Thursday, July 3, 2014

BPA Found to Activate Breast Cancer Cells and Interfere with Treatment

Last week at the annual joint meeting of the International Society of Endocrinology and the Endocrine Society of Chicago, a team from Duke University in North Carolina presented an abstract indicating that Bisphenol-A (BPA) is linked to the speed of progression of inflammatory breast cancer as well as rendering the treatment for the cancer less effective.

BPA, along with many other man-made chemicals, has become quite prevalent in our environment, and have been shown to possess estrogen-like characteristics which have led to significant human health problems.  BPA, in addition to many similar endocrine disruptors, can be found in many different products, including the plastic in water bottles, the thermal paper for printers, and countless other products made from plastic and epoxy resins.

Inflammatory breast cancer is much more aggressive and rare compared with other cancers, and is also one of the more difficult cancers to treat due to the fact that it is often not diagnosed until a much more advanced stage. 

Dr. Scott Sauer and his team from Duke University presented their data at a recent meeting and found that BPA was the most active endocrine disruptor in the breast cancer cells study, and BPA actually increases the rate of inflammatory breast cancer cell growth and spread/proliferation.  Specifically, BPA increased pEGFR and pERK levels in EGFR-activated breast cancer cells, as well as increased expression of a few antioxidants in these same cells, the levels of which are important in the proliferation and spread the cancer.

A common treatment for inflammatory breast cancer, lapatinib, basically functions to inhibit both pEGFR levels and GPER expressions, however, this study by the Duke group found that BPA effectively negated the actions of lapatinib, and basically rendered the drug ineffective.  In other words, BPA increased pEGFR levels in the breast cancer cells much more quickly and efficiently than the treatment drug could counteract, thereby indicating that BPA not only can speed up the growth and spread of inflammatory breast cancer, but it also makes the cells effectively resistant to the current therapy used today.

Sunday, June 29, 2014

Low-Dose BPA Paper In Toxicological Sciences Fatally Flawed & Should Be Retracted: Plagued By Massive Errors & Poor Design. Contaminated Controls Raise Issues About Federal Breeding Colony Integrity

By Lewis Perdue and Rebecca L. Yeamans (Corresponding author:
NOTE: An earlier version of this paper originally appeared on on Feb., 24, 2014.
This version is enormously expanded to address peer-review suggestions from multiple prominent researchers. Those who helped improve this paper who wish to remain un-named because the direct and un-nuanced data and opinions expressed here may cause funding, political or other undesirable issues.
However, we are enormously grateful for their help, assistance and encouragement.

Please click this link for a .pdf version of this post.
Bisphenol A (BPA) has become nearly ubiquitous in our environment and can be found in many different products, including the plastic in water bottles and baby bottles, thermal paper for printers, and even in dental sealants and medical devices including intravenous fluid and chemotherapy bags and tubing(26,27,28,29,30,31).
Thousands of studies have been published that examine the levels of BPA and other endocrine disruptors present in the environment along with the mechanisms and pathways those chemicals may take to affect or harm living things.There is, however, considerable controversy concerning negative health effects of so-called “low-dose” exposures.
One recent study, published in the journal Toxicological Sciences, stated as its goals the desire to help shed light on the conflicting body of evidence. Unfortunately, that study, "Toxicity Evaluation of Bisphenol A Administered by Gavage to SPRAGUE-DAWLEY Rats from Gestation Day 6 through Postnatal Day 90(1)"is fatally flawed.
The study(1) by Delclos et al., concluded that low-dose BPA is not harmful. However, that conclusion cannot be scientifically justified by the experiment as conducted. This study suffers from numerous and massive errors including; by the eventual admission of the authors(1); the violation of one of the scientific method’s paramount experimental rules: the control subjects were contaminated by the chemical substance being evaluated.
Additionally, while the study authors claim to have no idea of the BPA contamination source(1), an examination of the paper and a current understanding of the science indicate numerous avenues of contamination that are obvious, well-established, and should have been considered in any careful experiment design and conduct.
This letter will explore a number of those sources and their consequences in more detail below, but it merits consideration at this stage that one possible contamination source could jeopardize results of experiments underway in the very substantial, multi-agency program known as the Consortium Linking Academic and Regulatory Insights on BPA Toxicity (CLARITY-BPA).

Test Animal Contamination Concern For CLARITY-BPA
Delclos et al. state that the test animals in their experiment were obtained from the NTP breeding colony(1). If so, then their contaminated controls may also hold significance for the scores of investigators participating CLARITY-BPA.
“CLARITY-BPA is a collaborative effort between NTP and NIEHS with support from FDA to conduct a perinatal 2-year guide- line chronic rodent toxicity study on BPA(95).”
The program is designed to investigate “scientific uncertainties about BPA’s health effects to better inform regulatory decision-making. …The CLARITY-BPA consortium is made up of NCTR staff, NIEHS and NTP staff, and 12 extramural grantees(95).”
The core guideline- compliant study is being conducted at FDA’s National Center for Toxicological Research (NCTR) CLARITY-BPA investigators, both with government at universities, must use rats from the NTP breeding colony(95).”
The unknown source of the BPA contamination of controls raises the issue of whether the animals in the NTP breeding colony are regularly monitored for BPA and other endocrine disruptors.
Ongoing and regular population sampling by NTP would alert breeders to potential contamination. Prior to release, batch samplings would assure the receiving investigators of the purity of their test animals.
It is unknown whether the NTP breeding colony has monitoring protocols in place that adequately monitor test animals and assure investigators that the test subjects are uncontaminated and appropriate for experimentation.
Avoidable Errors Accumulate
In addition to the contamination error, the study fails on an accumulation of other serious errors:
  • Potential contamination by other endocrine-disrupting compounds
  • Unknown Combination Effects Of Stressors
  • Use of oral gavage which introduces non-chemical stressors
  • Use of oral gavage which fails to recreate appropriate BPA Absorption
  • Inappropriate Rat Strain
  • Poor choice of outcome measures
  • Failure to use current science in BPA and Endocrine Disruptor Compound (EDC) research
  • Erroneous claim that BPA is “weak” estrogen
  • Failure to identify well-known exogenous source(s) of BPA contamination
  • Failure to identify well-known exogenous source(s) and estrogenic activity of equipment and supplies
  • Failure to measure BPA levels in any of the animals except in the test cohort at the end of the trial
  • Failure to measure other exogenous estrogenic compounds in test animals
  • Use of oral gavage
  • Wrongly examining toxicity when timing is a bigger issue
  • Failure to include disclosure of conflicts

Sunday, April 6, 2014

Rock-A-Bye Baby Gone Bad? Crib Mattresses Found to Emit Harmful VOCs

Anyone with experience raising a baby knows that they sleep a lot.  Sure, they DON’T sleep a lot as well, particularly on multiple occasions throughout the night leaving mom and dad often very sleep-deprived the next day.  In fact, I often liken my experiences with my two geriatric dogs to raising an infant—lots of sleeping, lots of pooping, and lots of projectile vomiting.

Other than eating, crying, and filling up their diapers with what can only be described at times to be made from Lucifer himself, babies sleep.  They don’t really have much control nor coordination of their muscles in the very early months, nor do they need to allocate their time to multitask a job, hobbies, or doing taxes, so what is there to do other than sleep? 

In fact, in the first three years of life, babies are known to sleep around 12-13 hours per day, compared with 8 hours (or less, for many of us with busy schedules) for adults.

With so much time devoted to sleep, what we place our babies to snooze on should be safe, obviously, right?  Well, one recent study showed that the mattresses used in babies cribs are a big source of potentially hazardous airborne chemicals called volatile organic compounds (VOCs), exposing the sleeping infant to harmful chemical compounds that have been linked to a wide range of health problems1.

The average run-of-the-mill crib is made up of a layer of polyurethane or polyester foam padding within a waterproof plastic cover for protection.  Since much of the chemicals used to create these crib mattresses are plastic-based, studies have found that these cribs are likely sources of VOCs, and are linked to sensory issues, breathing problems, and reduced airflow in mice2.

Intake of VOCs in infants may be greater than it would be for an adult experiencing the same level of exposure.  Per day, babies inhale an order of magnitude more air than adults do, suggesting that infants will inhale significantly more VOCs than an adult in the same room.

Other studies have found that infant exposure to VOCs is linked to negative impacts on the developing immune system of the child, increased risk of asthma, and increased risk of allergies in exposed children3.

Using controlled environmental chambers to avoid any contamination from the outside environment, this most recent study examined both brand new and used mattresses at two different temperatures (23oC and 36oC) and if VOCs are emitted at levels that are potentially harmful for the sleeping baby.  Additionally, since getting a real baby for this kind of test is highly unethical, the researchers used a “baby dummy” instead that was set at the approximate temperature of a living breathing infant to get as realistic as possible of a scenario.

The study confirmed what previous studies have found, in that as the temperature of the room increased from 23oC to 36oC, VOCs emitted from the mattresses increased significantly.  In fact, VOC levels were about double at 36oC than what they were at 23oC, suggesting that VOC exposure may be greater during the summer than during the winter (provided the room does not have air conditioning).

The study also found that new crib mattresses emitted about 4 times higher levels of VOCs than older used mattresses.

Additionally, many of the mattress covers were able to reduce the VOC levels in the air around the crib, however warned that a couple of the mattress covers actually INCREASED VOC levels in the air.
Lastly, depending upon the material, some mattress covers can act like a “VOC sink”, absorbing a lot of the compounds that would have otherwise escaped into the air.

Based on the VOC levels emitted by the crib mattresses during the experiment and how much the typical infant breathes while sleeping in the mattress, the sleeping baby could inhale 1μg/kg of VOCs (depending upon the temperature of the room).  If an adult were in the same room breathing the same air, they would inhale significantly less VOCs than the infant.

What can you do?

Many crib mattresses are made of plastic-based materials, and studies have linked these materials to increased VOC levels in the air around the crib.  This same source of VOCs has been linked to health problems in young children, including increased risk of asthma and allergies.  What can you do to help avoid or at least reduce the amount of VOCs your baby inhales while it sleeps?

1.       Maintain good air flow throughout the room.  If you live in a climate that allows it, keep the windows cracked a little and run a ceiling fan to help move any VOCs emitted from the mattress away from the sleeping baby.
2.       Use an older mattress.  This comes with some caveats, as some older mattresses actually contain some harmful flame retardants that also have been shown to emit dangerous VOCs in the air4.  If using an older mattress, use one that doesn’t have these flame retardants added (specifically polybrominated diphenyl ether or PBDE).
3.       Let the mattress “air out”.  Studies have shown VOC levels are significantly higher in brand new mattresses and gradually decrease over time.  Think about purchasing the mattress for your crib earlier on in the pregnancy and leave it out (and out of any packaging) in a well-ventilated room with bedding until it’s baby time.
4.       Find mattresses that are GreenGuard certified. Products that receive a GreenGuard certification5 must be made to reduce the harmful chemicals that contribute to indoor air pollution, like the VOCs emitted by plastic-based mattresses.  I can’t say for certain if these products are completely VOC-free, however, they should be significantly reduced.

Further reading:

1.       Boor, B.E., Järnström, H., Novoselac, A., and Xu, Y. 2014. Infant Exposure to Emissions of Volatile Organic Compounds from Crib Mattresses. Environmental Science and Technology 48: 3541-3549.
2.       Anderson, R.C., and Anderson, J.H. 2000. Respiratory toxicity of mattress emissions in mice. Archives of Environmental Health 55(1): 38-43.

3.       Franklin, P.J. 2007. Indoor air quality and respiratory health of children. Paediatric Respiratory Reviews 8: 281-286.

4.       Stapleton, H.M., Klosterhaus, S., Keller, A., Ferguson, P.L., van Bergen, S., Cooper, E., Webster, T.F., and Blum, A. 2011. Identification of flame retardants in polyurethane foam collected from baby products. Environmental Science and Technology 45(12): 5323-5331.

Sunday, February 9, 2014

Tesla Terror: Can That New Car Smell Kill You? Or Someone Else?

By Lewis Perdue

Driving with the windows down when you are tired may keep you awake in more ways than just the sounds and tactile effects of air currents. It could also keep you from being poisoned and, perhaps, prevent you from killing someone.

Take, for instance,  Navindra Kumar Jain, a 63-year-old retired Silicon Valley tech executive who told police that the intense new car smell of his Tesla S made him drowsy enough to fall asleep at the wheel.

When Jain lost control of the Tesla on Nov. 2, 2013, he killed 40-year-old librarian
Joshua Alper who had been riding a bicycle in a wide shoulder lane on Highway 1 north of Santa Cruz.

Most public reactions to Jain's claim have been met with derision and disbelief.

But scientific evidence, including a major one by Australia's CSIRO14, indicate that many of the chemicals given off by automotive dashboards, upholstery, wiring, adhesives and interior trim can offer the same consciousness-impairing and mind-altering effects as sniffing glue.

The CSIRO study and others have found that -- in addition to toluene, xylene, benzene and other Volatile Organic Counpounds (VOCs)(1-4) , there are phthalates (5-7), flame-retardants(11,12) and other Endocrine Disrupting Compounds that are outgassed from car interior materials and form the scummy film on windshields and windows.(5-7).

And, in a contra-Darwinian sense, people love the fragrance of these VOCs so much that they support an entire industry of sprays and air fresheners containing many of the same petrochemicals and EDCs. (See: shop on Google for new car smell)

Tuesday, February 4, 2014

Pesticide Exposure Linked to Alzheimer's Disease Risk

By Becca Yeamans

Alzheimer’s disease (AD), a very common neurological disease, has continued to see a growing trend over the past few decades, with projections increasing to up to 3-fold over the next four decades1.  Exactly what causes AD is still unknown, though there are many avenues of research where some progress is being made.  Due to the complexity of the disease, it’s been extremely difficult to find out what it is caused by, let alone a cure.  Studies have found links to AD in genetic, environmental, and lifestyle factors, which you can imagine would complicate the picture greatly with so much variability2.  So far, genetic factors have only been tied to less than half of diagnosed AD cases, leaving a majority of AD cases to be caused by environmental or lifestyle factors.

One earlier study strongly hinted at a connection between AD and pesticide exposure, specifically DDE, a metabolite of the organochlorine pesticide, DDT, showing that serum DDE levels in patients with AD were significantly higher than serum DDE levels of control (no AD) patients, in addition to a significant association between DDE levels and AD diagnosis3

Wishing to confirm (or refute) these findings with a larger sample size, collaborating researchers from Rutgers University, Emory University, and the University of Texas Southwestern Medical Center recently published a study examining the difference between brain and serum DDE levels, and also whether or not DDE or DDT had any effect on amyloid beta expression, the protein that is most commonly associated with AD4.

Wednesday, January 22, 2014

"When Good Eggs Go Bad": Mechanisms of Female Infertility

By Becca Yeamans

There are many ways by which a woman can be infertile, however, most of the time, the problems center around the formation and maturation of the egg (oogenesis).   Age at pregnancy is one of those factors that are often cited when discussing fertility rates among women, however, it still is debated exactly how maternal age plays into the fertility story and what can and does go wrong when a woman gets to be of a certain age while pregnant. 

In addition to age, external stimuli, such as estrogen-like compounds like BPA and other EDCs found in the environment as a result of the various plastics and processed materials in our lives which are designed to make life “easier”.

In 2008, two researchers from Washington State University in Pullman, WA put together a very comprehensive review paper illustrating the different ways in which human female infertility can occur, specifically focusing on the egg itself and the processes it must go through between formation and maturation that can run into problems and cause infertility.  This paper provides excellent framework for the mechanisms behind female infertility related to problems with egg development, which I will summarize briefly for you in this post and draw from periodically when making possible connections to endocrine disruptors in future posts.

Monday, January 20, 2014

EDCs Linked to Infertility and Endometriosis in Italian Women: More Fuel for the Fire

Endocrine disruptors, specifically Bisphenol-A (BPA), have been found in countless studies to contribute to a whole host of health problems, including female infertility.  To be classified as infertile, a couple must have failed at achieving pregnancy for at least one year of trying(1).  There are many causes of infertility, so finding one “smoking gun” to solve all infertility problems is all but impossible.  We can, however, investigate all of the different sources possible, including genetic, lifestyle, and occupational risk factors, to help find therapies to address each individual couple’s problems in hopes to one day halt these rising infertility rates across the globe(2, 3). 

A recent study in Italy, part of the larger “PREVIENI” cohort, aimed to more closely examine the role of EDCs in female reproductive health, looking in particular about more commonly known chemicals including BPA, PFOS, PFOA, DEHP, and MEHP (4).  These chemicals have been shown to be very persistent in the environment, in addition to their ability to accumulate to toxin levels in the body.