Tracking plastics’ breakdown products 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 ISTOCKPHOTO
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, fatloving 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.
Phthalates such as DEHP are used as plasticizers in various products, including intravenous tubing and bags. In addition to studying these compounds, researchers are investigating their breakdown products.
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 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
July 15, 2008 / Environmental Science & Technology ■ 5035
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. 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, women 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.
Interview
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
Lead exposure, brain damage, and adult behavior
ISTOCKPHOTO
Lead is a well-known toxicant for In a parallel study, brain imagat the Johns Hopkins Bloomberg the developing brain, and some ing expert Kim Cecil and her colSchool of Public Health. The eviprevious studies have indirectly leagues scanned the brains of 150 dence is convincing because the suggested a link between lead exof the 250 individuals from the researchers experimentally acposure and violent behavior. Now, original study, between the ages of counted for other potentially two 30-year-long studies by re19 and 24. confounding factors, she adds. searchers at the University of CinThe researchers found a signifiBy recording other factors—like cinnati provide the most direct cant loss in the brain volume of socioeconomic status, maternal links from prenatal and earcare, and a mother’s level ly childhood lead exposure of education and use of to a smaller brain size and drugs and alcohol—and a greater tendency for adult plugging these data into a criminal behavior. The studmultivariable model, the ies were published May 27 in researchers made sure the journal PLoS Medicine. that other variables did Between 1979 and 1984, not muddy the results. developmental psycholoNot only do the results gist Kim Dietrich and his illustrate the risks of lead colleagues recruited pregcontamination in poor, nant women living in leadinner-city neighborhoods, contaminated houses in but they also show the poor, inner-city neighborneed for a revision of safehoods and traced the levels Lead continues to be a problem in poor, inner-city neighbor- ty standards, say Dietrich, hoods, where old and flaking paint often exposes children of lead in their children’s Cecil, and Silbergeld. blood from the womb until to the toxic metal. The U.S. Centers for age six and a half. Disease Control and PreThen the team obtained crimipeople who had higher lead levels vention set the standard for connal records for the same kids, as as children. “What we found was cern at 10 µg/dL. Yet Cecil’s study adults, from when they turned that the frontal lobe was the region showed observable impacts at lev18 until their ages at the end of most affected with volume loss,” els as low as 4.6 µg/dL, she says. October 2005. They found that says Cecil. That is the part of the “There is no safe level,” says Cecil. increased lead levels in blood corbrain that reasons, judges, solves “You’re going to have some form related with higher arrest rates for problems, and controls impulses of injury when you’re exposed to violent crimes. and emotional responses. lead.” Dietrich adds, “We just need A spike in lead levels of 5 micro“This is not your usual study; to prevent exposures to this neurograms per deciliter (µg/dL) at age 6 it’s a very carefully designed toxicant. It’s time to start looking at increased the risk of getting arreststudy,” says Ellen Silbergeld, an this seriously.” ed as an adult by 50%. epidemiologist and lead expert —RHITU CHATTERJEE 5036 ■ Environmental Science & Technology / July 15, 2008
