Synergy

31 07 2014

I just read the article by Mark Winston in the New York Times (July 15, 2014) in which he talks about the “thousand little cuts” suffered by honeybees which has led to the catastrophic decline of these insects. (The article is reproduced at the end of this blog.) I had been thinking about synergy and this seems to fit right in.

Synergy means the interaction of two (or more) things that produce an overall effect that’s greater than – or different from – the sum of the individual effects. In other words, we cannot predict the whole simply by looking at the parts.   Even so, we are challenged to understand and predict the impacts that contaminants have on communities – when understanding the effect of a single contaminant on a single organism is daunting. There are almost unlimited variables that impact any situation.

The EPA tests chemicals for adverse health effects, which they assume will occur individually. But in the real world, we’re exposed to a medley of chemicals every day – from car exhaust, to cosmetics, clothing, pesticide sprays for agriculture or mosquitos, even smog. The fact that these exposures can react with each other, and in effect, make each other more toxic, is a newly emerging science. In 1996, the EPA was required for the first time to consider cumulative pesticide exposure under the Food Quality Protection Act (FQPA). The FQPA recognizes that real-world pesticide exposure doesn’t occur as a single discrete exposure to a single pesticide, but rather as a combination of several pesticides at once. For example, USDA data shows that apples sold in the United States contained 22 different pesticide residues, and peaches contained 40.[1]

I just discovered the term “co-carcinogen”, which means the additive or synergistic effect of two or more agents which leads to cancer. These “co-carcinogens” may not themselves be a carcinogen. For example, a study by the University of Minnesota published a paper about the cancer-promoting effects of capsaicin – found in foods that contain hot chili peppers. It’s complicated – if you’re interested, please click here.

Here’s an interesting story:

In the summer of 1985, 30 year-old Thomas Latimer was leading a good life in the suburbs of Dallas, TX. He was a vigorous, athletic man with a promising engineering career. On one particular Saturday afternoon, Mr. Latimer spent the day mowing the lawn, picking up the clippings and edging the walkways. After about an hour, he began to feel dizziness, nausea, tightness in his chest and a pounding headache. Ten days later, he felt even worse and went to see his doctor.

Over the next six years, Mr. Latimer found himself unable to exercise. He suffered from brain seizures. He visited 20 different doctors and underwent numerous tests to determine the source of his medical problems. His symptoms were consistent with organophosphate poisoning, most likely from the insecticide diazinon that had been applied to his lawn. But because his symptoms were so severe and the amount of pesticide he was exposed to was so low, the doctors continued to look for a complicating factor. After further research, a toxicologist, three neurologists and two neuro-ophthalmologists all concluded independently that the popular ulcer drug Tagamet that Mr. Latimer was taking had suppressed his liver, making him more susceptible to pesticide poisoning.

Alfredo A Sudan, a professor of neurology and ophthalmology at the University of Southern California, who conducted extensive tests evaluating an eye disorder that Mr. Latimer developed, estimates that taking a medication like Tagamet “can make a person 100 to 1,000 times more sensitive to organophosphate poisoning.”[2]

In 2001, researchers at Duke University’s Department of Pharmacology and Cancer Biology published a series of papers looking at the synergistic effects of DEET (the active ingredient in most insect repellants) and permethrin (a pesticides commonly used in community mosquite programs, as well as many household bug killers.) The purpose of the studies was to determine a possible link between pesticides and other chemicals used during the Persian Gulf War and the “Gulf War Syndrome” – a neurological disease. When DEET, permethrin and pyridostigmine bromide (a drug taken by soldiers to counteract toxic gas warfare chemicals) were administered alone – even at doses three times the level soldiers received – no effects were observed. But when the three chemicals were used in combination, test animals suffered neurological symptoms similar to the Gulf War veterans.[3]

Neurology experts give three possible reasons for the synergistic effects seen in the above experiments. First, the stress endured by animals when exposed to a combination of chemicals undermines the protective role of the blood brain barrier, allowing the level of toxics to cross into the brain to be 100 times higher. Second, tissue that has been exposed becomes more sensitive and receptive to other toxic substances. Third, certain chemicals bind to enzymes that detoxify the body, making the enzymes unavailable to protect the body from other intruding chemicals. Dr. Goran Jamal, a neurologist at the West London Regional Neuro-Science Center of the Imperial College of Medicine, makes the following comparison, “It’s like releasing 200 criminals in London and taking away the police officers that are usually on duty. There is bound to be some damage.”[4]

The organization Beyond Pesticides suggests a variety of tests: testing for interactions between pesticides commonly used in agriculture, between pesticides used in agriculture and food contaminants, for pesticides commonly found in drinking water, for pesticides and pharmaceuticals, and for pesticides that are likely to drift. However, this testing is probably unrealistic so the best approach might be to limit exposure – by limiting exposure you also limit synergistic health effects.

Here is Mark Winston’s article, “Our Bees, Ourselves”:

New York Times, Katie Scott

New York Times, Katie Scott

AROUND the world, honeybee colonies are dying in huge numbers: About one-third of hives collapse each year, a pattern going back a decade. For bees and the plants they pollinate — as well as for beekeepers, farmers, honey lovers and everyone else who appreciates this marvelous social insect — this is a catastrophe.

But in the midst of crisis can come learning. Honeybee collapse has much to teach us about how humans can avoid a similar fate, brought on by the increasingly severe environmental perturbations that challenge modern society.

Honeybee collapse has been particularly vexing because there is no one cause, but rather a thousand little cuts. The main elements include the compounding impact of pesticides applied to fields, as well as pesticides applied directly into hives to control mites; fungal, bacterial and viral pests and diseases; nutritional deficiencies caused by vast acreages of single-crop fields that lack diverse flowering plants; and, in the United States, commercial beekeeping itself, which disrupts colonies by moving most bees around the country multiple times each year to pollinate crops.

The real issue, though, is not the volume of problems, but the interactions among them. Here we find a core lesson from the bees that we ignore at our peril: the concept of synergy, where one plus one equals three, or four, or more. A typical honeybee colony contains residue from more than 120 pesticides. Alone, each represents a benign dose. But together they form a toxic soup of chemicals whose interplay can substantially reduce the effectiveness of bees’ immune systems, making them more susceptible to diseases.

These findings provide the most sophisticated data set available for any species about synergies among pesticides, and between pesticides and disease. The only human equivalent is research into pharmaceutical interactions, with many prescription drugs showing harmful or fatal side effects when used together, particularly in patients who already are disease-compromised. Pesticides have medical impacts as potent as pharmaceuticals do, yet we know virtually nothing about their synergistic impacts on our health, or their interplay with human diseases.

Observing the tumultuous demise of honeybees should alert us that our own well-being might be similarly threatened. The honeybee is a remarkably resilient species that has thrived for 40 million years, and the widespread collapse of so many colonies presents a clear message: We must demand that our regulatory authorities require studies on how exposure to low dosages of combined chemicals may affect human health before approving compounds.

Bees also provide some clues to how we may build a more collaborative relationship with the services that ecosystems can provide. Beyond honeybees, there are thousands of wild bee species that could offer some of the pollination service needed for agriculture. Yet feral bees — that is, bees not kept by beekeepers — also are threatened by factors similar to those afflicting honeybees: heavy pesticide use, destruction of nesting sites by overly intensive agriculture and a lack of diverse nectar and pollen sources thanks to highly effective weed killers, which decimate the unmanaged plants that bees depend on for nutrition.

Recently, my laboratory at Simon Fraser University conducted a study on farms that produce canola oil that illustrated the profound value of wild bees. We discovered that crop yields, and thus profits, are maximized if considerable acreages of cropland are left uncultivated to support wild pollinators.

means a healthier, more diverse bee population, which will then move to the planted fields next door in larger and more active numbers. Indeed, farmers who planted their entire field would earn about $27,000 in profit per farm, whereas those who left a third unplanted for bees to nest and forage in would earn $65,000 on a farm of similar size.

Such logic goes against conventional wisdom that fields and bees alike can be uniformly micromanaged. The current challenges faced by managed honeybees and wild bees remind us that we can manage too much. Excessive cultivation, chemical use and habitat destruction eventually destroy the very organisms that could be our partners.

And this insight goes beyond mere agricultural economics. There is a lesson in the decline of bees about how to respond to the most fundamental challenges facing contemporary human societies. We can best meet our own needs if we maintain a balance with nature — a balance that is as important to our health and prosperity as it is to the bees.[5]

 

 

 

 

[1] http://www.beyondpesticides.org/infoservices/pesticidesandyou/Winter%2003-04/Synergy.pdf

[2] Allen, Frank Edward. 1991. One Man’s Suffering Spurs Doctors to Probe Pesticide-Drug Link. The Wall Street Journal. October 14.

[3] Abou-Donia, M.B., et. al. 1996. Neurotoxicity resulting from coexposure to pyridostigmine bromide, DEET, and permethrin: Implications of Gulf War chemical exposures. J. Toxicol. Environ. Health 48:35-56.

[4] http://www.beyondpesticides.org/infoservices/pesticidesandyou/Winter%2003-04/Synergy.pdf

[5] Winston, Mark, “Our Bees, Ourselves”, New York Times, July 15, 2014, pg. A25

 





What will nanotechnology mean to you?

2 04 2014

A hot topic in the media right now is the toxicity of chemical flame retardants that are in our furniture and are migrating out into our environment.  Tests have shown that Americans carry much higher levels of these chemicals in their bodies than anyone else in the world, with children in California containing some of the highest levels ever tested.   According to Ronald Hites of Indiana University, these concentrations have been “exponentially increasing, with a doubling time of 4 to 5 years.”[1]  These toxic chemicals are present in nearly every home – packed into couches, chairs and many baby products including (but not limited to) mattresses, nursing pillows, carriers and changing table pads (scary!).  Recent studies have found that most couches in America have over 1 pound of the toxic chemical Chlorinated Tris inside them[2], even though it was banned in children’s pajamas over cancer concerns over a generation ago.[3]

Why the concern?  Fire retardant chemicals, called PBDE’s (polybrominated diphenyl ethers) have been linked to cancer, reproductive problems and impaired fetal brain development, as well as decreased fertility.  And even though they’ve been banned in the U.S. and European Union, they persist in the environment and accumulate in your body – and they’re still being used today.

So its probably no surprise that there is a mad scramble on to produce a fire retardant that does not impact our health or the environment.   The current front runners, touted as being “exceptionally” effective yet safer and more environmentally friendly than the current fire retardants, use nanotechnology – specifically “nanocoatings” and “nanocomposites”[4] .  These composites and coatings are based on what are called “multiwalled carbon nanotubes” or MWCNTs.

Based on a final report published by the U.S. EPA in September 2013 about the assessment of the risks of using these  MWCNTs, the EPA found that there will be releases of these MWCNTs into the environment throughout the life cycle of textiles – to our air and water during production,  in the form of abraded particles of the textiles falling into the dust in our homes, and in the disposal of furniture in municipal landfills or incineration facilities.[5]

While it is reasonable to propose that substituting nanomaterials for polybrominated diphenyl ether (PBDEs)  or chlorinated triss  and calling it “sustainable”, the fact is that no quantitative study has ever been done to support this assertion . [6]

Please don’t misunderstand me – I am all for finding safer alternatives to the current crop of chemical fire retardants (assuming I buy into the argument that we actually need them).  However, I don’t want us to jump from the frying pan into the fire by rushing to use a technology which is still controversial.  But the race is on:  the US patent office published some 4000 patents under “977 – nanotechnology” in 2012, a new record.

patents nanotech

Here’s an interesting video which helps to explain how nano works – and why we will need extensive study to absorb the many implications of this emerging science.

Consider these science fiction type scenarios of how nano can be used to profoundly change our lives:

  • “nanomedicine” offers the promise of diagnosis and treatment of a disease – before you even have the symptoms.  Or it promises to rebuild neurons for people with Alzheimers or Parkinson’s disease – and stem cells for whatever ails you!   Bone regeneration.  [7]
  • Surfaces can be modified to be scratchproof, unwettable, clean or sterile, depending on the application.[8]
  • Quantum computing.
  • Solar cells capturing the sun’s visible spectrum – as well as infrared photons –  doubling the solar energy available to us.  How about zero net carbon emissions.
  • Nanoscale bits of metals can detoxify hazardous wastes.
  • Clothing that recharges your cell phone as you stroll, or an implant that measures blood pressure powered by your own heartbeat.

And yet.  The unknowns are great, and as Eric Drexler has said, the story involves a tangle of science and fiction linked with money, press coverage, Washington politics and sheer confusion.  Scientists and governments agree that the application of nanotechnology to commerce poses important potential risks to human health and the environment, and those risks are unknown. Examples of high level respected reports that express this concern include:

  • Swiss Federation (Precautionary Matrix 2008)[9]
  • Commission on Environmental Pollution (UK 2008)[10];
  • German Governmental Science Commission (“SRU”)[11];
  • Public testimony sought by USA National Institute for Occupational Safety and Health (NIOSH, Feb 2011)[12] ;
  • OECD working group (since 2007)[13];
  • World Trade Organization (WTO)[14]
  • as well as several industrial groups and various non-governmental organizations.

Nanotechnology is already transforming many products – water treatment, pesticides, food packaging and cosmetics to name a few – so the cat is already out of the bag.  Consider this small example of the nano particle  argument:  When ingested the nanoparticles pass into the blood and lymph system, circulate throughout the body and reach potentially sensitive sites such as the spleen, brain, liver and heart.[15]   The ability of nanoparticles to cross the blood brain barrier makes them extremely useful as a way to deliver drugs directly to the brain.  On the other hand, these nanoparticles may be toxic to the brain.  We simply don’t know enough about the size and surface charge of nanoparticles to draw conclusions.[16]  In textiles, silver nano particles are used as antibacterial/antifungal agents to prevent odors.

But there are almost no publications on the effects of engineered nanoparticles on animals and plants in the environment.

So it’s still not clear what nanoscience will grow up to be – if it doesn’t kill us, it might just save us.


[2] Stapleton HM, et al. Detection of organophosphate flame retardants in furniture foam and U.S. house dust. Environ Sci Technol 43(19):7490–7495. (2009); http://dx.doi.org/10.1021/es9014019.

[3] Callahan, P and Hawthorne, M; “Chemicals in the Crib”, Chicago Tribune, December 28, 2012, http://articles.chicagotribune.com/2012-12-28/news/ct-met-flames-test-mattress-20121228_1_tdcpp-heather-stapleton-chlorinated-tris

[5] Comprehensive Environmental Assessment Applied to Multiwalled Carbon Nanotube Flame-Retardant Coatings in Upholstery Textiles: A Case Study Presenting Priority Research Gaps for Future Risk Assessments (Final Report), Environmental Protection Agency, http://cfpub.epa.gov/ncea/nano/recordisplay.cfm?deid=253010

[6] Gilman,  Jeffrey W., “Sustainable Flame Retardant Nanocomposites”; National Institute of Standards and Technology

[7] Hunziker, Patrick,  “Nanomedicine: The Use of Nano-Scale Science for the Benefit of the Patient” European Foundation for Clinical Nanomedicine (CLINAM) Basel, Switzerland 2010.

[9] Swiss National Science Foundation, Opportunities and Risks of Nanomaterials Implementation Plan of the National Research Programme NRP 64 Berne, 6 October 2009; see also Swiss Precautionary Matrix, and documents explaining and justifying its use, available in English from the Federal Office of Public Health.

[10] Chairman: Sir John Lawton CBE, FRS Royal Commission on Environmental Pollution, Twenty-seventh report: Novel Materials in the Environment: The case of nanotechnology. Presented to Parliament by Command of Her Majesty November 2008.

[11] SRU, German Advisory Council on Environment, Special Report “Precautionary strategies for managing nanomaterials” Sept 2011. The German Advisory Council on the Environment (SRU) is empowered by the German government to make “recommendations for a responsible and precautionary development of this new technology”.

[12] See: Legal basis and justification: Niosh recommendations preventing risk from carbon nanotubes and nanofibers ”post-hearing comments Niosh current intelligence bulletin: occupational exposure to carbon nanotubes and nanofibers Docket NO. NIOSH-161 Revised 18 February 2011; Testimony on behalf of ISRA (International Safety Resources Association) Before NIOSH, USA. Comments prepared by Ilise L Feitshans JD and ScM, Geneva, Switzerland. Testimony presented by Jay Feitshans, Science Policy Analyst; ISRA Draft Document for Public Review and Comment NIOSH Current Intelligence Bulletin: Occupational Exposure to Carbon Nanotubes and Nanofibers, Docket Number NIOSH-161-A.

[13] The OECD Working Party for Manufactured Nanomaterials (WPMN) “OECD Emission Assessment for Identification of Sources of release of Airborne Manufactured Nanomaterials in the Workplace: Compilation of Existing Guidance”, ENV/JM/MONO (2009)16, http://www.oecd.org/dataoecd/15/60/43289645.pdf. “OECD Preliminary Analysis of Exposure Measurement and Exposure Mitigation in Occupational Settings: Manufactured Nanomaterials” OECD ENV/JM/MONO(2009)6, 2009. http://www.oecd.org/dataoecd/36/36/42594202.pdf.
“OECD Comparison of Guidance on selection of skin protective equipment and respirators for use in the workplace: manufactured nanomaterials”, OECD ENV/JM/MONO(2009) 17, 2009. www.oecd.org/dataoecd/15/56/43289781.pdf.

[14] WHO Guidelines on “Protecting Workers from Potential Risks of Manufactured Nanomaterials” (WHO/NANOH), (Background paper) 2011

[15] Dixon, D., “Toxic nanoparticles might be entering human food supply, MU study finds”, August 22, 2013, http://munews.missouri.edu/news-releases/2013/0822-toxic-nanoparticles-might-be-entering-human-food-supply-mu-study-finds/

[16] Scientific Committee on Emerging and Newly Identified health Risks (SCENIHR), The European Commission, 2006

http://www.cnn.com/video/data/2.0/video/health/2013/01/25/sgmd-gupta-flame-retardants.cnn.html

http://www.cnn.com/video/data/2.0/video/health/2013/01/25/sgmd-gupta-flame-retardants.cnn.html





Sofa cushions – foam, soy foam or latex?

12 09 2013

So we have produced the frame and put in the suspension system.  Next in line are the cushions – something soft to sit on.

In an upholstered piece of furniture, the cushions need a filler of some kind.  Before plastics, our grandparents used feathers, horsehair or wool or cotton batting.  But with the advent of plastics, our lives changed.  Polyurethane foam was introduced as a cushion component in furniture in 1957 –  only a bit more than 50 years ago – and quickly replaced latex, excelsior, cotton batting, horsehair and wool because it was CHEAP!  Imagine – polyfoam cushions at $2 vs. natural latex at $7 or $8.  Price made all the difference.  Today, Eisenberg Upholstery’s website says that “easily 25% of all furniture repairs I see deal with bad foam or padding. The point is start with good foam and you won’t be sorry.”

Cushions are generally measured by two values:

  • The density or weight per cubic foot of polyurethane foam. The higher the number the more it weighs.   Foam that has a density of 1.8 foam, for example, contains 1.8 lbs of foam per cubic foot and foam that is 2.5 foam would have 2.5 lbs of foam per cubic foot.  Density for sofa cushions ranges between 1.6 and 5 or even 6.
  • The second measurement tells you the firmness of the foam  (called the IFD  – the Indentation Force Deflection). The IFD is the feel of the cushion, and tells you how much weight it takes to compress the foam by one third. The lower IFD will sit softer. The higher IFD will sit firmer.  IFD numbers range between 15 to 35

What many people don’t realize is that the density and firmness numbers go hand in hand – you can’t look at one without the other.  They are expressed as density/firmness, for example: 15/30 or 29/52.  The first, 15/15 means that 1.5 pounds of foam per cubic foot will take 30 pounds of weight to compress the foam 33%.  The second example means that 2.9 pounds per cubic foot of foam will take 52 pounds of weight to compress the block one third.

The foam is then wrapped with something to soften the edges – for example,  Dacron or polyester batting, cotton or wool batting or down/feathers.

Lowest quality sofas will not even wrap the (low quality) foam; higher quality sofas have cushions that are made from very high quality foam and wrapped in wool or down.  But as you will see, the foam is itself very problematic.

You will now commonly find in the market polyurethane foam, synthetic or natural latex rubber and the new, highly touted soy based foam.  We’ll look at these individually, and explore issues other than embodied energy :

The most popular type of cushion filler today is polyurethane foam. Also known as “Polyfoam”, it has been the standard fill in most furniture since its wide scale introduction in the 1960’s because of its low cost (really cheap!).  A staggering 2.1 billion pounds of flexible polyurethane foam is produced every year in the US alone.[1]

Polyurethane foam is a by-product of the same process used to make petroleum from crude oil. It involves two main ingredients: polyols and diisocyanates:

  • A polyol is a substance created through a chemical reaction using methyloxirane (also called propylene oxide).
  • Toluene diisocyanate (TDI) is the most common isocyanate employed in polyurethane manufacturing, and is      considered the ‘workhorse’ of flexible foam production.
    • Both methyloxirane  and TDI have been formally identified as carcinogens by the State of California
    • Both are on the List of  Toxic Substances under the Canadian Environmental Protection Act.
    • Propylene oxide and TDI are also among 216 chemicals that have been proven to cause mammary tumors.       However, none of these chemicals have ever been regulated for their potential to induce breast cancer.

The US Environmental Protection Agency (EPA) considers polyurethane foam fabrication facilities potential major sources of several hazardous air pollutants including methylene chloride, toluene diisocyanate (TDI), and hydrogen cyanide.   There have been many cases of occupational exposure in factories (resulting in isocyanate-induced asthma, respiratory disease and death), but exposure isn’t limited to factories: The State of North Carolina forced the closure of a polyurethane manufacturing plant after local residents tested positive for TDI exposure and isocyanate exposure has been found at such places as public schools.

The United States Occupational Safety and Health Administration (OSHA) has yet to establish exposure limits on carcinogenicity for polyurethane foam. This does not mean, as Len Laycock explains in his series “Killing You Softly”, “that consumers are not exposed to hazardous air pollutants when using materials that contain polyurethane. Once upon a time, household dust was just a nuisance. Today, however, house dust represents a time capsule of all the chemicals that enter people’s homes. This includes particles created from the break down of polyurethane foam. From sofas and chairs, to shoes and carpet underlay, sources of polyurethane dust are plentiful. Organotin compounds are one of the chemical groups found in household dust that have been linked to polyurethane foam. Highly poisonous, even in small amounts, these compounds can disrupt hormonal and reproductive systems, and are toxic to the immune system. Early life exposure has been shown to disrupt brain development.”

“Since most people spend a majority of their time indoors, there is ample opportunity for frequent and prolonged exposure to the dust and its load of contaminants. And if the dust doesn’t get you, research also indicates that toluene, a known neurotoxin, off gases from polyurethane foam products.”

I found this on the Sovn blog:

“the average queen-sized polyurethane foam mattress covered in polyester fabric loses HALF its weight over ten years of use. Where does the weight go? Polyurethane oxidizes, and it creates “fluff” (dust) which is released into the air and eventually settles in and around your home and yes, you breathe in this dust. Some of the chemicals in use in these types of mattresses include formaldehyde, styrene, toluene di-isocyanate (TDI), antimony…the list goes on and on.”

Polyurethane foams are advertised as being recyclable, and most manufacturing scraps (i.e., post industrial) are virtually all recycled – yet the products from this waste have limited applications (such as carpet backing).  Post consumer, the product is difficult to recycle, and the sheer volume of scrap foam that is generated (mainly due to old cushions) is greater than the rate at which it can be recycled – so it  mostly ends up at the landfill.  This recycling claim only perpetuates the continued use of hazardous and carcinogenic chemicals.

Polyfoam has some hidden costs (other than the chemical “witch’s brew” described above):  besides its relatively innocuous tendency to break down rapidly, resulting in lumpy cushions, and its poor porosity (giving it a tendency to trap moisture which results in mold), it is also extremely flammable, and therein lies another rub!

Polyurethane foam is so flammable that it’s often referred to by fire marshals as “solid gasoline.” When untreated foam is ignited, it burns extremely fast. Ignited polyurethane foam sofas can reach temperatures over 1400 degrees Fahrenheit within minutes. Making it even more deadly are the toxic gasses produced by burning polyurethane foam –  such as hydrogen cyanide. The gas was also implicated in the 2003 Rhode Island nightclub fire that killed 100 people, including Great White guitarist Ty Longley, and injured more than 200 others. Tellingly, a witness to that fire, television news cameraman Brian Butler, told interviewers that “It had to be two minutes, tops, before the whole place was black smoke.”   Just one breath of superheated toxic gas can incapacitate a person, preventing escape from a burning structure.

Therefore, flame-retardant chemicals are added to its production when it is used in mattresses and upholstered furniture.   This application of chemicals does not alleviate all concerns associated with its flammability, since polyurethane foam releases a number of toxic substances at different temperature stages. For example, at temperatures of about 800 degrees, polyurethane foam begins to rapidly decompose, releasing gases and compounds such as hydrogen cyanide, carbon monoxide, acetronitrile, acrylonitrile, pyridine, ethylene, ethane, propane, butadine, propinitrile, acetaldehyde, methylacrylonitrile, benzene, pyrrole, toluene, methyl pyridine, methyl cyanobenzene, naphthalene, quinoline, indene, and carbon dioxide.

According to the federal government’s National Institute of Standards and Technology, polyurethane foam in furniture is responsible for 30 percent of U.S. deaths from fires each year.

In conclusion, the benefits of polyfoam (low cost) is far outweighed by the disadvantages:  being made from a non-renewable resource (oil),  and the toxicity of main chemical components as well as the toxicity of the flame retardants added to the foam – not to mention the fact that even the best foams begin to break down after around 10 – 12 years of “normal use”.[2]

Now we see ads for a  new miracle product: a bio based foam made from soybeans, which is highly touted as “A leap forward in foam technology, conserving increasingly scarce oil resources while substituting more sustainable options,” as one product brochure describes it. Companies and media releases claim that using soy in polyurethane foam production results in fewer greenhouse gas emissions, requires less energy, and could significantly reduce reliance on petroleum. Many companies are jumping on the bandwagon, advertising their green program of using foam cushions with “20% bio based foam” (everybody knows we have to start somewhere and that’s a start, right?).  As Len Laycock,  CEO of Upholstery Arts (which was the first furniture company in the world to introduce Cradle to Cradle product cycle and achieve the Rainforest Alliance Forest Stewardship Council Certification),  says  – who wouldn’t sleep sounder with such promising news?   (I have leaned heavily on Mr. Laycock’s articles on poly and soy foam, “Killing You Softly”, for this post.)

As with so many over hyped ‘green’ claims, it’s the things they don’t say that matter most.  While these claims contain grains of truth, they are a far cry from the whole truth. So called ‘soy foam’ is hardly the dreamy green product that manufacturers and suppliers want people to believe.

To begin, let’s look at why they claim soy foam is green:

  1. it’s made from soybeans, a renewable  resource
  2. it reduces our dependence on fossil  fuels  by  both reducing the amount of fossil fuel needed for      the feedstock  and  by reducing the energy requirements needed to produce the foam.

Are these viable claims?

It’s made from soybeans, a renewable resource:  This claim is undeniably true.   But what they don’t tell you is that this product, marketed as soy or bio-based,  contains very little soy. In fact, it is more accurate to call it ‘polyurethane based foam with a touch of soy added for marketing purposes’. For example, a product marketed as “20% soy based” may sound impressive, but what this typically means is that only 20 % of the polyol portion of the foam is derived from soy. Given that polyurethane foam is made by combining two main ingredients—a polyol and an isocyanate—in approximately equal parts, “20% soy based” translates to a mere 10% of the foam’s total volume. In this example the product remains 90% polyurethane foam and by any reasonable measure cannot legitimately be described as ‘based’ on soy. If you go to Starbucks and buy a 20 oz coffee and add 2-3 soy milk/creamers to it, does it become “soy-based” coffee?

It reduces our dependence on fossil fuels: According to Cargill, a multi-national producer of agricultural and industrial products, including BiOH polyol (the “soy” portion of “soy foam”), the soy based portion of so called ‘soy foam’ ranges from  5% up to a theoretical 40% of polyurethane foam formulations. This means that while suppliers may claim that ‘bio foams’ are based on renewable materials such as soy, in reality a whopping 90 to 95%, and sometimes more of the product consists of the same old petro-chemical based brew of toxic chemicals. This is no ‘leap forward in foam technology’.

It is true that the energy needed to produce soy-based foam is, according to Cargill, who manufactures the soy polyol,  less that that needed to produce the polyurethane foam.  But the way they report the difference is certainly difficult to decipher:  soy based polyols use 23% less energy to produce than petroleum based polyols, according to Cargill’s LCA.   But the formula for the foam uses only 20% soy based  polyols, so by my crude calculations (20% of 50%…) the energy savings of 20% soy based foam would require only 4.6%  less energy than that used to make the petroleum based foam.  But hey, that’s still a savings and every little bit helps get us closer to a self sustaining economy and is friendlier to the planet.

But the real problem with advertising soy based foam as a new, miracle green product is that the foam, whether soy based or not, remains a “greenhouse gas spewing pretroleum product and a witches brew of carcinogenic and neurotoxic chemicals”, according to Len Laycock.

My concern with the use of soy is not its carbon footprint but rather the introduction of a whole new universe of concerns such as pesticide use, genetically modifed crops, appropriation of food stocks and deforestation.  Most soy crops are now GMO:  according to the USDA, over 91% of all soy crops in the US are now GMO; in 2007, 58.6% of all soybeans worldwide were GMO.  If you don’t think that’s a big deal, please read our posts on these issues (9.23.09 and 9.29.09).  The debate still rages today.  Greenpeace did an expose (“Eating Up The Amazon”) on what they consider to be a driving force behind Amazon rainforest destruction – Cargill’s race to establish soy plantations in Brazil.  You can read the Greenpeace report here, and Cargill’s rejoinder here.

In “Killing You Softly“, another sinister side of  soy based foam marketing is brought to light:

“Pretending to offer a ‘soy based’ foam allows these corporations to cloak themselves in a green blanket and masquerade as environmentally responsible corporations when in practice they are not. By highlighting small petroleum savings, they conveniently distract the public from the fact that this product’s manufacture and use continues to threaten human health and poses serious disposal problems. Aside from replacing a small portion of petroleum polyols, the production of polyurethane based foams with soy added continues to rely heavily on ‘the workhorse of the polyurethane foam industry’, cancer causing toluene diisocyanate (TDI). So it remains ‘business as usual ‘ for polyurethane manufacturers.”

Despite what polyurethane foam and furniture companies imply , soy foam is not biodegradable either. Buried in the footnotes on their website, Cargill quietly acknowledges that, “foams made with BiOH polyols are not more biodegradable than traditional petroleum-based cushioning”. Those ever so carefully phrased words are an admission that all polyurethane foams, with or without soy added, simply cannot biodegrade. And so they will languish in our garbage dumps, leach into our water, and find their way into the soft tissue of young children, contaminating and compromising life long after their intended use.

The current marketing of polyurethane foam and furniture made with ‘soy foam’ is merely a page out the tobacco industry’s current ‘greenwashing’ play book. Like a subliminal message, the polyurethane foam and furniture industries are using the soothing words and images of the environmental movement to distract people from the known negative health and environmental impacts of polyurethane foam manufacture, use and disposal.

Cigarettes that are organic (pesticide-free), completely biodegradable, and manufactured using renewable tobacco, still cause cancer and countless deaths. Polyurethane foam made with small amounts of soy derived materials still exposes human beings to toxic, carcinogenic materials, still relies on oil production, and still poisons life.

So what’s a poor consumer to do?  We think there is a viable, albeit expensive, product choice: natural latex (rubber). The word “latex” can be confusing for consumers, because it has been used to describe both natural and synthetic products interchangeably, without adequate explanation. This product can be 100% natural (natural latex) or 100% man-made (derived from petrochemicals) – or it can be a combination of the two – the so called “natural latex”.   Also, remember latex is rubber and rubber is latex.

  • Natural latex – The raw material for  natural latex comes from a renewable resource – it is obtained from the sap of the Hevea Brasiliensis (rubber) tree, and was once widely used for cushioning.  Rubber trees are cultivated, mainly in South East Asia,  through a new planting and replanting program by large scale plantation and small farmers to ensure a continuous sustainable supply of natural  latex.  Natural latex is both recyclable and biodegradeable, and is mold, mildew and dust mite resistant.  It is not highly  flammable and does not require fire retardant chemicals to pass the Cal 117 test.  It has little or no off-gassing associated with it.    Because natural rubber has high energy production costs (although a  smaller footprint than either polyurethane or soy-based foams [3]),  and is restricted to a limited supply, it is more costly than petroleum based foam.
  • Synthetic latex – The terminology is very confusing, because synthetic latex is often referred to simply as  “latex” or even “100% natural latex”.  It is also known as styrene-butadiene rubber  (SBR).   The chemical styrene is  toxic to the lungs, liver, and brain.  Synthetic additives are added to achieve stabilization.    Often however, synthetic latex  can be made of combinations of polyurethane and natural latex, or a  combination of 70% natural latex and 30% SBR.  Most stores sell one of these versions under the term “natural latex” – so caveat emptor!    Being  petroleum based, the source of supply for the production of  synthetic latex is certainly non-sustainable and diminishing as well.

Natural latex is breathable, biodegradeable,  healthier (i.e., totally nontoxic, and mold & mildew proof) and lasts longer than polyfoam – some reports say up to 20 times longer.

Is there really a question as to which to buy?


[1] DFE 2008 Office Chair Foam;  http://en.wikiversity.org/wiki/DFE2008_Office_Chair_Foam#Basics

[2] http://www.foamforyou.com/Foam_Specs.htm

[3] Op cit., http://en.wikiversity.org/wiki/DFE2008_Office_Chair_Foam#Basics





Fire retardants: the new asbestos

9 05 2013

My toxic couch:

I’d like to nominate flame retardant chemicals used in our furniture, fabrics and baby products – as well as a host of other products – as being in the running for the “new asbestos”. These chemicals (halogenated flame retardants, such as polybrominated diphenyl ethers) are commonly known as PBDE’s. An editorial in the Chicago Tribune, responding to the series published by that paper about flame retardants called “Playing with Fire” (click here to read the series), said the use of flame retardants is a public health debacle.

According to “Playing with Fire”, the average American baby is born with “10 fingers, 10 toes and the highest recorded level of flame retardants among infants in the world.” Many of these chemicals accumulate within the blood, fat, and even breast milk, causing a number of unknown health risks. One common ingredient in flame retardants, BDE-49, has recently been found to damage neural mitochondria, leading to brain damage. The same study also found evidence of autism effects being amplified by environmental factors.(1) The MIND Institute at UC Davis, responsible for the study, summarized it by saying the “chemical, quite literally, reduces brain power,” noting that the findings “bolster the argument that genetics and environment can combine to increase the risk of autism and other neurological disorders.”

These chemicals accumulate in human tissues – and they last a really long time . In addition, we’re being constantly re-exposed because they’re ubiquitous in the environment – they’re used for foam in cushions, but also in such things as baby strollers, carpeting, mattresses and electronics. These chemicals are also found in mother’s milk in every country of the world and in animals – from polar bears in the Arctic to hummingbirds in the Amazon.

In the United States, California has required flame retardants on everything from children’s pajamas to furniture. This standard is called Technical Bulletin 117, or TB 117, which was passed in 1975 and requires that polyurethane foam in upholstered furniture be able to withstand an open flame for 12 seconds without catching fire. Because California is such a large market, and also because there is no other state or federal standard, many manufacturers comply with the California rule, usually by adding flame retardants with the foam.

The startling and disturbing result of a published study in Environmental Health Perspectives is that Latino children born in California have levels of PBDE in their blood seven times higher than do children who were born and raised in Mexico.[2] In general, residents of California have higher rates of PBDE in their blood than do people in other parts of the United States – and people in the United States have levels of PBDE higher than anyone else in the world.

A home can contain a pound or more of fire retardants. These chemicals are similar in structure and action to substances such as PCBs and DDT that are widely banned. They leak out from furniture, settle in dust and are taken in by toddlers when they put their hands into their mouths. A paper published in Environmental Science & Technology [3] also finds high fire retardant levels in pet dogs. Cats, because they lick their fur, have the highest levels of all.

One troubling example is chlorinated Tris, a flame retardant that was removed from children’s pajamas in the 1970s largely based on research done by Dr. Arlene Blum, a biophysical chemist, after it was found to mutate DNA and identified as a probable human carcinogen. In the journal Environmental Science and Technology, new research published in 2011 shows that chlorinated Tris was found in more than a third of the foam samples tested – products such as nursing pillows, highchairs, car seats and changing pads.[4] Tris is now being used again at high levels in furniture being sold in California to meet the California standard.

The benefits of adding flame retardants have not been proved. Since the 1980s, retardants have been added to California furniture, yet from 1980 to 2004, fire deaths in states without such a standard declined at a similar rate as they did in California. And during a fire when the retardants burn, they increase the toxicity of the fire, producing dioxins, as well as additional carbon monoxide, soot and smoke, which are the major causes of fire deaths.

So why are we rolling the dice and exposing our children to substances with the potential to cause serious health problems when there is no proven fire safety benefit?

Under current law, it is difficult for the federal Environmental Protection Agency to ban or restrict chemicals – current federal oversight of chemicals is so weak that manufacturers are not required to label products with flame retardants nor are they required to list what chemicals are used.[5]. Even now, the agency has yet to ban asbestos!

And when a ban does go into effect, it’s usually severely restricted: for example, in the USA, BPA is now banned in baby bottles – but only in baby bottles. Many products tout the fact that they’re “BPA free” but that’s because the chemical has hit a nerve with consumers, who recognize that BPA isn’t a good thing to have in plastic water bottles, for example, so the manufacturers voluntarily restrict its use. Another example is lead, which has been banned in the USA in some products– paint and gasoline come quickly to mind – but is still used in others, such as plastics, printing, and dyes. New legislation restricts the amount of lead that can be present in products designed for children to 100 ppm, despite the fact that research shows that any detectable amount of lead can be harmful to kids.

The Consumer Product Safety Commission has been working on a federal flammability standard for upholstered furniture for 16 years. The current proposal would allow manufacturers to meet the flammability standard without fire retardants. An agency spokesman said that “additional research looking into consumer exposure and the impact of chemical alternatives is needed.”

California State Sen. Mark Leno sponsored California Senate Bill 147, the Consumer Choice Fire Protection Act, introduced in February, 2011. The bill called for an alternative furniture flammability standard that would give consumers the choice to purchase furniture that is fire-safe and nontoxic.

However, aggressive lobbying in the form of multimillion-dollar campaigns from “Citizens for Fire Safety” and other front groups funded by three bromine producers – Albemarle, Chemtura and Israeli Chemicals Ltd. – resulted in a defeat of this bill in March, 2011. Their main argument was that new flame retardants – similar in structure and properties to the old ones and lacking any health information – were safe. This despite opposition which included 30 eloquent firefighters, scientists, physicians and health officers representing thousands of Californians. But new life is again being breathed into this issue, and California has introduced a new TB117-2013 to address the problem by changing the testing parameters so as not to need flame retardants.

But stay tuned – the chemical industry has a lot at stake and they won’t go down without a fight.

Although we stopped most uses of asbestos decades ago, workers and others inadvertently exposed continue to die from its long-term effects. Let’s not add more chemicals to this sad list.

(1) Napoli E, Hung C, Wong S, Giulivi C., “Toxicity of the flame-retardant BDE-49 on brain mitochondria and neuronal progenitor striatal cells enhanced by a PTEN-deficient background” Toxicol Sci. 2013 Mar;132(1):196-210.
[2] Eskenazi, B., et al., “A Comparison of PBDE Serum Concentrations in Mexican and Mexican-American
Children Living in California”, http://ehp03.niehs.nih.gov/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1289%2Fehp.1002874
[3] Vernier, Marta and Hites, Ronald; “Flame Retardants in the Serum of Pet Dogs and in their Food”, Environmental Science and Technology, 2011, 45 (10), pp4602-4608. http://pubs.acs.org/action/doSearch?action=search&searchText=PBDE+levels+in+pets&qsSearchArea=searchText&type=within&publication=40025991
[4] Martin, Andrew, “Chemical Suspected in Cancer is in Baby products”, The New York Times, May 17, 2011.
[5] Ibid.





What’s the “new” asbestos?

1 05 2013

What does asbestos have to do with fabrics?

Asbestos has been used in fabrics for centuries – the story goes that Roman soldiers (or, depending on the story, wealthy Persians) would clean asbestos napkins by throwing them into the fire – and they’d emerge clean and white. During the Middle Ages, some merchants would sell crosses made of asbestos, which looked just like wooden crosses, and claim they were from the “true cross” – the very same cross on which Jesus Christ was crucified. To prove it they’d show that the cross wouldn’t burn.

Chrysotile or white asbestos is the form that was used almost exclusively by the textile industry. While some types of asbestos are characterized by brittle, needle-like fibers, chrysotile asbestos fibers are as soft and pliable as cotton or flax, which makes them ideal for weaving into cloth. The special characteristics of asbestos (nearly fireproof, chemical resistance, and high tensile strength) means that from the 19th through the 20th centuries, it was used a lot for specialty applications in fabrics, such as:

• Theater, school auditorium, and other public building curtains and seating upholstery fabrics
• Firefighter and industrial worker protective garments and gloves
• Boiler and blast furnace cloths and blankets
• Welding blankets
• Circus and camping tents
• Military textiles
• Laboratory worker protective garments
• Public building displays such as banners, signage, flags, and much more

Asbestos is an example of one of the common misconceptions people today have about products made with “natural” ingredients. You often see the word natural applied to products to make them more appealing, and by implication we think they’re good (or at least not bad) for us.

Asbestos is a 100% natural product – a naturally occurring mineral that was plentiful and therefore inexpensive. But asbestos is one of those “natural” ingredients that can never be good for us, unlike water – another natural ingredient that we need (but only so much of – you can drown in too much of this good thing).

The first documented case of asbestos-related ailments occurred in 1897, when a Viennese physician attributed emaciation and pulmonary problems to asbestos dust inhalation. The first documented case of an asbestos-related death was reported in 1906 when the autopsy of an asbestos worker revealed lung fibrosis. In 1917 several studies observed that asbestos workers were dying unnaturally young.

Because many fabrics produced from the 1940s to the 1970s were made with asbestos fibers, textile workers were especially at risk of asbestos exposure. In fact, in 1947, an industry group called the Asbestos Textile Institute (ATI) commissioned a study on the risks of asbestos to textile factory workers and found that the industry should re-examine its threshold limit for asbestos exposure. But it was never acted upon – because the ATI believed it would damage the industry if it was made public.(1)

As the United States and many European countries began to look at the environmental and occupational health regulations surrounding the use of asbestos in products, world production has been shifted to third world countries. Although use has decreased substantially since the 1980s, it has not been eliminated.(2) Worldwide, 54 countries (including those in the European Union) have banned the new use of asbestos, in whole or in part. But in the United States, asbestos is still legally used in over 3,000 different consumer products, predominantly building insulation (and other building materials) – in fact, only six categories of products can NOT contain asbestos: flooring felt, rollboard, and corrugated, commercial, or specialty paper.(3)

So today, asbestos remains in millions of structures throughout the United States, as many people find out (to their dismay) when they are planning to repaint their home or do other remodeling tasks and must deal with the EPA rules for safe disposal or removal of products which may contain asbestos. Millions of people are exposed at home or in their workplace by the monumental quantities of asbestos that remain in the built environment — like attic insulation in 30 million American homes, for instance — following decades of heavy use. It also remains heavily used in brake shoes and other products, directly exposing auto mechanics and others who work with the materials, and indirectly exposing consumers and workers’ families.

Today, many researchers and medical doctors have provided irrefutable evidence about the dangers of asbestos and asbestos exposure. When asbestos is broken up, its microscopic crystal particles can remain airborne for prolonged periods of time, and when inhaled can cause a multitude of health problems.

According to the United States Environmental Protection Agency, three of the major health effects associated with asbestos exposure include:

Asbestosis – a serious, progressive, long-term non-cancer disease of the lungs. It is caused by inhaling asbestos fibers that irritate lung tissues and cause the tissues to scar. The scarring makes it hard for oxygen to get into the blood. The latency period (meaning the time it takes for the disease to develop) is often 10–20 years. There is no effective treatment for asbestosis.
Cancer — Cancer of the lung, gastrointestinal tract, kidney and larynx have been linked to asbestos. The latency period for cancer is often 15–30 years.
Mesothelioma– Mesothelioma is a rare form of cancer that is found in the thin lining (membrane) of the lung, chest, abdomen, and heart. Unlike lung, cancer, mesothelioma has no association with smoking. The only established causal factor is exposure to asbesto fibers. The latency period for mesothelioma may be 20–50 years. The prognosis for mesothelioma is grim, with most patients dying within 12 months of diagnosis. This is why great efforts are being made to prevent school children from being exposed.

No safe level of minimum exposure has ever been established for asbestos. Many of the first cases of mesothelioma were persons who never directly handled asbestos as part of their jobs. An early case in South Africa occurred in a young girl whose job it was to empty the pockets of miners before dry cleaning their clothes. The asbestos dust in the miners’ pockets made her fatally ill.(4) People who have worked in plumbing, steel, insulation and electrical industries have very high chances of suffering from asbestos-related disease. In fact, they could have passed it on to their family members through the dust that could have clung to their shirts, shoes and other personal belongings.

Today, even though global asbestos use is down, there are more than 10,000 deaths per year due to the legacy of asbestos exposure.(5) Asbestos kills thousands more people each year than skin cancer, and kills almost as many people as are slain in assaults with firearms.
With the science to back up the claims that asbestos is a serial killer, and with global use on the downward swing, wouldn’t you think that deaths from asbestos exposure would be going down? No – the U.S. EPA reports that asbestos related deaths are increasing.

asbestos

Asbestos is an example of a substance that is deadly, but not for a long time after exposure: certain chemicals, such as asbestos, have extraordinarily long latency periods – in other words, time from exposure to time disease is noted can be 20 – 50 years. The ongoing increase in asbestos mortality in the US is due largely to this 20 to 50 year latency period, meaning that individuals exposed in the 1960s and 1970s are just now dying from their exposure. Better tracking accounts for the dramatic increase in mesothelioma mortality reported in 1999, but lung cancer deaths from asbestos are not reported at all, and asbestosis is still dramatically underreported even in worker populations where asbestos exposure is well established. Dr. Richard Lemen, a former assistant U.S. surgeon general, estimates the death toll from asbestos at 500,000 people in the next 30 years.(6) In a 2005 study, RAND similarly projected 432,465 asbestos-related cancer deaths from 1965 through 2029; this number excludes fatal cases of asbestosis.(7)

The legacy of asbestos, in the United States as in other countries such as the U.K. and Australia, is that the initial use of asbestos as a miracle fiber quickly gave rise to a burgeoning industry and adoption of asbestos in many products. This happened long before any detrimental health effects were known, so now, many years later, asbestos related disease is killing significant numbers of people. Environmental Health Perspectives last year published “The Case for a Global Ban on Asbestos”(8) We hope this is not a precursor for other epidemics of chemicals with a similar latency period – which is why so often we hear of this chemical or that being the “new asbestos”, such as nanotechnology, PBDE’s or climate-change litigation for example – because these were all widely adopted before being well understood, yet may well leave a legacy of death and destruction similar to that of asbestos. (Well, okay, litigation has not been known to kill directly, but you understand the point I’m trying to make.). And we keep harping on the fact that we continue to live with chemicals in many consumer products, including fabrics, that are full of chemicals that we know nothing about

Next week I’ll tell you what my nomination would be for the “new asbestos”.

(1)http://www.asbestos.net/exposure/risks/asbestos-industry-and-products
(2)In 2010, Washington State banned asbestos in automotive brakes starting in 2014.
(3)http://www.banasbestos.us/
(4)http://www.allaboutmalignantmesothelioma.com/asbestos-3-uses.htm
(5)Environmental Working Group, http://www.ewg.org/sites/asbestos/facts/fact1.php
(6)http://www.mcclatchydc.com/2010/07/21/97624/asbestos-us-legacy-may-be-half.html
(7) Ibid.
(8)http://ehp03.niehs.nih.gov/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1289%2Fehp.1002285





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.
[7] http://www.ourstolenfuture.org/Basics/keypoints.htm
[8] http://www.ourstolenfuture.org/NewScience/lowdose/2007/2007-0525nmdrc.html#lightbulb
[9] Shulevitz,Judith, op. cit.





Copper in the textile industry

14 03 2013

copperWe did a post on copper over two years ago. Here’s the post if you missed it then, because the information is still valid:

Copper is an essential trace element that is vital to life. The human body normally contains copper at a level of about 1.4 to 2.1 mg for each kg of body weight; and since the body can’t synthesize copper, the human diet must supply regular amounts for absorption. The World Health Organization (WHO) suggests that 10-12 mg/day may be the upper safe limit consumption.hhh

The fact that copper is essential to life is well known, but it’s also a toxic metal, and that toxicity, except for the genetic overload diseases, Wilson’s disease and hemochromatosis, is not so well known. Humans can become copper-toxic or copper-deficient, often because of “copper imbalance” (which can include arthritis, fatigue, insomnia, migraine headaches, depression, panic attacks, and attention deficit disorder) .

Copper has been used for centuries for disinfection, and has been important around the world in technology, medicine and culture.

Is copper in the environment a health risk?

The answer to this question is complex. Copper is a necessary nutrient and is naturally occurring in the environment in rocks, soil, air, and water. We come into contact with copper from these sources every day but the quantity is usually tiny. Some of that copper, particularly in water, may be absorbed and used by the body. But much of the copper we come into contact with is tightly bound to other compounds rendering it neither useful nor toxic. It is important to remember that the toxicity of a substance is based on how much an organism is exposed to and the duration and route of exposure. Copper is bioaccumulative – there are many studies of copper biosorption by soils, plants and animals. But copper in the environment, (such as that in agricultural runoff, in air and soil near copper processing facilities such as smelters and at hazardous waste sites) binds easily to compounds in soil and water, reducing its bioavailability to humans. On the other hand, many children are born with excessive tissue copper (reason unknown), and one of the ways we are told to balance a copper imbalance is to reduce your exposure to sources of copper! (see http://www.healingedge.net/store/article_copper_toxicity.html)

There are no studies on what this increased copper is doing to the environment. Copper is listed as an EPA Priority pollutant, a CA Air Toxic contaminant, and an EPA Hazardous air pollutant (see http://wsppn.org/PBT/nolan.cfm#What%20are%20PBTs?); it is also a Type II Moderate Hazard by the WHO Acute Hazard Ranking . There is NO DATA on its carcinogenity, whether it is a developmental or reproductive toxin or endocrine disruptor or whether it contaminates groundwater.

Today, because of its long use as a disinfectant and because it’s required for good health, many claims are being made about using copper in various products – including fabric. Copper-impregnated fibers have been introduced, which enables the production of anti-bacterial and self-sterilizing fabrics. These copper infused fabrics are marketed to be used in hospital settings to reduce infections, as an aid to help those suffering from asthma and allergies provoked by dust mites, and in socks to prevent athlete’s foot.

These copper impregnated fabrics are said to be safe, pointing to the low sensitivity of human tissue to copper, and because the copper is in a non-soluble form. Yet, that copper is safe because it is in a non soluble form was disproven by at least one study which tried to determine whether total copper or soluble copper was associated with gastrointestinal symptoms. It was found that both copper sulfate (a soluable compound) and copper oxide (insoluable) had comparable effects on these symptoms. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1240446/)

And then there’s this: “…(copper) toxicity is so general in the population that it is a looming public health problem in diseases of aging and in the aging process itself. Diseases of aging such as Alzheimer’s disease, other neurodegenerative diseases, arteriosclerosis, diabetes mellitus, and others may all be contributed to by excess copper (and iron). A very disturbing study has found that in the general population those in the highest fifth of copper intake, if they are also eating a relatively high fat diet, lose cognition at over three times the normal rate”.[1]

Sometimes safety is cited because of the widespread use by women of copper intrauterine devices (IUDs). But the copper IUD was developed only in 1970; that timeline would put those first users only in their 60s today. How can we know that the copper has not influenced any health problems these 60 somethings may now have? In addition, about 12% of women have the copper IUD removed because of increased menstrual bleeding or cramping.[2] There are also cases of increased menstrual cramping, acne, depression and other symptoms attributed to the copper IUD.[3] The fact that we keep ignoring is that the body, like our ecosystem, is a highly complex, interconnected system. It is extremely hard to single out any one element as contributing to a series of causes and effects.

Although copper does have documented antimicrobial properties, it is a broad spectrum antimicrobial – meaning that it kills the good guys as well as the bad. Many studies show that this is not necessarily the best approach to infection control. Kaiser Permanente issued a December 2006 memo with this bottom line: “Review of current scientific literature reveals no evidence that environmental surface finishes or fabrics containing antimicrobials assist in preventing infections.” In fact, their policy now is to prohibit any fabrics with antimicrobial finishes in their hospitals.

Copper impregnated fabrics are legally sold in the USA, because the EPA has not issued any regulations regarding use. The reality is they don’t have any data on which to base an exclusion of use. In the US we must prove toxicity before the EPA even begins to regulate chemicals – look at the case of lead. Other organizations have evaluated copper (including the EPA, see above).

So really the question is: what possible benefit do you hope to achieve by using a product with this antimicrobial finish? Although copper isn’t one of the most alarming chemicals used in textile processing, it seems to me the benefits just aren’t that compelling. I wouldn’t risk altering my DNA or subjecting myself to copper imbalance symptoms just to eliminate stains or odors.

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[1] Brewer, George J., “Risks of Copper and Iron Toxicity during Aging in Humans”, Chemical Research in Toxicology, 2010, 23 (2), pp. 319 – 326.
[2] Zieman M, et al. (2007). Managing Contraception for Your Pocket. Tiger, GA: Bridging the Gap Foundation.
[3] http://www.aphroditewomenshealth.com/forums/ubbthreads.php?ubb=showflat&Number=314954








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