In a forthcoming article in the Proceedings of the National Academy of Sciences, Patric Allard and Monica Colaiácovo use a nemotode (round worm) system to explore how BPA damages genetic processes in animals.

BPA ranks among the highest production volume chemicals with a global annual production scale of ≈4 million metric tons. It is commonly used in the manufacture of several polymers, including polycarbonate and epoxy resins. Thus, BPA is found in a variety of items such as plastic bottles, the lining of both food and beverage cans, and dental sealants. Consistent with its widespread presence, urinary BPA is detected in >90% of the population in the United States. Higher levels of urinary BPA have been correlated with cardiovascular diseases and diabetes and may be associated with an increased risk for miscarriages.

Their results?

Using these conditions, we observed a sixfold reduction in the mean number of eggs laid (increased sterility) and a dramatic increase in embryonic lethality (97.3%; n = 333) in worms exposed to 1 mM BPA compared with vehicle. Furthermore, none of the rare larvae observed either reached adulthood or survived after 3 d in culture (100% larval lethality). Taken together, these phenotypes indicate that BPA impairs C. elegans reproduction and are suggestive of errors in chromosome segregation.

Why was this?  They found that worms exposed to BPA had dysfunctional DNA repair mechanisms that ordinarily fix breaks in genetic material.  It turns out that BPA exerts hormone-like effects and turns off the gene that makes the DNA repair proteins.

Without these repairs, the animals were not able to produce eggs (in an important cell division process called meiosis) with normal genetic material.  This led to incorrect chromosome alignment and separation in the cell division of embryonic worms.

Bottom line:  Exposure to BPA caused these worms to become sterile and exhibit elevated emrbyonic mortality.

There’s always a challenge in using lab animal models to extrapolate to human health.  One of the main criticisms of these kinds of studies is that the exposure concentrations are different than what people are experience on a daily basis.  The authors address this (emphasis mine):

We examined the internal levels of BPA following our exposure protocol and found that worms contained on average 2 μg/g of unconjugated BPA. These levels were within the range or lower than the internal free BPA levels detected in maternal kidneys, liver, and uterus, as well as in fetal liver and total fetal homogenate of pregnant rats perfused with a single dose of BPA at 10 mg/kg. Data on nonblood tissue levels of BPA both in rodent models and in humans are scarce and intraorgan concentrations in the BPA study on mouse meiosis were not measured, making direct exposure comparison difficult. However, it is likely that both our results and those of Susiarjo and colleagues represent the reproductive outcome following elevated BPA exposure. Therefore, our studies bear relevance to occupational exposure studies in humans, and particularly to fetal and neonate exposure levels, as suggested by the up to 10 times higher levels of BPA detected in premature infants in neonatal intensive care units.

Patrick Allard and Monica P. Colaiácovo (2010). Bisphenol A impairs the double-strand break repair machinery in the germline and causes chromosome abnormalities Proceedings of the National Academy of Sciences : 10.1073/pnas.1010386107

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Photo Credit: thesoftlanding

In a fascinating new article in PLOS One (open access), Daniel Nettle asks why we see social gradients in preventative health behaviors:

People of lower socioeconomic position have been found to smoke more, exercise less, have poorer diets, comply less well with therapy, use medical services less, adopt fewer safety measures, ignore health advice more, and be less health-conscious overall, than their more affluent peers. Some of these behaviors can simply be put down to financial constraints, as healthy diets, for example, cost more than unhealthy ones, but socioeconomic gradients are found even where the health behaviors in question would cost nothing, ruling out income differences as the explanation.

As we often assume with environmental or nutritional issues, maybe simply helping to better educate people is all that’s needed? Probably not, as Nettle points out, and with an interesting twist:

Socioeconomic gradients in health behavior are not easily abolished by providing more information. Informational health campaigns tend to lead to greater voluntary behavior change in people of higher socio-economic position, and thus can actually increase socioeconomic inequalities in health, even whilst improving health overall. Thus, we are struck with what we might call the exacerbatory dynamic of poverty: the people in society who face the greatest structural adversity, far from mitigating this by their lifestyles, behave in such ways as to make it worse, even when they are provided with the opportunity to do otherwise.

What are some of the possible explanations for this pattern, and are they sufficient?

Underlying socioeconomic differences in health behavior are differences in attitudinal and psychological variables. People of lower socioeconomic position have been found to be more pessimistic, have stronger beliefs in the influence of chance on health, and give a greater weighting to present over future outcomes, than people of higher socioeconomic position. These explanations seem clear.

However, they immediately raise the deeper question: why should pessimism, belief in chance, and short time perspective be found more in people of low socioeconomic position than those of high socioeconomic position? These deeper questions are at the level which behavioral ecologists call ultimate, as opposed to proximate causation

To develop more of an ultimate explanation, Nettle hypothesized that lower socioeconomic groups are subject to greater hazard or environmental harm or even simply the perception of living a more hazardous life.  This, in turn, discourages healthy behavior.

To test this hypothesis, he developed a mathematical/statistical model predicting the probability of dying in a given year, which is a combination of extrinsic risks that people cannot control as well as intrinsic risks that they can control through modified health behavior.   Thus, people choosing to take the time to engage healthier opportunities reduce their mortality risk.  Now there’s a tradeoff, however, because the more time people choose to undertake healthy behavior, the less time is left over for leisure activities and other life events.

Overall survival is therefore a combination of all of these factors, which can easily be modeled by assuming a range of values for time spent on health vs. other activities to see what kinds of mortality outcomes arise.

Here are the interesting results he found…

If it is the case that lower socioeconomic position is associated with a greater rate of extrinsic hazards (an assumption which needs justifying, see below), then we should expect people to respond to lower socioeconomic position with reduced preventative health behavior, because the benefits of that behavior to them are indeed lessened. This would in turn make their health outcomes worse, and so the gradient in health outcomes should in general be steeper than the underlying gradient in extrinsic risk exposures. Thus, the observed pattern of substantial socioeconomic gradients in health, which are to a  significant extent mediated by differences in health behavior, is exactly what we would predict if people are behaving adaptively given the environment in which they live.

Previous research on social inequalities in health behavior has found that people faced with socioeconomic deprivation endorse a greater belief in the influence of chance on life outcomes, particularly in the domain of health, are more pessimistic, and devalue future outcomes relative to present ones more sharply, than people of higher socioeconomic position. The model presented here is not in any sense an alternative to these accounts. On the contrary, the model here suggests an ultimate reason why these proximal psychological patterns might persist, and the proximal psychological accounts suggest how the adaptive behavior might actually be delivered. Clearly, people do not perform exact actuarial calculations in deciding whether to adopt a particular health behavior. Instead, they presumably employ some simple evolved heuristics. In this case, these might include something like ‘to the extent you see bad and unpredictable health outcomes besetting your peers, worry about today rather than tomorrow’.

And here’s where the environmental link comes in:

Several lines of evidence suggest that the assumption that lower socioeconomic position is associated with a greater degree of extrinsic hazard may not be unreasonable. First, studies of health inequalities generally find that controlling for behavioral factors (smoking, diet, etc.) attenuates socioeconomic gradients in health outcomes, but does not abolish them entirely. Of course, this could simply mean that not enough controls have been included, but it could also suggest that there is a residuum of health hazard which is extrinsic and thus not responsive to individuals’ behavioral decisions. Second, there are some health risk factors whose spatial distribution is socioeconomically patterned, and which people living in more deprived areas can do very little to avoid save for not living there. The clearest examples are noise, lead, and air pollution in the form of fine particles and nitrogen oxides. The levels of these hazards are higher in poor neighbourhoods, and their effects on morbidity and mortality well established. Third, many studies have found effects of living in poor neighbourhoods on health outcomes, above and beyond the effects of individual level socioeconomic characteristics. For example, poorer neighbourhoods are associated with substantially increased chances of accidental death or homicide, and heart disease, even once individual characteristics are adjusted for. This suggests that there are hazards fundamentally associated with living in these areas, which affect whoever it is that lives there.

In general, the model presented here draws the focus of health policy away from merely providing information or exhorting behavioral change, and onto extrinsic mortality. As with other neo-material approaches to health inequalities, it reminds us of the need to address the fundamental economic inequities which mean that some neighbourhoods contain higher risks of pollution, toxicity, and accident than others. More specifically, it suggests that reducing these structural inequities will reap a double dividend. It will have a primary effect on mortality inequality, and also a secondary effect as people respond to the primary effect by increasing their health-promoting behavior. Indeed, the secular trend in health behavior amongst middle-class people could be interpreted in this way. As economic development has eliminated many of the uncontrollable sources of danger, individuals have increased their investment in behaviors that mitigate those risks which do respond to individual choice. We need to create a similar dynamic in the most disadvantaged areas.

However, whilst changing structural conditions is the most important priority, the model also suggests that it is worth paying attention to people’s perceptions of extrinsic mortality. That is, in poor communities, individuals may perceive the local environment to be extrinsically dangerous to a greater extent than is in fact true (for example, because they are affected by social stereotypes or media portrayals). The model suggests that the psychological mechanisms which underlie behavioral decisions should be responsive to perceived levels of extrinsic mortality. If these perceptions are unrealistic, then they may lead to excessive fatalism and consequent disinvestment in health behavior. Thus, researchers and practitioners could usefully examine the genesis and malleability of people’s perceptions of the extrinsic dangers of their environments, and the relationships of these to their health attitudes and health behaviors.

What I love about this article is how it situates problems of sociology, psychology, public health, and justice squarely in the context of the environment—both actual and perceived.  And it encourages those of us interested in public health and well being to borrow a page from people engaged in environmental justice and just sustainability initiatives.

I also like how this result dismantles traditional notions of environmentalism and public health and forces us to consider new ways of studying pervasive problems in our world, where environmental studies scholars collaborate more with sociologists, psychologists, and historians to understand the ultimate causes of linked social-environmental challenges.

Nettle, D. (2010). Why Are There Social Gradients in Preventative Health Behavior? A Perspective from Behavioral Ecology PLoS ONE, 5 (10) DOI: 10.1371/journal.pone.0013371

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Photo credit: postopp1

Two stories in today’s news:

(1) The Washington Post ran an article on the possible pesticide-child behavior link we examined in a previous post.

(2) CNN also picked up the recent report from the Environmental Working Group (video clip and printed story) on pesticide residues in produce:

The Dirty Dozen (may contain 47-67 pesticides per serving—EWG suggests buying or growing these organically)

• Celery
• Peaches
• Strawberries
• Apples
• Domestic blueberries
• Nectarines
• Sweet bell peppers
• Spinach, kale and collard greens
• Cherries
• Potatoes
• Imported grapes
• Lettuce

The Clean 15 (contain fewer or no pesticides—EWG suggests you can buy these conventionally grown)

• Onions
• Avocados
• Sweet corn
• Pineapples
• Mango
• Sweet peas
• Asparagus
• Kiwi fruit
• Cabbage
• Eggplant
• Cantaloupe
• Watermelon
• Grapefruit
• Sweet potatoes
• Sweet onions

The EWG shopper’s guide.

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Photo Credit:  http://www.flickr.com/photos/maheshkhanna/786837829/

Now that hurricane season is upon us, we’re learning this week from forecasters that it’s supposed to be a bad one:

Weather Services International predicted 18 named storms, 10 hurricanes and five intense hurricanes, rated as Category 3 storm with winds of 110-130 mph, or greater.

NBC ran a segment (video clip) asking what impacts hurricanes might have on the oil spill.  The clip mentions, among other things, that 2010 Atlantic sea surface temperatures are the warmest on record—not a good omen when it comes to hurricane intensity.

This is, potentially, a very serious situation for the Gulf states.   If a Katrina-like storm surge were to push the oil plume onto land, we would be looking at possible oil contamination of all of the affected land areas.  Imagine parking your car in your house and opening the oil pan drain plug, letting oil leak onto the floors and out onto your driveway, lawn, and streets.  Now do that for every car and home along the Gulf Coast that could be impacted by storm surge where the oil plume is close to shore.

This has to be keeping people at EPA and the Gulf Coast up at night.   It could be an environmental pollution disaster the likes of which we have never seen—Marshes, swamps, white-sand beaches, and coastal/vacation communities becoming a giant, oil-soaked, polluted brownfield.

One would think that witnessing this kind of unprecedented environmental disaster, and the potential for worse with the impending hurricane season, would help make the case for the transition to clean energy.  Indeed, this week we have seen the oil spill mentioned by President Obama and some members of Congress as motivation for a long-term energy strategy.

Don’t hold your breath.

Even these events—as bad as they appear in real life— can be externalized from the day-to-day lives of most people in unaffected areas.  Maybe that will change as this spill gets worse and we face the possibility of oil release for another few months, but right now, there is simply not enough outrage from the public demanding change in Washington, as Bob Herbert alluded to last week.  And John Kerry is right, halting drilling on the Gulf Coast isn’t going to happen.

So where does all this leave us in terms of climate change, energy, and oil spills?

I’m pretty pessimistic these days.  I’m not sure if anything short of a severe economic energy shock that hits ordinary people hard—similar to what we saw in 2006-2007—will bring us to a tipping point.  If the U.S. returns to $4-5/gallon gasoline and home heating oil, we will start seeing environmentalists, security hawks, the energy independence crowd, green jobs advocates, and everyday citizens realign once again.  Only then will there be a coalition large and loud enough to force Washington take on the political-economic might of the fossil fuel industry and their lobbyists.

If my guess is right, then we are probably still a few years away from seeing a serious move to clean energy—not until the economic recovery is further along, economies pick up speed, and the demand for oil and oil speculation kick back into high gear, causing oil prices to spike once more.  Fortunately, this time around—unlike 2006-2007—we will have better technology, including electric cars, which will help make the leap easier and more sustained (provided that people can afford them).

The Gulf Coast is unfortunately poised to become collateral damage as we wait for more significant economic drivers to make the clean energy transition happen.

I’m lucky to have had the chance to travel along the coast from New Orleans to Tampa in the spring of 2005 before Katrina hit and now this oil spill happened.  It’s a beautiful region.  For our friends and all of the wildlife living there, let’s just hope this is a mild hurricane season and that most of the oil stays in the deep sea where it will hopefully get removed by hungry bacteria.

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Photo credit: http://www.flickr.com/photos/joiseyshowaa/2392156164/

Bob Herbert’s column in today’s Times forces us to look in the mirror not only with regards to the Gulf oil spill but to the political-economic foundation of social and environmental problems in general:

The response of the Obama administration and the general public to this latest outrage at the hands of a giant, politically connected corporation has been embarrassingly tepid. We take our whippings in stride in this country. We behave as though there is nothing we can do about it.

The fact that 11 human beings were killed in the Deepwater Horizon explosion (their bodies never found) has become, at best, an afterthought. BP counts its profits in the billions, and, therefore, it’s important. The 11 men working on the rig were no more important in the current American scheme of things than the oystermen losing their livelihoods along the gulf, or the wildlife doomed to die in an environment fouled by BP’s oil, or the waters that will be left unfit for ordinary families to swim and boat in.

This is the bitter reality of the American present, a period in which big business has cemented an unholy alliance with big government against the interests of ordinary Americans, who, of course, are the great majority of Americans. The great majority of Americans no longer matter.

No one knows how much of BP’s runaway oil will contaminate the gulf coast’s marshes and lakes and bayous and canals, destroying wildlife and fauna — and ruining the hopes and dreams of countless human families. What is known is that whatever oil gets in will be next to impossible to get out. It gets into the soil and the water and the plant life and can’t be scraped off the way you might be able to scrape the oil off of a beach.

It permeates and undermines the ecosystem in much the same way that big corporations have permeated and undermined our political system, with similarly devastating results.

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Photo Credit: http://www.flickr.com/photos/chrisjman/3338514389/

European bee populations are on the decline worldwide.   Who cares?  These bees are major pollinators of crops and therefore perform, for free, a vital ecological service worth about $U.S. 14 billion per year.  Not to mention the many other species of non-crop flowering plants that reproduce with the help of insects like this.

The recent kind of decline is specific—only female worker bees disappear—and has been given the name colony collapse disorder (CCD).  Nobody has figured out why this is happening.  The potential list of culprits includes mites, viruses, synthetic chemicals, and other factors.

In an article this week in PLoS ONE, Christopher Mullin and colleagues explore further the potential link between pesticides and CCD.¹

Excerpts:

One third of honey bee colonies in the US were lost during each of the last three winters between ’06-’09. This alarming overwinter along with other losses of this primary pollinator, Apis mellifera L., as well as those of native pollinators, has been documented in North America and Europe. The most recent manifestation of this decline, Colony Collapse Disorder (CCD), has led to a significant collaborative effort involving several land grant universities, Departments of Agriculture and the USDA.

We have found 121 different pesticides and metabolites within 887 wax, pollen, bee and associated hive samples. Almost 60% of the 259 wax and 350 pollen samples contained at least one systemic pesticide, and over 47% had both in-hive acaricides fluvalinate and coumaphos, and chlorothalonil, a widely-used fungicide. In bee pollen were found chlorothalonil at levels up to 99 ppm and the insecticides aldicarb, carbaryl, chlorpyrifos and imidacloprid, fungicides boscalid, captan and myclobutanil, and herbicide pendimethalin at 1 ppm levels. Almost all comb and foundation wax samples (98%) were contaminated with up to 204 and 94 ppm, respectively, of fluvalinate and coumaphos, and lower amounts of amitraz degradates and chlorothalonil, with an average of 6 pesticide detections per sample and a high of 39. There were fewer pesticides found in adults and brood except for those linked with bee kills by permethrin (20 ppm) and fipronil (3.1 ppm).

The 98 pesticides and metabolites detected in mixtures up to 214 ppm in bee pollen alone represents a remarkably high level for toxicants in the brood and adult food of this primary pollinator. This represents over half of the maximum individual pesticide incidences ever reported for apiaries. While exposure to many of these neurotoxicants elicits acute and sublethal reductions in honey bee fitness, the effects of these materials in combinations and their direct association with CCD or declining bee health remains to be determined.

The high frequency of multiple pesticides in bee collected pollen and wax indicates that pesticide interactions need thorough investigation before their roles in decreasing bee health can be either supported or refuted. The large number of studies to date, are limited by being done on mostly one compound at a time, as well as using whole colonies where the timing of contaminated pollen intake and its utilization by the colony are difficult to interpret as a causal relationship. Laboratory studies have clearly indicated sublethal impacts on honey bee learning, immune system functioning, and synergism of insecticide toxicity by fungicides, yet combinations of herbicides with fungicides and insecticides in 3 or more component mixtures have not been studied.

The widespread occurrence of multiple residues, some at toxic levels for single compounds, and the lack of any scientific literature on the biological consequences of combinations of pesticides, argues strongly for urgent changes in regulatory policies regarding pesticide registration and monitoring procedures as they relate to pollinator safety. This further calls for emergency funding to address the myriad holes in our scientific understanding of pesticide consequences for pollinators. The relegation of bee toxicity for registered compounds to impact only label warnings, and the underestimation of systemic pesticide hazards to bees in the registration process may well have contributed to widespread pesticide contamination of pollen, the primary food source of our major pollinator. Is risking the $14 billion contribution of pollinators to our food system really worth lack of action?

¹Christopher A. Mullin, Maryann Frazier, James L. Frazier, Sara Ashcraft, Roger Simonds, Dennis vanEngelsdorp, Jeffery S. Pettis (2010). High Levels of Miticides and Agrochemicals in North American Apiaries: Implications for Honey Bee Health PLoS ONE

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Photo Credit:  http://www.flickr.com/photos/viamoi/ / CC BY-NC-ND 2.0

How do you turn a male frog into a female frog that breeds with other male frogs?   Expose them to herbicides that are routinely sprayed on agricultural fields worldwide.

Last year, Tyrone Hayes from UC Berkeley gave a talk at Bowdoin about his career’s work studying the impacts of endocrine-disrupting chemicals on amphibian development.

This week’s Early Edition of the Proceedings of the National Academy of Sciences features some of this research.¹

Excerpts:

Atrazine is one of the most widely used pesticides in the world. Approximately 80 million pounds are applied annually in the United States alone, and atrazine is the most common pesticide contaminant of ground and surface water. Atrazine can be transported more than 1,000 km from the point of application via rainfall and, as a result, contaminates otherwise pristine habitats, even in remote areas where it is not used.  In fact, more than a half million pounds of atrazine are precipitated in rainfall each year in the United States.

In addition to its persistence, mobility, and widespread contamination of water, atrazine is also a concern because several studies have shown that atrazine is a potent endocrine disruptor active in the ppb (parts per billion) range in fish, amphibians, reptiles, and human cell lines, and at higher doses (ppm) in reptiles, birds, and laboratory rodents. Atrazine seems to be most potent in amphibians, where it is active at levels as low as 0.1 ppb.  Although a few studies suggest that atrazine has no effect on amphibians under certain laboratory conditions, in other studies, atrazine reduces testicular volume; reduces germ cell and Sertoli cell numbers; induces hermaphroditism; reduces testosterone; and induces testicular oogenesis. Furthermore, atrazine contamination is associated with demasculinization and feminization of amphibians in agricultural areas where atrazine is used and directly correlated with atrazine contamination in the wild.

Using an experiment where his team exposed frogs to a 2.5 parts per billion atrizine solution, here’s what they found:

Atrazine-exposed males were both demasculinized (chemically castrated) and completely feminized as adults. Ten percent of the exposed genetic males developed into functional females that copulated with unexposed males and produced viable eggs. Atrazine exposed males suffered from depressed testosterone, decreased breeding gland size, demasculinized/feminized laryngeal development, suppressed mating behavior, reduced spermatogenesis, and decreased fertility. These data are consistent with effects of atrazine observed in other vertebrate classes. The present findings exemplify the role that atrazine and other endocrine-disrupting pesticides likely play in global amphibian declines.

The main implication of this chemically induced sex switching is that it has the potential to disrupt breeding and contribute to the amphibian declines observed worldwide:

Although many studies have focused on death from disease and its role in global amphibian declines and sudden enigmatic disappearances of populations, virtually no attention has been paid to the slow gradual loss of amphibian populations due to failed recruitment. The present study suggests several ways that exposure to endocrine disruptors such as atrazine may lead to population level effects in the wild and contribute to amphibian declines. Certainly, the inability to compete for females and the significant decline in fertility in exposed males, as reported in the present study, will have a direct impact on exposed populations.

¹Hayes, T. et al (2010) Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis). Proceedings of the National Academy of Sciences. doi:10.1073/pnas.0909519107

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Photo credit:  http://www.flickr.com/photos/arte/ / CC BY-NC 2.0

The Guardian is running a story by Juliette Jowit suggesting that the total cost of externalities for the 3,000 largest companies in the world could be as much as $US 2.2 trillion in 2008.  As the story points out, that’s a lot:

• more than the economies of all but 7 nations
• about one third the value of the profits of these companies

Excerpts (links by Jowit):

Later this year, another huge UN study – dubbed the “Stern for nature” after the influential report on the economics of climate change by Sir Nicholas Stern – will attempt to put a price on such global environmental damage, and suggest ways to prevent it. The report, led by economist Pavan Sukhdev, is likely to argue for abolition of billions of dollars of subsidies to harmful industries like agriculture, energy and transport, tougher regulations and more taxes on companies that cause the damage.

“What we’re talking about is a completely new paradigm,” said Richard Mattison, Trucost’s chief operating officer and leader of the report team. “Externalities of this scale and nature pose a major risk to the global economy and markets are not fully aware of these risks, nor do they know how to deal with them.”

“It’s going to be a significant proportion of a lot of companies’ profit margins,” Mattison told the Guardian. “Whether they actually have to pay for these costs will be determined by the appetite for policy makers to enforce the ‘polluter pays’ principle. We should be seeking ways to fix the system, rather than waiting for the economy to adapt. Continued inefficient use of natural resources will cause significant impacts on [national economies] overall, and a massive problem for governments to fix.”

Another major concern is the risk that companies simply run out of resources they need to operate, said Andrea Moffat, of the US-based investor lobby group Ceres, whose members include more than 80 funds with assets worth more than US$8tn. An example was the estimated loss of 20,000 jobs and $1bn last year for agricultural companies because of water shortages in California, said Moffat.

The field of nanotechnology is exploding, and many materials, such as titanium (Ti), are being shrunk and used in consumer products like sun tan lotions, cosmetics, and toothpaste.

It has been traditionally thought that inert materials like Ti won’t cause health issues because they don’t react with molecules in our cells.  New research from UCLA’s Jonsson Comprehensive Cancer Center published in Cancer Research suggests that this conventional wisdom may be flawed.

Ti appears to migrate throughout the body, causing DNA/chromosome breakage and inflammation (both of which are linked to cancer) and oxidative stress causing cell death.  Rather than chemically reacting with molecules in cells, the high surface area of the tiny particles appears to cause cell molecules to change.

The manufacture of TiO2 nanoparticles is a huge industry, Schiestl said, with production at about two million tons per year. In addition to paint, cosmetics, sunscreen and vitamins, the nanoparticles can be found in toothpaste, food colorants, nutritional supplements and hundreds of other personal care products.

Once in the system, the TiO2 nanoparticles accumulate in different organs because the body has no way to eliminate them. And because they are so small, they can go everywhere in the body, even through cells, and may interfere with sub-cellular mechanisms.

Photo credit:  http://www.flickr.com/photos/29487767@N02/ / CC BY-NC-SA 2.0

Every day, we are exposed to a cocktail of synthetic chemicals from consumer products.  How harmful are these?  In an earlier post, I described how risk analysis is an important scientific process for determining exposure, effects, and overall risk of these chemicals.

One thing missing from these analyses is how people respond to information about their chemical exposure.  In a recent issue¹ of the Journal of Health and Social Behavior, Rebecca Altman and colleagues addressed this by analyzing what they call the “exposure experience” of women in Cape Cod, MA—an area with elevated breast cancer rates.

What did they find?

As part of a larger analysis (Silent Spring Institute’s Household Exposure Study), they measured 120 homes for 89 chemicals that could affect hormones.  They also measured blood and urine concentrations in a sample of female residents.

They found that after receiving the chemical concentration data about their homes, participants concluded one or more of the following statements:

• Synthetic chemicals can be detected in household air and dust, and in human samples such as urine (e.g., “There’s chemicals everywhere in this place!”)
• Most homes have chemicals.
• Homes contain a variety of different chemical compounds.
• Even banned substances, such as the pesticide DDT, were detected.
• There are numerous sources for chemicals found in urine, blood, and household air and dust.
• Many common, household sources of chemical exposures are unregulated or understudied.

The response of many of the women included follow-up questions like

• Do these results signal a problem?
• What is “acceptable”?
• Where are these chemicals coming from?
• And, what should I do?

Altman and colleagues argued

In response to these circumstances, study participants reached out to others. As indicated in the previous excerpt, participants contacted the scientists, but they also queried friends and family (e.g., a friend with cancer, a daughter with a medical degree, or a son with scientific training). They shared study results with their physicians or oncologists. Some participants consulted Internet resources or local libraries. One participant copied the results for her landscaper, who had applied pesticides to her lawn and garden. Yet, as these participants reported, their friends and contacts—including their physicians—had few new insights to offer. Left unresolved were lingering questions: Participants’ narratives reflected puzzlement over how to interpret levels and make appropriate responses.

The research team noted that the participants were surprised by the number of chemicals detected in air and dust, and they weren’t sure where they could come from because the women perceived themselves using few chemicals.  It turns out, as Altman’s team discovered, they were actually using several products containing these chemical, illustrating the disconnect between consumer culture an its associated chemical exposure risks.

Another trend:  One of the first reactions of the participants was to attribute chemical levels to historical uses in the home, often citing the age of the home.  But, again, this reflects the tendency to look for explanations beyond current consumption patterns.

They also found that participants may have underestimated the threat of chemical concentrations in their homes.  When examining a graph showing the chemical concentrations in their home relative to all other participants’ homes and the EPA guideline level, many participants shrugged off their results as “average” when their home fell in the middle of the data values even when all of the data were above the EPA safety guideline.  As Altman noted,

[f]or most participants, this perception of “average-ness” allayed concerns of health risk.

When the participants were concerned about the levels of chemicals in their homes, Altman argued that they sometimes fell victim to bad mental models of what to do:

• technological fallacy—that it’s simply a matter of cleaning them up
• consumption fallacy—that it’s simply a matter of switching products, when in reality (1) it’s often not clear how to do this, (2) there may be no good alternatives for certain products, or (3) switching may do no good.   When one woman learned that she had pesticides in her urine, despite eliminating them from her home and eating organically, she was understandably shocked:
  It was overwhelming to know how many chemicals they found in my house, especially like I’ve already said, I’ve made really conscious efforts to eliminate so many things [pesticides]—my lawn, everything on the food that I eat. I have a water filtration system that cost me a thousand dollars to, you know, to purify my water. I’ve made so many, many little things like that … and to know that even so many years after my diagnosis, to know that I’m still being exposed. It’s overwhelming.

Interestingly, when confronted with the notion that chemical levels remained high even after efforts to reduce them, several of the participants began controlling them symbolically, for example, by dissociating pesticides sprayed in the neighborhood with those found in their homes or bodies.

Bottom line:

One of the conclusions that Altman draws is that scientists conducting risk analyses need to think about the context/starting assumptions that people have regarding scientific exposure data.  Specifically, it’s not enough for scientists to think about how to present uncertainty in the data; they also need to understand the “unique social and historical setting” in which the data are interpreted.

These stories make a compelling case that sociologists are (should be) an important part of the risk analysis process.

Related post: Do our daily routines put our health at risk?

¹Altman, R. (2008) Pollution comes home and gets personal: Women’s experience of household chemical exposure. Journal of Health and Social Behavior 49(4): 417-435.

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Photo credit:  http://www.flickr.com/photos/tzofia/ / CC BY-NC-ND 2.0