PBDEs are the new PCBs.

Introduced in the 1970's, they now show up in every living creature tested.

Levels are rising at an astounding pace in spite of bans on some formulations.

No other chemical is known to match the rate at which PBDE burdens are rising worldwide.

Research on PBDEs make it clear these chemicals cause serious health problems.

PBDEs are endocrine disruptors.

They are also

  • Carcinogenic
  • Cytotoxic
  • Excitotoxic
  • Genotoxic
  • Mutagenic
  • Neurotoxic
  • Teratogenic

PBDEs and their metabolites negatively impact

  • Adrenal glands
  • Blood-brain-barrier (BBB)
  • Brain
  • Cellular signaling pathways
  • Cerebrospinal fluid
  • Cholesterol
  • Cholinergic system
  • Chromosomes
  • DNA
  • Epididymis
  • Gender (feminization of males)
  • Glutathione
  • Heart
  • Hormones
  • Immune system
  • Liver
  • Mitochondria
  • Myelination
  • Neurodevelopment
  • Oxidative stress
  • Pregnancy (spontaneous abortion)
  • Prostate
  • Puberty (early in females and delayed in males)
  • Reproductive organs
  • Seminal vesicles
  • Sperm
  • Thyroid
  • Vitamin A
  • Weight (tends towards excess)

Effects have been seen at 2 ppb.

Effects can vary significantly between low and high doses, timing, and duration of exposure.

PBDEs were among the ~ 58,000 chemicals grandfathered into the Toxic Substances Control Act in 1976.

PBDEs are similar in structure to PCBs and dioxins.

Evidence shows they are similarly toxic.

BDE-153 structure similar to PCB and dioxinPCB-153 structure similar to PBDE and dioxinDioxin structure similar to PBDE and PCB

BDE-153, like PCB-153, is especially persistent because of the way its bromine atoms are attached to the molecular backbone.

This structure makes it difficult to metabolize, too.

Harm can occur at all ages, but developing fetuses and infants are affected the most.

Fetal exposure to a trace of PBDE causes behavioral problems later in life.

Reduced motor function

Impaired attentiveness

Poor learning and memory function

Some of these effects get worse with age.

PBDEs pass from mother to fetus through the placenta.

They also pass to the infant in breast milk.

PBDE levels have been monitored in blood, breast tissue, and breast milk:

Swedish researchers saw PBDE levels in human breast milk increase more than 50x between 1972 and 1997.

The level was doubling every 5 years.

Women in Vancouver, Canada, saw the level of PBDEs in breast milk increase 15x Between 1992 and 2002.

In the 1960s, breast tissue was archived from 420 women living in the San Francisco Bay Area.

Analysis detects no PBDEs in those samples.

Today, women living in the Bay Area have some of the highest PBDE levels in the world.

Younger mothers tend to have higher PBDE levels.

The level of PBDEs in dust at home correlates to the level of PBDEs in breast milk.

These are EPA standards for oral exposure to common PBDEs

Name Congener Oral RfD Exposure
TetraPBDE BDE–47 0.1 µg/kg/day 0.1 ppb
PentaPBDE BDE–99 0.1 µg/kg/day 0.1 ppb
HexaPBDE BDE-153 0.2 µg/kg/day 0.2 ppb
DecaPBDE BDE-209 7.0 µg/kg/day 7.0 ppb

PBDEs in breast milk generally exceed these values by at least 300x.

Note: even though all human breast milk is contaminated by PBDE and other chemicals, it is still the superior nutrition source for infants.

Many chemicals are lipid-soluble.

That means they dissolve into fats.

The body generates extra fat in response to such chemicals.

Making a place for these chemicals to be stored helps reduce their concentration elsewhere.

In other words, obesity can be a reaction to toxic body burden.

Eliminate the toxicants and the body no longer needs the extra fat.

"Dieting" to reduce fat has a problem.

Reducing the amount of fat increases the concentration of fat-soluble toxicants left behind.

Even without "dieting", chemicals stored in fat are not "tucked away" permanently.

They can be released back into circulation under many common conditions.

PBDEs are fat-soluble.

They migrate into the body's fatty places.

The more body fat a person has, the more time PBDEs remain inside that person.

PBDEs can stay inside a person for years.

PCBs are fat-soluble, too.

Scientists are concerned because people have more PBDEs than PCBs in their fat.

Americans carry 10x to 100x more PBDE than everyone else.

Canadians have the next highest levels.

By 2020 the median level for human PBDE burden is expected to reach 300 ppb.

That means half the population will have levels above 300 ppb.

Endocrine and thyroid dysfunction happen at 300 ppb.

Already some individuals have been found with levels near 10,000 ppb.

Children tend to carry higher concentrations of PBDEs than adults.

Sick cats can indicate the presence of human toxics.

An epidemic of feline hyperthyroidism is linked to household PBDEs.

This thyroid disease was rare in 1980 — today it is a leading cause of death in older cats.

Cats are fastidious about self-grooming.

They lick themselves thoroughly.

Consequently they ingest high levels of PBDE dust daily.

Chronic exposure to PBDEs disrupts thyroid activity.

The thyroid gland regulates many aspects of metabolism.

Cats experience increased appetite, weight loss, irritability, lethargy and diarrhea.

Based on weight...

...a cat and a 2-year-old child ingest similar concentrations of PBDE dust.

Animal studies mirror the increased PBDE levels found in humans — especially at the top of aquatic and terrestrial food chains.

In the 10-year period from 1989 to 1999, PBDE levels in San Francisco Bay seal blubber increased 100x.

In 2007, Chinese raptors had Deca levels of

Eggs 12,000 ppb
Muscle 31,700 ppb
Liver 40,900 ppb

Those peak levels are 270x higher than in European falcon eggs studied during the previous 10 years.

This study found that 5% of babies evaluated were born with overall PBDE concentrations 3x to 5x times higher than the median.

This pattern is repeated in every similar study.

PBDEs are slowly eliminated from the body.

Excretion ability decreases with repeated exposures.

This is significant because people are exposed to PBDEs every day.

Residue in food accounts for ~ 90% of pesticide, dioxin and PCB exposure.

Dust is the main route for PBDEs.

PBDEs mingle with dust.

Dust is inhaled.

Dust settles on food and water and gets ingested.

PBDEs are in dust everywhere.

Windows, tables, doors, floors.

Lawns, trees, fields.

Computers, desktops.


Clothes-dryer lint.

"Everywhere. We find them in the dust on top of mountains."

Infants and toddlers are most vulnerable.

They're closer to dust.

Crawling, handling, mouthing.

There are 209 different PBDE variations (congeners).

The most commonly used have been 'Penta', 'Octa', and 'Deca'.

These refer to the number of bromine atoms in their base structure:

Penta 5 bromine atoms
Octa 8 bromine atoms
Deca 10 bromine atoms

These degrade into smaller PBDE molecules with fewer bromine atoms.

The smaller (lighter) the PBDE molecule, the more toxic it is.

PBDEs are widely used as flame retardants.

PBDEs release bromine (Br) atoms when heated (debromination).


Debromination creates a very thin surface layer of Br gas.


This Br layer prevents oxygen from participating in combustion.


Reduced combustion prevents fire from spreading.

PBDE flame retardants are used in a wide array of products.

Familiar items include

Airplanes cabin walls
ceiling and floor panels
storage bins
engine components
Appliances alarm clocks
coffee makers
stove hoods
Automotive battery cases and trays
electrical connectors
electronic controls and panels
GPS systems
head rests
sun visors
Baby gear bassinets
car seats
Clothing footwear
various textiles
waterproofed items
Construction carpets
carpet pads
Electrical components adapters
battery packages
circuit boards
circuit breakers
electrical outlets
surge protectors
Foam products batting
Furniture beds
Electronics CD players
cell phones
DVD players
fax machines
remote controls

Polyurethane is easy for manufacturers to shape and it is inexpensive.

It is also highly flammable.

Wherever flexible polyurethane foam is used, PBDEs are likely to be found too.

Traditionally PBDEs have been added to the polyurethane mixture or applied as a coating to finished products.

Then the PBDEs escape and become part of environmental dust.

All forms of PBDE break down in real-world conditions.

Some of the processes include

• Heat

• Wastewater treatment

• Photodegradation in soil

• Decomposition by microorganisms

• Metabolism within animals and people

The resulting PBDEs have fewer bromine atoms.

They persist in the environment for decades.

Heat causes PBDE to migrate out of an object faster.

Devices that "warm up" — such as TVs and computers — are major sources of PBDE dust.

Hot vehicle interiors produce more free PBDEs than microenvironments like homes and offices.

Objects liberate increasing amounts of PBDE as they age.

Objects continue releasing PBDEs into the environment long after their usefulness and disposal.

Shredded vehicles, old furniture, and billions of other discarded items continuously add PBDEs to the environment.

Electronic waste (e-waste) has been noted to increase PBDE air levels by 100x.

PBDEs can travel great distances by winds and ocean currents.

Penta and Octa have been banned from most uses in Europe (2004) and the U.S. (2005).

It is clear these formulations break down into lighter, more toxic congeners.

But for years it has been argued that Deca is very stable.

No breakdown, no bioaccumulation, no harm.

But it turns out that DecaPBDE degrades, too.

PBDEs collect in rinse water.

Some of those PBDEs eventually cycle back into drinking water.

Or they end up in sewage destined for agricultural fertilizer, where they cycle back into the food we eat.

Even though dust is the main source for PBDE exposure, food does contribute to exposure.

It is easily found in

Fish Fresh and saltwater, shellfish
Meat Beef, chicken, pork, etc.
Dairy Milk, butter, cheese, ice cream

In North America, meat is the main food causing PBDE exposure.

In other parts of the world, fish is the main source.

Flame retardants are not a bad idea.

Suppressing fire can save lives and property.

But halogenated flame retardants are hazardous in ways that weren't understood at first.

Firefighters are acutely aware of toxic chemical danger.

Even if their gear protects them from immediate exposure during a fire, the gear becomes contaminated.

Exposure occurs later during cleanup and dress down.

Alternative flame retardants are often based on chlorine instead of bromine.

The health and environmental effects of chlorinated flame retardants have not been adequately studied.

One obvious concern with incinerated chlorines is the creation of dioxins.

Non-halogenated flame retardants are being developed.

Formulas include the use of

• Antimony oxides

• Bishydroxydeoxybenzoin (BHDB)

• Boron

• Melamine

• Melamine salts

• Metal hydroxides — such as magnesium hydroxide

• "nanoadditives"

• Phosphorus

• Silicon dioxide

• Silicones

Toxicity data is scarce for these newer flame retardants.

Some of the 'solutions' will become toxic burdens.

Others may be a true step forward.

PBDEs aren't the only brominated flame-retardants raising health concerns.

Others include

• Tetrabromobisphenol A (TBBPA)

• Hexabromocyclododecane (HBCD)

• Decabromodiphenyl ethane

Dechlorane Plus is another flame retardant found in household dust.

It is used primarily in cables and wires.

Dechlorane Plus is a produced in high volume — more than 1 million pounds annually.

Its chemical structure is similar to organochlorine pesticides such as





...all of which have been restricted or banned in the U.S.

Even if 100% of worldwide PBDE production halted today, millions of tons are already in the environment to contend with.

A complete ban will not occur in the foreseeable future.

PBDEs will continue being used in products such as

• Aircraft

• Industrial fabrics — for example draperies used in hotels and other commercial spaces

• Medical devices

• Military equipment

• Office furniture

• Space program equipment

• Items made from recycled materials

• Vehicles

PBDEs, PCBs, and methyl mercury are synergistically toxic with each other.

Very low exposures combine to induce more harm than expected.

Viral infection can change the uptake and distribution of PBDEs in tissue.

This can actually aggravate the viral disease.

Clearly PBDEs are toxic.

Health advocates, industry lobbyists, and government agencies are wrestling over whose interests will prevail.

Here is one example.

Consider these sites for further information