Waste More, Want More: The Adage of the Age of Electronics

written by Elise Miller, MEd
Director 

NOTE: While CHE primarily highlights emerging environmental health science, we also occasionally bring attention to how this new research is being applied (or not) to decision-making in the marketplace and regulatory policies. 
Every day new mountains are being born—not because of shifting plate tectonics but due to electronic waste, the fastest growing source of waste in the world. This is not news to most people, but what may be surprising is that many of the old computers and phones you thought you were being responsibly recycled are actually being shipped thousands of miles overseas. This is according Basel Action Network, which partnered with MIT to put geo-tracking devices in old electronics to see where they actually ended up. In their investigation, reported Monday, it was found that almost a third of old electronics taken in by even a couple of the most reputable electronic recycling companies in the US went to other countries—despite these companies stating explicitly that they did not allow this practice.
ewasteCreativeCommonsSnarkleMotion

photo from SnarkleMotion

Why is this a problem? Because we know that in many developing countries, the workers who take apart these electronics are often not protected from chronic exposure to toxic chemicals (such as arsenic, PVC, lead and mercury) in the products themselves, as well as to by-products (such as dioxin) from burning these materials. These chemicals are associated with an array of ailments, including neurological damage, certain cancers, and reproductive health problems. More concerning is that some of these workers are children, who are more vulnerable to these exposures and whose health may be impacted for their lifetimes. In addition, the diesel and other nonrenewable energy sources used to transport this waste are highly polluting and contribute to climate change.

Some nascent steps are being taken upstream to help rectify this situation. Apple, Inc., for example, issued a report last month stating the company will no longer use the following six toxic chemicals or chemical classes in their products: arsenic, beryllium, brominated flame retardants, lead, mercury and PVC/phthalates. While this is admirable (and the result of concerted market campaigns over the years), it is not exactly clear whether the chemical substitutes they have chosen are necessarily safer.

Ultimately it’s clear that we cannot buy, or even recycle, our way out of these problems. The current mounds of e-waste are full of non-biodegradable materials. E-waste is also part of the huge gyres of garbage circulating in our oceans and being consumed by fish that we then consume.
What we need are incentives to encourage a societal shift to a “waste not, want not” mentality. But the US, the largest producer of e-waste in the world, is generally driving in the opposite direction and prompting less-developed countries to consume emerging technology at ever-growing rates without any forethought being given to health-friendly disposal practices. There are a few things we can do, however. We can collectively demand that green chemistry be the basis for developing new electronic products. We can demands companies be accountable for the health and safety of their products throughout their life cycles, including the health and safety of those who make, use and dismantle them. And perhaps most important, we can model for our children and theirs that more is often not better—and in fact, less is often more.

Scientific Consensus Statements on the Role of Environmental Chemicals in Diabetes, Obesity, and Metabolism

written by Sarah Howard
Coordinator of the Diabetes-Obesity Working Group

Sarah Howard

Two worldwide gatherings of experts have published consensus statements on the role of environmental chemicals in diabetes, obesity, and metabolism:

The Parma Statement was based on a workshop held in Parma, Italy, in May 2014, and the Uppsala Statement was based on a workshop held in Uppsala, Sweden, in October 2015.

Both focus on guiding future scientific research in the field, but also contain recommendations for policy makers, health care providers, and other professionals. Both call for reducing environmental chemical exposures, especially in early life, to help prevent the development of metabolic problems later in life.

The sections below are direct quotes of some of the conclusions and recommendations from the Statements (the full text of both statements are available for free at the links above):

From the Parma Consensus Statement on Metabolic Disruptors

The Parma workshop helped to focus this emerging field by developing an overarching hypothesis for the role of environmental chemicals in the current worldwide epidemics of obesity, diabetes and related metabolic diseases. …The objective is both to indicate the strength of the current data and to provide a roadmap for further studies. A coherent, enhanced research agenda will help identify strategies to prevent metabolic diseases through actions that can be taken by individuals as well as public health agencies. History shows that prevention is always the best strategy. Increased understanding of the importance of the metabolic disruptor hypothesis to the epidemics of obesity and metabolic syndrome offers the potential for these diseases to be mitigated by modifying exposures, thereby creating a healthier environment for future generations.

Existing data lead us to predict that:

  • The effects of metabolic disruptors may be difficult to detect at the individual level due to human genomic variability creating a heterogeneous population requiring a genomic and statistical approach.
  • Some effects of metabolic disruptors may be transgenerational, requiring a multigenerational approach: a minimum of two generations for paternal line effects and three generations for maternal line effects.
  • Effects of metabolic disruptors will likely be dependent on the dose and route of exposure and may exhibit non-monotonic dose responses; this will require dose response studies and a pharmacokinetic approach.
  • We should expect effects to be due to multiple chemicals with varying half-lives, metabolism, persistence, tissue accumulation and target sensitivities; complete analysis will require a mixtures approach.
  • Certain metabolic disruptors will have specific actions, causing only obesity, diabetes or altered liver function whereas others will affect many aspects of metabolism leading to metabolic syndrome.
  • We are underestimating the importance of metabolic disruptors in obesity, diabetes, and metabolic syndrome because current research designs focus on studying one or a small subset of chemicals at a time, during limited windows of sensitivity, in single tissues (including only one adipose tissue) and often only endpoints related to a single disease outcome per study.
  • Reducing exposures to environmental chemicals and improving nutrition during development offers the possibility of preventing obesity and metabolic diseases.
  • The totality of environmental effects on obesity (drugs, chemicals, stress and nutrition) will likely be greater than the effects of genetic predisposition.”

From the Uppsala Consensus Statement on Environmental Contaminants and the Global Obesity Epidemic

In conclusion, since there are now numerous animal and epidemiological studies indicating that environmental pollutants could contribute to the global obesity epidemic, there is an urgent need to reduce the burden of environmental contaminants so that obesity does not become the normal outlook in the future. The workshop attendees concluded that public health efforts should focus on the importance of early obesity prevention by means of reducing chemical exposures, rather than only treating the established disease. Just as a bad start can last a lifetime and beyond, a good start can last a lifetime as well.

Recommendations for an Action Plan

Based on results discussed at the workshop, the authors suggested several actions that should be taken to restrict the potentially harmful effects of environmental contaminants on metabolism:

  • Increase research initiatives and funding to further explore mechanisms associated with chemical obesogen-induced metabolic disruptions, to examine mixtures, and to use exposure levels relevant to those encountered by human populations.
  • Educate physicians and other health care professionals regarding the effects of environmental contaminants on metabolism to increase the awareness of this problem, and how they could guide their patients, as well as the general population, to limit their exposure to these contaminants.
  • Ensure that knowledge of obesogenic environmental chemicals is incorporated into regulatory and policy making.
  • Demand that new chemicals that are to be released onto the market are tested in an appropriate fashion regarding their effects on metabolism.
  • Demand that all chemicals included in consumer products are disclosed in order to increase public awareness of their use and to provide individuals with the information they need to avoid exposures.
  • Find additional ways to increase public awareness about factors beyond caloric balance that are involved in obesity development, including the role of some environmental contaminants.
  • Increase awareness about the potential of these exposures to generate effects in future generations. This action item should also include education on how to avoid exposure to these contaminants.

Infectious and Non-infectious Diseases: The Lines Begin to Blur

written by Elise Miller, MEd
Director 

Deaths from noncommunicable diseases (NCDs) were estimated at 68% in 2012 globally, up from 60% in 2000, while deaths from infectious diseases are decreasing. This is according to the second edition of the World Health Organization’s report, “Preventing disease through healthy environments: a global assessment of the burden of disease from environmental risks“, published last month. The researchers found that environmental risk factors, including chemical exposures, pollutants in air, water and soil, climate change, and ultraviolet radiation, were primary contributors to these deaths.

What this tells us is the huge investment in preventing infectious diseases from philanthropic organizations, like the Bill and Melinda Gates Foundation, is making a real difference, particularly in low- and middle-income countries. This also suggests that we are not doing nearly enough to address far more intractable and pervasive concerns that lead to NCDs, such as ensuring people have clean drinking water. It’s easier to distribute vaccines than, say, stop the use of pesticides, take the lead out of pipes, or prevent coal-burning power plants from being built.

Enumerating the number of deaths also doesn’t account for the millions of people who suffer from chronic conditions that don’t necessarily lead to death, such as learning and developmental disabilities or reproductive health problems. Those of us working in the field of environmental health know that environmental risk factors can play a role in these as well, but the toll on individuals, communities, and societies is usually not as immediately obvious as from infectious diseases. This is because health outcomes from chronic and low-dose toxic exposures can take years or even decades to manifest.

In addition, what’s becoming increasingly clear is that deaths from infectious diseases and NCDs can’t always be divided into two neat categories. Instead, leading researchers are finding multiple contributors to disease often interact in a complex array of causal relationships. An infectious agent may be present, but other noncommunicable factors influence whether and what kind of disease may result. For example, endocrine disrupting chemicals can undermine the healthy functioning of the immune system, making a person more likely to contract an infectious disease.

Overall this means that even more deaths may be the result of exposure to environmental risk factors than is being currently calculated. If we increased funding for studies that could help us determine how multiple, interacting factors—including the chemical environment, viral agents, and socioeconomic status—result in disease and disability, we could then develop an algorithm to show the proportion of deaths that had both infectious and noninfectious contributors as well. And even more important, we could develop and invest in more effective upstream interventions that could decrease both.

To truly improve global health in the 21st century, the fact is we have to look beyond the rigidly defined categories and areas of expertise that have previously served to advance Western science. Instead, we now need to blur the lines some and explore the complexity of relationships between what we deemed earlier to be distinct and immutable. Systems approaches not only reflect the truth of our reality, but make it more likely that creative solutions will emerge that simultaneously address multiple, interacting factors to reduce disease incidence and boost resiliency and well-being. By doing so, perhaps 10 years from now when the third edition of WHO’s report is published, we could see the numbers for not only infectious diseases, but NCDs on the decline.

Which Chemicals Are Linked to Diabetes and Obesity? Perhaps More Than We Think.

written by Sarah Howard
Coordinator of the Diabetes-Obesity Spectrum Working Group

Sarah HowardResearchers from the National Institute of Environmental Health Sciences (NIEHS), EPA, research centers and universities have just published an article, Prioritizing environmental chemicals for obesity and diabetes outcomes research: a screening approach using toxcast high throughput data (Auerbach et al. 2016).

The intent of this project was to use new rapid screening methods to identify chemicals that may be able to affect biological processes linked to the development of diabetes and/or obesity. The researchers screened 1860 chemicals and found that, “the spectrum of environmental chemicals to consider in research related to diabetes and obesity is much broader than indicated from research papers and reviews published in the peer-reviewed literature.”

The chemicals screened include pharmaceutical drugs, chemicals already linked to diabetes or obesity development (as “signposts”), pesticide ingredients, chemicals found in consumer products, and some “green” chemicals. The biological processes that they tested for include insulin resistance, pancreatic islet and beta cell function, fat cell differentiation, and feeding behavior.

Overall, they found that the chemicals most highly ranked are generally not the ones being studied for potential effects on diabetes or obesity, in current laboratory or human research studies.

pillsThe “top 30” chemicals most likely to have effects on beta cells or islets include, for example, basic blue 7 dye (used to dye fabric), numerous pharmaceuticals, a few insecticides, a few herbicides, an “inert” pesticide ingredient, a flame retardant, a disinfectant, an air pollutant, a plasticizer, a few fragrances, a cosmetic ingredient, caffeine, a nitrosamine, and silica.

Now, before raising any alarms about these chemicals, please note:

  • some of the screening tests do not determine whether the effect was positive or negative—so chemicals/drugs with anti-diabetogenic effects for example, may show up high in the list of results;
  • most chemicals of the 85,000 in the marketplace were not included in this test, so we do not know how these chemicals compare to other chemicals;
  • we do not know how widespread exposures are to the chemicals listed in the “top 30”—they may be obscure and hardly ever used;
  • this study focused on obesity and type 2 diabetes, not type 1, due to a lack of  relevant biological assays in ToxCast (although chemicals that affect beta cells may be relevant for any type of diabetes); and
  • other studies have found that these screening tests may be inaccurate; results need to be tested further before any conclusions about these chemicals can be made. For example, researchers have found that ToxCast assays do not correlate well with laboratory studies on obesogens (Janesick et al. 2016).

The main point to take from this study is that numerous chemicals, largely unanalyzed for their potential effects on diabetes and obesity, have potential to play a role in these conditions. The study aimed to help develop hypotheses about which chemicals to test further, not to draw conclusions. Yet it also shows that the potential of chemicals to contribute to diabetes or obesity may be widespread.

Are the Glory Days Over for Glyphosate?

written by Elise Miller, EdM
Director 

The scientific evidence is mounting that glyphosate-based herbicides, which are the most heavily applied in the world, may not be the panacea for feeding the world’s hungry as its proponents have argued. A year ago the World Health Organization’s International Agency for Research on Cancer (IARC) concluded that glyphosate (also known by “Roundup”, one of its brand names) is “probably carcinogenic to humans.” Last month, over a dozen researchers published a Statement of Concern, asserting that regulations have not kept up with the emerging science on links between glyphosate exposure and human health concerns, particularly in light of the 100-fold increase in the use of the herbicide since the late 1970s. Just this past Monday, a new biomonitoring study was published that found the vast majority of Germans have glyphosate residues in their bodies, and a third of the population has levels 10 to 42 times higher than what is currently considered a safe threshold of exposure.

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Air Pollution and Weight Gain, Insulin Resistance and Metabolic Syndrome: Recent Findings

written by Sarah Howard
Coordinator of the Diabetes-Obesity Spectrum Working Group

Sarah HowardTwo studies published this month provided strong support for the idea that air pollution may cause weight gain, insulin resistance, and metabolic syndrome.

In the first study, pregnant rats exposed to Beijing’s air gained significantly more weight during pregnancy than those breathing filtered air. Their offspring (exposed pre- and postnatally) were also significantly heavier at 8 weeks of age.

In the second study, Mexican Americans living in Southern California exposed to ambient air pollutants had lower glucose tolerance, higher insulin resistance, and adverse blood lipid concentrations.  According to the authors, “the magnitudes of effect from a 1-[standard deviation] difference of [fine particulate matter] on metabolic outcomes were similar compared with the impact of a 1-unit change in percent body fat or [body mass index] BMI on the same metabolic outcomes.”

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Lead, Methane and Monetizing Natural Capital

written by Elise Miller, EdM
Director 
Widespread water contamination from lead in Flint, Michigan, and the huge methane leak in Aliso Canyon, California, have dominated media headlines in recent weeks. The oft-repeated response given to questions of why these situations weren’t addressed earlier has been: It would have been too costly. With this mindset, the government agencies and others responsible did not do anything, and even covered up how bad the situations were, until major health crises erupted. Of course these events are not anomalies. Sadly this is true for thousands of communities around the US and elsewhere because there is little economic incentive to invest in prevention-oriented actions.

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