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Tracking Plastic's Breakdown Products

Researchers examine the metabolites of a popular plasticizer in sewage sludge.

A rapidly growing body of research has raised concerns about the safety of phthalate plasticizers found in polyvinyl chloride (PVC) products, cosmetics, and medical devices. Now, scientists are gaining new insights by looking not just at the parent compounds but at their metabolites as well.

The most widely used plasticizer is DEHP, or di(2-ethylhexyl)phthalate, and millions of tons are produced annually, says Jim Nicell, an environmental engineer at McGill University (Canada). When added to PVC, DEHP lubricates the brittle polymer, providing it with the well-known flexibility that makes it ideal for use in building materials, household furnishings, and medical devices such as intravenous tubes and bags.

Because it is not chemically bound to the plastic polymer, fat-loving DEHP readily migrates out of products and is now ubiquitous in the environment, Nicell says. It has been found in human breast milk, blood, and urine as well as house dust, snow, and sewage sludge. The European Commission has classified DEHP as a priority organic pollutant and in 2006 proposed a water quality standard for DEHP of 1.3 micrograms per liter, Nicell adds. Denmark limits the concentration of DEHP in sludge used in agriculture to 50 milligrams per kilogram (mg/kg) dry weight.

"Environmental fate studies tend to focus on the parent compound, but the unanswered question is, what does it turn into?" Nicell asks. Expecting that DEHP would eventually degrade into CO2 and water, Nicell and his colleagues at McGill were surprised to find that soil microorganisms break down DEHP into metabolites that exhibit acute toxicity in standard tests.

Nicell's new study tracked for the first time the DEHP breakdown products in sewage sludge and found concentrations ranging from 1 to 228 mg/kg. "We don't have a handle on what is the long-term impact associated with exposure to minute concentrations, [when combined with] a whole bunch of other toxins or endocrine disrupters, on the health and reproductive health of organisms," Nicell says.

However, a burgeoning body of work on human exposure to DEHP has sprung up during the past 8 years, notes Russ Hauser, an epidemiologist at Harvard University. Humans oxidize DEHP into a different suite of metabolites compared with those from soil microorganisms, starting with MEHP (mono-ethylhexyl phthalate) and followed by four additional oxidative metabolites.

In an earlier study published in November 2006, Hauser and his colleagues measured the concentration of DEHP metabolites in urine samples collected from men at an infertility clinic and found a positive association of MEHP with DNA damage in sperm. "When we adjusted our statistical models for the oxidative metabolites, we found a strong and consistent signal for MEHP that would otherwise have been missed," Hauser says.

Scientists have been able to establish DEHP and its breakdown products as antiandrogenic in rodents, according to Shanna Swan, an epidemiologist at the University of Rochester. Exposure to DEHP in utero puts a damper on testosterone production in fetal male rats, which leads to undescended testicles, penile deformations, and a shorter anogenital distance.

The National Toxicology Program's Center for the Evaluation of Risks to Human Reproduction concluded (PDF Size: 4.46 MB) in November 2006 that DEHP in medical devices raises serious and significant concerns that normal development of the male reproductive tract in humans could be undermined.

In 2005, Swan and her colleagues looked for and found shortening of anogenital distance in human male infants, similar to that found in exposed rats; the effect was associated with higher exposures to four phthalates but not to DEHP. Swan is repeating the study with a larger sample size and more DEHP metabolites than in the earlier study.

Because of the known reproductive and toxic effects in animals, California has stepped in to regulate DEHP, explains Sam Delson, deputy director for external and legislative affairs at the California EPA. Beginning on January 1, 2009, California regulators will prohibit manufacturers from using DEHP in any toy or child-care article and will prohibit three other phthalates from being used in any toy or child-care article intended for use by children under 3 years of age, if the item can be placed in a child's mouth. The regulation is nearly identical to one finalized in the EU in 2006. The U.S. Congress is close to approving a bill (H.R. 4040) that would establish a federal ban on phthalates in children's toys.

The U.S. Food and Drug Administration (FDA) in 2002 recommended that hospitals use alternatives to DEHP-containing plastics for vulnerable populations such as premature baby boys, mothers pregnant with male fetuses, and boys nearing puberty, says Ted Schettler, science director for the Science and Environmental Health Network, an advocacy organization. To date, FDA has resisted calls from a coalition that includes the American Medical Association (the top advocacy group for doctors) and leading hospitals to require manufacturers to label medical devices that contain DEHP.

Given how much is known about the risks of DEHP from animal data and that we have some understanding of the molecular mechanisms, serious thought must be given to how to reduce human exposure, Hauser says. "Health Care Without Harm [an advocacy group] has a position stating that people shouldn't be exposed to DEHP and that we should be moving away from PVC medical devices to those made out of alternative materials," Schettler adds. —JANET PELLEY