Plastic (14 page)

For months, she plowed through thousands of studies about the impacts of pesticides and synthetic chemicals on the Great Lakes wildlife. She expected to see off-the-chart rates of cancer, the classic telltale mark of a toxin. Instead, the reports were filled with weird, eerie accounts of chicks wasting away, cormorants born with missing eyes and crossed bills, male gulls with female cells in their testes, and female gulls nesting together. It seemed "like a hodgepodge of disconnected information," Colborn later recalled in a book she coauthored,
Our Stolen Future.
But she sensed "that something important was lurking beneath the confusing surface."

To try to make sense of the data, she created an electronic spreadsheet, sorting the information by species and health effect. Looking over the array of symptoms—reproductive failures, immune problems, abnormal behaviors—she saw a pattern. Most could be traced to a dysfunction of the endocrine system, the complex network of glands that produce the hormones (such as estrogen, testosterone, thyroid hormone, human growth hormone) that govern growth, development, metabolism, and reproduction. This was a new and potentially profound type of environmental hazard—especially in light of another pattern Colborn was seeing in the data: the adult animals exposed to chemical toxins were mostly fine; the main health problems were in their offspring. Unlike typical toxins, these seemed to be acting as what she called "hand-me-down poisons."

Such transgenerational events weren't unknown. As Colborn was well aware, the drug DES, a powerful synthetic estrogen, had had a similar effect. The drug had been widely prescribed to women in the 1940s and '50s to prevent miscarriages. But years later, the children who had been exposed to the drug in the womb began experiencing a host of health problems. DES daughters had higher than normal rates of breast cancer and an extremely rare vaginal cancer, as well as reduced fertility and other reproductive problems, while DES sons were prone to undescended testicles and hypospadias (when the opening of the penis occurs along the shaft rather than the head).
The DES experience alerted scientists to the potential hazards of synthetic hormones.

But Colborn wasn't investigating a drug designed to mimic a hormone. Moreover, the pesticides and industrial chemicals she was examining had far wider circulation than DES. Her data suggested the frightening possibility that wildlife and people were being exposed to an entirely new kind of risk from widely used chemicals—one that challenged the Paracelsian paradigm that was the core tenet of regulatory testing. The poison wasn't solely in the dose; it could also be in the timing of exposure.

The implications of her hypothesis weighed heavily on Colborn's mind, and after finishing her report, she felt she couldn't just move on to another study. So she organized a meeting
in July 1991 at the Wingspread Conference Center in Racine, Wisconsin, pulling together twenty top researchers from various fields whose work had shaped her assessment and who had the collective expertise to consider her theory. The group members came from a range of disciplines—biology, endocrinology, immunology, toxicology, psychiatry, ecology, and anthropology—that rarely talked to one another. "I was scared to death!" Colborn recalled. "There I was, a brand-new PhD who knew only a handful of wildlife biologists."
But she pushed the group hard, working them from morning till night so they could get to know one another and make connections among their work. At the end of the weekend, the group agreed that, like the proverbial blind men feeling the elephant, each had been describing pieces of the same disturbing trend. They dubbed it "endocrine disruption."
Its hallmarks included three important findings often overlooked by traditional toxicological research: the effects could be transgenerational; they depended on the timing of exposure; and they might become apparent only as the offspring developed.

The first Wingspread conference identified about thirty chemicals as endocrine disrupters.
Today, the number may be anywhere from seventy to a thousand, depending on who is doing the counting. It's difficult to pin down because of the complex effects that result from interference with normal hormonal activity and the many mechanisms by which endocrine disrupters cause trouble.
For instance, by mimicking natural hormones, they can insinuate themselves into special receptors on cells that activate certain genes. Or they can block a natural hormone en route to its destination, preventing it from delivering its chemical message to the cellular receptor.
However many endocrine-disrupting chemicals there are, the ranks include several found in common plastics.

Aside from phthalates, one of the most infamous suspects at the moment is bisphenol A, the primary component of polycarbonate, a hard, clear plastic that's used to make a host of consumer items including baby bottles, compact discs, eyeglass lenses, and water bottles. Bisphenol A is also a basic ingredient of the epoxy resins used to line canned foods and drinks.
Unfortunately, the bonds holding these long molecules together can be weakened fairly easily. Hot water and detergents can loosen the links in the polymer daisy chain, and when that happens, small amounts of bisphenol A can slip free. So each time a polycarbonate bottle is washed, a little bit of BPA is unloosed and is able to leach out.
Scientists have known since the 1930s that bisphenol A acts as a weak estrogen, allowing it at least two possible ways to cause static in the body's normal hormonal conversations: by binding with estrogen receptors on cells and by blocking natural stronger estrogens from communicating with cells.
Either can disrupt how the body uses and produces natural estrogen.

By now hundreds of studies have suggested bisphenol A does just that in animals and humans. Researchers have reported the compound causes health effects in cells and animals that are similar to diseases becoming more common in people, such as breast cancer, heart disease, type 2 diabetes, obesity, and neurobehavioral problems such as hyperactivity.

Bisphenol A research has been hugely controversial, in part because the purported effects seen at very low doses don't show up at higher doses—a complete contradiction of Paracelsus's famous dictum. Yet it makes sense if you view the chemical as a hormone rather than as a typical poison in which the toxic effects increase with the amount of exposure. So said Frederick vom Saal, a reproductive endocrinologist at the University of Missouri, who pioneered much of the research on the molecule.
Hormones are produced in accordance with a finely tuned feedback system that's regulated by a pair of command-and-control glands in the brain, the pituitary and the hypothalamus. If the levels of a hormone get too high or too low, the hypothalamus relays that information to the pituitary, which in turn signals the gland that produces that hormone to gear up or slow down.
Because of that feedback loop, said vom Saal, "sex hormones cause opposite effects at high and low doses. That's what we teach undergraduates. At high doses, they turn off responses that they stimulate at low doses."

In the case of bisphenol A and a few other plastics, the worrisome element is an integral part of the molecular structure. Likewise, some critics consider polystyrene potentially dangerous because it is built from a monomer, styrene, that is a known neurotoxin and a suspected carcinogen, and a few studies have suggested styrene is also capable of migrating out of the polymer chain.

But most of the compounds that have experts worried are additives, chemicals such as phthalates that are blended into base polymers to confer desired properties. If they are only lightly linked to the daisy chains, they are apt to escape from the polymers. The phthalates in PVC, for instance, are drawn to lipids, or fats, and will fairly fly off the polymer chain so they can dissolve in those fatty molecules. Manufacturers rely on a vast assortment of fillers, fluffers, antioxidants, dyes, fire retardants, lubricants, stabilizers, plasticizers, and other additives to fine-tune their plastic products—so many that one reference book on polymer additives runs 656 pages long. So many that plastics additives themselves constitute a nearly thirty-seven-billion-dollar global market.

A few of the chemicals used in plastics—the phthalates found in IV bags; triclosan, an antibacterial found in kitchenware and toys; and the brominated fire retardants widely used in furniture—have already caught the attention of researchers and regulators. But that leaves hundreds, if not thousands, that we know little or nothing about. Witness the recent experience of German researchers who, much to their surprise, found that water bottles made of polyethylene terephthalate (PET) seemed to leach small amounts of one or more unknown compounds that mimic estrogen. "We knew there are plastics that release endocrine disrupters, but we didn't expect [to see that] in PET," study author Martin Wagner told me.
He didn't try to identify the compound causing the effect, but one possibility is antimony, a chemical catalyst used to make PET that has been shown to have estrogenic activity.

Unfortunately, there's no way for consumers to know what chemicals are in the plastic things we buy.
Manufacturers generally aren't required to list the ingredients of their plastic products. Indeed, given the long supply chain from raw polymer to finished product, most likely they don't know what's in the plastic resins they've used. (The resin codes on packaging were designed to aid recycling; they offer limited information, at best.) For the most part, consumers are as clueless as incubator babies about the plastics that surround us, a point that was driven home to me one day when I got a new plastic floor mat from OfficeMax.

It had a faintly chemical odor at the store, but after I left it in the car for a couple of hours while I ran other errands, the smell was overpowering. I pulled out the box and turned it all around, vainly hoping for some indication of what was in the mat. The box said only that it contained a blue chair mat with the helpful added note
chair not included.
It was a good bet the mat was vinyl, but I doubted the smell could be caused by any of the phthalates used in vinyl because, although they off-gas, they are odorless.
If you sniff an IV bag, you won't smell anything. Was the smell something I should be worried about or was it merely annoying? I had no way of knowing. When I later called OfficeMax, the company confirmed the mat was made of vinyl but could offer no more information. Allen Blakey, a spokesman for the Vinyl Institute, suggested the scent was due to inks and sulfides added to the plastic. "Some people love that smell," he said, adding that the odor dissipates after a few days.

I try not to be alarmist about these things, recognizing that my life is rife with more tangible risks. I grew up in a household of smokers and smoked for many years myself. I sometimes talk on my cell phone while driving. My house is prone to mold. I forget to put on sunscreen. After my trip to OfficeMax, I was going to get onto a freeway swimming in diesel particulates and exhaust, not to mention teeming with speeding cars. I considered dumping the floor mat, but then I'd be out thirty-nine dollars. In the end, I decided just to roll down the windows and wait for the wind to carry the smell away.

Many suspected endocrine disrupters interfere with estrogen. However, DEHP, the chemical found in IV bags and tubing, is an antiandrogen, meaning it interferes with testosterone and other masculinizing hormones coursing through the bodies of both men and women. Medical devices may be a significant source of exposure, but most of us come into contact with DEHP through its nonmedical deployment in such vinyl items as shower curtains, wallpaper, venetian blinds, floor tiles, upholstery, garden hoses, swimming-pool liners, rainwear, car upholstery and convertible tops, and the sheathing on cables and wires. It's been found in flip-flops and plastic shoes, modeling clay such as Fimo and Sculpey, yoga mats, cosmetics and nail polish, cleaning products, lubricants, and waxes,
not to mention household dust. But our primary exposure is through fatty foods, such as cheese and oils, which are particularly likely to absorb the chemical, though it is unclear whether that is happening via plastic packaging, the inks used in food wrapping, or during commercial preparation and processing. For instance, DEHP in milk has been traced to the tubing used by dairies.

Such ubiquity means the chemical can get into our systems through almost any route—by inhalation, ingestion, or absorption through the skin. Once the compound enters the bloodstream, it is broken down into smaller molecules, called metabolites. These metabolites are actually the toxic troublemakers. They're small enough to be absorbed by cells, including, most significantly, cells in the pituitary gland. The pituitary is the Leonard Bernstein of the endocrine system, the gland that conducts the complex symphony of hormonal releases by other glands and cells. DEHP takes a seat and promptly behaves like a wayward violin, introducing discordant sounds that clearly don't belong. Among other things, its metabolites stop the pituitary from producing a hormone that directs the testicles to make testosterone. When that occurs during sensitive periods of development, testosterone levels throughout the body can plummet, which in turn can trigger an avalanche of effects—at least in developing animals.

For example, researchers at the Environmental Protection Agency administered DEHP and another common phthalate, DBP, to male rats in utero during the period when sexual differentiation occurs; previous studies had focused on other phases of development. The scientists found that the chemicals caused dramatic changes in the fetuses' reproductive systems.
The pups were more likely to be born with undescended or missing testicles, low testosterone levels, and reduced sperm counts. They also were prone to a shortened distance between the anus and the penis, hypospadias (abnormal opening in the shaft of the penis), and other malformations. The cluster of symptoms was striking enough that the researchers gave it a name: the phthalate syndrome. In further studies, they found that afflicted rats were more likely to suffer impaired fertility and develop testicular tumors later in their lives. Though the effects are most pronounced in males, researchers found that female rat pups could also suffer from DEHP exposure, developing cysts on their ovaries and ceasing ovulation.