Archives for posts with tag: environmental health

From Earth Justice:

Each year, nearly one billion pounds of pesticides are sprayed into fields and orchards around the country. As the families who live nearby can tell you, those pesticides don’t always stay in the fields and orchards.

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Miller-McCune: America’s hidden diseases.

Millions of poor Americans living in distressed regions of the country are chronically sick, afflicted by a host of hidden diseases that are not being monitored, diagnosed or treated, researchers say. From Appalachia to the Mississippi Delta to the segregated inner cities of the Great Lakes and Northeast, they say, and from Navajo reservations to Latino communities along the U.S.-Mexico border, more than 20 chronic diseases are promoting the cycle of poverty in conditions of inadequate sanitation, unsafe water supplies and rundown housing. “These are forgotten diseases among forgotten people,” said Peter Hotez, a microbiologist at George Washington University, president of the Washington, D.C.-based Sabin Vaccine Institute and co-founder of the institute’s Global Network for Neglected Tropical Disease Control. “If these were diseases among middle-class whites in the suburbs, we would not tolerate them. They are among America’s greatest health disparities, and they are largely unknown to the U.S. medical and health communities.”  More . . .

The Pittsburgh Post-Gazette recently completed an amazing series of reports on the cancer clusters in Western Pennsylvania. Here is a sample from Day 2 of their 8-day series.

In many places around Western Pennsylvania residents see clusters of death and clusters of people sickened by cancer or heart and lung diseases.

And, like Lee Lasich, a Clairton resident, they’re frustrated that government health and environmental agencies don’t see them too, don’t do something about the problems and don’t take a tougher stance on enforcement of air pollution regulations.

* * *

The Pittsburgh Post-Gazette’s analysis of Pennsylvania Department of Health mortality data from 2000 through 2008 found that 14,636 more people died from heart and respiratory disease and lung cancer in 14 Western Pennsylvania counties than national rates would predict, or 12,833 after adjusting for excess smoking in the region. And the yearlong investigation found numerous people throughout the region who talked about what seemed like unnatural and unexplained clusters of illnesses and death in their communities.

This overlap of high mortality rates and pollution raises questions about whether there is a causal relationship. The question has not been definitively answered, but for the people who live among these clusters, the connection seems clear.

More . . .

When it comes to particulate pollution, what you can’t see can hurt you.

“The stuff now is more insidious but much harder to perceive,” said Lester B. Lave, the Carnegie Mellon University economics professor who pioneered pollution mortality research in the 1970s. “There is no rotten egg smell. There is no dirt. It is less easily perceived. People are usually astonished that Pittsburgh still is one of the worst, but air pollution is continuing.”

Studies estimate that pollution kills 20,000 to 60,000 each year in the United States. Even at the lower range, pollution deaths would equal the nation’s annual rate of homicides.

The upper range would equal traffic fatalities and suicides combined and rank pollution as the nation’s eighth leading cause of death, just behind diabetes — another disease pollution has been linked with — and just ahead of the combined category of influenza and pneumonia.

And what’s true about pollution deaths holds true about particulate pollution: Both remain largely imperceptible to the general public.

Science to the rescue

For the past 40 years, science time and again has implicated particle pollution as a major killer.

In 1970, Dr. Lave and Eugene B. Seskin for the first time calculated health damage from pollution. Their subsequent book, “Air Pollution and Human Health,” published in 1977, found not only “a close association between air pollution and mortality,” but determined the relationship to be substantial.

Drs. Lave and Seskin’s work stirred such controversy that it prompted an effort to get Dr. Lave fired from his teaching position. But their science stood the test of time and helped inspire major epidemiological studies in subsequent decades.

More . . .

Lindsey Konkel has just published an outstanding article on Environmental Health News.  Here is an excerpt:

When doctors told Wanda Ford her 2-year-old son had lead poisoning, she never suspected that the back yard in her low-income neighborhood was the likely culprit.

Ford knew that exposure to the heavy metal could be dangerous. So when she and her husband moved into the Lower Lincoln Street neighborhood, Ford, then pregnant, took steps to make sure their 100-year-old home was lead-free.

“We never thought to test the soil – my son played in the back yard all the time,” said Ford, whose son is now seven.

It’s long been known that children in poorer neighborhoods like Ford’s are more likely to be exposed to lead, industrial emissions, vehicle exhaust and other contaminants. Now, scientists are beginning to suspect that low-income children aren’t just more exposed – they actually may be more biologically susceptible to them, even at low levels.

A growing body of research suggests that the chronic stressors of poverty may fundamentally alter the way the body reacts to pollutants, especially in young children. Several studies have found that such stress may exacerbate the effects of lead on children’s developing brains, while others reported more asthma symptoms in kids with simultaneous exposure to air pollution and socioeconomic problems.

Everyone experiences stress occasionally; it can improve focus and performance to overcome obstacles at work, during athletic competitions, or in everyday life. But stress also can harm the body.

“When the stress is chronic and the stressors are out of our control, we experience it as a threat rather than a challenge,” said Dr. Rosalind Wright, a physician and epidemiologist at the Harvard School of Public Health. “This type of stress can have negative, lasting effects on key systems in the body. It’s like having the fight or flight response turned on all the time.”

Schools and homes next to refineries and Superfund sites, farm workers drinking toxic water, urban children breathing exhaust from congested streets. Many of these people are living in poverty or with low incomes, and they have to cope with socioeconomic problems as well as high exposure to pollutants. Scientists say living in such areas and facing financial strain, racial issues and high crime rates can wear down the systems responsible for controlling immunity and hormones. Hormones needed for proper brain development may be altered, or the immune system may continually release inflammatory molecules into the blood.

“This may make you more susceptible to everything else around you, including pollution,” said Jane Clougherty, an exposure scientist and epidemiologist at the University of Pittsburgh Graduate School of Public Health.

One + one = four

Stress, when combined with certain pollutants, may produce a much greater health effect than either stress or pollution alone.

“It would be like adding one and one together and getting three or four,” said Dr. Ted Schettler, science director of the Science and Environmental Health Network, a non-profit organization focused on applying science to promote health. “Socioeconomic status may affect underlying biology, making exposure to certain chemicals more adverse for the poorer kid.”

In Worcester, about 40 miles west of Boston, nearly one in five residents lives below poverty level, almost double the Massachusetts average, according to 2010 U.S. Census data. Its median household income is roughly 30 percent lower than the state’s.

Worcester is representative of many old manufacturing towns across the country. “With a decline in manufacturing, you get a decline in certain types of pollution, but you are also left with ongoing problems such as lead contamination in soil, which is typical of a lot of older American towns and cities,” said Katherine Kiel, an environmental economist at the College of the Holy Cross in Worcester. “Low-income housing is often built where property is cheapest. Unfortunately, these areas often have more pollution.”

Socioeconomic stress “may make you more susceptible to everything else around you, including pollution.  Jane Clougherty, University of PittsburghThe eaves of Ford’s home – one of Worcester’s iconic triple-decker apartment houses – are blackened by soot from trucks and cars. From her front porch, she can see the on-ramp to the interstate highway that bisects the city.

“This feels like a depressed town. There are a lot of neglected, dilapidated places. It’s not very child-friendly,” said Ford, who is not using her real name for fear that her son will be bullied at school about his learning disabilities.

Ford is black, as is roughly 12 percent of Worcester. One small study published last year found that women in Boston who faced racial discrimination and community violence had higher levels of a stress hormone linked to preterm births.

Gang activity and a drug raid at a house nearby have brought community violence close to home. “My husband and I didn’t see it at first when we moved here, but it’s pervasive,” said Ford.

Rates of violent crimes in Worcester are about 17 percent higher than the national average. In 2010, there were roughly 471 assaults, armed robberies and murders per 100,000 inhabitants in Worcester. The national average for that same period was 404 violent crimes per 100,000 people, according to the FBI’s Uniform Crime Reports.

She worries constantly about the safety of her kids. Four of them, all under the age of 15, live at home.

When her son was born in 2004, he seemed healthy. “Looking back, there were signs of developmental delays early on, like he drooled too much, but we didn’t think much of it,” she said.

When he was 2, his doctor found that his blood lead levels were elevated, though they fell below the commonly defined threshold for effects of lead. Ten micrograms per deciliter has traditionally been defined as the harmful level, but recently the Centers for Disease Control and Prevention lowered it to five, recognizing that effects can occur at lower levels.

Synergy between lead and stress

With lead pollution, “the toxicity of lead may be stronger in a child also exposed to the stress of poverty,” said Dr. Robert Wright, a pediatrician and environmental health scientist at the Harvard School of Public Health, and husband of Rosalind Wright.

Lead exposure, which has been linked to reduced IQs, attention problems and aggressive behavior, may be more detrimental to low-income kids than to children in families with higher incomes. Children in Boston began to show reduced IQ at blood lead levels as low as six micrograms per deciliter, while kids from families with more financial resources only began to show cognitive deficits at levels greater than 10, according to one study.

“If this synergy exists between stress and lead, from a biological perspective, it’s plausible this link exists between stress and other neurotoxic pollutants, such as mercury and polychlorinated biphenyls (PCBs) as well,” said Robert Wright.

For years, toxicologist Deborah Cory-Slechta of University of Rochester and her colleagues have studied the combined effects of lead and stressful conditions on lab rats. Lead plus stress had effects on their learning ability and brains that did not occur with either of those factors alone, according to their research.

Researchers are trying to tease apart why chronic stress may make some pollutants more harmful. Both human and animal studies suggest that it can throw key systems of the body out of whack. At a young age, it may create hormonal shifts that permanently alter the way the body responds to future stresses, including chemical exposures. It also may weaken the immune system or trigger inflammation.

“Inflammation is central to a lot of chronic diseases we worry about today,” including respiratory diseases such as asthma, Clougherty said.

In one study, young male laboratory rats put under chronic stress showed a rapid, shallow breathing pattern when inhaling polluted air – unlike rats exposed only to the pollution.

The researchers created a stressful environment by placing the young male rat in the home cage of an older, dominant male twice a week. The stressed rats had higher levels of molecules associated with inflammation in their blood.

Also, in East Boston, children who were previously exposed to community violence were more likely to show signs of asthma when breathing traffic-related air pollution than children in less violent neighborhoods. “This suggests a model where stress impacts the child’s susceptibility to pollution,” said Clougherty.

In addition to asthma, this may make low-income children more predisposed to diabetes, heart disease and even dementia later in life.

Kids living with violence also may experience more wear and tear on their DNA, damage that has been linked to disease later in life, according to a Duke University study published in April.

Susceptibility starts in the womb. Exposure to stress and pollution before birth and during early childhood may be particularly harmful because “both may alter development of the brain, lungs and nervous system during these critical periods,” said Rosalind Wright.

This raises an important question: Are people protected by policies that just consider their chemical exposures without looking at their living conditions, too? Many scientists think not.

Increased risks due to social status are “a critically important but neglected area within risk assessment, and should be incorporated in the future,” Harvard epidemiologists Joel Schwartz and David Bellinger and Johns Hopkins’ Thomas Glass wrote in a 2011 report.

Schettler said “this new understanding has the potential to change the way we think about interventions for low-income children.”

More.

From Wired:

Since returning home from Iraq and Afghanistan, an untold number of soldiers have come down with puzzling health problems. Chronic bronchitis. Neurological defects. Even cancer. Many of them are pointing the finger at a single culprit: The open-air “burn pits” that incinerated trash — from human waste to computer parts — on military bases overseas.

Pentagon officials have consistently reassured personnel that there was no “specific evidence” connecting the two. But now, only days after Danger Room uncovered a memo suggesting that Army officials knew how dangerous the pits were, an animal study is offering up new scientific evidence that links burn pits to depleted immune systems.

“The dust doesn’t only appear to cause lung inflammation,” says Dr. Anthony Szema, an assistant professor at Stony Brook School of Medicine who specializes in pulmonology and allergies, and the researcher who led this latest study. “It also destroys the body’s own T-cells.” Those cells are at the core of the body’s immune system, “like a bulletproof vest against illnesses,” Szema tells Danger Room. When they’re depleted, an individual is much more prone to myriad conditions.

For scientists, trying to establish a definitive connection between those diffuse health problems and the pits has been exceedingly difficult to do. Most notably because the Department of Defense, as a report issued by the Institutes of Medicine noted last year, didn’t collect adequate evidence — like what the pits burned and which soldiers were exposed — for researchers to draw any meaningful conclusions about the impact of the open-air incinerators. Szema’s study is only on 15 mice, so it’s by no means definitive. But it is an important first step.

Regardless, it’s becoming increasingly clear that Pentagon officials were aware of the risk posed by the pits. Another memo (.pdf), written by Lt. Col. Darrin Curtis in 2006 and obtained by Danger Room, warned of “an acute health hazard” to personnel stationed at Iraq’s Balad air base. “It is amazing,” he noted, “that the burn pit has been able to operate … without significant engineering controls being put in place.”

But as recently as yesterday, when asked about the leaked Army memo obtained by Danger Room (which cited a risk of ”long-term adverse health conditions” from the pits), Pentagon spokesperson George Little told reporters that “we do not have specific evidence that ties these kinds of disposal facilities to health issues.”

Perhaps not. But researchers just got way, way closer. A team, led by Dr. Szema at Stony Brook University, this week revealed to Danger Room the results of their ongoing investigations that are trying to directly link health problems to the air emitted by burn pits. And the results should cause those who served near the pits — which burned trash at most major bases in Iraq and Afghanistan during at least some period over the last decade — to be concerned.

More.

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.

The Chicago Tribune has just published a brilliant collection of articles, documents, charts, and videos that Upstream readers shouldn’t miss.  Here is the video for Part 4 of their series on EPA’s inefficacy in regulating toxic chemicals.

Regulators have allowed generation after generation of flame retardants onto the market without thoroughly assessing the health risks. One chemical touted as safe is now turning up in wildlife around the world. Read »


The Chicago Tribune has just published a brilliant collection of articles, documents, charts, and videos that Upstream readers shouldn’t miss.  Part 3 of their series looks at the troubling role of industry in science.

Companies that make flame retardants say science shows their products prevent fire deaths and are safe to use, but the research they often cite is either seriously flawed or grossly misrepresented. Read »

The Chicago Tribune has just published a brilliant collection of articles, documents, charts, and videos that Upstream readers shouldn’t miss.  Here is the video for Part 2 of their series on the troubling role of the tobacco industry.

With cigarettes starting deadly fires, tobacco companies created a new scapegoat — the furniture going up in flames — and invested in a national group of fire officials that would deliver the message. Read »

The Chicago Tribune has just published a brilliant collection of articles, documents, charts, and videos that Upstream readers shouldn’t miss.  Here are the opening paragraphs of the first article in the series.

Dr. David Heimbach knows how to tell a story.

Before California lawmakers last year, the noted burn surgeon drew gasps from the crowd as he described a 7-week-old baby girl who was burned in a fire started by a candle while she lay on a pillow that lacked flame retardant chemicals.

“Now this is a tiny little person, no bigger than my Italian greyhound at home,” said Heimbach, gesturing to approximate the baby’s size. “Half of her body was severely burned. She ultimately died after about three weeks of pain and misery in the hospital.”

Heimbach’s passionate testimony about the baby’s death made the long-term health concerns about flame retardants voiced by doctors, environmentalists and even firefighters sound abstract and petty.

But there was a problem with his testimony: It wasn’t true. . . .

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The Chicago Tribune has just published a brilliant collection of articles, documents, charts, and videos that Upstream readers shouldn’t miss.  Here is the video introduction to their outstanding series.

The average American baby is born with 10 fingers, 10 toes and the highest recorded levels of flame retardants among infants in the world. The toxic chemicals are present in nearly every home, packed into couches, chairs and many other products. Two powerful industries — Big Tobacco and chemical manufacturers — waged deceptive campaigns that led to the proliferation of these chemicals, which don’t even work as promised.


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.

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From New York Times:

Obesity and the form of diabetes linked to it are taking an even worse toll on America’s youths than medical experts had realized. As obesity rates in children have climbed, so has the incidence of Type 2 diabetes, and a new study adds another worry: the disease progresses more rapidly in children than in adults and is harder to treat.

“It’s frightening how severe this metabolic disease is in children,” said Dr. David M. Nathan, an author of the study and director of the diabetes center at Massachusetts General Hospital. “It’s really got a hold on them, and it’s hard to turn around.”

Before the 1990s, this form of diabetes was hardly ever seen in children. It is still uncommon, but experts say any increase in such a serious disease is troubling. There were about 3,600 new cases a year from 2002 to 2005, the latest years for which data is available.

The research is the first large study of Type 2 diabetes in children, “because this didn’t used to exist,” said Dr. Robin Goland, a member of the research team and co-director of the Naomi Berrie Diabetes Center at Columbia University Medical Center in New York. She added, “These are people who are struggling with something that shouldn’t happen in kids who are this young.”

Why the disease is so hard to control in children and teenagers is not known. The researchers said that rapid growth and the intense hormonal changes at puberty might play a part.

The study followed 699 children ages 10 to 17 at medical centers around the country for about four years. It found that the usual oral medicine for Type 2 diabetes stopped working in about half of the patients within a few years, and they had to add daily shots of insulin to control their blood sugar. Researchers said they were shocked by how poorly the oral drugs performed because they work much better in adults.

The results of the study and an editorial were published online on Sunday by The New England Journal of Medicine.

The findings could signal trouble ahead because poorly controlled diabetes significantly increases the risk of heart disease, eye problems, nerve damage, amputations and kidney failure. The longer a person has the disease, the greater the risk. So in theory, people who develop diabetes as children may suffer its complications much earlier in life than previous generations who became diabetic as adults.

“I fear that these children are going to become sick earlier in their lives than we’ve ever seen before,” Dr. Nathan said.

But aggressive treatment can lower the risks.

“You really have to be on top of these kids and individualize therapy for each person,” said Dr. Barbara Linder, a senior adviser for childhood diabetes research at the National Institute of Diabetes and Digestive and Kidney Diseases, which sponsored the new study.

Sara Chernov, 21, a college senior from Great Neck, N.Y., learned that she had Type 2 diabetes when she was 16. Her grandfather had had both legs amputated as a result of the disease, and one of the first questions she asked was when she would lose her legs and her eyesight.

A doctor scolded her for being fat and told her she had to lose weight and could never eat sugar again. She left the office in tears and did not go back; soon after, she joined the study at Columbia. Like many of the children in the program, she did not even know how to swallow a pill.

Ms. Chernov believes that the disease “is not a death sentence,” she said, if she is careful about controlling her blood sugar. But it has been a struggle. Her family tends to be overweight, she sometimes craves sweets and she has orthopedic problems that have required surgery and have made it hard for her to exercise. She is also being treated for high blood pressure.

A few weeks ago, because her blood sugar shot up despite the diabetes pills she was taking, Ms. Chernov began using insulin.

Most of the participants in the study came from low-income families: 42 percent had yearly incomes under $25,000, and 34 percent below $50,000. About 40 percent were Hispanic, 33 percent black, 20 percent white, 6 percent American Indian and less than 2 percent Asian. Poor people and minority groups have some of the highest rates of obesity and diabetes in both adults and children.

Dr. Phil Zeitler, an author of the study and a professor of pediatrics at the University of Colorado, Denver, said many participants lived with a single parent or guardian and, like Ms. Chernov, came from families with a history of diabetes and had relatives with kidney failure or amputations.

“They’re wrapped up in a lot of family chaos,” Dr. Zeitler said, calling them a “challenging population” with a lot of stress in their lives, on top of the normal chaos of the teenage years.

Type 2 diabetes used to be so rare in children that it was called adult-onset diabetes. Type 1, a much less common form, was most likely to strike children and teenagers, and was called juvenile diabetes. Both forms of the disease cause high blood sugar, but their underlying causes are different.

Type 1 occurs because the patient’s own immune system mistakenly destroys the cells in the pancreas that make insulin, a hormone needed to control blood sugar levels. Patients have to take insulin.

Type 2 is thought to be brought on by obesity and inactivity in people who have a genetic predisposition to develop the disease when they gain weight. And they may also have an inborn tendency to put on weight. The pancreas still makes insulin, though not enough, and the body does not use insulin properly — a condition called insulin resistance. High blood pressure and cholesterol often come with the disease. Initial treatments include dietary changes, exercise and oral medicines, but many people eventually need insulin.

Doctors began noticing an alarming increase in Type 2 cases in children in the 1990s, especially among blacks and Hispanics from poorer families. The problem had started even earlier in American Indians, who have had sharp increases in obesity in recent years.

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Is eating organic more expensive? In the long-run the answer would be NO. Synthetic pesticides or fertilizers used on vegetables and fruits affects our health. Pesticides have demonstrably elevated rates of asthma, leukemia, and prostate cancer.

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