APPENDIX II-BS: Permethrin Persists for Years in Household
Dust: Costner, et al, “Sick of Dust: Chemicals in Common Products—A Needless
Health Risk in Our Homes,”
Safer Products Project.
This appendix is copied from:
http://www.safer-products.org/downloads/Dust%20Report.pdf
Chemicals in Common Products—
A Needless Health Risk in Our Homes
Pat Costner, Beverley Thorpe & Alexandra McPherson Safer Products
P R O J E C T
M A R C H 2 0 0 5
Sick of Dust
Chemicals in Common Products—
A Needless Health Risk in Our Homes
Pat Costner, Beverley Thorpe & Alexandra McPherson
M A R C H 2 0 0 5
Safer Products P R
O J E C T
S I C K O F D U S T : C H E M I C A L S I
N C O M M O N P R O D U C T S 2
Sick of Dust
Chemicals In Common
Products —
A Needless Health Risk In
Our Homes
Acknowledgments to all the state groups who
took part in the dust sampling and report reviews:
� Ecology Center, Michigan
� Washington Toxics
Coalition
� Oregon Environmental
Council
� The Alliance for a
Healthy Tomorrow, Massachusetts
� Citizens Environmental
Coalition,
�
� Center for Environmental
Health,
� The Silicon Valley Toxics Coalition,
We wish to particularly thank the following
foundations for their support
� John Merck Fund
� Panta Rhea Foundation
� Homeland Foundation
� Overbrook Foundation
� Mitchell Kapor Foundation
� New York Community Trust
We also thank Lowell Center for Sustainable
Production,
Pesticide Action Network and Silent Spring
Institute.
A project of Clean Production Action
A U T H O R S
� Pat Costner
� Beverley Thorpe
� Alexandra McPherson
P R O D U C T I O N C R E D I T S
CONCEPT/DESIGN/PRODUCTION
David Gerratt/Nonprofi tDesign.com
CHEMICAL HOUSE ILLUSTRATION
John Klossner
LOGO & PRODUCT ICON ILLUSTRATIONS
Nate Walker
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 3
T A B L E O F C O N T E N T S
5 Executive Summary
7 Why We Tested for Hazardous Chemicals in
House Dust
13 What We Found
Findings and summary of concern for each
chemical class
Phthalates
Alkylphenols
Pesticides
Polybrominated Diphenyl Ethers
Organotins
Perfl uorinated Chemicals
27 Why Our Regulatory System Is Failing Us
31 Europe’s New Chemical Policy: REACH
35 Product Manufacturers and Retailers Respond
to Chemical Risks
41 We Can Do Better: The Way Forward to Safe
Chemicals
46 Report Endnotes
49 Appendix I
Hazardous chemicals found in dust samples
Additional Chemical Information
Phthalates
Alkylphenols and Alkylphenol Ethoxylates
Pesticides: Permethrins, Pentachlorophenol and
DDT
Polybrominated Diphenyl Ethers (PBDEs)
Organotins
Perfl uorinated Chemicals
66 Appendix II
Ranking of Companies and Retailers:
An overview of their chemicals policies
74 Appendix III
Analytical methods
83 Appendices Endnotes
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 4
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 5
E X E C U T I V E S U M M A R Y
The fi rst U.S. study to test house- he fi rst U.S. study to test
household
dust for a new and wide
variety of chemicals found
disturbing evidence of toxic
chemicals in ordinary homes across the
country. The study documents a range of
country. The study documents a range of
hazardous chemicals found in household dust
hazardous chemicals found in household dust
in 70 homes in seven states. All the
chemicals in 70 homes in seven states. All the chemicals
found are toxic and harmful to the immune and
found are toxic and harmful to the immune and
reproductive systems in animal tests. The
chem- reproductive systems in animal tests. The chemicals
are used in mass quantities in electronic
icals are used in mass quantities in electronic
products, cosmetics, vinyl fl ooring, uphol-
products, cosmetics, vinyl fl ooring, upholstery
and other everyday products that many stery
and other everyday products that many
people wrongfully assume are safe. Babies and
young children are particularly at risk from
exposure to these chemicals.
This study shows that the US federal
regulatory
system has failed in protecting people from
exposure to hazardous chemicals including
toxic fl ame retardants, pesticides, and
hormone disrupting chemicals. Exposure to these
chemicals is unnecessary and avoidable.
Europe is overhauling chemical legislation to protect
public health and promote the production of
safer chemicals and products. Some US
states across the country are working to pass
protective legislation for safer alternatives.
Progressive companies such as Dell, IKEA,
Herman Miller and Shaw Carpets have achieved
success in fi nding safer chemicals for their
product lines. But to date, the U.S. federal government
has taken little action and the majority of
US companies have no policies in place
to favor safer chemicals and production
methods.
This report documents the presence of
hazardous chemicals in household dust, the
health risks associated with the chemicals
and the products they are found in. The report
also ranks brand name companies and retailers
on their use of hazardous chemicals and reveals
the fundamental changes that are needed to
bring American chemical regulation up
to a level that will protect our basic health
and that of future generations.
Key Findings
1. All composite samples were contaminated by
all six of the chemical classes we investigated:
phthalates, pesticides, alkylphenols,
brominated fl ame retardants, organotins and
perfl uorinated compounds. This is the fi rst
U.S. study to document levels of organotins
and perfl uorinated compounds in household dust.
2. Toxic chemicals are brought into our homes
through ordinary consumer products including
vinyl fl ooring, foam cushions, pest control
products, fabrics, and cookware. Most
of the chemicals found in this study have also
been detected in breast milk as well as
blood and/or urine.
Hazardous chemicals are regularly used as
additives in
consumer goods, yet our current system of regulation allows
them to continue to be brought into our homes
in products.
(See page 9 for a full description of our
“Chemical House.”)
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 6
In order to leave a legacy for the next generation worthy
of our abilities, we need to generate billions of dollars of new
public and private investment in clean energy technologies.
A key assumption of this report is that a more thoughtful
and widespread engagement on innovation approaches and
opportunities is needed to attract new capital to this sector.
3. Hazardous chemicals in house dust adds to
our ongoing exposure to synthetic chemical
contaminants in water, air and food. Each
composite sample contained hormone disrupting
chemicals together with chemicals associated
with allergies, impaired nervous and
immune systems, cancer, reproductive and
developmental effects.
4. Some companies have demonstrated that the
transition to safer chemicals and material
use is feasible and profi table. The report
showcases four companies that searched for and
found safer chemicals for their product
lines. A transition to safe chemical use should be
a priority across all product sectors.
The study participants cannot be blamed for
contaminating
their homes with these toxic chemicals.
Rather, blame must be
placed squarely on the shoulders of the U.S.
regulatory system,
which allows dangerous chemicals to be put
into consumer products,
does not require even minimal safety testing
for the majority
of chemicals currently in use, and has
virtually no prohibitions in
place to reduce exposure to chemicals known
to cause harm. The
U.S. chemical industry must also take
responsibility for failing to
replace chemicals of known toxicity with
safer substitutes. Manufacturers of cosmetics, furniture,
computers, fl ooring and other products must also
take responsibility to ensure
that their products are safe and free of
harmful chemicals.
The American people deserve to be safe in our
own homes, and should be able to purchase
products without unwittingly exposing
ourselves and our children to substances that
can cause cancer and disrupt development.
This study provides solid evidence that the federal
government, US states, and US industry must
take immediate action to replace harmful
chemicals with safe substitutes.
Recommended Actions
1. The federal government must phase out the
most hazardous chemicals from production
and use. Comprehensive data on chemicals used
in commerce should be required and
toxicity information should be used as a
basis to replace the most hazardous chemicals
with safer substitutes. These include
chemicals linked to cancer, hormone disruption,
developmental and reproductive harm.
2. States should take strong action now to
phase out chemicals with known or likely hazards.
A number of states are currently considering
bans on the toxic fl ame retardants PBDEs,
which have been found in house dust as well
as in breast milk. States should also support
businesses using safer processes and
chemicals.
3. The chemical industry should supply
environmental and human health data for untested
chemicals currently in production and
immediately phase out the production of those
chemicals linked to cancer, hormone
disruption, developmental or reproductive harm.
The chemical industry should begin an
aggressive adoption of Green Chemistry Principles.
4. Retailers and product manufacturers should
establish substitution plans for all high risk
chemicals, placing a priority on chemicals
detected in this study. Design strategies exist
to help companies use safe chemicals.
This study provides solid evidence
that the federal government, US
states, and US industry must take
immediate action to replace harmful
chemicals with safe substitutes.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S F
O R A H E A L T H Y H O M E S A F E R P R O D U C T S P R O J E C T : A L T E R
N A T I V E S F O R A H E A L T H Y H O M E 7
Chemical contamination is now
global—reaching even polar regions
where no chemical production
or use takes place. Hazardous
chemicals are in our rain, rivers, oceans,
air and food. Our exposures routes are
many. Toxic chemicals in our environment
build up in the food chain. We can be
particularly
exposed through chemicals in food
at the top of the food chain such as meat,
eggs, fi sh and dairy which can be
contaminated
from pesticide use on crops and chemically
contaminated sewage sludge spread
on land, as two examples. Communities can
be exposed more directly and in greater
volumes from manufacturing plant emissions
or pesticide use on farms. Children
are the most vulnerable because they are
more exposed and their nervous, immune
and reproductive systems are still
developing.
Their responses to hormone signals
from endocrine disruptors can lead to
permanent
alterations of their organ systems.
Once upon a time, household dust was
just a nuisance. In a pinch, it was swept
under
the rug. No more. Today house dust is a
toxic menace. House dust is a time capsule
of chemical contaminants that come into
the home. Since most people spend about
69–90 percent of their time indoors,2,3 there
is ample opportunity for frequent and
prolonged
exposure to the dust and its load
of contaminants.
This dust study and previous others provide
evidence of the widespread presence of
hazardous chemicals in household products.
Chemicals migrate, leach out of, or otherwise
escape from consumer products during
W H Y W E T E S T E D F O R C H E M I C A L S I N H O U S E D U S
T W H Y W E T E S T E D F O R C H E M I C A L S I N H O U S E D U S T
� Household dust is a potentially signifi cant source
for both dermal and ingestion exposure
to hazardous
chemicals present in the home.� 1
normal use leading to their accumulation
in the dust of every household tested.
Plasticizers, fl ame retardants, and
surfactants
are just some examples of chemicals
that are brought home in everyday products
People have no way of knowing that these
contaminants are in the products they buy
and
bring home, much less that these “stealth”
contaminants will end up in the air and dust
in their homes.
as ingredients that are seldom listed on the
as ingredients that are seldom listed on the
labels. These products that are presumed to
labels. These products that are presumed to
pose no toxic threat include furniture, car-
pose no toxic threat include furniture, carpets,
televisions, computers, shampoos, and pets,
televisions, computers, shampoos, and
fl ooring. People have no way of knowing fl
ooring. People have no way of knowing
that these contaminants are in the products
that these contaminants are in the products
they buy and bring home, much less that they
buy and bring home, much less that
these “stealth” contaminants will end up
these “stealth” contaminants will end up
in the air and dust of their homes. Why are
in the air and dust of their homes. Why are
manufacturers putting toxic chemicals in
manufacturers putting toxic chemicals in
and on the products they sell for household
and on the products they sell for household
and personal use when, sooner or later, those
and personal use when, sooner or later, those
chemicals become household contaminants
chemicals become household contaminants
that threaten the health of their customers?
that threaten the health of their customers?
Why don’t the government agencies that Why
don’t the government agencies that
are supposed to protect public health stop
are supposed to protect public health stop
the sale of such products? the sale of such
products?
North Americans spend about 69–90 percent
of their time indoors, most of that at cent
of their time indoors, most of that at
home. home.4 A study in the Seattle
area found that
children spent 66 percent of their time in-
children spent 66 percent of their time indoors
at home and 21 percent indoors away doors at
home and 21 percent indoors away
from home, while the elderly spent 83–88 from
home, while the elderly spent 83–88
percent of their time indoors at home.
percent of their time indoors at home.5 No
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 8
Photo: Fuel Cell Energy
wonder house dust is an important pathway
of toxic exposures especially for children
whose risk from dust-borne contaminants
may be 40 times higher than that of adults.
As they play and crawl on the fl oor,
children
skin and mucous membranes; cancer of a
variety of tissues and organs; and
developmental
effects.8
For this study, six groups of contaminants
were selected that represent only a
small portion of the wide range of chemicals
that may be found in our homes. The
chemical intruders that were detected are:
• Phthalates are
used primarily as plasticizers
in fl exible polyvinyl chloride (PVC)
plastic (commonly known as vinyl), which
accounts for 80–90 percent of the world
plasticizer consumption.9 Phthalates are
also used in nail polishes, hair sprays,
and as solvents and perfume fi xatives in
various other products,10 as well as in the
enteric coatings of some medications.11
• Alkylphenols are
mainly used to make
alkylphenol ethoxylates found in household
and industrial cleaners, paints,
textile and leather treatments, pulp
and paper processing, and agricultural
chemicals.12,13
• Pesticides are
directly released, indoors
and outdoors, to get rid of insects, weeds
and molds. They are also incorporated
into soaps and household cleaning products,
paints, wall papers, etc. They are
also applied to carpets, textiles, and
other products prior to sale.
• Polybrominated diphenyl ethers are used
as fl ame retardants primarily in plastics,
especially polyurethane foam and high
impact polystyrene, but also in paints,
textiles and electronics.14,15
• Organotins are
used as additives for
polyvinyl chloride (PVC); as stabilizers in
PVC pips, as catalysts in the production
of rigid polyurethanes and silicones; as
fungicides and miticides in agriculture;
and as preservatives/antifoulants on
wood surfaces, in closed-circuit cooling
towers and in marine paints.16 Additives
for PVC account for about 70 percent of
organotin use.17
• Perfl uorinated surfactants: Perfl uorooctanyl
sulfate (PFOS) and perfl uorooctanoic
acid (PFOA) are used in fl oor
polishes, photographic fi lm, denture
All of these chemicals migrate, leach out
of, or
otherwise escape from consumer products
during
normal use. Most have been reported as
contaminants
in indoor air and household dust as well as
in the
breast milk, blood and other tissues of
humans.
may take in fi ve times as much dust while
their immature organs and immune system
make them more vulnerable to toxic insults.6
What are the chemical intruders in the
dust? For this study, we chose six chemical
classes for analysis beause they are all
listed
as Chemicals for Priority Action within the
OSPAR Convention. This international
convention represents 15 countries in the
North East Atlantic and includes
international
observers such as the Organization
for Economic Cooperation and Development
(OECD). The mission of the OSPAR
convention is to protect the marine
environment
through measures which include
“every endeavour to move towards the target
of the cessation of discharges, emissions
and losses of hazardous substances by the
year 2020.” OSPAR and previous international
conventions have monitored the increase
of the most hazardous chemicals in
the marine environment for almost two
decades, collected data on effects, and
continued
to advocate pollution prevention
measures within industry sectors that use
these chemicals.
These chemicals are listed as Chemical
for Priority Action because most, if not all,
are toxic in various ways. For example, all
six groups we tested include chemicals that
are endocrine disruptors or hormone
disruptors
which can cause adverse health
effects in humans and animals or their
offspring.
7 Many of the chemicals are associated
with allergic responses; suppressed or
hyperactive immune systems; impaired
respiratory,
cardiovascular; nervous, and reproductive
systems; irritated or infl amed
TVs & Computers
Electronic products
can contain
brominated fl ame
retardants (PBDEs)
which disrupt the
nervous system. American women
have the highest global levels of
PBDEs tested for in breast milk.
Electronic products and cables can
be made of PVC (vinyl) which contains
phthalates. Phthalates can be
toxic to the reproductive system and
are linked to increased incidences
of childhood asthma. PVC also uses
organotins which are toxic to the
immune and reproductive system.
Carpeting & Flooring
Kitchen and bathroom fl oors are
often made of vinyl (Polyvinyl Chloride
—PVC). Carpets can also be backed
with PVC. PVC releases phthalates,
reproductive toxins, which are linked
to increased incidences of childhood
asthma. PVC can
also contain organotins which are toxic to
the immune
and reproductive system. Carpets can contain
PBDEs,
a brominated fl ame retardant, and PFOAs, a
perfl uorinated
chemical. Both are global contaminants.
PBDEs
disrupt the nervous system and American
women have
the highest levels tested for in breast
milk. PFOAs are
highly persistent and known to cause cancer
in
animal tests.
Furniture
Furniture foam and
textiles can contain
PBDEs and PFOAs –
perfl uorinated chemicals.
Both are global
contaminants. PBDEs disrupt the
nervous system and American women
now have the highest levels tested for
in breast milk. PFOAs are highly persistent
and known to cause cancer
in animal tests.
Mattresses
Mattresses
can contain
PBDEs—a
brominated
fl ame retardant.
PBDEs are found widely
in the environment. They
disrupt the nervous system
and American women now
have the highest levels
tested for in breast milk.
Retailers
Many retailers who
sell household products
do not screen their
products for chemicals
known to present risks
to the environment or human health.
Retailers currently sell pesticides,
electronics,
rugs, furniture, and vinyl that
contain chemicals known to adversely
affect the reproductive sytem or cause
cancer in animal studies. Some retailers
have drawn up lists of prohibited chemicals
which they instruct their suppliers
to avoid but most retailers have no
chemical policy.
Personal Care/Cosmetics
Many personal
care products
(shampoo, perfume,
soap, make
up) contain and
release phthalates and alkylphenols.
Phthalates can be toxic to the reproductive
system and are linked
to increased incidences of childhood
asthma. Alkylphenols can
disrupt the hormone and reproductive
system.
Chemical
House
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 9
Pesticides
Pesticides are
used in pet
products and
applied in and
around homes for
insect control. They are also used
in carpets to prevent infestations
of insects and dust mites. Many
pesticides previously taken off
the market are still present in our
food and bodies. Many pesticides
sold today are linked to disruption
of the hormone and reproductive
system as well as being suspected
carcinogens.
Chemical
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 10
cleaners, shampoos, herbicides, insecticides,
and adhesives in a wide range of
products, as well as for surface treatment
of clothing and carpets and cookware.
PFOA is the best-known of the PFCs because
it is used to make Tefl on, Goretex,
and other oil-, water- and stain-resistant
materials used in many common items
including nonstick frying pans, utensils,
stove hoods, stainproofed carpets, furniture,
and clothes. PFOA is also used in
fi re-fi ghting foams, mining and oil well
surfactants, and the manufacture of
other fl uoropolymers.18, 19, 20, 21 PFOS is
considered to be the fi nal degradation
product of many of the commercially
used perfl uorinated chemicals and is
the predominant perfl uorinated acid
found in most environments that have
been studied.22
The majority of these chemicals are
also persistent: they don’t break down
readily in the environment, especially in
indoor environments, or in people’s bodies.
Those that do break down relatively quickly
are released into the environment in
quantities so large that they are constantly
present. For example, an adult’s body will
metabolize 50 percent of a single dose of
phthalates in about 12 hours. Nevertheless,
Hoppin et al. (2002) found little variation
in the day-to-day concentrations of phthalate
metabolites in women’s urine apparently
because of their constant daily exposure
to phthalates.23
Many of these chemicals are also
bioaccumulative:
they accumulate in the bodies
of organisms, some in fat tissues, others in
specifi c organs such as the liver and
kidney.
As a result, they build up and biomagnify
in the food chain. This means that organisms
at the top of the food chain have the
highest exposure. This includes humans,
especially the developing fetus exposed in
its mother’s womb, and the nursing infant
exposed by its mother’s breastmilk.
All of these chemicals migrate, leach
out of or otherwise escape from consumer
products during normal use and most have
been reported as contaminants in indoor
air and household dust as well as in the
breastmilk, blood and other tissues of
humans. They are also known to occur in
other media such as sewage sludge, water
resources, sediments, and freshwater and
in other living creatures, such as ocean
fi sh, birds, and marine mammals.
No one can say for sure what effects
these chemicals have on human populations.
But effects noted in animal tests and
the pervasiveness of these chemicals in our
environment give us ample warning that
we must immediately substitute these
chemicals.
The inherent hazards of these chemicals
may be contributing to the increase
in cancers and in some childhood diseases,
and to observed changes in fertility.
The degree to which these
trends can be linked to hazardous
chemicals exposure is not the
main issue. The real question is
why should we take chances when
safer chemicals and substitute
materials exist?
For example, it is estimated that nearly
12 million children (17%) in the United
States under age 18 suffer from one or more
learning, developmental, or behavioral
disabilities.
These are clearly the result of complex
interactions among chemical, genetic and
social-environmental factors that infl uence
children as they develop. But whatever the
combination of causes, the fact is that many
disabilities such as asthma, and attention
defi cit disorder are increasing among our
children.
• Asthma is the second most
prevalent
chronic condition among children. It
results in approximately 14 million days
of missed school each year. In 1980,
3.6% of children had asthma. By 1995,
the prevalence had increased to 7.5%,
or approximately 5 million children.24
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 11
Chemical Class Product Use Health Concerns
Polybrominated
diphenyl ethers
(Brominate Flame
Retardants)
PBDEs are applied to textiles or
incorporated into
plastics, foams and components of electrical
goods
to prevent or retard the spread of fi re.
They are
found in polyurethane foam products, foam
padding
in furniture, textiles, electrical
appliances, televisions
and computers.
These global contaminants persist for
long periods of time in the environment,
build up in the body, mimic thyroid
hormones,
and accumulate in breast milk.
US women have highest global levels of
these chemicals in breast milk.
Phthalates 80–90% of Phthalates are used in fl exible PVC
(vinyl) products such as wall coverings, fl
ooring,
furniture, shower curtains, clothing,
raincoats, shoes,
and toys. They are also used to make paint,
medical
equipment, pesticides, and personal care
products
such as perfume, nail polish, hairspray.
These global contaminants build up in
the body and disrupt the reproductive
system in animals studies, particularly
in male offspring. They are found in
higher concentrations in infertile men
and contribute to asthma and respiratory
problems in children.
Organotin
Compounds
Organotins are used primarily as heat and
light
stabilizers in PVC. They are found in PVC
water
pipes, PVC food packing materials, glass
coatings,
polyurethane foams and many other consumer
products.
Very poisonous even in small amounts,
these can disrupt the hormone and
reproductive
system and are toxic to the immune
system. Early life exposure in
animals can disrupt brain devlopment.
Alkylphenols Alkylphenols are used primarily as raw materials for
the manufacture of alkylphenol ethoxylates.
Alkylphenol
ethoxylates are used as non-ionic
surfactants,
emulsifi ers, lubricants or anti-oxidants in
laundry detergents, textiles, leather,
paints, disinfecting
cleaners, all-purpose cleaners, spot
removers,
hair-coloring, cosmetics, adhesives, some
plastics
and pesticides. Nonylphenol is used as a
spermicide.
These chemicals are widely recognized
to mimic natural estrogen hormones
leading to altered sexual development in
some organisms. They can affect sperm
production in mammals and may disrupt
the human immune system.
Perfl uorinated
Organics
(PFOA/PFOS)
PFOA is used to make Tefl on, Goretex, and
other
oil-, water- and stain-resistant materials
that are
used in many common items, including
nonstick
frying pans, utensils, stove hoods,
stainproofed carpets,
furniture and clothes. PFOS is thought to be
the main, fi nal degradation product of many
of
the perfl uorinated chemicals released into
the environment.
These chemicals are pervasive in the
blood of the general US population and
are now global contaminants. They are
potentially carcinogenic and caused damage
to organ function and sexual development
in lab animals. It takes over four
years to excrete half the amount of this
chemical from organs and human tissue,
therefore continuous exposure adds
high concern.
Pesticides Pesticides are applied in and around homes for
controlling infestations of various insects.
They are
applied to carpets, pre- and post-sale, to
prevent or
retard infestations of insects and dust
mites.
Pesticides are global contaminants
that can persist for long periods of time
in the environment. They can have adverse
effects on the hormone system
and be carcinogenic.
T A B L E 1
Chemicals Tested for In Dust, Their Product
Use and Health Concerns
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 12
T A B L E 2
Contaminant Groups and Their Member
Chemicals
• Attention defi cit hyperactivity disorder
(ADHD) is the most commonly diagnosed
childhood psychiatric disorder in
the United States. Recent evidence suggests
the prevalence may be as high as
17% for all school children. In effect,
the US has seen a 6-fold increase in
ADHD between the years 1985 (0.7 million
cases) and 2000 (4–5 million cases).25
The use of Ritalin, a stimulant widely
prescribed to treat hyperactivity and
attention
defi cits, has increased from 2.5
times to 5 times between 1990 and 1995.
By 2000 it was estimated that 15% of
school age children, or an estimated
8 million children, use Ritalin.26
Over the last decade, there has been a
wealth of research on changes in sexual
maturation and fertility
• It has been suggested that girls in the
United States are entering puberty earlier
than the age suggested in standard
pediatric textbooks and earlier than
previous studies.27
• A 1992 study reported a 40% decline
in sperm count over the second half of
the 20th century and generated much
controversy.28 Subsequent studies show
sperm counts have decreased signifi -
cantly in some areas and held steady
in others. There are no reports of
signifi cant increases in sperm count.
Mathematically this means there has
been an overall average decline.29
The degree to which these trends can be
linked to hazardous chemicals exposure is
not the main issue. The real question is why
should we take chances? It makes no sense
to continue to use known toxic and persistent
chemicals in commerce when safer
chemicals and substitute materials exist.
Where is our country’s innovation in safe
chemical production and sustainable
product design?
Alkylphenols and alkylphenol ethoxylates
4-nonylphenol
nonylphenol monoethoxylate
nonylphenol diethoxylate
4-octylphenol
octylphenol monoethoxylate
octylphenol diethoxylate
4-tert-methylbutylphenol
methylbutylphenol tert
Pesticides and related chemicals
chlorpyrifos
á-chlordane
(alpha-chlordane)
ă-chlordane
(gamma-chlordane)
2-bis(4-chlorophenyl)-1,1,1-trichloroethane
4,4-DDT
diazinon
dicofol + 4,4’-dichlorobenzophenone
(breakdown product)
dieldrin
methoxychlor
pentachloronitrobenzene
pentachlorophenol
cis-permethrin permethrin cis
trans-permethrin permethrin trans
piperonyl butoxide
propoxur
Perfl uorinated chemicals
perfl uorooctanoic acid
perfl uorooctanyl sulfonate
Phthalate esters
dimethyl phthalate
diethyl phthalate
di-n-propyl phthalate propyl
phthalate n
diisobutyl phthalate
di-n-butyl phthalate butyl
phthalate n
butylbenzyl phthalate
di(2-ethylhexyl) phthalate
[bis(2-ethylhexyl)phthalate]
Polybrominated diphenyl ethers (PBDEs)
2,2’,4,4’-tetrabromodiphenyl ether (BDE 47)
2,2’4,4’,5-pentabromodiphenyl ether (BDE 99)
2,2’,4,4’,6-pentabromodiphenyl ether (BDE 100)
2,2’, 4,4’, 5,5’-hexabromodiphenyl ether (BDE
153)
2,2’,4,4’5,6’-hexabromodiphenyl ether (BDE
154)
2,2’,3,4,4’,5’,6-heptabromodiphenyl ether (BDE
183)
decabromodiphenyl ether (BDE 209)
Organotins
monobutyltin
dibutyltin
tributyltin
tetrabutyltin
dioctyltin
tricyclohexyltin
triphenyltin
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 13
W H A T W E F O U N D
To investigate the presence of
hazardous chemicals in common
house dust we took dust samples
from vacuum bags in ten homes
in each of seven states (California, Maine,
Massachusetts, Michigan, New York, Oregon,
and Washington) to analyze for six classes
of well known hazardous chemicals. In all
samples 44 chemicals were tested for:
• seven phthalate esters,
• seven polybrominated diphenyl ethers
(PBDEs),
• 14 pesticides (including
pentachlorophenol),
• seven alkylphenol compounds,
• seven organotin compounds, and
• two perfl uorinated chemicals.
To our knowledge, the results presented
in this study for organotins and perfl
uorinated
chemicals are the fi rst to be reported
for dust collected from U.S. homes.
House dust is an important indicator of
indoor semi-volatile and non-volatile
contaminants.
30 It is also a very heterogeneous
material. Concentrations of chemical
contaminants
in house dust can vary dramatically
from home to home, room to room,
season to season, with frequency and
intensity
of cleaning, with the type of fl ooring,
etc.31,32,33,34 Consequently, it is not
surprising
that the concentrations of each of the
contaminant
groups and their member chemicals
varied considerably in this study, as
shown in Tables 3 and 4.
Thirty-fi ve of the 44 target chemicals
were measured in one or more of the seven
composite dust samples. In addition to
these target chemicals, it is virtually
certain
that many other toxic contaminants, such
as linear alkylbenzene sulfonates,35 polyaromatic
hydrocarbons (PAHs), heavy metals,36
dioxins,37 PCBs,38,39 etc., were present in
these samples and would have been detected
if they had been tested for in dust samples.
These chemicals have been detected in
other house dust studies.
The average contribution of each of the
six contaminant groups to the total
concentration
of target contaminants in the dust
is shown in Figure 1. In each of the seven
dust samples, phthalates were highest in
concentration, followed, in descending order,
by alkylphenols, pesticides, polybrominated
diphenyl ethers (PBDEs), organotins
and perfl uorinated chemicals.
Total Concentration
µg/g, parts per million (ppm)
Contaminant Group Maximum Minimum Average
Phthalate esters 552 294 424
Alkylphenols and alkylphenol ethoxylates 51.4
14.6 26.7
Pesticides 33.9 5.7 12.6
Polybrominated diphenyl ethers 12.5 3.6 8.9
Organotins 0.911 0.388 0.631
T A B L E 3
Summary of Analytical Results by
Contaminant Group, Across All Samples
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 14
Occurrence
Average
concentration
Minimum
concentration
Maximum
concentration
ěg/g, parts per million
(ppm)
Phthalates
dimethyl phthalate 1/7 0.038* <rl 0.272
diethyl phthalate 7/7 1.41 0.74 3.58
di-n-propyl phthalate 0/7 <rl <rl <rl
diisobutyl phthalate 7/7 3.79 1.61 8.35
di-n-butyl phthalate 7/7 20.15 7.80 49.5
butylbenzyl phthalate 7/7 69.37 42.1 137
di(2-ethylhexyl) phthalate 7/7 329.45 215 425
Alkylphenols
4-Nonylphenol 7/7 5.141 3.740 10.500
Nonylphenol monoethoxylate 7/7 7.611 3.720
14.800
Nonylphenol diethoxylate 7/7 9.890 5.850
17.900
4-Octylphenol 0/7 <rl <rl <rl
Octylphenol monoethoxylate 7/7 1.003 0.394
3.410
Octylphenol diethoxylate 7/7 1.870 0.395 8.550
4-t-methylbutylphenol 7/7 0.373 0.154 0.962
Pesticides
4,4’-DDT 7/7 0.504 0.0913 1.89
alpha-chlordane 1/7 0.020* <rl 0.138
gamma-chlordane 1/7 0.020* <rl 0.140
chlorpyrifos 1/7 0.029* <rl 0.205
diazinon 0/7 <rl <rl <rl
dicofol 0/7 <rl <rl <rl
dieldrin 1/7 0.103 <rl 0.720
methoxychlor 4/7 0.191 <rl 0.532
pentachloronitrobenzene 0/7 <rl <rl
<rl
pentachlorophenol 7/7 1.246 0.0481 7.310
cis-permethrin 7/7 3.34 0.607 11.6
trans-permethrin 7/7 6.41 1.30 21.0
piperonyl butoxide 7/7 0.69 0.147 2.18
propoxur 2/7 0.037* <rl 0.13
T A B L E 4
Summary Analytical Results for Individual
Contaminants in All Samples
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 15
Polybrominated Diphenyl Ethers
TetraBDE (BDE 47) 7/7 2.10 0.550 5.24
PentaBDE (BDE 99) 7/7 1.70 0.474 4.129
PentaBDE (BDE 100) 4/7 0.259 <rl 0.762
HexaBDE (BDE 153) 2/7 0.314 <rl 0.376
HexaBDE (BDE 154) 2/7 0.278 <rl 0.325
HeptaBDE (BDE 183) 0/7 <rl <rl <rl
DecBDE (BDE 209) 7/7 4.66 0.901 10.0
Organotins
Monobutyltin 7/7 0.2063 0.1060 0.3614
Dibutyltin 7/7 0.2493 0.1158 0.3215
Tributyltin 7/7 0.0798 0.0447 0.1931
Tetrabutyltin 0/7 <rl <rl <rl
Di-n-octyltin 7/7 0.1096 0.0717 0.1985
Tricyclohexyltin 0/7 <rl <rl <rl
Triphenyltin 0/7 <rl <rl <rl
Perfl uorinated Chemicals
Perfl uorooctanoic acid 7/7 0.0787 0.0185
0.2051
Perfl uorooctanyl sulfonate 7/7 0.4244 0.0764
1.1709
* The mean value cannot be regarded as representative with such a
small number of determinations.
<rl = less than limit of quantifi cation
F I G U R E 1
Average Contribution of Each
Group of Chemical Contaminants
in the Total Concentration of
All Chemicals Tested for in Seven
Composite House dust Samples Phthalates
89.6%
Alkylphenols
5.6%
Pesticides
2.6%
Polybrominated
Diphenyl Ethers
1.9%
Organotins
0.13%
Perfluorinated
Chemicals
0.10%
Note: This graph represents only the
contributions of the six categories
of chemicals tested in this study to
the sum total concentration of all 44
chemicals detected. The percentages
are not an indication of content in
total dust quantity nor of all chemicals
potentially present in house dust.
Occurrence
Average
concentration
Minimum
concentration
Maximum
concentration
ěg/g, parts per million
(ppm)
T A B L E 4
Summary Analytical Results for Individual
Contaminants in All Samples CONTINUED
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 16
Phthalates
Five of the seven phthalates selected for
analysis
were present at quantifi able concentrations
in all of the dust samples, as shown in
Table 3.
Phthalates are used primarily as plasticizers
for polyvinyl chloride (PVC) plastic,
commonly known as vinyl. Most phthalates
(80–90%) are used in vinyl products from
which they continuously off-gas. On average,
DEHP accounted for 78 percent of the total
concentration of the target phthalates in
the dust samples and 69 percent of the total
concentration of the 44 contaminants.
DEHP is present in PVC (vinyl) products
such as wall coverings, tablecloths, fl oor
tiles,
furniture upholstery, shower curtains, garden
hoses, swimming pool liners, rainwear,
baby pants, dolls, some toys, shoes,
automobile
upholstery and tops, packaging fi lm
and sheets, sheathing for wire and cable,
medical tubing, and blood storage bags.
450
400
350
300
250
200
150
100
50
0
µg/g, parts per pillion
(ppm)
FIGURE 2
Occurrence of Phthalates in All Dust
Samples:
The Minimum and Maximum Concentrations Are
Indicated by the Range Bar
di-n-propyl phthalate
diethyl phthalate
dimethyl phthalate
diisobutyl phthalate
di-n-butyl phthalate
butylbenzyl phthalate
di(2-ethylhexyl) phthalate
Maximum
Mean
Minimum
� PVC is neither a biological nor technical nutrient.
It is a nightmare.�
Michael Braungart, Director, McDonough
Braungart
Design Chemistry and EPA Green Chemistry
Award Winner
quoted in Healthy Building News. March, 2005
The remaining small share of phthalates
(that not added to PVC) is used in personal
care products such as skin creams,
hairsprays,
lotions, nail polish, and fragrances, and in
a variety of other products including
adhesives,
caulks, detergents, electrical capacitors,
inks, solvents, lubricating oils, paints, and
pharmaceuticals.
While environmental releases of industrial
chemicals are most commonly associated
with their manufacture and disposal,
it is estimated that more than 75 percent
of phthalate releases to the environment
occurs during the use of products that
contain phthalates. DEHP releases to air
from PVC fl ooring, for example, have been
documented.
• Children exposed to household dust with
the greatest concentations of DEHP were
more likely to have asthma than children
exposed to the lowest concentrations of
that phthalate.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 17
700
600
500
400
300
200
100
0
micrograms/gram (ug/g),
parts per million (ppm)
FIGURE 3
Phthalates — Mean Concentrations of Target
Pthalates in House Dust
in this study and those reported by Al
Bitar (2004), Costner et al. (2004),
Rudel et al. (2003), and Santillo et al.
(2003)
Mean, 7
samples
Belgium Brazil Cape Cod,
MA
UK
di(2-ethylhexyl)
phthalate
butylbenzyl
di-n-butyl phthalate
diisobutyl phthalate
di-n-propyl phthalate
diethyl phthalate
dimethyl phthalate
• Exposure to phthalates has also been
associated with premature breast development
in female children. A study on
premature breast development in female
children aged 6 months to 8 years found
phthalate esters in 68% of serum samples
from the patients.
• Phthalates have also been linked to
deteriorated
semen quality, low sperm counts,
and poor sperm morphology in men. In
a study, concentration of phthalate esters
was signifi cantly higher in
infertile men compared with
controls. Phthalates may be
instrumental in the deterioration
of semen quality in
infertile men.
• Animal studies have found
that phthalates pass from
the mother through the
placenta to the fetus, and
through breastmilk to the
newborn.
For a summary of occurrence
and more detailed information
and referenced discussion on
health effects, see Appendix I.
30
25
20
15
10
5
0
micrograms/gram (ug/g),
parts per million (ppm)
FIGURE 4
Alkylphenols and Alkylphenol Ethoxylates —
Mean Concentrations
of Target Compounds in House Dust in this
study and those reported
by Rudel et al. (2003)
Mean
7 Samples
Cape Cod,
MA
4-t-mehylbutylphenol
Octylphenol
diethoxylate
Octylphenol
monoethoxylate
4-Octylphenol
Nonylphenol
diethoxylate
Nonylphenol
monoethoxylate
4-Nonylphenol
Alkylphenols
All seven alkylphenols and alkylphenol
ethoxylates
selected for analysis were detected
in all samples. A summary of occurrence
and effects is given below.
Alkylphenols (APs) are used primarily as
raw materials for the manufacture of
alkylphenol
ethoxylates (APEs).
The major uses of APEs are as industrial
and institutional cleaning products and
household
cleaning products. They are also used
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 18
in paper and pulp production and de-inking
agents in paper recycling; emulsifying agents
in latex paints, pesticide and herbicide
formulations,
and fi berglass and polystyrene
products; as additives in cosmetics and in
polyvinyl chloride used for food packaging;
fl otation agents, industrial cleaners, cold
cleaners for cars, and in the textile
industry.
Nonylphenol (NP) is the active ingredient
in spermicides and NP or a derivative is also
apparently used in food wrapping fi lms,
foodcontacting
plastics, and some toys, because
the chemical has been found to leach from
these materials and products.
Nonylphenol is regarded as a ubiquitous
environmental contaminant. Nonylphenol
has also been detected in umbilical cords in
Japan confi rming that this chemical is
passed from the mother to the developing
fetus through the placenta. A very recent
study in Germany has found nonylphenol
in breastmilk confi rming that this chemical
also passes from mother to nursing infant.
• The most widely recognized hazard associated
with alkylphenols is their ability to
mimic natural estrogen hormones. The
estrogenicity of alkylphenols has been
known for years. As estrogenic compounds,
alkylphenols have been shown
to reduce testicular function in rats
potentially
leading to altered sexual development.
This may have implications for
other organisms as well.
• Preliminary studies suggest that
nonylphenol
may also disrupt the human
immune system.
For a more detailed and referenced discussion
see Appendix I.
� We have now acqired a fateful power to alter and
destroy nature. But man is a part of
nature, and his war
against nature is inevitably a war
against himself.�
Rachel Carson, author of Silent Spring, who
fi rst raised
awareness of the toxicity and persistence of
DDT pesticides,
quoted on CBS News, 1964
Pesticides
This group of target chemicals included
eleven pesticides and one synergist
(piperonyl
butoxide). Each of the dust samples
contained quantifi able concentrations of
fi ve compounds: 4,4’-DDT, pentachlorophenol,
cis-permethrin, trans-permethrin, and
piperonyl butoxide. A summary of occurrence
and effects is given below. For a
more detailed and referenced discussion
see Appendix I.
Permethrin
Permethrin, a synthetic pyrethroid, is used
to kill pest insects in agriculture, home
pest
control, forestry, and in public health
programs,
including head lice control. It was
fi rst marketed in 1973. Worldwide, the
dominant
use of permethrin is on cotton, accounting
for about 60 percent (by weight)
of the permethrin used. In the U.S., almost
70 percent of the permethrin used in
agriculture
is used on corn, wheat, and alfalfa
It is widely used in U.S. homes, yards and
gardens. Permethrin, like all synthetic pyreS
A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S F
O R A H E A L T H Y H O M E 19
30
25
20
15
10
5
0
micrograms/gram (ug/g), parts per million
(ppm)
FIGURE 5
Pesticides — Mean Concentrations of
Targeted Pesticides in House
Dust in this study and those reported by
Rudel et al. (2003)
Mean
7 Samples
Cape Cod,
MA
piperonyl butoxide
trans-permethrin
cis-permethrin
pentachlorophenol
pentachloronitrobenzane
methoxychlor
dieldrin
dicofol
diazinon
chlorpyrifos
gamma-chlordane
throids, kills insects by strongly exciting
their nervous systems.
Because of its ubiquitous use, the Food
and Drug Administration’s monitoring program
routinely fi nds permethrin on food.
In 2001, it was the 8th most commonly
detected
pesticide with DDT being number 1,
despite DDT being banned in 1972.
• The immune system appears to be a sensitive
target for permethrin activity.
• Permethrin also affects both male and
female reproductive systems.
• According to the EPA, permethrin is a
possible human carcinogen. The EPA
found that permethrin increased the frequency
of lung tumors in female mice,
and increased the frequency of liver tumors
in male and female mice.
Piperonyl butoxide
Piperonyl butoxide is used in formulations
of permethrin, other pyrethrins and
pyrethroids
as a synergist to increase the effectiveness
of the insecticides. As such, it is
sometimes relied upon as an indicator of
the presence of permethrin and other
pyrethroids.
It does not, by itself have pesticidal
properties. However, when added to insecticide
mixtures their potency is increased
considerably
• The US EPA has classifi ed piperonyl
butoxide
as a possible human carcinogen.
Pentachlorophenol
In the U.S., most exposure to
pentachlorophenol
(PCP) comes from its past use on
treated wood and soil. From 1987 to 1993,
the EPA recorded releases of PCP to land
and water, mostly from treated wood and
military munitions factories, totaling nearly
100,000 pounds. PCP has been limited since
1984 to use by certifi ed applicators for
certain
purposes. It is still used as a preservative
on wooden utility poles, railroad ties and
wharf pilings. It is also still used in
California,
mostly on almonds and structural
pest control.
In 2001, DDT was
the most commonly
detected pesticide
on food despite being
banned in 1972.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 20
• The EPA has determined that
pentachlorophenol
is a probable human carcinogen
and the International Agency for Cancer
Research classifi es it as possibly carcinogenic
to humans.
DDT
DDT is no longer registered for use in the
United States. However, it is still used in
other (primarily tropical) countries for
malaria
control. It is classifi ed in EPA’s Toxicity
Class II, moderately toxic. DDT was banned
from use in the United States in 1972, and
remains banned barring public health
emergency (e.g., outbreak of malaria).
Because of its ubiquitous past use, the
Food and Drug Administration’s monitoring
program routinely fi nds DDT on food.
In 2001, it was the most commonly detected
pesticide. In a recent body burden study by
the Centers for Disease Control and
Prevention
(CDC), scientists found DDT in blood
of 99% of those sampled—the highest incidence
of any pesticide sampled.
Of the quantity of the pesticide used in
1970–72, over 80 percent was applied to
cotton
crops, with the remainder being used
predominantly on peanut and soybean
crops. The decline in DDT usage was the
result of increased insect resistance; the
development
of more effective alternative pesticides;
and growing public concern over
adverse environmental side effects. DDT is
not metabolized very rapidly by animals; it
is deposited and stored in the fatty tissues.
The biological half-life of DDT is about
eight
years and is still a ubiquitous contaminant.
• DDT and its breakdown products are
considered hormone disruptors.
• The Centers for Disease Control have
reported a relation between DDT and
the likelihood of preterm birth.
Polybrominated
Diphenyl Ethers (PBDEs)
Three of the seven PBDEs that were selected
for analysis—BDE 47, BDE 99, and BDE
209—were present at quantifi able
concentrations
in all dust samples. As shown in
Figures 6 and 7, the decabrominated diphenyl
ether, BDE 209, predominated in our
samples and had the highest mean
concentration,
followed by BDE 47 and BDE 99.
On average, these three PBDEs accounted
for 95 percent of the total concentration
of this contaminant group. A summary of
occurrence and effects is given below. For
a more detailed and referenced discussion
see Appendix I.
More than 70 brominated chemicals
or groups of chemicals are used as fl ame
retardants in plastics, textiles and other
materials. Polybrominated diphenyl ethers
(PBDEs) are one of the three groups that
dominate the market for fl ame retardants.
PBDEs are applied to or incorporated into
many common household products, such as
furniture, carpeting, mattresses,
televisions,
coffee makers and hair dryers.
Decabromodiphenyl
ether (Deca-BDE or BDE 209) is
most commonly used in plastics and textiles,
Of the quantity
of DDT used in
1970–72, over
80 percent
was applied to
cotton crops.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 21
BDE 99
(a pentaBDE)
19%
BDE 47
(a tetraBDE)
24%
BDE 100
(a pentaBDE)
3%
BDE 153
(a hexaBDE)
1%
BDE 154
(a hexaBDE)
1%
BDE 209
(DecaBDE)
52%
12
10
8
6
4
2
0
micrograms/gram (ug/g),
parts per million (ppm)
FIGURE 7
Polybrominated Diphenyl Ethers — Mean
Concentrations of Target PBDEs
in House Dust in this study and those
reported by Al Bitar (2004), Rudel et al.
(2003), Santillo et al. (2003), and
Stapleton et al. (2005)
Mean,
7 samples
Belgium Cape Cod,
MA
UK Washington,
D.C.
DecaBDE (BDE 209)
HeptaBDE (BDE 183)
HexaBDE (BDE 154)
HexaBDE (BDE 153)
PentaBDE (BDE 100)
PentaBDE (BDE 99)
TetraBDE (BDE 47)
F I G U R E 6
Contributions of Individual PBDEs to
Total PBDE Concentration, Across All
Samples
in electrical components and in styrene
rubbers used in carpet backing and furniture.
Sunlight and UV light can degrade
BDE 209 to form less brominated BDEs,
such as the pentabromodiphenyl ethers
(penta-BDEs).
PBDEs have been found in air, water,
fi sh, birds, marine mammals, and humans
In many cases, their concentrations are
increasing
over time. Diet is regarded as the
most likely route of PBDE exposure for the
general population. However, air inside
homes and offi ces can carry PBDE
concentrations
that are estimated to be almost ten
times higher than levels in the air outside
the buildings. Moreover, house dust has
been identifi ed as an important pathway
of PBDE exposure for young children.
Studies of breast milk in the U.S. have
found PBDE concentrations from 10 to more
than 100 times higher than those in Europe.
Moreover, contrary to claims by PBDE
producers that BDE 209 (deca) is neither
mobile nor bioavailable, recent studies have
identifi ed BDE 209 in 20 to 80 percent of
breast milk samples. A recent study indicates
that PBDEs in Swedish breast milk began to
decrease in 1997, possibly due to a voluntary
phase-out of penta-BDE. BDE 209 has also
been identifi ed as the dominant PBDE in
several U.S. food groups.
• In studies with laboratory animals, mice
and rats exposed to one or more PBDEs
have shown a wide variety of effects
including
evidence of hormone disruption,
reproductive/developmental toxicity including
neurotoxicity, and cancer.
• Common metabolites of the PBDEs are
reported to compete strongly with the
thyroid hormone, thyroxin, raising the
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 22
potential for a broad range of effects on
growth and development, including permanent
neurobehavioral impacts, comparable
to the thyroid disrupting effects
of PCBs.
• Laboratory animals exposed to PBDEs
during the period immediately before or
after birth exhibited behavioral changes
when they reached adulthood. These
changes included marked hyperactivity
and learning and memory defi cits
• During exposure in newborn mice
PBDEs, including BDE 209, have been
shown to distribute throughout the body
and concentrate in the brain. They induce
developmental neurotoxic effects
in adult mice that worsen with age and
lead to abnormal behaviour.
� At pharmacologic levels, butyltins might
contribute to the onset of
developmental disorders
of the male reproductive system.�
Doering at al. (2002)
Organotins
Of the seven organotins analyzed, four
were quantifi ed in all samples:
monobutyltin,
dibutyltin, tributyltin, and di-n-octyltin.
To our knowledge this is the fi rst study to
analyze for organotins in household dust
in the US. A summary of occurrence and
effects is given below. For a more detailed
and referenced discussion see Appendix I.
Major use of organotins began some 40
years ago in parallel with mass production
nanograms/gram (ng/g),
parts per billion (ppb)
FIGURE 8
Organotins — Mean Concentrations of Target
Organotins in House Dust
Samples from this study and those reported
by Al Bitar (2004), Costner et al.
(2004), and Fromme et al. (2005)
Triphenyltin
Tricyclohexyltin
Di-n-octyltin
Tributyltin
Dibutyltin
Monobutyltin
2500
2000
1500
1000
500
0
Mean,
7 samples
Belgium Brazil Germany
of PVC plastic (vinyl). Between 1955 and
1992, organotin production increased by
a factor of ten and reached about 40,000
metric tons per year in 1996. Mono- and
dialkyltins account for 81 percent of total
organotin use: 76 percent used as heat and
light stabilizers for PVC and 5 percent as
catalysts for polyurethane and silicone elastomers.
The remaining organotin uses consist
mainly of tributyl-, triphenyl- and
tricyclohexyltin,
about 10 percent of which is
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 23
used as antifouling biocides, and 8 percent
as pesticides.
Organotins are found in PVC water pipes,
PVC food packing materials, glass coatings
and polyurethane foams. Other uses, mainly
of butyltin, include rigid PVC profi les and
sidings, venetian blinds, rain gutters,
window
profi les and, in particular in the U.S.,
building sidings. Organotins also occur in
textile products that contain polymer parts,
such as t-shirts with prints, sanitary
napkins,
bandaids and diapers. They are used as
fungicides
on textiles that are exposed to extreme
conditions such as canvas.
Organotins were found in 50 percent
of ordinary plastic products purchased in a
Japanese supermarket—diaper covers, sanitary
napkins, polyurethane gloves, cellophane
wrap, dishwashing sponges and baking
parchments.
Organotins were also found in the
cookies baked on the parchment. Another
study in Japan found organotins in children’s
PVC toys—face masks, balls, soft toys and
food toys. Organotins have also been detected
in drinking water transported through
PVC pipes. Elevated levels of organotins,
particularly tributyltin, have also been
found in PVC fl ooring and, at somewhat
lower concentrations, in carpets.
Organotins are found widely in the
environment.
They have been detected in air
and precipitation, freshwater resources,
ocean water, soils and sediments. Organotins,
particularly tributyltin (TBT), have
been identifi ed in many species including
mollusks, fi sh, marine and freshwater birds,
marine mammals,as well as various terrestrial
mammals.
• Organotins are toxic at relatively low
levels of exposure and fi ndings suggest
that chronic, low-level exposure to
dibutyltins
(DBT) in human populations may
have toxic impacts on both the immune
and nervous systems. At lower doses, triphenyltins
(TPT) exposure during pregnancy
resulted in behavioral changes in
the offspring.
• Tributyltins (TBT) and triphenyltins
(TPT) are all listed as poisons and described
as respiratory toxins, fetotoxins,
reproductive toxins, immunotoxins, possible
carcinogens, skin and respiratory
irritants, and allergens.
• Organotins are known to damage the
immune system in mammals. They are
transported through the placenta, as
demonstrated by their adverse developmental
effects
• In a 1999 study, organotins were tested
in the blood of people living in Michigan:
monobutyltin (MBT) was present in 53
percent of the samples; dibutyltin (DBT),
81 percent; and tributyltin (TBT), 70
percent.
• DBT is neurotoxic to mammalian brain
cells and has been shown to cause toxic
effects on the immune system at
concentrations
comparable to those reported in
human blood. DBT had neurotoxic effects
at levels that were lower than those
reported in human blood and some forty
times lower than the lowest toxic
concentration
of trimeth-yltin, a known neurotoxicant.
Organotins are found in PVC water pipes, PVC
food packing
materials, glass coatings and polyurethane
foams.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 24
Perfl uorinated Chemicals
(PFOS and PFOA)
All dust samples contained quantifi able
concentrations of the two target perfl
uorinated
chemicals—perfl uorooctanoic acid
(PFOA) and perfl uorooctanyl sulfonate
(PFOS). PFOS concentrations were highest
in all samples, with a mean of 424 ppm and
a range of 76.4 to 1,170 ppm, while the mean
concentration of PFOA was 78.7 ppm with
a range of 18.5 to 205 ppm. To our knowl-
600
500
400
300
200
100
0
nanograms/gram (ng/g), parts per billion (ppb)
FIGURE 9
Perfluorinated Chemicals — Mean
concentrations of
Perfluorooctanyl Sulfonate (PFOS) and
Perfluoroctanoic
Acid (PFOA) in House Dust in this study and
those
reported by Moriwaki et al. (2003)
Mean
7 Samples
Japan
PFOS
PFOA
� PFOA is detectable in the blood of most humans
and animals worldwide, which is
problematic because
it is only slowly eliminated in
mammals, is potentially
toxic, has no known metabolic or
environmental degradation
pathway, and is potentially
carcinogenic.�
Ellis et al. 2005
edge this is the fi rst study to detect PFOA
and PFOS in household dust in the US. A
summary of occurrence and effects is given
below. For a more detailed and referenced
discussion see Appendix I.
The two perfl uorinated chemicals (PFCs)
that were selected for analysis in our study
are only two of the already quite large and
still growing number of perfl uorinated
chemicals
(PFCs) that are manufactured and/or
found in the environment. PFOA is the
bestknown
of the PFCs because it is used to make
Tefl on, Goretex, and other oil-, water- and
stain-resistant materials that are used in
many common items, including nonstick
frying pans, utensils, stove hoods,
stainproofed
carpets, furniture, and clothes.
PFOA and PFOS may also be formed as
products of the degradation of other PFCs.
Polytetrafl uoroethylene (PTFE) also
known as polyvinyl fl uoride, is commonly is
commonly uoride
marketed as Tefl on. This use accounted
for 60–65 percent of all fl uoropolymer
consumption in the US., Western Europe
and Japan in 2001.
These chemicals are used in soil, stain,
grease, and water-resistant coatings for
textiles,
carpet, cookware and automobiles.
PFOA is also used widely in fi re-fi ghting
foams. PFOS has been used in refrigerants,
surfactants, polymers, pharmaceuticals, fl
ame
retardants, lubricants, adhesives, cosmetics,
paper coatings, and insecticides. The U.S.
manufacturer, 3M, discontinued PFOS
production in 2000.
PFCs are pervasive contaminants in the
global environment. PFOS and other PFCs
are found in freshwater and marine mammals,
fi sh, birds, shellfi sh, and domestic
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 25
cattle. Although contamination is global,
including remote locations in the Arctic
and North Pacifi c Oceans, concentrations
of PFCs are relatively greater in or near the
more populated and industrial regions.
• A number of studies have found PFCs to
be pervasive contaminants in the blood
of the general population of the U.S.
• It was known as early as 1975 that fumes
from hot pans coated with Tefl on
(polytetrafl
uoroethylene (PTFE) can kill
pet birds. Broiler chicks have died after
exposure to polytetrafl uoroethylenecoated
light bulbs.
• Exposed to PFOS, female rats showed
loss of appetite, interrupted estrus cycles,
and elevated stress hormone levels. PFOS
was found to accumulate in brain tissue,
particularly the hypothalamus, suggesting
that PFOS crosses the blood-brain
barrier and may interfere with reproductive
hormones.
• One recent review noted that studies in
monkeys, rats, fi sh and humans have
found that subchronic exposure to PFOS
led to signifi cant weight loss, reduced
serum cholesterol, and reduced thyroid
hormones.
• In rats, rabbits and mice, developmental
effects of exposure to PFCs include reduced
fetal weight, cleft palate, delayed
ossifi cation of bones and cardiac
abnormalities.
• Recent laboratory studies with PFOA
involving
rats have shown low birth weight,
small pituitary gland, altered maternal
care behavior, high pup mortality, and
signifi cant changes in the brain, liver,
spleen, thymus, adrenal gland, kidney,
prostate, and testes.
Breastfeeding Is Still Best for Baby
Breastmilk is one of the most important
contributors to infant health.
—US Surgeon General
While many of the chemicals we found in house
dust
have also been detected in human breast milk,
this should
not discourage mothers from
breastfeeding.
Breast milk is a good indicator
of the chemicals the fetus
is exposed to during pregnancy.
Because of the high
fat content of breast milk,
some chemicals can be more
easily detected in breast milk
than in blood. PBDEs, for example
are fat-loving chemicals
that would require a much
larger quantity of blood than
breast milk to obtain an accurate measurement.
Most doctors agree that the benefi ts of
breastfeeding
are crucial to the developing infant. Breast
milk is the
best nutrition for infants. It also provides
important
hormones, protective immune factors, and
promoters
for the development of the brain and nervous
system.
Breastfeeding also reduces the incidence of
anemia
and some gynecologic cancers in women,
including
premenopausal breast cancer.
Formula feeding does not eliminate children’s
exposure
to toxic chemicals. Children are exposed to signifi
cant
levels of chemicals, regardless of whether
they are breastfed,
through food, the household environment, and
from
contaminants that cross the placenta while a
fetus is
still developing.
Exposures to chemicals during pregnancy
generate
more concerns than have exposures through
breastfeeding.
Chemical exposures before birth have been
shown
to have adverse health effects, but common
exposures
through breastfeeding have not been shown to
cause
harm.
For more information, see Why breastfeeding is best
for babies?
by Physicians for Social Responsibility by
Physicians for Social Responsibility http://psr.igc.org/BFeasyeng2pg.10.18.pdf.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 26
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 27
W H Y O U R R E G U L A T O R Y S Y S T E M I S F A I L I N G U S
� ...it seems to me that if you wait until all the frogs
and toads have croaked their last to
take some action,
you’ve missed the point...�
One Frog Can Make a Difference—Kermit’s
Guide to Life in the 90’s
R.P. Riger, Jim Henson Productions Inc. 1993
The previous sections have documented
the inherent hazards of
six widely used chemical classes.
Most of these chemicals are still
used in products today. Even those that have
been restricted, such as DDT, will remain in
the environment for decades to come due
to their persistence and bioaccumulation.
But what about the known hazardous chemicals
that are legally allowed to be used in
everyday products and that end up in our
air, water, food, household dust, and bodies?
Why are manufacturers putting toxic
chemicals in and on the products they sell
for household and personal use when, sooner
or later, those chemicals can become
household
contaminants that threaten the health
of their customers? And why do hazardous
chemicals continue to be used in products
when safer, feasible alternatives exist?
Surveys show that most people believe
that chemicals contained in the products
they buy every day have been tested and
shown to be safe or government would not
allow them to be sold.40 Unfortunately, the
reality is far from this perception.
The problem rests in our current chemical
regulatory system—the high burdens it
places on government agencies to take action
to protect health as well as the lack of
incentives
to develop safer chemicals and
products.
How did this situation arise and why is
our government doing nothing to rectify
this worrying state of affairs? The growth
of the chemical industry after World War II
saw the proliferation of a wide range of
synthetic
chemicals, which were, for the most
part, unregulated.
It was only in the late 1970s that the
federal government enacted the Toxics
Substance
Control Act (TSCA) to regulate industrial
chemicals used in commerce. The
law provided authority
to the U.S. EPA to
require health and
use data on chemicals
in commerce, to review
applications for
new chemicals coming
on to the market,
and to control chemicals
that may be dangerous
to health or
the environment. Unfortunately, those
chemicals that were on the market prior to
1979—amounting to more than 99% by volume
of the chemicals on the market today
—were considered automatically “registered”
and reviewed—in other words, safe until
proven dangerous. For the EPA to restrict
one of these chemicals (all of the industrial
chemicals reviewed in this report were on
the market prior to 1979), the EPA must
demonstrate that there is a signifi cant risk
to health, that the benefi ts of regulation
(for health) outweigh the costs to industry,
and that they are chosing the least
burdensome
form of regulation to meet a goal.
When the EPA tried to severly restrict
the sale of asbestos in 1990, after ten years
of research, the 5th Circuit Court of Appeals
struck down EPA’s regulation stating that
they had not reached the threshold for
Surveys show that most people
believe that chemicals contained in
the products they buy every day have
been tested and shown to be safe or
government would not allow them
to be sold. Unfortunately, the reality
is far from this perception.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 28
requiring a phase-out of this known toxic
material. Because of these burdens, it is
nearly impossible for the EPA to restrict
chemicals on the market. As such, the EPA
has restricted fewer than 10 chemicals in
25 years.
Even data collection activities for existing
chemicals have been limited. In 1998, the
U.S. EPA published a report demonstrating
analyses in Europe have shown a severe lack
of information on chemical use and toxicity
throughout product supply chains, such
that chemical manufacturers may not even
know how their chemicals are being used.
For new chemicals coming on the market
since 1979, companies must complete
a “pre-manufacture notifi cation” including
information on the chemical and any
toxicological,
use, or exposure information that
may be available. The EPA has an opportunity
to review this information at the premanufacture
stage (before any marketing
has occurred). This pre-manufacture review
allows the EPA to raise concerns about
chemicals
before they are produced and funds
spent on marketing and manufacturing.
However,
because no actual testing is required
for new chemicals, the EPA is often required
to review these chemicals on the basis of
computer models. And because no additional
testing is required of new chemicals
as their production is initiated and
increased,
once those new chemicals reach the market,
EPA’s power to regulate them is greatly
diminished.
A similar situation exists in pesticide
regulation.
American and international agencies
have established maximum exposure
levels, above which they recognize signifi
cant
cause for concern about increased risk of
both cancer and non-cancer effects. While
there are some differences in the thresholds
established by different health and
environmental
agencies, the levels of exposure triggering
concern are generally extremely low.
These “acceptable” levels are not necessarily
safe because they are determined in
toxicity tests that consider only single
chemicals.
In the real world, we are exposed to
a multitude of chemicals simultaneously.
In fact, most pesticides are sold as
mixtures.
Thus, toxicity studies of the effects of
individual
chemicals on laboratory animals can
never be truly representative of actual
exposures.
In addition, many studies do not take
into account special periods of vulnerability
such as childhood or pregnancy, where a
single, very low dose of a chemical at a
certain
time could cause permanent damage
to the fetus or developing child.41
that over 93% of high production volume
chemicals (those produced over one million
pounds per year) lacked some basic screening
level health data. As a result of this report
and another by the Environmental Defense
Fund, the chemical industry
entered into a voluntary
initiative, called
the High Production
Volume Chemical Challenge.
This effort will
provide substantial basic
toxicological data for a
large percentage of the
2800 chemicals produced
over one million pounds per year.
Nonetheless,
the data being collected by industry does
not address many health effects of concern.
The voluntary program does not cover the
more than 6,000 chemicals currently used
annually in quantities between 10,000
and 1 million pounds.
Further, it does not include exposure
data and information on how chemicals are
used throughout supply chains, which is
critical for prevention efforts. Industry
The lack of power to
regulate existing chemicals
provides a strong
disincentive for manufacturers
to develop
safer chemicals.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 29
Alaska
The Anchorage School District bans the use
of pesticides linked to health or
environmental
damage
California
Penta-BDE and Octa-BDE to be banned.
PROP 65 demands labeling of CMRs for consumer
products. Banned pharmaceutical
uses of lindane. At least fi ve school
districts
in CA ban the use of pesticides linked to
health or environmental damage.
Colorado
The Boulder Valley School District bans the
use of pesticides linked to health or
environmental
damage.
Hawaii
Legislation banning PBDEs
Illinois
Pending legislation to ban pharmaceutical
uses of lindane
Maine
Penta-BDE and Octa-BDE banned as
of 2006. Deca-BDE banned as of 2008.
Mercury is banned.
Massachusetts
Pending legislation to fi nd safer
alternatives
for ten hazardous chemicals, including PBDEs,
DEHP, and some pesticides. Pending
legislation to mandate the use of safer
cleaning products in many public buildings.
Legislation to require comprehensive toxics
use reduction for large user segments. Boston
passed a dioxin free purchasing resolution
to avoid PVC use. MA state law bans
the use in schools or daycares of pesticides
that are considered known, likely, or probable
carcinogens, inert ingredients with
toxicological
concerns, or any products used for
purely aesthetic reasons. The law also
limits use of pesticides indoors.
Michigan
Legislation banning Penta-BDE and Octa-BDE
by 2006. Stakeholder Task Force on all Deca-
BDE. PBDEs and mercury guidelines in state
purchasing contracts.
Minnesota
Pending legislation to ban the herbicide
atrazine
New York
Penta-BDE and Octa-BDE to be banned by
2006. Deca-BDE phase out for review. Pending
legislation to ban pharmaceutical uses
of the pesticide, lindane. PVC fl ooring is
excluded
as an eligible material for the state
green building tax due to its release of
harmful
chemicals throughout its life cycle. NY’s
second largest city, Buffalo, passed a
PBT-free
purchasing resolution. At least fi ve school
districts, including NYC, have adopted
policies
that limit the use of pesticides for
aesthetic purposes or ban some highly
toxic pesticide categories.
Oregon
Pending legislation in the 2005 Oregon
Legislature to phase out the sale of products
containing brominated fl ame retardants.
Oregon’s most populous county, Multnomah
County, adopted the precautionary principle
in 2004 to help reduce the use of toxic
substances.
Executive Order to achieve zero
discharge of persistent chemicals by 2020.
The Portland schools do not allow the use
of known or likely carcinogens.
Washington
Executive order to phase out PBTs prioritizing
25 high priority chemicals. Legislation
pending
to ban all PBDEs as part of the PBT Executive
Order. Seattle passed a PBT-free purchasing
resolution. Passed mercury reduction
legislation. Six school districts and four
cities
in WA ban the use of pesticides linked to
health or environmental impacts.
T A B L E 5
States Move to Protect Public Health and
the Environment
in the Absence of Federal Governance
Leadership
Note: CMRs refer to carcinogens, mutagens and
reproductive toxics. PBTs refer to persistent,
bioacummulative and toxic substances.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 30
The lack of power to regulate existing
chemicals provides a strong disincentive for
manufacturers to develop safer chemicals.
While the EPA has developed some innovative
initiatives in Green Chemistry, Design
for Environment, and pollution prevention,
these are generally small, underfunded, and
marginal to the EPA’s toxics program. In
agriculture, a similar
situation exists. Last
year, the US Department
of Agriculture
awarded $4.5 million
in research
grants for the Integrated
Organic Program
but investment
on organic R&D and
promotion equals
0.1 percent of total
federal agriculture
grants.42 In essence,
our regulations fail
to promote sustainability
and innovation.
Currently, the
Senate is examining
the Green Chemistry
Research and Development
Act which
would increase federal
research and
development into
this science. This
Act was proposed by
Rep. Phil Gingrey (R-GA) and is supported
by the American Chemical Society. Such
initiatives
are indeed welcome but they must
be part of a comprehensive overhaul of the
current Toxic Substance Control Act to
make the goal of safe chemicals production
the core mission of chemical management.
For chemicals regulation to be effective,
the EPA needs the authority to collect and
act on accumulating information , including
an ability to require safer substitutes for
chemicals that are of high concern. As the
regulations currently exist this is virtually
impossible to do because the burden of
proof is put on the regulators to prove harm
rather than for the chemical industry to
demonstrate that they have adequately
examined
a full range of potential risks and
shown the chemical can be used safely.
Our chemical management in the U.S.
needs a modern and effective overhaul to
urgently fi ll the data gaps, act on early
warnings
to substitute chemicals and chemical
classes of high concern, and promote
innovation
in green chemistry and safe chemical
use by companies.
In the absence of a federal overhaul of
chemical policy, and faced with a lack of
chemical industry accountability and weak
federal regulatory powers, some state
governments
are taking action. These actions
include procurement guidelines for products
free of persistent, bioaccumulative or
toxic chemicals; hazardous chemical phaseout
programs; toxic use reduction planning
requirements; and labeling requirements
such as California’s Proposition 65. The
U.S. Federal Government must respect the
right of states to enact strong laws to
protect
their citizens from dangerous chemicals.
These approaches are building momentum
for national reform. It is essential that
states continue to develop policies that
target inherently hazardous chemicals for
substitution along with an aggressive program
to work with downstream chemical
users to fi nd and implement safer substitute
materials. This applies not only to
industrial
chemical use but to agricultural uses as well.
Currently, the Senate is examining
the Green Chemistry Research
and Development Act which would
increase federal research and
development into this science.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 31
At the World Summit for Sustain- t the World Summit for Sustain- Aable Development, the global able Development, the global Acommunity including the United Acommunity including the United
States adopted the “Generational States adopted the “Generational Goal” to
guide chemical policy development
and protect public health. This is an
evolution
of European policy which in 1995 stated
the goal of preventing pollution to the North
Sea “… by continuously reducing discharges,
emissions, and losses of hazardous substances
thereby moving towards the target
of their cessation within one generation (25
years) with the ultimate aim of
concentrations
in the environment near background
values for naturally occurring substances
and close to zero concentrations of manmade
synthetic substances.”
Increasing recognition that hazardous
chemicals were migrating out of products,
that waste was becoming increasingly toxic,
that large data gaps existed for the bulk of
chemicals in commerce, and that regulatory
powers to substitute chemicals were limited
forced the European Union to examine its
chemical regulatory system. Europe, home
to the largest chemical market in the world,
faced a situation whereby 70% of the
chemicals
that have been evaluated under the
new chemicals program since 1981 have
one or more dangerous properties.43
Even though the Europe Union had
restricted a variety of hazardous chemicals
from production and use, the community
and experts realized that a chemical by
chemical
approach took too long and could
E U R O P E ’ S N E W C H E M I C A L P O L I C Y : R E A C H
� At the very least, we recommend that where synthetic chemicals
are found in elevated concentrations
in biological fl uids
such as breast milk and tissues of
humans, marine mammals
or top predators, regulatory steps be
taken to remove them
from the market immediately.�
Royal Commission on Environmental Pollution,
UK—Chemicals in Products, 2003
• Known and probable carcinogens, mutagens
and reproductive toxicants and preparations
containing them.
• Mercury in electronics
• Lead in electronics
• Phthalate Esters in
small toys
• Cadmium
• Hexavalent Chromium in electronics
• Nickel in jewelry
• Polybrominated diphenyl ethers
• Polybrominated biphenyls in textiles and
electronics
• Copper chromate arsenic
• Tributyl tin
• Azo dyes in textiles
• Pentachlorophenol
• Creosote
• Organostannic compounds
• Trichloroethane
• Hexachloroethane
• Tetrachloroethane
• Short chain chlorinated parrafi n
Chemicals Currently Restricted or Banned
in the European Union Market
Source: Integrated Chemicals Policy, Lowell
Center for Sustainable
Production, University of Massachusetts,
Lowell
Note: text in bold denotes chemicals
analyzed for and found in dust
never adequately address the thousands of
chemicals that needed to be investigated.
This provided added incentive to re-think
its chemical management program and
focus it to create better safe guards for
public health.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 32
Europe’s new draft chemicals management
program, entitled REACH, is set for
enactment in 2006 or 2007. This far-reaching
policy would require the Registration,
Evaluation and Authorization of Chemicals
(REACH) to close the large loophole in
information
and regulate chemicals of high
concern.
In effect, REACH would require that industry
publicly provide basic health, safety
and environmental impact data for over
30,000 high volume chemicals—many of
Toxic Substances Control Act Proposed
Regulations in REACH
TSCA is based on proving harm before acting—
the burden of proof rests on the government to
demonstrate that a chemical “will present an
unreasonable risk” before the EPA can limit
the
use of particular chemical.
REACH is based on a precautionary approach—
industry has the burden of testing and
assuring safety
of all the chemicals they use. Governments can
severely restrict substances based on their
inherent
dangers and adequate evidence of harm.
The EPA only regulates chemicals put on the
market since 1981—this amounts to less than
1% by volume of chemicals on the market.
REACH does not differentiate between new and
existing chemicals—all chemicals produced in
amounts greater than one ton will be regulated
(estimated 30,000 chemicals). This levels the
playing
fi eld between old and new chemicals.
TSCA only requires that manufacturers submit
available toxicity data and registration for
new
chemicals and even then can only require
testing when the agency believes the chemical
might be problematic.
REACH requires basic human and environmental
toxicity information for all new and existing
chemicals.
In effect, it forces the chemical industry to
be
accountable for all their product lines
manufactured
prior to the 1980s and still in commerce
today.
Under TSCA it is very diffi cult for the EPA
to
restrict the use of existing chemicals that
are
highly toxic and found to be linked to cancer,
reproductive problems and/or persisting and
accumulating in the environment and human
bodies (the EPA has restricted less than 10
chemicals in the past 25 years).
REACH will require authorization for the use
of
inherently harmful materials, which include
chemicals
that are known or probable carcinogens,
reproductive
toxins, mutagens as well as chemicals that
persist
and accumulative in the environment and our
bodies
and endocrine disrupting chemicals. The use of
these
materials will be restricted and the list will
be publicly
available.
TSCA allows large quantities of chemicals to
be
used in everyday products without any health
or
ecological data.
REACH does not allow chemicals* to be put on the
market unless data is provided (no data, no
market).
TSCA is fully paid for by taxpayer dollars.
Industry will partly pay for REACH through registration
fees.
*Carcinogenic (cancer causing), Mutagenic (causes mutations in
cells), Reproductive Toxin (linked to birth defects), Persistent
(resists breakdown), Bioaccumulative (magnifi
es up the food chain), Teratogenic (linked to birth defects), Endocrine
Disruptor
(disrupts the hormonal system)
which are widely used in everyday consumer
products. Those chemicals which are
demonstrated
to be of high concern would need
to get authorization (like regulation for
drugs) in order to be produced and used.
Authorization would only occur if strict
controls,
and proof of socio-economic need
could be demonstrated. Many believe the
rigorous procedure of getting a chemical
authorized would, in fact, lead to the search
for safer substitutes. Others, such as the
Nordic countries and some companies,
T A B L E 6
A Comparison of the US versus Proposed New
European Chemicals Regulation
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 33
are lobbying hard to have any authorized
chemical the focus of immediate substitution
with safer chemicals.44
The American Chemistry Council
and the Bush Administration Lobby
Against Reform
Through international efforts, such as the
global Stockholm Convention on Persistent
Organic Pollutants (POPs) and Europe’s
REACH legislation, many governments are
adopting integrated approaches to replace
high risk chemicals with safer alternatives.
Unfortunately, the United States is playing
an active role in undermining this process.
At home, the Administration has tried to
use ratifi cation of the Stockholm Convention
as an excuse for restricting the ability
of the EPA and state governments to regulate
future POPs.
Abroad, the US government, largely led
by the State Department and Department
of Commerce have aggressively lobbied
against REACH threatening trade violations
and citing poorly researched economic impact
analysis created by the American Chemistry
Council (ACC). ACC’s predictions
of billions of dollars of
lost sales is countered by the
European Commission’s assessment
that the cost to the chemical
industry of pro-viding data
on their chemicals is estimated
to cost around 2.3 to 5.2 billion
Euros over 11 years of implementation.
This is equal to 0.15 percent of
annual profi ts from chemical sales, or about
50 cents per European each year.45
Not once have US government offi cials
recognized the economic and public health
benefi ts of REACH. The European Commission
has calculated that REACH will save
an estimated 50 billion Euros in health
benefi
ts over the next 30 years and the prevention
of 4300 cases of cancer.
The Environmental
Protection Agency has
restricted less than
10 chemicals in the
past 25 years.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 34
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 35
P R O D U C T M A N U F A C T U R E R S A N D R E T A I L E R S
R E S P O N D T O C H E M I C A L R I S K S
Using hazardous chemicals in
products is ultimately bad business
practice and future thinking
companies have been making
the transition to safer chemical use.
However consumer information about the
type of chemicals in household products is
very limited. People have no way of knowing
if contaminants are in the products they
buy and bring home, much less if these
“stealth” contaminants will end up in the air
and dust in their homes. We have no product
labeling or product registers to consult.
In the absence of such information,
advocacy and consumer groups have been
testing and researching company chemical
policies.
While collecting and analyzing the dust
from households across the country, Clean
Production Action sent questionnaires46 to
a sample of leading manufacturers and
retailers
asking them if they use the chemicals
targetted in this study. We were also inter-
Human Health Criteria Ecological Health
Criteria
Carcinogenicity Algae toxicity
Teratogenicity Bioaccumulation
Reproductive toxicity Climatic relevance
Mutagenicity
Content of halogenated organic
compounds
Endocrine disruption Daphnia toxicity
Acute toxicity Fish toxcity
Chronic toxicity Heavy metal content
Irritation of skin/mucous membranes
Persistence/biodedgradation
Sensitization
Other (water danger list, toxicity to soil
organisms, etc.)
Other relevant data (e.g., skin penetration
potential, fl ammability, etc.)
Human and
Ecological Health
Criteria Included
in McDonough-
Braungart’s
Design Consultancy
Materials
Assessment
Protocol
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 36
ested to better understand the challenges
companies might face in transitioning out
of these chemicals.
We developed a color coding system
based on previous surveys47 to help consumers
understand companies chemical policies.
We based the color coding on company answers
to the questionnaire, on information
available on their website, or through public
announcements the company or retailer
might have made.
The results of our company ranking are
contained in Appendix II.
Industry Leaders
Products do not need to contain hazardous
chemicals. Innovation in healthy materials
is a profi table reality. We showcase four
companies
who searched for and found safer
chemicals for their product lines. There
are many more like them who believe safe
materials are possible and profi table.
These companies
• Identify known or suspected hazardous
chemicals for immediate substitution
with safer alternatives.
• Work with employees and suppliers to
experiment and search for new materials
and designs; and
• Engage with public stakeholders and
disclose information to consumers.
� Herman
Miller ( ( www.hermanmiller.com)
Based in Western Michigan, Herman Miller,
a residential and commercial furniture
manufacturer has been quietly integrating
sustainability into their business practices.
Their commitment to redesigning their new
products is providing consumers with
materials
that are safer and cleaner throughout
their life cycle. Their design strategies are
driven by an aggressive sustainability
agenda to be met by 2020.
Dubbed “Perfect Vision,” the effort
establishes
signifi cant, measurable corporate
sustainability targets to be achieved
by the year 2020, including:
• Zero landfi ll
• Zero hazardous waste generation
• Zero air and water emissions from
manufacturing
• Company buildings constructed to a minimum
LEED Silver certifi cation
• And the use of 100 percent green energy
to meet its power needs.
“Emerging technologies are enabling
us to actively pursue our sustainability
goals,
and I’m convinced we’ll meet them,” says
Environmental Affairs Manager Paul Murray,
noting that in a number of areas Herman
Miller already is closing in on these
objectives.
48
One key component to Herman Miller’s
strategy is the McDonough Braungart’s
Cradle to Cradle Design Protocol to assess
the potential hazards of materials and
chemicals
proposed for new products.49 For
more information visit www.mbdc.com
and and www.greenblue.org.
These criteria are used to screen materials
and chemicals for the safest choices in
product design.
Herman Miller’s Mirra chair is an example
of a new product designed to use materials
that rank well in the assessment protocol.
Polyvinyl chloride (PVC) plastic(vinyl),
brominated fl ame retardants and other
materials of concern were replaced with
safer alternatives. If current suppliers
where
unable to meet the new environmental
Herman Miller
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 37
standards necessary for the product, they
searched for new suppliers who could. This
has important ramifi cation across supply
chains by rewarding those suppliers working
to produce and deliver safer materials
and chemicals. In addition to hazard
assessments,
Herman Miller also designs for reuse
and recycling to achieve their zero landfi ll
goal.
� Shaw
Inc. (www.shawfl oors.com)
Back in December of 2003, Shaw Inc, the
world’s largest carpet manufacturer in the
world, based in Dalton, Georgia, launched
a new environmental policy to change the
way in which they design products. This
meant fi nding a new set of materials that
could be safely reused and recycled
continuously
into new products. It also meant moving
out of PVC (vinyl) and other materials
and chemicals that pose a risk to human
health. Their vision below signifi es their
commitment to change.
Shaw Industries, Inc. recognizes that
merely preserving and conserving the natural
bounty of the earth will not make us a
sustainable corporation. A truly sustainable
carpet industry must mimic nature’s organic
cycle of life, death, and rebirth. The
answer does not lie in limiting growth, but
in encouraging the kind of growth that is
cradle-to-cradle, returning carpet to carpet
endlessly.
Toward that end, Shaw has adopted these
productive policies and practices.50
• Environmental sustainability is our
destination
and cradle-to-cradle is our path.
Our entire corporation and all stakeholders
will value and share this vision.
• Through eco-effective technology we will
continuously redesign our products, our
processes, and our corporation.
• We will take responsibility for all that we
do and strive to return our products to
technical nutrient cycles that virtually
eliminate the concept of waste.
• We will plan for generations, while accepting
the urgency of the present. We
are committed to the communities where
we live and work. Our resources, health,
and diversity will not be compromised.
• We look forward to a solar-powered future
utilizing the current solar income of the
earth, anticipating declining solar costs
and rising fossil fuel costs as technology
and resource depletion accelerate.
• We will lead our industry in developing
and delivering profi table cradle-to-cradle
solutions to our free-market economy.
Economy, equity, and ecology will be
continually optimized.
• Honesty, integrity, and hard work remain
our core values. We will continue to deliver
unsurpassed safety, quality, beauty,
performance, and value to our customers.
Using McDonough Braungart’s Cradle
to Cradle Design Protocol, the company not
only designs for recyclability, but also
prioritizes
the use of materials and chemicals that
are safer for human health and the
environment.
To affi rm their commitment to their
new environmental policy, Shaw launched
EcoWorx® Backing—the industry’s
fi rst 100%
non-PVC backing for carpets (see attributes
below). At comparable cost, using the best
available technologies and materials for
performance
and human health, Shaw established
a new precedent that will lead others
to change.
Shaw Inc.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 38
EcoWorx ® ® Backing
Backing 51 Backing51 • Recyclable into more EcoWorx® backing
• Thermoplastic compound containing
no chlorine to off-gas in a fi re and no
phthalate plasticizers to migrate into the
environment
• Equal to or better than PVC backing in
all performance categories
• 40% lighter weight than PVC, lowering
transport costs and carbon monoxide
emissions
• Extremely low in VOCs (exceeds protocols
for Green Label Certifi cation under
CRI’s Indoor Air Quality Program), available
with a low-VOC releasable adhesive
• Class I fi re rated, rating for smoke
generation
far superior to PVC
• Available on any modular tile or six-foot
style with no upcharge, no minimum,
and no overage
• Offered with a high-performance Lifetime
No-Failure Warranty
100% recyclable into more EcoWorx®
backing through granulation and return
to the extrusion process
In addition to EcoWorx®, Shaw also used
MBDC’s Cradle to Cradle protocol to design
Eco Solution Q ® ® fi ber—a safer carpet fi
ber.
Combining the two products creates a 100%
recyclable carpet that Shaw will pick up free
of charge at the end of life and reuse and
recycle back into new carpets. As with Herman
Miller, one product at a time, they are
establishing new design paradigms that not
only negate the need for harmful chemicals,
but also reduce the need for landfi lls, and
other waste sites.
� IKEA
(www.ikea.com)
For more than 60 years IKEA has been
perfecting
ways of creating low prices—manufacturing
as inexpensively as possible building
our own stores, fl at-packing furniture
for customers to put together themselves.
But IKEA’s responsibilities do not stop
there.
We also want the products to be free of
hazardous
substances. And we don’t want the
wood in bookcases, tables or other products
in the store to come from areas where forests
are being devastated.52
IKEA, headquartered in Sweden, is increasing
its presence in the United States
giving consumers access to products that
are affordable yet made with the intention
of being hazard free. This has meant
establishing
a comprehensive restricted substances
list for all of their suppliers, banning
materials
like PVC (vinyl), and chemical classes
like brominated fl ame retardants. Every
IKEA product is designed with the goal of
being hazard free throughout its life cycle.
In areas where a safer material or chemical
IKEA
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 39
does not exist, IKEA establishes an
aggressive
research and development program to
fi nd a safer alternative. In 1999, the
company
phased out brominated fl ame retardants
but found it had to use a chlorinated
organohalogen as a replacement in one of
its product lines. Since then it has been
researching
non-halogenated substitutes to
continue the transition to safer materials
that function well and meet international
fi re standards.
What makes IKEA unusual is that they
have been doing this long before
environmental
issues were on the map as a corporate
priority and necessity to maintaining
competitiveness. IKEA has not been afraid
to work collaboratively with NGOs such as
Greenpeace, Friends of the Earth and
World Wildlife Fund. In 2002, they signed
the Friends of the Earth UK’s Risky Chemical
Pledge committing to:
• Using offi cial lists, identify which
manmade
chemicals are suspected of building
up in peoples bodies (bioaccumulation),
or interfering with the hormone, immune
or nervous systems.
• Produce a strategy to identify which of
its own brand and branded products
contain these chemicals.
• Produce a timeline to phase out these
chemicals from its own-brand products,
with the aim of eliminating them in 5
years, starting with those chemicals,
which pose the greatest threat.
• Put pressure on manufacturers of
branded products to do the same.
• Report publicly on progress on an
annual basis.
IKEA is a world leader in sustainability.
They are the only retailer in the United
States offering consumers affordable
products ranging from beds, to shelves, to
couches and rugs that can be safely brought
into the home with the assurance that
chemical
exposure is prevented to the greatest
extent possible for technologies available
today.
� Dell (www.dell.com)
“Achieve an Environmentally Focused Culture53” Culture
Dell, the largest computer manufacturer in
the world, based in Austin, Texas, has
responded
to the needs and demands of their
increasingly young, socially and
environmentally aware consumer base.
Electronic manufacturers have developed
restricted substances lists, largely due to
emerging European restrictions on certain
hazardous substances. However, a few such
as Dell, go beyond government regulations
by listing halogenated plastics, and PVC
plastic—materials long believed to release
high risk chemicals throughout their life
cycle for phase out.
“Dell’s vision is to create a company culture
where environmental excellence is second
nature. Our mission is to fully integrate
environmental stewardship into the business
of providing quality products, best-in-class
services, and the best customer experience
at the best value. The following
environmental
policy objectives have been established
to achieve our vision and mission.”
Dell
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 40
Design Products With the Environment in
Mind
• Design products with a focus on: safe
operation
throughout the entire product
life cycle, extending product life span,
reducing energy consumption, avoiding
environmentally sensitive materials,
promoting
dematerialization, and using
parts that are capable of being recycled
at the highest level
• Set expectations of environmental
excellence
throughout Dell’s supply chain.
Their position on brominated fl ame
retardants also exceeds European Union
mandated industry standards. While most
companies work to comply with the European
Restriction on Hazardous Substances,
which bans only PBDEs by 2006, Dell’s
products are already PBDE free and plans
to phase out the entire class of brominated
fl ame retardants… “our publicly-stated goal
is to eliminate (all other) brominated fl ame
retardants in desktop, notebook, and server
chassis plastic parts by year-end 2004.”54
Dell’s Restricted Materials Specifi
cation/
Supplier Programs
In order to meet global environmental
product requirements, Dell developed a
restricted materials specifi cation to
encompass
all raw materials, parts, components or
products that are ultimately incorporated
into the product that Dell markets. For
outsourced
manufacturers, this includes products
produced by the manufacturer on behalf
of Dell. The following list of materials
represent examples of substances that
Dell has reduced or eliminated in certain
applications:
• Asbestos and its compounds
• Cadmium and its compounds
• Chlorofl uorocarbons (CFCs)
• Chloroparaffi ns, short-chained
(10–13 carbon chain)
• Chromium VI and its compounds
• Halogenated plastics
• Hydrochlorofl uorocarbons (HCFCs)
• Lead and its compounds
• Mercury and its compounds
• Nickel and its compounds
• Polybrominated biphenyls (PBBs) and
their ethers/oxides (PBDEs, PBBEs)
• Polychlorinated biphenyls (PCBs) and
terphenyls (PCTs)
• Polyvinyl chloride (PVC)
Dell has also committed to taking their
products back at the end of life “to reuse,
recycle and dispose of safely.”
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 41
To prevent hazardous chemical
exposures from everyday products
found in our own homes, we need
major changes in government
policy, industry practice and individual
consumer behavior.
For too long we have been exposed to
chemicals in common household products
with little or no information. This situation
can not continue. The national regulatory
system has failed to protect consumers,
citizens and children from the unintended
consequences of exposure to small doses of
harmful chemicals from multiple sources.
The federal Toxic Substance Control Act
needs to be replaced with a new chemicals
policy that will:
• Require Safer Substitutes and Solutions
—seek to eliminate hazardous chemical
use and emissions by altering production
processes, substituting safer chemicals,
redesigning products and systems, and
rewarding innovation. Safer substitution
includes an obligation on the part of the
public and private sectors to invest in
research
and development for sustainable
chemicals, products, materials, and
processes.
W E C A N D O B E T T E R : The Way Forward to Safe
Chemicals
• Phase-out Persistent, Bioaccumulative,
or Highly Toxic Chemicals—prioritize
for elimination chemicals that are slow to
degrade, build up in the bodies of humans
and wildlife, or are highly hazardous
to humans or the environment.
• Give the Public and Workers the Full
Right-To-Know—label products that contain
hazardous chemicals, list quantities
of hazardous chemicals used in agricul-
� It will be
obvious when chemists have fulfi lled their singular historic
obligation to promote sustainability…. Every newly graduated
chemist will have
a thorough understanding of the fundamentals of sustainability
ethics, toxicity and
ecotoxicity and will know how to avoid pollution when designing
chemicals and
chemical processes. Chemists will have developed non-polluting
affordable technologies
suitable for mass distribution that can convert solar to
electrical and chemical energy
with high effi ciency. Through the properly informed design of
chemicals and chemical
processes, an economically vibrant, safe technology base will
have been invented
that is attractive to industry while being neither toxic nor
ecotoxic. �
Terry Collins, Director, Institute for Green
Chemistry, Carnegie Mellon University, USA.
Quoted in Green Chemistry,
August 2003
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 42
• Require Comprehensive Safety Data for
All Chemicals—assume that a chemical
is highly hazardous unless comprehensive
safety data are available for the
chemical and require manufacturers to
provide this data by 2015 for a chemical
to remain on the market—this is the
principle of “No Data, No Market.”
• Take Immediate Action to Protect
Communities and Workers—When
communities and workers are exposed to
levels of chemicals that pose an immediate
health hazard, immediate action is
necessary to eliminate these exposures.
Our chemical industry could be designing
a whole new set of chemicals that are
safer and ultimately benefi cial for human
health and the environment with expertise
that already resides in our universities and
institutes.
Step One
Safer Chemistry—Companies can assemble a list of high risk
chemicals and Companies can assemble a list of high risk chemicals and Safer Chemistry
substance by substance phase them out of their
products.
Step Two
Green Chemistry—The chemical industry can learn the guiding
principles of what The chemical industry can learn the guiding principles of
what Green Chemistry
consitutes toxicity and potential hazards by
reviewing the large body of resarch and
studies in toxicology and pharmacology. Then
they can use these principles to design
chemicals less likely to be hazardous.
Step Three
Ecological Chemistry—The chemical industry and university
researchers can identify The chemical industry and university researchers can
identify Ecological Chemistry
those chemicals commonly employed by natural
systems to support life and study
the processes by which organisms make these
safe materials. These principles then
become the basis on which to design safe
chemicals and materials.
Source: Adapted from Making Safer Chemicals, Ken Geiser, Lowell Center for Sustainbale
Production,
Aujgust 2004.
The Transition to Safe Chemicals
ture and in manufacturing facilities, and
provide public access to safety data on
chemicals.
• Act on Early Warnings—act to prevent
harm when credible evidence exists that
harm is occurring or is likely to occur,
even when some uncertainty remains regarding
the exact nature and magnitude
of the harm.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 43
Ten Things You Can Do for a Toxic-Free
Future
The public, consumers, industry and elected
offi cials can hasten the move to safe
chemicals
use in society and we suggest ten steps
below:
1Get Involved-—contact
your local or
state environmental group working to
advance safe chemical production and ask
them how you can help their efforts (for the
seven states partnering on this project,
please
see contact info below. For other states,
please visit www.besafenet.com). These and
other national groups will be promoting
the passage of the Green Chemistry Bill
and working to reform federal chemical
regulations.
California
Center for Environmental Health
www.cehca.org
Silicon Valley Toxics Coalition
www.svtc.org
Maine
Environmental Health Strategy Center
www.preventharm.org
Massachusetts
The Alliance for a Healthy Tomorrow
www.healthytomorrow.org
Michigan
Ecology Center
www.ecocenter.org
New York
Citizens Environmental Coalition
www.cectoxic.org
Oregon
Oregon Environmental Council
www.oeconline.org
Washington
Washington Toxics Coalition
www.watoxics.org
2Don’t buy products made of polyvinyl
chloride plastic (PVC), or ‘vinyl’—this
includes vinyl fl oors, vinyl shower curtains
and imitation leather goods such as vinyl
bags and toys. PVC requires a cocktail of
chemicals such as phthalates and organotins
tested for in this study. Vinyl plastic uses
the
number 3 to distinguish it from other
plastics
(or you can call the company to fi nd
out what kind of plastic it is). Visit the
Healthy Building Network to fi nd PVC-free
building materials (www.healthybuilding.net)
and Greenpeace International data base of
PVC alternatives (www.greenpeace.org. au/pvc/).
3Use natural forms of pest control in
your home and gardens. For information
visit the Pesticide Action Network’s website
at www.panna.org/resources/advisor. dv.html. html
Also visit www.beyondpesticides.org. org
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 44
4Buy curtains, carpets or furniture that
are free of brominated fl ame retardants
or perfl uorinated chemicals. Contact companies
directly to ask if they use these chemicals
in their products. See www.safer-products.
org
for more information. In addition, you for
more information. In addition, you can replace carpets with wood fl oors, cork
tiles, linoleum and area rugs. For more
information
visit www.healthybuilding.net
and and www.greenpeace.org.au/pvc/.
5Next time you buy cosmetics, choose
products that are free of suspect
chemicals. Visit the Safe Cosmetics Campaign
to fi nd brand name companies that
are phasing out harmful chemicals
(www.safecosmetics.org).
6Purchase your electronic products
from companies that avoid brominated
fl ame retardants (BFR). You can fi nd
a list of companies which are leading the
fi eld at www.computertakeback.org and and www.
cleanproduction.org
or visit our website at or visit our website
at www.safer-products.org. Also ask companies Also ask companies org
when they intend to phase out the use
of PVC cables.
7Initiate a safer chemicals program
in government procurement
of all products and services at the
local or state level for bulk purchases
of computer and electronic goods,
and other product sectors outlined in
our report. Initiate pesticide-free bylaws
for all public spaces, and a phase
out of vinyl use in all public buildings
and furnishings.
8The same can be done in the
private and institutional sector.
If your employer buys in bulk from
suppliers, fi nd out about their chemicals
policy. At a minimum your company
should have a strict phase out date for
all Chemicals for Priority Action and a
timeline
for transitioning to safer materials. It
is imperative that buyers source non-PVC
plastic (vinyl) for building materials and
consumer products. Big buyers can infl uence
the market in a way that individual
consumers can not.
9If you are a retailer ask your buyers to
implement a safer chemicals agreement
with their suppliers and make your policy
public. Responsible retailers such as IKEA
have implemented a strict chemicals policy
which they enforce through frequent spot
checks on their products. Other retailers
have joined retailer consortiums to exert
more pressure on their chemical suppliers.
Post your chemicals policy on the web,
through product labelling or through other
forms of direct communication with your
consumers.
Prioritize local and organic food
in school cafeterias, hospitals and
other institutional settings. Initiate pesticide-
free bylaws in your local community.
10
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 45
More Resources
Clean Production Action (www.cleanproducti
on.org), working with state partners, launched
the Safer Products Project to generate public
support for safe chemicals. We intend
to give updates to people who wish to stay
informed via our website at www.saferproducts.
org.
The following websites provide a wealth
of information and an invitation to join in
the movement to promote safe chemicals
production and use.
Vinyl, also called PVC, uses a wide variety
of toxic ingredients. When burned in fi res,
incinerators or accidentally, as in house
fi res, PVC will form dioxin as a byproduct
—the most toxic compound ever synthesized.
For information and further links
to information on PVC visit:
• www.healthybuilding.net
• Greenpeace International data base
of PVC alternatives
www.greenpeace.org.au/pvc/
• www.myhouseisyourhouse.org
• www.besafenet.com
• www.grrn.org
Pesticides. Find safer alternatives at:
• www.panna.org/resources/advisor.dv.html
• www.beyondpesticides.org
Cosmetics. Find who is using safer
chemicals at:
• www.safecosmetics.org
Cleaning Products. Find out which products
contain hazardous chemicals at:
• www.net.org/health/cabcon_results.vtml
Electronics. The Computer Take-Back
Campaign can tell you who is ‘taking it back
and making it clean” at www.computertakeback.
org. Also visit the Silicon Valley Toxics Coalition
for information about materials in
electronics at www.svtc.org
Clean Production. For information on how
manufacturing plants and product designers
are moving to safer chemicals visit:
• www.cleanproduction.org
• www.bluegreen.org
• www.mbdc.com
• www.sustainableproduction.org
• www.epa.gov/greenchemistry
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 46
1 Edwards, R., Yurkow, E., Lioy, P., 1998.
Seasonal
deposition of housedusts onto household
surfaces. Sci. Total Environ. 224: 69–80.
2 Klepeis NE, Nelson WC, Ott WR, Robinson
JP, Tsang AM, Switzer P et al. 2001. The
national human activity pattern survey
(NHAPS): a resource for assessing exposure
to environmental pollutants. J Expo Anal
Environ Epidemiol 11:231-252. Available
at http://www.exposurescience.org/pub/
preprints/LBNL-47713.pdf
3 Oleskey, C., McCally, M., A Guide to
Biomonitoring of Industrial Chemicals.
New York: Center for Children’s Health and
the Environment, Mount Sinai School of
Medicine.
4 Wilford, B., Harner, T., Zhu, J., Shoeib,
M.,
Jones, K., 2004 Passive sampling survey of
polybrominated diphenyl ether fl ame
retardants
in indoor and outdoor air in Ottawa,
Canada: Ijplications for sources and
exposure.
Environ. Sci. technol. 38: 5313-5318.
5 Liu L- JS, Box M, Kalman D, Kaufman J,
Koenig
J, Larson T, et al. 2003. Exposure assessment
of particulate matter for susceptible
populations in Seattle; Environ Health
Perspect
111: 909- 918.
6 Roberts, J., Clifford, W., Glass, G.,
Hummer,
P., 1999. Reducing dust, lead, dust mites,
bacteria,
and fungi in carpets by vacuuming.
Arch. Environ. Contam. Toxicol. 36: 477-484.
7 Rudel, R., Camann, D., Spengler, J., Korn,
L.,
Brody, J., Phthalates, alkylphenols,
pesticides,
polybrominated diphenyll ethers, and other
endocrine-disrupting compounds in indoor
air and dust. Environ. Sci. Technol. 2003.
37:
4543-4554.
8 M. Maroni, B. Seifert, T. Lindvall (Eds.),
Indoor Air Quality: a Comprehensive
Reference Book, Elsevier, Amsterdam, 1995.
9 Bizzari, S., Gubler, R., Kishi, A., 2003.
CEH
Report: Plasticizers. ceh.sric.sri.com/Public/
Reports/576.0000/
10 U.S. Food and Drug Administration, 2001.
Phthalates and Cosmetic Products. U. S. Food
and Drug Administration, Center for Food
Safety and Applied Nutrition, Offi ce of
Cosmetics
and Colors Fact Sheet. http://
vm.cfsan.fda.gov/~dms/cos-phth.html
11 Hauser, R., Duty, S., Godfrey-Bailey, L.,
Calafat,
A., 2004. Medications as a source of human
exposure to phthalates. Environ. Health
Perspect. 112:751–753.
E N D N O T E S
12 U.S. Environmental Protection Agency,
2001.
Removal of Endocrine Disruptor Chemicals
Using Drinking Water Treatment Processes.
EPA/ 625/ R- 00/ 015 . Washington, D.C.:
USEPA Offi ce of Research and Development
13 Losey, B., 2003. The Future of Nonylphenol
Ethoxylates in Nonwovens. Presented at
International
Nonwovens Technical Conference
2003. The Alkylphenols & Ethoxylates
Research
Council, http: www.aperc.org.
14 Johnson, A., Olson, N., 2001. Analysis and
occurrence of polybrominated diphenyl
ethers in Washington State freshwater fi sh.
Arch. Environ. Contam. Toxicol. 41: 339-344.
15 Huwe, J., Hakk, H., Lorentzsen, M., 2002.
A
mass balance feeding study of a commercial
octabromodiphenyl ether mixture In rats.
Organohalogen Compounds. 58:229-232.
16 Suresh, B., Schlag, S., Yoneyama, M., 2002.
CEH Report: Organometallics. http://
ceh.sric.sri.com/Public/Reports/681.7000/
17 Hock, M., 2001. Organotin compounds in
the environment – an overview. Applied
Geochemistry 16: 719-743.
18 Key, B., Howell, R., Criddle, C., 1997.
Fluorinated organics in the biosphere.
Environ. Sci. Technol. 31: 2445-2454.
19 Kissa, E., “Fluorinated Surfactants.”
Dekker,
New York, 1994.
20 Moriwaki, H., Takata, Y., Arakawa, R.,
2003.
Concentrations of perfl uorooctane sulfonate
(PFOS) and perfl uorooctanoic acid (PFOS)
in vacuum clean dust collected in Japanese
homes. J. Environ. Monit. 5: 753-757.
21 Lehmler, H.-J., 2005. Synthesis of
environmentally
relevant fl uorinated surfactants—
a review. Chemosphere. In Press.
22 So, M., Taniyasu, S., Yamashita, N.,
Giesy, J.,
Zheng, J., Fang, Z., Im, S., Lam, P., 2004.
Perfl uorinated compounds in coastal waters
of Hong Kong, South China, and Korea.
Environ.Sci.Technol. 38: 4056-4063
23 Hoppin, J., Brock, J., Davis, B., Baird,
D.,
2002. Reproducibility of urinary phthalate
metabolites in fi rst morning urine samples.
Environ Health Perspect; 110:515–8.
24 Center for Disease Control and Prevention.
National Center for Environmental Health.
Asthma Speaker’s Kit. Asthma Prevalence
by Age 1980-1996. Visited on the web Feb 25,
2005 at http://www.cdc.gov/asthma/speakit/
epi.htm
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 47
25 Rich Mayes, University of Richmond, VA.
Rise
of ADHD Prevalence and Psychostimulant
Use: A Historical Perspective, Presented at
the 130th Annual Meeting of the American
Public Health Association, 11 Nov 2002.
26 DeGrandpre R. Ritalin Nation. Norton: New
York, 1999 quoted in Ted Schettler et al.,
Physicians
for Social Responsibility and the Clean
Water Fund, In Harm’s Way: Toxic Threats
to Child Development, May, 2000.
27 Herman-Giddens, ME, EJ Slora, RC
Wasserman,
CJ Bourdony, MV Bhapkar, GG Koch
and CM Hasemeir. 1997. Secondary sexual
characteristics and menses in young girls
seen
in offi ce practice: a study from the
pediatric
research in offi ce settings network.
Pediatrics
99(4):505-512. Cited in www.ourstolenfuture.org
28 Carlsen, E., A Giwercman, N Keiding, N
Skakkebćk. 1992. Evidence for Decreasing
Quality of Semen During Past 50 Years.
British Medical Journal 305:609-613.
29 For an overview of studies visit: www.
ourstolenfuture.org/NewScience/reproduction/
sperm/humansperm.htm
30 Butte, W., Heinzow, B., 2002. Pollutants
in
house dust as indicators of indoor
contamination.
Rev. Environ. Contam. Toxicol. 175: 1-46.
31 Maertens, R., Bailey, J., White, P., 2004.
The
mutagenic hazards of settled house dust:
A review. Mutation Research 567: 401-425.
32 Simoni, M., Carrozzi, L., Baldacci, S.,
Scognamiglio, A., Pede, F., Sapigni, T., Viegi,
G., 2002. The Po River ( North Italy) indoor
epidemiological study: Effects of pollutant
exposure on acute respiratory symptoms and
respiratory function in adults. Arch.
Environ.
Health 57: 130–136.
33 Lioy, P., Freeman, N., Millette, J., 2002.
Dust:
A metric for use in residential and building
exposure assessment and source
characterization.
Environ Health Perspect 110:969–983.
34 Clausen, P., Hansen, V., Gunnarsen, L.,
Afshari, A., Wolkoff, P., 2004. Emission of
Di-2-ethyhexyl phthalate from PVC fl ooring
into air and uptake into dust: emission and
sorption experiments in FLEC and CLIMPAQ.
Environ. Sci. Technol. 38: 2531-2537.
35 Vejrup, K., Wolkoff, P., 2002. Linear
alkylbenzene
sulfonates in indoor fl oor dust. Sci.
Total Environ. 300: 51-58.
36 Maertens, R., Bailey, J., White, P., 2004.
The mutagenic hazards of settled house dust:
A review. Mutation Research 567: 401-425.
37 Tang, K., Nace, C., Lynes, C., Maddeloni, M.,
Laposta, D., Callahan, K., 2004. Characterization
of background concentrations in Upper
Manhattan, New York apartments for select
contaminants identifi ed in World Trade
Center
dust. Environ. Sci. Technol. 38: 6482-6490.
38 Rudel, R., Camann, D., Spengler, J., Korn,
L.,
Brody, J., Phthalates, alkylphenols,
pesticides,
polybrominated diphenyll ethers, and other
endocrine-disrupting compounds in indoor
air and dust. Environ. Sci. Technol. 2003.
37:
4543-4554.
39 Lioy, P., Freeman, N., Millette, J., 2002.
Dust:
A metric for use in residential and building
exposure assessment and source
characterization.
Environ Health Perspect 110:969–983.
40 Fairbank, Maslin, Maullin &
Associates—
PBT Opinion Research Report,
www.safealternatives.org
41 Schafer, Kristin, et al. Chemical Trespass
Pesticides in Our Bodies and Corporate
Accountability. Pesticide Action Network
North America May 2004. Available at
http://panna.org/campaigns/docsTrespass/
ChemTresMain(screen).pdf
42 Lipson, Mark. Searching for the “O-Word”:
Analyzing the USDA Current Research
Information
System for Pertinence to Organic
Farming. Organic Farming Research Foundation.
1997
43 European Commission, Extended Impact
Assessment, COM(2003) 1171/3 (Oct. 29,
2003), pg. 27.
44 International Chemical Secretariat. What
We Need From REACH. January, 2005.
45 Ackerman and Massey, The True Costs of
REACH, Global Development and Environment
Institute, Tufts University (2004).
46 See www.cleanproduction.org
for questionnaire. for questionnaire. 47 For
consistency, we are using the same system
Greenpeace used internationally in their dust
campaigns so that we can highlight double
standards. (www.greenpeace.co.uk
click onto click onto toxics campaign and
then ‘chemical house’)
48 www.hermanmiller.com/CDA/SSA/News/Story/
0,1585,a10-c407-n322,00.html
49 Source: McDonough, et al., 2003, “Applying
the Principles of Green Engineering to
Cradleto-
Cradle Design,” Environmental Science
and Technology.
50 www.designweave.com/DWEnvironmental.shtml
51 www.designweave.com/DWEnvironmental.shtml
52 Social and Environmental Responsibility,
IKEA’s brochure
53 www1.us.dell.com/content/topics/global.aspx/
corp/environment/en/program_policy?c=us&l=en
&s=corp&~section=000
54 www1.us.dell.com/content/topics/global.aspx/
corp/environment/en/prod_design?c=us&l=en&s
=corp&~section=011
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 48
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 49
A P P E N D I X I : Results of Chemicals
Tested For, Occurrence, and Health Concern
Target Chemicals Uses References
Phthalates 80 – 90 percent of all phthalates are used in fl exible PVC
products,
or vinyl – wall coverings, fl ooring,
furniture, shower curtains, clothing,
raincoats, shoes, toys, etc. The rest are used
in paint, medical
equipment, pesticides, and personal care
products (perfume, nail
polish, hairspray). DEHP is the predominant
phthalate in fl exible PVC
products, while DEP and DBP are used most
often in personal care
products. Phthalates are also found in
recycled paper products.
1, 2
Alkylphenols
and Alkylphenol
ethoxylates
Alkylphenols are used primarily as raw
materials for the manufacture
of alkylphenol ethoxylates. Alkylphenol
ethoxylates are used as nonionic
surfactants, emulsifi ers, lubricants or
anti-oxidants in laundry
detergents, textiles, leather, paints,
disinfecting cleaners, all-purpose
cleaners, spot removers, hair-coloring,
cosmetics, adhesives, some
plastics and pesticides. Nonylphenol is used
as a spermicide.
3
Polybrominated
diphenyl ethers
PBDEs are applied to textiles or incorporated
into plastics, foams and
components of electrical goods to prevent or
slow the spread of fi re.
They are found in polyurethane foam products,
foam padding in furniture,
textiles, electrical appliances, televisions
and computers. Decabrominated
diphenyl ether, BDE 209, is used solely as a
fl ame retardant
in the hard, dense plastics of consumer
electronics products (~ 80%
production volume) and in the latex back coating
of fl ame retardant
upholstery textiles (~20 % production volume).
4,5,6
Pesticides Pesticides are applied in and around homes for controlling
infestations
of various insects; applied to carpets, pre-
and post-sale, to prevent
or or slow infestations of insects, dust
mites, and mold. They are also
added to soaps, paints, and household
cleaners. Inside uses of
chlorpyrifos and diazinon recently restricted
by the EPA due to health
concerns. In agricultural areas, pesticides
from neighboring agricultural
use can drift into homes and schools.
Organotins Organotins are used to the greatest extent as heat and light
stabilizers
in PVC. They are found in PVC water pipes, PVC
food packing
materials (e.g., dioctyltin), glass coatings
(e.g., butyltin trichloride),
polyurethane foams and many other consumer
products. They also
serve as catalysts for the manufacture of
polyurethane and silicone
elastomers; as antifouling agents for ships
and boats; as biocides
and fungicides applied to or incorporated in carpets
and paints or
applied to fruits and vegetables; as surface
disinfectants for wood,
paper, textiles, paints and some electrical
equipment. Monomethyltin,
dimethyltin, butyltin and octyltin are the
most widely used of the
organotins.
7, 8
— c o n t i n u e d —
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 50
Photo: Fuel Cell Energy
Perfl uorinated
Surfactants
PFOA and PFOS are used as fl oor polishes,
photographic fi lm, denture
cleaners, shampoos, herbicides, insecticides, and
adhesives in a
wide range of products, as well as surface
stain-resistant coatings for
fabrics, carpets, and paper and as a coating
for cookware. PFOA is
the best-known of the PFCs because it is used
to make Tefl on, Goretex,
and other oil-, water- and stain-resistant
materials used in many
common items, including nonstick frying pans,
utensils, stove hoods,
stainproofed carpets, furniture, and clothes.
PFOA is also used in fi re-
fi ghting foams, mining and oil well
surfactants, and the manufacture
of other fl uoropolymers. PFOS is thought to
be the main, fi nal degradation
product of many of the perfl uorinated
chemicals released into
the environment.
9, 10, 11
Phthalates
Five of the seven phthalates selected for
analysis were
present at quantifi able concentrations in
all of the
dust samples, as shown in Table 2.
Di-(2-ethylhexyl) phthalate (DEHP) was
present
in all of the samples. With a mean
concentration of
329 ppm, DEHP was predominant among not only
the phthalates but also all 44 contaminants. No
federal
or state agencies have established regulatory
limits on
levels of DEHP in house dust. However, even
the lowest
DEHP concentration measured, 214 ppm, exceeds
the acceptable limit of 44 ppm DEHP in
residential
soils established by the State of Connecticut.12 On
average, DEHP accounted for 78 percent of the
total
concentration of the target phthalates in the
dust
samples and 69 percent of the total
concentration
of the 44 contaminants.
While this study found mean concentrations of
1.4
ppm and 329 ppm for diethyl phthalate (DEP)
and
di(2-ethylhexyl) phthalate (DEHP)
respectively, Rudel
et al. (2003) reported higher mean
concentrations
for both, 8.5 ppm for DEP, and 506 ppm for
DEHP,
in their study of dust from some 120 homes on
Cape
Cod, Massachusetts.
As shown in Figure 2, butylbenzyl phthalate
(BBP)
(in the literature, this chemcial also
appears as benxylbutyl
phthalate or BBzP) had the second highest
concentration
among the phthalates and accounted, on
average, for 16 percent of the total mass of
phthalates.
With a mean concentration of 69 ppm, BBP also
ranked second highest among all 44
contaminants.
Di-n-butyl phthalate was detected in all
samples
with an average concentration of 20.15 ppm.
Dimethyl phthalate (DMP) was found at a very
low
concentration in only one of the seven
samples while
di-n-propyl phthalate (DPP) was below
detection levels
in all samples.
Rudel et al. (2003) did not assay for
dimethyl
phthalate but did assay for the following
phthalates
that were not target analytes in the current
study: dicyclohexyl
phthalate, 2.98 ppm; di-n-hexyl phthalate,
2.6
ppm; and di-n-pentyl phthalate (<rl).
In this study, diisobutyl phthalate was found
at an
average concentration quite similar to that
reported
by Rudel et al. (2003). However, much higher
concentrations
of this phthalate were found in house dust
from Belgium, Brazil and the U.K. This may
refl ect
different patterns of phthalate use in
products made
and used in those countries.
Figure 3 shows the fi ndings of the current
study
with respect to phthalates in comparison to
those of
other studies of house dust from Belgium;13 Brazil;14
Cape Cod, Massachusetts;15 and the United Kingdom.16
The non-US studies also tested for some
phthalates
that were not selected for analysis in this
study.
In house dust from
Belgium, Al Bitar (2004) found
as follows: dicyclohexyl phthalate, 1.7 ppm;
di-noctyl
phthalate, 55.7 ppm; di-isononyl phthalate,
162.9 ppm; and di-isodecyl phthalate, 66 ppm.
In house dust from the
U.K., Santillo et al. (2003)
also reported di-isononylphthalate (48.5 ppm)
and
di-isodecylphthalate (20.8 ppm).
In house dust from
Brazil, Costner et al. (2004) reported
dicyclohexyl phthalate (0.62 ppm), di-n-octyl
phthalate (1.4 ppm), di-isononyl phthalate
(71.2
ppm) and di-isodecyl phthalate (93 ppm).
Phthalates—Production, Use, Occurrence
and Effects
“PVC is neither a biological nor technical
nutrient.
It is a toxic nightmare.”
—Michael Braungart, Director,
McDonough Braungart Design Chemistry and
EPA Green Chemistry Award Winner
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E S A F E R P R O D U C T S P R O J E C T : A L T E
R N A T I V E S F O R A H E A L T H Y H O M E 51
51 Global production of phthalates is an estimated 3.5
million metric tons per year,17 of which 80-90 percent
is used as additives in fl exible polyvinyl
chloride (PVC)
plastic—commonly known as vinyl.18 Roughly 50 percent
of the market share for phthalates is
accounted
for by di(2-ethylhexyl) phthalate (DEHP),19 at least 95
percent of which is added to PVC to give it
fl exibility.20
DEHP is present in PVC (vinyl) products such
as wall
coverings, tablecloths, fl oor tiles,
furniture upholstery,
shower curtains, garden hoses, swimming pool
liners,
rainwear, baby pants, dolls, some toys,
shoes, automobile
upholstery and tops, packaging fi lm and
sheets,
sheathing for wire and cable, medical tubing,
and
blood storage bags.21
The remaining small share of phthalates not
added
to PVC is used in personal care products such
as skin
creams, hairsprays, lotions, nail polish, and
fragrances,
and in a variety of other products including
adhesives,
caulks, detergents, electrical capacitors,
inks, solvents,
lubricating oils, paints, and pharmaceuticals.22,23,24
While environmental releases of industrial
chemicals
are most commonly associated with their
manufacture
and disposal, it is estimated that more than
75
percent of phthalate releases to the
environment occur
during the use of products that contain
phthalates.
25 Clausen et al. (2004) documented releases to
air of DEHP from PVC fl ooring.26 In studying phthalate
emissions from PVC skirting, PVC fl ooring,
and
other materials, Afshari et al. (2004)
concluded: 27
“Plasticizers used in surface materials
indoors can be
detected in the indoor air and human
exposure to plasticizers
can be expected. This study shows that the
concentration
of phthalates in indoor air is independent
of
ventilation rates and the area of surface
materials containing
plasticizers, i.e. a small area of
plasticizer containing
products emits almost as much as a large
area.
Therefore, if the surface materials
contain plasticizers,
it is impossible to avoid the phthalates
in indoor
air.” [emphasis added] .”
[emphasis added] Phthalates are among the
most ubiquitous synthetic
chemicals in the environment28 and are nearly always
found at some concentration in virtually all
people
and wildlife.29 Phthalates are found in
the air and dust
in homes and offi ces.30
Occurrence of Phthalates
and Their Metabolites in People
Exposure to phthalates has been associated
with
• asthma and other respiratory problems,
rhinitis
and eczema in children;
• premature breast development in female
children;
and
• deteriorated semen quality, low sperm
counts, and
poor sperm morphology in men;
Findings of the studies described below can
be summarized
as follows:
• Phthalates and their metabolites are
common, if
not ubiquitous, contaminants in the bodies of
U.S.
men, women and children;
• A metabolite of diethyl phthalate, which is
used in
personal care products, is present at higher
levels
in the urine of U.S. adults who are 20 years
old and
older;
• Metabolites of DEHP, DBP and benzylbutyl
phthalate
occurred at higher concentrations in the
urine
of the youngest people tested, children aged
6 to
11 years;
Studies in Germany found
evidence that DEHP
concentrations exceeded U.S. EPA’s reference
dose
in almost one-third of the people tested and
were
about twice as high among very young
children, ages
2 to 6 years, as among their parents and
teachers;
80–90 percent of all phthalates are used as
additives in fl exible polyvinyl chloride
(PVC)
plastic—or ‘vinyl’ products such as wall
coverings, tablecloths, fl oor tiles,
furniture
upholstery, shower curtains, garden hoses,
swimming pool liners, rainwear, baby pants,
dolls, some toys, shoes, automobile
upholstery
and tops, packaging fi lm and sheets,
sheathing for wire and cable, medical
tubing,
and blood storage bags. They are now one
of the most widespread sysnthetic chemicals
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 52
Among 30 pregnant women
in New York City and
30 in Krakow, Poland, all had measurable
concentrations
of four phthalates—diethyl phthalate (DEP),
dibutyl phthalate (DBP), diethylhexyl
phthalate
(DEHP), and butyl benzyl phthalate (BBzP)—in
their personal air and metabolites of these
same
phthalates in their urine;
A study in Italy found DEHP
and/or its metabolite,
monoethylhexyl phthalate (MEHP) in more than
80 percent of the cord blood samples from 84
births.
Pregnancy durations tended to be shorter for
those
in which MEHP was present in the cord blood;
Several phthalate
metabolites were detected in
pooled breastmilk samples from the U.S.
Exposure to phthalates
has been associated with
— asthma and other respiratory problems,
rhinitis
and eczema in children;
— premature breast development in female
children; and
— deteriorated semen quality, low sperm
counts,
and poor sperm morphology in men;
In a study of urine phthalate levels in 2,541
U.S.
residents, the Centers for Disease Control
(CDC)
found evidence of widespread exposure, with
higher
concentrations in women. Concentrations of monoethyl
phthalate, a metabolite of diethyl phthalate,
were almost two times higher in the urine of
people
aged 20 years and older than in children aged
6 to 11
years. Diethyl phthalate is used in products
such as
fragrances, soaps, and hand lotions. The highest
levels
of metabolites for DEHP, DBP and benzylbutyl
phthalate
were found in the urine of the youngest
people
tested, children aged 6 to 11 years. In fact,
the concentrations
of monobenzyl phthalate, a metabolite
of benzylbutyl phthalate, were more than
three times
higher in the children’s urine. Benzylbutyl
phthalate
is used in products such as adhesives,
sealants, and
car care products.31
In Germany, Koch et al. (2003) concluded that
the
general population is exposed to DEHP to a
much
higher extent than previously believed,
noting that
31 percent of their subjects had DEHP values
that
exceeded the U.S. EPA reference dose. They
concluded
as follows: 32
“This is of greatest importance for public
health since
DEHP is not only the most important phthalate
with
respect to its production, use and
occurrence and omnipresence
but also the phthalate with the greatest
endocrine
disrupting potency.”
In a later analysis of DEHP metabolites in
urine,
Koch et al. (2004) estimated the internal
exposure of
nursery school children, aged 2–6 years, to
DEHP to
be about twice that of their parents and
teachers.33
In a study of pregnant women – 30 in New York
City and 30 in Krakow, Poland, Adibi et al.
(2003)
measured concentrations of four phthalates in
personal
air and the metabolites of these same
phthalates
in urine. These phthalates—diethyl phthalate
(DEP),
dibutyl phthalate (DBP), diethylhexyl
phthalate
(DEHP), and butyl benzyl phthalate
(BBzP)—were
present in 100 percent of the air samples and
their
metabolites in 100 percent of urine samples.
Their
results demonstrate considerable phthalate
exposures
during pregnancy among these women and
indicate
that inhalation is an important route of
exposure.34
Animal studies have found that phthalates
pass from
the mother through the placenta to the fetus
and
through breastmilk to the newborn.
A study by Latini et al. (2003) found
detectable DEHP
and/or its metabolite monoethylhexyl
phthalate
(MEHP) in the cord blood of 88% of 84
newborns in
Italy. MEHP-positive newborns showed a
signifi cantly
lower gestational age compared with
MEHP-negative
newborns. Their fi ndings confi rm that human
exposure
to DEHP can begin in utero and suggest that
phthalate exposure is signifi cantly
associated with a
shorter pregnancy duration.35 Calafat et al. (2004) detected
several phthalate metabolites in three pooled
human breast milk samples in the U.S.,
suggesting
that phthalates can be incorporated into
breast milk
and transferred to the nursing infant. Three
of the
phthalate metabolites and three oxidative
metabolites
were detected in all three pooled samples.36 Animal
studies have also found that phthalates pass
from the
mother through the placenta to the fetus and
through
breastmilk to the newborn.37,38,39
Effects of Exposure to Phthalates
and Their Metabolites in People
As illustrated by the studies discussed
below, exposure
to phthalates and their metabolites have been
associated
with a broad range of health effects:
• asthma and other respiratory problems,
rhinitis
and eczema in children;
• premature breast development in female
children;
and
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F O R A H E A L T H Y H O M E 53
• deteriorated semen quality, low sperm
counts, and
poor sperm morphology in men.
Children exposed to household dust with the
greatest concentrations of di(2-ethylhexyl)
phthalate
(DEHP) were 2.9 times as likely to have
asthma
as were children exposed to the lowest
concentrations
of that phthalate.
According to Jaakkola et al. (1999) and Řie
et al
(1997), the presence of plasticizers in
surface materials
indoors can increase the risk of bronchial
obstructions,
asthma, and perhaps the susceptibility to
respiratory
infections.40,41 The later noted that
indoor inhalation
of DEHP-adsorbed particulate matter could be
as or
more important than inhalation of vapor phase
DEHP. 42 Bornehag et al. (2004)
found that children
exposed to household dust with the greatest
concentrations
of di(2-ethylhexyl) phthalate (DEHP) were
2.9 times as likely to have asthma as were
children exposed
to the lowest concentrations of that
phthalate.
Similarly, children in homes with the
greatest concentrations
of butyl benzyl phthalate were 3.0 and 2.6
times as likely as the other children to have
rhinitis
and eczema, respectively.43
The concentration of phthalate esters was
signifi cantly higher in infertile men
compared
with controls and they may be instrumental
in the
deterioration of semen quality in infertile
men.
A study on premature breast development
(thelarche)
in female children aged 6 months to 8 years
found
phthalate esters in 68% of serum samples from
the
thelarche patients. The phthalate esters with
the most
common commercial uses, DEHP and DBP, were
detected
in the highest concentrations. For those
samples
with high concentrations of DEHP, one of the
major
DEHP metabolites, mono(2ethylhexyl)phthalate
(MEHP), was also detected. DEHP was detected
in
only 14% of the control samples in lower
concentrations.
A more sensitive analysis of eight thelarche
samples
allowed detection of a further two
phthalates, DMP
and DEP, in two and three samples,
respectively.44
A study on premature breast development in
female
children aged 6 months to 8 years found
phthalate
esters in 68% of serum samples from the
patients.
Duty et al. (2002) explored whether general
levels
of phthalates in the U.S. population were
associated
with altered semen quality and found
suggestive
evidence of associations between high
mono-benzyl
phthalate (MBzP) levels and low sperm counts,
and
between high mono-methy phthalate (MMP) and
poor sperm morphology. Mono-n-butyl phthalate
(MBP), MBzP and MMP were associated with
altered
semen quality. 45 In another related
study, Duty et al.
(2003) found that urinary monoethyl phthalate
(MEP),
at environmental levels, is associated with
increased
DNA damage in sperm.46 Rozati et al. (2002) found
that the concentration of phthalate esters
was signifi -
cantly higher in infertile men compared with
controls
and concluded that they may be instrumental
in the
deterioration of semen quality in infertile
men without
an obvious mechanism of action.47
Effects of Exposure to Phthalates
and Their Metabolites in Laboratory Animals
Some phthalates and their metabolic products
act
functionally as anti-androgens during the
prenatal
period.48, 49, 50 Developmental effects in
males include
reduction in androgen-dependent tissues—in
the
reproductive organs such as seminal vesicles,
epididymus,
prostate, and anogenital distance.51,52,53,54 Furthermore,
exposure of rats prenatally and during
suckling
to DEHP and DBP has produced irreversible
testicular
damage at dose levels that caused only
minimal effects
in adult animals.55,56,57,58
Numerous studies have shown that some
phthalates
are toxic to embryos and cause developmental
malformations
in the offspring of exposed rodents. DEHP
has these effects in mice. It is also toxic
to rat embryos
at dose levels that are not toxic to the
mother.59,60 DBP
generally is toxic to the fetus of rats and
mice in the
absence of maternal toxicity, and it has
harmful developmental
effects only at doses high enough to be toxic
to the mother.61 In very recent studies,
rats exposed to
DBP during pregnancy and shortly after birth,
a number
of effects were seen in the male offspring
including:
decreased anogenital distance, absent or
underdeveloped
epididymis and seminal vesicles, cleft penis
(hypospadias), decreased reproductive organ
weights,
and widespread germ cell loss in the testis.
In contrast,
vaginal opening, age at fi rst estrus, and
estrous cyclicity
were not affected in the female offspring
indicating
that DBP does not mimic estrogenic but rather
acts as
an anti-androgen.62
Exposure during gestation and through
breastmilk
to large doses of dibutyl phthalate (DBP) and
its
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 54
metabolite, monobutyl phthalate (MBP), causes
male
reproductive tract malformations in rats.63,64 DBP reduces
the production of testosterone by the fetal
testis
through an anti-androgenic mechanism.65 Exposure
to high doses of DBP results in spontaneous
abortion
of rat pups, demasculinization of baby male
rats, and
decreased testicle size in rats, mice, ferrets,
and
guinea pigs.66,67
In male rats, high doses of DEHP have
resulted in
decreased testicle weights and smaller
tubules.68 The
DEHP metabolite, mono-2-ethylhexyl phthalate
(MEHP) may be the active agent.69,70
Although fewer studies have been carried out
on
female animals, existing studies suggest that
long-term
exposures of adult female rats result in
adverse effects,
including effects on the ovulation cycles and
cysts of
the ovaries.71 A recent study suggests
that DEHP,
through MEHP, suppresses the production of
the
hormone estradiol in the ovary, interfering
with egg
production.72
Several phthalates can also be carcinogenic
in
rodents.73,74,75 DEHP, DBP, and their
monoester metabolites
appear to have the greatest potential
toxicity.
DEHP is a peroxisome proliferator
hepatocarcinogen
in rodents,76 but the relevance of
carcinogenicity by
this mechanism in humans is being debated.77,78,79
Alkylphenols
Six of the seven alkylphenols and alkylphenol
ethoxylates
selected for analysis were detected in all samples.
These chemicals were the second most abundant
group of contaminants.
Nonylphenol diethoxylate was present at the
highest
concentration in six of seven samples. The
combined
concentrations of 4-nonylphenol, nonylphenol
monoethoxylate
and nonylphenol diethoxylate accounted
for 75–95 percent of the total concentrations
of this
group of contaminants. 4-Nonylphenol is
widely known
as an endocrine disruptor and is one of the
major
metabolites of the nonylphenol ethoxylate
surfactants.
Octylphenyl monoethoxylate and octylphenol
diethoxylate were detected in all samples,
but 4-octylphenol
was not quantifi able in any. As shown in
Figure
4, Rudel et al. (2003) reported a low
concentration of
4-octylphenol in their Cape Cod study.
Similarly, Santillo
et al. (2003) found 4-octylphenol at a low
concentration,
0.3 ppm, in only one sample in their study of
house dust in the U.K.
While bisphenol-A was not selected as an
analyte in
this study, Al Bitar (2004) detected this
compound at
2.2 ppm in Belgian house dust.
Alkylphenols and Alkylphenol Ethoxylates—
Production, Use, Occurrence and Effects
Alkylphenols (APs) are used primarily as raw
materials
for the manufacture of alkylphenol
ethoxylates (APEs).
They are also used in the preparation of
phenolic resins,
polymers, heat stabilizers, antioxidants, and
curing
agents. Almost half of global APE production
takes
place in the U.S. 80 With a total U.S. production of
more than 500 million pounds per year,
nonylphenol
ethoxylates account for about 80 percent of
total APE
use. Most of the remaining production
consists of
octylphenol ethoxylates.81
APs are also formed as degradation products
of
APEs. During wastewater treatment, APEs are
degraded
to form APs. In the liver, enzymes break down
the
toxic APEs to form APs.82
The most widely recognized hazard associated
with
alkylphenols is their ability to mimic
natural estrogen
hormones. This can lead to altered sexual
development
in some organisms.
The major uses of APEs are: industrial
applications,
55 percent; industrial and institutional
cleaning products,
30 percent; household cleaning products, 15
percent;
and other uses, less than 1 percent. 83 APEs are
used as nonionic surfactants in detergents;
applied as
dispersing agents in paper and pulp production
and
de-inking agents in paper recycling;
emulsifying agents
in latex paints, pesticide and herbicide
formulations,
and fi berglass and polystyrene products; as
wetters in
peats; as additives in cosmetics and in
polyvinyl chloride
used for food packaging; fl otation agents,
industrial
cleaners, cold cleaners for cars, and in the
textile
industry; in the form of
tris(nonylphenol)phosphates
as antioxidants in plastics. Nonylphenol is
the active
ingredient in spermicides. Nonylphenol or a
derivative
is also apparently used in food wrapping fi
lms, foodcontacting
plastics, and some toys because the chemical
has been found to leach from these materials
and
products.84,85,86,87,88,89,90
Nonylphenol is regarded as a ubiquitous
environmental
contaminant.91,92
Occurrence of Alkylphenols and
Alkylphenol Ethoxylates in People
There is very little information on the
occurrence of
alkylphenols and alkylphenol ethoxylates in
people.
Thus far, the Centers for Disease Control and
Prevention
(CDC) has chosen not to included alkylphenols
and alkylphenol ethoxylates in their
biomonitoring
program, as refl ected in the agency’s
National Report
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 55
on Human Exposure to Environmental Chemicals
of
2001 and the succeeding 2003 report.93,94 This will also
be the case in the CDC’s upcoming third
report. 95
In a very recent study, Calafat et al. (2005)
analyzed
archived urine samples from a reference
population
of 394 people in the U.S. and found
4-nonylphenol in
51 percent of the samples and bisphenol A in
95 percent
of the samples at concentrations of 0.1 parts
per
billion (ppb) or more.96 Scientists in Japan found
quantifi able concentrations of 4-nonylphenol
and
4-tert-octylphenol in human
plasma octylphenol in human plasma tert 97 but not in urine.98
Nonylphenol has also been detected in
umbilical cords
in Japan,99 confi rming that this
chemical is passed
from the mother to the developing fetus
through the
placenta. A very recent study in Germany has
found
nonylphenol in breastmilk100 confi rming that this
chemical can also pass from the mother to her
nursing infant.
Health Effects of Exposure to Alkylphenols
and Alkylphenol Ethoxylates in People
No studies were found of the health impacts
in people.
However, the most widely recognized hazard
associated
with APs, both nonylphenol and octylphenol,
is their
ability to mimic natural estrogen hormones.
This can
lead to altered sexual development and impact
reproduction
in some organisms.
Hazards to human health are not yet well defi
ned,
although a number of studies with animals,
such as
those described below, serve to highlight
concerns
that are very relevant to public health.
Effects of Exposure to Alkylphenols and
Alkylphenol Ethoxylates in Laboratory Animals
Most laboratory studies of the effects of
alkylphenols
and alkylphenol ethoxylates have explored
their
potential roles as endocrine disruptors and
associated
reproductive and developmental effects. For
example,
the ability of alkylphenols to mimic estrogen
has been
known for years.101 As such, alkylphenols have been
shown to reduce testicular function in rats.102 Of several
alkylphenols and alkylphenol ethoxylates
tested,
tertiary octylphenol showed the highest
estrogenic
activity.103
The estrogenicity of alkylphenols has been
known
for years and, as estrogenic compounds,
alkylphenols
have been shown to reduce testicular
function in
rats.
Both nonylphenol and octylphenol show
estrogenic
and anti-androgenic activities.104,105 Although nonylphenol
has the lower binding affi nity to estrogen
receptors, it exerts more estrogenic potency
because
serum has a more protective effect against
octylphenol.
This is an important fi nding to consider
when
comparing levels in the diet and actual
effects of
these and other estrogen mimics.106,107
The reproductive and developmental effects of
alkylphenols are illustrated in two low-dose
developmental
studies in rodents:
• Sharpe et al. (1995) showed that exposure
before
and after birth to octylphenols caused a
reproducible
and consistent decrease in testicular size
and
daily sperm production in rats during a
relatively
short period;108 and
• A multigenerational mouse study
demonstrated
that nonylphenol affected both the parents
and
offspring, most notably by diminishing the
size of
male reproductive organs, reducing sperm
quality
and decreasing fertility.109
Preliminary studies suggest that nonylphenol
may
also disrupt the human immune system. For
example,
in laboratory studies, nonylphenol inhibits
the production
of a chemical that attracts and activates an
important group of white blood cells.110 In mice, nonylphenol
also increases the production of a specifi c
chemical messenger in T lymphocytes and
increases
levels of certain antibodies. This suggests
that nonylphenol
may enhance allergic responses because both
the chemical messenger and the antibody are
key
factors in allergies.111
Dietary exposure of female rats to
octylphenol
throughout pregnancy and lactation can
interfere
with sexual development of male offspring by
changing
sexual behavior and decreasing adult body
weight,
testis weight, and the average diameter of
the seminiferous
tubules.112 Similar evidence has
come from studies
with newborn rats,113,114,115,116,117,118,119 and from
studies where the exposure has been carried
out for
longer periods into adulthood.120, 121
The estrogenic potency of octylphenol is
evidenced
by persistent estrus in females exposed in
adulthood
to octylphenol122 and caused the
production of an
hormone related to milk production
(prolactin) both
in the adult males123 and after newborn exposure124 as
well as in several other study
models.125,126,127,128,129,130
In a three-generation study with pigs,
octylphenol
exposure extended pregnancy length, induced
basel
cell proliferation in the cervical epithelium
of the
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 56
parental generation, accelerated onset of
puberty,
and reduced litter size in the fi rst
generation females.
In the fi rst generation offspring of female
pigs treated
with the low dosage of octylphenol, onset of
puberty
was accelerated. When fi rst generation young
female
and male pigs originating from sows treated
with high
dosages of octylphenol were bred, the litter
size was
reduced. When several alkylphenols and
alkylphenol
ethoxylates were tested, tertiary octylphenol
tended
to exhibit the highest estrogenic activity.131
Pesticides
“We have now acquired a fateful power to
alter
and destroy nature. But man is a part of
nature, and
his war against nature is inevitably a war
against
himself.”
—Rachel Carson, author of Silent Spring,
who fi rst raised awareness of the toxicity
and persistence
of DDT pesticides, quoted on CBS News, 1964
This group of chemicals included eleven
pesticides
and one synergist (piperonyl butoxide).
Together,
these chemicals were the third most abundant
of the
six groups of contaminants. Each of the dust
samples
contained quantifi able concentrations of fi
ve compounds:
4,4’-DDT, pentachlorophenol, cis-permethrin,
trans-permethrin, and piperonyl butoxide.
Only one
of the samples contained quantifi able
concentrations
of the two chlordane isomers and dieldrin.
Chlorpyrifos
also occurred in only one sample. Three of
the target
pesticides—diazinon, dicofol and
pentachloronitrobenzene—
were not present at quantifi able
concentrations in any of the samples.
Combining the concentrations of both
permethrin
isomers, this pesticide had the highest mean
concentration
(9.7 ppm) of all targeted pesticides in six
samples.
Pentachlorophenol had the highest
concentration,
7.3 ppm, in the seventh sample, and the
second
highest mean concentration,1.246 ppm, in the
six
sample dominated by permethrin.
Piperonyl butoxide had the third highest mean
concentration in this contaminant group, 0.69
ppm.
This chemical is used as a synergist in
formulations of
permethrin, other pyrethrins and pyrethroids
to increase
the effectiveness of the insecticides.132 As such
it is sometimes relied upon as an indicator
of the
presence of permethrin and other pyrethroids.133
As shown in Figure 5, Rudel et al. (2003)
also reported
major contributions by permethrin and
piperonyl
butoxide.134 However, the latter
chemical was
present at a far higher concentration, 15.8
ppm, in
the dust from Cape Cod than the mean
concentration
found in this study. It is possible that
because our
samples were composited (all 10 of the
samples put
together), the variations was lessened.
Pesticides: Permethrins, Piperonyl butoxide,
Pentachlorophenol and DDT
Permethrin, a synthetic pyrethroid, is used
to kill pest
insects in agriculture, home pest control,
forestry, and
in public health programs, including head
lice control.
It was fi rst marketed in 1973. Worldwide,
the dominant
use of permethrin is on cotton, accounting
for
about 60 percent (by weight) of the
permethrin
used.135 In the U.S., almost 70
percent of the permethrin
used in agriculture is used on corn, wheat,
and
alfalfa.136 It is widely used in
U.S. homes, and yards
and gardens. Permethrin, like all synthetic
pyrethroids,
kills insects by strongly exciting their
nervous systems.
Because of its ubiquitous use, the Food and
Drug
Administration’s monitoring program routinely
fi nds
permethrin on food. In 2001, it was the 8th
most commonly
detected pesticide137 with DDT being number 1.
Human and animal health effects
Experiments with laboratory animals indicate
that the
immune system “appears to be a sensitive
target for
permethrin activity.” Ingestion of permethrin
reduces
the ability of immune system cells called
T-lymphocytes
to recognize and respond to foreign proteins.
Doses
equivalent to 1/100 of the LD50 , inhibited
T-lymphocytes
over 40 percent. Permethrin ingestion also
reduced
the activity of a second type of immune
system
cell, natural killer cells, by about 40
percent.138 In tests
using mouse cell cultures, permethrin had
similar
effects on the immune system via the
inhibition of two
kinds of lymphocytes.139 Researchers concluded that
“the immune system is exquisitely
sensitive…at exposure
levels that cause no overt toxicity.”
Based on tests with laboratory animals, it
appears
children may be more sensitive to permethrin
than
adults. Permethrin is almost 5 times more
acutely
toxic to 8-day-old rats than it is to adult
rats.140
Experiments with laboratory animals indicate
that
the immune system appears to be a sensitive
target
for permethrin activity. Permethrin also
affects both
male and female reproductive systems.
Permethrin affects both male and female
reproductive
systems. It binds to receptors for androgen,
a male sex
hormone, in skin cells from human males,
causing
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 57
researchers to “advise protection from any
form of
contact or ingestion of the pyrethroids.”141 Permethrin
was mutagenic in three tests with human cell
cultures,
one with hamster cells, and one with fruit fl
y larvae.
In cultures of human lymphocytes (white blood
cells),
permethrin exposure caused an increase in
chromosome
aberrations, chromosome fragments,142 and
DNA lesions143 often linked to cancer
development.
According to the EPA, permethrin is a
possible
human carcinogen.144 The EPA found that permethrin
increased the frequency of lung tumors in
female
mice, and increased the frequency of liver
tumors in
male and female mice.145 The World Health Organization
reports that permethrin increased the
frequency
of lung tumors in females in two out of the
three mouse
studies it reviewed. Lung tumors increased
with increasing
permethrin exposure in the third study, but
the increase was not statistically signifi
cant.146
Piperonyl butoxide is used in formulations of permethrin,
other pyrethrins and pyrethroids as a
synergist
to increase the effectiveness of the
insecticides As
such it is sometimes relied upon as an
indicator of the
presence of permethrin and other pyrethroids.
It does
not by itself have pesticidal properties.
However, when
added to insecticide mixtures, their potency
is increased
considerably. Pyrethrin with piperonyl
butoxide kills
parasites and their eggs. Together they are
used to
treat scabies and lice infestations of the
head, body,
and pubic area. Pyrethrin with piperonyl
butoxide
does not prevent these infestations.
Piperonyl butoxide is a potent inhibitor of a
family
of enzymes (Cytochrome P450) that helps to
break
down many pesticides and is considered the
principal
detoxifi cation pathway for these chemicals.
Hindering
this detoxifi cation process allows higher
concentrations
of the active insecticide to remain within
the
target animal for a longer period.
It is still being debated whether the
substance is
oncogenic, mutagenic, or teratogenic in
humans. The
EPA has classifi ed piperonyl butoxide as a
possible
human carcinogen.147
Pentachlorophenol
In the U.S., most exposure to
pentachlorophenol
(PCP) comes from PCP its past use on treated
wood
and soil. From 1987 to 1993, the EPA recorded
releases
of PCP to land and water, mostly from treated
wood
and military munitions factories, totaling
nearly
100,000 pounds.148
PCP uses have been limited since 1984 to use
by
certifi ed applicators for certain purposes
such as a
preservative on wooden utility poles,
railroad ties and
wharf pilings.149 It is also still used in
California, mostly
on almonds and structural pest control.150
Health Effects
Technical grade PCP is frequently
contaminated with
dioxins and hexachlorobenzene151 making it diffi cult
to differentiate between the health effects
that are
due to pentachlorophenol itself and those
caused
by its common contaminants.
It is unclear whether exposure of the
developing
fetus to pentachlorophenol will result in
birth defects
or other developmental effects in people, but
laboratory
animals exposed to high levels during
development
experience health effects including low body
weight, decreased growth and skeletal
problems.152
PCP is a suspected endocrine disruptor,
interfering
with the natural function of estrogen,
androgen and
thyroid hormones.
The EPA has determined that pentachlorophenol
is
a probable human carcinogen and the
International
Agency for Cancer Research classifi es it as
possibly
carcinogenic to humans.153,154
DDT
DDT is no longer registered for use in the
United
States, although it is still used in other
(primarily
tropical) countries for malaria control. It
is in the EPA
Toxicity Class II, moderately toxic. DDT was
banned
from use in the United States in 1972, and
remains
banned barring public health emergency (e.g.,
outbreak
of malaria).155 The early popularity of
DDT, a
member of the chlorinated hydrocarbon group,
was
due to its reasonable cost, effectiveness,
persistence,
and versatility. During the 30 years prior to
its cancellation,
a total of approximately 1,350,000,000 pounds
of DDT was used domestically.
After 1959, DDT usage in the U.S. declined
greatly,
dropping from a peak of approximately 80
million
pounds in that year to just under 12 million
pounds in
the early 1970s. Of the quantity of the
pesticide used
in 1970-72, over 80 percent was applied to
cotton
crops, with the remainder being used
predominantly
on peanut and soybean crops. The decline in
DDT
usage was the result of increased insect
resistance; the
development of more effective alternative
pesticides;
growing public concern over adverse
environmental
side effects; and increasing government
restrictions
on DDT use.156
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 58
Occurrence and Effects
Even though current dietary levels are quite
low, past
and current exposures may result in
measurable body
burdens due to its persistence in the body.
There is
evidence that DDT causes reproductive effects
in test
animals. DDT is not metabolized very rapidly
by animals;
instead, it is deposited and stored in the
fatty
tissues. The biological half-life of DDT is
about eight
years; that is, it takes about eight years
for an animal
to metabolize half of the amount it
assimilates. If ingestion
continues at a steady rate, DDT builds up
within the animal over time. In a recent body
burden
study by the Centers for Disease Control and
Prevention
(CDC), scientists found DDT in blood of 99%
of
those sampled—the highest incidence of any
pesticide
sampled.157
Research by Cohn et al. reveals an unexpected asso- reveals an unexpected asso- al
ciation between DDT and delays in pregnancy
in the
daughters of exposed women, 30 years after
birth.
This is the fi rst scientifi c report ever of
a link between
DDT and reproductive outcome in women exposed
to
the contaminant in the womb. Their
statistical assessment
indicates that the association is unlikely to
be a
result of chance.158
We are still learning the consequences of
past
DDT use. Strong hints that there might be
more yet
to learn surfaced recently, when Centers for
Disease
Control scientists reported a striking
relation between
DDT and the likelihood of preterm birth.159 Longnecker
et al. demonstrate a powerful association be- demonstrate a powerful
association be- al
tween levels of the breakdown product of DDT,
DDE,
in mothers’ serum and the likelihood of
premature
birth. The higher the contamination level,
the more
likely was preterm birth. They also show that
contamination
is linked to the baby’s size, with babies
more
likely to be small for their gestational age
when born
to mothers with higher DDE levels.
More information on DDT & malaria is
available at:
http://www.panna.org/campaigns/docsPops/docsPops_
030317.dv.html
Polybrominated diphenyl ethers
“This stuff is everywhere”
— Dr. Jake Ryan, Health Canada
PBDEs were fourth in abundance among the
contaminant
groups. Three of the seven PBDEs that were
selected for analysis—BDE 47, BDE 99, and BDE
209
—were present at quantifi able concentrations
in all
dust samples. BDE 100 (penta) reached
quantifi able
concentrations in four samples, and BDE 153
and
BDE 154 (hexa), in two samples. No quantifi
able
levels of BDE 183 were found in any of the
samples.
As shown in Figure 7, decabrominated diphenyl
ether, BDE 209, predominated in 4 of the 7
samples
and, as shown in Figure 6, had the highest
mean concentration,
followed by BDE 47 and BDE 99. On average,
these three PBDEs accounted for 95 percent of
the total concentration of this contaminant
group.
As shown in Figure 7, a higher mean
concentration
of total PBDEs, 9.524 ppm, was found in this
study
than by Stapleton et al. (2005)160 in their study of
house dust from the Washington, DC area, 5.65
ppm.
However, BDE 209 was the largest contributor
in both
cases. The apparent lack of similarity to the
fi ndings
by Rudel et al. (2003) are due primarily to
differences
in the PBDEs selected for analysis, e.g., the
Rudel
study did not test for BDE 154 , BDE 183, and
BDE
209. Also, while total PBDEs in UK and
Belgian dust
fell within the range of those measured in
this study,
the PBDE “profi le” was very different in
that decabromodiphenyl
ether (BDE 209) accounted for a far larger
share of total PBDE concentrations in the
European
samples. This may be attributed to mandated
and voluntary
actions in the European Union to phase out
the use of those PBDEs that were thought to
pose
greater health threats.
Polybrominated Diphenyl Ethers—
Production, Use, Occurrence and Effects
“The accumulation and ongoing increase in
the
levels of PBDEs calls for immediate measures
to
stop the environmental pollution and human
exposure to PBDEs.”
—Noren and Meironyte, 2000.161
More than 70 brominated chemicals or groups
of
chemicals are used as fl ame retardants in
plastics, textiles
and other materials. Polybrominated diphenyl
ethers (PBDEs) are one of the three groups
that dominate
the market for fl ame retardants.162 In 1999, total
global production of the three major
commercial
PBDE products was 67,125 metric tons:
deca-BDE,
82 percent; penta-BDE, 13 percent; and
octa-BDE,
6 percent; and penta-BDE, 13 percent.
Ninety-eight
percent of penta-BDE is used in North
America.163
PBDEs are applied to or incorporated into
many
common household products, such as furniture,
carpeting,
mattresses, televisions, coffee makers, and
hair
dryers.164 Decabromodiphenyl ether
(Deca-BDE or
BDE 209) is most commonly used in plastics
and textiles,
in electrical components, and in styrene
rubbers
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 59
used in carpet backing and furniture.165 Sunlight and
UV light can degrade BDE 209 to form less
brominated
BDEs, such as the pentabromodiphenyl ethers
(penta-BDEs).166
PBDEs have been found in air, water, fi sh,
birds,
marine mammals, and humans, and in many
cases,
concentrations are increasing over time.167 Diet is regarded
as the most likely route of PBDE exposure for
the general population.168 However, air inside homes
and offi ces can carry PBDE concentrations
that are
estimated to be almost ten times higher than
levels in
the air outside the buildings.169 Moreover, house dust
has been identifi ed as an important pathway
of PBDE
exposure for young children.170 Despite the ubiquity
of PBDEs, information on their toxicology is
limited.171
Occurrence of Polybrominated Diphenyl Ethers
in People
The Centers for Disease Control and
Prevention
(CDC) does not monitor PBDEs in the U.S.
population.
No data on PBDE levels are given in CDC’s
National
Report on Human Exposure to Environmental
Chemicals of 2001 or the succeeding 2003
report,172,173
and PBDE data will not be included the CDC’s
upcoming
third report.174
Many other studies have found PDBEs in human
breast milk,175,176, 177,178,179,180 blood,181,182 umbilical cord
blood, 183, 184 and adipose tissue.185,186,187,188 Interestingly,
the German national biomonitoring program
found that men had PBDE levels from 20 to 75
percent
higher than women, depending on the sampling
year.189
PBDE concentrations in human serum and breast
milk have been increasing at exponential
rates for
more than two decades.190,191,192,193 During the period
of 1972 to 1997, levels of organochlorine
contaminants
in the breast milk of Swedish mothers were
falling
while PBDE concentrations were rising.194 However,
a recent study indicates that PBDEs in
Swedish breast
milk began to decrease in 1997, possibly due
to a
voluntary phase-out of penta-BDE.195
Studies of breast milk in the U.S. have found
PBDE
concentrations 10 to more than 100 times
higher than
those in Europe.196,197,198 Moreover, contrary to claims
by PBDE producers that BDE 209 (deca) is
neither
mobile nor bioavailable, three recent studies
have
identifi ed BDE 209 in 20 to 80 percent of
breast milk
samples.199,200,201 BDE 209 has also been
identifi ed as
the dominant PBDE in several U.S. food
groups.202
PBDE levels in mother’s milk and blood were
shown to have a strong correlation with PBDE
levels
in fetal blood in a study carried out in
Indianapolis,
Indiana, where maternal and fetal blood
levels were
20–106 times higher 203 than the levels reported previously
in Swedish mothers and infants 204 and 20 times
higher than Norwegian blood samples.205 Twentythree
women from the San Francisco Bay Area were
found to have PBDE concentrations in adipose
tissue
from their breasts higher than have been
reported
to date in human tissues. 206
The tetrabrominated PBDE congener, BDE-47,
is the most abundant PBDE congener in all
human
samples tested, making up 53–65% of total
PBDEs
detected. The other major congeners include,
BDE-99, 100, 153, and 154.207,208,209
Effects of Polybrominated Diphenyl Ethers in
Human
Several relatively dated studies cited by
Darnerud
(2003) found no effects: no skin
sensitization was observed
among human volunteers exposed to decaBDE
products and no effects were noted in four
epidemiologic
studies of workers from workplaces where fl
ame
retardants were used.210
However, in a U.S. study, workers exposed to
PBBs
and PBDEs during manufacture had
higher-than-normal
rates of primary hypothyroidism and signifi
cant
reductions in conducting velocities in
sensory and motor
neurons were reported. However no conclusions
were drawn about the causative role of PBBs
and/or
PBDEs.211
A study of fi sh consumers in the Baltic
region found
that higher levels of BDE 47 were weakly
associated
with lower plasma levels of the thyroid
hormone, thyrotropin.
212 The researchers noted that the weak positive
correlation could have been due to chance.
However
the fi ndings of the U.S. study suggest that
the
correlation may not have been a chance
occurrence.
Effects of Polybrominated Diphenyl Ethers
in Other Species
Laboratory studies indicate that some PBDEs
may trigger
dioxin-like responses, although at
concentrations
that are far higher than those required for
the most
potent dioxin congener.213 Similarities have also been
drawn to the PCBs, with PBDEs associated with
birth
defects, liver and kidney damage, thyroid
imbalances
and neurological damage to animals and
humans.
In studies with laboratory animals, mice and
rats
exposed to one or more PBDEs have shown a wide
variety of effects including evidence of
endocrine
disruption,214,215,216,217,218 reproductive/developmental
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 60
toxicity including neurotoxicity,219,220,221,222 and cancer.223
Mice exposed to some PBDEs three or ten days
after
birth exhibited changes in spontaneous
behavior
(locomotion, rearing, and total activity)
when twomonths
old, while post-natal exposure to other PBDEs
resulted in impaired learning and memory.224,225,226
Such effects are similar to those seen after
exposure
to DDT or PCBs.227
Generally, the pentaBDEs seem to cause
adverse
effects at lower doses while much higher
doses of
decaBDE are required to produce effects. The
more
critical effects of pentaBDEs are on neurobehavioural
development and thyroid hormone levels. Both
rats
and rabbits exhibited fetal
toxicity/teratogenicity following
exposure to octaBDEs and changes in thyroid,
liver and kidney morphology after exposure to
decaBDE.
At very high levels, decaBDE was carcinogenic
in animals.
However, IARC (1990) considers decaBDE not
to be classifi able with regard to
carcinogenicity in
humans.228 Other PBDEs have shown
genotoxic effects
in mammalian cell lines, which suggests that
they may
be cancer promoters. 229
After neonatal exposure to PBDE 99 and PBDE
153, adult mice also exhibited learning and
memory
effects. The induction of permanent
aberration in
spontaneous behaviour was induced during
limited
period of the neonatal brain development.230,231 The
altered spontaneous behaviour also worsened
with
age.232,233 Developmental neurotoxic
effects after neonatal
exposure to PBDE 209 are suggested to be
caused
by a metabolite.
Common metabolites of the PBDEs are reported
to
compete strongly with the thyroid hormone,
thyroxin
raising the potential for a broad range of
effects on
growth and development, including permanent
neurobehavioral impacts, that are comparable
to
the thyroid disrupting effects of PCBs.
PBDEs are thought to have low acute toxicity.
However
chronic exposure to low levels during
gestation
and via lactation can cause irreversible
changes in development.
Studies with laboratory animals indicate
that PBDEs are transferred from the mother to
the
fetus via the placenta and from the mother to
the nursing
offspring through breast milk.234,235,236,237,238,239,240
Following gestational and/or lactional
exposure, offspring
show signs of thyroid disruption and
developmental
neurotoxicity,241,242,243,244,245,246 as well as other
endocrine and genetic effects.247,248,249,250,251,252,253
Laboratory animals exposed to PBDEs during
the
perinatal period exhibited exhibited
behavioral
changes when they reached adulthood. These
changes included marked hyperactivity and
learning and memory defi cits.
Chronic exposure, particularly during
gestation,
can interfere with brain and skeletal
development in
rats 254 and lead to permanent
neurological effects.255
Common metabolites of PBDEs are reported to
compete
strongly with the thyroid hormone, thyroxin,
raising the potential for a broad range of
effects on
growth and development, including permanent
neurobehavioral
impacts, comparable to the thyroid disrupting
effects of PCBs. (Meerts et al. 1998, 2000,
2001). Other researchers have also raised the
possibility
that, considering the structural similarity
of PBDEs
with PCBs and the known health effects of
PCBs, the
two groups of chemicals could work through
the same
mechanism to cause developmental
neurotoxicity.256
When mice are exposed shortly after birth, PBDEs,
including BDE 209, have been shown to
distribute
throughout the body and concentrate in the
brain.
They induce developmental neurotoxic effects
in
adult mice that worsen with age and lead to
abnormal
behaviour. 257 For example, laboratory
animals exposed
to PBDEs during the perinatal period
exhibited
exhibited behavioral changes when they
reached adulthood.
These changes included marked hyperactivity258,259 hood. hyperactivity
and learning and memory defi cits.260
A range of PBDEs show estrogenicity in human
cells lines and bind to the estrogen
receptors.261 PBDEs
are also metabolized to form
hydroxylated-PBDEs that
are even more potent estrogen mimics.262
Organotins
As far as we could establish, this is the fi
rst time that
organotins were analyzed in American
household
dust. Of the seven organotins that were
tested, four
were quantifi ed in all samples:
monobutyltin, dibutyltin,
tributyltin, and di-n-octyltin. The other
three—
tetrabutyltin, tricyclohexyltin and
triphenyltin—were
below reportable limits in all samples. The
total concentration
of all selected organotins ranged from 388
to 911 parts per billion (ppb). Monobutyltin
was the
predominant organotin in three samples and
dibutyltin
dominated in three samples. In the remaining
sample, the concentrations of these two
compounds
were almost the same.
As shown in Figure 8, total organotin
concentrations
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 61
in this study are in the same general range
as the mean
value reported by Costner et al. (2004) in
dust from
Brazil and by Fromme et al. (2005)263 in dust from
German homes. However, they are markedly
lower
than the total mean concentrations reported
by Al
Bitar (2004) for Belgian dust samples.
Monooctyltin was not selected as an analyte
in this
study. However, Fromme et al. (2005) found
this compound
at a mean concentration of 10 ppb in house
dust in Germany and Costner et al. (2004)
reported
a mean of 62.5 ppb in house dust in Brazil.
Organotins—Production, Use, Occurrence
and Effects
“At pharmacologic levels butyltins might
contribute
to the onset of developmental disorders of
the male
reproductive system.”
— Doering et al. (2002) 264
No information on current production rates for
organotins
was found. However, major use of organotins
began some 40 years ago in parallel with mass
production
of PVC plastic (vinyl).265 Between 1955 and
1992, organotin production increased by a
factor of
ten266 and, reached about
40,000 metric tons per year
in 1996.267 Mono- and dialkyltins
account for 81 percent
of total organotin use: 76 percent used as
heat
and light stabilizers for PVC and 5 percent
as catalysts
for polyurethane and silicone elastomers. The
remaining
total organotin use consists mainly of
tributyl, triphenyl-
and tricyclohexyltin, about 10 percent of
which
is used as antifouling biocides and 8 percent
as pesticides.
268,269
Organotins are found in PVC water pipes, PVC
food packing materials (e.g., dioctyltin),
glass coatings
(e.g., butyltin trichloride), polyurethane
foams.270
Other uses, mainly of butyltin, include rigid
PVC pro-
fi les and sidings. Venetian blinds, rain
gutters, window
profi les and, in particular in the U.S.,
building sidings.271
Organotins also occur in textile products
that contain
polymer parts, such as t-shirts with prints,
sanitary napkins,
bandaids and diapers and they are used as
fungicides
on textiles that are exposed to extreme
conditions,
such as canvas. 272 Organotins were found in 50
percent of ordinary plastic products
purchased in a
Japanese supermarket—diaper covers, sanitary
napkins,
polyurethane gloves, cellophane wrap,
dishwashing
sponges and baking parchments. Organotins
were
also found in the cookies baked on the
parchment.273
Another study in Japan found organotins in
children’s
PVC toys—face masks, balls, soft toys and
food toys.274
Organotins have also been detected in
drinking water
transported through PVC pipe.275,276,277,278 Elevated
levels of organotins, particularly tributyltin,
have also
found in PVC fl ooring and somewhat lower
concentrations
in carpets.279
Organotins are found in ambient air and
precipitation,
280,281 freshwater resources, ocean water, soils and
sediments.282,283,284 Organotins, particularly
tributyltin
(TBT), have been identifi ed in many species
including
mollusks, fi sh, marine birds, marine
mammals,
and freshwater birds,285 as well as various terrestrial
mammals.286 In short, these
chemicals are ubiquitous
in the environment.287
Occurrence of Organotins in Humans
The Centers for Disease Control and
Prevention
(CDC) does not monitor organotins in the U.S.
population.
No data on organotin levels are given in
CDC’s
National Report on Human Exposure to
Environmental
Chemicals of 2001 or the succeeding 2003
report,288,289 and organotins will not
be included the
CDC’s upcoming third report.290
Few studies of the occurrence of organotins
in
human tissues are available. However, in a
1999 study,
organotins were tested in the blood of people
living in
Michigan: monobutyltin (MBT) was present in
53 percent
of the samples; dibutyltin (DBT), 81 percent;
and
tributyltin (TBT), 70 percent. Concentrations
were
in the order of MBT > DBT > TBT. The fi
ndings were
taken to suggest exposure to MBT and DBT,
which
are used in a variety of consumer products.291
Organotins occurred with less frequency in
blood
samples from the Environmental Specimen Bank/
Human Specimen Bank in Germany: MBT was
measurable
in 17 percent of the samples; DBT in 3
percent;
and no other organotins were detected.292 Organotins
have also been detected in the liver tissues
of people
in Japan,293 Poland,294 and Denmark.295 Methyltins
have also been detected in human urine296
Effects of Organotins in Humans
Human fatalities from widespread poisoning
with
organotin occurred in France and Algeria in
1954 when
Stalinon capsules, containing 15 mg of
diethyltin,
were used to treat staphylococcal skin
infections.297
Accidental poisoning with trimethyltin has
resulted
in memory defi cits, seizures, altered
emotional affect,
hearing loss, disorientation, and death.
Limited
evidence suggests that mono- and dimethyl tin
are
neurotoxic in humans.298
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 62
Effects of Organotins in Other Species
Organotins are toxic at relatively low levels
of exposure.
Tributyltins (TBT) and triphenyltins (TPT)
are
all listed as poisons and described as
respiratory toxins,
fetotoxins, reproductive toxins,
immunotoxins, possible
carcinogens, skin and respiratory irritants,
and
allergens.299,300 TPT interferes with the
cell components
responsible for moving chromosomes into place
before
a cell divides and acts synergistically with
pentachlorobiphenyl,
a PCB, to induce abnormal chromosome
arrangements in mitosis at very low
concentrations.301
The relative toxicities of the butyltins are
often considered
to be TBT > DBT > MBT.302 However, DBT is
more toxic than TBT to certain enzyme
systems,303,304
and DBT is more toxic than TBT to the immune
systems in fi sh.305
Studies have reported that MBT, DBT, and TBT
act
synergistically when exposed in combination
(ie. their
combined effects is more pronounced than the
effects
of each one added together). Butyltin
compounds in
blood have also been reported to be able to
interact
with other classes of contaminants such as
organochlorines
to lead to adverse effects.306
Organotins are also toxic to the immune
system in
rats and other mammals.307 The immune system toxicity
of DBT, TBT and triphenyltin stems from their
capacity for destroying or limiting the
functionality of
various white blood cells.308,309,310,311,312,313,314.315,316 DBT
is frequently shown to be more toxic to the
immune
system than TBT.317,318
DBT is neurotoxic to mammalian brain cells.319
DBT has been shown to exert toxic effects on
the immune
system at concentrations comparable to those
reported in human blood.320 DBT also had toxic effects
on the nervous system at levels that were
lower
than those reported in human blood and some
forty
times lower than the lowest toxic
concentration of trimethyltin,
a known neurotoxicant.321 These fi ndings
suggest that chronic, low-level exposure to
DBT in
human populations may have impacts on both
the
immune and nervous systems.
Organotins are transported through the
placenta,
as demonstrated by their adverse
developmental
effects.322 A recent study suggests
some in utero developmental
effects may result from the impacts of
relatively
low doses of TBT on maternal thyroid
function.
Effects included: reduced maternal weight
gain; increased
post-implantation loss; decreased litter
sizes;
decreased fetal weights; delayed fetal
skeletal development;
and abnormalities in genital development in
male fetuses.323
Some of the reproductive and developmental
effects of organotins on mice and rats
summarized
in a recent review are: 324
• TPT caused decreased fertility due to
degenerative
changes in testicular tissue and ovarian
impairment.
• Triphenyltin chloride (TPTCl) and
diphenyltin
chloride (DPTCl) exposure during early
pregnancy
caused implantation failure.
• TPT exposure during pregnancy caused
embryonic/
fetal death, suppressed fetal growth at doses
toxic
to the mother, and, at lower doses, resulted
in
behavioral changes in the offspring.
• Maternal exposure to tributyltin chloride
(TBTCl)
decreased weights of male reproductive
organs,
decreased sperm counts, decreased serum
estradiol
levels, delayed vaginal opening, impaired
estrous
cyclicity, and increased female anogenital
distance
in the offspring. Given during early
pregnancy,
TBTCl or dibutyltin chloride (DBTCl) resulted
in
implantation failure.
• Maternal exposure to TBT resulted in
embryonic/
fetal deaths, suppressed fetal growth and
cleft palate
at doses toxic to the mother and, at lower
doses,
behavioral changes in offspring.
• DBT produced fetal malformations.
Perfl uorinated Chemicals
All dust samples contained quantifi able
concentrations
of the two target perfl uorinated
chemicals—perfl uorooctanoic
acid (PFOA) and perfl uorooctanyl sulfonate
(PFOS). PFOS concentrations were highest in
all
samples, with a mean of 424 ppm and a range
of 76.4
to 1,170 ppm, while the mean concentration of
PFOA
was 78.7 ppm with a range of 18.5 to 205 ppm.
As illustrated in Figure 9, the mean total
PFOS/
PFOA concentration, 503 ppb, found in this
study is
quite close to that reported by Moriwaki et
al. (2003)
for house dust in Japan. However, PFOS was,
by far,
the largest contributor to the total
concentration of
these two perfl uorinated chemicals in the
dust samples
of the present study, while PFOA was largest
in
dust samples from Japan. PFOS is generally
regarded
as the fi nal product of degradation for
other perfl uorooctanyl
compounds. The difference in the PFOS/
PFOA ratios of these two groups of house dust
samples
may conceivably refl ect earlier use of perfl
uorinated
surfactants in consumer products in the U.S.
and, consequently, greater opportunity for
these
substances to degrade to PFOS.
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 63
Perfl uorinated Chemicals—Production,
Use, Occurrence and Effects
PFOA is detectable in the blood of most
humans
and animals worldwide, which is problematic
because
it is only slowly eliminated in mammals, is
potentially
toxic, has no known metabolic or
environmental degradation
pathway, and is potentially carcinogenic.
— Ellis et al., 2005 325
The two perfl uorinated chemicals (PFCs) that
were
selected as analytes for this study—perfl
uorooctanoic
acid (PFOA) and perfl uorooctane sulfonate
(PFOS)—
are only two of the already quite large and
still growing
number of PFCs that are manufactured and/or
found in the environment. PFOA is the
best-known of
the PFCs because it is used to make Tefl on,
Goretex,
and other oil-, water- and stain-resistant
materials used
in many common items, including nonstick
frying
pans, utensils, stove hoods, stainproofed
carpets, furniture,
and clothes.326
PFOA is used to make fl uoropolymers, which
had a
global consumption rate of 112 thousand
metric tons
valued at $2.1 billion in 2001,327 and fl uoroelastomers,
with a global consumption rate of 15 thousand
metric
tons valued at $700 million in 2002.328 Polytetrafl uoroethylene
(PTFE or vinyl fl uoride), commonly marketed
as Tefl on, accounted for 60-65 percent of
all fl uoropolymer
consumption in the US., Western Europe and
Japan in 2001.329 DuPont has almost 50
percent of the
global market share for fl uoropolymers,330 while the
U.S. accounts for 45 percent of the world’s
fl uoroelastomer
consumption.331 PFOA and PFOS may also
be
formed as products of the degradation of
other PFCs.
Both fl uoropolymers and fl uoroelastomers
are used
in soil, stain, grease, and water-resistant
coatings for
textiles, carpet, cookware and automobiles.
PFOA is
also used widely in fi re-fi ghting foams.
PFOS has been
used in refrigerants, surfactants, polymers,
pharmaceuticals,
fl ame retardants, lubricants, adhesives,
cosmetics,
paper coatings, and insecticides. However,
the
U.S. manufacturer, 3M, discontinued PFOS
production
in 2000.332
Relatively high concentrations of some PFCs
have
been found in the indoor air of homes. In
Canada,
three PFCs were detected in indoor air of two
homes
and a laboratory at concentrations about 100
times
higher than in outdoor air. A PFC that is
widely used
as a stain repellent on carpets was the most
abundant
of the three PFCs in both indoor and outdoor
air.333
A later, more comprehensive study involving
more
than 50 homes confi rmed that some PFCs are
present
in indoor air at very high concentrations.334
A PFC that is found as a by-product in oil-
and
water-repellent coatings for paper and
paperboard
used for food packaging was detected in more
than
55 percent of composite fast food samples in
Canada.
This PFC is also used as a pesticide in the
U.S.335
PFCs are pervasive contaminants in the global
environment.
PFOS and other PFCs are found in freshwater
and marine mammals, fi sh, birds, shellfi sh,
and
domestic cattle.336,337,338,339,340,341,342,343 Although distribution
is global, including remote locations in the
Arctic
and North Pacifi c Oceans, concentrations of
PFCs are
relatively greater in or near the more populated
and
industrial regions.
It was known as early as 1975 that fumes
from hot
pans coated with polytetrafl uoroethylene
(PTFE,
Tefl on) can kill pet birds. Broiler chicks
have died
after exposure to polytetrafl
uoroethylene-coated
light bulbs.
Occurrence of Perfl uorinated Chemicals in
Humans
The Centers for Disease Control and
Prevention
(CDC) does not monitor PFCs in the U.S.
population.
No data on PFC levels are given in CDC’s
National
Report on Human Exposure to Environmental Chemicals
of 2001 or the succeeding 2003 report,344,345 and no PFCs
will be included the CDC’s upcoming third
report.346
However, U.S. EPA has proposed that CDC
include
PFOS, PFOA and other perfl uorinated
chemicals in
the next national study.347
A number of studies have found PFCs to be
pervasive
contaminants in the blood of the general
population
of the U.S. A broad survey of individual
blood
samples from adult Red Cross blood donors,348 children
from a clinical trial, 349and a group of elderly people
from Seattle, Washington.350 A number of studies of
fl uorochemical production workers found PFC
levels
in blood that were, on average,20-30 times
higher than
the concentrations found in the general
population.
351,352,353,354
For very thorough and detailed descriptions
of the
fi ndings of these studies as well as
potential health impacts
and other aspects of the perfl uorinated
chemicals,
see the Environmental Working Group report,
“PFCs:
A Family of Chemicals That Contaminate the
Planet,”
and related materials at http://www.ewg.org/reports/
pfcworld/
PFCs are also found in the blood of the
general
populations of Italy, Colombia, Brazil,
Belgium, Poland,
India, Malaysia, and Korea355 as well as Sweden,356,357
Japan,358 and in indigenous peoples
in Northern
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 64
Canada.359 PFCs are also found in
the liver tissue
of the general U.S. population.360
The presence of PFCs in cord blood has been
demonstrated,361,362 indicating that these
chemicals
pass from the mother through the placenta to
the developing
fetus.363 PFCs have been detected
in human
breast milk in one very limited study that
found fewer
specifi c PFCs at concentrations below those
in blood
serum.364 This study, a study with
rats,365 and a study
of wood mice366 all indicate that PFCs
are passed
from mother to breastfeeding infant.
Effects of Perfl uorinated Chemicals in Humans
The following text is excerpted from the
summary
and conclusions of the OECD hazard assessment
of
PFOS and its salts: 367
“Several occupational studies have been
conducted
on volunteers at the 3M plants in Decatur,
Alabama
and Antwerp, Belgium.… In a mortality study,
which
followed workers for 37 years, mortality
risks for most
of the cancer types and non-malignant causes
were not
elevated. However, a statistically signifi
cant risk of
death from bladder cancer was reported.
Three male
employees in the cohort died of bladder
cancer (0.12
expected), and all of them had been employed
at the
plant for more than 20 years. All of them
had also
worked in high exposure jobs for at least 5
years. In
order to screen for morbidity outcomes, an
“episode of
care” analysis was undertaken for employees
who had
worked at the plant between 1993 and 1998.
Many
different types of cancer and other
non-malignant conditions
were examined. Increased risks were not
reported
for most of the conditions or did not reach
statistical
signifi cance. However, an increased risk of
episodes
was reported for neoplasms of the male
reproductive
system, the overall category of cancers and
benign
growths, and neoplasms of the
gastrointestinal tract.
These risk ratios were highest in employees
with the
highest and longest exposures to fl
uorochemicals.”
Effects of Perfl uorinated Chemicals in Other
Species
It was known as early as 1975 that fumes from
hot
pans coated with polytetrafl uoroethylene
(PTFE,
Tefl on) can kill pet birds, and broiler
chicks have
died after exposure to polytetrafl uoroethylenecoated
light bulbs.368
In 1979, 3M administered four doses of PFOS
to
monkeys and all the monkeys in all treatment
groups
died within weeks.369 Note that as mentioned above,
3M did not discontinue production of this
chemical
until 2000.
A study of female laboratory rats indicates
that
PFOS can affect the neuroendocrine system.
Exposed
to PFOS, female rats evidenced loss of
appetite, interrupted
estrus cycles, and elevated stress hormone
levels. PFOS was found to accumulate in brain
tissue,
particularly the hypothalamus, suggesting
that PFOS
crosses the blood-brain barrier and may
interfere with
reproductive hormones through the
pituitary-hypothalamus
process that stimulates their production.370
One recent review noted that studies in
monkeys,
rats, fi sh and humans have found that
subchronic exposure
to PFOS led to signifi cant weight loss,
liver toxicity,
reduced serum cholesterol, and reduced
thyroid
hormones. In rats, rabbits and mice,
developmental
effects included reduced fetal weight, cleft palate,
edema,
delayed ossifi cation of bones and cardiac
abnormalities.371
Exposure of rats and mice to PFOS during
pregnancy
resulted in both toxic effects to the mother
and
birth defects in the offspring. Exposed
mothers exhibited
a broad range of effects: dose-dependent
suppression
of maternal weight gain, reduced maternal
thyroid
hormone levels (thyroxine and
triiodothyronine);
reduced maternal serum triglycerides; and
marked
enlargement of the liver at higher doses.
PFOS was
detected in the livers of rat fetuses at
levels about half
of those of their mothers. Among the
resulting birth
defects were cleft palate, generalized edema,
ventricular
septal defect, and enlargement of the right
atrium.372
The follow-up study found that PFOS exposure
during
pregnancy severely compromised survival of
the offspring,
caused delays in growth and development, and
was accompanied by reduced thyroid hormone
levels.
At the highest PFOS dosages, 95 percent of
the newborn
rats and mice died within 24 hours of birth.
Survival improved at lower dosages.373
Wood mice from a nature reserve near two fl
uorochemical
facilities in Belgium PFOS-contaminated
areas in Belgium showed an age-dependent
increase
in PFOS concentrations in liver tissue,
increased liver
weights at high PFOs concentrations in the
liver, decreased
serum triglyceride levels with increased PFOS
exposure, evidence of possible liver damage,
and evidence
of maternal PFOS transfer to the young during
pregnancy and/or lactation.374
Recent laboratory studies with PFOA involving
rats
show low birth weight, small pituitary gland,
altered
maternal care behavior, high pup mortality,
and signifi
cant changes in the brain, liver, spleen,
thymus,
adrenal gland, kidney, prostate, testes and epididymides.
375
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 65
Color Code Rating Description
Gold Star Company adheres to the Safer Chemicals Pledge
Green Company avoids the use of the Priority OSPAR1 list of chemicals in their product line; this
is stated to us via the questionnaire or
through detailed information about their chemical
policy on their website.
Yellow Company is transitioning out of one or more high priority
chemicals - this is stated to us
via the questionnaire or through detailed
information about their chemical policy on their
website or through publications.
Orange Company has not replied to the questionnaire, has no detailed
information about chemical
policy on their website but has recently made
a public announcement to phase out
one or more of the OSPAR group of chemicals.
Red Company has not replied nor gives any detailed information online
to their consumers
about their chemical policy.
Explanation of Color Coding in Company Ranking
A P P E N D I X I I : Company Rankings on
Chemical Policies
* OSPAR (1992) List of Chemicals for Priority
Action are internationally recognized chemicals of high concern which
North Atlantic European countries have
committed to eliminate over the long term (www.ospar.org)
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 66
Cosmetic Manufacturers
Color Code Company Incorporation of a
Sustainable Chemicals Policy Contact Information
Yellow Aveda In accordance with the company’s Material Use
Guidelines, Aveda is working to eliminate the
use
of any materials considered persistent organic
toxins.
http://www.aveda.com/
contactus/
contactus.tmpl
Yellow Unilever Unilever is committed to phasing out phthalates in
products sold in the USA. The company has
adopted
improved screening methodologies to avoid the
use
of chemicals that disrupt the endocrine
system. The
company does not use alkylphenols in European
products, it is unclear whether or not US products
contain these chemicals.
http://
www.unilever.com/
home/contactus/
/Orange L’Oreal L’Oreal is
committed to phasing out phthalates. The
company does not have a public chemical policy
to
ensure that their suppliers replace
alkylphenols and
other chemicals of concern with safer
alternatives.
http://www.loreal.com/_
en/_ww/tools/
index.aspx?contact/
contact_1.aspx
Orange Revlon Revlon is committed to phasing out phthalates. The
company does not have a public chemical policy
to
ensure that their suppliers replace
alkylphenols and
other chemicals of concern with safer
alternatives.
http://www.revlon.com/
information/
contactform.asp
Orange Estee
Lauder
Inc.
Estee Lauder Inc. is committed to phasing out
phthalates. The company does not have a public
chemical policy to ensure that their suppliers
replace
alkylphenols and other chemicals of concern
with
safer alternatives.
http://
www.elcompanies.com/
htm/frameset/frm_
m5.htm
Orange Procter &
Gamble
Procter and Gamble is committed to phasing out
phthalates. The company does not have a public
chemical policy to ensure that their suppliers
replace
alkylphenols and other chemicals of concern
with
safer alternatives.
http://www.pg.com/
getintouch/index.jhtml
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 67
Retailers
Color Code Company Incorporation of a
Sustainable Chemicals Policy Contact Information
Yellow IKEA
Most of the OSPAR high priority chemicals are
not used in IKEA products. IKEA has phased out
the use of brominated fl ame retardants (BFRs)
in mattresses, carpets, and furniture. IKEA is
still working to phase out BFRs in their
lighting
fi xtures. With the exception of cables, IKEA
phased out all uses of PVC by 1996, thereby
signifi cantly reducing and often eliminating
the
use of phthalates and organotins. They have a
phthalate ban on all children’s products. IKEA
bans pesticides from their products. IKEA also
bans the use of carcinogens in their products.
http://info.ikea-usa.com/
IKEAContactUs/
Contact.aspx
Red Target Target does not have a public chemical policy
to ensure that their suppliers avoid OSPAR and
other chemicals recognized as posing a risk to
human health.
1-800-440-0680
Red Sears Sears does not have a public chemical policy
to ensure that their suppliers avoid OSPAR and
other chemicals recognized as posing a risk to
human health.
1-800-349-4358
Red Walmart Walmart does not have a public chemical policy
to ensure that their suppliers avoid OSPAR and
other chemicals recognized as posing a risk to
human health.
1-800-WAL-MART
Red Home
Depot
Despite partnerships with Natural Step and a
commitment to green alternative products, Home
Depot does not have a public chemical policy
to
ensure that their suppliers avoid OSPAR and
other
chemicals recognized as posing a risk to human
health.
1-800-553-3199
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 68
Televisions
Color Code Company Chemical Policy in the US
Contact Info
Yellow Samsung
Electronics
Samsung Electronics is committed to phasing
out brominated fl ame retardants by the end of
2005. The company is also committed to fi
nding
safer alternatives for other OSPAR chemicals
including phthalates, and organotins as well
as
replacing materials such as PVC that release
chemicals of concern.
http://www.samsung.com/
ContactUs/ContactUs.htm
Yellow Sony Sony has a public policy to transition out of all
applicable OSPAR chemicals. For brominated
fl ame retardants, Sony is committed to
replacing
them with halogen free alternatives, including
TBBPA. Sony restricts the use of PVC in
certain applications and has started to use
biobased plastics in some of their products.
http://esupport.sony.com/
feedback/feedback.html
Orange Panasonic Despite a strong commitment to increase the
use of halogen free (PVC free) plastics and
lead-free solders, Panasonic does not have
a clear chemicals policy for other hazardous
materials. In Europe, they will introduce
chlorine
free wiring within 2005 and eliminate the use
of PVC by the end of March 2006. It is unclear
whether or not this is a global commitment.
http://www.panasonic.
com/environmental/
contact_us.asp
Orange Philips Despite a strong commitment to sustainability
and the removal of lead from their products,
Philips does not have a clear public policy on
thier use of other hazardous materials in US
products. In Europe, Philips is committed to
removing brominated fl ame retardants by 2006,
but it is unclear whether or not this is a
global
commitment.
1-888-744-5477
Red JVC JVC does not have a public chemical policy
to ensure that their suppliers avoid OSPAR and
other chemicals recognized as posing a risk to
human health.
1-800-252-5722
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 69
Computers
Color Code Company Chemical Policy Contact
Info
Yellow Dell Dell has a public policy to transition out of all
applicable OSPAR chemicals. Brominated fl ame
retardants (BFRs) in Dell’s desktops, notebooks,
and server chassis plastic parts were to be
replaced
by year-end 2004. Dell is committed to
replacing
BFRs, including TBBPA, with halogen free
alternatives.
Dell is working to avoid PVC and all
halogenated
plastics, which will reduce phthalate and
organotin exposure.
Tel: 888-560-8324
Yellow Hewlett
Packard
HP has a public policy to transition out of
some
OSPAR chemicals. HP has replaced deca-BDE with
a halogen free alternative, but is not
committed to
non-halogenated alternatives for other BFRs,
such
as TBBPA. HP restricts the use of PVC in
certain
applications.
http://welcome.hp.com/
country/us/en/contact/
email_2.html
Yellow Apple Apple has a public policy to transition out of most
OSPAR chemicals. Apple is committed to phasing
out all PBDEs, but does not commit to a
halogen
free alternative for Deca. Apple does not have
a
phase-out target for TBBPA. Apple does not
have a
policy to restrict the use of plastics, such
as PVC
that contribute to phthalate and organotin
exposure.
https://www.apple.com/
contact/
Yellow IBM IBM has a public policy to transition out of some
OSPAR chemicals. In 1991, IBM phased out all
PBDEs, but has no defi ned commitment to
replace
TBBPA with safer alternatives. IBM does not
have
a policy to restrict the use of plastics, such
as PVC
that contribute to phthalate and organotin
exposure.
https://www.ibm.com/
contact/us/en/query
Orange Toshiba Toshiba is in compliance with the Restriction
of Hazardous Substances Directive(RoHS), which
means it is phasing out PBDEs—brominated fl
ame
retardants. Depsite a comprehensive website
dedicated
to Toshiba’s environmental initiatives, it is
unclear whether or not they are globally
phasing
out other hazardous chemicals besides those
targeted in the RoHS Directive.
http://www.toshiba.
com/taisnpd/contactus/
email.html
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 70
Mattresses
Color Code Company Chemical Policy Contact
Information
Green IKEA IKEA has phased out the use of brominated fl ame
retardants (BFRs) and phthalates in
mattresses.
IKEA also bans the use of carcinogens in their
products.
http://info.ikea-usa.com/
IKEAContactUs/Contact.aspx
Orange Serta As of January 2005, Serta plans to have their
mattresses free of brominated fl ame retardants
(BFRs). Serta does not have a public chemical
policy to ensure that their suppliers avoid
OSPAR
and other chemicals recognized as posing a
risk
to human health.
customer.service@serta.com
Orange Sealy In the US, Sealy does not have a public chemical
policy to ensure that their suppliers avoid
OSPAR
and other chemicals recognized as posing a
risk
to human health. In England, Sealy is
committed
to moving away from OSPAR chemicals.
1-800-MY-SEALY
Red Simmons Simmons does not have a public chemical policy
to ensure that their suppliers avoid OSPAR and
other chemicals recognized as posing a risk to
human health.
1-877-399-9397
Red Sears-OPedic
Sears does not have a public chemical policy
to ensure that their suppliers avoid OSPAR and
other chemicals recognized as posing a risk to
human health.
1-800-349-4358
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 71
Carpets and Flooring
Color Code Company Chemical Policy Contact
Information
Green IKEA IKEA has phased out the use of brominated
fl ame retardants (BFRs) in carpets.
IKEA bans the use of PVC in most of
its products, which reduces and in some
cases eliminates the use of organotins
and phthalates. IKEA also bans the
use of carcinogens in their products.
http://info.ikea-usa.com/
IKEAContactUs/Contact.aspx
Yellow Shaw Shaw Inc. is committed to using MBDC’s
Cradle to Cradle protocol* to replace
persistent bioaccumulative toxins with
safer alternatives. EcoWorx® Backing,
their new carpet back does not
contain PVC.
http://www.shawfl oors.com/about/ about
Shaw/Contact_Shaw.asp
Yellow Interface Interface is committed to moving away
from petro-based materials to avoid the
release and use of harmful chemicals.
Their Ingeo™ carpet line uses bio-based,
plant-derived fi bers and their i2™ fl ooring
products was designed using biomimicry
to ensure safe material use that
can be reused and recycled infi nitely.
http://66.110.208/contactus.
aspx?source=interfaceinc
Red Mohawk Mohawk does not have a public
chemical policy to ensure that their
suppliers avoid OSPAR and other
chemicals of concern.
mohawkind@mohawkind.com
* McDonough Braungart Design Chemistry
(www.mbdc.com)
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 72
Furniture
Color Code Company Chemical Policy Contact
Information
Yellow IKEA IKEA has eliminated brominated fl ame
retardants and is working to replace
persistent bioaccumlative chemicals
with safer alternatives in all their product
lines
http://info.ikea-usa.com/
IKEAContactUs/Contact.aspx
Yellow Herman
Miller
Herman Miller is committed to using
MBDC’s Cradle to Cradle protocol*
to replace persistent bioaccumulative
chemicals with safer alternatives in all
their product lines. As a result, their
new chair, MIRA, does not contain
BFRs or PVC.
www.Hermanmiller.com
1-888 443 4357
Yellow Steel
Case
Steel Case is committed to using MBDC’s
Cradle to Cradle protocol to replace
persistent bioaccumulative chemicals
with safer alternatives for all their
product lines.
http://www.steelcase.com/na
/askus.aspx?f=13918&p=18518
Red Century
Furniture
Century Furniture does not have a public
chemical policy to ensure that their suppliers
avoid OSPAR and other chemicals
recognized as posing a risk to human
health.
webcs04@centuryfurniture.com
Red La-Z-Boy La-Z-Boy does not have a public chemical
policy to ensure that their suppliers avoid
OSPAR and other chemicals recognized
as posing a risk to human health.
http://www.la-z boy.com/contactus/
* McDonough Braugart Design Chemistry
(www.mbdc.com)
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 73
T A B L E 7
The Twelve Principles of Green Chemistry
1. Prevention
It is better to prevent waste than to treat or
clean up
waste after it has been created.
2. Atom Economy
Synthetic methods should be designed to
maximize the
incorporation of all materials used in the
process into the
fi nal product.
3. Less Hazardous Chemical Syntheses
Wherever practicable, synthetic methods should
be designed
to use and generate substances that possess
little
or no toxicity to human health and the
environment.
4. Designing Safer Chemicals
Chemical products should be designed to effect
their
desired function while minimizing their
toxicity.
5. Safer Solvents and Auxiliaries
The use of auxiliary substances (e.g.,
solvents, separation
agents, etc.) should be made unnecessary
wherever
possible and innocuous when used.
6. Design for Energy Effi ciency
Energy requirements of chemical processes
should be
recognized for their environmental and
economic impacts
and should be minimized. If possible,
synthetic methods
should be conducted at ambient temperature and
pressure.
7. Use of Renewable Feedstocks
A raw material or feedstock should be
renewable rather
than depleting whenever technically and
economically
practicable.
8. Reduce Derivatives
Unnecessary derivatization (use of blocking
groups,
protection/deprotection, temporary modifi
cation of
physical/chemical processes) should be
minimized or
avoided if possible, because such steps
require additional
reagents and can generate waste.
9. Catalysis
Catalytic reagents (as selective as possible)
are superior
to stoichiometric reagents.
10. Design for Degradation
Chemical products should be designed so that
at the end
of their function they break down into
innocuous degradation
products and do not persist in the
environment.
11. Real-time analysis for Pollution
Prevention
Analytical methodologies need to be further
developed to
allow for real-time, in-process monitoring and
control prior
to the formation of hazardous substances.
12. Inherently Safer Chemistry for Accident
Prevention
Substances and the form of a substance used in
a chemical
process should be chosen to minimize the
potential
for chemical accidents, including releases,
explosions,
and fi res.
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 74
Introduction
Numerous organic chemicals have been detected
in
house dust, both in the United States (Camann
et al.,
2002; Rudel et al., 2003) and in the United
Kingdom
(Santillo et al., 2003). Clean Production
Action contracted
with an EPA-accredited laboratory (name
provided
on request) to measure the concentrations of
selected chemicals in composited dust samples
from
ten households from each of seven states of
the
United States. The laboratory is currently
certifi ed by
the National Environmental Laboratory
Accreditation
Program and possesses the ISO 9001:2000
Certifi cate
of Registration. The chemicals which were
targeted
are 7 phthalate diesters, 7 brominated
diphenyl ethers,
13 pesticides, 7 alkylphenol compounds and
pentachlorophenol,
7 organotins, and 2 perfl uorinated organics;
the specifi c chemicals are identifi ed in
Table 1.
The laboratory determined the concentrations
of
each of these chemicals in the composite dust
sample
from each state.
Methods and Materials Sieving
and Compositing of Bag Dust Samples
Bag dust samples from ten households in each
of
seven states (CA=California,
MA=Massachusetts,
ME=Maine, MI=Michigan, NY=New York,
OR=Oregon,
and WA=Washington) were received at the
laboratory
between September 28 and October 18, 2004,
and
stored frozen until sieving. A composite
sieved dust
sample was prepared from the ten designated
bag
dust samples from each state. Each designated
bag
from a state was opened consecutively and
about 30 g
of dust from 9 specifi c representative
locations was
passed through a cleaned 150-um stainless
steel sieve,
to obtain a 3.0 g weighed aliquot of each fi
ne dust.
The ten 3.0 g aliquots were then combined and
passed
twice through the sieve to create a
homogenized state
composite, which was then split into separate
2.0 g
aliquots (including those labeled N=Neutrals,
P=Phenols,
F=PFOA/PFOS, and O=Organotins) for the
necessary
extractions and analyses. At least one 2 g
dust aliquot
was fortifi ed with all the target analytes
of a specifi c
method before extraction and analysis, in
order to
A P P E N D I X I I I : Analytical Methods and
Data Quality of Chemical
Concerntrations Measured in Household Dust Composites from Seven
U.S. States
26 Neutral Chemicals*
(by GC/MS on 60 m column):
• 7 Phthalate Diesters: dimethyl (DMP),
diethyl
(DEP), di-n-propyl (DPP), diisobutyl (DiBP),
di-nbutyl
(DnBP), butylbenzyl (BBzP), di(2-ethylhexyl)
(DEHP)
• 6 Brominated Diphenyl Ethers: BDE 47, BDE
99,
BDE 100, BDE 153, BDE 154, BDE 183
• 13 Pesticides: chlorpyrifos,
alpha-chlordane,
gamma-chlordane, 4,4’-DDT, diazinon, dicofol +
4,4’-dichlorobenzophenone (breakdown product),
dieldrin, methoxychlor,
pentachloronitrobenzene,
cis-permethrin, trans-permethrin, piperonyl
butoxide, propoxur
Decabrominated Diphenyl Ether (BDE 209)
(by GC/MS on 15 m column):
8 Phenolic Chemicals* (by GC/MS):
• 7 Alkylphenol Compounds: 4-nonylphenol
(4NP),
nonylphenol monoethoxylate, nonylphenol
diethoxylate,
4-octylphenol (4OP), octylphenol
monoethoxylate,
octylphenol diethoxylate,
4-(1,1,3,3-tertmethylbutyl)
phenol (4TMBP)
• Pentachlorophenol
7 Organotins (by GC/MS):
• 7 Organotins: monobutyltin (MBT), dibutyltin
(DBT),
tributyltin (TBT), tetrabutyltin (TeBT),
dioctyltin
(DOT), tricyclohexyltin (TCHT), triphenyltin
(TPT)
2 Perfl uorinated Organics
(by LC/MS negative electrospray):
• Perfl uorooctanoic acid (PFOA), Perfl
uorooctanyl
sulfonate (PFOS)
* The laboratory extracted and analyzed split
composited fine
(<150 um) dust samples for the targeted
compounds, generally
as described in Rudel et al (2003).
T A B L E 1
Target Chemicals in Dust Survey
for Clean Production Action
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 75
assess the extraction effi ciency of each
target analyte
from dust.
Extraction and Analytical Methods
Neutral-extracted Chemicals. Approximately 2 g of
sieved fi ne dust was spiked with fi ve
extraction surrogates,
equilibrated for 30 minutes at room
temperature,
then Soxhlet-extracted fi rst using 6% ether
in
hexanes and then hexane:acetone (1:1), for 16
hours
each. The extracts were combined and concentrated
to 10 mL, from which 1 mL was removed for
cleanup.
The cleaned eluent was concentrated to a fi
nal volume
of 2 mL with 10% ether in hexanes.
Analysis for the 26 neutral target chemicals
was
performed using an Agilent 6890/5973 GC/MS in
selected ion monitoring (SIM) mode, as
described
by Rudel et al (2003). A 60 m x 0.25 mm i.d.
ZB-5MS
column was used as the GC analytical column.
The
GC/MS instrument was scanned to monitor 2 or
4
selected ions per analyte. Quantifi cation
was performed
using labeled compounds similar to the
analytes
as internal standards. Analysis for BDE-209
was
performed by GC/MS/SIM using a DB-5MS 15 m
x 0.25 mm GC column.
Phenolic Chemicals. Approximately 2 g of sieved fi ne
dust was acidifi ed, spiked with
2,4,6-tribromophenol
as the extraction surrogate, equilibrated for
30 minutes
at room temperature, and extracted by
sonication
with dichloromethane. The extract was
solvent-exchanged
to hexane at a fi nal volume of 20 mL.
Target phenols in extracts and calibration
standards
were converted to their silyl derivatives
prior to
GC/MS analysis. Analysis for the 8 phenolic
chemicals
was performed using an Agilent 6890/5973
GC/MS
in selected ion monitoring (SIM) mode, as
described
by Rudel et al (2003). A 30 m x 0.25 mm i.d.
DB-5MS
column was used as the GC analytical column.
Quanti-
fi cation was performed using
3,4,5-trichlorophenol
as the internal standard.
Perfl uorooctanoic Acid (PFOA) and Perfl
uorooctanyl
Sulfonate (PFOS). Approximately 2 g of sieved fi ne
dust was sonicated in a polyethylene
container for 30
minutes in 10 mL of methanol for the
extraction of
PFOA and PFOS. The samples were then
centrifuged
and ~ 1 mL of the extract was removed for
LC/MS
analysis. Perfl uorononanoic acid (PFNA) was
added
prior to extraction as a surrogate to monitor
the
extraction effi ciency of the compounds.
Analysis was
performed using liquid chromatography/mass
spectrometry
(LC/MS). Analytical conditions were based
on reverse phase HPLC separation with
negative
mode electrospray ionization mass
spectrometry.
Quantitation was performed using the external
standard
method.
Organotins. Approximately 1 g of sieved fi ne dust was
extracted by shaking in 4 mL diethyl
ether:hexanes
(4:1) with 0.1% tropolone for the organotin
compounds.
Tri-n-propyltin chloride was added prior to
extraction
as a surrogate to monitor the extraction effi
ciency of
the compounds. The samples were then
centrifuged
and 2 mL of the extract was removed for
derivatization.
The 2 mL aliquot was derivatized using
n-pentylmagnesium
bromide (Grignard reagent) to form
volatile pentyl derivatives suitable for
GC/MS analysis.
The derivatized extract was diluted two-fold
prior to
GC/MS analysis. Calibration standards were
derivatized
in the same manner.
Analysis was performed using GC/MS. A six
point
calibration standard curve ranging from 0.4 –
0.01
µg/mL was used to quantitate the compounds in
the
extract. Due to the different salt forms of
organotins
available, the concentration values were
based solely
on the cation portion of the compound. For
example,
tri-n-butyltin chloride was used in the
calibration standard
but the concentrations were calculated based
on
tri-n-butyltin only. The WA and CA dust
samples were
selected as matrix spike samples. Tetrabutyltin
was recovered
in both samples. Most of the recoveries of
the
organotin compounds ranged from 10–40% with
the
exception of monobutyltin with recoveries
less than 10%.
Data Reporting Qualifi ers. Data reporting qualifi ers
were used to report special circumstances
that may
affect interpretation of the analyte=s value
for a
sample:
U (< detection limit) Analyte not
detected. Nominal
DL = lowest standard/3.0
B Analyte present in solvent blank. Blank
value not
subtracted.
BS Blank subtracted. Analyte level in solvent
blank
subtracted from measured level.
E Analyte amount is elevated due to
interference
peak
J Imprecise quantifi cation: amount below
lowest
standard
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 76
Evaluation of Analytical Data Quality
Solvent Blanks
A solvent blank was processed through all
extraction
steps for each extraction method and analyzed
along
with the dust samples. The solvent blank
results were
evaluated. The only target chemicals present
in the
solvent blanks were diethyl phthalate (DEP)
(at 2.31
ug/extract) and di(2-ethylhexyl) phthalate
(DEHP)
(at 2.26 ug/extract) in the neutrals method
solvent
blank, and 4-nonylphenol (4NP) (at 4.69
ug/extract)
in the phenols method solvent blank. There is
no indication
of laboratory-introduced contamination for
any of the other targeted chemicals.
Blank Subtraction
If 2 grams of dust had been extracted, the
detected
solvent blank contaminant levels are
equivalent to
1.15 ug/g of DEP, 1.13 ug/g of DEHP, and 2.35
ug/g
of 4NP. Lab-introduced DEHP (of about 1.13
ug/g)
contributed less than 1% to the DEHP
composite dust
measurements, which ranged from 216 ug/g to
425
ug/g. However, lab-introduced DEP (of about
1.15
ug/g) contributed substantially to the
measured DEP
composite dust measurements, which ranged
from
1.89 ug/g to 4.73 ug/g. Similarly,
lab-introduced 4NP
(of about 2.35 ug/g) contributed considerably
to the
measured 4NP composite dust measurements,
which
ranged from 6.08 ug/g to 12.86 ug/g. The fi
nal corrected
concentrations of diethyl phthalate,
di(2-ethylhexyl)
phthalate, and 4-nonylphenol were obtained by
subtracting the solvent blank concentrations
of DEP,
DEHP, and 4NP from the measured dust
concentrations
of these chemicals, in order to adjust for
the laboratory-
introduced levels, as indicated by the
solvent
blanks. After blank subtraction, the
corrected dust
concentrations of the state composites ranged
from
0.74 ug/g to 3.58 ug/g for DEP, and from 3.74
ug/g
to 10.5 ug/g for 4NP.
Surrogate Recovery
Extraction surrogate compounds were spiked
into
each dust sample and QC sample before
extraction
by each method to indicate the adequacy of
the extraction
procedure. The fi ve neutrals extraction
surrogates
were decachlorobiphenyl for the
organochlorines,
chlorfenvinphos for the organophosphate
pesticides, and dibenzyl phthalate, diphenyl
isophthalate,
and diphenyl phthalate for the phthalate
diesters
and brominated diphenyl ethers. Recovery of
the
extraction surrogates in each extracted
sample was
evaluated. Recoveries of each of the fi ve
neutrals surrogates
ranged between 50% and 109% in the seven
composite dust samples, indicating adequate
neutral
extraction. Recovery of 2,4,6-tribromophenol,
the phenols
surrogate, was good (87% to 98%) from most
dust
composites, but very low from the MA (22%)
and MI
(45%) composites. Low recovery of
2,4,6-tribromophenol
may indicate ineffi cient extraction of
pentachlorophenol
from the MA and MI composites. Recovery
of perfl uorononanoic acid (PFNA), the PFOA/
PFOS surrogate, was generally elevated (102%
to
192%) from the dust composites, but indicates
that
PFOA and PFOS were completely extracted from
the
dust. Recovery of tri-n-propyltin, the
organotin surrogate,
was low but consistent (55% to 65%) from the
dust composites, indicating equivalent
organotin extraction
of each state dust composite, but recovery of
tri-n-propyltin was lower (32.5%) in both
organotin
matrix spikes.
Dust Matrix Spike Recoveries
At least one matrix spike of all targeted
analytes was
prepared into a composite dust aliquot and
extracted
and analyzed by each method, and the spike
recoveries
of each analyte were calculated. One matrix
spike
(of the NY composite dust) with all neutrals-
and phenols-
targeted analytes was performed and analyzed.
Two matrix spikes (of the NY and OR composite
dusts) with PFOA and PFOS were performed and
analyzed.
Two matrix spikes (of the CA and WA composite
dusts) with the seven organotins were
performed
and analyzed. The dust matrix spike
recoveries obtained
for every targeted analyte by its extraction
method were evaluated. Most neutral targeted
compounds
were extracted quite effi ciently (70% to
130%)
from the NY composite neutrals matrix spike,
although
recoveries were low for DEP (54%) and BDE 153
(62%) and were high for piperonyl butoxide
(305%),
DEHP (237%), butylbenzyl phthalate (215%),
transpermethrin
(185%), and cis-permethrin (176%). All
targeted phenolic compounds were extracted
quite
effi ciently (80% to 136%) from the NY
composite
phenols matrix spike, with the exception of
the low
recovery of pentachlorophenol (52%). The
matrix
spike recovery of 4-n-nonylphenol (80%) was
used to
estimate the recovery of the multi-component
4-nonylphenol
(4NP). Recoveries of PFOA were good (69%
and 98%) from the NY and OR composite perfl
uorinated
organic matrix spikes, but PFOS recoveries
were
elevated (176% and 197%). Recoveries of
tetrabutylS
A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S F
O R A H E A L T H Y H O M E 77
tin were good (95% and 100%) from the CA and
WA
composite organotin matrix spikes, but
recovery of
the other six organotins was very poor but
consistent
from the CA and WA organotin matrix spikes.
The
mean recoveries were 37% for tributyltin, 26%
for
di-n-octyltin, 26% for dibutyllin, 23% for
tricyclohexyltin,
14% for triphenyltin, and only 1% for
monobutyltin.
Another organotin extraction method gave
similar
matrix spike recoveries and similar measured
dust
concentrations as the reported organotin
results.
Accuracy of Measured Concentrations in Dust
Composites Deduced from Matrix Spike
Recoveries
Per the laboratory’s recommendation, the
reported
concentrations of the targeted chemicals in
dust were
not adjusted for the matrix spike recoveries.
Instead,
the matrix spike recoveries were used to
assess the accuracy
of the measured concentrations of the
targeted
neutrals chemicals, phenolic chemicals, PFOA
and
PFOS, and organotin chemicals in the seven
state
composite fi ne dust samples. The
blank-subtraction
corrected concentrations (denoted with the fl
ag BS)
were reported and used for diethyl phthalate,
di(2-
ethylhexyl) phthalate, and 4-nonylphenol, as
recommended
by the laboratory.
The dust matrix spike recoveries obtained
provide
an indication of the accuracy of the reported
chemical
concentrations in the state dust composite
samples.
The reported dust concentrations are probably
quite
accurate for those chemicals which were
extracted
effi ciently. However, the reported dust
concentrations
may be overestimates for chemicals with high
matrix
spike recoveries (piperonyl butoxide, DEHP,
butylbenzyl
phthalate, trans-permethrin, cis-permethrin,
and
PFOS) and underestimates for chemicals with
low
matrix spike recoveries (DEP, BDE 153,
pentachlorophenol,
tributyltin, di-n-octyltin, dibutyllin,
tricyclohexyltin,
triphenyltin, and monobutyltin). Since the
recoveries of some chemicals vary
considerably from
different dust matrices (Rudel et al., 2003) due
to the
variable composition of house dust, the
degree of
over-estimation or under-estimation in the
reported
dust concentrations of a chemical may also
vary
across the dust samples.
References
Camann DE, Colt JS, and Zuniga MM.
Distributions and
Quality of Pesticide, PAH, and PCB
Measurements in Bag
Dust from Four Areas of USA. In: Proceedings of Indoor Air
2002, H. Levin, ed., Santa Cruz, CA, 2002, Vol. 4, pp 860-864.
Rudel RA, Camann DE, Spengler JD, Korn LR,
Brody JG,
2003. Phthalates, Alkylphenols, Pesticides,
Polybrominated
Diphenyl Ethers, and Other
Endocrine-Disrupting Compounds
in Indoor Air and Dust. Environ. Sci. Technol., 37 37 Technol
(20), 4543-4553.
Santillo D, Labunska I, Davidson H, Johnston
P, Strutt M,
Knowles O, 2003. Consuming Chemicals:
Hazardous chemicals
in house dust as an indicator of chemical
exposure in
the home. Greenpeace Research Laboratories,
Department
of Biological Sciences, University of Exeter,
Exeter, UK
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U C
T S 78
Phthalates µg/g, parts per million
(ppm)
CA ME NY WA OR MI MA
Mean, 7
samples
Belgium Brazil
Cape
Cod, MA
UK
dimethyl phthalate <rl 0.272 <rl <rl
<rl <rl <rl 0.039 1.5 1.4 na 0.12
diethyl phthalate 0.74 0.74 3.58 1.07 1.41 0.86
1.47 1.41 10 2.5 8.5 12.2
di-n-propyl phthalate <rl <rl <rl
<rl <rl <rl <rl <rl na na <rl. <rl
diisobutyl phthalate 8.35 3.01 3.80 3.05 4.49
1.61 2.20 3.79 74.6 29 2.92 52
di-n-butyl phthalate 13.0 10.5 28.0 20.8 49.5
7.8 11.4 20.15 32.4 52.2 27.3 50.2
butylbenzyl phthalate 137 71.4 64.2 56.9 42.1
49.9 63.9 69.4 195.8 3.2 124 56.5
di(2-ethylhexyl) phthalate 393 425 342 338 301
292 215 329 338.7 241.5 506 191.5
Belgium—Al Bitar (2004) also assayed
dicyclohexy phthalate (1.7 ppm), di-n-octyl phthalate (55.7 ppm), di-isononyl
phthalate (162.9 ppm),
and di-isodecyl phthalate (66 ppm), but did
not assay di-n-propyl phthalate
Cape Cod, MA—Rudel et al. (2003) also assayed
dicyclohexyl phthalate (2.98 ppm), di-n-hexyl phthalate (2.6 ppm), di-n-pentyl
phthalate (<rl),
but did not assay dimethyl phthalate.
U.K.—Santillo et al. (2003) assayed
di-isononylphthalate (48.5 ppm) and di-isodecylphthalate (20.8 ppm),
Brazil—Costner et al. (2004 also assayed
dicyclohexyl phthalate (0.62 ppm), di-n-octyl phthalate (1.4 ppm), di-isononyl
phthalate (71.2 ppm),
and di-isodecyl phthalate (93 ppm), but did
not assay di-n-propyl phthalate.
Phthalates
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 79
Alkylphenols µg/g, parts per million
(ppb)
CA WA MI OR MA NY ME
Mean, 7
samples
Cape Cod,
MA
4-Nonylphenol 5.830 8.550 5.430 10.500 3.950
3.740 3.820 5.974 2.73
Nonylphenol monoethoxylate 14.800 9.290 8.470
4.670 6.820 5.520 3.720 7.613 2.58
Nonylphenol diethoxylate 17.900 12.300 8.730 8.180
9.340 6.930 5.850 9.890 7.87
4-Octylphenol <rl <rl <rl <rl
<rl <rl <rl – 1.00
Octylphenol monoethoxylate 3.410 0.571 1.010
0.486 0.483 0.667 0.394 1.003 0.33
Octylphenol diethoxylate 8.550 0.570 1.610
0.532 0.395 0.786 0.649 1.870 0.44
4-t-methylbutylphenol 0.962 0.391 0.291 0.222
0.400 0.190 0.154 0.373 na
Cape Cod, MA - Rudel et al (2003) also assayed
nonylphenol ethyoxycarboxylate (2940 ppb) but did not assay
4-t-methylbutylphenol
Alkylphenols
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 80
Pesticides µg/g, parts per million (ppm)
OR ME MA WA MI NY CA
Mean, 7
samples
Cape Cod,
MA
4,4’-DDT 0.0913 0.327 1.89 0.308 0.364 0.188
0.363 0.504 0.971
alpha-chlordane <rl <rl <rl <rl
<rl <rl <rl 0.020 0.328
gamma-chlordane <rl <rl <rl <rl
<rl <rl 0.138 0.020 0.383
chlorpyrifos 0.21 <rl <rl <rl <rl
<rl <rl 0.029 2.54
diazinon <rl <rl <rl <rl <rl
<rl 0.140 0.505
dicofol <rl <rl <rl <rl <rl
<rl <rl 0.058
dieldrin <rl <rl <rl <rl <rl
<rl 0.720 0.103 0.132
methoxychlor <rl 0.326 0.164 <rl 0.532
0.313 <rl 0.334 1.08
pentachloronitrobenzene <rl <rl <rl
<rl <rl <rl <rl na
pentachlorophenol 0.444 7.310 0.0481 0.0968
0.126 0.553 0.148 1.246 1.13
cis-permethrin 11.6 2.09 3.42 2.28 2.04 1.34
0.607 3.34 2.68
trans-permethrin 21.0 3.52 7.67 4.52 4.17 2.67
1.31 6.41 5.03
piperonyl butoxide 0.572 0.325 0.345 0.553
0.147 0.705 2.18 0.69 15.8
propoxur <rl <rl <rl <rl 0.129
<rl 0.130 0.037 0.691
Cape Cod, MA – Rudel et al. (2003) also
assayed 4,4’-DDD (0.031 ppm), 4,4’-DDE (0.036 ppm), alachlor (0.002 ppm),
aldrin (<rl),
atrazine (<rl), bendocarb (0.781 ppm),
carbaryl (1.43 ppm), carbofuran (<rl), chlorothalonil (0.153 ppm),
3,5,6-trichloro-2-pridinol
(0.987 ppm), cyanazine (<rl), cypermethrin
(1.61 ppm), endrin (<rl), heptachlor (0.010 ppm), lindane (0.017), malathion
(0.033 ppm),
HPTE (<rl), methyl parathion (0.16 ppm),
metalachlor (<rl), nitrofen (<rl), parathion (<rl), o-phenylphenol
(0.345 ppm), prometon
(0.001 ppm), simazine (<rl), and trifl
uralin (<rl)
Pesticides
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S
F O R A H E A L T H Y H O M E 81
Polybrominated
diphenyl ethers
µg/g, parts per million (ppm)
OR WA CA MI MA NY ME
Mean, 7
samples
Belgium
Cape
Cod, MA
UK
Washington,
D.C.
BDE 47, a tetraBDE 1.37 5.24 3.22 1.84 1.82
0.674 0.550 2.10 0.026 0.719 0.223 1.220
BDE 99, a pentaBDE 1.06 4.13 2.67 1.27 1.68
0.595 0.474 1.70 0.054 1.290 0.044 1.700
BDE 100, a pentaBDE <rl 0.762 0.509 0.229
0.315 <rl <rl 0.454 0.006 0.166 na 0.274
BDE 153, a hexaBDE <rl 0.376 0.251 <rl
<rl <rl <rl 0.314 0.002 0.538 0.034 0.181
BDE 154, a hexaBDE <rl 0.325 0.231 <rl
<rl <rl <rl 0.296 <rl na na 0.156
BDE 183, a heptaBDE <rl <rl <rl
<rl <rl <rl <rl -– <rl na 0.192 0.031
BDE 209, decaBDE 10.04 0.90 3.51 6.35 5.72
3.59 2.53 4.66 4.401 na 9.820 2.090
Belgium—Al Bitar (2004) also assayed
octabromodiphenyl ether (no detects), hexabromo cyclododecane (4.8 ppm), and
tetrabromobisphenol A (0.068 ppm)
Cape Cod, MA—Rudel et al. (2003) did not assay
BDE 154, BDE 183, or BDE 209, but assayed for PCB-52 (0.165 ppm), PCB-105
(0.248 ppm), and PCB-153 (0.538 ppm).
UK—Santillo et al. (2003) assayed BDE-28 (4.14
ppb), hexabromocyclododecane (3158 ppm), and tetrabromobisphenol-A (116 ppm),
but did not assay BDE 100 and BDE154.
Washington, D.C.—Stapleton et al. (2005) also
assayed BDE-28 (21 ppm).
Polybrominated Diphenyl Ethers
S I C K O F D U S T : C H E M I C A L S I N C O M M O N P R O D U
C T S 82
Organotins ng/g, parts per billion (ppb)
ME OR WA MI MA NY CA Mean, 7
samples
Belgium Brazil Germany
Monobutyltin 205.1 361.4 227.8 219.2 106.0
184.8 140.1 206.3 567.0 90.0 160.0
Dibutyltin 314.7 321.5 204.2 236.6 265.4 186.7
115.8 235.0 1417.0 252.5 510.0
Tributyltin 193.1 44.8 99.4 49.2 55.6 71.7
44.7 79.8 280.0 56.7 20.0
Tetrabutyltin <rl <rl <rl <rl
<rl <rl <rl –
Di-n-octyltin 198.5 76.4 108.8 71.7 128.8 95.8
87.6 109.7 113.0 187.5 20.0
Tricyclohexyltin <rl <rl <rl <rl
<rl <rl <rl – na na na
Triphenyltin <rl <rl <rl <rl
<rl <rl <rl – na 17.5 na
Germany—Fromme et al (2005) also assayed
monooctyltin (10 ppb) but did not assay tricyclohexyltin or triphenyltin
Belgium—Al Bitar et al. (2004) also assayed
monooctyltin and tetrabutyltin but did not assay tricylclohexyltin or
triphenyltin
Brazil—Costner et al (2004) also assayed
monooctyltin (62.5 ppb) and tetrabutytin (zero detects) but did not assay
tricyclohexyltin
U.K.—Santillo et al.(2003)also assayed
monooctyltin (450.6 ppb) and tetrabutyltin (zero detects).
Organotins
Perfl uorinated
Chemicals
ng/g, parts per billion (ppb)
CA ME MA MI NY OR WA
Mean, 7
samples
Japan
PFOA 127.8 66.5 18.5 68.3 31 33.5 205.1 78.7
380
PFOS 413.5 76.4 104.8 243.8 431.1 1170.9 530
424.4 200
Perfl uorinated Chemicals
S A F E R P R O D U C T S P R O J E C T : A L T E R N A T I V E S F
O R A H E A L T H Y H O M E 83
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3 Betts, K., 2003. Are US Homes a Haven for
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Environ. Sci. Technol. 407A-411A. Nov. 1,
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4 Rudel in Betts, K., 2003. Are US Homes a
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Nov. 1, 2003.
5 Butt, C., Diamong, M., Truong, J., 2004.
Spatial distribution
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Ontario
as measured in indoor and outdoor window
organic
fi lms. Environ. Sci. Technol.2004,
38,724-731.
6 American Chemistry Council’s Brominated
Flame Retardant
Industry Panel for the Voluntary Children’s
Chemical
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the Peer Consultation Meeting on
Decabromodiphenyl
Ether. 2-3 April, 2003, Cincinnati, Ohio.
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H., 2004.
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dust in
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H., 2004.
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Fluorinated
organics in the biosphere. Environ. Sci.
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2445-2454.
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11 Moriwaki, H., Takata, Y., Arakawa, R., 2003.
Concentrations
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perfl uorooctanoic
acid (PFOS) in vacuum clean dust collected
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753-757.
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on the Web.
States and Territories. Washington, D.C:
http//www.
esweb.bna.com/. Bureau of National Affairs,
Inc.
13 Al Bitar, F., 2004. Hazardous chemicals in
Belgian house
dust. Brussels: Greenpeace Belgium.
14 Costner, P., Butcher, J., Peters, R.,
2004. Hazardous
Chemicals in Brazilian House and Offi ce
Dust. Sao
Paulo: Greenpeace Brazil.
15 Rudel, R., Camann, D., Spengler, J., Korn,
L., Brody, J.,
2003. Phthalates, alkylphenols, pesticides,
polybrominated
diphenyl ethers, and other
endocrine-disrupting
compounds in indoor air and dust. Environ.
Sci. Technol.
37: 4543-4553.
16 Santillo, D., Labunska, I., Davidson, H.,
Johnston, P.,
Strutt, M., Knowles, O., 2003. Consuming
chemicals:
Hazardous chemicals in house dust as an
indicator of
chemical exposure in the home.
GRL-TN-01-2003.
Exeter, UK: Greenpeace Research Laboratories.
E N D N O T E S
17 Bornehag, C.-G., Sundell, J., Weschler,
C., Sigsgaard,
T., Lundgren,B., Hasselgren, M.,
Hagerhed-Engman, L.,
2004. The association between asthma and
allergic symptoms
in children and phthalates in house dust: A
nested
case–control study. Environ Health Perspect
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Pat Costner, Beverley Thorpe & Alexandra McPherson
Safer Products
P R O J E C T
The American people deserve to be safe
in our own homes and should be able to
purchase
products without unwittingly exposing
ourselves and our
children to substances that can cause cancer
and disrupt
normal and healthy development. This study
provides solid
evidence that the federal government, U.S.
states and
U.S. industry must take immediate action to
replace
harmful chemicals with safe substitutes.
California
Center for Environmental Health
528 61st Street, Suite A
Oakland, CA 94609
Tel: (510) 594-9864
www.cehca.org
Silicon Valley Toxics Coalition
760 North First Street
San Jose CA 95112
Tel: (408) 287-6707
www.svtc.org
Maine
Environmental Health
Strategy Center
P.O. Box 2217
Bangor, Maine 04402
Tel: (207) 827-6331
www.preventharm.org
Massachusetts
Clean Water Action
36 Bromfi eld St.
Suite 204
Boston, MA 02108
Tel: (617) 338-8131
www.cleanwateraction.org/ma
Michigan
Ecology Center
117 N. Division St.
Ann Arbor, MI 48104
Tel: (734) 761·3186
www.ecocenter.org
New York
Citizens Environmental Coalition
33 Central Avenue
Albany, NY 12210
Tel: (518) 462-5527
www.cectoxic.org
Oregon
Oregon Environmental Council
222 NW Davis Street, Suite 309
Portland, OR 97209
Tel: (503) 222-1963
www.oeconline.org
Washington
Washington Toxics Coalition
4649 Sunnyside Ave. N, Suite 540
Seattle, WA 98103
Tel: (206) 632.1545
www.watoxics.org
Sick of Dust
Chemicals in Common Products—
A Needless Health Risk in Our Homes
Clean Production Action
P. O. Box 153, Spring Brook, NY 14140
Tel: 716-805-1056
www.cleanproduction.org