potential health hazard.
Summary of Findings Flexible PVC harms indoor air quality. Flexible vinyl products appear
to contribute to the health hazards of poor indoor air by releasing phtha-
lates and facilitating the growth of hazardous molds.
PVC products release phthalates into the building environment.
Phthalate levels in indoor air in buildings with PVC are typically
many times higher than in outdoor air. Phthalate accumulation in
suspended and sedimented indoor dusts are particularly high, with
concentrations in dust as high as 1,000 parts per million.
PVC phthalate exposure may be linked to asthma. In laboratory
animals, metabolites of phthalates used in vinyl cause asthma-like
symptoms through a well-described inflammatory mechanism. Three
separate epidemiological studies have found that human exposure to
PVC in building interiors causes significantly elevated risks of asthma
and other pulmonary conditions, including bronchial obstruction,
wheezing, pneumonia, prolonged cough, and irritation of the nasal
passages and eyes.
PVC products can release heavy metals into the building
Metal stabilizers, particularly lead, cadmium, and organ-
otins, can be released from vinyl products. Significant quantities of
Vinyl has been cited as the lead have been found to be released from vinyl window blinds into air interior building material and from PVC pipes into water. Toxicological effects of these sub-stances include neurological, development, and reproductive damage.
most likely to facilitate the growth of toxic molds.
Vinyl wall covering encourages toxic mold growth. Because vinyl
wall coverings form a barrier impermeable to moisture, they encourage
the growth of molds on wall surfaces beneath the vinyl, particularly in
buildings where air conditioning or heating systems produce significant
temperature and humidity differentials between rooms and wall cavi-
ties. Some molds that grow beneath vinyl produce toxic substances
that are released into indoor air and are suspected causes of severe
human health problems. Numerous liability suits are active on the link
between vinyl-produced molds and respiratory and neurological symp-
toms among exposed persons. Vinyl has been cited as the interior
building material most likely to facilitate the growth of these molds.
Environmental Impacts of Polyvinyl Chloride Building Materials Workers and communities are exposed to toxic substances due to PVC
In the production of PVC, many thousands of tons per year of
the feedstocks ethylene dichloride (EDC) and vinyl chloride monomer
(VCM) are released into the workplace and into local environments.
PVC feedstocks cause cancer and other health impacts. Both EDC
and VCM cause cancer in laboratory animals; VCM is classified as a
known human carcinogen and EDC is a probable human carcinogen.
Increased risks of liver cancer and brain cancer have been docu-
mented among workers exposed to VCM. They are toxic to the nerv-
ous system and cause a variety of other impacts on human health
There is preliminary evidence that workers involved in the manufac-
ture of PVC products may have elevated risks of testicular cancer.
There is no safe VCM exposure level. Although workplace expo-
sures in U.S. chemical and plastics facilities have been significantly
reduced from the levels of the 1960s, there is no threshold below
which VCM does not increase the risk of cancer, so current exposures
in the U.S. continue to pose cancer hazards to workers. Further,
occupational exposure to VCM remains extremely high in some facil-
ities in Eastern Europe and Asia.
VCM production facilities are major polluters. Severe contamina-
tion of communities and waterways in the vicinity of VCM produc-
tion facilities has been documented. In Louisiana, significantly
elevated levels of dioxins have been found in the blood of people liv-
ing near a VCM facility, several communities have been evacuated
due to VCM contamination of groundwater, and extremely high lev-
els of highly persistent, bioaccumulative by-products attributable to
VCM production have been found in local waterways. In Europe,
VCM production facilities have caused severe regional contamina-
tion with dioxins and other by-products.
Chlorine production consumes enormous amounts of energy.
Chlorine production is one of the world's most energy-intensive indus-
trial processes, consuming about 1 percent of the world's total electricity
output. Chlorine production for PVC consumes an estimated 47 billion
Summary of Findings kilowatt hours per year—equivalent to the annual total output of eightmedium-sized nuclear power plants.
Chlorine production causes mercury pollution. The mercury-based
process for producing chlorine accounts for about a third of world chlo-
rine production. In this process, very large quantities of mercury are
released into the environment. Mercury is now a global pollutant that
causes severe reproductive, developmental, and neurological impacts at
low doses. The vinyl lifecycle is associated with the continuing release of
Even in Europe, where PVC many tons of mercury into the environment each year.
recycling is more advanced PVC is extremely difficult to recycle. Very little PVC is recycled, and
than in the United States, this situation is unlikely to change in the foreseeable future. Because eachPVC product contains a unique mix of additives, post-consumer recy- less than 3 percent of cling of mixed PVC products is difficult and cannot yield vinyl products post-consumer PVC is with equivalent qualities to the original. Even in Europe, where PVCrecycling is more advanced than in the United States, less than 3 percent recycled, and most of this of post-consumer PVC is recycled, and most of this is merely "downcy- is merely "downcycled." cled" into other products, which means there is no net reduction in theproduction of virgin PVC. By 2020, only 9 percent of all post-consumerPVC waste in Europe is expected to be recycled, with a maximum poten-tial of no more than 18 percent.
PVC is one of the most environmentally hazardous consumer materi-
als ever produced.
The PVC lifecycle presents one opportunity after
another for the formation and environmental discharge of organochlo-
rines and other hazardous substances. When its entire lifecycle is consid-
ered, it becomes apparent that this seemingly innocuous plastic is one of
the most environmentally hazardous consumer materials produced, creat-
ing large quantities of persistent, toxic organochlorines and releasing
them into the indoor and outdoor environments. PVC has contributed a
significant portion of the world's burden of persistent organic pollutants
and endocrine-disrupting chemicals—including dioxins and phthalates—
that are now present universally in the environment and the bodies of the
human population. Beyond doubt, vinyl has caused considerable occupa-
tional disease and contamination of local environments as well.
Environmental Impacts of Polyvinyl Chloride Building Materials In summary, the feedstocks, additives, and by-products of the PVC lifecy-cle are already present in global, local, and workplace environments atunacceptably high levels. Efforts to reduce the production and release ofthese substances should be environmental and public health priorities. The hazards posed by It is time to phase out PVC building materials. The hazards posed by
dioxins, phthalates, met- dioxins, phthalates, metals, vinyl chloride, and ethylene dichloride arelargely unique to PVC, which is the only major building material and the als, vinyl chloride, and eth- only major plastic that contains chlorine or requires plasticizers or stabi- ylene dichloride are largely lizers. PVC building materials therefore represent a significant andunnecessary environmental health risk, and their phase-out in favor of unique to PVC. It is time to safer alternatives should be a high priority.
phase out PVC building PVC is the antithesis of a green building material. Efforts to speed adop- tion of safer, viable substitute building materials can have significant, tan-gible benefits for human health and the environment.
Summary of Findings

PURPOSE OF THIS REPORT The purpose of this report is to present information on the environmentaland health hazards associated with the lifecycle of polyvinyl chloride plastic(PVC; commonly known as vinyl). This report is not intended as a completereview of all aspects of the PVC lifecycle; rather, the most important evidenceindicating that PVC poses important hazards to health and the environmenthave been surveyed from a perspective consistent with the precautionary prin-ciple. Individual chapters on the manufacture, use and disposal of vinylproducts discuss the formation, release, exposure, and health implications ofhazardous substances during the manufacture, use, and disposal of vinylproducts are considered, as well as energy consumption associated with PVCproduction. The final chapter presents background information on scientificand economic issues relevant to vinyl and persistent organic pollutants,including a detailed discussion of the environmental hazards of dioxin-likecompounds and phthalate plasticizers, two particularly hazardous classes ofsubstances associated with the vinyl lifecycle. In the United States, building and construction applications account for anestimated 75 percent of all vinyl consumption.1 In the European Union, 60percent of vinyl is used in building and construction applications, with anadditional 25 percent in appliances, electronics, and furniture.2 In this report,hazards specific to building and construction uses are highlighted wheneverpossible; however, many of the hazards of the vinyl lifecycle are general to allPVC uses and will be discussed in that context. Because many of the hazardsassociated with PVC are global in scale, this report takes an international per-spective on vinyl markets and environmental impacts. Further, significantquantities of vinyl and vinyl products are imported, so decisions on buildingmaterials in the United States have implications for environmental quality andworker and community health wherever PVC is manufactured.
Environmental Impacts of Polyvinyl Chloride Building Materials TOXIC RELEASES THROUGHOUT THE LIFECYCLE OF PVC The PVC lifecycle is marked by three major stages—manufacture, use,and disposal (figure 1). Environmental hazards of vinyl productioninclude the formation and release of toxic substances and the consump-tion of energy and resources in any and all of these steps.
Figure 1 The lifecycle of PVC
Stages are shown in boxes;
regular type and arrows show material flows

Chlor-alkali process Ethylene dichloride (EDC) Heavy and light "ends" VCM synthesis (pyrolysis) (wastes to disposal or other synthesis processes) Vinyle chloride monomer (VCM) Plasticizers, stablizers, etc.
Molding and manufacturing Vinyl products (i.e.,pipes) Manufacture
PVC manufacture is comprised of five major steps—ethylene and chlo-
rine gas production, feedstock production, polymerization, formulation
or compounding, and molding.
1. Ethylene and chlorine gas production—ethylene gas (purified from petro- leum or natural gas) and chlorine gas (synthesized from sea salt by high-energy electrolysis) are two basic materials for vinyl production.
2. Feedstock production—ethylene dichloride (EDC, also known as 1,2- dichloroethane) can be produced from chlorine and ethylene by chlori-nation or oxychlorination. In chlorination, ethylene and chlorine arecombined to produce EDC. Hydrogen chloride formed as a by-product in this reaction is then combined with more ethylene to pro-duce additional EDC in a process known as oxychlorination. EDC isthen converted into vinyl chloride monomer (VCM; the chemical nameof which is chloroethylene), by a reaction called pyrolysis. 3. Polymerization—VCM molecules are linked together to yield polyvinyl chloride, typically a white powder. 4. Formulation or compounding—pure PVC is mixed with other chemi- cals—stabilizers, plasticizers, colorants, and the like—to yield a usableplastic with desired properties. In its pure form, PVC is not particu-larly useful: it is rigid and brittle, and it gradually catalyzes its owndecomposition when exposed to ultraviolet light. For PVC to be madeinto useful products, additives must be mixed with the polymer tomake it flexible, moldable, and long lasting.3 PVC additives include arange of toxic compounds, but the most environmentally important ofthese are the phthalate plasticizers and metal-based stabilizers—lead,cadmium, organotins, zinc, and other compounds. 5. Molding—the formulated plastic is molded to produce the final prod- uct, such as a bottle, floor tile, or pipe. Usage
The second major stage in the PVC lifecycle is the use of vinyl products.
The duration of the product's useful life may be short (PVC packaging,
with a lifetime measured in days or weeks) or moderate (PVC floor tiles
or roofing materials, which have an average lifetime of 9 to 10 years).4
Environmental Impacts of Polyvinyl Chloride Building Materials Environmental hazards during this stage include the release of toxic sub-stances into the indoor or outdoor environment from the vinyl productor during accidental combustion, especially where large quantities ofPVC are used, such as vinyl roofing membranes or siding. The American Public Finally, after its useful life, the vinyl product is disposed of, typically inincinerators or landfills. Environmental impacts at this stage include the Health Association long-term persistence of vinyl products in land disposal facilities, the adopted a consensus product being leached of hazardous substances, and the formation andrelease of unintended combustion by-products when vinyl is incinerated resolution that hospitals or processed in a secondary smelter for recycling metal products. Only a should "reduce or small portion of vinyl is recycled, a process that can lead to the dispersalof hazardous additives into the environment or a greater range of con- eliminate their use of PVC sumer products.
plastics" wherever feasible due to the global health INTERNATIONAL ACTION TO ELIMINATE PVC and environmental UNEP POPs agreement
impacts of the PVC In the fall of 2000, international negotiations were completed on the firstlegally binding instrument to address global contamination by persistent organic pollutants (POPs).5 The agreement, which will require each generation in particular.
nation to eliminate the production of POPs, represents a fundamentalshift from the present control and disposal techniques used to managechemicals. Although the treaty takes initial action on just 12 pollutants, itincludes provisions for additional substances to be addressed in thefuture. Four of these pollutants are produced in significant quantities dur-ing the vinyl lifecycle (table 1).
International analyses
Currently there is considerable international concern and activity to
restrict PVC consumption for environmental reasons. In 1995, for exam-
ple, the American Public Health Association adopted a consensus resolu-
tion that hospitals should "reduce or eliminate their use of PVC plastics"
wherever feasible due to the global health and environmental impacts of
the PVC lifecycle—dioxin generation in particular.6 In a study of all
major packaging materials for the Council of State Governments in the
Table 1 Persistent organic pollutants addressed by UNEP's
International POPs Agreement

Hexachlorobenzene (HCB)* Polychlorinated Biphenyls (PCBs)* Polychlorinated dibenzo-p-dioxins (PCDDs)* Polychlorinated dibenzo-furans (PCDFs)** Produced at one or more points during the lifecycle of PVC. Source: UNEP 1997.
United States, the independent Tellus Institute found that PVC is themost environmentally damaging of all plastics.7 A lifecycle analysis by theDanish EPA found that the common plastics polyethylene, polypropy-lene, polystyrene, polyethylene terephthalate (PET), and ethylene-propylene diene synthetic rubber are all clearly preferable toPVC in terms of resource and energy consumption, accident risk, andoccupational and environmental hazards, including chemical exposure.8 Restrictions in the EU
Almost all European Union nations have restrictions on uses of PVC. These
restrictions address concerns about dioxin exposure, release of phthalate sof-
teners, or the difficulty of recycling and waste disposal. Among the most
far-reaching policies are those of Sweden, whose parliament voted in 1995
to gradually eliminate soft and rigid PVC. In 1996, Sweden called for a vol-
untary industry phase-out of all PVC production. In 1999, it adopted a bill
that includes mandatory provisions to eliminate use of PVC with hazardous
additives—including phthalates and lead—and to substitute PVC use with
other materials wherever feasible. From 1994 to 1999, this program had
reduced total PVC use in Sweden by 39 percent.9
Environmental Impacts of Polyvinyl Chloride Building Materials Denmark established a national strategy to address the environmentalhazards of PVC, including a tax on PVC of $0.30 U.S. per kilogram, ahigher tax on phthalates, a prohibition on the incineration of PVC, andan order to substitute alternative materials for all non-recyclable PVC use.
The German Environmental Protection Agency (UBA) has called for anend to the use of phthalates and the gradual phase-out all uses of flexiblePVC.10 Due to the concern for dioxin generation, UBA has also called fora ban on the use of PVC in applications susceptible to fire.11 The policy in the Netherlands is to reduce the use of PVC in products that are notrecycled and to eliminate the use of phthalate plasticizers and lead stabi- lizers in PVC. The European Union has begun an official process to Berlin and Bonn—and six review the environmental hazards of PVC and to establish appropriatepolicy measures to safeguard the environment.12 states have written policies to phase-out or Restrictions elsewhere in the world
Not all action on PVC is restricted to Europe. India's Ministry of the
restrict PVC.
Environment and Forests has established rules that ban the incinerationof PVC and other chlorinated plastics in medical waste incinerators.
Singapore has informed the Secretariat of the Basel Convention on thetransboundary movement of hazardous waste that it considers PVC-containing waste and PVC-coated cables to be hazardous waste thatare therefore banned from import or export.13 Restriction on PVC use in construction
Numerous local and regional governments have specific policies to avoid
PVC in construction.14 In Germany, 274 communities—including Berlin
and Bonn—and six states have written policies to phase-out or restrict PVC.
The Netherlands' four largest cities—Amsterdam, Den Haag, Rotterdam,
and Utrecht—have specifications to avoid PVC whenever possible in con-
struction. Fifty-two cities in Spain have declared themselves "PVC-free,"
with specific strategies to substitute safer alternatives for PVC construction
materials. Basel, Switzerland, has guidelines for the use of environmentally
friendly materials, listing PVC as environmentally harmful and a candidate
for substitution whenever possible. In Austria, seven of nine states and a
large number of municipalities have restrictions on PVC. The city of Linz
has reportedly achieved an 85 percent PVC phase-out in public buildings,
and the Vienna subway and Vienna Ost hospital were constructed without
Numerous major construction projects have reduced or eliminated PVCentirely. In an effort to utilize green building practices, the Sydney 2000Olympics established a commitment "to minimizing and ideally avoidingthe use of chlorine-based products such as PCBs, PVC, and chlorine-bleached paper."15 PVC use was eliminated or radically reduced in theconstruction of the hotel, Olympic village, stadium, and many otherstructures. Seville's guidelines for the 2004 Olympics specify that "we Nearly all of the world's must avoid the use of PVC in construction, infrastructure, accessories andany other complements in Olympics facilities."16 The headquarters for major car manufacturers, the Danish society of Engineers has been built without PVC, as has the including BMW, Daimler- new European headquarters for Nike in Hilversum. Many buildings inthe United Kingdom, including the new Tate Gallery of Modern Art, Benz, Ford, General have been designed and built to minimize or eliminate PVC use.17 Motors, Honda, Nissan, Many private firms have also taken steps to restrict or substitute PVC Opel, Toyota, and products.18 The Swedish construction firms HM and Svenska Bostder Volkswagen AG have have announced that they are phasing out PVC use. In Japan, the elec-tronics manufacturers AEG, Electrolux, Matsushita, Ricoh, Sharp, Sony- policies to reduce or Europe, and Vorwerk have PVC phase-out policies. German Telekom, eliminate the use of PVC Nippon, and Sumitomo Electric Industry have policies to avoid PVC usein cable manufacture. The furniture and décor manufacturers and retail- in automobiles.
ers Eco AB, EWE Kuechen (Austria), IKEA, and Innarps AB have poli-cies to avoid PVC products. In transportation, nearly all of the world'smajor car manufacturers, including BMW, Daimler-Benz, Ford, GeneralMotors, Honda, Nissan, Opel, Toyota, and Volkswagen AG have policiesto reduce or eliminate the use of PVC in automobiles. PVC restrictions in toys
Particularly urgent and widespread action has focused on PVC toys, due
to concern for exposure of children to phthalate plasticizers in flexible
PVC. In the late 1990s, government ministries in Denmark and the
Netherlands found that substantial quantities of phthalates are released
from PVC into saliva from vinyl teethers and chew toys. As a result, these
countries, along with ministries in Austria, Belgium, Finland, France,
Germany, Greece, Italy, Norway, Spain, and Sweden, sought bans on the
use of soft PVC in toys. In 1997, a number of European toy retailers and
manufacturers suspended sales of PVC teething rings or announced plans
Environmental Impacts of Polyvinyl Chloride Building Materials to eliminate all vinyl from their toy lines. In late 1998, when a wave ofpublicity on the issue hit the U.S. press, Mattel, Toys-R-Us, and severalother U.S. toy makers and retailers announced that they would stop sell-ing certain vinyl toys.19 Subsequently, the U.S. Consumer Product SafetyCommission called on the toy industry to voluntarily stop making vinylchewing toys that contained phthalates.20 In 1999, the EuropeanCommission finalized an emergency ban on six phthalate plasticizersfound in soft PVC toys. Although toys represent a small fraction of totalPVC consumption, the trend away from vinyl use in toys is significant forthe entire industry. As one plastics industry spokesman commented, "Inthe long run, the industry will go the way toys go."21 PVC AND THE CASE AGAINST ORGANOCHLORINES EDC, PVC, VCM, and the by-products formed during the vinyl lifecycleare members of a large class of problematic chemicals called organochlo-rines—organic (carbon-based) substances that also contain one or moreatoms of chlorine. The debate over PVC takes place in the context ofbroader concern about the class of organochlorines—regarded by many asthe most environmentally problematic class of synthetic substances.22 PVCis the only major plastic used in buildings that contains chlorine. Chlorine-free plastics include polyethylene (PE), polypropylene (PP), polyethyleneterephthalate (PET), acrylonitrile-butadiene-styrene (ABS) copolymer, eth-ylene vinyl acetate (EVA), and numerous others. Polyurethane, polycarbon-ate, and epoxy resins are chlorine-free plastics that are currentlymanufactured via the organochlorine intermediates chlorohydrin,epichlorohydrin, phosgene, and propylene, but technologies are beingdeveloped to produce these plastics through chlorine-free routes.23 The proper course of action for addressing organochlorines is controver-sial. Some organizations and analysts, including the American PublicHealth Association and the International Joint Commission (a binationaladvisory body of the United States and Canadian governments chargedwith protection of the Great Lakes ecosystem), have called for a gradualphase-out of all uses of chlorine and organochlorines. Others, includingthe chemical industry and the Society of Toxicologists, have advocatedcontinuing the current system of chemical-by-chemical regulation.24 Decisions about the use of PVC in building materials do not require theproper course of action on all organochlorines to be resolved. The ques-tion of vinyl should be seen, however, in the context of concern about theclass of chemicals of which PVC is perhaps the most important member.
Vinyl and its feedstocks have the largest production volume, by far, of allorganochlorines. Further, a vast variety of other organochlorines are pro-duced in considerable quantities during the lifecycle of vinyl. Many ofthese by-products are known to be hazardous; many more have not been specifically identified or evaluated for their environmental behavior and addressed by United toxicity, and an understanding of the general characteristics oforganochlorines is relevant to predicting their hazards.
Nations Environmental Programme (UNEP), all Concern about organochlorines began with the recognition that theytend to dominate all major lists of "priority pollutants." For example, of are organochlorines, and the 12 POPs addressed by United Nations Environmental Programme four are produced by the (UNEP), all are organochlorines, and four are produced by the PVC life-cycle (see table 1). Of the 11 chemicals on the International Joint PVC lifecycle.
Commission's Critical Track of hazardous pollutants in the Great Lakes,eight are organochlorines, as are 168 of the 362 Great Lakes contami-nants on the IJC's Secondary Track.25 Organochlorines are prominent onEPA's list of common groundwater pollutants and of contaminants athazardous waste sites, and they constitute the majority of the list ofknown endocrine disrupting chemicals.26 Systematic problems with organochlorines
Further analysis has revealed why organochlorines are so problematic.
Organochlorines tend to have several characteristics, all of which derive
from fundamental chemical properties of the chlorine atom. The same
properties that make chlorine and organochlorines useful in industrial
applications, in fact, are responsible for their environmental hazards.
Reactivity of chlorine: Chlorine gas is extremely reactive, combiningquickly and randomly with any organic matter it contacts. This propertymakes it an effective bleach, disinfectant, and chemical feedstock, but alsoresults in the generation of a diverse mixture of by-products, typicallycontaining hundreds or thousands of organochlorines—including diox-ins—whenever chlorine is used.27 Environmental Impacts of Polyvinyl Chloride Building Materials Persistence. The chlorine atom is extremely electronegative, which meansit exerts a strong pull on the electrons it shares with carbon atoms in anorganochlorine—significantly stronger than the hydrogen atom it usuallyreplaces. The addition of chlorine to organic molecules therefore changesthe chemical stability of the resulting substance—often stabilizing butsometimes destabilizing it, depending on the structure of the parent com-pound. In most cases, the resulting organochlorine is far less reactive thanthe original substance; organochlorines that do break down usuallydegrade into other organochlorines, which may be more persistent andtoxic than the original substance. Stability makes organochlorines usefulas plastics, solvents, and refrigerants—applications for which long-lifeand fire-resistance are virtues. This same property, however, makes theseorganochlorines persistent in the environment and therefore likely toaccumulate and become globally distributed. In some cases, organochlorines become more unstable and reactive thanthe parent compound, making them useful as chemical intermediates.
But this property also makes them more easily converted in the body totoxic and reactive metabolites (other organochlorines), which can thenproceed to damage DNA or other essential molecules in cells.28 Chlorine'simpact on the stability of organic molecules thus has one of two oppositeeffects, depending on the structure of the parent compound—and bothare problematic from an environmental health perspective. Bioaccumulation. One factor that determines the solubility of a substancein water or fat is its molecular size: the larger a molecule, the more it dis-rupts interactions among water molecules and the greater the tendencyfor the substances to be nondissolvable in water. The chlorine atom isvery large—several times larger than an atom of carbon, hydrogen, oroxygen—so chlorination significantly increases the size of organic mole-cules and as a result almost invariably increases solubility in fats and oils.
The increase in fat solubility applies to the chlorination of virtually anyorganic substance, and increases with each chlorine atom added.29 Thus,for example, tetrachloroethylene, hexachlorobenzene andoctachlorodibenzofuran, are about one hundred, one thousand, and onebillion times more oil-soluble, respectively, than their chlorine-freeanalogs (figure 2). Oil-solubility makes organochlorines useful as solvents Figure 2 Effect of chlorine on oil solubility and
bioaccumulation on organic chemicals

y (octanol-water co-ef Number of chlorine atoms on molecule Note: In all groups, chlorination increases the tendency of a chemical to dissolve fats and oils, and each chlo-rine atom has a greater effect. Blank cells indicate no data available.
Source: HSDB 1997.
Environmental Impacts of Polyvinyl Chloride Building Materials and dielectric fluids, but it is directly responsible for the tendency tobioaccumulate. The American Public Toxicity. Organochlorines tend to be overwhelmingly toxic. The Health Association has American Public Health Association has concluded that "virtually allorganochlorines that have been studied exhibit at least one of a range of concluded that "virtually serious toxic effects, such as endocrine dysfunction, developmental all organochlorines that impairment, birth defects, reproductive dysfunction and infertility,immunosuppression and cancer, often at extremely low doses, and many have been studied exhibit chlorinated organic compounds…are recognized as significant workplace at least one of a range of hazards."30 According to a comprehensive independent review of thou-sands of individual organochlorines, chlorination of organic chemicals "is serious toxic effects, such almost always associated with an increase in the toxic potential. Only as endocrine dysfunction, rarely does chlorination produce no increase or even a decrease in effects.
This observation applies for all kinds of toxic effect (acute, subchronic, and chronic toxicity; reproductive toxicity; mutagenicity; and carcino- impairment, birth defects, genicity)."31 The general toxicity of organochlorines makes them usefulas pesticides and antibiotics, but also hazardous to humans and wildlife reproductive dysfunction once they enter the environment.
immunosuppression and cancer, often at extremely 1. Geiser 2000. 2. European Commission 2000.
3. Tukker et al. 1995.
4. Schneider and Keenan 1997.
5. United Nations Environment Programme 2000.
6. APHA 1996.
7. Tellus Institute 1992.
8. Christaensen et al. 1990. PVC was not judged demonstrably inferior under certain criteria (such as energy useand accident potential during manufacture) to polyurethane, acrylonitrile-butadiene-styrene, and aluminum.
9. KemI 2000; Greenpeace International 2000.
10. European Commission 2000.
11. UBA 1992.
12. European Commission 2000.
13. Greenpeace International 2000.
14. Greenpeace International 2000.
15. Quoted in Greenpeace International 2000.
16. Quoted in Greenpeace International 2000.
17. Greenpeace International 2000.
18. Greenpeace International 2000.
19. Warren 1998; New York Times 1998.
20. Mayer 1998.
21. Warren 1998.
22. Thornton 2000; Collins 2001; International Joint Commission 1992; APHA 1994. 23. For a discussion of chlorine-free synthesis technologies, see discussion and references in Thornton 2000.
24. Karol 1995.
25. Great Lakes Water Quality Board 1987.
26. Burmaster and Harris 1982; Miller et al. 1991; Guillette and Crain 1999.
27. See discussion and references in Thornton 2000.
28. Henschler 1994.
29. Solomon et al. 1993. 30. APHA 1994.
31. Henschler 1994.
PRODUCTION OF CHLORINE The PVC lifecycle begins with the production of chlorine gas in thechlor-alkali process. Electricity is passed through a solution of brine toproduce sodium hydroxide (also called alkali or caustic soda) and chlorinegas in a fixed ratio of 1.1 to 1. Because chlorine gas and sodium hydrox-ide react with each other on contact, the key to the process is to separateimmediately the chlorine from the alkali in a specially designed elec-trolytic chamber, called a cell. There are three types of chlor-alkali cells inuse, which differ in the ways that chlorine and alkali are separated fromeach other. The mercury process, the oldest and most energy-intensive of the threeprocesses for chlorine production, involves two connected cells. In thefirst cell, salt is split into chlorine gas and sodium at the cell's positive ter-minal (called the anode); the sodium forms an amalgam with a layer ofliquid mercury, which then flows into another cell, where it reacts withwater to form sodium hydroxide and hydrogen gas. The mercury processis banned in Japan, but 35.5 percent of chlorine production worldwide isby this method, with 14 percent of chlorine in North America and 65percent of that in Western Europe produced by this technology as of1994. In Western Europe, the Oslo-Paris Commission on the NortheastAtlantic has recommended that mercury cells be phased out, so the pro-portion of mercury-related chlorine is expected to decline.1 In the asbestos diaphragm process, brine enters the cell and is split at theanode, yielding chlorine gas and sodium ions. The ions then flowthrough a semi-permeable asbestos barrier to the other pole, where theyreact with water to form sodium hydroxide and hydrogen gas. Chlorine,which cannot pass through the membrane, remains near the anode. The Environmental Impacts of Polyvinyl Chloride Building Materials diaphragm method was developed after the mercury process and, as of1994, accounted for 77 percent of all chlorine production in the UnitedStates and 25 percent in Europe.2 The remaining 7 percent of chlor-alkali production is based on the mem-brane process, the most recently developed of the three methods. Themembrane technique is similar to the diaphragm process, except that asynthetic membrane rather than asbestos is used to separate the compart- Chlorine gas produced ments in which chlorine and alkali are formed. The membrane process each year for vinyl uses slightly less energy and yields products of higher purity than theother kinds of cell, but retrofitting a chlorine plant with membranes is production carries expensive. Because most chlor-alkali plants in the United States and between 1,400 and 7,200 Europe were built decades ago, few use the membrane process. But mostnew facilities—particularly those in Asia and Latin America—are now constructed with it.3 persistent and toxic The world chlor-alkali industry produced nearly 39 million metric tons of chlorine in 1997; 27 percent of that was made in the United States.
by–products — including There are 42 chlor-alkali facilities in the United States, but more than 70percent of production capacity is located at just 12 large plants in the HCB, hexachloroethane Gulf Coast region of Louisiana and Texas.4 Because vinyl accounts for (HCE), PCBs, OCS, more than 40 percent of all chlorine consumption, it is reasonable to esti-mate that the same proportion of the environmental impacts of chlorine production—releases of toxic substances and energy demand—is associ- the world's economy.
ated with the vinyl lifecycle.
Dioxin and other organic by-products
From the moment that chlorine gas is formed in the chlor-alkali cell, it will
react with any organic matter present to form organochlorines. For this rea-
son, manufacturers purify raw materials and equipment surfaces carefully to
remove as much organic material as possible. Nevertheless, carbon-containing
substances remain as trace impurities—in plastic materials or from the
graphite electrodes used in some types of chlor-alkali cells.5 Chlorine com-
bines with these organic contaminants to form persistent organochlorine by-
products, such as HCB and hexachloroethane (HCE), which are found in the
chlorine product itself.6 Chlorine gas can also be contaminated with PCBs,
octachlorostyrene (OCS), and tetrachlorobenzene. The concentrations are
moderate—40 to 210 parts per billion (ppb)7 —but the quantities are signifi-cant: based on the levels found, the chlorine gas produced each year carriesbetween 1.6 and 8.2 tons of these highly persistent and toxic by-productsinto the world's economy.8 Based on an attributable fraction of 40 percent,the chlorine used for vinyl contains between 1,400 and 7,200 pounds ofthese substances annually.
Severe contamination of Much greater quantities of organochlorine contaminants are deposited inchlorine production wastes. Swedish researchers have identified high con- fish and sediments with centrations of dioxins and furans9 in the sludges from spent graphite elec- OCS—an extremely trodes used in chlor-alkali cells,10 and high levels of polychlorinateddibenzofurans have been found in the blood of Swedish chlor-alkali work- ers.11 The levels were up to 650 ppb, with TEQ values up to 28 ppb.
bioaccumulative POP— (Because dioxin-like compounds cause toxicity through a common mecha-nism, mixtures of these substances can be expressed relative to the toxicity has been documented of TCDD, the most toxic dioxin, as TCDD-equivalents (TEQ). To calcu- late the TEQ value for a mixture, the quantity of each substance is multi-plied by its toxicological potency relative to TCDD, and the TEQ is the American chlorine sum of these weighted quantities. A mixture with a calculated TEQ of 1 microgram is expected to have toxicity equal to 1 microgram of TCDD.) Severe contamination of fish and sediments with OCS—an extremelypersistent, bioaccumulative POP—has been documented near eightNorth American chlorine producers. Additionally, large-scale OCS con-tamination of sediments in Lake Ontario has been traced to disposal ofspent chlor-alkali electrodes.12 OCS is now a global contaminant, withconsiderable levels found in the Canadian arctic—and chlor-alkali manu-facture is considered an important source of that contamination.13 As a result of these problems, all chlor-alkali plants in North America andmany in Europe replaced graphite electrodes with titanium substitutesduring the 1970s and 1980s—a move that industry and governmentassumed eliminated the formation of organochlorine by-products. Butrecent data indicate that even the most modern chlor-alkali plants pro-duce dioxin-like compounds. With graphite eliminated, traces of organicchemicals are still present, primarily from plastic pipes and valves thatrelease small quantities of their materials into the cell. A 1993 study by Environmental Impacts of Polyvinyl Chloride Building Materials Swedish scientists found dioxins and furans in the sludge and plastic pip-ing from a modern chlor-alkali plant with titanium electrodes at levelsnear 5 ppt (TEQ).14 Subsequent Swedish research found significantquantities of chlorinated dibenzofurans in the sludge from a chlor-alkaliplant with titanium electrodes, apparently due to chlorination of organiccompounds in the rubber linings of the cell.15 In 1997, the UKEnvironment Agency confirmed that a chlor-alkali plant owned by ICIChemicals and Polymers, which replaced its graphite electrodes around1980, continues to release dioxins in its wastewater.16 Mercury releases
Most of the mercury used in mercury chlor-alkali cells is recycled, but sig-
nificant quantities are routinely released into the environment via air, water,
products, and waste sludges. In the 20th century as a whole, chlor-alkali
production has been the largest single source of mercury releases into the
environment.17 As recently as the 1980s, the chlorine industry was second
only to fossil fuel combustion as a mercury source in Europe.18
Many mercury-cell plants have been retired in the past two decades, andcontrols on existing plants have improved, but chlor-alkali facilitiesremain a source of mercury pollution. The chlorine industry is the largestmercury consumer in the United States; it is presumably even moreimportant in Europe, where the mercury cell process is more common.19According to the Chlorine Institute (an industry organization) the chlor-alkali industry in the United States consumes 176,769 pounds of mer-cury per year.20 By definition, materials consumed are not recycled butare released directly to the environment, into wastes, or in the productitself. Without providing documentation, the Vinyl Institute has arguedthat only 20 percent of the chlorine produced by the mercury process inthe United States is used to produce PVC.21 Based on these two figures,vinyl manufacture in the United States alone is associated with the releaseof more than 35,000 pounds (about 16 metric tons) of mercury into theenvironment each year. The U.S. industry's figures probably significantly underestimate actual mercury releases. More detailed estimates, derived by superior mass-balance accounting methods, are available based on studies conducted Table 2 Mercury releases from the world chlor-alkali industry, 1994
Metric tons of mercury per year1
PVC attributable portion2
Total consumption Discharges to water Contaminants in products 1. Assuming 39 million metric tons per year of chlorine production worldwide, of which 35.5 percent was produced by the mercury process. 2. Assuming that PVC accounts for 40 percent of chlorine consumption worldwide and that an equal fraction of the chlorine produced in mercury cells isused for PVC; the Vinyl Institute has argued that the attributable fraction for mercury is 20 percent in the United States.
Note: These data are based on mass balances prepared by the chlorine industry for facilities in Europe and may not accurately represent global averages. Source: Ayres 1997. by Euro-Chlor, the trade association of the European chlorine industry.22This information indicates that the world chlor-alkali industry consumedabout 230 tons of mercury in 1994; this is the quantity not recycled butlost from production processes each year. Exactly where the mercury goesremains controversial, but if we extrapolate from the Euro-Chlor estimates,about 30 tons were released directly into the air and water, 5 tons remainedas a contaminant in the product, more than 150 tons were disposed onland, and 36 tons could not be accounted for (table 2). Based on these fig-ures and an attributable fraction of 40 percent, the PVC lifecycle is associ-ated with the consumption of 92 metric tons of mercury (202,400 pounds)per year, of which the majority is released into air, water, or landfills. If weuse the Vinyl Institute's U.S.-based estimate that 20 percent of the chlorineproduced by the mercury process is used to produce PVC, production ofchlorine for vinyl would account for the release of 46 tons per year of mer-cury each year. The actual worldwide totals are likely to be even highersince the well-regulated facilities of Europe are not likely to be representa-tive of those in other regions of the world.
Mercury is an extremely toxic, bioaccumulative global pollutant.
Mercury compounds cause irreversible health damage to wildlife andhumans—especially to developing children, resulting in birth defects,impaired neurological development, kidney damage, and severe neuro-logical destruction.23 The most tragic and infamous example of mercury Environmental Impacts of Polyvinyl Chloride Building Materials pollution happened in Minimata, Japan, where the Chisso Chemicalcompany routinely dumped mercury-contaminated waste into the localbay from the 1930s to the 1960s. Fish in Minimata Bay bioaccumu-lated mercury to levels 40 to 60 times higher than those in nearbyecosystems, and the local population—among whom a diet of fishplayed a key role—suffered high mercury exposures. In the early 1950s,symptoms of chronic mercury poisoning, including neurological toxic-ity, paralysis, coma, and death began to appear in adults in the commu- The PVC lifecycle is nity, and a horrifying outbreak of severe birth defects and mental associated with the retardation occurred in children. Ultimately, mercury poisoning killedhundreds and injured more than 20,000 people in the Minimata area.24 consumption of 92 metric Chlor-alkali production is not traditionally assumed to have been the tons of mercury (202,400 source of the Chisso's mercury releases because the company had beenusing mercury as a catalyst in fertilizer production since the 1930s. As pounds) per year, of which one history of the event points out, however, Chisso began using the the majority is released mercury process to make chlorine for PVC plastic in 1952. In 1953,symptoms of mercury poisoning began to appear in the local popula- into air, water, or landfills.
tion, and over the next four years the number of victims correlated withChisso's growing production volume of vinyl chloride.25 This patternsuggests that mercury releases from the chlor-alkali process are likely tohave played a role in the Minimata epidemic. Today, mercury exposure remains a major environmental health problem.
According to a recent report by the U.S. National Academy of Science,"Individuals with high [mercury] exposure from frequent fish consump-tion might have little or no margin of safety—in other words, exposuresof high-end consumers are close to those with observable adverse effects.
Those most at risk are children of women who consumed large amountsof fish and seafood during pregnancy. The committee concludes that therisk to that population is likely to be sufficient to result in an increase inthe number of children who struggle to keep up in school and who mightrequire remedial classes or special education."26 Mercury cells are now banned in Japan and are gradually being phasedout in the United States and Europe as well, but releases of mercuryremain a problem. In the 1980s, for instance, a major British chlor-alkalifacility was found to be discharging up to 100 kilograms per day of mer- cury into local waterways; more than a decade later, mercury levels in thesediment remained extremely high.27 In Italy, elevated levels of mercuryin air, soil, and plant tissues have been found in the vicinity of a mercury-based chlor-alkali plant owned by the Solvay Company.28 In India, a1990 study of waterways around a chlorine facility documented severemercury contamination of fish and sediments.29 The global chlor-alkali Major energy consumption
Chlorine production requires enormous amounts of energy. Chlor-alkali
industry consumes about electrolysis is one of the most energy-intensive industrial processes in the 117 billion kilowatt-hours world. The production of one ton of chlorine requires about 3,000 kilo-watt-hours of electricity, and the global chlor-alkali industry consumes of electricity each year, about 117 billion kilowatt-hours of electricity each year.30 This quantity equivalent to the annual is about 1 percent of the world's total demand for electricity,31 costs about$5 billion per year,32 and is equivalent to the annual power production of power production of about about 20 medium-sized nuclear power plants.33 As a major energy con- 20 medium-sized nuclear sumer, chlorine chemistry contributes considerably to all the environ-mental problems—global warming, air pollution, acid rain, mercury power plants.
emissions, generation of radioactive and other wastes from the mining,processing, and consumption of nuclear fuels, and so on—that are associ-ated with energy production. Based on an attributable fraction of 40 percent of chlorine demand, thechlorine consumed in vinyl production is associated with electricityconsumption of approximately 47 billion kilowatt-hours per year. On aper mass basis, production of chlorine to make one ton of PVC con-sumes about 1,800 kilowatt-hours of electricity, based on the fact thatpure PVC is 59 percent chlorine by weight. Additional energy is con-sumed in the chemical synthesis of EDC, VCM, and PVC and in theproduction of additives in the vinyl product. An estimate of the totalenergy consumption required for the manufacture of PVC is beyondthe scope of this document.
Environmental Impacts of Polyvinyl Chloride Building Materials SYNTHESIS OF EDC AND VCM Releases of EDC and VCM carcinogens
Large quantities of EDC and VCM are released directly into the environ-
ment during the production of feedstocks for PVC. Because at least 95
percent of the world's annual production of 24 million tons of VCM goes
into PVC, these releases are almost entirely attributable to vinyl products.
Undoubtedly, extremely large quantities of EDC and VCM are releasedinto the air and water each year. As part of the U.S. Toxics ReleaseInventory (TRI), manufacturers of PVC and its feedstocks self-reportedemissions of 887,000 and 798,000 pounds of VCM and EDC, respectively,directly into the environment in 1998; an additional 2 million pounds ofVCM and 27 million pounds of EDC were reported sent to sewage treat-ment plants or off-site waste facilities.34 These figures may significantlyunderestimate actual releases, however, because of widely recognized prob-lems with the TRI database. Reported emissions are not based on actualmonitoring of releases, and estimation methods vary greatly among facili-ties. Most importantly, TRI release estimates are self-reported by the indus-try and are thereby subject to no independent verification. More valid figures come from estimates made by the Norwegian govern-ment in 1993. Based on a detailed mass balance conducted at aNorwegian facility, specific estimates of per-ton releases of EDC andVCM from vinyl manufacture were made (table 3). Extrapolating theseestimates using 1990 vinyl production figures,35 we can calculate that thePVC industry releases at least 100,000 tons each of EDC and VCM intothe air each year—plus more than 200 tons of EDC and 20 tons of VCMinto surface water. Worldwide VCM production has increased by about50 percent in the past decade,36 which increases the associated estimatesof total releases by a similar fraction. The actual total may be even highersince this estimate was extrapolated from emissions at a single facility inNorway: manufacturers in many other nations have less advanced pollu-tion control equipment and less careful plant operation than this rela-tively modern, well-regulated facility.
Table 3 Releases of EDC and VCM in PVC production stages;
Norwegian government estimates, 1993

Grams released per ton of product
EDC to air
EDC to water
VCM to air
VCM to water
EDC synthesis (1 ton) VCM synthesis (1 ton) PVC polymerization (1 ton) – Indicates releases <1 g/ton.
Source: SFT 1993. EDC and VCM are not particularly persistent—but both are highlytoxic. Releases of these compounds therefore pose the greatest hazards forcommunities and ecosystems near EDC/VCM manufacturing facilities.
The facility studied in Norway, for instance, releases 40 to 100 tons ofEDC each year directly into the local atmosphere.37 In the United States,some 12.5 million people are exposed to EDC emissions from chemicalmanufacturing facilities, according to the National Institute forOccupational Safety and Health. Workers in plants that manufacturePVC or its feedstocks receive the highest exposures to these compoundsin workplace air—81,000 U.S. workers are regularly exposed to vinylchloride, while 77,000 are exposed to EDC.38 According to the International Agency for Research on Cancer and theU.S. National Toxicology Program, VCM is a known human carcinogen,and EDC is a probable human carcinogen. Studies of workers exposed toVCM have shown an unambiguous increase in liver cancer. Four out offive studies also report an increased risk of brain cancer that is statisticallysignificant in a combined analysis.39 Both EDC and VCM cause a varietyof other toxic effects, including immune suppression, liver damage, neu-rological toxicity, and testicular damage.40 Since the carcinogenicity of VCM was established, government regula-tions have required considerable reductions in worker VCM exposure. Inthe United States, workplace VCM levels within the 1–5 ppb range arenow required—orders of magnitude lower than typical concentrations ofthe 1950s and 1960s—but much higher levels continue to occur in facili- Environmental Impacts of Polyvinyl Chloride Building Materials ties elsewhere.41 For example, a recent survey found that workers in Asiaand Eastern Europe are typically exposed to VCM at levels up to 1,000times the typical U.S. concentrations. In China, the air in dormitories forplastics industry workers and their families contains VCM levels thatexceed the permissible workplace level in the United States.42 Although occupational exposure to EDC and VCM has declined significantlyin the United States, even the much lower levels that now characterize the domestic vinyl industry remain a matter of concern, because there appears to be no safe dose of these compounds. The mechanisms by which EDC andVCM cause cancer have been elucidated, and it is now clear that both sub- irreversible damage to stances are genotoxic—causing irreversible damage to DNA. Indeed, VCM DNA—and are not likely to has been shown to form chemical bonds with DNA, leading to mutationsthat abolish natural controls over cell differentiation and proliferation.43 have a threshold below Currently accepted biological theory indicates that mutations in a single cell which they do not can result in the development of a malignant tumor; similarly, a single mole-cule of a genotoxic substance can damage DNA. Carcinogens such as VCM increase the risk of therefore are not likely to have a threshold below which they do not increase the risk of cancer. That is, any exposure to this carcinogen poses some risk ofcancer, and the magnitude of the risk increases with the level of exposure.44The same is true of other health impacts mediated by DNA damage, includ-ing certain birth defects and genetic diseases. Thus, reduced levels of EDCand VCM in U.S. PVC production facilities reduce but do not eliminate theoccupational health risks from these chemicals.
The health effects of community EDC and VCM exposure remain largelyunstudied. It is clear, however, that severe environmental contamination andsocial disruption have occurred in several communities near EDC and VCMproduction facilities. As an example, Reveilletown, Louisiana, was once asmall African-American community adjacent to a EDC/VCM facility ownedby Georgia-Gulf. In the 1980s, after a plume of vinyl chloride in groundwa-ter began to seep under homes in the area, a number of residents complainedof health problems and brought a lawsuit against the company. In 1988,Georgia-Gulf agreed to an out-of-court settlement that provided for the per-manent evacuation of the community but sealed the court records andimposed a gag order on the plaintiffs. One hundred six residents were relo-cated and Reveilletown has since been demolished.45 The next year, as concern about air and groundwater pollution grewaround Dow Chemical's EDC/VCM facility five miles from Reveilletownin the small town of Morrisonville, near Plaquemine, Louisiana, Dowbegan to buy out and relocate citizens there in a pro-active program toavoid exposure, liability, and bad press. Morrisonville, too, is now all butabandoned.46 On the other side of the state, in Lake Charles, Louisiana,PPG and Vista Chemical manufacture EDC and VCM, which, alongwith by-products of their synthesis, now contaminate water and sedi-ments in the Calcasieu Estuary.47 Residents here continue to occupy theirhomes, drink local water, and eat fish from the area's polluted bayous.
Because many EDC/VCM manufacturing facilities are located in com-munities with poor and/or minority populations, this stage of the PVClifecycle has considerable environmental justice impacts.
Formation of PCBs and other organochlorine by-products
EDC/VCM synthesis generates large quantities of persistent, bioaccumu-
lative by-products. EDC is made in two ways: ethylene is chlorinated
with chlorine gas, or ethylene is oxychlorinated with hydrogen chloride
that has been formed as a waste in other synthesis processes. Most EDC
producers use both methods in a linked cycle, since chlorination of ethyl-
ene generates hydrogen chloride as a by-product, which can then be used
in oxychlorination. Both processes yield a complex mixture of reaction
products, which are then distilled to yield three batches of materials: the
distilled EDC product, the light ends (those substances more volatile
than EDC), and the heavy ends (less volatile than EDC). The waste
quantities are quite large—about two kilograms each of heavy and light
ends for each ton of EDC produced. Based on these figures, world EDC
synthesis by the oxychlorination process produces at least 30,000 tons per
year each of light and heavy ends.48
In general, the heavy ends are discarded and the light ends reprocessed inother chemical reactions. EDC goes on to be pyrolyzed—heated in theabsence of oxygen—to yield VCM. By-products formed in this processinclude chlorinated ethanes, chlorobenzene, chlorobutadiene, ethylenes,methanes, and large amounts of complex but uncharacterized wastetars.49 According to industry sources, the total amount of chemical wastesproduced in the various processes involved in EDC/VCM synthesis is Environmental Impacts of Polyvinyl Chloride Building Materials estimated as between 3 to 10 percent of the VCM yield—a staggering570,000 to 1.9 million tons of by-products each year.50 The heavy ends contain most of the persistent and toxic by-products. Noacademic or government studies have sought to identify all the com-pounds present in these wastes, but there are data from industry and envi-ronmental groups. In 1990, Dow Chemical analyzed its EDC heavy endsand found them to be about 65 percent chlorine, including large quanti- EDC oxychlorination ties of highly persistent, bioaccumulative, and toxic substances: 302 ppmPCBs, 0.3 percent HCE, 1.2 percent hexachlorobutadiene (HCBD), and results in the worldwide 30.6 percent unidentified compounds.51 If Dow's analysis is representa- tive of heavy ends in general, then EDC oxychlorination results in theworldwide production of a remarkable 20,000 pounds of PCBs each year, remarkable 20,000 even though these compounds were banned from intentional production pounds of PCBs each some 20 years ago.52 year, even though these The vinyl industry claims that these by-products are "contained" within compounds were banned the production equipment and thereby never released into the environ-ment. But releases and contamination have clearly occurred. In 1993, chemists from the Greenpeace laboratory at the University of Exeter ana- production some 20 years lyzed material from a number of European EDC/VCM manufacturers.
Soil and gravel samples taken near a Swedish oxychlorination reactor con- tained a wide variety of persistent organochlorines in the high ppm range,and HCB and HCBD were present at the remarkable levels of 1.9 and0.6 percent by weight.53 The following year, Greenpeace obtained sam-ples of heavy ends from several U.S. EDC/VCM manufacturers and hadthem analyzed by the Exeter laboratory. In one sample from BordenChemical, 174 organochlorines were identified, including a wide varietyof highly chlorinated substances with a range of chemical structures,many of them highly persistent, bioaccumulative, and toxic.54 Dioxin and furan formation
With PCBs and HCB in the wastes from PVC production, it is no sur-
prise that the structurally related and extremely hazardous dioxins and
furans are found in significant quantities, as well. Dioxins have been
detected in the wastes from VCM synthesis. In research at a chemical
plant in Russia, substantial quantities of dioxins and furans were identi-
fied in the wastewater and wastewater sludge from the pyrolytic produc-tion of VCM from EDC—as well as in the waste incinerator emissions.55But the largest quantities of dioxin are formed in the production of EDCby oxychlorination. As the British chemical company ICI made clear in asubmission to the government, the formation of dioxin in this process isinevitable and unpreventable: It has been known since the publication of a paper in 1989 that these The formation of dioxin in oxychlorination reactions generate polychlorinated dibenzodioxins this process is inevitable (PCDDs) and polychlorinated dibenzofurans (PCDFs). The reactionsinclude all of the ingredients and conditions necessary to form and unpreventable.
PCDD/PCDFs, i.e., air or oxygen, a hydrocarbon (ethylene, etc.),chlorine or hydrogen chloride, a copper catalyst, an ideal tempera-ture, and an adequate residence time. It is difficult to see how any ofthese conditions could be modified so as to prevent PCDD/PCDFformation without seriously impairing the reaction for which theprocess is designed.56 The 1989 paper to which ICI was referring was the work of a group ofchemists at the University of Amsterdam who simulated the oxychlorina-tion process in the laboratory and found dioxin formation at a rate thatwould make this method of producing EDC one of the world's largest—ifnot the largest—sources of dioxin.57 These authors estimated that 419grams of dioxin TEQ are formed per 100,000 tons of EDC produced—arate equivalent to more than 60,000 grams of dioxin (TEQ) per year fromthe world vinyl industry.58 Although not all the dioxins created would bereleased directly into the environment, this quantity is more than 50 timesthe annual dioxin emissions from all trash incinerators in the UnitedStates—the largest known source of U.S. dioxin emissions. It is also doublethe 25,000 grams of dioxin (TEQ) per year that EPA estimates are carriedinto the environment by contaminated pentachlorophenol59—the largestidentified source of dioxin to any environmental medium.
This research generated considerable public and scientific concern. As aresult, the vinyl industry began its own sampling program. In 1993, theNorwegian PVC manufacturer Norsk-Hydro confirmed that itsEDC/VCM synthesis plant produced dioxins but claimed the quantities Environmental Impacts of Polyvinyl Chloride Building Materials were hundreds of times lower than the Dutch study had predicted.60 Howmuch dioxin is actually formed remains uncertain, because both studieshave strengths and weaknesses. On one hand, the Dutch analysis may bea more accurate indicator of total dioxin generation because theresearchers captured and analyzed all the material outputs from the oxy-chlorination process. The Norwegian report, like any study of a full-scalefacility, inevitably missed some of the by-products, which are directedinto too many different equipment surfaces, products, recirculating mate-rials, and wastes to be completely assessed in a large-scale industrial con-text. On the other hand, the Dutch study was a laboratory simulation,and the industry analysis took place at a real production facility; theremay be reasons why the simulation caused more dioxin to form than areal-world synthesis of EDC.
Dioxin releases in wastes
Whatever the exact quantities, there can be no doubt that dioxin genera-
tion occurs in far from negligible amounts. In 1994, government scien-
tists found dioxins at high concentrations (up to 414 ppb TEQ) in
sludges from a fully modernized EDC/VCM plant in Germany, refuting
the claim that only outdated EDC/VCM technologies produce dioxin.61
The same year, ICI Chemicals and Polymers found that its vinyl chloride
plant in Runcorn, UK, was producing large quantities of dioxin—not as
much as the Dutch studies predicted but substantially more than Norsk-
Hydro had estimated. Most of the dioxins at ICI were deposited in
heavy-end wastes, and smaller quantities were released directly into the air
and water.62
In the United States, wastes from Vulcan Chemical's EDC plant inLouisiana have been found to contain dioxins and furans at the concentra-tion of 6.4 ppm (TEQ), which makes them among the most dioxin-con-taminated wastes ever discovered, on a par with wastes associated with themanufacture of Agent Orange.63 In 2000, Norwegian scientists reportedfinding "extremely high" concentrations of dioxins and furans—26.6 ppm(60.7 ppb TEQ)—in the sludges from a VCM/EDC manufacturing plant.
Considerable quantities of dioxins and furans had migrated from an on-sitedisposal facility for these sludges into groundwater, a nearby brook, and theGulf of Finland in the Baltic Sea. Dioxin and furan levels in several fish species in the region of the plant were 2 to 9 times higher than levels in fishcaught from a relatively uncontaminated local comparison area.
Considerable quantities of PCBs were also found in sediments near the plantand were attributed to the production of EDC/VCM.64 The wastes from EDC synthesis have one of two major destinations. Insome facilities, wastes are used in the manufacture of chlorinated sol-vents—wherein the contaminants end up in the wastes or products from Residents in the Mossville those processes. In other facilities, the wastes are disposed of, usually by area—located across the incineration. (A discussion of environmental releases from this practicefollows). But not all by-products of EDC/VCM synthesis end up in the road from a large vinyl hazardous wastes—some escape directly into the environment. Dioxins chloride manufacturing have been detected in wastewater discharges and air emissions from anumber of EDC/VCM plants,65 and local and regional contamination of facility—have blood levels water, sediments, and shellfish has been linked to EDC/VCM manufac- of dioxins and furans turers in Europe and the United States.66 For example, severe dioxin con-tamination of sediments in Italy's Venice Lagoon has been linked to an (TEQ) averaging nearly EDC/VCM manufacturing facility.67 In the Netherlands, levels of dioxins three times those of a in sediment samples in the River Rhine jump dramatically immediatelydownstream from an EDC/VCM manufacturing plant.68 The levels are so high, in fact, that the majority of dioxins in Rhine sediments down-stream from the plant—all the way to the river's mouth, and in the entireNorth and Wadden Seas—appear to be attributable to the facility.69 These dioxin releases contribute not only to environmental contamina-tion but also to human exposure. In Lake Charles, Louisiana, the U.S.
Centers for Disease Control reported that residents in the Mossvillearea—located across the road from a large vinyl chloride manufacturingfacility—have blood levels of dioxins and furans (TEQ) averaging nearlythree times those of a comparison population (an increase that was statis-tically significant at the 95 percent confidence level). Eggs from chickensraised in the area were found to contain dioxins and furans at levels nearlydouble those in store-bought eggs; but the sample size was too small forstatistical significance to be evaluated. The study did not evaluate specifi-cally whether the increased dioxin levels were due to releases of dioxinfrom the EDC/VCM synthesis, from on-site incinerators for productionwastes, or from some other process at facilities in the area.70 Environmental Impacts of Polyvinyl Chloride Building Materials Other by-products are also present near chemical plants that make PVCfeedstocks. In Lake Charles, Louisiana, the National Oceanic andAtmospheric Administration (NOAA) found high levels of persistentorganochlorines in the water, sediment, and fish of bayous nearEDC/VCM facilities owned by PPG and Vista Chemical. According toNOAA, the geographical pattern of contamination indicates that PPG isthe primary cause of high levels of organochlorines in the water and sedi-ment. In one portion of the estuary near PPG's facility, concentrations ofHCB, HCBD, and HCE exceeded 1,000 ppm in sediment; in some sam-ples, these three by-products represented from 0.1 percent to an extraor-dinary 4.8 percent of the sediment's total mass.71 POLYMERIZATION, COMPOUNDING, AND MOLDING Polymerization of VCM to make pure PVC is a more diffusely structuredindustry than EDC/VCM synthesis, with smaller quantities of productmade at a greater number of facilities. No estimates of the total quantity ofVCM released into the workplace and the local environment in these stagesare available. Traditionally, worker exposure in this sector has been assumedto be higher than in any other process.72 As previously discussed, numerousstudies of the health of workers in PVC polymerization facilities have beenconducted, and they have established a causal connection to angiosarcomaof the liver and revealed statistically significant excesses of brain cancer andneurological effects among VCM-exposed workers. In the United States,worker exposure in this sector has declined in recent decades.
Occupational health & phthalates
Release of phthalates into the environment and occupational exposure to
these substances is another issue in the later manufacturing stages of the
vinyl lifecycle. In 1997, chemical and plastics industries in the United
States reported releasing 213,621 pounds of the plasticizer diethylhexyl
phthalate (DEHP) directly into the air, plus 71,004 pounds into the
land.73 Occupational exposures can be significant: in one plastics molding
facility, DEHP levels have been measured at 11,500 nanograms per cubic
meter, thousands of times higher than the levels typically found in out-
door air.74 According to the National Toxicology Program, "workers may
be exposed to relatively high concentrations during the compounding ofDEHP with PVC resins. The major route of exposure is inhalation."75 Cancer risk from PVC manufacturing
There are few direct studies of health impacts and phthalate exposure in
the PVC manufacturing industry. Two studies by a research group in
Sweden indicate an increased risk of testicular cancer among workers in
PVC manufacturing industries. In the first study, a variety of occupa-
Occupational work with tional exposures were investigated for a possible link to testicular cancer.
Work in plastics production was found to cause a 2.9-fold increase in therisk of testicular cancer.76 The second study tested and clarified the rela- associated with a 5.6-fold tionship between plastics work and testicular cancer. In this report, using increase in the risk of a case-control study of 163 men with testicular cancer and 326 withoutthe condition, occupational work with PVC plastic was associated with a seminoma—a form of 5.6-fold increase in the risk of seminoma—a form of testicular cancer testicular cancer.
that occurs later in life and may thus plausibly be caused by occupationalexposure. The increased risk was statistically significant and highestamong those men with the greatest cumulative exposures. No significantincreases in the testicular cancer rate were seen among men who workedwith other types of plastics. Because exposure to endocrine-disruptingcompounds can lead to testicular cancer, the authors hypothesized thatexposure to phthalates used as plasticizers in PVC—some of which areknown endocrine disrupters and testicular toxicants—may be the specificcause of the increased risks.77 These results contrast with those of aDanish study that found no relationship between work in cable manufac-ture—a large consumer of PVC—and testicular cancer.78 DISPOSAL OF EDC/VCM WASTES The organochlorine-rich heavy ends produced by EDC/VCM manufac-ture are regulated as a hazardous waste in the United States. The majorityof these are disposed of by incineration, usually in on-site furnaces at theproduction facility. In theory, a properly designed and operated incinera-tor converts organochlorines by oxidation into carbon dioxide, hydrogenchloride, and water. Real-world combustion systems, however, never takethis reaction to completion for all the compounds fed into them. Mostcompounds are completely oxidized, but some fraction escapes unburned, Environmental Impacts of Polyvinyl Chloride Building Materials and a larger portion is converted into new organic compounds, calledproducts of incomplete combustion (PICs). According to EPA's technicalreview document on hazardous waste incineration, "The complete com-bustion of all hydrocarbons to produce only water and carbon dioxide istheoretical and could occur only under ideal conditions…Real worldcombustion systems…virtually always produce PICs, some of which havebeen determined to be highly toxic."79 Dioxin and other byproduct formation in incinerators
By-products form in incinerators for the same reasons as in chemical
manufacturing: multiple reaction pathways, local optima that lead to sta-
ble by-products, and deviations from optimal conditions. In incineration,
the problems are particularly acute—wastes are complex mixtures of
diverse materials that can never be uniformly blended. Further, combus-
tion is by nature a stochastic process of bond breakage and formation; at
high temperatures, most of the molecules will be completely oxidized, but
some will follow alternative reaction pathways and emerge as PICs.
Transient variations and upsets are a particular problem with incinerators.
Good management can reduce but never eliminate the production of
PICs, as EPA's analysis made clear:
[Deviations from optimum] usually are a consequence of a rapid per-turbation in the incinerator resulting from a rapid transient in feedrate or composition, failure to adequately atomize a liquid fuel, excur-sions in operating temperature, instances where the combustible mix-ture fraction is outside the range of good operating practice, orinadequate mixing between the combustibles and the oxidant…Theamount and composition of PICs will depend in a complex andunpredictable way on the nature of the perturbation.80 The type of incinerator and how well it is operated will affect the magni-tude of the PICs released, but the production of chlorinated PICs—including the most hazardous ones like the dioxins and furans—is auniversal and inevitable outcome whenever chlorinated wastes areburned. As the British Department of the Environment noted,"Comprehensive tests have established that all waste incinerators, inde-pendent of type of incinerator or waste composition, are likely to produce all of the possible 75 PCDD and 135 PCDF isomers and congeners, aswell as about 400 other organic compounds."81 By-products form from diverse and unpredictable reactions not only inthe furnace but also in the cooler zones, where control over combustionconditions is nearly irrelevant.82 Dioxins can even form in pollution con-trol devices or smokestacks, where chlorine gas, hydrochloric acid, ororganochlorine precursors come in contact with organic compounds in Incinerators not only fly ash. This process, called de novo dioxin formation, is greatly acceler- destroy organochlorines, ated if iron or copper catalysts are present, as they are in EDC/VCMwastes and municipal trash.83 they also manufacture This means that incinerators not only destroy organochlorines, as they aresupposed to, but also manufacture them. EPA estimates that PICs formedin the incineration process number in the thousands.84 Of these, somehave been characterized, and the rest remain unidentified. Laboratorytests show that burning methane—the simplest possible hydrocarbon—inthe presence of a chlorine source produces more than 100 organochlorinePICs. These by-products, ranging from chlorinated methanes to dioxins,are produced by a set of reactions thought to be common to all incinera-tion processes in which chlorine is present.85 It is much more challengingto analyze PICs in the stack gas of real-world incinerators, but more than50 organochlorines or groups of organochlorines have been identified inthe emissions of hazardous waste incinerators—ranging from the struc-turally simple carcinogen carbon tetrachloride to highly persistent andbioaccumulative compounds like chlorinated hexanes, dioxins, ethers,furans, naphthalenes, PCBs, phenols, and thiophenes.86 As in other aspects of the vinyl lifecycle, the identified compounds arejust the beginning. At hazardous waste incinerators, the most comprehen-sive research burns have identified about 60 percent of the total mass ofunburned hydrocarbons in incinerator stack gases, and most field testshave had far less success in identifying the PICs emitted.87 There is goodreason to be concerned about these mystery compounds because at leastsome appear to be in the same toxicological family as dioxins. Germanresearchers measuring the dioxin-like toxicity of trash incinerator fly ash Environmental Impacts of Polyvinyl Chloride Building Materials using a biological test found that toxicity was up to five times greater thancould be accounted for by the amount of dioxins, furans, and PCBs inthe ash.88 The remaining dioxin-like effect was presumably caused byscores of other compounds—such as chlorinated naphthalenes, diphenylethers, thiophenes, and many others—that can cause similar health effectsbut were not specifically measured.
Efficient incineration and high emissions
An incinerator burning The total quantity of PICs and unburned wastes emitted from incineratorsis not known precisely, but it appears to be large. In the United States, haz- EDC/VCM manufacturing ardous waste incinerators must pass a trial burn that requires them to wastes may be certified demonstrate a destruction and removal efficiency (DRE) of 99.99 percent ofthe organic compounds fed to them, which means that no more than 0.01 as achieving 99.99 percent of several test chemicals fed into the furnace may be measured in percent DRE when, in stack emissions. But high DREs do not mean that the environment is pro-tected, for several reasons. fact, it is emitting huge quantities of unburned EDC heavy ends are burned in such immense quantities that even if allincinerators achieved 99.99 percent DRE, they would still emit more and partially burned than 6,600 pounds per year of unburned hazardous wastes into the air in the United States alone.89 Much greater amounts of organochlorines are released as PICs.
"Destruction" means only that the chemical tested was transformed intosome substance other than the original compound, and PICs are notcounted against the 99.99 percent DRE figure. EPA's Science AdvisoryBoard has estimated that the total quantity of PICs that hazardous wasteincinerators emit to the air may be up to 1 percent of the organic matterfed to them.90 This estimate suggests that incineration of heavy endsfrom vinyl manufacture would emit some 660,000 pounds of PICs eachyear.
Still more unburned wastes and PICs are transferred to the land or waterwhere the ash, sludge, and effluent from incinerators are disposed of.
These quantities are not included in a DRE, which reflects not onlydestruction of waste chemicals but also their removal by pollution control devices. An incinerator with a filter that captures 95 percent of the dioxinin the stack gas deposits 20 times more dioxin in its ash than it emits intothe air, without any effect on the calculated DRE.
DREs are calculated from an incinerator's performance when burningtest chemicals that are fed in high concentrations, but two EPA stud-ies have found that substances in low concentrations burn much lessefficiently. Chemicals that are present in wastes in the ppb or ppmrange—such as the dioxins, PCBs, and many other by-products inEDC/VCM wastes—are subject to destruction efficiencies as low as99 percent, implying that significant amounts of these hazardous sub-stances will escape intact from incinerators.91 DREs measured in trial burns are unlikely to reflect emission ratesduring routine operation because trial burns involve the combustionof simplified mixtures of pure chemicals under carefully controlled,closely scrutinized conditions. In daily use, incinerators generally per-form less efficiently, due to the complexity of real-world wastes andthe frequency of upsets, operator error, and equipment malfunction.92Further, the standard trial burn protocol allows the measurement ofemissions to stop when the feed of waste chemicals to the incineratorstops, but emissions can continue for days, resulting in total emissionsof unburned wastes that are orders of magnitude greater—and DREsfar lower—than those measured during the trial burn.93 For these reasons, an incinerator burning EDC/VCM manufacturingwastes may be certified as achieving 99.99 percent DRE when, in fact, itis emitting huge quantities of unburned and partially burned wastes intothe environment.
Environmental Impacts of Polyvinyl Chloride Building Materials FAILURE OF THE VINYL INSTITUTE'S SELF-CHARACTERIZATION OF DIOXIN RELEASES The Vinyl Institute (VI) has argued that its role in dioxin formation isminimal, primarily based on its own study, called the "dioxin self-characterization."94 In this report, the Vinyl Institute concludes thatthe U.S. PVC industry releases about 13 grams of dioxin (TEQ) per yearto the environment. This estimate is also the basis for the Vinyl Institute's Pathways that contain the contention that vinyl production is responsible for only a small fraction largest amounts of dioxin of identified dioxin releases in the United States.95 were completely ignored.
There are three reasons to be skeptical of the industry's reassurancesabout its dioxin emissions: Even if the Vinyl Institute's estimate is accurate, 13 grams of dioxinper year is still highly significant, justifying action to reduce vinylconsumption. U.S. EPA's current standard for the acceptable dailydioxin intake of an average adult (weighing 70 kg) is 0.153 billionthsof a gram per year.96 Based on its own estimates, then, the vinylindustry's annual releases of dioxin into the environment equal theacceptable annual dose for about 85 billion people. (Not all of thedioxins released by the industry will result in direct human exposures,of course. The point of this calculation is to demonstrate that,because dioxin is so exquisitely toxic, a quantity of dioxin that appearssmall on a mass basis is in fact extremely significant from a toxicologi-cal perspective.) The Vinyl Institute's figures on its dioxin releases are likely to be grossunderestimates because they omit the majority of the dioxin pro-duced during the vinyl lifecycle. The industry's self characterizationanalyzed several potential pathways for dioxin release, finding low tomoderate quantities of dioxins and furans in samples of EDC, PVCproducts, air emissions, and wastewater and sludge from its treat-ment. But numerous pathways that contain the largest amounts ofdioxin—along with many PVC-related processes that are majordioxin sources—were completely ignored. No data, for example, weregathered on dioxin contamination of chemical streams that re-circulate in the manufacturing process, of light ends and otherwastes used in other synthesis processes, and—most importantly,because these are known to be so severely contaminated—heavy ends,tars, and other hazardous wastes that are sent to disposal facilities.
Nor did the program address what is apparently the largest PVC-related dioxin source—the burning of vinyl in incinerators, smelters,and accidental fires. Thus, the industry's estimates are grossly incom-plete and do not effectively refute the argument that the lifecycle of The Vinyl Institute report PVC is a major dioxin source.
did not address what is The Vinyl Institute's estimates have not been independently verified.
apparently the largest In this self-characterization, the PVC industry decided when and PVC-related dioxin where to take samples, how to collect them, how to analyze dioxincontent, which data to present, and how to interpret this data before source—the burning of submitting their results to EPA. While an independent panel vinyl in incinerators, reviewed the submission, the industry chose which data the panelsaw. Information about the samples—including which facility they smelters, and accidental came from—was completely confidential, so neither reviewers nor the public had the opportunity to determine whether sampling times andlocations accurately represented typical dioxin releases. Most impor-tantly, no one was able to independently evaluate, confirm, or act onthe information. It would be naïve to take at face value the industry's own estimates of themagnitude of its releases of dioxin—a substance that is the subject ofmajor public concern and regulatory activity—particularly when thoseestimates conflict with a large body of information gathered by independ-ent sources, such as those cited above.
Notes1. Leder et al. 19942. Leder et al. 1994.
3. Leder et al. 1994.
4. Leder et al. 1994; see also Thornton 2000.
5. Schmittinger et al. 1986.
6. HSDB 1997.
7. Hutzinger and Fiedler 1988.
8. My calculation of annual loadings assumes world production of 39 million metric tons of chlorine each year(Leder et al. 1994). 9. Polychlorinated dibenzofurans (PCDFs, or furans) are structurally related to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, known colloquially as dioxin), the best studied and most hazardous of the dioxin-like com-pounds, a large group of structurally and toxicologically related group of compounds that includes not only Environmental Impacts of Polyvinyl Chloride Building Materials the furans but also some PCBs, chloronaphthalenes, and many others), together referred to as dioxins ordioxin-like compounds. 10. Rappe et al. 1991.
11. Svennson et al. 1993.
12. Kaminski and Hites 1984.
13. Barrie et al. 1997.
14. Andersson et al. 1993.
15. This research is summarized in Versar, Inc. 1996 and EPA 1998.
16. Environment Agency 1997.
17. Lindqvist et al. 1991.
18. Lindqvist et al. 1991; Pacyna and Munch 1991.
19. Ayres 1997.
20. Chlorine Institute 2000.
21. Burns 2000.
22. The data from Euro-Chlor, presented in Ayres 1997, are the most comprehensive available. The data arebased on a mass balance method, so that all mercury consumed is accounted for in one way or another. My cal-culation of total mercury releases from the chlor-alkali industry uses this range and assumes 39 million tonsglobal chlorine production,35.5 percent through the mercury process (Leder et al. 1994). The actual total may behigher, since many plants are not likely to be as well operated as those in Europe. Euro-Chlor's estimates ofreleases to water and air (0.2 and 1.9 grams of mercury per ton of chlorine, respectively) are somewhat lower thanestimates made by other parties. One review estimates mercury releases at 3 grams per ton of chlorine for a newchlor-alkali plant, and 10 grams per ton of chlorine for a well-operated existing facility (Schmittinger et al. 1986).
Real-world plants in Germany have been found to release 19 grams per ton (SRI International 1993).
23. ATSDR 1998.
24. Harada 1995; Davies 1991.
25. Hill and Holman 1989.
26. National Academy of Sciences 2000.
27. Airey and Jones 1970; Johnston et al. 1993.
28. Maserti and Ferrara 1991.
29. Panda et al. 1990.
30. Energy requirements vary somewhat among the chlor-alkali cell types: the mercury cell requires 3310-3520 kilowatt-hours per ton of chlorine, the diaphragm 2,830 kilowatt-hours per ton, and the membraneprocess 2,520 kilowatt-hours per ton. Based on the proportion of each cell type in the world industry, theaverage energy requirement for the industry overall is slightly under 3,000 kilowatt-hours per ton (SRIInternational 1993).
31. SRI International 1993.
32. Assuming an average global cost of 4.2 cents per kilowatt-hour for chlor-alkali customers (SRIInternational 1993).
33. In the United States, 109 nuclear plants generated 673 billion kilowatt-hours of electricity, for an averageof about 6 billion kilowatt-hours per plant per year (Energy Information Administration 1996).
34. National Institutes of Health 1998. 35. Production estimates are 29,137 kilotons EDC per year, 18,495 kilotons of VCM per year, and 18,135 kilo-tons of PVC per year (SRI International 1993).
36. Kielhorn et al. 2000.
37. SFT 1993.
38. ATSDR 1993; ATSDR 1995.
39. Kielhorn et al. 2000.
40. ATSDR 1993; ATSDR 1995.
41. Kielhorn et al. 2000.
42. Kielhorn et al. 2000.
43. Kielhorn et al. 2000.
44. Pitot and Dragan 1991.
45. Bowermaster 1993.
46. Bowermaster 1993.
47. Curry et al. 1996.
48. My calculations assume that about 15 million metric tons per year of EDC produced by oxychlorination(half of world production (SRI International 1993), assuming integrated oxychlorination and direct chlorina-tion process in 1.1 molar ratios). Heavy and light ends are assumed to be produced at the rate of 2 kilogramseach per ton, based on the fact that production of 168,796 tons of EDC in Sweden per year results in the gen-eration of 335 and 333 tons per year of heavy and light ends, respectively (TNO Centre for Technology andPolicy Studies 1996). This figure is slightly lower than that of Rossberg et al. (1986), who estimate 2.3 and 2.9kilogram heavy and light ends per ton of VCM produced, respectively. Use of more recent figures for globalPVC production rates (Kielhorn et al. 2000) increases this estimate by about 50 percent.
49. Rossberg et al. 1986.
50. The lower estimate is from Papp 1996. The upper estimate is from Rossberg et al. 1986, assuming synthe-sis of EDC in integrated chlorination/oxychlorination facility plus pyrolysis to VCM, and includes releases toair, water, heavy ends, and light ends, except nitrogen gas vented to the atmosphere and aqueous streams.
51. Dow Chemical 1990.
52. This calculation assumes global production of 32 kiltons of EDC heavy ends per year, as discussed in thesection above. Use of more recent figures for global PVC production rates (Kielhorn et al. 2000) wouldincrease this estimate by about 50 percent.
53. Johnston et al. 1993.
54. Costner et al. 1995.
55. Khizbullia et al. 1998.
56. ICI Chemicals and Polymers 1994.
57. Evers 1989. 58. Based on early 1990s world production of EDC by oxychlorination of about 15 million tons per year (seenote above).
59. EPA 1998.
60. The conclusions from this study are summarized in SFT 1993.
61. Lower Saxony Ministry of Environmental Affairs 1994.
62. Total dioxin generation associated with EDC/VCM synthesis was estimated at 27 grams (TEQ) per200,000 tons of VCM, for a dioxin generation rate of 13.5 grams (TEQ) per 100,000 tons—substantiallymore than the Norwegian estimate but less than the Dutch figure. If production at the same plant of perc andtrichloroethylene from the heavy ends of EDC oxychlorination are included, the estimate of dioxin formationincreases to 500 grams TEQ per year from this plant alone. Based on this estimate, all oxychlorinationprocesses would constitute one of the world's largest sources of dioxin (Environment Agency 1997).
63. Costner et al. 1995.
64. Isosaari et al. 2000.
65. DTI 1995; Environment Agency 1997; SFT 1993.
66. Contamination in the UK is described by Environment Agency 1997; in Germany by Lower SaxonyMinistry of Environmental Affairs 1994; and in the United States by Curry et al. 1996.
67. Ramacci et al. 1998.
68. Evers et al. 1988.
69. Evers et al. 1993; Evers et al. 1996.
70. U.S. Centers for Disease Control 1999.
71. Curry et al 1996.
72. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
73. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
74. Rudell et al. forthcoming.
75. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
76. Hardell et al. 1998.
77. Hardell et al. 1997; Ohlson and Hardell 2000.
78. Hansen 2000.
79. EPA 1990.
80. EPA 1989.
81. UKDOE 1989. 82. Dellinger et al. 1988; EPA 1994b.
83. Gullett 1990.
84. EPA 1989.
85. Eklund et al. 1988. Similarly, combustion under well-controlled laboratory conditions of trichloroethyl-ene, another relatively simply organochlorine, produces a variety of persistent organochlorine PICs, includinghexachloropentadiene, highly chlorinated benzenes and indenes, PCBs, and the dioxin-like chlorofulvalenes(Blankenship et al. 1994).
86. Trenholm and Lee 1986; Trenholm and Thurnau 1987; Dellinger et al. 1988; Chang et al. 1988; EPA1987a and 1987b; Wienecke et al. 1995. 87. EPA 1990.
88. Markus et al. (1997) used a calibrated bioassay to quantify the activity of the cytochrome p4501A1enzyme, which is induced by dioxin and serves as a "sensitive and selective" marker of dioxin exposure. Thetotal dioxin-like toxicity of the fly ash exceeded that predicted by the quantity of dioxins, furans, and PCBs inthe sample by a factor of two to five.
89. Assuming incineration of 30,000 tons of EDC heavy ends per year.
90. EPA SAB 1985.
91. Kramlich et al. 1989; Trenholm et al. 1984.
92. See, for instance, the 1986 analysis by U.S. EPA engineers (Staley et al. 1986), which concluded, "Thereare several problems with the permitting process [based on trial burns]. First, the trial burn data only indicatehow well the incinerator was operating during the time that the data were being taken, typically only a periodof a few days. No information is obtained on how the incinerator might respond if fuel, or especially waste,conditions change. Waste streams vary widely in composition and one incinerator may burn many differenttoxic substances over its useful life, resulting in unavoidable and frequent changes in waste feed conditions. Itis difficult to generalize the results of a trial burn to predict how the composition of the incinerator exhaustwill change under these varying conditions."93. Licis and Mason 1989. 94. Vinyl Institute 1998. 95. Burns 2000.
96. EPA 1985. The "acceptable" dose (0.006 pg/kg of body-weight/day) is the daily exposure that poses a cal-culated lifetime cancer risk of one per million.
Environmental Impacts of Polyvinyl Chloride Building Materials Use of PVC Products
Use of PVC Products PVC is not bioavailable, so the polymer itself is not toxic during use. Butvinyl products are not pure PVC; they contain both accidental contami-nants and chemical modifiers that are added to the plastic on purpose,and some of these may pose health hazards. Moreover, PVC productsoften encounter reactive conditions—accidental fires in particular—thatcan transform the plastic into hazardous by-products. BY-PRODUCT FORMATION Some portion of the diverse organochlorine by-products created in thesynthesis of EDC/VCM end up in the PVC itself. In May 1994, theSwedish Environmental Protection Agency found that pure PVC plasticfrom two Swedish producers contained dioxins, furans, and PCBs at con-centrations ranging from 0.86 to 8.69 ppt TEQ.1 In 1995, the UK gov-ernment found dioxins and furans in the same range in PVC foodpackaging items, including cling film and bottles for oils and beverages.2Subsequently, the U.S. Vinyl Institute and the European plastics indus-tries conducted their own studies, both of which identified trace quanti-ties of some dioxin congeners in some samples of PVC plastic.3 The levelswere very low, but any quantity of dioxin in consumer products is a mat-ter of concern.
INDOOR AIR QUALITY: RELEASE OF TOXICANTS Because chemical additives are present in PVC in large amounts, they areparticularly problematic. PVC additives include a range of toxic com-pounds, but the most important of these are the phthalate plasticizers andmetallic stabilizers. Phthalates can make up a large portion—up to 60percent by weight—of the final vinyl product.4 Flexible PVC—including Environmental Impacts of Polyvinyl Chloride Building Materials flooring, roofing membranes, and wall coverings—accounts for morethan half of all vinyl demand, while the remainder is rigid, unplasticizedmaterials such as pipes and siding.5 Stabilizers—including lead, cad-mium, organotins, and other compounds—are used to extend the life ofPVC products exposed to light, and they are typically present in lowerbut still significant concentrations. About 5.4 million tons of phthalatesand 156 thousand tons of lead are used each year in the worldwide pro-duction of PVC.6 Vinyl accounts for more than 90 percent of the total Vinyl accounts for more consumption of phthalates, so the health and environmental impacts of than 90 percent of the phthalates are overwhelmingly attributable to PVC.7 total consumption of The additives are not chemically bonded to the PVC polymer but are phthalates, so the health mixed into the plastic during its formulation. Over time, these additivesleach out of vinyl products, entering the air, water, or other liquids with and environmental which the product comes in contact. When PVC containers and films are impacts of phthalates are used to hold food products, plasticizers migrate out of the plastic and accu-mulate in foods, especially fatty ones like cheese and meats.8 The common practice of storing blood and drug formulations in PVC bags causes phtha- lates to leach into the container's contents, which can result in substantialshort-term phthalate exposures for the recipient.9 Newborn infants receiv-ing a single blood transfusion have been found to have extremely high levelsof phthalates in their systems.10 When exposure is repeated, blood levels ofphthalates can be 100 to 1,000 times greater than "background" and canreach levels at which liver damage and birth defects can occur in animals.11Phthalates are also released in significant quantities into saliva when smallchildren suck on vinyl toys and teethers.12 Release of phthalate plasticizers
Of particular relevance to the health and environmental impacts of build-
ing materials is the release of phthalates into indoor air from flexible
PVC. The plastics industry has argued that most phthalates have low
vapor pressures; therefore they are not expected to volatilize much.13 But
this prediction is not borne out by experience: empirical data make clear
that phthalates are released in considerable amounts from vinyl products
into the indoor atmosphere. For example, DEHP levels in indoor air
average 20 to 103 nanograms per cubic meter, compared to 0.3 to 4.0
nanograms per cubic meter in outdoor air.14 As one review concluded,
Use of PVC Products "Phthalates are typically present in indoor air at much higher concentra-tions than outdoor air due to their high concentrations in consumerproducts and building materials."15 According to figures cited by theNational Toxicology Program, inhalation accounts for about 15 percentof the average adult's daily intake of DEHP.16 The relatively low vapor pressure of most phthalates may explain theirtendency to be present on dust particles in higher concentrations than inthe vapor phase. One U.S. study of indoor dust and air samples takenfrom homes and offices found substantial levels of all phthalates tested.
Levels were highest of DEHP and butyl benzyl phthalate (BBP), whichwere present in dust at the remarkably high mean levels of 315 and 117ppm, respectively.17 Another recent study of indoor air in Norwegian resi-dences had similar findings, reporting an average of 960 ppm (including640 ppm of DEHP and 110 ppm of BBP) on sedimented dust particlesand 1,180 ppm (more than 0.1 percent) on suspended dust particles.18This study also found that a large portion of the phthalate-contaminateddust particles were small enough to be taken into the airway and lungs.
As discussed later, phthalates impair reproduction and development, andsome are suspected carcinogens. Phthalate connections to asthma and other conditions
The high levels of phthalates in indoor air suggest the possibility that
these compounds may contribute to the risk of asthma—the cases of
which have been steadily increasing in recent decades—particularly
among children. In 1997, an analysis of phthalate levels in indoor air
pointed out that MEHP—the primary metabolite of DEHP—induces
bronchial hyper-reactivity in rats, presumably by its ability to bind to and
activate the receptor for prostaglandin D2, a locally-acting hormone that
triggers inflammation. This report concluded, "We propose that the
increase in asthma is due to contributory factors of environmental chemi-
cals in general, and specifically DEHP through its primary hydrolysis
product MEHP, which affects the bronchial contracting receptors and
thereby generates a hyper reactive condition in the lungs. This will
increase the risk of a pathological development in addition to aggravation
of the effects of other environmental agents."19
Environmental Impacts of Polyvinyl Chloride Building Materials Three epidemiological studies have tested this hypothesis and found evi-dence that exposure to PVC in building interiors increases the risk ofasthma and related conditions. The first study of 251 Norwegian childrenwith bronchial obstruction, with an equal number of healthy children forcomparison, found that the presence of PVC flooring in the home wasassociated with a statistically significant 1.9-fold increase in the risk ofbronchial obstruction. Further analysis revealed a dose-response relation-ship between the amount of PVC and other plasticizer-containing materi- PVC flooring in the home als in the home and the risk of this condition—a finding that increases was associated with a sta- confidence that the association between exposure and risk is not a spurious one.20 tistically significant 1.9- fold increase in the risk of A larger follow-up study in Finland found that children in homes withPVC flooring or wall covering were significantly more likely to suffer from asthma, persistent wheezing, pneumonia, prolonged cough, andphlegm in the airway. The researchers concluded, "Emissions from plasticmaterials indoors may have adverse effects on the lower respiratory tractsof small children…our findings provide additional evidence that indoorplastic materials may emit chemicals that have adverse effects on thelower respiratory tracts of small children…and warrant further attentionto the types of plastic materials used in interior decoration."21 A third study focused on the presence of certain breakdown products ofDEHP in indoor air. This report by Swedish researchers examined theprevalence of symptoms of eye and nasal irritation, as well as biochemicalindicators of inflammation and secretion in these tissues, in relation tothe presence of 2-ethyl-1-hexanol (EH) in indoor air. EH is the primarybreakdown product of DEHP in damp conditions, which sometimesoccur when floors or walls that are covered with an impermeable layer ofvinyl become wet. The study examined the staff of four nursing homes—three with PVC flooring, and one without. Workers in the two buildingswith damp PVC surfaces were exposed to higher levels of EH and hadsignificantly increased symptoms of nasal and ocular irritation, as well asof biochemical indicators. Other indoor air factors could not explain thefinding, as levels of formaldehyde, molds, bacteria, ozone, and NO were low in all four buildings. The authors concluded, "Emissions related tothe degradation of DEHP due to dampness in the floors…may affect the Use of PVC Products mucous membranes in the eyes and nose, decrease tear film stability andincrease the occurrence of ocular and nasal symptoms. The low occur-rence of both symptoms and signs in the building with special materialsand design illustrates that it is possible to construct a new building with aminimum of adverse effects on nasal and ocular membranes."22 This evidence does not prove that PVC is a major cause of asthma, but it Vinyl wall coverings are justifies concern about the role of indoor exposure to phthalate plasticizersin relation to this widespread condition and action to reduce exposures.
said to be the major cause of mold and mildew in Toxic mold growth
Vinyl's tendency to trap dampness can create another indoor air prob-
interiors, according to sev- lem—the growth of toxic molds. Some molds produce toxic and/or aller- eral building industry genic products, particularly among sensitive individuals. These molds donot normally grow indoors but can grow on persistently damp surfaces that contain nutrients (including gypsum and sheetrock), if they are suit-ably warm and protected from drying out. Repair of the mildewed mate-rial has cost millions of dollars, and liability claims are on the rise forproperty damage and personal injury caused by mold growing insidebuildings, including headaches, skin rashes, memory loss, respiratoryproblems, lung disease, and brain damage.23 Vinyl wall coverings, becausethey are impermeable to water vapor, are said to be the major cause ofmold and mildew in interiors, according to several building industrysources.24 The vinyl industry confirms that vinyl wall coverings have cre-ated this situation in many buildings; PVC acts as "a vapor barrier thattraps moisture inside the wall cavity, where it condenses against the rela-tively cool inside surface of the wall. Prolonged exposure to these condi-tions will result in deterioration of the gypsum board."25 The industrysuggests that use of permeable membranes on the outside wall part of thecavity and prevention of moisture infiltration can help reduce the risk ofmildew growth.26 Because dampness and condensation can occur insidevinyl-sealed walls from temperature and humidity differentials producedby heating and air conditioning systems, however, at least one authorita-tive building industry source recommends avoiding vinyl wall coveringsaltogether to prevent mold and mildew growth.27 Environmental Impacts of Polyvinyl Chloride Building Materials Releases of lead and other stabilizers
Metal stabilizers are also released from PVC products. Significant releases of
lead have been documented from PVC window blinds,28 leading to a warn-
ing by the U.S. Consumer Product Safety Commission. Lead is also known
to leach into water carried in PVC pipes that contain lead stabilizers.29
But lead continues to be used in building-related materials, as are otherhazardous additives. Lead stabilizers are commonly used in pipes, vinyl Lead is an infinitely per- cables, and window profiles, although their use is greater in Europe than sistent substance and is in the United States.30 Lead accounts for nearly 70 percent of all vinylstabilizers in Europe, with consumption of more than 51,000 tons of lead exquisitely toxic to the in PVC annually, based on 2000 estimates by the European Union.31 developing brain—even in Lead is an infinitely persistent substance and is exquisitely toxic to thedeveloping brain—even in tiny amounts. In November 2000, the Danish tiny amounts.
government took action to ban the use of virtually all lead compounds,including those in PVC cables, gutters, pipes, roofing, and windows, byno later than 2003.32 PVC is also associated with other toxic metals. According to the EuropeanCommission, 50 tons (110,000 pounds) of cadmium—also a highly neuro-toxic and infinitely persistent metal—are used in vinyl each year in Europe,although quantities are declining. Consumption of organotin compounds invinyl is estimated at 15,000 tons, mostly in rigid films, roofing materials, andclear rigid construction sheeting.33 Organotins used in vinyl can suppress theimmune systems, cause birth defects, damage the liver, bile duct, and pan-creas, and may pose hazards to the aquatic organisms when released into theenvironment.34 Further, the mono- and di-butyl tin compounds used in PVCare contaminated with tributyl tin (TBT), a potent endocrine-disruptingcompound that has caused major damage to marine wildlife populations.35 ACCIDENTAL COMBUSTION RELEASES The possibility of fire is another major hazard associated with the use ofPVC products. Vinyl manufactures often stress the materials' fire resistantproperties—due to the high fraction of chlorine in PVC—as an advan-tage for hospitals, schools, and other public buildings. In fact, chlorine'sresistance to combustion represents a hazard, not a benefit. Use of PVC Products Hydrochloric gas releases
PVC is now ubiquitous in modern buildings and vehicles. When vinyl
burns, the primary combustion products are carbon dioxide, hydrochloric
acid, and water. In several major fires, hydrochloric acid has caused severe
burns to skin, eyes, and lungs and is an important cause of toxicity to
firefighters and persons exposed to fumes and smoke. It can also cause
severe damage to computers and other equipment.36 When large masses
of PVC are present—as in vinyl siding or roofing membranes—the haz-
ards may extend to building occupants and the surrounding community.
The hazards of PVC in fires have prompted action or positions by a num-ber of expert organizations. The U.S. military has adopted specifications toavoid PVC-jacketed cables in aircraft, space vehicles, and enclosures inwhich offgassing may occur in the event of fire.37 In the United Kingdom,the Fire Brigades Union (FBU) has stated, "The FBU is now particularlyconcerned about the safety of PVC based building materials that are used inthe construction and fitting out of buildings when involved in fire."38 TheInternational Association of Firefighters has stated, Because of its majority chlorine content, when PVC burns in firestwo hazardous substances are formed which present acute and chronichazards to fire fighters, building occupants, and the surroundingcommunity. These are hydrogen chloride gas and dioxin. Hydrogenchloride is a corrosive, highly toxic gas that can cause skin burns andwhen comes into contact with the mucous lining of the respiratorytract creates hydrochloric acid, which can cause severe respiratorydamage. Exposure to a single PVC fire can cause permanent respira-tory disease. Dioxin is an unintentional by-product of PVC combustion, andwould most likely be left behind in ash and debris from a PVC fire.
While only small amounts of dioxin may be formed as the result ofburning PVC, it is one of the most toxic substances known to science.
Dioxin is a known human carcinogen and has been linked to repro-ductive disorders, immune suppression, and endometriosis, and otherdiseases in laboratory animals.
Environmental Impacts of Polyvinyl Chloride Building Materials Due to its intrinsic hazards, we support efforts to identify and usealternative building materials that do not pose as much risk as PVCto firefighters, building occupants or communities.39 Dioxin formation
Accidental fires provide very poor combustion conditions, so substantial
amounts of dioxin and other organochlorines form as products of incom-
plete combustion in a vinyl fire.40 Indeed, the combustion conditions in an
In Germany after a fire in a accidental fire, where gases do not mix thoroughly and materials cool rap- kindergarten that con- idly as they escape from the flame, are considered optimal for the rapid pro-duction of dioxins.41 As a result, all accidental fires in buildings containing tained substantial quanti- PVC are likely to generate dioxins and other persistent, bioaccumulative ties of PVC, scientists organochlorines. For example, in Germany after a fire in a kindergartenthat contained substantial quantities of PVC, scientists measured dioxin measured dioxin levels in levels in indoor soot at concentrations of 45,000 ppt (TEQ)—almost 300 indoor soot at concentra- times greater than the German government's health standard. This situationrequired the building's interior to be completely stripped of PVC—all tions of 45,000 ppt (TEQ) floors, ceilings, wall coverings, furnishings, and so on—sandblasted, and —almost 300 times greater remediated by hazardous waste experts before children were allowed toenter again.42 Dioxins have also been identified in the residues from burn- than the German govern- ing automobiles, railway coaches, and subway cars.43 ment's health standard.
Even a small amount of dioxin from each of the 621,000 structural firesand 421,000 vehicle fires in the United States each year could substan-tially contribute to dioxin contamination of the environment.44 TheGerman EPA and the German Environment Ministers have called for theuse of substitutes for PVC in all areas susceptible to fire, but PVC use inconstruction continues to grow on a global basis.45 As a result, a stockpileof PVC, waiting to burn, is accumulating in immense quantities.
Worldwide, more than 400 million tons of PVC are "in stock"—that is,in use in various applications, mostly construction-related, and suscepti-ble to fire at some point.46 The Vinyl Institute has argued that PVC firesare probably a relatively small contributor to the total dioxin burden,based on a study that quantified dioxin levels in soot residues within alimited radius of a fire at a plastics facility.47 But more than 90 percent ofthe dioxins produced in a structural fire are in the gaseous phase andescape into the atmosphere,48 and an additional amount is transported Use of PVC Products beyond the local area, so this study is likely to have underestimated totaldioxin emissions by at least a factor of ten. EPA has concluded that thedata are currently inadequate to make a firm quantitative estimate of thecontribution of accidental structural fires to national dioxin emissions.49 While many small fires taken together may constitute an importantsource of organochlorines, a single fire at a large commercial building,disposal site, PVC factory, or warehouse can generate large quantities ofpollutants. A home contains at most a few hundred kilograms of PVC,50but a large building may contain much more. For example, a vinyl-linedroof on an average-sized school contains more than 10 tons of PVC,51and a plastics warehouse or landfill may have hundreds of tons on-site.
After a fire at a plastics warehouse in Binghamton, New York, dioxin lev-els in soil on the site were found to be more than 100 times greater thanother samples from the same community.52 Elevated dioxin levels havealso been reported in a university building after an interior fire in a lec-ture hall that contained PVC components.53 According to the EuropeanCommission, fires are estimated to account for 6.6 percent of all dioxinemissions from identified sources (table 4).
Lead and phthalate releases
PVC fires not only create dioxins and other organochlorines, they also
release additives held in the plastic. The world stock of PVC in use con-
tains a staggering 3.2 million tons of lead and 83 million tons of
phthalates.54 Since lead cannot be destroyed by combustion, accidental
fires represent an important potential source of lead exposure—a hazard
that looms larger as more and more PVC accumulates worldwide in
building applications.
Notes1. SEPA 1994.
2. MAFF 1995.
3. Wagenaar et al. 1996; Carroll et al. 1996. 4. DTI 1995.
5. These figures are for Western Europe (European Commission 2000); in the U.S., where unplasticized vinylsiding is more widely used, the relevant figure may be slightly lower.
6. My calculations are extrapolated from the figures for Sweden, where the lead input into PVC equals 0.653percent of total PVC production, and the phthalate input equals 22.6 percent (TNO Centre for Technologyand Policy Studies 1996), assuming 24 million tons of PVC production worldwide.
7. TNO Centre for Technology and Policy Studies 1996.
8. DTI 1995.
9. Pearson and Trissel 1993; Goldspiel 1994.
Environmental Impacts of Polyvinyl Chloride Building Materials 10. Plonait et al. 1993.
11. Dine et al. 2000; National Toxicology Program Center for the Evaluation of Risks to HumanReproduction 2000a.
12. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a and2000c.
13. American Chemistry Council 2000.
14. Rudell 2000.
15. Rudell 2000.
16. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
17. Rudell et al. forthcoming.
18. Oie et al. 1997.
19. Oie et al. 1997.
20. Jaakola et al. 1999.
21. Jaakola et al. 2000.
22. Wieslander et al. 1999. 23. Hsieh 2000.
24. Lstiburek and Carmody 1994; Downs 2001.
25. Vinyl Institute 2000.
26. Vinyl Institute 2000.
27. Lstiburek and Carmody 1994. 28. Chicago Tribune 1996.
29. DTI 1995.
30. European Commission 2000.
31. European Commission 2000. 32. ENDS 2000. 33. European Commission 2000.
34. European Commission 2000; Ema et al 1996; Merkord et al 2000; De Santiago and Aguilar-Santelises1989.
35. Kemi 2000.
36. Markowitz et al. 1989; Markowitz 1989; Wallace 1990.
37. U.S. Navy 1986.
38. Cameron 1996.
39. Duffy 1998.
40. Wirts et al. 1998; Christman 1989; Theisen et al. 1989.
41. TNO Centre for Technology and Policy Studies 1996.
42. Fiedler et al. 1993.
43. Versar, Inc. 1996. 44. Versar, Inc. 1996.
45. UBA 1992; German Environment Ministers 1992.
46. I have extrapolated from figures for Sweden (TNO Centre for Technology and Policy Studies 1996),which indicate that the stock of PVC in use (2 million tons) equals 22.47 years of current PVC production. Ihave assumed a similar stock-to-production ratio worldwide, and annual PVC production of 19.1 million tonsper year (DTI 1995). Use of more recent figures for global PVC production would increase this estimate sub-stantially (Kielhorn et al. 2000).
47. Carroll 1995.
48. Versar 1996; EPA 1998.
49. EPA 1998.
50. Carroll 1995.
51. Assuming a roof size of 80,000 square feet and a mass of 0.31 pounds of vinyl roofing membrane persquare foot (Cummings 2001).
52. Schecter and Kessler 1996. 53. Deutsch and Goldfarb 1988.
54. I have extrapolated from figures for Sweden (TNO Centre for Technology and Policy Studies 1996),which indicate that the stock of PVC in use (2 million tons) equals 22.47 years of current PVC production,which contains 15,000 tons of lead 288 thousand tons of phthalates. I have assumed a similar stock-to-pro-duction ratio worldwide, and annual PVC production of 19.1 million tons per year (DTI 1995). Use of morerecent figures for global PVC production rates (Kielhorn et al. 2000) would increase this estimate by about 50percent.
Use of PVC Products Disposal of PVC Products
Disposal of PVC Products The final stage of PVC's lifecycle creates the most severe environmentalhazards. About 30 to 50 percent of the vinyl produced annually—some 8to 12 million tons per year worldwide—ends up in the trash stream.1EPA has estimated that at least 1.5 million tons of PVC are disposed ofannually in the United States.2 Although some building materials have arelatively long lifetime, significant quantities of vinyl are disposed of ascutaways in preconsumer waste and, ultimately, in demolition or renova-tion wastes when a product's useful lifetime ends. Construction productsare often thought of as a long-life sector of PVC use, but vinyl productsin commercial interiors—often renovated well before their componentsare physically spent—have relatively short lifetimes.
THE FAILURE OF RECYCLING One thing is true everywhere: very little postconsumer PVC is recycled. Asubstantial portion of preconsumer PVC—scraps and cuttings from man-ufacturing stages—is recycled, but the quantities of preconsumer wasterepresent a small amount of the PVC waste stream. Recycling postcon-sumer PVC is extremely difficult because vinyl products are mixtures ofPVC and additives, and each specific formulation is uniquely suited to itsapplication. In virtually all post-consumer vinyl recycling, many formula-tions are mixed together, destroying the special properties of each. As aresult, recycled post-consumer PVC is always of lower quality than theoriginal material, so it can be used only in products without strict mate-rial requirements, such as fence posts and speed bumps.3 Since recycled PVC is almost never used to make a new version of theoriginal product, down-cycling is a better term for the process than recy-cling.4 An example of true recycling is the reprocessing of paper: the oldfibers are used to make new paper products, and a new tree does not need Environmental Impacts of Polyvinyl Chloride Building Materials to be cut down. In contrast, a new vinyl wall covering or floor tile mustbe made of new plastic. Down-cycling does not reduce the amount ofPVC produced each year or the total quantity of PVC building up on theplanet. The illusion of recycling actually increases the global PVC burdenby finding new uses for old PVC while creating a positive image for aproduct that can be neither safely disposed of nor truly recycled. As theEuropean Commission put it, while true recycling has obvious environ-mental benefits, "the environmental advantages of the down-cycling of The American Association mixed plastics for the production of products which substitute concrete,wood, or other non-plastic applications are less certain."5 of Postconsumer Plastics Recyclers announced in In the European Union countries, less than 3 percent of postconsumer PVCwaste is recycled—the majority of which is actually down-cycling of cable 1998 that its attempts to and packaging wastes. According to a 2000 report by the European recycle PVC had failed Commission, "high-quality mechanical recycling for post-consumer [vinyl]wastes is still in a preliminary stage and exists only for a few product groups and that it would and with low quantities."6 Sweden, a nation with an ambitious and effecting henceforth view vinyl recycling program, had a total PVC recycling rate of just 2 percent in 1999,nearly all of it preconsumer waste.7 The European Commission projects that products as unrecyclable only 9 percent of all PVC waste is likely to be recycled by 2020, with a max- contaminants in the imum potential of no more than 18 percent.8 Such low recycling rates, evenwith time to develop an ambitious program, indicate that PVC is not and municipal waste stream.
cannot be a green building material. The American Association of Postconsumer Plastics Recyclers announcedin 1998 that its attempts to recycle PVC had failed and that it wouldhenceforth view vinyl products as unrecyclable contaminants in themunicipal waste stream.9 There are also concerns about the potential environmental hazards of PVCrecycling. Mechanical recycling of PVC can release additives, includingphthalates and stabilizers, which may then be dispersed into the recycledproducts, into the environment, or, if they are captured, disposed of on landor in incinerators. The European Commission has recognized significant con-cerns about the presence of lead and cadmium stabilizers in PVC productsthat are recycled and their subsequent dispersal into a greater range of con-sumer products.10 Disposal of PVC Products LAND DISPOSAL LEACHATES AND FIRES A significant portion of discarded PVC ends up in landfills, and almostall the remainder is burned—the exact proportions vary from one coun-try to another. In landfills, there are three concerns about PVC disposal.
First, the persistence of PVC, which typically lasts for centuries in a land-fill, presents a significant burden in terms of the demand for landfillspace. Second, the release of additives in the plastic can contaminate EPA estimates that landfill groundwater. Because phthalates and metals are not chemically bonded to fires may emit on the the polymer, they can leach out of disposed products into landfillleachate, eventually contaminating groundwater.11 order of 1,000 grams of dioxins and furans (TEQ) Third, fires can occur during or after the disposal process, releasing haz-ardous substances into the air, including dioxins and metals. In into the air each year in Hamilton, Ontario, for example, after some 200 tons of PVC burned at a the United States, plastics recycling facility, samples of ash, soot, and tree leaves from the firearea were found to contain elevated quantities of dioxins.12 Of particular potentially making them concern are landfill fires, which occur with some regularity at landfills the largest U.S. dioxin and waste storage sites where large quantities of PVC are present. Data ondioxin releases from landfill fires are limited, but EPA estimates that land- sources to the air.
fill fires may emit on the order of 1,000 grams of dioxins and furans(TEQ) into the air each year in the United States, potentially makingthem the largest U.S. dioxin sources to the air.13 Role of PVC in incineration
Dioxin releases: In every inventory of dioxin sources in the world, trash
incinerators and other combustion sources account for the majority of
identified dioxin releases into the environment (table 4), and PVC is the
predominant source of dioxin-generating chlorine in these facilities. In
municipal waste incinerators, PVC contributes at least 80 percent of the
organically-bound chlorine and 50 to 67 percent of the total chlorine
(organochlorines plus inorganic chloride) in the waste stream—although
it makes up only about 0.5 percent of the trash stream by weight.14 In the
United States, an estimated 200,000 to 300,000 tons of PVC is inciner-
Environmental Impacts of Polyvinyl Chloride Building Materials Table 4 Inventoried dioxin sources in North America, Europe, and the world
Percent of all releases from inventoried sources

Source type
United States 1
European Union2 United States 3
Great Lakes4
* Municipal waste incinerators Ferrous metals production * Copper smelting * Medical waste incinerators Forest, brush, straw fires * Accidental fires Wood and coal combustion Hazardous waste incineration Dioxin-contaminated chemicals * Uncontrolled trash incineration Cement kilns (no hazardous waste) * Dioxin sources in which PVC is a major chlorine donor. NA = quantitative estimate not available. 1. Percent of all identified releases to air of PCDD/F (TEQ) based on median estimates for year 1995. Hazardous waste incineration estimate includesreleases from cement kilns that burn hazardous wastes, as well as boilers and industrial furnaces. 2. Percent of all identified releases to air in the European Union. 3. Percent of identified emissions of total PCDD/F to the air in the United States as of 1989. Municipal waste incinerators include apartment incinera-tors. Accidental fires include structural fires, PCB fires, and PCP fires. 4. Percent of identified emissions of PCDD/F (TEQ) to the air that reach the Great Lakes. 5. Percent of identified PCDD/F releases (TEQ) to the air. Estimate for hazardous waste incineration includes cement kilns burning hazardous waste; esti-mate for cement kilns does not. Estimate for forest, brush, straw fires includes all biomass combustion, including wood. Source: U.S. EPA 1998; Hanberg et al. 1999; Thomas and Spiro 1995; Cohen et al. 1995; Brzuzy and Hites 1996a.
Note: There are numerous additional dioxin sources for which none of the inventories made a quantitative estimate, due to inadequate data. Sources arelisted from largest to smallest, by the percent contribution in EPA's inventory, except for sources with NA in that column, which were ordered accordingto their contribution in the EU inventory. Sources with less than 1 percent contribution in all inventories are not shown. ated in trash burners every year.15 Large quantities of PVC also go tomedical waste incinerators, where PVC accounts for 5 to 18 percent ofthe waste stream—more than 90 percent of the organic chlorine, andmore than 80 percent of the total chlorine content of medical waste.16 Astable 4 shows, combustion sources in which PVC is a major source ofchlorine—and therefore of dioxin formation—make up the bulk of theworld's major dioxin sources identified to date. In fact, sources in whichPVC is the dominant chlorine donor account for 77 percent of all inven-toried dioxin emissions in the U.S. and 50 percent in Europe. Unidentified PICs: Without a doubt, burning vinyl is a source of dioxin.
Numerous laboratory combustion tests involving pure PVC (or purePVC in the presence of metal catalysts) produce considerable amounts of Disposal of PVC Products dioxin.17 No one has attempted to identify the full range of by-productsthat form when PVC burns, but 45 organochlorines—including persist-ent and toxic chlorinated benzenes, naphthalenes, PCBs, PCDFs, phe-nols, and styrenes—have been found in the combustion products whenthe closely related plastic polyvinylidene chloride (PVDC; commonlyknown as Saran Wrap) is incinerated.18 In municipal waste As in many other processes, the identified compounds are just the begin-ning. In municipal incinerators, the most thorough analysis to date iden- incinerators, PVC tified several hundred PICs, including 38 organochlorines—chlorinated contributes at least 80 benzenes, ethylenes, methanes, PCBs, and others—but 58 percent of thetotal mass of PICs remained unidentified.19 As noted above, a consider- percent of the organically- able portion of these mystery compounds are likely to be hazardous, and bound chlorine in the at least some are known to cause dioxin-like toxicity.
waste stream.
Lead and other additives : Incinerators also release additives contained inPVC products into the environment. An estimated 45,000 tons of leadstabilizers in PVC enter the world's municipal trash each year, based onSwedish figures.20 Because lead cannot be destroyed by incineration, alllead that enters an incinerator ultimately enters the environment via stackemissions, ash, scrubber effluent, or wastewater sludges. Incinerators arenow the largest source of lead emissions into the environment; PVC isresponsible for about 20 percent of the lead in the waste stream, accord-ing to Swedish figures.21 In the European Union, vinyl contributes from1 to 28 percent of the lead and 10 percent of the cadmium enteringmunicipal waste incinerators.22 Backyard burning : Not all vinyl burning takes place in high-tech incinera-tors. In developing countries and rural areas of industrial nations, openburning of waste is a common method to rid trash and debris. A recentstudy by U.S. EPA and the New York Department of EnvironmentalConservation indicates that backyard burning of trash in barrels canresult in massive emissions of toxic chemicals, including chlorinated ben-zenes, methanes, phenols, as well as dioxins and furans. Emissions ofdioxins and furans per pound of waste burned were 12,000 to 75,000times higher than emissions from an optimally operated modern trashincinerator.23 Further, when more PVC was burned, average releases of Environmental Impacts of Polyvinyl Chloride Building Materials dioxin and all other chlorinated PICs rose substantially; the experimentdid not include enough replications for the statistical significance of theincrease to be evaluated. Although it is unlikely that construction or dem-olition waste from commercial buildings will be disposed of by uncon-trolled burning, materials used in residential construction in rural areasand developing countries may be. The rapidly expanding use of vinyl indeveloping nations, where expensive means of waste management are notavailable, has the potential to cause a major increase in worldwide emis-sions of dioxins.
Smelter releases : Some spent metal products that contain vinyl—includingmaterials used in buildings such as cables and electronics equipment—arerecycled or reprocessed in smelters, and these facilities are also majordioxin sources. Secondary copper smelters, for example, recover copperfrom PVC-coated wire and cable and PVC-containing telephone cases.
High dioxin emissions have been measured at these facilities, which areconsidered major dioxin sources in most inventories.24 Most importantly,removing some of the vinyl sheathing before cables are fed to the smeltersreduces dioxin emissions considerably.25 Secondary steel smelters havealso been found to emit large quantities of dioxin, in part because theyrecover metal from scrap automobiles that contain PVC.26 Secondary leadsmelters release dioxin and other organochlorines, too, due to the feed oflead automobile batteries with internal PVC parts. In the United States,however, PVC has been recently phased out of this application, so EPAno longer considers lead smelters an important dioxin source.27 Dioxin formation and PVC—
evidence from combustion experiments
Following an aggressive effort by the chemical and plastics industry, an
apparent controversy has developed over whether burning PVC in incin-
erators results in increased dioxin emissions. The data, however, strongly
support the view that dioxin forms when PVC and other organochlorines
burn, and further that burning more PVC (or other organochlorines)
results in the formation of more dioxin. This is not to say that the
organochlorine content of the waste is the only factor involved in dioxin
formation; facility design, operating conditions, and the presence of cata-
lysts also play major roles. Chlorine is a requirement for dioxin synthesis,
Disposal of PVC Products and preventing the introduction of organochlorines into incinerators isthe best means to prevent dioxin formation. Conversely, because burningPVC is known to produce dioxin, burning more PVC will produce moredioxin, and burning less PVC will reduce dioxin generation.
Dioxin cannot be formed without a chlorine source, so emissions fromincinerators must be the result of burning organochlorines, burning salt,or some combination of the two. To suggest that organochlorines are notimportant dioxin precursors requires burning organochlorines to producelittle or no dioxin and the combustion of inorganic chloride salts to be Chlorine is a requirement the predominant source of dioxin. Several lines of evidence indicate that for dioxin synthesis, and organochlorines—particularly PVC—are the most important and mostpreventable cause of dioxin emissions from combustors.
The first line of evidence comes from numerous well-conducted studiesin the laboratory. Results from the laboratory are particularly convincing organochlorines into because, unlike trial burns at full-scale incinerators, they allow combus- incinerators is the best tion conditions, emissions, and input materials to be carefully controlledand accurately monitored. Studies of this type indicate that burning PVC means to prevent dioxin is clearly an important dioxin source.
The German EPA has found that burning PVC or otherorganochlorines produces dioxin—with concentrations in ashresidues ranging from 3.2 to 662 ppt (TEQ). But combustion ofseveral types of organochlorine-free but chloride-containing cotton,paper, wood, or wool does not produce dioxin above the detectionlimit of 0.1 ppt28 (table 5).
Two separate studies by Danish researchers have found that burningpure PVC produces dioxin. Under some conditions, the quantitiesformed are quite large.29 A 2000 report by Japanese researchers found that adding 4 percent PVCto a mixture of chlorine-free materials in a lab-scale incinerator had an"intense effect in dioxin emissions"—a more than 10-fold increase.
Adding an equal quantity of salt caused at most a two-fold increase.30 Environmental Impacts of Polyvinyl Chloride Building Materials Table 5 Dioxins in ash from burning organochlorines and chloride
containing materials

Total PCDD/F (ppt)
Materials not known to contain organochlorines PVC plastic (pure) PVC flooring material PVC window frame material PVC cables (copper) PVC cables (no copper) PVC gloves, hose, pipes, tape Polychlorobutadiene (neoprene) plastic Materials containing other organochlorines Bleached coffee filters Linuron pesticide Source: Theisen 1991.
Disposal of PVC Products When newspaper or chlorine-free plastics are burned in a labora-tory-scale incinerator, dioxin generation is extremely low. WhenPVC is added to the mix, dioxin levels in fly ash increase by a fac-tor of 200 to 1,200—compared to a 13- to 45-fold increase whensalt is added.31 Numerous well-conducted When PVC is added to a mixture of chloride-containing coal andbark, dioxin concentrations in the residues increase by a factor of 10 studies indicate that to 100; the more PVC added, the higher the dioxin concentration.32 Adding PVC during combustion of natural chloride-containing wood particularly PVC—are the products increases dioxin levels in the ash by 15 to 2,400 times.
most important and most When large quantities of chemical hardeners containing inorganicchloride are added, dioxin levels rise somewhat, but are still 3 to 350 preventable cause of times lower than when PVC is included in the mix.33 A Swiss study dioxin emissions from confirmed these results, finding that dioxin levels in fly ash from theburning of waste wood that has been glued, painted, or otherwise processed are up to 2,000 times higher than in ash from the burningof natural wood.34 Combustion of a mixture of coal and salt produces trace quantities ofdioxins and furans in the off-gas, but when elemental chlorine isadded to the mix, total dioxin formation increases 130-fold.35 Burning chloride-containing vegetable matter does not producedetectable PCDD/Fs, but including PVC or chlorine gas along withthe plant material does.36 The same pattern exists for other organochlorines. Finnish researchershave found that burning perchloroethylene in a laboratory combus-tion reactor produces more dioxins, chlorobenzenes, and chlorophe-nols than burning sodium chloride.37 An American study found thatformation of dioxin precursors rises as the proportion of organochlo-rines in the waste increases,38 while three others have found thatadding salt to a combustion reaction has no detectable effect ondioxin formation.39 Environmental Impacts of Polyvinyl Chloride Building Materials In full-scale or pilot-scale incinerators (units smaller than commercialburners but similar in design), the evidence also supports a relationshipbetween burning organochlorines and creating dioxin, but there are alsosome contradictory studies, possibly due to the difficulty of analyzingcomplex input and output streams and adjusting for fluctuatingoperating conditions: The Danish EPA has found that doubling the PVC content of an incin-erator's waste input increases dioxin emissions by 32 percent, while dou-bling the chloride content increases dioxin emissions by a muchsmaller margin.40 A team of Japanese researchers has reported on two separate sets ofexperiments that showed burning a mixture of PVC and polyethyl-ene—in which PVC is the only chlorine source—produces substan-tial quantities of dioxin.41 Two groups of researchers from Finland have found that dioxin levelsin stack gas or fly ash are very low when a mixture of coal and chlo-rine-free plastics is burned, but rise substantially when PVC is addedto the mix.42 A 1996 study for the Dutch Environment Ministry reported that whenboth PVC and chloride-containing compostable matter are removedfrom municipal waste, emissions of chlorophenols—indicator com-pounds for dioxin formation—were extremely low. When 20 percent ofthe original amount of compostables was added back into the mix, emis-sions did not increase, but when 30 percent of the original amount ofPVC was added along with the compostables, chlorophenol emissionsapproximately doubled.43 A series of studies at a pilot-scale incinerator at the University ofFlorida has documented a clear relationship between the feed of PVCand the emission of chlorophenols. The authors summed up theirfindings: "These experimental, phenomenological and theoreticalstudies of toxic emissions from incineration all support the physicallyintuitive hypothesis that reduction of chlorinated plastics in the inputwaste stream results in reduction of aromatic chlorinated organic Disposal of PVC Products emissions. We are convinced that, when all other factors are heldconstant, there is a direct correlation between input PVC and outputPCDD/PCDF and that it is purposeful to reduce chlorinated plasticsinputs to incinerators."44 German scientists have found that removing PVC sheathings fromcopper cables before they are recycled in copper smelters causes dioxinemissions to drop precipitously.45 Four studies have found that the addition of PVC-containing"refuse-derived fuel" to incinerators burning salt-containing organicmatter like wood chips or peat results in significant increases indioxin formation.46 According to a 2000 study by Japanese researchers, adding PVC to amixture of chlorine-free matter in a pilot-scale incinerator increasesdioxin emissions substantially; when more PVC is added, moredioxin is formed.47 In some of these studies, a relationship was seen in the air emissions butnot in the fly ash, or vice versa, reinforcing the difficulty of establishingstatistically significant relationships in the complex context of burningreal wastes in large incinerators.
Two widely cited studies, one by the New York Department ofEnvironmental Conservation48 and the other by the European plasticsindustry,49 have come to the opposite conclusion, finding no relationshipof dioxin emissions at individual trash incinerators with PVC content ofthe waste burned. Neither of these investigations controlled or adjustedfor other factors that affect dioxin formation, including facility type,operating conditions, or other characteristics of the waste feed. This over-sight radically weakens any study's ability to detect a potential relation-ship between PVC and dioxin formation. Indeed, an EPA reanalysis ofthe data from the New York study found that when combustion condi-tions were adjusted for, emissions of dioxins and furans increased as PVCcontent of the waste rose.50 Environmental Impacts of Polyvinyl Chloride Building Materials A recent Swedish investigation found that dioxin formation is directlyrelated to chlorine content, but only when chlorine levels in the fuelexceed 0.5 percent, as they do in most modern waste streams. Changes inchlorine content below this level had no statistically significant effect ondioxin emissions.51 These results could indicate that there is a thresholdbelow which chlorine has no impact on dioxin levels, but it is equallypossible that the failure to find a correlation at low chlorine levels is anartifact of the limits of chemical and statistical analysis: as levels of bothchlorine and dioxin decrease, measurement error and statistical fluctua-tions become more and more important, swamping a fading signal under From a policy perspective, a growing chorus of noise. it does not really matter Salt combustion and dioxin formation
how much dioxin salt Some studies indicate that burning large quantities of salt can produce combustion can produce.
dioxin. For instance, paper mills often burn logs that have been soaked insaltwater, and these incinerators have much higher concentrations of If we want to prevent dioxin in their emissions than burning unsoaked wood.52 The Swedish dioxin formation in report discussed above found that it did not matter whether the chlorinecame in organic or inorganic form—both gave rise to dioxin in approxi- incinerators, we need to mately equal amounts.53 One of the Japanese studies also found that burning large quantities of salt in a lab-scale incinerator could result insubstantial dioxin emissions.54 Another study found that burning PVC caused a much greater increase in dioxin formation than salt did,although the two substances caused similar increases in dioxin whenmunicipal incinerator fly ash—which contains a wide range oforganochlorines and other compounds—was included in the mix.55 These results conflict with the findings of the other studies discussedabove, so the importance of salt in dioxin formation in incineratorsremains an open question. From a policy perspective, however, it doesnot really matter how much dioxin salt combustion can produce. Ifburning chloride results in negligible dioxin emissions, then dioxin out-put depends almost entirely on the organochlorine content of the waste.
Lowering the input of organochlorines is necessary to reduce the forma-tion of dioxin. If, on the other hand, burning salt can produce dioxin inamounts comparable to the burning of PVC and other organochlorines,then dioxin generation depends on the waste's total level of chlorine Disposal of PVC Products (organic plus inorganic). Lowering the quantity of organochlorines in thewaste will then reduce the total chlorine level and reduce dioxin forma-tion. Either way, if we want to prevent dioxin formation in incinerators,we need to stop burning organochlorines.
The VI's ASME study is Whatever the quantities, salts are ubiquitous in organic matter and can- deeply flawed for several not be removed easily from production, commerce, or the waste stream.
reasons—and does not In contrast, PVC use is highly preventable. Alternatives for most uses arecurrently available, ranging from traditional materials to chlorine-free provide an adequate basis polymers.56 Any program to eliminate dioxin generation at the source to dismiss the many should include provisions to reduce the use and combustion of PVC.
studies that do establish a Vinyl Institute's flawed ASME dioxin study
link between dioxin To rebut evidence linking incineration of vinyl to dioxin formation, theVinyl Institute (VI) frequently cites a single study, purportedly by the generation and the American Society of Mechanical Engineers (ASME), a professional soci- combustion of PVC and ety representing 125,000 mechanical engineers worldwide, "[which]found little or no correlation between chlorine input and dioxin emis- sions from incinerators."57 This study is deeply flawed for several rea-sons—and it does not provide an adequate basis to dismiss the manystudies that do establish a link between dioxin generation and the com-bustion of PVC and other organochlorines.
ASME study is biasedSeveral vinyl industry documents shed light on the purpose and origins ofthe ASME report. Just before U.S. EPA released its draft DioxinReassessment in 1994, the Vinyl Institute commissioned the public rela-tions firm Nichols-Desenhall Communications to prepare a CrisisManagement Plan for the Dioxin Reassessment. According to the plan,"EPA will likely conclude that the incineration of chlorinated compoundsis the single largest known contributor of dioxin…We believe that PVCwill be specifically mentioned and potentially slated for further regula-tion." In order to "prevent punitive regulation of PVC by EPA, Congress,or the state legislatures," the plan advised the Vinyl Institute how to pres-ent itself in the media and "strongly urge[d] VI to aggressively defend theindustry's credibility through the use of third party sources todebunk…EPA's misleading claims."58 Environmental Impacts of Polyvinyl Chloride Building Materials The industry took the advice of its public relations firm. In 1994, the VinylInstitute's Incineration Task Force hired the consulting firm Rigo and Rigo,Inc. to prepare an "independent" analysis, which found that the amount ofdioxin released by incinerators has no relation to the amount of chlorinatedorganic materials fed into them.59 The Vinyl Institute arranged to have thereport published as a product of the prestigious ASME, an independent pro-fessional organization. According to Vinyl Institute documents, one of theleaders of the Vinyl Institute's Incineration Task Force, Dick Magee, was alsoan active ASME member; Magee brokered an arrangement in which theVinyl Institute would hire and fund Rigo to write a report that would bereleased under the ASME banner. According to an internal Vinyl Institutememo from 1994, the purpose of ASME's involvement was to create theillusion of "third-party" authority, and that the Rigo report was conceived,carried out, and rewarded in a spirit of public relations, not unbiased analy-sis. The memo reads: The Vinyl Institute has created an Incineration Task Force in antici-pation of adverse EPA actions regarding dioxins and furans…DickMagee brought forward a proposal from the American Society ofMechanical Engineers to hire Rigo & Rigo Associates, Inc., ofCleveland, OH. The purpose of ASME as the contractor is to provideunassailable objectivity to the study… The Incineration Task Group interviewed Dr. H. Gregory (Greg)Rigo, principal of Rigo & Rigo Associates, Inc. by phone and foundhim to be extremely knowledgeable about incineration and to haveseveral proprietary databases VI had not discovered. He is also userfriendly, i.e., willing to set his priorities to our needs, and appears tobe sympathetic to Plastics, Vinyl, PVC, and Cl2… The ASME proposal calls for $130,000 for the Rigo & Rigo/ASMEstudy. Since there are many unanswered questions regarding dioxins andsince VI may want to use Greg Rigo as an expert witness or advocate totalk about the report, I am proposing an additional $20,000 as a contin-gency fund, for a total of $150,000 to be fully funded by VI.60 Disposal of PVC Products Methodological flawsThe methodology of the Rigo report is no less flawed than its origins,undermining the reliability of its claim that burning organochlorines isnot related to dioxin formation. The study was not experimental, so itcould not directly refute the existence of a chlorine-dioxin link. Instead ofgenerating new data, the authors compiled existing trial burn measure-ments from a large number of incinerators, statistically analyzed the rela-tionship between indicators of chlorine feed and dioxin releases, and The study's data and concluded that there was no statistically significant relationship between methods on dioxin output the two. A statistical analysis of this type is particularly sensitive to designproblems: if the putative cause and effect are not measured accurately, or and chlorine input were if confounding factors are not taken into account, then a meaningful rela- flawed in several ways, tionship is likely to go undetected. In fact, the study's data and methodson dioxin output and chlorine input were flawed in several ways, suggest- suggesting that it's failure ing that it's failure to detect a causal link is more likely an artifact of bad to detect a causal link is study design than a meaningful finding that no relationship betweenchlorine and dioxin actually exists: more likely an artifact of 1. The Rigo study failed to take account of differences among facilities.
bad study design than a Chlorine input is not the only factor that determines the magnitude meaningful finding that of dioxin emissions from incinerators; combustion conditions, thetypes and quantities of substances in the waste, and other variables no relationship between also affect the amount of dioxin that will be released. Because of this chlorine and dioxin complexity and constant fluctuations of many factors, statistical rela-tionships between stack emissions and indicators of waste input or actually exists.
combustion conditions can seldom be established, even at individualincinerators.61 Massively compounding this problem, Rigo used datafrom a large number of incinerators operating under widely variableconditions, but did not control or adjust for differences in facilitytype, operating parameters, waste type, or other factors. A statisticalsummary of data from many different facilities, with no attempt tocontrol or adjust for confounding factors, cannot be expected todetect a signal within such extensive noise. Even a strong relationshipbetween organochlorine input and dioxin output is likely to go unde-tected in a study designed in this manner. 2. The Rigo study also used data from unreliable sources. The emissions data in Rigo's analysis came almost exclusively from trial burns Environmental Impacts of Polyvinyl Chloride Building Materials designed for permitting purposes, without the proper kinds of con-trols and measurements necessary to evaluate the relationship betweenchlorine input and output. Moreover, trial burn data are notoriouslyproblematic. First, with their highly simplified designs, these trials donot accurately represent the way incinerators operate in the realworld, when waste composition and operating conditions constantlyfluctuate. Further, they do not measure the much larger quantity ofchemicals that are released after the feed of waste to the incineratorhas stopped.62 In fact, many trial burns have conducted their evalua-tions of low- or no-chlorine wastes after chlorinated wastes have beenburned, so the later stack samples become contaminated by continu-ing emissions from earlier runs. The use of results from trial burns ofthis sort thoroughly scrambles any relationship that might otherwisehave been recognizable between chlorine input and dioxin input. 3. Rigo's study relied on the wrong kinds of measurements. To investi- gate a link between the amounts of organochlorines burned and theamount of dioxin produced by incinerators, Rigo should have exam-ined the statistical relationship between the mass of organochlorinesfed to an incinerator and the mass of dioxins released. Instead, thestudy tracked "surrogate" measures for both of these parameters,measuring the concentration of hydrogen chloride (HCl; the primaryby-product of organochlorine combustion) in the stack gas as a roughindicator for the mass of organochlorines in the feed; as a surrogatefor the mass of dioxin released, it examined the concentrations ofdioxin in the stack gas.63 The problem is that concentrations do notaccurately represent quantities, for several reasons: If the total flow of stack gas increases (as it generally will if morewaste, and thus more chlorine, is fed to the incinerator), the concen-trations of dioxin in the gas may decrease, even if a larger amount ofdioxin is being emitted.
Stack gas measurements omit pollutants directed into fly ash, bottomash, and scrubber water, so changes in the efficiency of pollution con-trol devices can reduce the concentration of dioxin in stack emissionswhile total dioxin formation increases. Control devices can alsoreduce the concentration of HCl while total organochlorine input Disposal of PVC Products rises. (Because pollution control devices have different capture effi-ciencies for dioxin and hydrochloric acid, the concentrations of thesematerials in the stack gas after it passes through this equipment willnot reflect the ratios of the amounts that were actually produced bythe incinerator). Hydrogen chloride is formed not only by the combustion oforganochlorines but also by the burning of chloride salts. It is there-fore not a reliable indicator of the amount of organochlorines fed toan incinerator. The variables that Rigo analyzed are thus grossly inappropriate substitutesfor the quantities that are truly of interest; Rigo's failure to find a relation-ship between the surrogates he used says nothing about whether a linkactually exists between organochlorine input and dioxin generation.
All the flaws discussed above cripple the ASME study's ability to establisha link between chlorine and dioxin. A finding of "no relationship" is onlyas good as a study's power to detect a relationship, and in this case thatpower can only be described as pathetically weak. On the basis of Rigo'sanalysis, no reliable inferences can be drawn about whether a relationshipexists between the amount of organochlorines burned and the amount ofdioxin formed in an incinerator. With more than twenty well-designedstudies coming to the opposite conclusion—that burning PVC and otherorganochlorines produces dioxins, and burning less reduces dioxins—Rigo's findings are far from persuasive. The weight of evidence from labo-ratory, pilot, and full-scale tests clearly establishes that vinyl is animportant source of dioxin in incinerators, fires, and combustion-basedrecycling facilities, which together are responsible for the majority ofidentified dioxin releases in the world.
PVC and dioxin relationship—historical evidence
The theory that burning organochlorines like PVC is an insignificant
dioxin source and that salt is responsible for incinerator emissions of
dioxin implies several specific predictions, none of which turn out to be
true. First, if salt is a more important dioxin source than burning
organochlorines, forest fires should result in large dioxin releases because
Environmental Impacts of Polyvinyl Chloride Building Materials plant matter is rich in salt. According to research by chemists at IndianaUniversity, however, dioxin levels in the sediment of a U.S. lake, thewatershed of which suffered a major forest fire in 1937, show no changewhatsoever around or after the time of the fire.64 More recently, scientistsin Spain analyzed samples of salt-containing vegetation and soil thatburned in four different 1998 forest fires; the burned materials showedno increase in dioxin levels compared to background levels, leading theresearchers to conclude, "Natural fires seem not to be an importantsource of dioxin-like compounds."65 The second prediction implied by industry's salt theory is that historical The theory that burning levels of dioxin should track trends in the burning of salt, not the produc- organochlorines like PVC tion and incineration of organochlorines—but they do precisely thereverse. Several studies have analyzed the dioxin and furan content of is an insignificant dioxin mummified and frozen remains of people who lived several hundred to source and that salt is several thousand years ago, including individuals from cultures thatcooked over indoor fires and were exposed to considerable amounts of responsible for incinerator combustion emissions. These studies have found that dioxin levels (meas- emissions of dioxin ured as TCDD-equivalents) in ancient tissues were no more than 1 to 2percent of the amount found in modern humans, and even this amount implies several specific could represent contaminants deposited in the samples in modern times, predictions, none of which especially during handling and analysis.66 turn out to be true.
Dioxin levels in sediment cores from lakes and seas in North Americaand Europe also indicate that organochlorines and not the burning ofsalt are responsible for the bulk of dioxin emissions (figure 3). Everystudy conducted to date shows that dioxin levels were extremely lowbefore the 20th century when chlorine and organochlorine productionbegan, despite the fact that natural and industrial combustion processeswere abundant in this period. Sediments in Swedish lakes show no meas-urable dioxin before 1945,67 and those in the Great Lakes show nonebefore 1920.68 In the Baltic, dioxins and furans were present in a sedi-ment sample dated to 1882, but the levels were 20 times lower than thepeak concentrations in 1978.69 A study of two lakes in Germany's BlackForest found that sediments from the seventeenth and eighteenth cen-turies contained small quantities of dioxins and furans—77 and 34 timeslower than the maximum concentrations from this century. Expressed as Disposal of PVC Products Figure 3 Dioxin deposition in European sediments
Note: The vertical axis shows concentrations of total dioxins and furans (ppt) in sediment cores from theBaltic (circles) and two German lakes—the Wildsee (triangles) and the Herrenweiser See (squares), expressedas a percentage of the highest levels measured in each location. In all locations, levels were extremely low priorto the advent of chlorine chemistry, and they rise rapidly thereafter. Source: Juttner et al 1997; Kjeller and Rappe 1995.
TCDD-equivalents, the ratios were even higher: 310 and 90 timesgreater in modern than in pre-chlorine sediments.70 In New York's GreenLake, small quantities of dioxins and furans are present in layers fromthe late 1800s, but at concentrations 1,500 times lower than those foundin the 1960s.71 Only with the advent of chlorine chemistry and the incineration of its prod-ucts and by-products did dioxin levels begin to rise. In all samples, dioxinconcentrations began to increase slowly in the early decades of this century,then shot up rapidly from the 1940s to the 1970s—rising 25-fold or morebetween 1935 and 1970, then declining somewhat thereafter.72 This patternis consistent with the rise of chlorine chemistry, which peaked in the 1960s Environmental Impacts of Polyvinyl Chloride Building Materials Figure 4 Dioxin deposition in European sediments
Every study conducted to date shows that dioxin levels were extremely low before the 20th century oduction and coal consumption when chlorine and production began.
Source: Juttner et al 1997; Kjeller and Rappe 1995.
or 1970s, followed by restrictions on dioxin-contaminated pesticides andchlorinated gasoline additives went into effect. Although these trends follow the production of chlorine, they do noteven approximately track the history of combustion of salt, either indus-trial or natural. One study of dioxin trends in Great Lakes sedimentsfound that dioxin levels do not follow trends in combustion of coal—practiced on a massive scale long before dioxin concentrations began torise—but they do correspond closely to the rise of the chlorine chemicalindustry (figure 4). These results suggest that industrial combustionprocesses—including coal-fired power plants, furnaces for heating, railengines, steel mills, and other industries powered by coal (which contains Disposal of PVC Products chloride salts)—have never been major sources of dioxin. The authors ofthe Great Lakes studies summarized their results so succinctly that theyare worth quoting at length: There is an abrupt increase in PCDD and PCDF concentrations around1940…Starting at this time, the production of chlorinated organic com-pounds such as chlorobenzenes and chlorophenols increased substan-tially. These compounds are used in a variety of products, including Dioxin concentrations building supplies, herbicides, and packaging. Much of these materials began to increase slowly in eventually become incorporated in solid wastes. The trend for the pro-duction of chloro-organic compounds is similar to the sedimentary the early decades of this PCDD and PCDF profiles. The agreement between these two trends is century, then shot up convincing despite the uncertainties introduced by sediment mixing andthe errors inherent in the dating and quantitation techniques…It is clear rapidly from the 1940s to that the high levels of dioxins and furans found in presently accumulat- the 1970s consistent with ing sediments are not due to the advent of fire.73 the rise of chlorine If organochlorines have nothing to do with dioxin emissions, then why were dioxin levels in the environment non-existent or minusculebefore the chemical industry began to produce them? In particular,why were dioxin levels so low during the 19th century when combus-tion of chloride-containing materials such as coal and wood was at itspeak? These data make abundantly clear that the majority of dioxin inthe environment is due to the production, use, and disposal of chlo-rine gas and organochlorines.
In conclusion, while it is likely that some dioxin can be formed by thecombustion of chloride-containing salts, the available evidence indicatesthat industrially produced materials containing organochlorines—PVC inparticular—are the dominant cause of dioxin generation in incinerators.
More importantly, these materials are the most readily preventable causeof dioxin formation. Salts are naturally ubiquitous, but we can choose tostop producing, using, and burning organochlorines. As the DanishTechnical Institute has written, "It is most likely that the reduction of thechlorine content of the waste can contribute to the reduction of thedioxin formation, even though the actual mechanism is not fully understood."74 Environmental Impacts of Polyvinyl Chloride Building Materials PVC is the major chlorine source in the majority of the combustion facilitiesthat dominate inventories of dioxin sources. The production and use of PVCalso contributes to dioxin pollution. It therefore appears that PVC is responsi-ble for more dioxin generation than any other single product. As more andmore vinyl installed in buildings over the preceding decades enters the wastestream for disposal, the potential for dioxin generation grows accordingly.
Any program to eliminate dioxin generation at the source—a public healthimperative—should include provisions to reduce the use of PVC in applica-tions susceptible to accidental fire or disposal by combustion.
Notes1. TNO Centre for Technology and Policy Studies 1996.
2. Franklin Associates 1997. 3. European Commission 2000.
4. DTI 1995.
5. European Commission 2000.
6. European Commission 2000.
7. KemI 2000.
8. European Commission 2000.
9. APR 1998.
10. European Commission 2000.
11. European Commission 2000.
12. Hamilton-Wentworth 1997; Socha et al. 1997. Socha et al. notes that dioxin levels in tree leaves downwindfrom the fire were 7 to 100 times above normal. Apparently, pollutants on the leaves were washed from the leavesinto the general environment by rain, because levels on leaves declined significantly after the first post-fire rainstorm.
13. EPA 1998.
14. Danish EPA 1993; Ecocycle Commission of the Government of Sweden 1994; DTI 1995; TNO Institute ofEnvironmental and Energy Technology 1994.
15. This assumes U.S. municipal waste incinerator capacity of 48 million tons per year (Versar 1996), 80 percentcapacity utilization, and PVC content of 0.5 to 0.8 percent.
16. According to two studies, 9.4 percent (Marrack 1988) and 15 percent (Hasselriis and Constantine 1993) ofinfectious red-bag waste in the U.S. is PVC, and as much as 18 percent of non-infectious hospital wastes are PVC(Hasselriis and Constantine 1993). In Denmark, PVC accounts for about 5 percent of all medical waste (DTI1995). See also Green 1993.
17. Christmann et al. 1989; Theisen et al. 1989; Theisen 1991.
18. Yasuhara and Morita 1988. See also Blankenship et al. 1994.
19. Jay and Stieglitz 1995.
20. I have extrapolated from the relevant figures for Sweden, where 249 tons of PVC enter the waste stream eachyear (TNO Centre for Technology and Policy Studies 1996), assuming 19.1 million tons of PVC productionworldwide, each year (DTI 1995).
21. TNO Centre for Technology and Policy Studies 1996.
22. European Commission 2000.
23. Lemieux 1997. PCDD/F emissions (total) from an avid recycler with high PVC content in their waste averaged269.6 micrograms per kilogram of waste burned; from a non-recycler with much lower quantities of PVC, andPCDD/Fs averaged 44.30 ug/kg of waste. There were only two runs for each type of trash, so conclusions about therole of PVC in dioxin emissions are tentative. EPA contrasted these high levels of dioxin emissions to those from amunicipal waste combustor, which EPA estimated at 0.0035 ug/kg of waste. This figure may be lower than manyincinerators in the real world, but the point that uncontrolled burning of waste produces relatively high quantities ofdioxin is almost certainly correct. My estimate of the number of households required to produce the same amountof PCDD/Fs assumes, as EPA's report does, an incinerator burning 182,000 kilograms of waste per day, as com-pared to an average of 4.9 kilograms per day in non-recycling households.
24. Christmann 1989; EPA 1994a; Versar, Inc. 1996.
25. Christmann et al. 1989.
26. Lahl 1994; Schaum et al. 1993; EPA 1994b; Aittola et al. 1993.
27. Versar, Inc. 1996.
28. Theisen 1991.
29. Christman 1989; Vikelsoe and Johansen 2000.
30. Ishibashi et al. 2000. 31. Takasuga et al. 2000. When fly ash from a municipal incinerator was added to the mix, baseline concentrationsof dioxin were higher, and, as discussed below, addition of PVC or salt yielded similar increases in dioxin levels.
32. Kopponen et al. 1992.
Disposal of PVC Products 33. Kolenda et al. 1994; Wilken 1994.
34. Wunderli et al. 2000.
35. Mahle and Whiting 1980.
36. Liberti et al. 1983. 37. Halonen et al. 1995.
38. Altwicker et al. 1993. In this study, increasing the feed of organically-bound chlorine results in a substantiallyhigher ratio of chlorophenols to chlorobenzenes in the combustion products; chlorophenols are considered precur-sors for dioxin formation.
39. Bruce et al. (1991) found that addition of potassium chloride, sodium chloride, or calcium chloride to a com-bustion reaction had no effect on the quantities of dioxins and furans formed and deposited in the fly ash. Addink etal. (1998) added sodium chloride to fly ash and found that it did not participate in the de novo formation of dioxinsand furans. Lenoir et al. (1991) burned sodium chloride with polyethylene in a fluidized bed combustor and foundno effect on the amount of dioxins and furans emitted.
40. Danish Environmental Protection Agency 1993.
41. Tamade et al. 2000; Yoneda et al. 2000.
42. Mattila et al. 1992; Ruuskanen et al. 1994; Frankenhauser et al. 1993. 43. This study by Kanters et al. (1996) focused on emissions of chlorophenols as a surrogate for dioxin, due to thedifficulty and expense of dioxin sampling and analysis.
44. Wagner and Green 1993; this study also measured emissions of chlorophenols as a dioxin surrogate.
45. Christmann et al. 1989.
46. Vesterinen and Flyktmann 1996; Halonen et al. 1993; Hutoari and Vesterin 1996; Manninen et al. 1996. In allof these studies, dioxin levels in fly gas or flue gas increased with increasing feed of refuse-derived fuel to the burner,which was significantly higher in chlorine content than the organic matter used in comparison runs. 47. Hatanaka et al. 2000.
48. Visalli 1987.
49. Mark 1994.
50. EPA 1988.
51. Wikstrom et al. 1996.
52. Pandompatam et al. 1997.
53. Wikstrom et al 1996.
54. The report of Hatanaka et al. (2000) also found that NaCl and PVC resulted in similar increases in dioxin for-mation, although the unusually high concentration of NaCl added was thought to have resulted in less optimalcombustion conditions, possibly increasing dioxin emissions indirectly.
55. Takasuga et al. 2000.
56. Thornton 2000. 57. Burns 2000.
58. Burnett 1994. 59. Rigo et al. 1995. 60. Goodman 1994. 61. Illustrating this point, even carbon dioxide, a widely accepted indicator of combustion conditions, is not consis-tently related to the emission of unburned wastes, according to Staley et al. 1986 and EPA 1990. 62. Licis and Mason 1989. 63. Rigo analyzed Hydrogen chloride in stack gas for municipal and medical waste incinerators. For hazardous wasteincinerators, his analysis was based on the percent chlorine in the waste feed, a parameter that also does not reflectthe mass of chlorine. If the percent of chlorine stays the same and total waste feed is increased, then the mass of chlo-rine feed will increase but would not have been noted using Rigo's approach. Further, increasing the waste feed typi-cally increases the stack gas flow rate, which will tend to reduce dioxin concentrations even if the mass of dioxinemitted increases.
64. Brzuzy and Hites 1996b.
65. Martinez et al. 2000.
66. Schecter 1991; Ligon et al. 1989; Schecter et al. 1988; Tong et al. 1990.
67. Reviewed in Alcock and Jones 1996.
68. Czuczwa and Hites 1986; Czuczwa et al. 1984; Czuczwa and Hites 1985.
69. Kjeller and Rappe 1995.
70. Juutner et al. 1997.
71. Reviewed in Alcock and Jones 1996. Echoing these findings, EPA scientists, in a study of 11 lakes in remoteparts of the U.S., found that PCDD/F concentrations in pre-1930 sediments were at most one-tenth the levels inmore recent layers (Cleverly et al. 1996).
72. Brzuzy and Hites 1996b.
73. Czuczwa and Hites 1984. Additional data are reported in Czuczwa and Hites 1986 and 1985.
74. DTI 1995.
Environmental Impacts of Polyvinyl Chloride Building Materials Background
Persistent Organic Pollutants (POPs)

Background on Persistent OrganicPollutants (POPs) In recent years, there has been extensive scientific and political activity ontoxic pollutants, their global distribution, and their effects on highlyexposed populations and the general public. An understanding of thatcontext strengthens the case for action to restrict PVC in building appli-cations, and action on PVC would in turn strengthen internationalefforts to reduce persistent toxic pollution at the source. GLOBAL DISTRIBUTION OF POPs Recently the first global agreement to eliminate sources of persistentorganic pollutants (POPs) has been negotiated. The POPs treaty is, inlarge part, a response to scientific research in the past decade that hasidentified a variety of synthetic chemical pollutants that are now globallydistributed in the environment and food web, have damaged wildlifepopulations, and may have caused large-scale human health damage.1Global contamination has occurred because many synthetic chemicals arepersistent in the environment, resisting natural degradation processes formonths, years, or even decades. As a result, even substances that are dis-charged at a relatively slow rate build up to higher levels over time and aredistributed widely by air and water. Because many synthetic organic sub-stances are derived from petrochemicals, they are oil soluble and thereforebioaccumulate—they build up in the fatty tissues of living things andmultiply in concentration as they move up the food chain. Some bioaccu-mulative substances reach concentrations tens of millions of times greaterthan their levels in the ambient environment in species high on the foodweb, including humans.2 Releases of persistent and/or bioaccumulative substances since the expan-sion of synthetic chemical manufacturing after World War II has resulted in Environmental Impacts of Polyvinyl Chloride Building Materials the global accumulation of POPs in areas remote from any known sourcesof these substances, including the high Arctic,3 the isolated rainforests ofSouth America and Africa,4 and remote regions of the deep oceans.5 In theArctic, where long residence times, cold temperatures, and long food chainscombine to enhance the persistence and bioaccumulation of organic chemi-cals, body burdens of humans and wildlife are as much as an order of mag-nitude greater than in temperate latitudes of industrialized nations.6 "Acceptable" substances Although research and policy have focused primarily on a handful of sub-stances—dioxins, PCBs, and about a dozen organochlorine pesticides— global contamination cannot be reduced to a few "bad actors." In the bioaccumulate cannot be Great Lakes, 362 synthetic chemicals have been "unequivocally identi-fied" in the water, sediments, and food chain. The list includes the infa- integrated into natural mous POPs, but it also contains a full spectrum of less familiar cycles. The ecosystem's substances, from solvents and chemical intermediates to a host of com-plex industrial specialty chemicals, by-products, and breakdown assimilative capacity for products.7 By-products of chlorinated chemical manufacture and disposal are present in measurable quantities in the Canadian Arctic8 and over theremote Atlantic Ocean,9 and a variety of chlorinated benzenes are compo- nents of rain and snow.10 Chlorinated solvents, refrigerants, and their substances is therefore environmental degradation products have become truly ubiquitous con-taminants of the atmosphere and vegetation.11 zero, and the only "acceptable" discharge is With the environment and food web ubiquitously contaminated, itshould come as no surprise that people are contaminated as well. Human exposures come through inhalation, drinking water, and eating food. Forhighly bioaccumulative substances, the vast majority of the average indi-vidual's exposure—in excess of 90 percent—comes through the food sup-ply, primarily from animal products.12 At least 700 xenobiotic organicchemicals are present in the adipose tissues of the general population ofthe United States.13 Close to 200 organochlorine by-products, metabo-lites, pesticides, plastic feedstocks, solvents, and specialty chemicals havebeen specifically identified in the blood, breath, fat, milk, semen, or urineof the general U.S. and Canadian populations—people with no specialworkplace or local exposures to these substances. Fat-soluble chemicalsthat have accumulated in a woman's body easily cross the placenta and areconcentrated in breast milk. Background on Persistent Organic Pollutants (POPs) The now-ubiquitous global presence of synthetic chemicals—in large-scale production for just over than half a century—supports a simpleinference: substances that persist or bioaccumulate cannot be integratedinto natural cycles. Discharged in even small amounts, these chemicalsbuild up gradually in the environment and in living things. Givenenough time, even small "acceptable" discharges reach unacceptable lev-els. The ecosystem's assimilative capacity for persistent or bioaccumula-tive substances is therefore zero, and the only "acceptable" discharge isalso zero. Any amount greater than zero must be expected to lead tosome degree of long-term, large-scale contamination. For this reason,strategies designed to eliminate the materials and processes that producepersistent or bioaccumulative substances are far superior to those thatattempt to control, manage, or dispose of persistent chemicals after theyhave been produced.
ENDOCRINE DISRUPTION What are the impacts of universal exposure to POPs on the health ofpeople and wildlife? Important discoveries have emerged in the pastdecade from toxicology, epidemiology, and ecoepidemiology on the haz-ards of low-dose exposure. Traditionally, toxicological studies havefocused on frank manifestations of toxicity at relatively high doses, suchas cancer, organ damage, paralysis and tremors, structural birth defects,and death. Recently, however, it has been discovered that many syntheticchemicals can, at minute doses, result in subtle but significant deficits inan organism's functional capacities, such as fertility, immunity, cognitionand intelligence. Many of these effects occur as the consequence of a newly recognized setof toxicological mechanisms—disruption of the body's endocrine sys-tem.14 The endocrine system comprises the hormones, the glands thatproduce them, and the response of diverse tissues to these substances.
Hormones are the body's natural signaling molecules, circulating in theblood in low concentrations (typically in the ppt range) and triggeringcascades of gene expression that control essential aspects of development,behavior, immunity, reproduction, and the maintenance of homeostasis.
Environmental Impacts of Polyvinyl Chloride Building Materials In the past decade, a flurry of research has identified dozens of industrialand agricultural chemicals that disrupt the endocrine system. Somemimic or block the activity of the body's endogenous hormones by inter-acting directly with the hormone receptor molecules mediating theresponse of cells to hormones—such as the steroids estrogen, testosterone,progesterone, and the stress hormones cortisol. Others change the rate atwhich the body produces or excretes its own hormones, causing unnatu-rally low or high levels of steroid, retinoid, and thyroid hormones. Still The U.S. National others disrupt local signaling mechanisms that are critical to develop- Academy of Sciences ment, brain function, and the immune response, including growth fac-tors, neurotransmitters (molecules that mediate communication among concluded that adverse brain cells), and cytokines (intercellular signaling molecules that regulate immune function). The U.S. National Academy of Sciences has reviewed the evidence on neurological, and endocrine disruption and concluded that adverse developmental,immunological, neurological, and reproductive effects have occurred in reproductive effects have human populations, wildlife, and laboratory animals as a consequence of occurred in human exposure to hormonally active compounds found in the environment.15According to the Academy, effects observed include functional and struc- populations, wildlife, and tural abnormalities of the reproductive tract, reduced fertility, behavioral laboratory animals as a changes, reduced cognitive ability, and immune suppression. Many stud-ies of wildlife have shown associations between health impacts and expo- consequence of exposure sure to endocrine disrupting substances, including in large ecosystems to hormonally active like the Great Lakes and Baltic Sea with pollutant concentrations that areincreased above universal levels by less than an order of magnitude. There compounds found in the is evidence that the health of the general public may have been compro- mised by universal exposure to these substances, but the Academy did notreach consensus on this point. The panel noted that the degree of supportfor this hypothesis depends on perspectives that are informed by values,including the standard of proof that should be satisfied before conclu-sions about public health are drawn, what kinds of effects are worthy ofconcern, and how scientific findings about effects on one species or stageof life should be extrapolated to others.
Background on Persistent Organic Pollutants (POPs) DIOXIN AND RELATED COMPOUNDS Occurrence and exposure
The most intense scientific activity has focused on 2,3,7,8-tetra-
chlorodibenzo-p-dioxin (TCDD, also known colloquially as dioxin) and
other structurally similar compounds that act through a similar toxicolog-
ical mechanism (called, collectively, dioxin-like compounds). Research on
A typical nursing infant in dioxins is particularly relevant to the PVC debate because of the evidence the United States receives that the PVC lifecycle is a major source of dioxins.
a daily dioxin dose 92 Dioxins are extremely persistent substances that break down slowly if at times greater than that of all in the environment. Dioxins are also powerfully bioaccumulative andare now globally distributed in the ambient environment and food web.
the average adult.
They can be detected in the tissues and fluids of the entire U.S. popula-tion. They are cleared from the body extremely slowly: U.S. EPA esti-mates an average half-life for TCDD in humans of more than 7 years; thebody burden of the average adult therefore increases throughout life asthe substance gradually accumulates in fatty tissues. Dioxins are passedtransgenerationally with great efficiency; a typical nursing infant in theUnited States receives a daily dioxin dose 92 times greater than that of theaverage adult.16 Health impacts of dioxin
In 2000, U.S. EPA released its Dioxin Reassessment,17 a comprehensive
scientific summary and analysis of research in dioxin toxicology and epi-
demiology, and has come to the following conclusions:
Epidemiological and laboratory studies have established that dioxin isa human carcinogen, echoing the findings of both the U.S. NationalToxicology Program and the International Agency for Research onCancer.18 Dioxin is the most potent synthetic carcinogen ever tested, caus-ing increases in specific cancers and cancers of all sites at extremelylow doses. In utero exposures to small quantities of dioxin are associ-ated with increased cancer of hormone-responsive organs (such asmammary glands) when the exposed animal reaches adulthood.
Environmental Impacts of Polyvinyl Chloride Building Materials The general public's exposures to dioxin pose a calculated cancer risk inthe range of one per 100 to one per 1,000—at least 1,000 times greaterthan the usual acceptable risk.19 People who eat greater than averagequantities of meat or fish are subject to even higher cancer risks.
(EPA's estimates are based on numerous assumptions and may or maynot accurately reflect actual risks.) Dioxin's non-cancer effects may be of even greater concern than itscarcinogenicity. Dioxin is a potent endocrine-disrupting substance, inter-acting with an intracellular receptor and disrupting the action ofgonadotropins, retinoic acid, steroid hormones, thyroid hormone,and growth factors at extremely low doses. Exposure to even a singletiny dose before birth can lead to profound effects on development ofthe brain and reproductive system, with effects including impairedcognitive ability and IQ, reduced sperm density, smaller or mal-formed reproductive organs and structures, and impaired sexualbehavior. Dioxin is a powerful immune suppressant, interfering with immunefunction and increasing susceptibility to infectious disease atextremely low doses.
The current body burden of the general human population is already ator near the level at which dioxin has been found to cause a variety ofeffects in laboratory animals and human populations, including cogni-tive defects, endometriosis, hormonal changes, immune suppression,reduced sperm count, and impaired development of the male andfemale reproductive systems.20 There is no evidence of a threshold dose of dioxin below which no adversehealth impacts occur. For all responses that have been studied—includ-ing expression of target genes, growth of pre-malignant liver tumors,and changes in circulating levels of thyroid hormones—the best esti-mate of dose-response relationships at low levels of dioxin is that theseverity of the impact is roughly proportional to the magnitude ofdioxin exposure.21 Background on Persistent Organic Pollutants (POPs) Supporting the view that there is no practical threshold for dioxin toxic-ity, several studies have discovered that almost infinitesimally low doseshave significant biological effects. For example, when rats are given a sin-gle dose of TCDD as low as 64 billionths of the animal's body weight onday 15 of pregnancy, the behavior, function, and sexual development oftheir male offspring are compromised.22 Dioxin's immunotoxicity hasbeen documented at even lower levels. Doses of TCDD as low as 2.5 Doses of TCDD as low as parts per quadrillion—equivalent to a mere 10 molecules per cell—com-pletely abolish the ability of cultured immune cells to respond to signals 2.5 parts per quadrillion— to proliferate and mount an immune defense.23 In whole animals, dioxin equivalent to a mere 10 produces immunotoxicity at concentrations in the spleen about five timeslower than this—on the order of just two molecules per cell.24 If there is a molecules per cell— threshold for dioxin, it is so low that it is irrelevant for the purposes of completely abolish the environmental policy and health protection.
ability of cultured immune In addition to these findings, evidence from wildlife suggests a significant cells to respond to signals current environmental health hazard from dioxin contamination. A largenumber of ecoepidemiological studies have established that bioaccumu- to proliferate and mount lated dioxin-like compounds have caused large-scale epidemics of devel- an immune defense.
opmental impairment, endocrine disruption, immune suppression, andreduced fertility in mammals, fish, and birds in the Baltic Sea, the GreatLakes, and the Wadden Sea.25 Together, these findings indicate that we cannot assume that the general public has any margin of safety for dioxin exposure. Indeed, it is possi-ble—though not proven—that dioxin-like compounds already contributeto society-wide rates of cancer, endometriosis, immune suppression,impaired cognitive development, and infertility. From a public healthperspective, universal dioxin exposure is already too high by a consider-able margin. Further releases of dioxins into the environment should beeliminated wherever technically feasible.
Trends in dioxin contamination
Trends in dioxin levels in the environment support the conclusion that
measures to reduce dioxin generation through material substitution can
effectively reduce contamination and human exposure. Numerous studies
of soils and sediment in Europe and North America show that dioxin lev-
Environmental Impacts of Polyvinyl Chloride Building Materials els were very low before the 20th century (figure 3). They began to riseslowly around the turn of the century and then increased rapidly from1940 to 1970, the period during which the chlorine industry expandedmost rapidly.26 Then, during the 1970s, many governments restricted theuse of leaded gasoline (which contains chlorinated additives and thus pro-duces dioxin when burned) and major applications of some dioxin-contaminated pesticides, including 2,4,5-T and pentachlorophenol. Inthe same period, the U.S. Clean Air Act and similar legislation in other If there is a threshold for nations required a wide range of industrial facilities (such as chemical dioxin, it is so low that it is plants, incinerators, and steel mills) to install particulate-reducing pollu-tion control devices, which are likely to have reduced dioxin emissions to irrelevant for the purposes the air, as well. Following those actions, dioxin releases to the air—as of environmental policy measured by dioxin accumulation in plant foliage27—declined by nearly80 percent between the late 1970s and the early 1990s. As one might and health protection.
expect, dioxin levels in the milk of cows, which eat foliage, subsequentlydeclined, falling by about 25 percent between 1990 to 1994.28 Becauseannual sediment layers primarily reflect the deposition of dioxin from theair into surface waters, dioxin concentrations in most samples of marineand freshwater sediment also declined.29 But declining deposition rates do not necessarily mean a lower total bur-den of pollutants in the environment. Sediment layers provide a reason-ably reliable record of the quantity of a substance that settles to thebottom of a body of water in any year, which roughly indicates theamount that entered the water in that year. The annual flux of persistentcompounds, however, is not directly related to the total environmentalburden; if the rate at which one puts marbles into a jar declines from 100per year to 50, the total number of marbles in the jar will continue toincrease. For a record of the total amount of dioxin that has accumulatedin the environment over time, soils are better indicators than sediments,because pollutants from the recent and the distant past stay near the topof the soil, rather than being buried in annual layers. British scientistshave found that dioxin levels in soil, unlike those in sediments andfoliage, continued to increase without interruption right through the1980s and into the early 1990s. They concluded, "PCDD/Fs are persist-ent in soils, such that declines in atmospheric deposition may not resultin a decline in the UK PCDD/F burden for some time. It may be that Background on Persistent Organic Pollutants (POPs) even with the anticipated declines in the primary emissions of PCDD/Fsover the next decade, the rate of deposition may still exceed the rate ofloss from soils."30 Human and wildlife tissues reflect the same pattern, with a delay becauseof the persistence of these compounds in our bodies. Dioxin levels in sev-eral species of wildlife in the Great Lakes declined during the late 1970s, These pollutants are so 1980s, and early 1990s.31 By 1993, however, levels of dioxins in the eggsof Great Lakes trout had stopped falling, reaching, in the words of one persistent that, so long as group of researchers, "a steady state or a very slow decline."32 No human releases continue tissue analyses are available from the early decades of this century, butdioxin levels in people from the United States increased steadily during somewhere, the global the 1960s. Following the regulatory actions of the 1970s, levels declined environmental burden of during the 1980s.33 Concentrations continued to fall in most Europeannations during the 1990s, although the data for the United States are declines slowly, if at all.
There are no reliable projections of future trends in dioxin levels.
Apparently, the successful actions of the past have had their effect, how-ever. According to Swedish scientists, the declines are history, not a con-tinuing trend. "During the last twenty years an overall decrease in thelevels [of dioxin in human tissues] is recorded. The major part of thisdecrease dates back to the late 1970s and the early 1980s. The situationof today seems to be quite constant and resembles what has been foundfor PCB. Analyses of human breast milk show a similar trend."35 InGermany, dioxin levels in human milk have stopped falling and increasedslightly in the late 1990s.36 All this information suggests a pattern with clear implications for policy.
Action to reduce production and use of dioxin-generating substances hasreduced emissions to the environment of these compounds. On localand regional scales, contamination of the environment and the tissues ofliving organisms has fallen in response, with the speed of the declinevarying among different kinds of sampled material. But these pollutantsare so persistent that, so long as releases continue somewhere, the globalenvironmental burden of these compounds declines slowly, if at all. If weallow releases to continue at a reduced rate, concentrations will stop Environmental Impacts of Polyvinyl Chloride Building Materials declining when a new steady state is reached. If we want to reducehuman and wildlife exposure, we should reduce the use of dioxin-gener-ating materials rapidly. Because infinitesimal doses of dioxin are enoughto cause health damage, the only level of dioxin exposure that should beconsidered acceptable from a public health perspective is zero. If wewant to prevent the accumulation of dioxins and other persistent toxicchemicals in the global environment, we need to stop environmentalreleases altogether. Because infinitesimal doses of dioxin are enough to cause health damage, the only level of dioxin exposure that Concern has recently focused on phthalates, a class of compounds used asplasticizers in flexible PVC. Phthalates are organic chemicals used to should be considered make vinyl plastic flexible, and they can make up a large portion—up to acceptable from a public 60 percent by weight—of the final product.37 Flexible PVC—includingflooring and wall coverings—accounts for just more than half of all vinyl health perspective is zero.
demand, while the remainder is rigid, unplasticized materials like pipesand siding.38 PVC accounts for the vast majority of all phthalate con-sumption, and phthalates are the dominant class of plasticizers used insoft vinyl products.39 An estimated 50 percent of all phthalates producedare used in building and interior materials.40 About 5.4 million tons ofphthalates are used in vinyl products worldwide each year.41 Vinyl is theonly major plastic that requires phthalates to be flexible.
Four specific phthalates are used extensively in PVC and are relevant tothis discussion: diethylhexyl phthalate (DEHP; U.S. production near 2million tons per year), diisononyl phthalate (DINP; 178,000 tons peryear), butylbenzyl phthalate (BBP; production not reported), anddiisodecyl phthalate (DIDP; 135,000 tons per year). In addition, di-n-octyl phthalate is formed as a by-product of the production of otherphthalates that are used in PVC and is released to the environment dur-ing the manufacture and use of flexible PVC.42 The other commerciallyimportant phthalates dibutyl phthalate (DBP) and dioctyl phthalate(DOP) are not used appreciably in PVC.
Background on Persistent Organic Pollutants (POPs) Fate, occurrence, and exposure
Phthalates are moderately persistent in the environment. They can be
degraded biologically or chemically in the presence of air in days or
weeks; in anaerobic conditions, like those often found in groundwater,
little if any degradation occurs, with a hydrolysis half-life of 2000 years.43
Because phthalates are soluble in fat, they quickly adsorb into sediments
or enter the food chain, where they can bioaccumulate.44 Although some
Because phthalates are phthalates are partially metabolized in humans, DEHP tends to bioaccu-mulate in aquatic invertebrates and fish. Bioconcentration factors meas- fat-soluble, they cross the ured in fish range from 42 to 2680, indicating that fish swimming in placenta easily and water contaminated with DEHP accumulate in their tissues levels ofDEHP that are up to thousands of times greater than the concentration concentrate in breast milk.
Because of this behavior and the large quantities produced, phthalateshave become ubiquitous environmental contaminants, present in air,water, fish, and human tissues on a global basis.46 Because most phtha-lates are more soluble in fat than air or water, levels in outdoor air andwater are typically low, although considerably higher levels of somephthalates occur in indoor air;47 levels of DEHP and metabolites in ani-mal and human tissues can be quite high, reaching concentrations higherthan such infamous pollutants as PCBs and DDT.48 For the general population, the greatest exposures to phthalates comethrough the food supply, with the highest levels in fatty foods like dairy,fish, meat, and oils, although indoor air contributes substantially aswell.49 Because of their higher rate of food consumption per kilogram ofbody weight, children ages 6 months to 4 years receive the highest expo-sures to phthalates, with a daily dose of DEHP (19 micrograms per kilo-gram of body weight) that is more than three times that of the averageadult.50 A recent U.S. Centers for Disease Control study analyzed urinesamples from the general U.S. population and found surprisingly highlevels of metabolites of BBP, DEHP, DINP, and DnOP (137, 21.5, 7.3,and 2.3 ppb, respectively), reflecting "considerable exposure" to thesecompounds, as well as other phthalates.51 Because phthalates are fat-soluble, they cross the placenta easily and concentrate in breast milk.52The authors of the CDC study concluded, "Some individual exposures Environmental Impacts of Polyvinyl Chloride Building Materials are substantially higher than previously estimated for the general popula-tion," and these "data indicate a substantial internal human dose of DBP,DEP, and BBP, [the metabolites of which] are of particular concernbecause of their developmental and reproductive toxicity in animals."53 Health impacts
Phthalates are well-recognized developmental and reproductive toxicants.
DEHP is the most studied member of the class, and in studies of a variety
Phthalate exposure in of species of laboratory animals, relatively high doses of DEHP producestructural birth defects, developmental delay, and intrauterine death.
utero or during childhood DEHP also reduces estrogen levels, fertility, and ovarian weight, and it suppresses ovulation in female rodents. In males, DEHP causes testicularlesions, reduced androgen levels, and atrophy of the testes. Exposure in utero or during childhood is particularly problematic—developmental developmental effects effects occur at doses up to 100 times lower than those that producereproductive toxicity in the adult.54 Exposure of a pregnant mother rat to occur at doses up to 100 DBP or DEHP disrupts the development of her male offspring's repro- times lower than those ductive system; effects include reduced synthesis of testosterone by thefetal testis, loss of sperm-producing cells, and abnormal development of that produce reproductive the testes, epididymes, and prostate.55 Extremely low levels of MEHP toxicity in the adult.
(100 nanomolar, or less than 30 ppb)—approximately the same level asfound in the urine of the general U.S. population56—cause significantdamage to cultured sperm-producing cells of developing rat testes.57 The general human population is exposed to levels of DEHP that justifypublic health concern. EPA's reference dose (RfD) for DEHP is 20 micro-grams per kilogram of body-weight per day.58 An RfD is the "acceptable"exposure level, predicted by EPA based on toxicological studies, at whichsignificant risk of health effects will not occur. But the average daily dosein the United States for children ages 6 months to 4 is 19 micrograms perkilogram of body weight, approximately the same as EPA's RfD.59 Andresearchers at the Centers for Disease Control have estimated that thedaily DEHP exposure of adults in the general U.S. population, based onthe 95th percentile and maximal levels found in the general population'surine, is as high as 3.6 and 46 micrograms per kilogram per day—in thesame range as EPA's RfD, and considerably higher for some individuals.60 Background on Persistent Organic Pollutants (POPs) These results make clear that the general public's DEHP exposure allowslittle or no clear margin of safety. Furthermore, EPA's RfD for DEHP wasestablished in 1986 based on a 1953 study that examined changes in liverweight in rodents exposed to DEHP, supplemented by other studies from1982 and 1984. This RfD was calculated before any of the relevant studiesof the effects of chronic low-level exposure to DEHP and metabolites onreproduction and development were published. Since these types of impactsmay occur at substantially lower doses than liver damage, even the RfD The general public's DEHP may not represent a truly safe dose.61 It is therefore prudent from a public exposure allows little or health perspective to reduce exposures to DEHP as rapidly as possible.
no clear margin of safety.
Considerably less research has been conducted on the toxicity of otherphthalates, but some data are available. Like DEHP, BBP is a male repro-ductive toxicant, causing testicular lesions, reduced sperm counts, andincreased infertility at relatively high doses in adult males—but virtuallyno data are available on impacts on the development of the reproductivesystem.62 Monobutyl phthalate, a metabolite of BBP, causes cryp-torchidism (failure of the testes to descend) when exposure occurs inutero.63 Much more data needs to be gathered before the full suite ofeffects caused by each phthalate, together with the dose required to pro-duce these effects at different stages of development, will be understood. In 2000, an expert committee convened by the National ToxicologyProgram reported its review of the evidence on the reproductive anddevelopmental toxicity of phthalates. The panel compared the doses ofDEHP that produce developmental toxicity in animals to the levels towhich infants and toddlers in the general U.S. population are routinelyexposed, and concluded a "concern that exposure may adversely affectmale reproductive tract development."64 The panel also examined expo-sure that occurs across the placenta and via breast milk and concluded,"The panel has concern that ambient oral DEHP exposures to pregnantor lactating women may adversely affect the development of their off-spring." Based on the available data, the panel expressed low, minimal, ornegligible concern about other phthalates.
There are few epidemiological data concerning the impacts of phthalateson human development and reproduction. One study suggests that Environmental Impacts of Polyvinyl Chloride Building Materials phthalate exposure of the general population may be related toendocrine disruption and altered reproductive development in girls. InPuerto Rico, the incidence of premature breast development (early the-larche, defined as breast development during the period from 2 to 8years of age) is quite high (about 1 percent of the population) and hasbeen rising rapidly in recent decades. This phenomenon cannot beexplained by changes in nutrition or exposure to hormones used in agri-culture,65 and a similar trend has been documented in the UnitedStates.66 Exposure to endocrine-disrupting compounds is one plausibleexplanation, because estrogens trigger breast development in girls. Acase-control study of girls from the general Puerto Rican populationfound that the levels of phthalates in the blood of girls with prematurebreast development were 5.9 times higher levels than in girls withoutpremature development. Levels of DEHP, which accounted for morethan 80 percent of the total phthalates measured in the girls' blood, were6.4 times higher among girls with premature thelarche. This study doesnot prove that phthalates caused the precocious sexual development, but,as the authors concluded, it suggests that the estrogenic or otherendocrine-disrupting effects of phthalates may have contributed to theepidemic of early thelarche.67 Some phthalates may be carcinogens. According to the NationalToxicology Program (NTP), DEHP is "reasonably anticipated to be ahuman carcinogen" based on consistent findings of liver cancer in labora-tory animals. There has been some debate about whether the mechanismof carcinogenicity in rodents is relevant to humans. Based on this issue,the International Agency for Research on Cancer now lists DEHP as ananimal carcinogen but as unclassifiable with regard to human carcino-genicity. But the NTP has not adopted this view, and scientists at theNational Institute for Environmental Health Scientists have criticized theIARC's action as lacking a sound scientific basis in current understandingof DEHP's mechanism of toxicity.68 TRENDS IN PVC MARKETS Polyvinyl chloride plastic was first marketed in 193669 but did not beginto play a major role in building construction until the 1950s. Production Background on Persistent Organic Pollutants (POPs) grew rapidly from the 1960s through the 1980s, and has now reachedmore than 30 million tons per year. This estimate includes the non-PVCcomponents of vinyl products, such as plasticizers and stabilizers; produc-tion of pure polyvinyl chloride is now estimated at approximately 24 mil-lion metric tons per year worldwide.70 Vinyl is the largest use of chlorinein the world, accounting for more than 40 percent of all chlorine use inthe United States, with a similar or slightly greater proportion globally.71 Few materials have infiltrated modern life as ubiquitously as PVC, and Few materials have construction represents the largest sector of vinyl applications. In the past infiltrated modern life as fifty years, vinyl—the only major plastic that contains chlorine—hastaken the place of ceramics, metals, textiles, and wood in a range of build- ubiquitously as PVC, and ing products, including exterior siding, floor tiles, pipes, wall coverings, construction represents window frames, and wire and cable sheathings. PVC is also used in appli-ance casings, furniture, shower curtains, toys, upholstery, and other the largest sector of vinyl household items, as well as in automobile and other vehicle components, medical devices, office supplies, and packaging. Today, PVC is not only the largest but also the fastest growing use ofchlorine in the world. In fact, it is the only major chlorine applicationstill increasing in the world's wealthy nations, and it is growing particu-larly rapidly in developing countries.72 The reasons for the industry'saggressive expansion of PVC markets lie in the economics of the produc-tion of chlorine and its coproduct, sodium hydroxide (caustic soda oralkali). Alkali is a profitable and environmentally unproblematic sub-stance that is used as a source of sodium and hydroxide ions in a widevariety of industries. The majority of the world's alkali is produced bychlor-alkali electrolysis, in which chlorine and sodium hydroxide are pro-duced together in a fixed ratio. Chlorine is a hazardous gas, so it cannotbe safely stored; the chemical industry therefore can only produce asmuch alkali as there are markets for chlorine. In recent years, as numer-ous uses of chlorine (for example, pulp and paper, refrigerants, and sol-vents) have been restricted for environmental reasons, a chlor-alkaliimbalance has developed, requiring the industry to create new markets forchlorine in order to continue potential sales in alkali markets.73According to an analyst for the chlor-alkali manufacturer Elf-Atochem,"There is a logical progression toward permanent imbalance between Environmental Impacts of Polyvinyl Chloride Building Materials caustic supply and demand. Domestic chlorine consumption and chlori-nated exports will set operating rates for U.S. chlor-alkali capacity, withthe EDC/VCM/PVC chain leading the way."74 The industry's strategy to rectify the chlor-alkali imbalance is the aggres-sive expansion of markets for PVC and the feedstocks from which it ismade—already the major global sinks for chlorine. For the past severaldecades, PVC production and consumption has grown at a remarkablepace, but recently PVC markets in industrialized nations have neared sat-uration. Vinyl has already replaced so many traditional materials, thatgrowth in vinyl in these countries is now no greater than annual increasesin gross national product.75 This rate of growth is not nearly enough to The reasons for the offset the loss of chlorine demand in sectors that have been restricted so industry's aggressive the industry has focused on expanding exports of PVC and its feedstocksto developing nations.76 U.S. net exports of EDC, PVC, and VCM now expansion of PVC markets contain about two million tons of chlorine per year—more than 15 per- lie in the economics of the cent of total chlorine production—and were expected to grow by a stun-ning 14 percent in 1998 alone.77 The major recipients are Latin America production of chlorine and and Asia, where PVC consumption is expected to grow at annual rates of its coproduct, sodium 7 percent or more per year, leading to a doubling of demand eachdecade.78 Why these countries? As an executive of a major Japanese PVC company explained, vinyl is a uniquely marketable product for exportbecause poor countries need to reach only minimal levels of economicand technological development before they can be encouraged to buyplastic, and these nations usually have few environmental regulations: Demand for PVC in the high-population developing countries willgrow rapidly after their GNP per capita reaches $500 per year. Onthe other hand, in the world's major industrialized countries whereper capita GNP is over $10,000/year, the use of PVC has come closeto its maturity, and the growth rate of PVC may not be as much asthe GNP growth rate. The concern about the disposal of waste mate-rial is one of the reasons for advanced society to refrain from excessiveuse of plastics.79 The rapid increase in vinyl consumption in developing countries meansthat, despite slow growth in PVC consumption in the wealthy nations, Background on Persistent Organic Pollutants (POPs) global demand for PVC will rise from 22 million tons per year in 1996 to28 million tons per year 2000—an annual growth rate of more than 6percent.80 According to one industry analyst, The most important structural changes [in the chlorine industry]will be concentration of growth in emerging markets and restructur-ing in industrialized markets: potential loss of 10–30 percent of cur-rent customers in industrialized markets; continued shutdown ofinland plants linked to declining uses; three quarters of globaldemand growth in developing countries; increase in VCM and PVCtrade and potential tripling in volume of global EDC trade. Itappears unlikely at this point that lost markets will offset growth forPVC and other uses.81 Notes1. Thornton 2000; Colborn et al. 1996. 2. Tatsukawa and Tanabe 1990; Allan et al. 1991.
3. Gregor and Gummer 1989; Patton et al. 1991; Barrie et al. 1997.
4. Simonich and Hites 1995.
5. Ono et al. 1987. 6. Dewailly et al. 1993; Norstrom et al. 1990. 7. Great Lakes Water Quality Board 1987.
8. Barrie et al. 1997.
9. Fuhrer and Ballschmitter 1998. 10. Brun et al. 1991. 11. DeLorey et al. 1998; Makhijani and Gurney 1995; Plumacher and Schroder 1993.
12. EPA 2000a. 13. Onstot et al. 1987. 14. National Research Council 2000; Guillette and Crain 1999.
15. National Research Council 2000. 16. EPA 2000a.
17. EPA 2000a.
18. McGregor et al. 1998; National Toxicology Program 2001.
19. Following EPA's usual approach, this risk estimate is based on the upper bound of the 95 percent confi-dence interval for the carcinogenic potency of dioxin. The potency is derived from both human and animalstudies. 20. See discussion in EPA 2000a, as well as DeVito et al. 1995 and Tryphonas 1995. 21. See also Tritscher et al. 1994; Kohn et al. 1996; Portier et al. 1996.
22. Peterson et al. 1992.
23. Neubert and colleagues (1991) documented this effect in primate lymphocytes at TCDD concentrationsas low as 10-14 moles per liter.
24. Kerkvliet (1994) reports that TCDD concentrations in the spleen as low as 2 x 10-15 moles per liter causedimmunotoxicity in laboratory rats.
25. See for example Olsson et al. 1994. Reijnders 1986; de Swart et al. 1996; Giesy et al. 1994a and 1994b.
26. Alcock and Jones (1996) provide an excellent review of dioxin trends. Specific papers include Czuczwaand Hites 1984, 1985 and 1986, Czucwa et al. 1984, Juttner et al. 1997, Kjeller and Rappe 1995, Kjeller etal. 1991, and Kjeller et al. 1996. 27. Kjeller et al. 1996.
28. Reviewed in Alcock and Jones 1996.
29. Sediment cores from two Black Forest lakes, for example, show a contradictory pattern. One shows thatdioxin levels in the layer dated 1985–1992 were lower than in that from the period 1964–1985. The other,however, shows that dioxin levels in 1982–1992 were higher than in 1960-1982. (Juttner et al. 1997).
30. Alcock and Jones 1996. Kjeller et al. 1991 also provide a useful discussion.
31. Allan et al. 1991. Alcock and Jones (1996) also review studies that suggest a decline in PCDD/Fs in Balticwildlife during the same period.
Environmental Impacts of Polyvinyl Chloride Building Materials 32. Huestis et al. 1997.
33. Stanley et al. 1990.
34. LaKind et al. 2001.
35. Johansson 1993.
36. Furst 2000.
37. DTI 1995.
38. These figures are for Western Europe (European Commission 2000).
39. DTI 1995.
40. Oie et al. 1997.
41. My calculations are extrapolated from the figures for Sweden, where the phthalate input into PVC equals22.6 percent (TNO Centre for Technology and Policy Studies 1996), assuming 24 million tons of vinyl pro-duced per year worldwide.
42. National Toxicology Program 2000.
43. HSDB 1997.
44. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a, 2000b,and 2000c.
45. HSDB 1997.
46. Giam et al. 1978;, Blount et al. 2000; HSDB 1997. 47. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
48. Giam et al. 1978; National Toxicology Program Center for the Evaluation of Risks to HumanReproduction 2000a.
49. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
50. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
51. Blount et al. 2000.
52. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
53. Blount et al. 2000.
54. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
55. Gray et al. 1999; Lambright et al. 2000.
56. Blount et al. 2000.
57. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
58. EPA 2000b.
59. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
60. Kohn et al. 2000. The median exposure level was estimated to be 0.71 micrograms per kilogram per day.
61. EPA 2000b. 62. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000b.
63. Imajima et al. 1997.
64. National Toxicology Program Center for the Evaluation of Risks to Human Reproduction 2000a.
65. Colon et al. 2000.
66. Hermann-Giddens et al. 1997.
67. Colon et al. 2000.
68. Melnick 2001.
69. Taylor 1957; Aftalion 1991.
70. Kielhorn et al. (2000) report global vinyl chloride production capacity of 27 million tons per year.
Assuming 95 percent utilization of VCM in PVC and 95 percent operating rates, global PVC production islikely to be about 24 million tons per year.
71. Leder et al. 1994.
72. Growth is expected in a few much smaller applications, such as phosgene for polycarbonate and propylenechlorohydrin for propylene oxide, but the increases in these chlorine uses are less than one-tenth the growthexpected in PVC (Mears 1995).
73. Leder et al. 1994.
74. Tullos 1995.
75. Endo 1990.
76. Leder et al. 1994.
77. Mears 1995.
78. Waltermire 1996.
79. Endo 1990.
80. Svalander 1996.
81. Tittle 1995.
Background on Persistent Organic Pollutants (POPs)

The PVC lifecycle presents one opportunity after another for the forma-tion and environmental discharge of organochlorines and other hazardoussubstances. When its entire lifecycle is considered, it becomes apparentthat this seemingly innocuous plastic is one of the most environmentallyhazardous consumer materials produced, creating large quantities of per-sistent, toxic organochlorines and releasing them into the indoor and out-door environments. PVC has contributed a significant portion of theworld's burden of persistent organic pollutants and endocrine-disruptingchemicals—including dioxins and phthalates—that are now present uni-versally in the environment and the bodies of the human population.
Beyond doubt, vinyl has caused considerable occupational disease andcontamination of local environments as well.
In summary, the feedstocks, additives, and by-products of the PVC lifecy-cle are already present in global, local, and workplace environments atunacceptably high levels. Efforts to reduce the production and release ofthese substances should be environmental and public health priorities.
The hazards posed by dioxins, phthalates, metals, vinyl chloride, and eth-ylene dichloride are largely unique to PVC, which is the only majorbuilding material and the only major plastic that contains chlorine orrequires plasticizers or stabilizers. PVC building materials therefore repre-sent a significant and unnecessary environmental health risk, and theirphase-out in favor of safer alternatives should be a high priority.
PVC is the antithesis of a green building material. Efforts to speed
adoption of safer, viable substitute building materials can have signif-
icant, tangible benefits for human health and the environment.

Environmental Impacts of Polyvinyl Chloride Building Materials Addink, R., F. Espourteille, and E.R. Altwicker. 1998. Role of inorganic chlorine in the formation of poly- chlorinated dibenzo-p-dioxins/dibenzofurans from residual carbon on incinerator fly ash. EnvironmentalScience and Technology 32:3356–3359.
Aftalion, F. 1991. A History of the International Chemical Industry. Translated by O.T. Benfey. Philadelphia: University of Pennsylvania Press.
Airey, D., and P.D. Jones. 1982. Mercury in the River Mersey, its estuary and tributaries during 1973 and 1974. Water Research 16:565–577.
Aittola, J.P., J. Paasivirta, and A. Vattulainen. 1993. Measurements of organochloro compounds at a metal reclamation plant. Chemosphere 27:65–72.
Alcock, R.E., and K.C. Jones. 1996. Dioxins in the environment: a review of trend data. Environmental Science and Technology 30:3133–3143.
Allan., R, D., Peakall, V. Cairns, J. Cooley, G. Fox, A. Gilman, D. Piekarz, J. van Oostdam, D. Villeneuve, and M. Whittle. 1991. Toxic Chemicals in the Great Lakes and Associated Effects, Volume I: ContaminantLevels and Trends. Ottawa: Environment Canada.
Altwicker, E.R., R.K.N.V. Konduri, C. Lin, and M.S. Milligan. 1993. Formation of precursors to chlorinated dioxin/furans under heterogeneous conditions. Combustion Science and Technology 88:349–368.
American Chemistry Council. 2000. Response of the Phthalate Esters Panel of the American Chemistry Council to a briefing paper submitted by Joe Thornton, Ph.D., acting under the direction of the Centerfor Maximum Potential Building Systems and the Healthy Building Network. Arlington, VA, AmericanChemistry Council.
Andersson, P., K. Ljung, G. Soderstrom, and S. Marklund. 1993. Analys av Polyklorerade Dibensofuraner och Polykloerarde Dibensodioxiner i Processprover fran Hydro Plast AB. Umea, Sweden: Institute ofEnvironmental Chemistry, University of Umea.
APHA (American Public Health Association). 1996. Resolution: Prevention of dioxin generation from PVC plastic use by health care facilities. Adopted at APHA Annual Meeting, New York, November.
———. 1994. Resolution 9304: Recognizing and addressing the environmental and occupational health problems posed by chlorinated organic chemicals. American Journal of Public Health 84:514–515.
APR (Association of Postconsumer Plastics Recyclers). 1998. APR takes a stand on PVC. Press release.
Washington, DC, April 14.
ATSDR (Agency for Toxic Substances and Disease Registry). 1998. Toxicological Profile for Mercury (update). Washington, DC: U.S. Public Health Service.
———. 1995. Toxicological Profile for Vinyl Chloride (update). Washington, DC: U.S. Public Health ———. 1993. Toxicological Profile for 1,2-Dichloroethane. Washington, DC: U.S. Public Health Service. Ayres, R. 1997. The life-cycle of chlorine, part I: chlorine production and the chlorine-mercury connection.
Journal of Industrial Ecology 1:81–94.
Badr, M.Z. 1992. Induction of peroxisomal enzyme activities by di-2-ethylhexylphthalate in thyroidectomized rats with parathyroid replants. Journal of Pharmacology and Experimental Therapy 263:1105–1110.
Barrie, L., R. Macdonald, T. Bidleman, M. Diamond, D. Gregor, R. Semkin, W. Strachan, M. Alaee, S.
Backus, M. Bewers, C. Gobeil, C. Halsall, J. Hoff, A. Li, L. Lockhart, D. Mackay, D. Muir, J.
Pudykiewicz, K. Reimer, J. Smith, G. Stern, W. Schroeder, R. Wagemann, R. Wania, and M. Yunker.
1997. Chapter 2: Sources, occurrence and pathways. In: J. Jensen, K. Adare, R. Shearer eds. CanadianArctic Contaminants Assessment Report. Ottawa: Indian and Northern Affairs Canada.
Blankenship, A., D.P.Y. Chang, A.D. Jones, P.B. Kelly, I.M. Kennedy, F. Matsumura, R. Pasek, and G.S.
Yang. 1994. Toxic combustion by-products from the incineration of chlorinated hydrocarbons and plas-tics. Chemosphere 28:183–196.
Blount, B.C., M.J. Silva, S.P. Caudill, et al. 2000. Levels of seven urinary phthalate metabolites in a human reference population. Environmental Health Perspectives 108:979–982.
Bowermaster, J. 1993. A town called Morrisonville. Audubon 95(4):42–51.
Bruce, K.R., L.O. Beach, and B.K. Gullett. 1991. The role of gas-phase Cl2 in the formation of PCDD/PCDF during waste combustion. Waste Management 11:97–102.
Brun, G.L., G.D. Howell, and H.J. ONeill. 1991. Spatial and temporal patterns of organic contaminants in wet precipitation in Atlantic Canada. Environmental Science and Technology 25:1249–1261. Brzuzy, L.P., and R.A. Hites. 1996a. Global mass balance for polychlorinated dibenzo-p-dioxins and dibenzo- furans. Environmental Science and Technology 30:1797–1804.
———. 1996b. Response to comment on global mass balance for polychlorinated dibenzo-p-dioxins and dibenzofurans. Environmental Science and Technology 30:3647–3648.
Burmaster, D., and R. Harris. 1982. Groundwater contamination: an emerging threat. Technology Review Burnett, R. 1994. Crisis management plans for the dioxin reassessment. Memorandum and enclosures from Vinyl Institute executive director to Vinyl Institute (VI) executive board members and VI issues manage-ment committee members. Morristown, NJ: Vinyl Institute, September 6.
Burns, T.F. 2000. Comments on LEED CI Draft Proposed Rating System. Morristown, NJ: Vinyl Institute.
Burress, C. 2000. Berkeley group wants toxic ban: city asked to stop dumping of carcinogens. San Francisco Chronicle, October 3.
Cameron, K. 1996. Statement of the Fire Brigades Union on PVC in buildings. Surrey, UK, September 30.
Carroll W. 1995. Is PVC in House Fires the Great Unknown Source of Dioxin? Washington DC: The Vinyl Carroll, W.F., F.E. Borelli, P.J. Garrity, R.A. Jacobs, J.W. Lewis, R.L. McCreedy, and A.F. Weston. 1996.
Characterization of dioxins and furans from ethylene dichloride, vinyl chloride, and polyvinyl chloridefacilities in the United States: resin, treated wastewater and ethylene dichloride. OrganohalogenCompounds 27:62–67.
CDC (U.S. Centers for Disease Control). 1999. Health Consultation: Exposure Investigation Report, Calcasieu Estuary, Lake Charles, Calcasieu Parish, Louisiana. Washington DC: Department of Health and HumanServices.
Chang, D., M. Richards, and G. Huffman. 1988. Studies of POHC DE during simulated atomization failure in a turbulent flame reactor. In: Land Disposal, Remedial Action, Incineration and Treatment of HazardousWaste, Proceedings of the Fourteenth Annual Research Symposium. Cincinnati: U.S. Environmental Protec-tion Agency Hazardous Waste Engineering Laboratory (EPA 600/9–88/021). Chicago Tribune. 1996. Hazardous lead levels exist in plastic, vinyl miniblinds. July 8:A7. Chlorine Institute. Production of chlor-alkali chemicals. Washington DC: The Chlorine Institute, 1991.
———. 2000. Third Annual Report of the Chlorine Institute to U.S. EPA and Environment Canada.
Washington, DC: May.
Christanesen, K., A. Grove, L.E. Hansen, L. Hoffman, A.A. Hensen, K. Pommer, and A. Schmidt. 1990.
Environmental Assessment of PVC and Selected Alternative Materials. Copenhagen: Danish Ministry of theEnvironment. Christmann, W. 1989. Combustion of polyvinyl chloride—an important source for the formation of PCDD/PCDF. Chemosphere 19:387–392.
Christmann, W., K.D. Koppel, H. Partscht, and W. Rotard. 1989. Determination of PCDDs/PCDFs in ambient air. Chemosphere 19:521–6.
Cleverly, D., M. Monetti, L. Phillips, P. Cramer, M. Heit, S. McCarthy, K. O'Rourke, J. Stanley, and D.
Winters. 1996. A time-trends study of the occurrences and levels of CDDs, CDFs and dioxin-like PCBsin sediment cores from 11 geographically distributed lakes in the United States. OrganohalogenCompounds 28:77–81.
Cohen M, Commoner B, Eisl H, Bartlett P, Dickar A, Hill C, Quigley J, Rosenthal J. Quantitative Estimation of the Entry of Dioxins, Furans, and Hexachlorobenzene into the Great Lakes from Airborneand Waterborne Sources. Flushing, NY: Center for the Biology of Natural Systems, Queens College, CityUniversity of New York, 1995.
Colborn, T., D. Dumanoski, and J.P. Myers. 1996. Our Stolen Future. New York: Dutton, 1996.
Collins, T. 2001. Towards sustainable chemistry. Science 291:48–50.
———. 2000. A call for a chlorine sunset: the hazards of organochlorines require that they be eliminated.
Colon, I., D. Caro, C. Bourdnoy, and O. Rosario. 2000. Identification of phtahalte esters in the serum of young Puerto Rican girls with premature breast development. Environmental Health Perspectives108:895–900. Costner, P. 1997. The Burning Question: Chlorine and Dioxin. Washington DC: Greenpeace USA.
Costner, P., C. Cray, G. Martin, B. Rice, D. Santillo, and R. Stringer. 1995. PVC: A Principal Contributor to the U.S. Dioxin Burden. Washington DC: Greenpeace USA.
Cummings, M. 2001. Personal electronic mail communication with B. Walsh of the Healthy Building Network, May 9.
Environmental Impacts of Polyvinyl Chloride (PVC) Building Materials Curry, M.S., M.T. Huguenin, A.J. Martin, and T.R. Lookingbill. 1996. Contamination Extent Report and Preliminary Evaluation for the Calcasieu Estuary. Silver Spring, MD: National Oceanic And AtmosphericAdministration. Czuczwa, J.M., and R.A. Hites. 1986. Airborne dioxins and dibenzofurans: sources and fates. Environmental Science and Technology 20:195–200.
———. 1985. Historical record of polychlorinated dioxins and furans in Lake Huron Sediments. In: L.H.
Keith, C. Rappe, and G. Choudhary, eds. Chlorinated Dioxins and Dibenzofurans in the TotalEnvironment II. Boston: Butterworth, 1985:59–63.
———. 1984. Environmental fate of combustion-generated polychlorinated dioxins and furans.
Environmental Science and Technology 186:444–449.
Czucwa, J.M., B.D. Veety, and R.A. Hites. 1984. Polychlorinated dibenzo-p-dioxins and dibenzofurans in sediments from Siskiwit Lake, Isle Royale. Science 226:568–569.
Danish Environmental Protection Agency. 1993. PVC and Alternative Materials, English translation.
Copenhagen: Danish Environmental Protection Agency. Davies, F.C.W. 1991. Minimata disease: A 1989 update on the mercury poisoning epidemic in Japan.
Environmental Geochemistry and Health 13:35–38.
De Santiago, A., and M. Aguilar-Santelises. 1999. Organotin compounds decrease in vitro survival, prolifera- tion and differentiation of normal human B lymphocytes. Human Experimental Toxicolology 18:619–24.
de Swart, R.L., P.S. Ross, J.G. Vos, and A.D.M.E. Osterhaus. 1996. Impaired immunity in harbour seals (Phoca vitulina) exposed to bioaccumulated environmental contaminants: Review of a long-term feedingstudy. Environmental Health Perspectives 104 (Supplement 4):823–828. Dellinger, B., P. Taylor, D. Tiery, J. Pan, and C.C. Lee. 1988. Pathways of PIC formation in hazardous waste incinerators. In: Land Disposal, Remedial Action, Incineration and Treatment of Hazardous Waste,Proceedings of the Fourteenth Annual Research Symposium. Cincinnati: U.S. EPA Hazardous WasteEngineering Research Laboratory (EPA 600/9–88/021). DeLorey, D., D. Cronn, and J. Farmer. 1988. Tropospheric latitudinal distributions of CF2Cl2, CFCl3, N20, CH3CCl3, and CCl4 over the remote Pacific Ocean. Atmospheric Environment. 22:1481–1494. Denmark Skatteministeriet. 2001. Taxes on polyvinylchloride and phthalate act. Available at: Deutsch, D.G., and T.D. Goldfarb. 1988. PCDD/PCDF contamination following a plastics fire in a univer- sity lecture hall building. Chemosphere 12:2423–2431.
DeVito, M.J., L.S. Birnbaum, W.H. Farland, and T. Gasiewicz. 1995. Comparisons of estimated human body burdens of dioxinlike chemicals and TCDD body burdens in experimentally exposed animals.
Environmental Health Perspectives 103:820–831.
Dewailly, E., P., Ayotte, S. Bruneau, C. Laliberte, D.C.G. Muir, and R.J. Norstrom. 1993. Inuit exposure to organochlorines through the aquatic food chain in Arctic Quebec. Environmental Health Perspectives101:618–620.
Dine, T., M. Luyckx, B. Gressier, et al. 2000. A pharmacokinetic interpretation of increasing concentrations of DEHP in hemodialysed patients. Medical Engineering and Physics 22:157–165.
Dow Chemical. 1990. Waste Analysis Sheet: Heavy Ends from the distillation of Ethylene Dichlorine in Ethylene Dichloride Production. Plaquemine, LA, February 21.
Downs, P. 2001. Mold and Mildew. Available at: DTI (Danish Technical Institute). 1995. Environmental Aspects of PVC. Copenhagen, November. Duffy, R.M. 1998. Letter to Concord School Board Members. International Association of Fire Fighters.
Washington DC, April 14.
Ecocycle Commission of the Government of Sweden. 1994. PVC: A Plan to Prevent Environmental Impact. Stockholm: Ecocycle Commission, 104.
Eklund, G., J. Pedersen, and B. Stromberg. 1988. Methane, hydrogen chloride, and oxygen form a wide range of chlorinated organic species in the temperature range 400 C–950 C. Chemosphere 173:575–586.
Ema, M., T. Iwase, Y. Iwase, N. Ohyama, and Y. Ogawa. 1996. Change of embryotoxic susceptibility to di-n- butyltin dichloride in cultured rat embryos. Archives of Toxicology 70:742–8. Endo, R. 1990. World demand for PVC (presentation materials). The Second World Chlor-alkali Symposium. Washington, DC, September.
ENDS. 2000. Denmark defies EU opposition to ban lead. ENDS Daily, 14 November.
Energy Information Administration, Office of Coal, Nuclear, Electric and Alternate Fuels. 1996. Electric Power Annual 1995, Volume I. Washington, DC: U.S. Department of Energy (DOE/EIA-0348(95)/1,Distribution Category UC-950).
Environment Agency. 1997. Regulation of Dioxin Releases from the Runcorn Operations of ICI and EVC.
Warrington, UK.
EPA (U.S. Environmental Protection Agency). 2000a. Exposure and Health Assessment for 2,3,7,8- Tetrachlorodibenzo-p-dioxin (TCDD) and Related Compounds (review draft). Washington, DC: U.S.
EPA Office of Research and Development.
———. 2000b. Integrated Risk Information System, record for Bis (2-ethylhexyl)phthalate. Available at: ———. 1998. The Inventory of Sources of Dioxin in the United States (review draft). Washington, DC: U.S.
EPA, Office of Research and Development (EPA/600/P–98–002a), 1998.
———. 1994a. Health Assessment Document for 2,3,7,8- tetrachlorodibenzo-p-dioxin and Related Compounds, Volumes I–III, Review Draft. Washington, DC: U.S. EPA, Office of Research andDevelopment (EPA/600/BP–92–001). ———. 1994b. Estimating Exposures to Dioxin-like Compounds, Volumes I–III (review draft). Washington, DC: U.S. EPA, Office of Research and Development (EPA/600/6–88–005).
———. 1990. Standards for owners and operators of hazardous wastes incinerators and burning of hazardous wastes in boilers and industrial furnaces; proposed and supplemental proposed rule, technical corrections,and request for comments. 55 Federal Register 82, April 27.
———. 1989. Background Document for the Development of PIC Regulations from Hazardous Waste Incinerators. Washington, DC: U.S. Environmental Protection Agency, Office of Solid Waste.
———. 1988. Specific Comments on the Food and Drug Administration's Evaluation on the Environmental Issues Associated with the Proposed Rule on PVC. Washington, DC: U.S. EPA, Office of FederalActivities, May 23. ———. 1987a. National Dioxin Study: Report To Congress. Washington, DC: U.S. EPA, Office of Air Quality Planning and Standards (EPA/530–SW–87–025).
———. 1987b. National Dioxin Study Tier 4—Combustion Sources: Engineering Analysis Report, Washington, DC: U.S. EPA Office of Air Quality Planning and Standards (EPA/450–84––014h).
———. 1985. Health Assessment Document for 2,3,7,8- tetrachlorodibenzo-p-dioxin. Washington, DC: U.S. EPA Office of Health and Environmental Assessment (EPA/600–8–84/014f).
EPA SAB (U.S. Environmental Protection Agency, Science Advisory Board). 1985. Report on the Incineration of Liquid Hazardous Wastes by the Environmental Effects, Transport and Fate Committee.
Washington, DC.
European Commission. 2000. Green Paper: Environmental Issues of PVC (COM (2000)469, 26/7/2000).
Evers, E. 1989. The formation of polychlorinated dibenzofurans and polychlorinated dibenzo-p-dioxins and related compounds during oxyhydrochlorination of ethylene. Amsterdam: University of Amsterdam, Department ofEnvironmental and Toxicological Chemistry.
Evers, E.H.G., K. Ree, and K. Olie. 1988. Spatial variations and correlations in the distribution of PCDDs PCDFs and related compounds in sediments from the river Rhine. Chemosphere 17:2271–2288.
Evers, E.H.G., H. Klamer, R. Laane, and H. Govers. 1993. Polychlorinated dibenzo-p-dioxin and dibenzofu- ran residues in estuarine and coastal North Sea sediments: sources and distribution. EnvironmentalToxicology and Chemistry 12:1583–1598.
Evers, E.H.G., R.W.P.M. Laane, G.J.J. Groeneveld, and K. Olie. 1996. Levels, temporal trends and risk of dioxins and related compounds in the Dutch aquatic environment. Organohalgen Compounds28:117–122.
Fiedler, H., O. Hutzinger, and J. Hosseinpour. 1993. Analysis and remedial actions following an accidental fire in a kindergarten. Organohalogen Compounds 14:19–23. Frankenhaeuser, M., H. Manninen, I. Kojo, J. Ruuskanen, T. Vartiainen, R. Vesterinen, and J. Virkki. 1993.
Organic emissions from co-combustion of mixed plastics with coal in a bubbling fluidized bed boiler.
Chemosphere 27:309–316.
Franklin Associates 1997. Characterization of Municipal Solid Waste in the United States: 1996 Update (EPA-530-R-97-015) Quoted in Hammer Consulting 1998. It's Perfectly Clear: The Case against PVCPackaging. Boston: Masspirg Education Fund, April.
Fuhrer, U., and K. Ballschmitter. 1998. Bromochloromethoxybenzenes in the marine troposphere of the Atlantic ocean: a group of organohalogens with mixed biogenic and anthropogenic origin. EnvironmentalScience and Technology 32:2208–2215.
Furst, P. 2000. PCDD/PCDFs in human milk: still a matter of concern? Organohalogen Compounds Geiser, K. 2000. Presentation materials. Organizing Meeting of the Healthy Building Network. Bolinas, CA, German Environment Ministers. 1992. Impacts on the Environment from the Manufacture, Use and Disposal and Substitution of PVC. Hamburg: German Joint Federal-State Committee on Environmental Chemicalsfor the German Environmental Ministers. Giam, C.S., H.S. Chan, G.S. Neff, and E.L. Atlas. 1978. Phthalate ester plasticizers: a new class of marine pollutant. Science 199:419–421.
Environmental Impacts of Polyvinyl Chloride (PVC) Building Materials Giesy, J.P., J.P. Ludwig, and D.J. Tillitt. 1994a. Deformities in birds of the Great Lakes region: assigning causality. Environmental Science and Technology 28:128a–134a.
———. 1994b. Dioxins, dibenzofurans, PCBs and wildlife. In: A. Schecter, ed. Dioxins and Health. New York: Plenum, 249–308.
Gilbertson, M.G., T. Kubiak, J. Ludwig, and G. Fox. 1991. Great Lakes embryo mortality, edema, and defor- mities syndrome (GLEMEDS) in colonial fish-eating birds: similarity to chick edema disease. Journal ofToxicology and Environmental Health 33:455–520.
Goldspiel, B.R. 1994. Pharmaceutical issues: preparation, administration, stability, and compatibility with other medications. Annals of Pharmacotherapy 28:S23–S26.
Goodman, D. 1994. Memorandum: Incineration task force. Washington, DC: Morrisville, NJ, August 22.
Gray, L.E., C. Wolf, C. Lambright, P. Mann, M. Price, R.L. Cooper, and J. Ostby. 1999. Administration of potentially antiandrogenic pesticides (procymidone, linuron, iprodione, chlozolinate, p,p'-DDE, andketoconazole) and toxic substances (dibutyl- and diethylhexyl phthalate, PCB 169, and ethane dimethanesulphonate) during sexual differentiation produces diverse profiles of reproductive malformations in themale rat. Toxicology and Industrial Health 15:94–118.
Great Lakes Water Quality Board. 1987. 1987 Report on the Great Lakes Water Quality. Windsor, ON: International Joint Commission. Green, A.E.S. 1993. The future of medical waste incineration. In: A.E.S. Green, ed. Medical Waste Incineration and Pollution Prevention. New York: Van Nostrand Reinhold:170–207. Greenpeace International. 2000. PVC-Free Future: A Review of Restrictions and PVC-Free Policies Worldwide.
Gregor, D., and W. Gummer. 1989. Evidence of atmospheric transport and deposition of organochlorine pes- ticides and plychlorinated biphenyls in Canadian Arctic snow. Environmental Science and Technology23:561–565.
Guillette, L.J., and D.A.Crain, eds. 1999. Environmental Endocrine Disruption: An Evolutionary Approach.
London: Taylor and Francis.
Gullett, B.K. 1990. The effect of metal catalysts on the formation of poychlorinated dibenzo-dioxin and poly- chlorinated dibenzofuran precursors. Chemosphere 20:1945–52.
Halonen, I., J. Tarhanen, T. Kopsa, J. Palonen, H. Vilokki, and J. Ruuskanen. 1993. Formation of polychlo- rinated dioxins and dibenzofurans in incineration of refuse derived fuel and biosludge. Chemosphere26:1869–1880.
Halonen, I., J. Tarhanen, T., Ruokojarvi, K. Tuppurainen, and J. Ruuskanen. 1995. Effect of catalysts and chlorine source on the formation of organic chlorinated compounds. Chemosphere 30:1261–1273.
Hamilton-Wentworth (Regional Municipality of Hamilton-Wentworth, Ontario). 1997. Public Health Statement on Plasti-met Fire. Hamilton, Ontario. Available at [http://www.hamilton-went.on.ca].
Hammer Consulting. 1998. It's Perfectly Clear: The Case against PVC Packaging. Boston: Masspirg Education Fund, April.
Hanberg, A. 1999. Compilation of EU Dioxin Exposure and Health Data. Oxfordshire: AEA Technology plc and European Commission DG Environment.
Hansen, J. 1999. Risk for testicular cancer after occupational exposure to plastics. International Journal of Harada, M. 1995. Minimata disease: methyl mercury poisoning in Japan caused by environmental pollution.
Critical Reviews in Toxicology 25:1–24.
Hardell, L., A. Nasman, C.G. Ohlson, and M. Fredrikson. 1998. Case-control study on risk factors for testic- ular cancer. International Journal of Oncology 13:1200–1303.
Hardell, L., C.G. Ohlson, and M. Frerikson. 1997. Occupational exposure to polybinyl chloride as a risk fac- tor for testicular cancer evaluated in a case control study. International Journal of Cancer 73:828–830.
Harris, C.A., P. Henttu, M.G. Parker, and J.P. Sumpter. 1997. The estrogenic activity of phthalate esters in vitro. Environmental Health Perspectives 105:802–811.
Hasselriis, F., and L. Constantine. 1993. Characterization of today's medical waste. In: A.E.S. Green, ed.
Medical Waste Incineration and Pollution Prevention. New York: Van Nostrand Reinhold, 37–52.
Hatanaka, T., T. Imagawa, and M. Takeuchi. 2000. Formation of PCDD/Fs in artificial solid waste incinera- tion in a laboratory-scale fluidizedbed reactor: influence of contents and forms of chlorine sources inhigh-temperature combustion. Environmental Science and Technology 34:3920–3924.
Heindel, J.J.and R.E. Chapin. 1989. Inhibition of FSH-stimulated cAMP accumulation by mono(2-ethyl- hexyl)phthalate in primary rat Sertoli cell cultures. Toxicology and Applied Pharmacology 97:377–385. Henschler, D. 1994. Toxicity of chlorinated organic compounds: effects of the introduction of chlorine in organic molecules. Angewandte Chemie International Edition (English) 33:1920–1935.
Herman-Giddens, M.E., E.J. Slora, R.C. Wasserman, C.J. Bourdony, M.V. Bhapkar, G.G. Koch, and C.M.
Hasemeier. 1997. Secondary sexual characteristics and menses in young girls seen in office practice: astudy from the Pediatric Research in Office Settings Network. Pediatrics 99:505–512.
Hill, G., and J. Holman. 1989. Chemistry in Context, Third Edition. London: Nelson Publishers, 266–269.
HSDB (Hazardous Substances Databank). 1997. Bethesda, MD: National Library of Medicine.
Hsieh, S. 2000. Will toxic mold be the next asbestos? Lawyers Weekly 853.
Huestis, S.Y., M.R. Servos, and D.G. Dixon. 1997. Evaluation of temporal and age-related trends of chemi- cally and biologically generated 2,3,7,8-tetrachlorodibenzo-p-dioxin equivalents in Lake Ontario trout,1977–1993. Environmental Toxicology and Chemistry 16:154–164.
Hutari, J., and R. Vesterinen. 1996. PCDD/F emissions from co-combustion of RDF with peat, wood waste, and coal in FBC boilers. Hazardous Waste and Hazardous Materials 13:1–10.
Hutzinger, O. 1986. Dioxin danger: incineration status report. Analytical Chemistry 586:633–642.
Hutzinger, O., and H. Fiedler. 1988. Formation of Dioxins and Related Compounds in Industrial Processes.
Pilot Study on International Information Exchange on Dioxins and Related Compounds #173. Brussels:NATO Committee on the Challenges of Modern Society.
ICI Chemicals and Polymers, Ltd. 1994. Report to the Chief Inspector HMIP Authorization AK6039, Improvement Condition, Part 8, Table 8.1, Item 2—Formation of Dioxins in Oxychlorination: Significancefor Human Health and Monitoring Proposals. Runcorn, UK: ICI Chemicals and Polymers Safety andEnvironment Department, April.
Imajima, T., T. Shono, O. Zakaria, and S. Suita. 1997. Prenatal phthalate causes cryptorchidism postnatally by inducing transabdominal ascent of the testis in fetal rats. Journal of Pediatric Surgery 32:18–21.
International Joint Commission. 1992. Sixth Biennial Report on Great Lakes Water Quality. Windsor, Ontario.
Ishibashi, N., Y. Yoshihara, K. Nishiwaki, S. Okajima, M. Hiraoka, and J. Shudo. 2000. The effects of organic- and inorganic-chloride in municipal solid wastes on dioxins formation and emission.
Organohalogen Compounds 46:122–125.
Isosaari, P., T. Kohonen, H. Kiviranta, J. Tuomisto, and T. Vartiainen. 2000. Assessment of levels, distribu- tion and risks of polychlorinated dibenzo-p-dioxins and dibenzofurans in the vicinity of a vinyl chloridemonomer production plant. Environmental Science and Technology 34:2684–2689.
Jaakkola, J.J., P.K. Verkasalo, and N. Jaakkola. 2000. Plastic wall materials in the home and respiratory health in young children. American Journal of Public Health 90:797–799.
Jaakkola, J.J., L. Oie, P. Nafstad, G. Botten, S.O. Samuelsen, and P. Magnus. 1999. Interior surface materials in the home and the development of bronchialobstruction in young children in Oslo, Norway. AmericanJournal of Public Health 89:188–192.
Jay, K., and L. Stieglitz. 1995. Identification and quantification of volatile organic components in emissions of waste incineration plants. Chemosphere 30:1249–1260.
Jobling, S., T. Reynolds, R. White, M.G. Parker, and J.P. Sumpter. 1995. A variety of environmentally per- sistent chemicals, including some phthalate plasticizers, are weakly estrogenic. Environmental HealthPerspectives 103:582–587.
Johansson, N. 1993. PCDD/PCDF and PCB: the Scandinavian situation. Organohalogen Compounds Johnston, P.A., S. Trondle, R. Clayton, and R. Stringer. 1993. PVC—The Need for an Industrial Sector Approach to Environmental Regulation. GERL Technical Note 04/93. Exeter: University of Exeter EarthResources Center.
Juttner, I., B. Henkelmann, K.W. Schramm, C.E.W. Steinberg, R. Winkler, and A. Kettrup. 1997.
Occurrence of PCDD/F in dated lake sediments of the Black Forest, Southwestern Germany.
Environmental Science and Technology 31:806–812.
Kaminsky, R., and R.A. Hites. 1984. Octachlorostyrene in Lake Ontario: sources and fates. Environmental Science and Technology 18:275–279.
Kanters, M.J., R. Van Nispen, R. Louw, and P. Mulder. 1996. Chlorine input and chlorophenol emission in the lab-scale combustion of municipal solid waste. Environmental Science and Technology 30:2121–2126.
Karol, M.H. Toxicological principles do not support the banning of chlorine. 1995. Fundamental and Applied Toxicology 24:1-2.
KemI (Kemikalienspektionen). 2000. PVC—utveckling mot en miljoanpassad PVC. Translated by Greenpeace KEMI (Swedish Chemicals Inspectorate). 2000. Summary of Report 6/00: Organotin Stabilizers in PVC— Assessment of Risks and Proposals for Risk Reduction Measures. Stockholm.
Kerkvliet, N.I. 1994. Immunotoxicology of dioxins and related chemicals. In: A. Schecter, ed. Dioxins and Health. New York: Plenum, 199–217.
Khizbullia, F., I. Muslymova, I. Khasanova, L. Chernova, and J. Abdraschitov. 1998. Evaluation of polychlo- rinated dibenzodioxins and dibenzofurans emissions from vinylchloride-monomer production.
Organohalogen Compounds 26:225–229.
Kielhorn, J., C. Melber, U. Wahnschaffe, A. Aitio, and I. Mangelsdorf. 2000. Vinyl chloride: still a cause for concern. Environmental Health Perspectives 108:579–588.
Environmental Impacts of Polyvinyl Chloride (PVC) Building Materials Kjeller, L.O., and C. Rappe. 1995. Time trends in levels, patterns, and profiles for polychlorinated dibenzo-p- dioxins, dibenzofurans, and biphenyls in a sediment core from the Baltic proper. Environmental Scienceand Technology 29:346–355.
Kjeller, L.O., K.C. Jones, A.E. Johnston, and C. Rappe. 1996. Evidence for a decline in atmospheric emis- sions of PCDD/Fs in the UK. Environmental Science and Technology 30:1398–1403.
———. 1991. Increases in the polychlorinated dibenzo-p-dioxin and -furan content of soils and vegetation since the 1840s. Environmental Science and Technology 25:1619–1627.
Kohn, M.C., F, Parham, S.A. Masten, C.J. Portier, M.D. Shelby, J.W. Brock, and J.W. Needham. 2000.
Exposure estimates for phthalates. Environmental Health Perspectives 108(10).
Kohn, M.C., C.H. Sewall, G.W. Lucier, and C.J. Portier. 1996. A mechanistic model of effects of dioxin on thyroid hormones in the rat. Toxicology and Applied Pharmacology 136:29–48.
Kolenda, J., H. Gass, M. Wilken, J. Jager, and B. Zeschmer-Lahl. 1994. Determination and reduction of PCDD/F emissions from wood burning facilities. Chemosphere 29:1927–1938.
Kopponen, P., R. Torronen, J. Ruuskanen, J. Tarhanen, T. Vartiainen, and S. Karenlampi. 1992.
Comparison of cytochrome P4501A1 induction with the chemical composition of fly ash from combus-tion of chlorine containing material. Chemosphere 24:391–401.
Kramlich, J.C., E.M. Poncelet, R.E. Charles, W.R. Seeker, G.S. Samuelsen, and J.A. Cole. 1989. Experimental Investigation of Critical Fundamental Issues in Hazardous Waste Incineration. Research Triangle, NC: U.S.
Environmental Protection Agency Industrial Environmental Research Lab (600/2–89–048).
Lahl, U. 1994. Sintering plants of steel industry: PCDD emission status and perspectives. Chemosphere LaKinjd, J.S., C.M. Berlin, and D.Q. Naiman. 2001. Infant exposure to chemicals in breast milk in the United States: what we need to learn from a breast milk monitoring program. Environmental HealthPerspectives 109:75–88.
Lambright, C., J. Ostby, K. Bobseine, V. Wilson, A.K. Hotchkiss, P.C. Mann, and L.E. Gray. 2000. Cellular and molecular mechanisms of action of linuron: an antiandrogenic herbicide that produces reproductivemalformations in male rats. Toxicological Sciences 56:389–399.
Leder, A., E. Linak, R. Holmes, and T. Sasano. 1994. CEH Marketing Research Report: Chlorine/Sodium Hydroxide. Palo Alto: SRI International.
Lemiuex, P.M. 1997. Evaluation of Emissions from the Open Burning of Household Waste in Barrels: Volume 1, Technical Report. Washington, DC: U.S. Environmental Protection Agency Office of Research andDevelopment, Control Technology Center (EPA–600–R–97–134a).
Lenoir, D., A. Kaune, O. Hutzinger, G. Mutzenrich, and K. Horch. 1991. Influence of operating parameters and fuel type on PCDD/F emissions from a fluidized bed incinerator. Chemosphere 23:1491–1500.
Liberti, A., G. Goretti, and M.V. Russo. 1983. PCDD and PCDF formation in the combustion of vegetable wastes. Chemosphere 12:661–663. Licis, I.J., and H.B. Mason. 1989. Boilers cofiring hazardous waste: effects of hysteresis on performance meas- urements. Waste Management 9:101–108.
Ligon, W.V., S.B. Dorn, and R.J. May. 1989. Chlorodibenzofuran and chlorodibenzo-p-dioxin levels in Chilean mummies dated to about 2800 years before the present. Environmental Science and Technology23:1286–1290.
Lindqvist, O., K. Johansson,, M. Aastrup, A. Andersson, L. Bringmark, G. Hovsenius, L. Hakanson, A.
Iverfeldt, M. Meili, and B. Timm. 1991. Mercury in the Swedish environment: recent research on causes,consequences and corrective methods. Water Air Soil Pollution 55:1–32.
Lower Saxony Ministry of Environmental Affairs. 1994. Data report and press release, dioxin data from ICI facility, Wilhelmshaven, Germany, March 22. Lstibureck, J.W. and J. Carmody. 1994. Moisture Control Handbook: Principles and Practices for Residential and Small Commercial Buildings. New York: Van Nostrand Reinhold. MAFF (Ministry of Agriculture, Food, and Fisheries/Food Safety Directorate). 1995. Dioxins in PVC food packaging: Food Surveillance Information Sheet Number 59. London.
Mahle, N., and L. Whiting. 1980. Formation of chlorodibenzodioxins by air oxidation and chlorination of bituminous coal. Chemosphere 9:693–699.
Makhijani, A. and K.R. Gurney. 1995. Mending the Ozone Hole. Cambridge: MIT Press.
Maloney, E.K., and D.J. Waxman. 2000. Trans-Activation of PPARa and PPARg by structurally diverse envi- ronmental chemicals. Toxicology and Applied Pharmacology 161:209–218.
Manninen, H., A. Perkio, T. Vartiainen, and J. Ruuskanen. 1996. Formation of PCDD/PCDF: effect of fuel and fly ash composition on the formation of PCDD/PCDF in the co-combustion of refuse-derived andpackaging-derived fuels. Environmental Science and Pollution Research 3:129–134.
Mark, F. 1994. Energy Recovery through Co-combustion of Mixed Plastics Waste and Municipal Solid Waste.
Hamburg: Association of Plastics Manufacturers in Europe.
Markowitz, J.S. 1989. Self-reported short-and long-term respiratory effects in PVC-exposed firefighters.
Archives of Environmental Health 44:30–33.
Markowitz, J.S., E.M. Gutterman, S. Schwartz, B. Link, and S.M. Gorman. 1989. Acute health effects among firefighters exposed to a polyvinyl chloride (PVC) fire. American Journal of Epidemiology 129:1023–1031.
Markus, T., P. Behnisch, H. Hagenmaier, K.W. Bock, and D. Schrenk. 1997. Dioxin-like components in incinerator fly ash: a comparison between chemical analysis data and results from a cell culture bioassay.
Environmental Health Perspectives 105(12):475–481. Marrack, D. 1988. Hospital red bag waste: an assessment and management recommendations. Journal of the Air Pollution Control Association 38:1309–1311.
Martinez, M, J. Diaz-Ferrero, R. Marti, F. Broto-Puig, L. Comellas, and M.C. Rodriguez-Larena. 2000.
Analysis of dioxin-like compounds in vegetation and soil samples burned in Catalan forest fires.
Comparison with the corresponding unburned materials. Chemosphere 41:1927–1935.
Maserti, B.E. and R. Ferrara. 1991. Mercury in plants, soil, and atmosphere near a chlor-alkali complex.
Water, Air, and Soil Pollution 56:15–20.
Masuyama, H., Y. Hiramatsu, M. Kunitomi, T. Kudo, and P.N. MacDonald. 2000. Endocrine disrupting chemicals, phthalic acid and nonylphenol, activate pregnane X receptor-mediated transcription. MolecularEndocrinology 14:421–428.
Mattila, H., T. Virtanen, T. Vartiainen, and J. Ruuskanen. 1992. Emissions of polychlorianted dibenzo-p- dioxins and dibenzofurans in flue gas from co-combustion of mixed plastics with coal and bark.
Chemosphere 25:1599–1609.
Mayer, C.E. 1998. CPSC won't seek phthalate ban; agency asks that the chemicals not be used in some toys.
Washington Post, December 2, C16. McGregor, D.B., C. Partensky, J. Wilbourn, and J.M. Rice. 1998. An IARC evaluation of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans as risk factors in human carcinogenesis.
Environmental Health Perspectives 106 (Supplement 2):755–760.
Mears, C.L. 1995. Presentation materials for: Where will the chlorine industry be in ten years? Conference on The Changing Chlorine Marketplace: Business Science and Regulations. New Orleans, April.
Melnick, R.L. 2001. Is peroxisome proliferation an obligatory precursor step in the carcinogenicity of Di(2- ethylhexyl)phthalate (DEHP)? Environmental Health Perspectives 109:437–444.
Merkord, J., H. Weber, G. Kroning, and G. Hennighausen. 2000. Antidotal effects of 2,3-dimercapto- propane-1-sulfonic acid (DMPS) and meso-2,3-dimercaptosuccinic acid (DMSA) on the organotoxicityof dibutyltin dichloride (DBTC) in rats. Human Experimental Toxicology 19:132–7. Miller, A.B., D. Bates, T. Chalmers, M.J. Coye, J. Froines, D. Hoel, J. Schwartz, P. Schulte, D.L. Davis, L.M.
Poore, and P. Adams. 1991. Environmental Epidemiology: Public Health and Hazardous Wastes.
Washington, DC: National Academy Press.
National Academy of Sciences, Committee on the Toxicological Effects of Methyl Mercury. 2000.
Toxicological Effects of Methyl mercury. Washington, DC: National Academy Press.
National Institutes of Health. 1998. U.S. Toxics Release Inventory for 1998. Available at [http://www.med- National Research Council. 2000. Hormonally Active Agents in the Environment. Washington, DC: National National Toxicology Program. 2001. Ninth Report on Carcinogens (Revised January 2001). Washington, DC: U.S. Department of Health and Human Services.
National Toxicology Program Center for the Evaluation of Risks to Human Reproduction. 2000a. NTP- CERHR Expert Panel Report on Di(2-ethylhexyl)phthalate. Washington, DC: U.S. Department of Healthand Human Services.
———. 2000b. NTP-CERHR Expert Panel Report on Butylbenzylphthalate. Washington, DC: U.S.
Department of Health and Human Services.
———. 2000c. NTP-CERHR Expert Panel Report on Di-isononylphthalate. Washington, DC: U.S.
Department of Health and Human Services.
Neubert, R., U. Jacob-Muller, H. Helge, R. Stahlmann, and D. Neubert. 1991. Polyhalogenated dibenzo-p- dioxins and dibenzofurans and the immune system: 2. In vitro effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on lymphocytes of venous blood from man and a non-human primate (Callithrixjacchus). Archives of Toxicology 65:213–219.
New York Times. 1998. Toys-R-Us halting sale of some infant products. November 14, C4. Norstrom, R.J., M. Simon, and D.C.G. Muir. 1990. Polychlorinated dibenzo-p-dioxins and dibenzofurans in marine mammals of the Canadian North. Environmental Pollution 66:1–19.
Ohlson, C.G., and L. Hardell. 2000. Testicular cancer and occupational exposures with a focus on xenoestro- gens in polyvinyl chloride plastics. Chemosphere 40:1277–1282.
Oie, L., L.G. Hersough, and J.O. Madsen. 1997. Residential exposure to plasticizers and its possible role in the pathogenesis of asthma. Environmental Health Perspectives 105:972–978.
Olsson, M., B. Karlsson, and E. Ahnland. 1994. Diseases and environmental contaminants in seals from the Baltic and Swedish west coast. Science of the Total Environment 154:2317–227.
Environmental Impacts of Polyvinyl Chloride (PVC) Building Materials Ono, M., N. Kanna, T. Wakimoto, and R. Tatsukawa. 1987. Dibenzofurans: a greater global pollutant than dioxins? Evidence from analyses of open ocean killer whale. Marine Pollution Bulletin 18:640–643.
Onstot, J., R. Ayling, and J. Stanley. 1987. Characterization of HRGC/MS Unidentified Peaks from the Analysis of Human Adipose Tissue, Volume I: Technical Approach. Washington, DC: U.S. EnvironmentalProtection Agency Office of Toxic Substances (560/6–87–002a).
Pacyna, J.M., and J. Munch. 1991. Anthropogenic mercury emission in Europe. Water, Air, and Soil Pollution Pagnetto, G., F. Campi, K. Varani, A. Piffanelli, G. Giovannini, and P.A. Borea. 2000. Endocrine-disrupting agents on healthy human tissues. Pharmacology and Toxicology 86:24–29.
Panda, K.K., M. Lenka, and B.B. Panda. 1990. Monitoring and assessment of mercury pollution in the vicin- ity of a chlor-alkali plant. Science of the Total Environment 96:281–296.
Pandompatam, B., Y. Kumar, I. Guo, and A.J. Liem. 1997. Comparison of PCDD and PCDF emissions from hog fuel boilers and hospital waste incinerators. Chemosphere 35:1065–1073.
Papp, R. 1996. Organochlorine waste management. Pure and Applied Chemistry 68:1801–1808.
Patton, G.W., M.D. Walla, T.F. Bidleman, and L.A. Barrie. 1991. Polycyclic aromatic and organochlorine compounds in the atmosphere of northern Ellesmere Island. Canadian Journal of Geophysical Research 96(D6):10867–10877.
Pearson, S.D., and L.A. Trissel. 1993. Leaching of diethylhexyl phthalate from polyvinyl chloride containers by selected drugs and formulation components. American Journal of Hospital Pharmacology50:1405–1409.
Peterson, R.E., R.W. Moore, T.A. Mably, D.L. Bjerke, and R.W. Goy. 1992. Male reproductive system ontogeny: effects of perinatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. In: T. Colborn and C.
Clement, eds. Chemically-Induced Alterations in Sexual and Functional Development: The Wildlife/HumanConnection. Princeton: Princeton Scientific Publishing, 175–194.
Pitot, H.C., and Y.P. Dragan. 1991. Facts and theories concerning the mechanisms of carcinogenesis. FASEB Plonait, S.L., H. Nau, R.F. Maier, W. Wittfoht, and M. Obladen. 1993. Exposure of newborn infants to di- (2-ethylhexyl)-phthalate and 2-ethylhexanoic acid following exchange transfusion with polyvinyl chloridecatheters. Transfusion 33:598–605.
Plumacher, J., and P. Schroder. 1993. Accumulation and fate of C2-chlorocarbons and trichloroacetic acid in spruce needles from an Austrian mountain site. Organohalogen Compounds 14:301–302.
Portier, C.J., C.D. Sherman, M. Kohn, L. Edler, A. Kopp-Schneider, R.M. Maronpot, and G. Lucier. 1996.
Modeling the number and size of hepatic focal lesions following exposure to 2,3,7,8-TCDD. Toxicologyand Applied Pharmacology 138:20–30.
Ramacci, R., G. Ferrari, and V. Bonamin. 1998. Sources of PCDDs/PCDFs from industrial and municipal waste water discharges and their spatial and temporal distribution in the sediments of the Venice lagoon.
Organohalogen Compounds 39:91–95.
Rappe, C., L.O. Kjeller, and S.E. Kulp. 1991. Levels, profile and pattern of PCDDs and PCDFs in samples related to the production and use of chlorine. Chemosphere 23:1629–1636.
Reijnders, P.J.H. 1986. Reproductive failure in common seals feeding on fish from polluted coastal waters.
Rigo, H., A. Chandler, and W. Lanier. 1995. The Relationship between Chlorine in Waste Streams and Dioxin Emissions from Combustors. New York: American Society of Mechanical Engineers.
Rossberg, M., W. Lendle, A. Togel, E.L. Dreher, E. Langer, H. Rassaerts, P. Kleinshmidt, H. Strack, U. Beck, K.A. Lipper, T. Torkelson, E. Loser, and K.K. Beutel. 1986. Chlorinated hydrocarbons. In: W. Gerhartz,ed. Ullman's Encyclopedia of Industrial Chemistry, Fifth Edition. New York: VCH Publishers,A6:233–398.
Rudell, R. 2000. Polycycling aromatic hydrocarbons, phtahalates, and phenols. In: Spangler, J.D., McCarthy, J.F., Samet, J.M., eds. Indoor Air Quality Handbook. New York: McGraw-Hill, 34.1–34.26.
Rudell, R.A., P.W. Geno, G. Sun, A. Yau, J.D. Spengler, J. Vallarino, and J.G. Brody. Forthcoming.
Identification of selected hormonally active agents and animal mammary carcinogens in commercial andresidential air and dust samples. Journal of Air and Waste Management Association. Ruuskanen, J., T. Vartiainen, L. Kojo, H. Manninen, J. Oksanen, and M. Frankenhauswer. 1994. Formation of polychlorinated dibenzo-p-dioxins and dibenzofurans in co-combustion of mixed plastics with coal:exploratory principal component analysis. Chemosphere 28:1989–1999.
Schaum, J., D. Cleverly, M. Lorber, L. Phillips, and G. Schweer. 1993. Sources of dioxin-like compounds and background exposure levels. Organohalogen Compounds 14:319–326. Schecter, A. 1991. Dioxins in humans and the environment. In: Biological Basis for Risk Assessment of Dioxins and Related Compounds. Banbury Report 35:169–214.
Schecter, A., and H. Kessler. 1996. Dioxin and dibenzofuran formation following a fire at a plastic storage warehouse in Binghamton, New York in 1995. Organohalogen Compounds 27:187–190. Schecter, A., A. Dekin, N.C.A. Weerasinghe, S. Arghestani, and M.L. Gross. 1988. Sources of dioxins in the environment: a study of PCDDs and PCDFs in ancient frozen Eskimo tissue. Chemosphere 17:627–631.
Schmittinger, P., L.C. Curlin, T. Asawa, S. Kotowski, H.B. Beer, A.M. Greenberg, E. Zelfel, and R.
Breitstadt. 1986. Chlorine. In: W. Gerhartz, ed. Ullman's Encyclopedia of Industrial Chemistry, FifthEdition. New York: VCH Publishers, A6:399–480. Schneider, K.G., and A.S. Keenan. 1997. A documented historical performance of roofing assemblies in the United States. Proceedings of the Fourth International Symposium on Roofing Technology. U.S. NationalRoofing Contractors Association.
SEPA (Swedish Environmental Protection Agency). 1994. Sample reports 610s09 and 0610s017: PVC suspen- sion/PVC plastic and PVC suspension used to make PVC. Stockholm: Swedish Environmental ProtectionAgency, May 5. SFT (Norwegian State Pollution Control Authority). 1993. Input of organohalogens to the convention area from the PVC industry. Submission to the Oslo and Paris Commissions, Oslo, November. Simonich, S.L., and R.A. Hites. 1995. Global distribution of persistent organochlorine compounds. Science Socha, A., S. Abernethy, B. Birmingham, R. Bloxam, S. Fleming, D. McLaughlin, and D. Spry. 1997.
Plastimet Inc. Fire, Hamilton, Ontario, July 9–12, 1997. Ottawa: Ontario Ministry of Environment andEnergy.
Solomon K, Bergman H, Huggett R, Mackay D, McKague B. 1993. A Review and Assessment of the Ecological Risks Associated with the Use of Chlorine Dioxide for the Bleaching of Pulp. WashingtonDC: Alliance for Environmental Technlogy.
SRI International. 1993. The Global Chlor-Alkali Industry: Strategic Implications and Impacts. Zurich.
Staley, L., M. Richards, G. Huffman, and D. Chang. 1986. Incinerator Operating Parameters which Correlate with Performance. Cincinnati: U.S. EPA Hazardous Waste Engineering Research Laboratory (EPA600/2–86–091).
Stanley, J.S., R.E. Ayling, P.H. Cramer, K.R. Thornburg, J.C. Remmers, J.J. Breen, J. Schwemberger, H.K.
Kiang, and K. Watanabe. 1990. Polychlorinated dibenzo-p-dioxin and dibenzofuran concentration levelsin human adipose tissue samples from the continental United States collected from 1971 to 1987.
Chemosphere 20:895–892.
Svalander, J.R. 1996. Presentation materials on pursuing new horizons: taking PVC beyond the millennium.
PVC ‘96 New Perspectives Conference. Brighton, UK, April.
Svensson, B.G., L. Barregard, G. Sallsten, A. Nilsson, M. Hansson, and C. Rappe. 1993. Exposure to poly- chlorinated dioxins and dibenzofurans from graphite electrodes in a chloralkali plant. Chemosphere27:259–262.
Takasuga, T., T. Makino, K. Tsubota, and N. Takeda. 2000. Formation of dioxins (PCDDs/PCDFs) by dioxin-free fly ash as a catalyst and relation with several chlorine sources. Chemosphere 40:1003–1007.
Tamade, Y., T. Ikeguchi, Y. Yagi, K. Yoneda, and K. Omori. 2000. Generation of dioxins from waste plastics combustion in a fluidized bed incinerator. Organohalogen Compounds 46:166–169.
Tatsukawa, R., and S. Tanabe. 1990. Fate and bioaccumulation of persistent organochlorine compounds in the marine environment. In: D.J. Baumgartner, and I.M. Dudall, eds. Oceanic Processes in MarinePollution, Volume 6. Malabar, FL: RE Krieger, 39–55.
Taylor, F. 1957. A History of Industrial Chemistry. New York: Abelard Schuman.
Tellus Institute. 1992. CSG/Tellus Packaging Study for the Council of State Governments, U.S.
Environmental Protection Agency, and New Jersey Department of Environmental Protection andEnergy. Boston.
Theisen, J. 1991. Untersuchung der Moglichen Umweltgefahrdung Beim Brand Von Kunststoffen (Investigation of Possible Environmental Dangers Caused by Burning Plastics). Berlin: German Umweltbundesamt(104–09–222). Theisen, J., W. Funcke, E. Balfanz, and J. Konig. 1989. Determination of PCDFs and PCDDs in fire acci- dents and laboratory combustion tests involving PVC-containing materials. Chemosphere 19:423–428. Thomas V, Spiro C. An estimation of dioxin emissions in the United States. Toxicology and Environmental Chemistry 50:1-37, 1995. Thornton, J. 2000. Pandora's Poison: Chlorine, Health, and a New Environmental Strategy. Cambridge: MIT Tittle, W.L. 1995. Presentation materials for: Where will the chlorine industry be in ten years. Conference on The Changing Chlorine Marketplace: Business Science and Regulations. New Orleans, April.
TNO Centre for Technology and Policy Studies. 1996. A PVC substance flow analysis for Sweden: Report for Norsk-Hydro. Apeldoorn, Netherlands.
TNO Institute of Environmental and Energy Technology. 1994. Sources of Dioxin Emissions into the Air in Western Europe. Brussels: Eurochlor.
Environmental Impacts of Polyvinyl Chloride (PVC) Building Materials Tong, H.Y., M.L.O. Gross, A. Schecter, S.J.Monson, and A. Dekin. 1990. Sources of dioxin in the environ- ment: second stage study of PCDD/Fs in ancient human tissue and environmental samples. Chemosphere20:987–992.
Trenholm, A., and C.C. Lee. 1986. Analysis of PIC and total mass emissions from an incinerator. In: Land Disposal, Remedial Action, Incineration, and Treatment of Hazardous Waste, Proceed-ings of the TwelfthAnnual Research Symposium. Cincinnati: U.S. Environmental Protection Agency Hazardous WasteEngineering Research Laboratory (EPA 600/9–86/022).
Trenholm, A., and R. Thurnau. 1987. Total mass emissions from a hazardous waste incinerator. In: Land Disposal, Remedial Action, Incineration, and Treatment of Hazardous Waste, Proceedings of the ThirteenthAnnual Research Symposium. Cincinnati: U.S. Environmental Protection Agency Hazardous WasteEngineering Laboratory (EPA/600/9–87/015).
Trenholm, A., P. Agorman, and G. Jungclaus. 1984. Performance Evaluation of Full-Scale Hazardous Waste Incinerators, Volume I: Executive Summary. Cincinnati: U.S. Environmental Protection Agency, IndustrialEnvironmental Research Lab.
Tritscher, A.M., G.S. Clark, and G.W. Lucier. 1994. Dose-response effects of dioxins: species comparison and implications for risk assessment. In: A. Schecter, Dioxins and Health. New York: Plenum, 227–248. Tryphonas, H. 1995. Immunotoxicity of PCBs (Aroclors) in relation to Great Lakes. Environmental Health Perspectives 103 (Supplement 9):35–46.
Tukker A., J.L.B. eGroot, and P. van de Hofstadt. 1995. PVC in Europe: Environmental Concerns, Measures and Markets. Apeldoorn, Netherlands: TNO Policy Research Group. Tullos, B.G. 1995. Presentation materials for: The caustic/chlorine relationship. Conference on The Changing Chlorine Marketplace: Business Science and Regulations. New Orleans, April.
UBA (German Federal Office of the Environment). 1992. Environmental Damage by PVC: An Overview.
UKDOE (United Kingdom Department of the Environment). 1989. Dioxins in the Environment: Pollution Paper #27. London.
United Nations Environment Programme. 2000. Final Report: UNEP/POPS/INC.4/5—Report of the Intergovernmental Negotiating Committee for an International Legally Binding Instrument for ImplementingInternational Action on Certain Persistent Organic Pollutants on the Work of its Fourth Session, Bonn, 20–25March, Geneva.
U.S. Navy. 1986. Military Specification Sheet: Insulation sleeving, electrical, heat shrinable, polyvinyl chlo- ride, flexible, crosslinked and noncrosslinked. MIL–I–23053/2C, May 1.
———. 1979. Military Specification Sheet: Insulation sleeving, electrical, heat shrinkable, polyvinyl chloride, flexible, crosslinked and noncrosslinked. MIL–I–23053/2C, Amendment 1, October 19.
Versar, Inc. 1996. Formation and Sources of Dioxin-like Compounds: A Background Issue Paper for U.S. Environmental Protection Agency, National Center for Environmental Assessment. Springfield, VA: Versar.
Vesterinen, R., and M. Flyktmann. 1996. Organic emissions from co-combustion of RDF with wood chips and milled peat in a bubbling fluidized bed boiler. Chemosphere 32:681–689.
Vikelsoe, J., and E. Johansen. 2000. Estimation of dioxin emissions from fires in chemicals. Chemosphere Vinyl Institute. 2000. Vinyl by Design: Vinyl wallcovering. Available at: [http://www.vinylbydesign.com/wall- ———. 1998. Vinyl Institute Dioxin Characterization Program Phase I Report. Morristown, New Jersey: Vinyl Visalli, J.R. 1987. A comparison of dioxin, furan and combustion gas data from test programs at three MSW incinerators. Journal of the Air Pollution Control Association 3712:1451–1463.
Wagenaar H, Langeland K, Hardman R, Sergeant Y, Brenner K, Sandra P, Rappe C, Tiernan T. Analyses of PCDDs and PCDFs in virgin suspension PVC resin. Organohalogen Compounds 27:72-74, 1996.
Wagener, K.B., C.D. Batich, and A.E.S. Green. 1993. Polymer substitutes for medical grade polyvinyl chlo- ride. In: A.E.S. Green, ed. 1993. Medical Waste Incineration and Pollution Prevention. New York: VanNostrand Reinhold, 155–169.
Wagner, J., and A. Green. 1993. Correlation of chlorinated organic compound emissions from incineration with chlorinated organic input. Chemosphere 26:2039–2054. Wallace, D. 1990. In the Mouth of the Dragon. Yonkers: Consumers Union.
Waltermire, T. 1996. Presentation materials for: The vinyl plastics industry. Goldman, Sachs Fourth Annual Chemical Investor Forum. New York, May.
Warren, S. 1998. Toy makers say bye-bye to "plasticizers." Wall Street Journal, November 12.
Wienecke, J., H. Kruse, U. Huckfeldt, W. Eickhoff, and O. Wasserman. 1995. Organic compounds in the flue gas of a hazardous waste incinerator. Chemosphere 30:907–913.
Wieslander, G., D. Norback, K. Nordstrom, R. Walinder, and P. Venge. 1999. Nasal and ocular symptoms, tear film stability and biomarkers in nasal lavage, in relation to building-dampness and building design inhospitals. International Archive of Occupational and Environmental Health 72:451–461.
Wikstrom, E., G. Lofvenius, and C. Rappe. 1996. Influence of level and form of chlorine on the formation of chlorinated dioxins, dibenzofurans, and benzenes during combustion of an artificial fuel in a laboratoryreactor. Environmental Science and Technology 305:637–1644.
Wilken, M. 1994. Dioxin Emissions from Furnaces, Particularly from Wood Furnaces. Berlin: Engineering Group for Technological Environmental Protection for the German Environmental Protection Agency,February.
Wirts, M., W. Lorenz, and M. Bahadir. 1998. Does co-combustion of PVC and other plastics lead to enhanced formation of PCDD/F? Chemosphere 37:1489–1500.
Wunderli, S., M. Zennegg, et al. 2000. Determination of polychlorinated dibenzo-p-dioxins and dibenzo- furans in solid residues from wood combustion by HRGC-HRMS. Chemosphere 40:641–649.
Yasuhara, A., and M. Morita. 1988. Formation of chlorinated aromatic hydrocarbons by thermal decomposi- tion of vinylidene chloride polymer. Environmental Science and Technology 22:646-650.
Yoneda, K., Y. Yagi, T. Ikeguchi, Y. Tamade, and K. Omori. 2000. Behaviour of dioxins and precursors in industrial waste incineration. Organohalogen Compounds 46:170–173.
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ADVANCES IN ORBITAL INFLAMMATION Nora V. Laver, MD Ocular Pathology Laboratory New England Eye Center Tufts Medical Center Boston, Massachusetts Learning objectives 1. To discuss the most important inflammatory orbital lesions and their clinical frequency. 2. To familiarize the audience with the most prevalent infectious orbital pathologies. 3. To compare and contrast the most important inflammatory orbital lesions, including Grave's orbitopathy, inflammatory pseudotumor, infections and other diseases.


A Drug Abuse Prevention Guide For Teens Table of Contents Introduction:Substance Abuse Guide For Teens 1 Part One:Today's Drug Problem 2Extent of Problem 2 Drugs of Abuse 3• Cannabis • Heroin • Cocaine 4• Methamphetamine • Prescription Drugs 5• GHB • Ecstasy 6 • LSD • PCP • Ketamine 7• Anabolic Steroids • Inhalants • Over the Counter (OTCs) 8