APEOs and NPEOs in textiles

24 01 2013

Alkylphenol ethoxylates (APEOs – often called alkyphenols or alkylphenyls) are surfactants which have an emulsifying and dispersing action, so they have good wetting, penetration, emulsification, dispertion, solubilizing and washing characteristics. This makes them suitable for a very large variety of applications: they’ve been used for over 50 years in a wide variety of products. In the textile industry, they are used in detergents and as a scouring, coating or waterproofing agents, in printing pastes and adhesives, and in dyeing. The most important APEO or alkylphenol ethoxylates for the textile industry are NPEO (nonylphenol ethoxylates) and OPEO (octylphenol ethoxylates) due to their detergent properties, but there are a big family. About 90% of the produced APEO are in fact NPEO.

The three critical issues in making APEOs and NPEOs in the environment of particular concern are:

  1. They are everywhere. They’re in receipts, canned foods and couches, paint and spot cleaners. They’re in the dust in our homes, our blood and urine, in breast milk and in the cord blood of newborns. Concentrations of NP and its parent compound NPEO have been measured worldwide in surface waters, sediments, sewage, the atmosphere, aquatic organisms, and even in typical human food products. And most disturbingly, these concentrations of APEOs are on the rise.(1) The U.S. EPA has noted rising levels of alkylphenols in water samples taken from streams and rivers throughout the U.S.
  2. The life cycles indicate long term, continued environmental contamination. APEOs are slow to biodegrade and they tend to bioaccumulate. They also move up the food chain and ultimately to us. Though APEOs themselves are not carcinogenic, teratogenic or mutagenic, research has shown that when they do degrade, their byproducts have a higher toxicity, estrogenic activity, persistence and tendence to bioaccumulate than APEOs themselves.(2)
  3. They have been shown to be toxic to aquatic organisms and an endocrine disruptor in higher animals, and therefore they pose a risk to humans. As an environmental hormone disruptor, these new substances can invade the human body through a variety of channels, with estrogen-like effects, and are harmful to normal hormone secretion, leading to reduced sperm count in men. Research published in the September 2006 edition of Toxicological Sciences shows that the human placenta responds to alkylphenyls in the first trimester.(3) The result may be early termination of pregnancy and fetal growth defect.(4)

Think of using fish to replace the proverbial canary in the coal mine. Because most mills do not treat their wastewater, the effluent containing these APEOs is discharged directly into our groundwater, where it is a major source of hormone disruption in fish species. The classic example is intersex attributes in fish (suppression of testes growth in males), with other reproductive effects and anomalies; in one study, egg production of zebrafish, exposed to wastewater effluent contaminated with APEOs, was reduced by up to 89.6% (5) ; other studies found a reduced percentage of fertilized eggs, reduced embroyo survival, and abmormal embroys (6) . These results and other studies indicate that the reproductive potential of native fishes may be compromised in wastewater-dominated streams due to the presence of alkylphenyls (7). Other studies have determined that fish, when exposed to these environmental estrogens, cannot regulate their internal homeostasis (called osmoregulation, which is related to the ability of fish to prevent dehydration or waterlogging , and buffers them against the effect of fresh or sea water). These studies of APEOs in US rivers have led scientists to conclude that fish are currently being impacted – they’re our canaries.

  1. Researchers at UC Davis  found that offspring of  fish in San Francisco estuary had underdeveloped brains, inadequate energy supplies and dysfunctional livers. They grew slower and were smaller than offspring of hatchery fish raised in clean water.

    Researchers at UC Davis found that offspring of fish in San Francisco estuary had underdeveloped brains, inadequate energy supplies and dysfunctional livers. They grew slower and were smaller than offspring of hatchery fish raised in clean water.

Wastewater treatment facilities theoretically have the capabilities of effectively breaking down APEOs, but they are often not designed to remove them from the effluent. Most often sewer sludge contains these APEOs.

In the U.S., these chemicals are basically unregulated, nor is there any restriction on their use. The US Environmental Protection Agency (EPA) has focused research efforts on determining acceptable levels of these compounds in water and identified NPEs as well as the chemical nonylphenol (NP) for further study because of concern about their impact on the environment and us. Why has nothing been done? Because as you might imagine, this is big business, and the chemical lobby has not only impeded regulation but has even tried to block research.(8) The lack of action on the part of environmental regulators in the United States stems largely in part from the research conducted by the Alkylphenol and Ethoxylate Research Council formed by the Chemical Manufacturers Association to conduct studies on APEO (APE Research Council, 2001). To date this panel has disputed all claims that NP concentrations in waterways of the United States are above concentrations where a significant effect would be realized. The Alkylphenol and Ethoxylate Research Council also contests the estrogenic potential of NP (APE Research Council, 2001) (9).

In Europe, the use of NPEO has been banned or voluntarily restricted since 1986. Since 1998, the use of APEO in detergents has been forbidden in Germany – and since January 2005 the EU directive 2003/53/ EG has forbidden the use of NPEO in higher concentrations than 0.1% in product formulations. However it will take years before there is progress in phasing out APEOs completely, as was done by Norway in 2002.(10)

Although forbidden in the EU, many companies have production sites or suppliers outside Europe, where the use of NPEO is not forbidden. Textile eco-labels such as the EU flower and Öko-Tex 1000 have also forbidden the use of APEOs.

But voluntary certifications and the prohibition in some countries is not enough to stem the tide, as Greenpeace found recently. Their Detox Campaign was designed to expose the links between clothing brands, their suppliers and toxic water pollution around the world. The Greenpeace studies found that these NPEs aren’t just expelled into wastewater – they also remain in the finished textile. The chemicals found in the finished clothing of top name brands (Calvin Klein, Levi’s and Victoria’s Secret, among others) included nonylphenol ethoxylates (NPEs). Concentrations of NPEOs were found in 89 garments (just under two thirds of those tested) at levels ranging from just above 1 part per million up to 45000 parts per million in the top name brand items tested (Calvin Klein, Levi’s, Victoria’s Secret, H&M, Gap among others) (11); over 20% of the items tested had more than 100 parts per million.

To see the PBS series on Frontline entitled “Poisoned Waters”, click here.

[1] Zoller, Uri, “Endocrine disrupting APEOs in Isreal/Palestinian water resrouces: What should it take to prevent future pollution?”, http://www.researchgate.net/publication/228493491_ENDOCRINE_DISRUPTING_APEOs_IN_ISRAELIPALESTINIAN_WATER_RESOURCES_WHAT_SHOULD_IT_TAKE_TO_PREVENT_FUTURE_POLLUTION
[2] Wessels, Denise, “Policy Brief: Endocrine Disrupters in Wastewater Alkylphenol Ethoxylates and the City of Indianapolis Combined Sewer System”,
[3] Bechi, N., Estrogen-Like Response to p-Nonylphenol in Human First Trimester Placenta and BeWo Choriocarcinorna Cells, Toxicological Sciences, 93(1), 75-8 1 (September, 2006).http:lltoxsci.oxford~ournals.org/cgi/content~full/93/1l75.
[4] Potential adverse effects of NP and NPEs on human health is also discussed in Vazquez-Duhalt, Nonylphenol, an integrated vision of a pollutant, Applied Ecology and Environmental Research 4(1): 1-25 ISSN1589 1623, http:lIwww.ecology.kee.hu~pdf/O401~001025.pdf. Widespread exposure of the U.S. population to NP has been demonstrated. Calafat, A., Kuklenyik Z., Reidy J., Cauhll S., Ekong J., Needham L. 2005. Urinary Concentrations of Bisphenol A and 4-Nonylphenol in a Human Reference Population. Environmental Health Perspectives Vol. 113, p. 391. NP at high doses has been llnked to breast cancer in mice. BBC News. 2005. Chemical Link to Breast Cancer.http:llnews.bbc.co.uW1/hl/healthl676129.strnin 612005.
[5] Tyler, C.R. and Routledge, E.J., “Oestrogenic effects in fish in English rivers with evidence of their causation”, Dept. of Biology and Biochemistry, Brunel University, UK, Pure and Applied Chemistry, Vol 70, No. 9 pp. 1796-1804, 1998.
[6] Dickey, Philip, “Troubling Bubbles: Alkylphenol ethoxylate surfactants”, Washington Toxics Coalition
[7] “Response to comments submitted by the Alkylphenols and ethoxylates research council”, by Victoria Whitney, Deputy Director, Division of Water Quality, State Water Resources Control Board, Sacramento, California, June 20, 2011 ALSO SEE: Tyler, C.R. and Routledge, E.J., “Oestrogenic effects in fish in English rivers with evidence of their causation”, Dept. of Biology and Biochemistry, Brunel University, UK, Pure and Applied Chemistry, Vol 70, No. 9 pp. 1796-1804, 1998.
(8) Kristof, Nicholas, “Warnings from a Flabby Mouse”, New York Times, January 19, 2013.
[9] Porter, A. and Hayden, N., “Nonylphenol in the Environment: A Critical Review”, Dept of Civil and Encironmental Engineering, University of Vermont.
[10] Norris, David and Carr, James, “Endocrine Disruption: Biological Bases for Health Effects in Wildlife and Humans”, Oxford University Press, 2006
[11] http://www.greenpeace.org/international/en/publications/Campaign-reports/Toxics-reports/Big-Fashion-Stitch-Up/

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What are PBDE’s and why should I be concerned?

21 07 2010

PBDE’s are chemical compounds that are used as flame retardants.  They can be found in almost anything that carries an electrical current or is highly flammable.  They’re in, for example, your TV, your computer, your cellphone,  your car, your toaster and your sofa. 

PBDE stands for polybrominated diphenyl ether – a compound which contains bromine atoms.  PBDE’s come in different forms, depending on the number and location of the bromine atoms.   There are 209 possible variations.  Often in the U.S. PBDE’s are marketed with trade names such as DE-60F or Saytex 102E (among others).  Variations of the polybrominated diphenyl ethers (PBDE’s)  include pentabrominated diphenyl ethers (pentaBDE’s); octabrominated diphenyl (octaBDE) and decabrominated diphenyl ethers (decaBDE’s).   Penta and Octa BDE’s are on the way out worldwide (are actually no longer produced in the US), but the chemical industry is waging a fierce fight to retain the use of the third major PBDE compound, Deca, which is the most widely used of the PBDE’s – about 50 million pounds a year in the U.S. alone.

PBDEs are released into the environment during manufacturing operations, as products containing these chemicals degrade, or when the products containing the PBDE’s  are disposed.

WHY SHOULD I BE CONCERNED?

SHORT ANSWER:   PBDE’s are everywhere, they accumulate and they spread.  And they’re really not good for us.

LONGER ANSWER:

Demand for flame retardants is up:  The average “escape time” that a person has to get out of a burning home has dropped from 17 minutes in 1975 to only 3 minutes today, according to a study by Underwriters Laboratories released in October 2007.  The reason for this is that plastics, from which so much of our consumer products are made, are made from oil, which is actually considered an accelerant in fires.  And synthetic fabrics (according to the UL study) produce hotter fires and more toxic smoke than natural fiber furnishings. The higher fire load of consumer products and home decorations has effectively made home fires so dangerous that fire alarms sounding will often not provide adequate time for occupants to escape. The flame retardants for plastics therefore have become more critical than ever before. Increasingly stringent fire codes and flammability requirements, especially in building materials and consumer products, are driving demand for flame retardants steadily higher.

PBDE use has increased 40% from 1992 to 2003, and is forecast to grow by at least 3% per year from 2011;   they are ubiquitous in consumer products.

Food is the major source of exposure for many contaminants, including DDT and PCBs.   But food doesn’t seem to be the culprit in this case: Since PBDEs are used as additive flame-retardantsand do not bind chemically to the polymers, they leach fromthe surface of the product and easily reach the environment.  In fact, The Environmental Working Group calculations show that dust is likely to be a more important PBDE exposure route for children than food, as PBDEs migrate from furniture and electronics into house dust.

And they don’t stay put:  Sit down on a foam cushion and you’re releasing countless, invisible PBDE particles. When the TV gets hot, still more escape and land in the dust in our homes. They rinse off our clothes in the laundry and run down the shower drain, winding up in sewage that’s applied to farm fields as fertilizer.

And what about all that plastic in the ocean gyres or in landfills?  It is slowly leaching PBDE’s.

These chemicals have characteristics that make them intrinsically hazardous to humans and other animals:  they are stable (persistent), they are fat seeking and they have the potential to act as endocrine disruptors.  What is meant by these sorta innocuous sounding terms is:

  1. persistent:  they bioaccumulate, or build up, in fish and cats and Orcas and foxes – and people.  Our bodies cannot get rid of these contaminates, so our levels just increase over time.  We eat PBDEs when they contaminate our food, particularly meat and dairy products. They latch on to dust and other particles, so we breathe them in, or ingest them when dust settles on food or when children stuff their fingers into their mouths. Scientists look for PBDEs in breast milk because the chemicals stick to fat. In 1999, Swedish researchers reported that PBDE levels in women’s breast milk had increased 60-fold between 1972 and 1997.  Similar dramatic increases were documented in California harbor seals, ringed seals from the Arctic, gull eggs from the Great Lakes and human blood from Norway.   PBDE pollution has been found essentially everywhere scientists have looked: in the tissues of whales, seals, birds and bird eggs, moose, reindeer, mussels, eels, and fish; in human breast milk, hair, fat and blood; in hot dogs and hamburgers and the cheese we put on them;  in twenty different countries and remote areas such as the North Sea, the Baltic Sea and the Arctic Ocean, on top of mountains and under the sea.
  2. fat seeking: this causes them to magnify up the food chain, increasing in concentration at each successively higher  level. Once PBDE’s are released into the environment, they invariably find their way into humans, including pregnant women, where they pass  to the developing fetus in utero or through the breast milk to the nursing infant.  As evidence of fetal exposure, the infant at birth has levels of PBDE’s that are up to 25% of maternal levels.  And researchers have found that children’s PBDE levels are about 2.8 times higher than their mothers. Research in animals shows that exposure to brominated fire retardants in-utero or during infancy leads to more significant harm than exposure during adulthood, and much lower levels of PBDEs are needed to cause harm to infants and children than to adults.
  3. endocrine disruptors: Many of the known health effects of PBDEs are thought to stem from their ability to disrupt the body’s thyroid hormone balance, which plays an essential role in brain development.  Laboratory animals showed deficits in learning and memory with exposure to PBDE’s.   Studies of mice showed that a single exposure to PBDEs caused permanent behavioral aberrations that worsened as the mice got older.  One study, for instance, found that women whose levels of T4 measured in the lowest 10 percent of the population during the first trimester of pregnancy were more than 2.5 times as likely to have a child with an IQ of less than 85 (in the lowest 20 percent of the range of IQs) and five times as likely to have a child with an IQ of less than 70, meeting the diagnosis of “mild retardation.”
    1. In addition to their effects on thyroid hormones and neurological development, PBDEs have been linked to a gamut of other health impacts in laboratory animals, from subtle to dramatic.  In-utero exposures have  been associated with serious harm to the fetus, including limb malformation, enlarged hearts, bent ribs,  delayed bone hardening, and lower weight gain. The malformations of the fetus were consistently seen at levels much lower than doses harmful to the mouse mothers.
    2. Only one commercial PBDE mixture has been tested for its ability to cause cancer, in a single study more than 15 years ago. High doses of Deca given to rats and mice caused liver, thyroid and pancreas tumors.

What does all of that mean, exactly?  

Personal choices can make a difference. Buying furniture, fabric, cell phones or computers made without PBDEs is definitely a vote for a non-toxic future. But personal choices can only go so far – and the crisis is great.   PBDEs, like other contaminant issues, are at least as much a social as a personal issue and challenge. You can help your kids not only with your buying habits, but also by modeling social action for environmental change, and by campaigning for a non-toxic future, the kind of future where mother’s milk will regain its purity.