Are biosolids safe?

25 08 2015

In a recent email from the Green Science Policy Institute, Arlene Blum mentioned that she was just back from Fluoros 2015, which aims to examine the “state of the science” on fluorinated organic compounds in the environment. Her take away was that many of these fluorinated compounds (like those found in fire retardants)  are found in vegetables such as lettuce, tomatoes and strawberries. The assumption is that these man-made chemicals are found in our vegetables because biosolids were used as fertilizer and reclaimed water was used for irrigation.

How does this happen?

First we have to know what a biosolid is: Bascially, biosolids are made from treated sewage sludge, under another (less prejudicial) name. According to the U.S. Environmental Protection Agency, biosolids are “nutrient-rich organic materials”, which contain useful amounts of plant nutrients such as nitrogen, phosphorus and micronutrients. Because it is made from treated sewage, it’s considered safe for use as fertilizer or land reclamation, and about 50% of all biosolids produced in the U.S. are being used as fertilizer, though only about 1% of cropland has biosolids applied.  But the use is growing because the cost to farmers is far less than for chemical fertilizers – by a factor of 4![1]   They can also be composted and sold for use on lawns and home gardens.

Sounds like a dream, right? Using  sewage sludge as fertilizer is a sweet way to get rid of the mountain of sludge produced in the U.S. each year.   Sludge management is an integral part of any municipal waste management system. The most common disposal method is incineration (which has its own problems) and landfills, storage in huge sludge ponds, dried in the sun or dumped in the oceans. But ocean dumping, which created vast dead moon-scapes on the ocean floor, was halted by the Ocean Dumping ban of 1987. Thus the policy of disposing of sludge by spreading it on agricultural land (a policy given the name “land application”) was born.     biosolidsGOC

The problem with biosolids is that most municipal treatment facilities are not able to remove the many chemicals found in sewage. The four main categories of potential pollutants – nutrients, pathogens, toxic organics, and heavy metals – behave differently and cannot all be managed by any single kind of treatment. The goal of “safe management” of such a complex toxic mixture cannot be met at a reasonable cost.

The EPA itself conducted the national Sewage Sludge Survey (NSSS) in 1988 to get information on pollutants found in treated biosolids. They found dozens of hazardous substances, including heavy metals, organics, PBDE’s, pharmaceuticals, steroids and hormones[2] in ALL the sludge samples the EPA took around the USA.

Rolf Halden is a professor at Arizona State University, member of the adjunct faculty at Johns Hopkins and an expert on the environmental impacts of industrial chemicals. His lab recently used treated sewage sludge to identify and prioritize persistent bioaccumulative chemicals.[3] The study found that chemicals contributed between 0.04% – 0.15% of the total dry mass of biosolids produced in the USA annually, which is equivalent to 2,866 – 8,708 tons of chemicals. The top individual chemicals found included:

  • Brominated fire retardants
    • DecaBDE
    • pentaBDE
    • 1,2-bis(2,4,6 tribromophenoxy
    • ethane
  • Surfactants
    • Nonylphenol (NP) and their ethoxylates (NPEOs) – both used in textile processing
  • Antimicrobials
    • Triclosan and triclocarban
  • Antibiotics
    • Azithromycin
    • Ciprofloxacin
    • ofloxacin

The Centers for Disease Control and Prevention (CDC) did a comprehensive exposure assessment of environmental chemicals found the U. S. population. They found about 139 organic chemicals in human blood, serum, urine and tissue samples. About 70% of the chemicals found in biosolids are also found in humans.

New studies have shown that:

  • Sewage sludge is mutagenic (it causes inheritable genetic changes in organisms), but no one seems sure what this means for human or animal health. Regulations for the use of sewage sludge ignore this information.
  • Two-thirds of sewage sludge contains asbestos. Because sludge is often applied to the land dry, asbestos may be a real health danger to farmers, neighbors and their children. Again, regulations don’t mention asbestos.
  • Governments issue numeric standards for metals. However, the movement of metals from soils into groundwater, surface water, plants and wildlife – and of the hundreds of other toxins in sludge – are poorly understood.
  • Soil acidity seems to be the key factor in promoting or retarding the movement of toxic metals into groundwater, wildlife and crops. The National Research Council (NRC) of the National Academy of Sciences gives sewage sludge treatment of soils a clean bill of health in the short term, “as long as…acidic soils are agronomically managed.” However the NRC acknowledges that toxic heavy metals and persistent organic pollutants can build up in treated soils.
  • There is good reason to believe that livestock grazing on plants treated with sewage sludge will ingest the pollutants – either through the grazed plants, or by eating sewage sludge along with the plants. Sheep eating cabbage grown on sludge developed lesions of the liver and thyroid gland. Pigs grown on corn treated with sludge had elevated levels of cadmium in their tissues. An AP story published in 2008 documented that milk sold throughout the U.S contained high levels of thallium (the primary toxin in rat poison), which had been present in the sewage sludge spread on crops fed to dairy cows.[4]
  • Small mammals have been shown to accumulate heavy metals after sewage sludge was applied to forestlands.
  • Insects in the soil absorb toxins, which then accumulate in birds.
  • It has been shown that sewage sludge applied to soils can increase the dioxin intake of humans eating beef (or cow’s milk) produced from those soils.
  • Traces of prescription drugs and household chemicals were found deep in the soil as a result of a couple of decades of use of biosolids as fertilizer.[5]

A study done in Sweden found that scientists have found antibiotic resistant “super bugs” in sewage sludge; they’re sounding the alarm about the danger of antibiotic resistant genes passing into the human food chain. Of the samples collected, 79% tested positive for the drug-resistnat vancomycin-resistant enterococci (VRE)

Astonishingly, in a November, 1990 edition of the United States Federal Register, the Environmental Protection Agency (EPA) had this to say of sewage sludge: “Typically, these constituents may include volatiles, organic solids, nutrients, disease-causing pathogenic organisms (bacteria, viruses, etc.), heavy metals and inorganic ions, and toxic organic chemicals from industrial wastes, household chemicals and pesticides.”

Not all contaminants are created equal:  some chemicals are stored in the human body, and others pass through it.  Some break down in our digestive system, and others don’t.  Each person is different, with a different body size, stage of development and metabolism.   The same chemical may wreak devastating effects if a pregnant woman eats it but may go unnoticed if eaten by a man.  And remember, chemicals are synergistic, and very little is known about interactions between low levels of large numbers of chemicals.  As an example, take the chemical triclosan, one of the antimicrobials that Rolf Halden’s lab found in highest quantities in treated sludge. Triclosan has been used for several decades in antibacterial products like soaps, deodorants and cosmetics.  It is also nearly universally found in sewage sludge.  A recently published study found that soybeans planted in soil containing triclosan took the triclosan up into their beans.

Triclosan is a suspected endocrine disruptor and recent CDC reports show more than a 40 percent increase in triclosan levels in the urine of Americans over a recent two-year period.  The amount in our bodies can’t be blamed entirely on sewage sludge; humans can absorb triclosan through their skin and those who use triclosan-containing toothpastes put the chemical directly into their mouths.   But at what point does exposure to triclosan become more than an individual body can bear?

According to the EPA, about half of all sewage sludge is applied to land, but it is only applied to about one percent of the nation’s farmland.  The likely result is that, if dangers do lurk in the sludge applied to land, we rarely find out about them.

Most people’s chances of eating enough tainted food from farms that apply sewage sludge as fertilizer to cause an acute reaction are pretty slim.  The chance that anyone who got sick would be able to correctly trace his or her illness back to the farm and to sewage sludge is even smaller.  However, a lack of easily traceable acute illnesses does not prove that sewage sludge is safe.  Health harm due to exposure to low levels of toxins over a long period of time is no more acceptable than acute problems, even if they are less obvious.

As a consumer, the only sure way to avoid food grown in sewage sludge is to buy organic food (or grow your own).  If you are a gardener and you wish to avoid sewage sludge fertilizers or composts, avoid any product that says it contains “biosolids.”  Last, if you wish to keep sewage sludge from being spread on farm fields near where you live, you can take action locally to make it illegal in your city or county.

[1] “Davison, Janet, “Earth Day: Is sewage sludge safe for farm fields?”, CBC news Canada, April 22, 2014.

[2] EPA , “Targeted National Sewage Sludge Survey Statistical Analysis Report”, revised April, 2009

[3] Halden, Rolf et al; “Wastewater treatment plants as chemical observatories to forecase ecological and human health risks of manmade chemicals”, Scientific Reports, January 2014

[4] Hellprin, John and Vineys, Kevin: “Sewage-based fertilizer safety doubted”, USA Today; 3.6.2008

[5] Bienkowski, Brian, “Farm sludge contaminates soil with drugs, other chemicals”, Environmental Health News, May 2014.


Endocrine disruptors – in fabric?

11 04 2013

jeansThis post was published about two years ago, but it’s time to re-run it, because Greenpeace has published its expose of the endocrine disruptors (APEOs and NPEOs) they found in garments produced by major fashion brands (like Levis, Zara, Calvin Klein and others). Click here to read their report.
Many chemicals used in textile processing – and elsewhere in consumer products – have been identified as “endocrine disruptors”. I never paid too much attention to “endocrine disruptors” because it didn’t sound too dire to me – I preferred to worry about something like “carcinogens” because I knew those caused cancer. I knew that endocrine disruptors had something to do with hormones, but I didn’t think that interfering with acne or my teenager’s surliness was much of a concern. Boy was I wrong.
What is an “endocrine disruptor”?
The Environmental Protection Agency defines an endocrine disruptor as an external agent that interferes in some way with the role of natural hormones in the body. (Hmm. Still doesn’t sound too bad.)
The endocrine system includes the glands (e.g., thyroid, pituitary gland, pancreas, ovaries, or testes) and their secretions (i.e., hormones), that are released directly into the body’s circulatory system. The endocrine system controls blood sugar levels, blood pressure, metabolic rates, growth, development, aging, and reproduction. “Endocrine disruptor” is a much broader concept than the terms reproductive toxin, carcinogen, neurotoxin, or teratogen. Scientists use one or more of these terms to describe the types of effects these chemicals have on us.
How do they work? This is from The Society of Environmental Toxicology and Chemistry (SETAC):

Humans and wildlife must regulate how their bodies function to remain healthy in an ever-changing environment. They do this through a complicated exchange between their nervous and endocrine systems. The endocrine systems in humans and wildlife are similar in that they are made up of internal glands that manufacture and secrete hormones. Hormones are chemical messengers that move internally, start or stop various functions, and are important in determining sleep/wake cycles, stimulating or stopping growth, or regulating blood pressure. Some of the most familiar hormones in humans or wildlife are those that help determine male and female gender, as well as control the onset of puberty, maturation, and reproduction. An endocrine disruptor interferes with, or has adverse effects on, the production, distribution, or function of these same hormones. Clearly, interference with or damage of hormones could have major impacts on the health and reproductive system of humans and wildlife, although not all of the changes would necessarily be detrimental.

But why the fuss over endocrine disruptors — and why now? After all, scientists had known for over fifty years that DDT can affect the testes and secondary sex characteristics of young roosters[1]. And for almost as long, it has been well known that daughters born to women who took the drug diethylstilbestrol (DES), a synthetic estrogen, early in their pregnancies had a greatly increased risk of vaginal cancer. [2]
And it has been known for over 25 years that occupational exposures to pesticides could “diminish or destroy the fertility of workers.”[3]

It wasn’t until Theo Colborn, a rancher and mother of four who went back to school at age 51 to get her PhD in zoology, got a job at the Conservation Foundation and began to put the pieces together that the big picture emerged. Theo’s job was to review other scientists’ data, and she noticed that biologists investigating the effects of presumably carcinogenic chemicals on predators in and around the Great Lakes were reporting odd phenomena:

  • Whole communities of minks were failing to reproduce;
  • startling numbers of herring gulls were being born dead, their eyes missing, their bills misshapen;
  •  and the testicles of young male gulls were exhibiting female characteristics.

Often, the offspring of creatures exposed to chemicals were worse off than the animals themselves. Colborn concluded that nearly all the symptoms could be traced to things going wrong in the endocrine system.
In 1991, Colborn called together a conference, whose participants included biologists, endocrinologists and toxicologists as well as psychiatrists and lawyers, at the Wingspread Conference Center in Racine, Wisconsin. They produced what become known as the “Wingspread Statement,” the core document of the endocrine-disruption hypothesis, in which these researchers concluded that observed increases in deformities, evidence of declining human fertility and alleged increases in rates of breast, testicular and prostate cancers, as well as endometriosis are the result of “a large number of man-made chemicals that have been released into the environment”.[4]
Endocrine disruption—the mimicking or blocking or suppression of hormones by industrial or natural chemicals— appeared to be affecting adult reproductive systems and child development in ways that far surpassed cancer, the outcome most commonly looked for by researchers at the time. Potential problems included infertility, genital abnormalities, asthma, autoimmune dysfunction, even neurological disorders involving attention or cognition. In one early study that Colborn reviewed, for instance, the Environmental Protection Agency (EPA) commissioned psychologists to study children whose mothers ate fish out of the Great Lakes. The researchers found that the children “were born sooner, weighed less, and had smaller heads” than those whose mothers hadn’t eaten the fish. Moreover, the more endocrine-disrupting chemicals that were found in the mother’s cord blood, the worse the child did on tests for things such as short-term memory. By age eleven, the most highly exposed kids had an average IQ deficit of 6.2.[5]
The endocrine disruptor hypothesis first came to widespread congressional attention in 1996, with the publication of the book Our Stolen Future – by Theo Colborn, Dianne Dumanoski and John Peterson Myers.[6]
In the years since the Wingspread conference, many of its fears and predictions have been fleshed out by new technologies that give a far more precise picture of the damage that these chemicals can wreak on the human body – and especially on developing fetuses, which are exquisitely sensitive to both the natural hormone signals used to guide its development, and the unexpected chemical signals that reach it from the environment.[7]
Thanks to a computer-assisted technique called microarray profiling, scientists can examine the effects of toxins on thousands of genes at once (before they could study 100 at a time at most). They can also search for signs of chemical subversion at the molecular level, in genes and proteins. This capability means that we are beginning to understand how even tiny doses of certain chemicals may switch genes on and off in harmful ways during the most sensitive period of development.
The endocrine disruption hypothesis has also unleashed a revolution in toxicity theory. The traditional belief that “the dose makes the poison” (the belief that as the dose increases, so does the effect; as the dose decreases, so does its impact) has proven inadequate in explaining the complex workings of the endocrine system, which involves a myriad of chemical messengers and feedback loops.
Experimental data now shows conclusively that some endocrine-disrupting contaminants can cause adverse effects at low levels that are different from those caused by high level exposures. For example, when rats are exposed in the womb to 100 parts per billion of DES, they become scrawny as adults. Yet exposure of just 1 part per billion causes grotesque obesity.[8] Old school toxicology has always assumed that high dose experiments can be used to predict low-dose results. With ‘dose makes the poison’ thinking, traditional toxicologists didn’t pursue the possibility that there might be effects at levels far beneath those used in standard experiments. No health standards incorporated the possibility.
Jerry Heindel, who heads a branch of the National Institute of Environmental Health Science (NIEHS) that funds studies of endocrine disruptors, said that a fetus might respond to a chemical at “one hundred-fold less concentration or more, yet when you take that chemical away, the body is nonetheless altered for life”. Infants may seem fine at birth, but might carry within them a trigger only revealed later in life, often in puberty, when endocrine systems go into hyperdrive. This increases the adolescent’s or adult’s chances of falling ill, getting fat, or becoming infertile – as is the case with DES, where exposure during fetal development doesn’t show up until maturity.
And not just the child’s life, but her children’s lives too. “Inside the fetus are germ cells that are developing that are going to be the sperm and oocytes for the next generation, so you’re actually exposing the mother, the baby, and the baby’s kids, possibly,” says Heindel.[9]
So it’s also the timing that contributes to the poison.
According to Our Stolen Future, “the weight of the evidence says we have a problem. Human impacts beyond isolated cases are already demonstrable. They involve impairments to reproduction, alterations in behavior, diminishment of intellectual capacity, and erosion in the ability to resist disease. The simple truth is that the way we allow chemicals to be used in society today means we are performing a vast experiment, not in the lab, but in the real world, not just on wildlife but on people.”
Now that I know what “endocrine disruptor” means, I’m not dismissing them any more as mere irritants.
[1] Burlington, F. & V.F. Lindeman, 1950. “Effect of DDT on testes and secondary sex
characteristics of white leghorn cockerels”. Proc. Society for Experimental Biology
and Medicine 74: 48–51.
[2] Herbst, A., H. Ulfelder, and D. Poskanzer. “Adenocarcinoma of the vagina: Association of maternal stilbestrol therapy with tumor appearance in young women,” New England Journal of Medicine, v. 284, (1971) p. 878-881.
[3] Moline, J.M., A.L. Golden, N. Bar-Chama, et al. 2000. “Exposure to hazardous substances
and male reproductive health: a research framework”. Environ. Health Perspect.
108: 1–20.
[4] Shulevitz,Judith, “The Toxicity Panic”, The New Republic, April 7, 2011.
[5] Ibid.
[6] Colborn, Theo, Dianne Dumanoski, and John Peterson Myers. Our Stolen Future: Are We Threatening Our Fertility, Intelligence, and Survival? A Scientific Detective Story. New York: Penguin. (1996) 316 p.
[9] Shulevitz,Judith, op. cit.

Can your fabric choices make you fat?

31 01 2013

We have all heard the stories of our “growing obesity epidemic” – especially in western nations. It’s an important national problem, and is partly responsible for our soaring health care costs. We often point to obesity as being caused by overeating, fast food, and/or sedentary lifestyles for those having a genetic predisposition to the disease. But the rates of obesity have escalated in such an exponential manner that the commonly held causes of obesity – overeating and inactivity – cannot explain the current obesity epidemic. A growing number of studies have suggested a new culprit: environmental rather than genetic causes.

Our world is different than it was 100 years ago. We have developed many synthetic organic and inorganic chemicals to make our lives easier – and used them in a fabulously wide range of products. In fact, you could say, as some do, that we’re living in a toxic soup of these chemicals. And those chemicals are changing us. Some of the chemicals changing us are called “endocrine disruptors” (which we discussed in last week’s post) since they interfere with the body’s hormone balance, which confuses the body. Initially, they caused concern because of their links to cancers and the malformation of sex organs. Those concerns continue, but the newest area of research is the impact that they have on fat storage.

It has been found that the developing organism (us!) is extremely sensitive to chemicals with estrogenic or endocrine disrupting activity and that exposure to these chemicals during critical stages of development may have permanent long-lasting consequences, some of which may not be expressed or detected until later in life.(1)

But back to obesity, which is what we’re concentrating on this week. (I know it’s difficult to stay on task, because these chemicals are synergistic, have multi-dimensional effects and often degrade into different substances altogether).

Nicholas Kristof, writing in the New York Times last weekend, talked about the results of a study which I found disturbing. Look at these two mice:

The only difference between these mice: The one at the top was exposed at birth to a tiny amount of an endocrine-disrupting chemical.  New York Times

The only difference between these mice: The one at the top was exposed at birth to a tiny amount of an endocrine-disrupting chemical. New York Times

According to Kristof, “they’re genetically the same, raised in the same lab and given the same food and chance to exercise. Yet the bottom one is svelte, while the other looks like, well, an American. The only difference is that the top one was exposed at birth to just one part per billion of an endocrine-disrupting chemical (2) . The brief exposure programmed the mouse to put on fat, and although there were no significant differences in caloric intake or expenditure, it continued to put on flab long after the chemical was gone.”

Bruce Blumberg, a developmental biologist at the University of California, Irvine, coined the term “obesogen” in a 2006 journal article to refer to chemicals that cause animals to store fat. Initially, this concept was highly controversial among obesity experts, but a growing number of peer-reviewed studies have confirmed his finding and identified some 20 substances as obesogens.

Manufacturers have already exploited obesogens by using them to fatten livestock, and by formulating pharmaceuticals to induce weight gain in grossly underweight patients. A study by Dr. Baillie-Hamilton presents the hypothesis that the current level of human exposure to these chemicals may have damaged many of the body’s natural weight-control mechanisms and that these effects, together with a wide range of additional, possibly synergistic, factors may play a significant role in the worldwide obesity epidemic.(3) And these changes continue generation after generation. It’s clear that the most important time for exposure is in utero and during childhood.(4)

The magazine Scientific American recently asked whether doctors should do more to warn pregnant women about certain chemicals.(5)  It cited a survey indicating that only 19% of doctors cautioned pregnant women about pesticides, only 8% about BPA (an endocrine disruptor in some plastics and receipts), and only 5% about phthalates (endocrine disruptors found in cosmetics and shampoos). Dr. Blumberg, the pioneer of the field, says he strongly recommends that people — especially children and women who are pregnant or may become pregnant — try to eat organic foods to reduce exposure to endocrine disruptors, and try to avoid using plastics to store food or water. “My daughter uses a stainless steel water bottle, and so do I,” he said.

Endocrine disruptors are found in fabrics – Greenpeace did a study of 141 clothing items purchased in 29 different countries from authorized retailers. Endocrine disruptors were found in 89 of the 141 articles tested. According to the report: “Overall, a variety of hazardous chemicals were detected within the broad range of high street fashion textile products analysed. These covered a diverse range of brands and countries of manufacture. These results indicate the ongoing – and in some cases widespread – use of hazardous chemicals in the manufacture of textile products openly marketed to consumers.”

It’s not clear whether most obesogens will do much to make an ordinary adult, even a pregnant woman, fatter (although one has been shown to do so). But what about our children, and their children? How does fabric processing impact my weight, or my child’s weight? Should I avoid certain processing chemicals in my own home?

The government made a tremendous impact on public health when it outlawed lead in gasoline. Now we need to make those same hard choices about doing without some of the things we’ve learned to like but which we know to be impacting our health. Support the Safe Chemicals Act and spread the word. This is too important to ignore.

[1] Newbold, R. R., Padilla-Banks, E., Snyder, R. J. and Jefferson, W. N. (2005), Developmental exposure to estrogenic compounds and obesity. Birth Defects Research Part A: Clinical and Molecular Teratology, 73: 478–480. doi: 10.1002/bdra.20147

[2] Newbold, R. R., Padilla-Banks, E., Snyder, R. J. and Jefferson, W. N. (2005), Developmental exposure to estrogenic compounds and obesity. Birth Defects Research Part A: Clinical and Molecular Teratology, 73: 478–480. doi: 10.1002/bdra.20147

[3] Baillie-Hamilton, PF, “Chemical toxins: a hypothesis to explain the global obesity epidemic”, Journal of Alternative and Complementary Medicine, April 2002,

[4] Blumberg, Bruce et al, “Transgenerational Inheritance of Increased Fat Depot Size, Stem Cell Reprogramming, and Hepatic Steatosis Elicited by Prenatal Obesogen Tributyltin in Mice”, Environmental Health Perspectives, January 15, 2013.

[5] Kay, Jane, “Should Doctors Warn Pregnant Women about Environmental Risks?”, Scientific American, December 10, 2012.

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?”,
[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)
[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, 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 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