Environmental Factor

June 2011


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Extramural papers of the month

By Jerry Phelps
June 2011

SRP logo Research Brief

Water purifier harnesses nanotechnology

Scientists at the University of Kentucky, with support from the NIEHS Superfund Research Program, have invented a water purifier that degrades chemical toxins without the addition of acids or other harmful chemicals. The device employs nanotechnology to generate hydroxyl radicals and could be used to provide safe, clean drinking water for the developing world and the U.S.

Two-thirds of all hazardous waste sites in the U.S. are contaminated with trichloroethylene (TCE). Along with trichlorophenol, TCE is responsible for drinking water contamination in much of the world. To remove these chemicals from drinking water is costly and requires the use of acids and other hazardous chemicals in large amounts. The Kentucky investigators first mix glucose with contaminated water and then let it pass through a nanostructured membrane embedded with glucose oxidase, an enzyme that produces hydrogen peroxide from glucose. A second membrane containing iron trapped in an acidic matrix converts the peroxide into hydroxyl radicals, which interact with and destroy the organic pollutants.

The investigators are currently filing for patents for the technology. The device could represent a major step forward in providing clean drinking water inexpensively in areas of the world where chemical contamination is prevalent.

Citation: Lewis SR, Datta S, Gui M, Coker EL, Huggins FE, Daunert S, Bachas L, Bhattacharyya D.(http://www.ncbi.nlm.nih.gov/pubmed/21606340) Exit NIEHS 2011. Reactive nanostructured membranes for water purification. Proc Natl Acad Sci U S A 108(21):8577-8582.

Elevated blood levels of flame retardants in Mexican-American children

NIEHS-funded epidemiologists at the University of California Berkeley report that levels of flame retardants are seven times higher in Mexican-American children living in California than children in Mexico. They report that levels of the flame retardant chemicals, polybrominated diphenyl ethers or PBDEs, are higher in these children than almost all other groups of children ever studied.

PBDEs are used in a variety of products, including padding in upholstered furniture, carpet pads, child car seats, mattresses, and clothing. Some of these products have been reported to contain as much as fifty percent of the chemicals by weight and they tend to have long lifespans. PBDEs do not bind chemically to the products they are used in. As the products age and degrade, the chemicals are released in the form of dusts. California has very high anti-flammability standards; these could have inadvertently led to high levels of PBDE-laden dusts in homes.

Prior research suggests that exposure to PBDEs is linked to infertility problems and thyroid hormone imbalances. The levels reported in this study represent a major challenge for California public health officials.

Citation: Eskenazi B, Fenster L, Castorina R, Marks AR, Sjödin A, Rosas LG, Holland N, Guerra AG, López-Carrillo L, Bradman A.(http://ehp03.niehs.nih.gov/article/info:doi/10.1289/ehp.1002874) 2011. A comparison of PBDE serum concentrations in Mexican and Mexican-American children living in California. Environ Health Perspect; doi:10.1289/ehp.1002874; [Online 15 April 2011].

Ah receptor activation delays development of chemical-induced mammary tumors

In a somewhat surprising finding, NIEHS-supported investigators report that exposure to tetrachlorodibenzo-p-dioxin (TCDD) prior to exposure to the known mammary tumor promoter dimethylbenz[a]anthracdene (DMBA), delays the development of breast cancer in mice and produces a lower overall incidence of breast tumors. The researchers conclude that the effect is caused by activation of the Ah receptor by TCDD.

The Ah receptor has been studied extensively because of its role in the toxic effects of dioxin-like compounds. However, recently there have been numerous reports that the receptor is involved in normal development, carcinogenesis, and cell cycle regulation.

Previous work has suggested that exposure to TCDD during pregnancy causes impaired mammary gland growth and development. Normal pregnancy-induced mammary differentiation has been shown to be protective against breast cancer. The investigators' initial hypothesis was that TCDD exposure would make the mice more susceptible to DMBA-induced tumor development.

In both pregnant and non-pregnant mice, TCDD treatment prior to exposure to DMBA caused a four-week delay in tumor formation and a lower tumor incidence throughout the six month study. No markers for tumor initiation differed between TCDD-treated and control mice. These findings suggest that Ah receptor activation causes the delay in tumor formation and could provide an opportunity for possible therapeutic interventions.

Citation: Wang T, Gavin HM, Arlt VM, Lawrence BP, Fenton SE, Medina D, Vorderstrasse BA.(http://www.ncbi.nlm.nih.gov/pubmed/20521247) Exit NIEHS 2011. Aryl hydrocarbon receptor activation during pregnancy, and in adult nulliparous mice, delays the subsequent development of DMBA-induced mammary tumors. Int J Cancer 128(7):1509-1523.

Risk of bladder cancer higher in diabetics

NIEHS Superfund Research Program grantees at Dartmouth Medical School report that a history of diabetes and taking oral medications for diabetes significantly increase a person's risk for developing bladder cancer. These findings are based on a case-control study in New Hampshire including nearly 600 people.

Recent research has demonstrated a link between diabetes and bladder cancer. However, these studies did not consider type or duration of diabetic therapy. The current study found that diabetics were more than twice as likely to develop bladder cancer as matched controls. The association was even stronger in diabetics with a history of the disease of more than 16 years. Their risk was more than 3½ times higher. Diabetics with a history of taking oral hypoglycemic medications were at more than three times greater risk for bladder cancer.

The researchers point out that their study was limited by their inability to differentiate between Type 1 and Type 2 diabetics. They conclude that more research is needed to determine the weighted effects of duration of diabetes and medication type on the risk of bladder cancer.

Citation: MacKenzie T, Zens MS, Ferrara A, Schned A, Karagas MR.(http://www.ncbi.nlm.nih.gov/pubmed/21425156) Exit NIEHS 2011. Diabetes and risk of bladder cancer: Evidence from a case-control study in New England. Cancer 117(7):1552-1556.

(Jerry Phelps is a program analyst in the NIEHS Division of Extramural Research and Training.)



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