Archives for category: Endocrine Disruptors

You can link to an illuminating podcast interview, titled “Better Living Through Chemistryfrom the Physicians for Social Responsibility (PSR), here.

Here is PSR’s brief description of the interview:

We depend on chemicals in consumer products to perform as expected, and to be safe. But our regulatory system is not adequately protecting us from potential hazards in our food cans, diapers, shower curtains, baby bottles, and other consumer products. Listen to Washington State PSR President, Dr. Steven Gilbert, a toxicologist, together with pediatric urologist and Phsicians for Social Responsibility (“PSR”) board member Dr. Rich Grady, discuss chemicals policy in an illuminating radio interview, touching on “chemical trespass,” the precautionary approach to chemical regulation, and the importance of state-level policy change. They also discuss the federal bills, currently before Congress, intended to modernize the Toxic Substances Control Act — including the need to strengthen these bills. The interview was aired on Seattle radio station KEXP on June 19, 2010.

Listen to the interview here (mp3, 10 MB).

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From BrandeisNow (an article about Upstream Contributors Ana Soto and Carlos Sonnenschein):

This year’s Jacob Heskel Gabbay Award goes to three researchers, Drs. Patricia Hunt, Ana Soto and Carlos Sonnenschein, who have dedicated decades to researching and identifying the effects of BPA in plastics on mamalian cells. The honoree will give their prize talks tomorrow, Oct. 22, in Rapaporte Treasure Hall, Goldfarb Library.

The potential dangers of BPA — bisphenol A — now cannot be disputed. More and more research shows effects of the estrogen-mimicking chemical that is frequently used in such items as plastic bottles, aluminum can linings, heat-activated register receipts and even some dental sealants.

In 2008, in an FDA report on BPA, the National Toxicology Program expressed “concern for effects on the brain, behavior, and prostate gland in fetuses, infants, and children at current human exposures to bisphenol A.” In July of this year the FDA announced that baby bottles and children’s drinking cups will no longer be allowed to contain BPA.

According to a New York Times report, a study of over 2,000 people found that more than 90 percent of them had BPA in their urine. Traces have also been found in breast milk, the blood of pregnant women and umbilical cord blood.

The Gabbay Award in Biotechnology and Medicine is given to scientists in academia, medicine, or industry whose work had outstanding scientific content and significant practical consequences in the biomedical sciences. The award consists of a $15,000 cash prize (to be shared in the case of multiple winners) and a medallion. Recipients travel to Brandeis University in the fall of each year to present a lecture on their work. It is followed by a dinner at which the formal presentation takes place.

The winners are:

  • Dr. Patricia Hunt, an internationally renowned geneticist, and a professor in the School of Molecular Biosciences at Washington State University. Her talk is titled:  “Making a Perfect Egg: How Age and the Environment Affect Our Reproductive Health”
  • Dr. Ana Soto, a professor of anatomy and cell biology at Tufts University School of Medicine. Her talk is titled: “BPA exposure, Development and Cancer”
  • Dr. Carlos Sonnenschein, a professor of anatomy and cell biology at Tufts University School of Medicine.  His talk is titled: “Social Impact of Scientific Discoveries: The Case of Endocrine Disruptors”

The Gabbay Awards were established in 1998, when the trustees of the Jacob and Louise Gabbay Foundation decided to create a new award in basic and applied biomedical sciences.

Nominations are solicited from selected scientists in industry and academia. A panel of distinguished researchers representing the biotechnology and pharmaceutical industries, as well as universities and schools of medicine, are assembled to consider nominations.

Because of their long association with Brandeis University, the trustees asked the Rosenstiel Basic Medical Sciences Research Center at Brandeis to administer the award.

Visit Ana Soto and Carlos Sonnenschein’s main Upstream page.

From NPR.org (an article about, and interview of, among others, Upstream Experts Leo Trasande and Frederica Perera):

BPA could be making kids fat. Or not.

That’s the unsatisfying takeaway from the latest study on bisphenol A — the plastic additive that environmental groups have blamed for everything from ADHD to prostate disease.

Unfortunately, the science behind those allegations isn’t so clear. And the new study on obesity in children and teens is no exception.

Researchers from New York University looked at BPA levels in the urine of more than 2,800 people aged 6 through 19. The team wanted to know whether those with relatively high levels of BPA were more likely to be obese.

But the results, published today in the Journal of the American Medical Association, didn’t offer a simple answer to that question.

Among white kids and teens, higher BPA levels were associated with more than twice the risk of obesity. With black and Hispanic youth, though, BPA levels didn’t make a difference.

“When we find an association like this, it can often raise more questions than it answers,” says the study’s lead author, Leonardo Trasande, an associate professor of pediatrics at New York University. There’s no obvious reason why one group of kids would be affected by BPA while another group wouldn’t, he says.

Also, there’s no way in this study to know whether BPA is actually causing kids to put on weight, says Frederica Perera, who directs the Columbia Center for Children’s Environmental Health. “Obese children may be simply eating and drinking foods that have higher BPA levels,” she says.

And even if BPA is playing a role in weight gain, it may be just one of many chemicals involved, Perera says.

“Our center has recently published a study showing that exposure to another group of endocrine disruptors, polycyclic aromatic hydrocarbons or PAH, was associated with obesity in the children,” Perera says. Those hydrocarbons are typically a part of air pollution in cities.

Some of the uncertainty about BPA may come because the researchers had no way of knowing how much exposure kids in the study may have had in the womb — the time many scientists believe chemical exposure is most likely to have a lifelong effect.

“Clearly we need a longer term study that examines exposure in the earliest parts of life,” Trasande says. Even so, he says, it may be time to rethink childhood obesity.

“Diet and physical activity are still the leading factors driving the obesity epidemic in the United States,” Trasande says. “Yet this study suggests that we need to also consider a third key component to the epidemic: environmental factors that may also contribute.”

* * *

Read entire story and transcript of NPR interview here.

From Harvard Gazette:

Life evolved in a toxic world long before humans began polluting it, according to a University of Massachusettsenvironmental toxicologist, who added that understanding life’s evolutionary response to environmental poisons can help people to fight destructive effects.

Emily Monosson, an adjunct professor in the UMass Department of Environmental Conservation and author of the book “Evolution in a Toxic World,” said that an understanding of both how rapidly and how slowly life can evolve to fight toxic pollutants is largely missing from toxicology, which is the science of understanding the effects of poisons on life, particularly human life.

Monosson, who spoke Thursday at Harvard’s Haller Hall in an event sponsored by the Harvard Museum of Natural History, said lessons from our evolutionary past that might help us avoid trouble have been ignored by toxicologists and industry alike.

Monosson said she wrote the book in an effort to get toxicologists to think differently about their field, which she said still uses tools that are 40 years old and badly need updating.

“The basic point of doing this book is to get toxicologists to look differently at our field,” Monosson said. “Toxicology needs to change.”

Examples abound on the ramifications of rapid evolution, she said. Bacteria reproduce so fast that they quickly evolve resistance to drugs used to treat disease, resulting in frightening new ailments such as multidrug-resistant tuberculosis. Similarly, insects can rapidly evolve resistance to pesticides, and weeds can evolve resistance to herbicides.

“Roundup Ready” soybeans offer an example where a better understanding of the rapidity of evolution might have helped, Monosson said. The soybean was genetically modified to be resistant to the herbicide Roundup, which could then be sprayed on soybean fields, where it would kill weeds but not the soybeans. Officials believed that the weeds would not become resistant to Roundup. But after blanket applications, it appears that some resistance is evolving.

Slow evolutionary change also holds lessons for toxicologists and industry, Monosson said. Estrogen receptors help to control the body’s use of the critical reproductive hormone. Some industrial chemicals bond with the receptor, widely disrupting reproduction of an array of creatures.

Estrogen receptors are highly conserved, meaning they are widespread among many kinds of creatures and have changed extremely slowly over time, an indication of their evolutionary importance. An understanding of that importance would have helped officials predict that chemicals interfering with them would have widespread and deleterious environmental effects, Monosson said.

“There’s a lot of problems we could have avoided if we understood the power of evolution in the presence of toxic chemicals,” Monosson said.

It is unknown how humans today will respond to the many chemicals, usually at low levels, that our bodies are carrying. Some of these chemicals may be harmless alone but could have interactions with other chemicals in our bodies, Monosson said.

“Those chemicals in us today weren’t in our grandparents,” Monosson said. “If we take an evolutionary approach to understand how systems evolved to detoxify chemicals, maybe we can learn how to do it [ourselves].”

A toxic Earth is nothing new to life, Monosson said. When life began 3.8 billion years ago, there were poisons all around. Besides the presence of metals and other toxins in the environment, early microbes were bombarded from above. The early Earth had little oxygen in the atmosphere and no protective ozone layer to shield the microbes from ultraviolet (UV) rays.

In response, early life evolved an enzyme, photolyase, to repair the UV damage to DNA. That enzyme, though lost in most mammals, remains widespread in other types of creatures.

Another early example involved oxygen, which is very reactive and on the early Earth acted like a poison. Life has since evolved to handle and depend on oxygen. One strategy evolved to break down hydrogen peroxide, a highly toxic chemical that forms naturally in the presence of oxygen, water, and UV rays. Early life developed an enzyme called catalase to detoxify hydrogen peroxide, accelerating the natural breakdown process from weeks to a fraction of a second.

In the future, climate change promises to alter the range of many creatures, putting them in new environments to which they’ll have to adapt. The ozone hole is exposing creatures to higher levels of UV radiation than they’re adapted to handle. And human-generated pollutants continue to be released into the environment, presenting an environmental challenge for a wide array of creatures.

Some, like Hudson River fish that have evolved to thrive despite the presence of polychlorinated biphenyls (PCBs), will evolve their own solutions, but others may need human intervention to handle an environment whose toxicity is changing much more rapidly than in the past.

“The problem today is that in a blink of time, we changed the Earth,” Monosson said. “We’ve added a lot of new synthetic chemicals and redistributed a lot of natural chemicals.”

Read entire article here.

Image by Kris Snibbe/Harvard Staff Photographer.

From the Myrtle Beach Sun News: Mutant fish: A puzzle in the water (by Claudia Lauer, September 29):

Longtime Bucksport residents know every curve in the dirt road leading to the Bull Creek boat landing.

* * *

Fishing and wading in the muddy waters is almost second nature for generations of residents who grew up as river folks, but something in the creek is starting to worry some residents.

A U.S. Geological Survey study released in September 2009 reported that 90 percent of the largemouth bass pulled from the creek during the study had male and were developing female reproductive cells. A year after the study was finished, residents still have questions about the effects of the fish on people and whether something in the water — the same water filtered for drinking water for many Horry County residents — is causing what biologists call endocrine disruption, which makes reproduction for the fish more difficult.

The problem is not confined to Bull Creek, but the Pee Dee Basin had the highest incidence of intersex fish in the study. The study looked at river basins all over the country and found that about half of them had some instances of intersex fish. The only river basin examined that didn’t show any problems was Alaska’s Yukon River Basin. In parts of the Mississippi River in Minnesota and the Yampa River in Colorado, 70 percent of the smallmouth bass had female signs. Scientists and residents say more research must be done to determine which of the many possible environmental contaminants to the water may be causing the issue in the fish and whether it’s something being done locally or upstream.

Steve Howell, like many of the lifelong residents, feels some ownership in the creek that he, his family and his friends have fished for generations.

“What about taking baths, drinking the water, cooking and etc. with the water from your tap that is coming straight out of the same river that is highly contaminated that it is screwing the fish up?” Howell said. “Since it is affecting the fish in such drastic ways as this, then what is it going to do to humans over a period of time, and why isn’t anyone or any group doing a study to try and find out?”

* * *

A number of contaminants have been suspected as the cause of the endocrine disruption. Researchers are studying the effects of livestock farming, of industrial chemicals, and of hormones and other chemicals that find their way into waste water. Hormones and birth control pills have become more commonplace and leave the human body in our waste.

* * *

Howell said he plans to continue fishing in the creek, but he’s wary of what the long-term effects could be.

“You want to know what is happening because if the water is doing that to the fish, then what happens to us?” he said. “What happens to women who are pregnant or babies that aren’t born yet? You want to know what they’re doing to make sure we’re safe and whether there’s more happening other than here’s this study and we don’t know why it’s happening or what it means.”

Read the entire article here.

From EurActiv:

Shanna H. Swan, a renowned scientist specialising in reproductive medicine, has warned about the health effects of endocrine disrupting chemicals (EDCs) known as phthalates which can end up in food via pesticides or plastics. In an interview with EurActiv, she calls on regulators to better protect consumers against those “hidden chemicals”.

Shanna H. Swan, PhD is Professor and Vice-Chair for Research and Mentoring Department of Preventive Medicine at Mount Sinai School of Medicine. Dr Swan is known for her work on the impact of environmental exposures on male and female reproductive health and has served on the National Academy of Science’s Committee on Hormone-Related Toxicants. She was speaking to EurActiv’s editor, Frédéric Simon.

You are a well-known scientist in the field of Endocrine Disrupting Chemicals (EDCs), which you have been researching for many years. What were your main findings?

The major findings I have are that certain EDCs – and I’ve looked specifically at pesticides, phthalates and Bisphenol A – are significantly related to human development, more strongly when exposure is foetal but also some adult exposures.

Has exposure tended to increase over time?

There are some studies of old stored samples. That’s the only way we can know about a person’s exposure. So to put this in context, unlike studies of smoking or pharmaceuticals where you can ask the person what their exposure was, you cannot learn anything – or very little – about a person’s exposure from EDCs by asking them what they do.

These are chemicals that are hidden – I call them stealth chemicals – and for this reason the only way we can know what the exposure was is to measure it in biological samples, either in urine or blood. Urine is usually easier and for various technical reasons preferable for the non-persistent chemicals.

When older samples are available and have been looked at, they have shown that levels were lower in the past. I can’t unfortunately be more specific but I could point you to some references.

So these go as far back as the 1960s?

There was one study in 1958 called the Collaborative Perinatal Project which had stored urine. There was a Kaiser California study in the early 60s which had stored samples. So these are very rare studies, they are the only ones.

In the most recent years some of the phthalates, for example DEHP, has decreased with the substitution. So we can pick up certain trends in use in these national samples of urinary metabolites.

Do we know precisely what the sources of exposure are?

For that, you have to go chemical by chemical. So if we restrict ourselves to phthalates, you still have to narrow that further because phthalates have different uses. Some phthalates are added to tubing to make it soft, particularly DEHP.

This is in the tubing in hospitals, in the tubing for milking cows, whenever you want a soft, flexible, plastic, you will take DEHP. Whatever is passing through that, particularly if it’s warm, it will absorb that. In this way we get exposure through material that has passed through this.

And also from milk?

It is measurable in milk, yes. So for DEHP, our dominant route of exposure is through food and there’s some in water. But you also get DEHP if you are in a medical department and hooked up to a tube.

Phthalates have been banned in some uses already such as toys, etc. So can we consider the problem solved?

Let me just go back for a second. Phthalate is a chemical class and so it’s important because you ask me if there are many exposures.

If we put cosmetics on our skin, our face – men, women, children, babies – we immediately get another phthalate in our body, which is DEP. And this is very clear. If we put hair spray or put a nail polish, then we inhale that phthalate which is primarily DBP.

So it’s a complicated story because we have many sources and many routes of exposure and also differing toxicity. Now, as for whether the problem is solved – not at all. We’ve only begun to solve the problem.

But there have been bans on some of the uses of phthalates which were of most concern, such as baby bottles…

No, this was Bisphenol A, it’s another chemical class. Think of it this way. Phthalates makes plastic soft, BPA makes plastic hard. So if you have one of these sports water bottles, those were made with BPA. Hard baby bottles, that’s BPA. Lining of tin cans, that’s also BPA. But Phthalates are on the soft side of the equation although they are both plasticisers.

Ok, so why do I say the problem is not solved? The primary elimination of phthalates has been from children’s toys. Certainly this is important but it does not protect the most sensitive organism, and that is the developing foetus.

So a toy is something you play with after birth, the pregnant mother is getting an exposure which is for the foetus much more potent than what the child will get with a toy.

By eliminating these phthalates from children’s toys – I think it is important, excellent, I certainly support it – but I would not do that at the expense of eliminating phthalates in products to which pregnant women are exposed. Because that is the most critical target for phthalates.

There has been a lot of controversy for many years over the health risks of low-dose exposure to chemicals such as phthalates. Looking at the science, is there any evidence to support this?

Let me say three things.

First of all, there is absolutely no doubt that tiny, tiny doses of hormones can permanently alter the development of the foetus – at the right time. You cannot look at the dose alone, you must look at the dose in a particular time window, because otherwise you don’t have the toxicity captured because that’s really a product of two things: Not just the dose but the timing as well.

The next thing is a story that isn’t obviously about chemicals but just to point out that we know from some human and many animal studies that when a rodent is in utero  (in the mother’s womb), each one of those is hooked up in the uterine horn and they will be located between two other pups.

So if you look at a male between two males, and a male between two females, you can measure how much testosterone is in those two males. And the difference is significant and measurable and very, very small. It’s about a drop in an Olympic-size swimming pool. That’s how small it is. It’s an extremely low dose, one part per trillion.

And what is the consequence of exposure to this?

The consequence is that the rodent that is a male between two males grows to be more aggressive, more masculine in behaviour and in his general development. He will have a stronger sperm count; he will be more fertile. And there’s no question about that, it has been shown in a number of species. And there are a number of supporting human studies. I only mention this as proof of principle that a very small amount of hormonal substance at the right time alters development.

Now let’s just go to the human situation. When people say, ‘Well the doses are too low,’ I say two things. One is, ‘Maybe so, but we are seeing effects’. So whatever dose it is, it seems to be doing something. There are probably close to 30 studies that find associations between phthalates and a variety of human health end points.

The counter-argument could be that these effects could be coming from something completely different.

Exactly. Not the counter argument, but a relevant, additional point is that, we are never exposed to one chemical. In fact a recent study found 200 chemicals on average in babies at birth.

That means that in utero the babies had 200 chemicals circulating in their bodies affecting their development, on average. The maximum in that study sample of ten was 287. So we are unquestionably exposed, and the foetuses as well.

So yes, there are many chemicals and statistically you can ask what are the associations with just DEHP metabolites, just DBP metabolites. But it’s not the most efficient way to do it. Better is to ask what about co-exposure to all of those? What about the cocktail effect?

Now, we cannot reasonably, with the sample sizes we have available, yet look at the 200 all together. But we could look at and do look at multiple exposures. So the fact that they may be quite low individually, we know that these doses add up, and so if you have several of these, you already add up to a much higher dose.

Do we know specific combinations that are particularly harmful?

Yes, among the DEHP metabolites, there are many of them, we currently look at four or five of them and can assess the sum of them. That’s one example but there are others.

This sounds quite scary. How should consumers behave or react? If my wife was pregnant what should I be telling her?

I get this question all the time. It’s a frustrating question because I can only give you a partial answer. On a simple side, I would tell her she could limit her exposure to harmful personal care products.

And the reason we can give this advice is that they have been looked at quite carefully by a number of NGOs, and specifically I point you to the Environmental Working Group website called ‘Not Too Pretty’, where they actually go through product by product and talk about the chemicals in them. That’s a nice tool for consumers.

You can also say, just a blanket precaution: Do not use air fresheners, do not spray things in your house, products and so on.

Where it gets more problematic is that even when we tell people all these things, only in rare situations can we remove these chemicals from their body. And one of the major reasons is that they are so deeply hidden, you can check the label on the lotion but you can’t check the label on your spaghetti sauce or on your bottle of milk and so on.

So we need to give consumers the tools to make informed choices. And at this point we don’t have those tools.

You mean labelling?

Labelling, yes, and also advice about behaviour – for example not to store in plastic, not to microwave in plastic.

What I tell people if you want to do the best you can, buy local produce, buy it unprocessed, buy it organic. There is a population in New York that does this, and that is the Old Order Mennonites [an anti-technology religious group similar to the Amish]. They’re quite severe, they grow everything themselves, they don’t drive in cars, they don’t use sprays… and they have very low levels of environmental chemicals.

And that has been scientifically measured?

Yes, we measured how many phthalates and phenols were in their urine and they had almost none. And it’s interesting because a couple of women did have peaks. One was a woman who used a hairspray. And you could see this because we asked what did you do before you came here and gave your urine? And this woman said, ‘Well, I was not supposed to but I used hairspray because I was going out.’ And there we see the peak for MBP in her urine.

And then another woman rode in a car even though they don’t do this normally and you see another peak. So in an extreme situation – which to most consumers is quite radical action – you can eliminate.

Another population was given regular food and then they fasted. Their urine was tested under the normal diet and after 48 hours of fasting and they had no DEHP in their urine at all.

Of course we can’t all fast! So I think we have to make it much easier for consumers to avoid these products.

In terms of chemical presence in food, there have been measures taken at EU level to reduce the use of pesticides. In France for example there is an objective of halving the use of pesticides by 2018, and there have been bans on aerial spraying and things like that. Are these steps sufficient to reduce the risk of contamination in food?

Well, removing pesticides certainly removes one source of exposure to EDCs – and a very important one, and I think this is great.

By the way, aside from phthalates, we found a number of pesticides and herbicides in the Midwest where they were associated with a lower sperm count. So these are acting as well. Also I should point out that phthalates are actually in pesticides – they are put in there to increase absorption.

So these measures to reduce pesticide use are certainly a good thing to do but it won’t do the whole job. As long as the food is processed in contact with phthalates or Bisphenol A, canned, shipped in plastic, stored in plastic or cooked in Teflon, there are just a lot of occasions along the way to pick endocrine-disrupting chemicals.

And pesticide removal is certainly a very important first step but then we have to worry about what happens to the food after it is picked and along the rest of the chain from farm to fork.

In Europe, we have minimum residue levels for pesticides in food below which ingestion is not considered to pose any risk for human health. Are you saying these should be lowered further?

I cannot comment on permissible level of pesticides. But I can comment on the question of a threshold. We have many examples in environmental science – the best I think is lead – that no matter how we keep dropping the permissible level, we see adverse effects still at a lower level.

And I think that what we have to keep in mind is that to some particular sensitive populations and particularly sensitive periods, perhaps the level has to be reduced further. But there will have to be some practical level – obviously we can’t remove everything entirely.

You may be aware that in Europe we have this REACH regulation on chemicals which is undergoing a review this year. Are you encouraging policymakers to tighten REACH even further?

For me the most important thing about REACH it that it alters the burden of proof. Of the 80,000 chemicals in commerce in the world, 62,000 were just blessed and assumed to be safe in the United States.

That is actually the default assumption still in the United States: That until a chemical is proven harmful it is assumed to be safe. This of course places the burden of proof on the consumer, to prove harm, which is not where the burden should be in my opinion. So generally shifting the burden of proof I think is extremely important and should be implemented in US policies as well.

The US must actually follow REACH if they are going to export to Europe. What has been the impact on the US industry the way you see it?

I can’t tell you that. I do know that that is not the default assumption in regulation. So whether they do something different to send things to Europe, I’m sure they have to, and I’m sure they do, but it is not what they accept as their burden to prove safety before a product is marketed.

As far as whether the regulation should be tightened, that is a very broad question. And what I have an opinion about is that I feel that endocrine disruption is a category deserving its own regulation. It’s different enough from reproductive toxicity and carcinogenicity. The risk assessment for endocrine disruption is different. The scientific issues are different enough that it would protect public health much further if we could deal with this as a class of chemicals. So that’s where I see maybe tightening up.

For you as a scientist, the link between endocrine-disrupting chemicals, the ones you have been studying, and lower fertility has been proven and is scientifically watertight? Can it be argued against?

Watertight? This is never the case, of course. There are still people here who argue cigarettes don’t cause lung cancer. Of course it will always be argued against.

I think we have now a lot of data that environmental chemicals can and do lower sperm count, impact time to conception, increase foetal loss in early pregnancy, affect pregnancy outcomes. Do we need more studies? Of course we do. But do we have enough information to act on these studies that we have? I say that we do.

More.

From Metro (quoting Upstream Expert, Dr. Carlos Sonnenschein):

The synthetic chemical bisphenol A, which is used in the linings of beer, soda and food cans, plus plastic water bottles, has been exposed as a hormone disrupter and linked to autism, cancer and other complications in the body. But it might be just the tip of the iceberg of toxic chemicals impacting us every day.

“There are 80,000 chemicals in everyday use that have never been tested,” says Dr. Carlos Sonnenschein of Tufts University School of Medicine’s Department of Anatomy and Cellular Biology. “It really is a nightmare.”

Despite decades of research supported by the National Institute of Environmental Health Sciences on the harmful effects of BPA and other endocrine disruptors, Dr. Sonnenschein says that “very little has been done about it where it counts for the public, that is, at the regulatory end (EPA, FDA).”

Dr. Sonnenschein urges the public to get involved in banning toxic ingredients because “nothing will change,” he says, “without protests before officials who run for local, state and national office. The public has an important stake in this.”

The potential effects of such ingredients are widespread: “Hormonal disruptors, at their most radical, cause fetal damage during pregnancy. There’s more incidence of breast cancer as there’s more exposure. [Pubescent girls] are particularly sensitive to exposure. But, throughout our lives, continuous exposure means the body is storing the chemicals in fat tissue,” Dr. Sonnenschein adds.

“Most people are fed up with all these chemicals. The evidence is there. It is time for the regulatory agencies to act to protect the people.”

BPA: here to stay

Despite a lawsuit from the international nonprofit Natural Resources Defense Council, the FDA recently ruled to continue allowing BPA in food packaging. The NRDC’s public health
program’s senior scientist, Dr. Sarah Janssen, responded in a statement, which in part read:

“We believe FDA made the wrong call. The agency has failed to protect our health and safety — in the face of scientific studies that continue to raise disturbing questions about the effects of BPA exposures, especially in fetuses, babies and young children. The FDA is out-of-step with scientific and medical research. This illustrates the need for a major overhaul of how the government protects us against dangerous chemicals.”

More.

From The DailyMail (quoting Upstream Expert Dr. Ana Soto):

Cancer fears have grown over a chemical widely used in plastic packaging and food-can linings after new research showed that it affected the development of monkey breasts.

Various studies have linked Bisphenol A (BPA) to breast cancer – and now teams at Washington State University and Tufts University have added weight to these findings.

They found that foetal exposure to the plastic additive alters mammary gland development in primates.

Lead author Patricia Hunt said: ‘Previous studies in mice have demonstrated that low doses of BPA alter the developing mammary gland and that these subtle changes increase the risk of cancer in the adult.

‘Some have questioned the relevance of these findings in mice to humans. But finding the same thing in a primate model really hits uncomfortably close to home.’

For the research the structure of newborn mammary glands from BPA-exposed and unexposed female rhesus macaques were compared.

Pregnant monkeys were fed a piece of fruit containing a small amount of BPA each day during the gestational period corresponding to the human third trimester of pregnancy, resulting in blood levels of BPA comparable to those of many humans today.

The researchers found that, at birth, the density of mammary buds was significantly increased in BPA-exposed monkeys, and the overall development of the mammary gland was more advanced compared to unexposed monkeys.

Previous studies have shown that exposing rodents to tiny amounts of BPA can alter mammary gland development, leading to pre-cancerous and cancerous lesions when the animals exposed in utero reach adult age.

The researchers said the primate research makes them confident that the rodent mammary gland is a reliable model to study developmental exposures to chemicals like BPA that disrupt a mammal’s estrogen activity.

Tufts University School of Medicine researcher Ana Soto said: ‘This study buttresses previous findings showing that foetal exposure to low xenoestrogen levels causes developmental alterations that in turn increase the risk of mammary cancer later in life.

‘Because BPA is chemically related to diethylstilbestrol, an estrogen that increased the risk of breast cancer in both rodents and women exposed in the womb, the sum of all these findings strongly suggests that BPA is a breast carcinogen in humans and human exposure to BPA should be curtailed.’

The research appears in the latest Proceedings of the National Academies of Sciences.

More.

From U.S. News and World Report, an article about Upstream expert, Dr. Frederica Perera’s most recent study:

Women exposed to higher levels of certain air pollutants while pregnant are more likely to have children with anxiety, depression and attention problems by ages 6 and 7, new research suggests.

“This study provides new evidence that prenatal exposure to air pollution at levels encountered in New York City can adversely affect child behavior,” said Frederica Perera, a professor of environmental health sciences and director of the Columbia Center for Children’s Environmental Health at the Columbia University Mailman School of Public Health.

She led the new study, published online March 22 in Environmental Health Perspectives.

The researchers looked at pollutants known as polycyclic aromatic hydrocarbons (PAH). They are created by the burning of fossil fuels and are common in urban environments. Traffic emissions are a major source of these pollutants.

The study is believed to be the first to link behavior problems in school-age children with two measures of prenatal PAH exposure: air concentrations and a PAH-specific marker found in mothers’ blood samples and umbilical cord blood. The PAH, inhaled by the mom during pregnancy, can cross the placenta, experts know.

Perera’s team followed the children of 253 inner-city women who gave birth between 1999 and 2006. None of the mothers smoked.

The researchers measured the concentrations of PAH in the environment of the mothers for 48 hours during trimester two or three. They also took blood samples from the mothers and the umbilical cords.

In addition, the women answered questions about their children’s behavior, including describing any attention problems, anxiety or depression. The attention problems would not qualify as attention-deficit/hyperactivity disorder, Perera noted.

The investigators found a link between higher PAH exposure levels and behavior problems. “Symptoms of anxiety and depression were 45 percent higher in the higher exposure group versus the lower,” Perera said. Attention problems were 28 percent greater in the higher PAH exposure group.

When the researchers took into account other sources of pollutants such as tobacco smoke and diet, the link remained. However, although the study found an association between prenatal PAH exposure and childhood behavior problems, it did not prove a cause-and-effect relationship.

The level of problems were those that could result in referral to a doctor for further evaluation, Perera noted.

Several mechanisms could explain the link, she said. Oxidative stress is one. Or, the chemicals may be “endocrine disrupters, which are capable of affecting the normal signaling that occurs in early brain development.”

Perera plans to follow the children until they are age 12.

“The study by itself is not convincing to me,” said Dr. Victor Klein, an obstetrician-gynecologist who specializes in high-risk pregnancies and is director of patient safety and risk reduction at North Shore-LIJ Health System in Great Neck, N.Y. He reviewed the study and said that “further research has to be done.”

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Read other Upstream posts about Dr. Perera’s work, including her Upstream interview videos, click here.

From The Independent:

Man-made chemicals present in homes, schools, offices, cars and food are probably contributing to the sharp rise in obesity and diabetes in western societies, according to a review of scientific literature published today.

Until now lifestyle factors such as lack of exercise and poor diet were believed to be the primary causes of the increased incidence of both conditions, whose proliferation has strained global health budgets.

While these remain undisputed factors, the review of 240 scientific papers by two leading experts, Professor Miquel Porta of Spain and Professor Duk-Hee Lee of South Korea, suggests chemicals in plastics and other surfaces play an important and avoidable role.

Their study assessed the impact of chemicals including the now banned PCBs, the plastic-softeners phthalates, and the plastic-hardener Bisphenol A, or BPA, a common substance in food packaging and plastic bottles which The Independent has written widely about. All 240 studies they reviewed – whether in test-tubes, on animals or on humans – had been peer-reviewed and published in scientific journals.

The paper, the Review of the Science Linking Chemical Exposures to the Human Risk of Obesity and Diabetes, found some of the chemicals appeared to have a causal effect on obesity, some on diabetes and some on both.

Many are endocrine disruptors, which can change human hormones, including the stimulation of appetite and fat storage and regulation of sugar.

* * *

One of the study authors, Professor Miquel Porta, of the Hospital del Mar Research Institute, Barcelona, said: “The epidemics in obesity and diabetes are extremely worrying.

“The role of hormone disrupting chemicals in this must be addressed. The number of such chemicals that contaminate humans is considerable.

“We must encourage new policies that help minimise human exposure to all relevant hormone disruptors, especially women planning pregnancy, as it appears to be the foetus developing in utero that is at greatest risk”.

* * *

BPA is commonly found in the plastic lining inside tinned foods, on thermal till receipts and in consumer electronics such as mobile phones and televisions, while phthalates are present in vinyl flooring, shower curtains and children’s toys.

CHEM Trust (Chemicals Health & Environment Monitoring Trust), the British pressure group which commissioned the research, urged the UK Government and the EU to press industry to find safer alternatives.

Elizabeth Salter Green, director of CHEM Trust, said: “If exposure to hormone disrupting chemicals is programming us to be fat, it is high time that public health policy takes into account cutting edge science. Obesity and diabetes are examples of the adverse health trends linked with endocrine disruption which need to be urgently addressed.

“We are talking about prevention, not cure here, and in this time of financial squeeze, anything that can help with prevention, reducing NHS spending, is a good idea.”

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From Environmental Health News:

A study raises concern about children’s exposure to mercury through fish eating, tying it for the first time to hormone changes that increase chronic stress and associated immune system dysfunction.

The mercury levels measured in the children were well below the levels considered a health risk by the U.S. Environmental Protection Agency.

This new study from Oswego County, New York, finds that higher mercury levels measured in the children’s blood are significantly associated with lower cortisol levels. The hormone cortisol is released in response to stress and is important for metabolism, immune responses and blood pressure. Its levels naturally fluctuate during the day – levels are higher in the morning and lower in the afternoon.

Even lower cortisol levels and responses can result in chronic stress even though stress increases the hormone’s level. The study’s results suggest that mercury exposure at levels commonly seen in fish eating populations may do this. It may act as a chronic stressor and disrupt the stress response. Chronic stress means the body doesn’t relax – cells continually function in high gear and do not return to a normal state. Long-term stress can have many negative health effects such as increased heart disease, more metabolic disorders and lowered immunity.

The findings are in line with prior studies in people and fish. The toxic metal increased inflammation in miners exposed to mercury. Animal studies find reduced cortisol levels in mercury-contaminated fish after capture stress.

Fish consumption is a major source both of beneficial omega-3 fatty acids and toxic mercury. Omega-3s benefit health by protecting against heart disease. Mercury is potentially harmful because it affects the brain and nervous system in children. Although there are fish advisories in many states, it is still uncertain whether the benefit of eating fish outweighs the potential harm in children.

To address the pros and cons of fish eating in children, the researchers examined 100 children from 9 to 11 years old in New York State. Parents reported children’s fish consumption, which was categorized as eating or not in the analysis. Blood mercury levels, blood lipids, cortisol in saliva and inflammation markers were measured. Blood lipids indicate future heart disease risk; cortisol reflects changes of stress response; and inflammation markers indicate immune response differences.

Fish eaters had higher HDL – or so called good cholesterol – related to lower heart disease risk, than non-fish eaters. However, the fish eaters also had much higher – almost three times higher – mercury levels than non-fish eaters (1.1 and 0.4 microgram per liter, respectively).

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AIRS THIS THURSDAY, JAN 12

We’re fat. Really fat. Almost 60% of Canadians are now either overweight or obese, and that figure is expected to climb even higher. But what if we have an excuse?

In Programmed to be Fat?, we explore controversial new science that suggests being overweight is not just the result of too much food, too little exercise, and genetics.  Exposure to environmental chemicals such as Bisphenol A, pesticides and herbicides during fetal development may be changing our physiology forever. That, say some scientists, could explain the alarming statistics on obesity – like the fact that the number of overweight infants rose 74% in just twenty years.  Scientists are now moving beyond their mice and rat studies, to test the theory in people.  In Programmed to Be Fat?, we will get the skinny on the science of fat.

Premiering January 12, 2012 on CBC TV’s “The Nature of Things” with David Suzuki.

Directed by Bruce Mohun, written by Bruce Mohun and Helen Slinger, produced by Sue Ridout, Helen Slinger and Sara Darling.

Preview below:

Vodpod videos no longer available.

From USA Today:

“All of our friends told us to cherish every moment,” Claudia says. “When I started planning her first birthday party, I remember crying and wondering where the time had gone.”

Even so, Laila’s parents never expected their baby to hit puberty at age 6.

They first noticed something different when Laila was 3, and she began to produce the sort of body odor normally associated with adults. Three years later, she grew pubic hair. By age 7, Laila was developing breasts.

Without medical treatment, doctors warned, Laila could begin menstruating by age 8 — an age when many kids are still trying to master a two-wheeler. Laila’s parents, from the Los Angeles area, asked USA TODAY not to publish their last name to protect their daughter’s privacy.

Doctors say Laila’s story is increasingly familiar at a time when girls are maturing faster than ever and, for reasons doctors don’t completely understand, hitting puberty younger than any generation in history.

About 15% of American girls now begin puberty by age 7, according to a study of 1,239 girls published last year in Pediatrics. One in 10 white girls begin developing breasts by that age — twice the rate seen in a 1997 study. Among black girls, such as Laila, 23% hit puberty by age 7.

“Over the last 30 years, we’ve shortened the childhood of girls by about a year and a half,” says Sandra Steingraber, author of a 2007 report on early puberty for the Breast Cancer Fund, an advocacy group. “That’s not good.”

Girls are being catapulted into adolescence long before their brains are ready for the change — a phenomenon that poses serious risks to their health, says Marcia Herman-Giddens, an adjunct professor at the University of North Carolina-Chapel Hill.

“This is an issue facing the new generation,” says Laila’s doctor, Pisit “Duke” Pitukcheewanont, a pediatric endocrinologist at Children’s Hospital of Los Angeles, who treats girls with early puberty. “Many parents don’t know what is going on.”

Researchers don’t completely understand why the age of puberty is falling, Herman-Giddens says. Most agree that several forces are at work, from obesity to hormone-like environmental chemicals. There’s no evidence that boys are maturing any earlier, says Paul Kaplowitz, author of Early Puberty in Girls.

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From American Scientist:

When research suggests that a single chemical may cause harm, public concern rises, as it has for the plastic additive bisphenol A (BPA) in recent years. But many more of the 83,000 or so humanmade chemicals used in the United States receive little attention. The possible effects of chemicals in combination get still less scrutiny, even though the potential that some chemicals will interact is high, given their numbers.

This may be due in part to the staggering amount of work required to discern those effects. It would be a very difficult task to keep up with research on all of these substances, much less evaluate their relative risk as new results appear. The U.S. Environmental Protection Agency (EPA) has put considerable effort into this under the Toxic Substances Control Act, but the Act has not been updated since its passage in 1976 and excludes many substances from the agency’s purview.

Substances that have the potential to disrupt development in an organism are of special concern. The results of exposure to such chemicals can range from birth defects to developmental irregularities that don’t appear until later in life. Determining whether a substance is an endocrine disruptor, how strongly it acts and at what concentrations, not to mention deciphering hormone pathways themselves, takes a great deal of time and resources. Studies in the lab can’t be directly extrapolated to real-life situations, but they can offer clues about new routes to explore, along with help in evaluating the risk posed by various chemicals.

Heather Patisaul, a biologist at North Carolina State University, studies the effects of BPA and other compounds suspected to disrupt hormonal processes, using female rats as models. “The biggest unknown,” she says, “is if human harm is indeed resulting from exposure to these chemicals at low doses. If it is, it requires a major paradigm shift in how we approach toxicology, because the current strategies are ill equipped to deal with endocrine disruptors.”

A new study adds several more pieces to the puzzle. In a September 2011 study in the Proceedings of the National Academy of Sciences of the U.S.A., Eunah Chung, Maria C. Genco, Laura Megrelis and Joan V. Ruderman chose a less known, but widely used, substance to investigate: triclocarban (3,4,4’-trichlorocarbanilide, or TCC).

TCC has been used as an antimicrobial in consumer products since the 1950s. A 2001 study found that it was present in 84 percent of antimicrobial bar soaps sold in the United States. It’s often mentioned in the same breath with triclosan: Both are halogenated carbons used in soaps and other products, but their chemical identities are unique. The EPA reports that between 1 and 10 million pounds of TCC were used in the United States in 2002. People who shower with soap containing TCC absorb it through their skin. It is metabolized quickly by humans but persists in surface waters and in sewage sludge that is spread on agricultural fields.

Ruderman and her coauthors looked at the gene aromatase-B (AroB) in the brains of developing zebrafish embryos. AroB is regulated by estrogen, among other compounds, and is expressed in subregions of the brain including the hypothalamus and preoptic areas. To determine what concentration of TCC to use, they tested a range, then chose one that did not show signs of developmental delay or toxicity. The 0.25 micromolar experimental concentration was about 1600 times higher than a high-end estimate of levels in surface waters in an industry report to the EPA, and about 12 times higher than a high-end estimate from a university-based study in Environmental Health Perspectives.

The team found that TCC had little effect on AroB when introduced without estrogen, but that it strongly enhanced the effects of introduced estrogen on the gene, with a twofold greater increase than that induced by estrogen alone. They also tested the effects of BPA and found that it induced the gene’s expression even without estrogen present.

Then the researchers exposed embryos to TCC and BPA together. Rather than amplifying the effect of the estrogen-mimicking BPA, TCC suppressed it: Its presence along with BPA resulted in about a twofold decrease in transcription of aromatase-B compared to embryos exposed to BPA alone.

“The experiments we did with BPA plus TCC were an example where each one has a positive effect on an estrogenlike process,” Ruderman says. “But you put them together and they are not additive—in fact in some ways they suppress each other.” It’s surprising that TCC would amplify estrogen’s effect but reduce the effect of an estrogen mimic—a reminder that chemicals in combination can act unpredictably.

In a 2008 study in Environmental Health Perspectives, Bruce Hammock, an entomologist at the University of California, Davis, and colleagues found that TCC enhanced estrogen- and testosterone-dependent gene expression by 2.5 times in human cells. “The major significance” of Ruderman’s study, he says, “is an elegant demonstration that there is the potential for two known environmental chemicals to synergize for an enhanced biological effect.” He thinks it’s unlikely that environmental exposure to both chemicals will be high enough to create such effects, but he notes, “This is a cautionary tale in terms of mixtures in general. As a society we are using thousands of high-volume chemicals with little regard to environmental or human health effects.”

More.

From the Maine Public Broadcasting Network:

Maine is among just a handful of states that require manufacturers to report the use of certain chemicals in their products. It also has the earliest deadine for companies to report. This week the results are in, and more than 650 products are on the list. Business representatives and state regulators say the reported presence of the chemicals does not indicate there’s a risk present. But health advocates say the list will help consumers protect their health from chemicals that leach out of products.

Listen to the four minute story here.

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