Study finds potential well water contaminants highest near natural gas drilling

Main Category: Water - Air Quality / Agriculture
Also Included In: Public Health
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Study finds potential well water contaminants highest near natural gas drilling

A new study of 100 private water wells in and near the Barnett Shale showed elevated levels of potential contaminants such as arsenic and selenium closest to natural gas extraction sites, according to a team of researchers that was led by UT Arlington associate professor of chemistry and biochemistry Kevin Schug.

The results of the North Texas well study were published online by the journal Environmental Science & Technology. The peer-reviewed paper focuses on the presence of metals such as arsenic, barium, selenium and strontium in water samples. Many of these heavy metals occur naturally at low levels in groundwater, but disturbances from natural gas extraction activities could cause them to occur at elevated levels.

"This study alone can't conclusively identify the exact causes of elevated levels of contaminants in areas near natural gas drilling, but it does provide a powerful argument for continued research," said Brian Fontenot, a UT Arlington graduate with a doctorate in quantitative biology and lead author on the new paper.

He added: "We expect this to be the first of multiple projects that will ultimately help the scientific community, the natural gas industry, and most importantly, the public, understand the effects of natural gas drilling on water quality."

Researchers believe the increased presence of metals could be due to a variety of factors including: industrial accidents such as faulty gas well casings; mechanical vibrations from natural gas drilling activity disturbing particles in neglected water well equipment; or the lowering of water tables through drought or the removal of water used for the hydraulic fracturing process. Any of these scenarios could release dangerous compounds into shallow groundwater.

Researchers gathered samples from private water wells of varying depth within a 13 county area in or near the Barnett Shale in North Texas over four months in the summer and fall of 2011. Ninety-one samples were drawn from what they termed "active extraction areas," or areas that had one or more gas wells within a five kilometer radius. Another nine samples were taken from sites either inside the Barnett Shale and more than 14 kilometers from a natural gas drilling site, or from sites outside the Barnett Shale altogether. The locations of those sites were referred to as "non-active/reference areas" in the study.

Researchers accepted no outside funding to ensure the integrity of the study. They compared the samples to historical data on water wells in these counties from the Texas Water Development Board groundwater database for 1989-1999, prior to the proliferation of natural gas drilling.

In addition to standard water quality tests, the researchers used gas chromatography - mass spectrometry (GC-MS), headspace gas chromatography (HS-GC) and inductively coupled plasma-mass spectrometry (ICP-MS). Many of the tests were conducted in the Shimadzu Center for Advanced Analytical Chemistry on the UT Arlington campus.

"Natural gas drilling is one of the most talked about issues in North Texas and throughout the country. This study was an opportunity for us to use our knowledge of chemistry and statistical analysis to put people's concerns to the test and find out whether they would be backed by scientific data," said Schug, who is also the Shimadzu Distinguished Professor of Analytical Chemistry in the UT Arlington College of Science.

On average, researchers detected the highest levels of these contaminants within 3 kilometers of natural gas wells, including several samples that had arsenic and selenium above levels considered safe by the Environmental Protection Agency. For example, 29 wells that were within the study's active natural gas drilling area exceeded the EPA's Maximum Contaminant Limit of 10 micrograms per liter for arsenic, a potentially dangerous situation.

The areas lying outside of active drilling areas or outside the Barnett Shale did not show the same elevated levels for most of the metals.

Other leaders of the Texas Gas Wells team were Laura Hunt, who conducted her post-doctoral research in biology at UT Arlington, and Zacariah Hildenbrand, who earned his doctorate in biochemistry from the University of Texas at El Paso and performed post-doctoral research at UT Southwestern Medical Center. Hildenbrand is also the founder of Inform Environmental, LLC. Fontenot and Hunt work for the EPA regional office in Dallas, but the study is unaffiliated with the EPA and both received permission to work on this project outside the agency.

Scientists note in the paper that they did not find uniformity among the contamination in the active natural gas drilling areas. In other words, not all gas well sites were associated with higher levels of the metals in well water.

Some of the most notable results were on the following heavy metals:

Arsenic occurs naturally in the region's water and was detected in 99 of the 100 samples. But, the concentrations of arsenic were significantly higher in the active extraction areas compared to non-extraction areas and historical data. The maximum concentration from an extraction area sample was 161 micrograms per liter, or 16 times the EPA safety standard set for drinking water. According to the EPA, people who drink water containing arsenic well in excess of the safety standard for many years "could experience skin damage or problems with their circulatory system, and may have an increased risk of getting cancer." Selenium was found in 10 samples near extraction sites, and all of those samples showed selenium levels were higher than the historical average. Two samples exceeded the standard for selenium set by the EPA. Circulation problems as well as hair or fingernail loss are some possible consequences of long-term exposure to high levels of selenium, according to the EPA. Strontium was also found in almost all the samples, with concentrations significantly higher than historical levels in the areas of active gas extraction. A toxicological profile by the federal government's Agency for Toxic Substances and Disease Registry recommends no more than 4,000 micrograms of strontium per liter in drinking water. Seventeen samples from the active extraction area and one from the non-active areas exceeded that recommended limit. Exposure to high levels of stable strontium can result in impaired bone growth in children, according to the toxic substances agency.

"After we put the word out about the study, we received numerous calls from landowner volunteers and their opinions about the natural gas drilling in their communities varied," Hildenbrand said. "By participating in the study, they were able to get valuable data about their water, whether it be for household or land use.

"Their participation has been incredibly important to this study and has helped us bring to light some of the important environmental questions surrounding this highly contentious issue."

The paper also recommends further research on levels of methanol and ethanol in water wells. Twenty-nine private water wells in the study contained methanol, with the highest concentrations in the active extraction areas. Twelve samples, four of which were from the non-active extraction sites, contained measurable ethanol. Both ethanol and methanol can occur naturally or as a result of industrial contamination. Historical data on methanol and ethanol was not available, researchers said in the paper.

The paper is called "An evaluation of water quality in private drinking water wells near natural gas extraction sites in the Barnett Shale formation." A Just Accepted version is available on the journal website.

Many from the research team are now conducting well water sampling in the Permian Basin region of Texas, establishing a baseline set of data prior to gas well drilling activities there. That baseline will be used for a direct comparison to samples that will be collected during and after upcoming natural gas extraction. The team hopes that these efforts will shed further light on the relationship between natural gas extraction and ground water quality.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our water - air quality / agriculture section for the latest news on this subject.

The paper is called “An evaluation of water quality in private drinking water wells near natural gas extraction sites in the Barnett Shale formation.” A Just Accepted version is available on the journal website.

Other co-authors include: Qinhong “Max” Hu, associate professor of earth and environmental sciences at UT Arlington; Doug D. Carlton Jr., a Ph.D. student in the chemistry and biochemistry department at UT Arlington; Hyppolite Oka, a recent graduate of the environmental and earth sciences master’s program at UT Arlington; Jayme L. Walton, a recent graduate of the biology master’s program at UT Arlington; and Dan Hopkins, of Carrollton-based Geotech Environmental Equipment, Inc.

Alexandria Osorio and Bryan Bjorndal of Assure Controls, Inc. in Vista, Calif., also are co-authors. The team used Assure’s Qwiklite™ system to test for toxicity in well samples and those results are being prepared for a separate publication.

The research published this week is representative of the important work going on at The University of Texas at Arlington, a comprehensive research institution with about 33,800 students and more than 2,200 faculty members in the heart of North Texas.

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Study finds druggable target for pulmonary hypertension

Main Category: Respiratory / Asthma
Also Included In: Hypertension;  Genetics
Article Date: 27 Jul 2013 - 0:00 PDT Current ratings for:
Study finds druggable target for pulmonary hypertension

Columbia University Medical Center (CUMC) scientists have identified new genetic mutations that can cause pulmonary arterial hypertension (PAH), a rare fatal disease characterized by high blood pressure in the lungs. The mutations, found in the gene KCNK3, appear to affect potassium channels in the pulmonary artery, a mechanism not previously linked to the condition. Cell culture studies showed that the mutations' effects could be reversed with a drug compound known as a phospholipase inhibitor. The study was published in the online edition of the New England Journal of Medicine.

"The most exciting thing about our study is not that we've identified a new gene involved in pulmonary hypertension, but that we've found a drug that can 'rescue' some mutations," said co-senior author Wendy K. Chung, MD, PhD, associate professor of pediatrics and medicine at CUMC. "In genetics, it's common to identify a gene that is the source of a disease. However, it's relatively rare to find potential treatments for genetic diseases."

PAH is a progressive disorder characterized by abnormally high blood pressure in the pulmonary artery, which reduces blood flow from the right side of the heart to the lungs. The heart can compensate by pumping harder, but over time this can weaken the heart muscle and lead to right-sided heart failure. Common symptoms of PAH include shortness of breath, dizziness, and fainting. About 1,000 new cases are diagnosed in the United States each year. The disorder is twice as common in females as in males. There is no cure for PAH and few effective treatments. Most patients with PAH die within 5-7 years of diagnosis.

Some cases of PAH are caused by inherited genetic defects. Most of these "familial" cases have been linked to mutations in a gene called BMPR2 (bone morphogenetic protein receptor, type II), which was identified simultaneously in 2000 by two independent research teams, one led by the late Robin Barst and Jane Morse, CUMC researchers. However, the majority of cases are idiopathic in origin (of unknown cause). Other forms of PAH can be triggered by autoimmune diseases, congenital heart defects, infections (such as schistosomiasis), and medications (such as the now-banned diet-drug combination commonly known as fen-Phen).

Dr. Chung and her colleagues discovered the new mutations by sequencing the exomes (the portion of the genome that codes information to make proteins) of families with PAH without identified mutations. KCNK3 mutations were found in 3.2 percent of those with familial disease and in 1.3 percent of those with idiopathic PAH.

The team found that the mutations alter the function of potassium channels by reducing the activity of these channels. Potassium channels help maintain the vascular tone of the pulmonary artery and help it respond to low levels of oxygen.

"We were surprised to learn that KCNK3 appears to play a role in the function of potassium channels in the pulmonary artery," said Dr. Chung. "No one had suspected that this mechanism might be associated with PAH." The other gene linked to the disorder, BMPR2, is thought to cause PAH by ultimately promoting growth and multiplication of smooth muscle cells in the pulmonary artery, thereby restricting blood flow.

Dr. Chung also found, working in collaboration with co-senior author, Robert S. Kass, PhD, the Alumni and David Hosack Professor of Pharmacology, chair of the department, and vice dean for research at CUMC, that the effects of the KCNK3 mutations could be reversed with an experimental phospholipase inhibitor called ONO-RS-082. The findings were made in cell cultures. Further study is needed to determine whether treatment with this or other drugs that affect potassium channels might be useful in the treatment of people with PAH, said Dr. Chung.

"KCNK3 mutations are a rare cause of PAH, so I don't want to oversell our findings," said Dr. Chung. "Still, it's exciting that we've found a mechanism that can lead to the disease that is a new, druggable target. It's also possible that targeting KCNK3 may be beneficial for patients who have PAH independent of their KCNK3 genetic status."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our respiratory / asthma section for the latest news on this subject.

The paper is titled, "A Novel Channelopathy in Pulmonary Arterial Hypertension." The other contributors are: Lijiang Ma, Danilo Roman-Campos, Eric D, Mélanie Eyries, Kevin Sampson, Florent Soubrier, Marine Germain, David-Alexandre Trégouët, Alain Borczuk, Erika Berman Rosenzweig, Barbara Girerd, David Montani, Marc Humbert, and James E. Loyd.

The authors declare no financial or other conflicts of interests.

The study was supported by grants from the National Institutes of Health (R01 HL060056, P01 HL072058, K23 HL098743, and R01 HL56810) and by a Vanderbilt Clinical and Translational Science Awards (UL1 RR024975) from the National Center for Research Resources.

Columbia University Medical Center

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Researcher finds way to convert blood cells into autoimmune disease treatment

Main Category: Immune System / Vaccines
Also Included In: Blood / Hematology;  Arthritis / Rheumatology;  Crohn's / IBD
Article Date: 19 Jul 2013 - 2:00 PDT Current ratings for:
Researcher finds way to convert blood cells into autoimmune disease treatment

Cells from one's own blood could be converted into a treatment for autoimmune diseases, like rheumatoid arthritis and Crohn's disease, based on the discovery of a Purdue University researcher.

Chang Kim, a professor of comparative pathobiology, has created a way to direct the differentiation of T-cells, a white blood cell that is a key player in the body's immune system. The method uses naive T-cells, immature cells from which all T-cells develop, and induces them to become suppressive T-cells that block the development of painful inflammation associated with autoimmune diseases.

Naive T-cells can be gathered from a patient's blood, treated and then re-injected, said Kim, who also is a university faculty scholar and member of Purdue's Center for Cancer Research and Weldon School of Biomedical Engineering.

"These cells are being directed to become a type of cell that is already present in our bodies, where a fine balance between inflammatory T-cells and suppressive T-cells is maintained," he said. "We are just tipping the scales in favor of suppressive T-cells to reduce inflammation. Because of this there are none of the toxic side effects associated with many immune-suppressive drugs. In addition, cells from one's own body aren't rejected and remain in the body much longer. Instead of taking a pill every day, this could lead to a treatment administered, for example, every six months."

Autoimmune diseases occur when the immune system attacks one's own body instead of fending off infection from viruses, bacteria and other foreign cells. An overactive immune system sends T-cells to healthy tissue and organs where they cause inflammation and tissue destruction.

Suppressive T-cells migrate to areas of inflammation and suppress the T-cells there without significantly lowering the number of T-cells in other areas of the body where they are needed for proper immune function, Kim said.

"Treatment with suppressive T-cells has the potential to be a much more precise and targeted regulation of immune function than what currently exists," he said. "Treating autoimmune diseases without compromising a patient's immune system has been a big problem in the field. We need to catch the thief without taking down the house, and this has that potential."

Kim discovered that naïve T-cells cultured in the presence of the hormone progesterone can be induced to become suppressive T-cells. This discovery and his work have been detailed in papers in the Journal of Immunology and the European Journal of Immunology. The group also filed a patent based on this work. The national Institutes of Health and the Crohn's and Colitis Foundation of America funded the research.

Studies in mice showed that about 500,000 suppressive T-cells are needed to have an effect on inflammation, Kim said.

"More work needs to be done to determine the appropriate dosage of cells for a human patient, but the amount of blood many people regularly donate would likely yield multiple treatments," he said.

Kim next plans to study at the molecular level how progesterone causes the cells to differentiate into suppressive T-cells and to uncover the proteins and protein receptors involved. An understanding of the molecular regulation of these cells could lead to a way to control their differentiation and function without using progesterone, he said.

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posted by Su Su on 20 Jul 2013 at 6:54 am

How long will this take to get it helping those suffering and on Big Drugs with deadly side effects? I would like to share with Chang Kim what I have learned about RA.

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Animal Study Finds Estrogen Enables Females To Respond Better To Stress

Main Category: Anxiety / Stress
Also Included In: Women's Health / Gynecology;  Psychology / Psychiatry
Article Date: 11 Jul 2013 - 1:00 PDT Current ratings for:
Animal Study Finds Estrogen Enables Females To Respond Better To Stress

The idea that females are more resilient than males in responding to stress is a popular view, and now University at Buffalo researchers have found a scientific explanation. The paper describing their study is published online in the high-impact journal, Molecular Psychiatry.

"We have examined the molecular mechanism underlying gender-specific effects of stress," says senior author Zhen Yan, PhD, a professor in the Department of Physiology and Biophysics in the UB School of Medicine and Biomedical Sciences. "Previous studies have found that females are more resilient to chronic stress and now our research has found the reason why."

The research shows that in rats exposed to repeated episodes of stress, females respond better than males because of the protective effect of estrogen. In the UB study, young female rats exposed to one week of periodic physical restraint stress showed no impairment in their ability to remember and recognize objects they had previously been shown. In contrast, young males exposed to the same stress were impaired in their short-term memory.

An impairment in the ability to correctly remember a familiar object signifies some disturbance in the signaling ability of the glutamate receptor in the prefrontal cortex, the brain region that controls working memory, attention, decision-making, emotion and other high-level "executive" processes.

Last year, Yan and UB colleagues published in Neuron a paper showing that repeated stress results in loss of the glutamate receptor in the prefrontal cortex of young males.

The current paper shows that the glutamate receptor in the prefrontal cortex of stressed females is intact. The findings provide more support for a growing body of research demonstrating that the glutamate receptor is the molecular target of stress, which mediates the stress response. The stressors used in the experiments mimic challenging and stressful, but not dangerous, experiences that humans face, such as those causing frustration and feelings of being under pressure, Yan says.

By manipulating the amount of estrogen produced in the brain, the UB researchers were able to make the males respond to stress more like females and the females respond more like males.

"When estrogen signaling in the brains of females was blocked, stress exhibited detrimental effects on them," explains Yan. "When estrogen signaling was activated in males, the detrimental effects of stress were blocked.

"We still found the protective effect of estrogen in female rats whose ovaries were removed," says Yan. "It suggests that it might be estrogen produced in the brain that protects against the detrimental effects of stress." In the current study, Yan and her colleagues found that the enzyme aromatase, which produces estradiol, an estrogen hormone, in the brain, is responsible for female stress resilience. They found that aromatase levels are significantly higher in the prefrontal cortex of female rats.

"If we could find compounds similar to estrogen that could be administered without causing hormonal side effects, they could prove to be a very effective treatment for stress-related problems in males," she says. She notes that while stress itself is not a psychiatric disorder, it can be a trigger for the development of psychiatric disorders in vulnerable individuals.

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Jing Wei, PhD, postdoctoral associate in the UB Department of Physiology and Biophysics, is first author and Eunice Y. Yuen, PhD, former research assistant professor in the same department, contributed equally. Other co-authors are Xiangning Li, PhD, postdoctoral associate, and Ping Zhong, PhD, research scientist in the same department; Ilia N. Karatsoreos of Washington State University; and Bruce S. McEwen of Rockefeller University.

The research was funded by the National Institute of Mental Health of the National Institutes of Health.

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