Pet Coke: Breakfast of Champions?

10373257433_2e008cabf6_o

Pet coke piles in Chicago as of 10/19/13 by Josh Mogerman, used via Creative Commons license

This morning NPR informed me that petroleum coke and the Koch brothers have struck again – this time in my hometown of Chicago.

Petroleum coke, adorably nicknamed pet coke, made headlines this past summer when it was improperly stored by Koch Carbon and billowed into homes and neighborhoods in Detroit, where I currently live.

But wait. That’s a lie. I live just outside of Detroit in a wealthier suburb, just as I grew up outside of Chicago in a tree-lined college town. That makes a big difference. No one would dream of dumping three-story-high piles of industrial soot in my current backyard or the one I played in as a child. Those neighborhoods are simply too wealthy, too powerful, too ready and willing to sue.

Communities near the pet coke storage sites in both Detroit and Chicago are hurting financially. We all know about the struggles of bankrupt Detroit, where it takes about an hour for emergency workers to respond to the direst 911 calls. Southeast Chicago, once an industrial hub, has faced many of the same challenges as Detroit. This year, both areas became dumping grounds for increasing quantities of pet coke (in some cases, without a permit).

That increase in pet coke is due to ramped-up tar sands drilling in Canada. Pet coke is a product of the tar sands refining process. Although it is too sooty to be used for energy here in the United States, countries like Mexico and China will buy it to use as fuel. That means neighborhoods like South Deering in Chicago wind up serving as holding stations for pet coke while companies sell it internationally and arrange for its transport. But this pet coke sits and waits in open-air piles. Strong gusts of wind cause black plumes of dust that travel into neighborhoods and homes.

View of a pet coke plume from the Detroit piles on 7/27/13, via 3860remerson on YouTube

The residents of these neighborhoods have found black dust coating their floors, countertops, and even food. They describe it getting into their eyes, mouths, and lungs. I find these exposures alarming. But Laurie C. McCausland, who represents the Koch brothers’ interests as the deputy general counsel for Koch Companies Public Sector, thinks that’s silly. According to WBEZ, Chicago’s NPR affiliate, McCausland says that overall pet coke is safe. WBEZ quotes her as follows:

“It’s unfair for people to be overly scared about this product. I think people just don’t have a lot of information.”

In a letter to the editor of the Chicago Tribune, Jim Watson, the Executive Director of the Illinois Petroleum Council, expressed a similar sentiment. He wrote:

“Extensive testing has revealed that petcoke has no observed carcinogenic, reproductive, or developmental effects in humans and a low potential to cause adverse effects on aquatic or terrestrial environments.”

I was curious if these statements were true. Has pet coke been extensively studied? And is the health concern surrounding pet coke just an instance of misinformed scaremongering like the anti-vaccination movement? I headed over to PubMed, the U.S. government’s comprehensive catalog of scholarly papers in science, health, and medicine. I searched for “petroleum coke” and got 56 results. Most of these papers had to do with 1) nifty chemical reactions you can do with pet coke, 2) how pet coke affects aquatic life, and 3) the health of people who make pet coke react with other potentially hazardous compounds for a living. I came across only three titles that appeared to be specific and relevant: one that assessed correlations between pet coke exposure and lung cancer in petroleum workers and two that tested the effects of pet coke exposure in mammalian animal models.

The most recent was published in the International Journal of Toxicology this year. The authors include representatives from ExxonMobil (first author), the American Petroleum Institute, and Shell (last author). From what I can tell, the remaining authors work for contract research laboratories (as in, paid by the oil companies). Another paper was published in Occupational & Environmental Medicine in 2012 by authors at ExxonMobil (first author) and Imperial Oil, although this study at least included collaborators from actual universities including McGill (last author). A third paper, published in 1987 in the American Journal of Industrial Medicine, was penned by representatives of Standard Oil, the American Petroleum Institute (last author), and two contract laboratory companies (first author). Not surprisingly, none of these papers conclude that pet coke is especially hazardous.

Even if I missed one (or even ten!) relevant articles in my search, I think it’s safe to say that the research is anything but “extensive.”  I haven’t yet combed through the three papers, nor am I the best person to evaluate their methods. Still, I do think it’s proper to question their impartiality and recommend that they be scrutinized by unbiased experts. We should also wonder if we are getting an accurate representation of such industry-funded research. When corporations and labs-for-hire come up with results they don’t like, they don’t have to (and often don’t) publish them. Yet when corporations do get a result that they like (for whatever reason, including a lack of statistical power), they are happy to publish it and thrust it into the hands of publicists and legal representatives like Ms. McCausland who tell us not to be silly; pet coke’s perfectly safe. That bias alone throws off a fair evaluation of the issue.

Residents of Southeastern Chicago on the pet coke,  via NRDCflix on YouTube

Modern (and ancient) history play like a broken record of chemicals, compounds, and practices that were harmless until suddenly they weren’t. Shoe stores once had x-ray machines so you could see how well your shoes fit – or just stare at your wiggling toe bones. We’ve seen the rise and fall of leaded paint and gasoline, asbestos, and thalidomide and now we’re learning about the dangers of plastics in our baby bottles and flame retardants in our cushions. There’s plenty of reason to suspect that pet coke exposure is no day at the health spa. Inhaled particulates irritate the airways and can, at the very least, exacerbate asthma and other respiratory illnesses. Analysis of the Detroit pet coke dust showed that it also contained the toxic elements vanadium and selenium, although it’s not clear whether residents were exposed at high enough levels to cause ill effects. (While we actually require trace amounts of selenium,  further exposure is toxic.)

It seems to me that we need more information. We need impartial toxicologists, epidemiologists, and other specialists to pore over the papers published on the topic and start conducting unbiased experiments of their own. And while we wait, we need to protect the residents who live in the shadow of pet coke. Pet coke piles should be enclosed so that the dust can’t escape into communities, schools, and homes.

I find myself wondering how much faith people like Laurie McCausland, Jim Watson, and Charles Koch truly put in those industry-funded studies on pet coke. Would they be willing to move their families into a community coated with pet coke? Or is it only safe enough for those families who can’t afford to live elsewhere?

Between permit oversights and unlawful air pollution, the Koch brothers’ companies may already have broken the law. But if they are putting vulnerable people’s health and well being at risk to make a buck? Well that truly is criminal.
______

Schnatter AR, Nicolich MJ, Lewis RJ, Thompson FL, Dineen HK, Drummond I, Dahlman D, Katz AM, & Thériault G (2012). Lung cancer incidence in Canadian petroleum workers. Occupational and environmental medicine, 69 (12), 877-82 PMID: 23077208

McKee RH, Herron D, Beatty P, Podhasky P, Hoffman GM, Swigert J, Lee C, & Wong D (2013). Toxicological Assessment of Green Petroleum Coke. International journal of toxicology PMID: 24179031

Plastic and the Developing Brain

7921839158_7ed88d6e80_o

When I was pregnant with my daughter, I had enough on my mind. I didn’t have much time to think much about plastic. I knew vaguely that plastics can release estrogen-mimicking substances like bisphenol A (BPA) into our food and I’d heard that they might cause genital defects in male fetuses. But once my husband and I had the 20-week ultrasound and knew we were having a girl, I thought I could stop searching for products in cardboard or glass. It was just too hard. Everything is packaged in plastic these days.

Apparently I jumped the gun.

Scientific papers warning about the hazards of prenatal exposure to BPA have been coming out in a steady stream, with a string of particularly damning ones appearing over the last 18 months in the Proceedings of the National Academy of Sciences. Last month one in particular caught my eye: a study of how prenatal BPA exposure changes the brain. The results were enough to make this neuroscientist pause.

While we tend to think of estrogens as the sex hormones that manage ovulation and pregnancy, these molecules also have powerful and direct effects on the brain. Many types of neurons have estrogen receptors on their outer surface. While there are several kinds of estrogen receptors in the brain, all bind to estrogens (and other molecules that resemble estrogens) and all trigger changes within their neurons as a result. These small changes can potentially add up to alter how entire neural circuits function. In fact, estrogens influence a wide range of skills and behaviors – from cognitive function to mood regulation and even fine motor control. While we don’t yet know why estrogens have such a broad and powerful influence on the brain, it does appear that we should think twice before mucking around with estrogen levels, particularly in the developing brain.

BPA and other compounds found in plastics resemble estrogens. The similarity is close enough to fool estrogen receptors, which bind to these foreign molecules and interpret them as additional estrogen. Although BPA has been used commercially as a dental sealant and liner for food containers (among many other uses) since the 1960s, the health consequences of this case of mistaken identity are just beginning to be understood.

In the PNAS paper published last month, a group of scientists headed by Dr. Frances Champagne at Columbia report the effect of prenatal BPA exposure on mice. They fed pregnant laboratory mice one of three daily doses of BPA (2, 20, or 200 μg/kg) or a control product without BPA. These are not high doses of BPA. Based on the amount of BPA found in humans, scientists estimate that we are exposed to about 400 μg/kg per day. The U.S. Food and Drug Administration reached their own estimate by testing the amount of BPA in various foods and then approximating how much of these people consume daily. Their calculations put the figure at around 0.19 μg/kg daily for adults. This discrepancy (400 versus 0.19) is one of many points of contention between the FDA, the packaging industry, and the scientific community on the subject of BPA.

Champagne and her colleagues fed their mice BPA on each of the twenty days of mouse gestation. (That’s right, ladies: mouse pregnancies last less than three weeks.) After each mouse pup was born, the scientists either studied its behavior or sacrificed it and examined its brain.

What did they find? Prenatal BPA exposure had a noticeable impact on mouse brains, even at the lowest dose. They found BPA-induced changes in the number of new estrogen receptors being made in all three brain areas they examined: the prefrontal cortex, hypothalamus, and hippocampus. These effects were complex and differed depending on the gender of the animal, the brain area, the BPA dose, and the type of estrogen receptor. Still, in several cases the researchers found a surprising pattern. Without BPA-exposure, female mice typically made more new estrogen receptors than their male counterparts. The same was true for mice given the highest BPA dose. But among pups exposed to the two lowest BPA doses, male mice made more estrogen receptors than females! This sex-difference reversal stemmed from changes in both genders; male mice made more estrogen receptors than normal at these doses while female mice made fewer than their norm.

Champagne and colleagues also observed and recorded several behaviors of the mice in different circumstances. For most behaviors, males and females were naturally different from one another.  Just as human boys tend to chase each other more than girls do, male mouse pups chased more than females. Unexposed male mice sniffed a new mouse more than unexposed females did. They showed more anxiety-like behavior in an open space and were less active in their home cages. Prenatal BPA treatment reversed these natural sex differences. Exposed female mice did more sniffing, acted more anxious, and ran around less than their exposed male counterparts. And at the highest prenatal BPA dose, the male mice chased each other as rarely as the females did. In one case, BPA treatment affected the two genders similarly; both sexes were less aggressive than normal at the two lower doses and more aggressive than normal at the highest dose.

Overall, the results of the study are complex and it might be easy to ignore them because they don’t seem to tell a straightforward tale. Yet their findings can be summed up in a single sentence: BPA exposure in utero has diverse effects on the mouse brain and later behavior. Not only does the BPA ingested by the mom manage to affect the growing fetus, but those effects persist beyond the womb and past the end of the exposure to BPA.

Some will dismiss these results because they come from mice. After all, how much do we really resemble mice? Yet studies in monkeys have also found that BPA affects fetal development. And while mice and monkeys excrete BPA differently, they clear it at a similar rate — to each other and to human women. Results from correlational studies in humans also suggest that BPA exposure during development affects mood, anxiety and aggressiveness to varying degrees (depending on the child’s gender).

Still, there’s a lot we don’t know about the relevance of this study for humans. At the end of the day, mice aren’t humans and no one has agreed on how much BPA pregnant women ingest. Moreover, Champagne and colleagues examined only a small subset of the neural markers and behaviors that BPA might affect in mice. Perhaps the changes they describe are the worst of BPA’s effects, or perhaps they are only the tip of the iceberg. We don’t yet know.

What’s the upshot of all this? You may want to err on the side of caution, particularly if you’re pregnant. Avoid plastics when possible. Be aware of other sources of BPA like canned foods (which have plastic liners) and thermal receipts. Do what you can do and then try not to let it stress you out. If you’re pregnant, you already have enough on your mind.

As for my daughter, she seems to be fine despite her plasticized third trimester. While she doesn’t do much sniffing, she does occasionally slap my husband or me in the face. It could be the BPA making her aggressive. I choose to blame it on her sassy genes instead.

__

Photo credit: .imelda on Flickr

ResearchBlogging.org

Kundakovic M, Gudsnuk K, Franks B, Madrid J, Miller RL, Perera FP, & Champagne FA (2013). Sex-specific epigenetic disruption and behavioral changes following low-dose in utero bisphenol A exposure. Proceedings of the National Academy of Sciences of the United States of America, 110 (24), 9956-61 PMID: 23716699

Pb on the Brain

6865041631_7bdcf0cc44_o

I’ve got lead on my mind. Lead the element, not the verb; the toxic metal that used to grace every gas tank and paint can in this grand country of ours. For the most part we’ve stopped spewing lead into our environment, but the lead of prior generations doesn’t go away. It lingers on the walls and windows of older buildings, on floors as dust, and in the soil. These days it lingers in my thoughts as well.

I started worrying about lead when my daughter became a toddler and began putting everything in her mouth. I fretted more when I learned that lead is far more damaging to young children than was previously thought. Even a tiny amount of it can irreversibly harm a child’s developing brain, leading to lower IQs, attention problems and behavioral disorders. You may never even see the culprit; lead can sit around as microscopic dust, waiting to be inhaled or sucked off of an infant’s fingers.

Public health programs use blood lead levels (BLLs) to evaluate the amount of lead in a child’s system and decide whether to take preventative or medical action. In the 1960s, only BLLs above 60 μg/dL were considered toxic in children. That number has been creeping downward ever since. In 1985 the CDC’s stated blood lead level of concern became 25 μg/dL and in 1991 it went down to 10. But last year the CDC moved the cutoff down to 5 μg/dL and got rid of the term “level of concern.” That’s because scientists now believe that any amount of lead is toxic. In fact, it seems as if lead’s neurotoxic effects are most potent at BLLs below 5 μg/dL. In other words, a disproportionately large amount of the brain damage occurs at the lowest doses. Recent studies have shown subtle intellectual impairments in kids with BLLs as low as 2 μg/dL (which is roughly the mean BLL of American preschoolers today). All great reasons for parents to worry about even tiny exposures to lead, no?

Yes. Absolutely. Parents never want to handicap their children, even if only by an IQ point or two. But here’s what’s crazy: nearly every American in their fifties, forties, or late-thirties today would have clocked in well over the current CDC’s cutoff when they were little. The average BLL of American preschoolers in the late ‘70s was 15 μg/dL – and 88% had BLLs greater than 10 μg/dL.

These stats made me wonder if whole generations of Americans are cognitively and behaviorally impaired from lead poisoning as children. Have we been blaming our intellectually underwhelming workforce on a mismanaged education system, cultural complacency, or the rise of television and video games when we should have been blaming a toxic metal element?

I was sure I wasn’t the first person to wonder about the upshot of poisoning generations of Americans. And lo and behold, a quick Google search led me to this brilliant article on Mother Jones from January. The piece chronicles a rise in urban crime that began in the ‘60s and fell off precipitously in the early-to-mid ‘90s nationwide. The author, Kevin Drum, walks readers through very real evidence that lead fumes from leaded gasoline were a major cause of the rise in crime (and that increased regulation restricting lead in gasoline could be credited for the sudden drop off.)

The idea certainly sounds far-fetched: generations of city-dwellers were more prone to violence as adults because they breathed high levels of lead fumes when they were kids. It doesn’t seem possible. But when you put the pieces together it’s hard to imagine any other outcome. We know that children of the ‘50s, ‘60s, and ‘70s had BLLs high enough to cause irreversible IQ deficits and behavioral problems (of which aggression and impulse control are particularly common). Why is it so hard to imagine that more of these children behaved violently when they became adults?

In the end, this terrible human experiment in mass poisoning has left me pondering two particular questions. First, what does it mean for generations of children to be, in a sense, retroactively damaged by lead? At the time, our levels were considered harmless, but now we know better. Does knowing now, at this point, explain anything about recent history and current events? Does it explain the remarkable intransigence of certain politicians or the bellicosity of certain talk show hosts, athletes, or drivers with a road rage problem? Aside from the crime wave, what other sweeping societal trends might be credited to the poisoning of children past? How might history have played out differently if we had all been in our right minds?

Finally, I’ve been thinking a lot about the leads and asbestoses and thalidomides of today. Pesticides? Bisphenol A? Flame retardants? What is my daughter licking off of those toys of hers and how is it going to harm her twenty years down the line? This is not just a question for parents. Think crime waves. Think lost productivity and innovation. Today’s children grow up to be tomorrow’s adults. Someday when we are old and convalescing they’ll take the reigns of our society and drive it heaven-knows-where. That makes child health and safety an issue for us all. We may never even know how much we stand to lose.

_____

Photo credit: Zara Evens

%d bloggers like this: