Painkillers, other drugs found in southern Ontario drinking water

Last Updated: Monday, March 24, 2008 | 3:41 PM ET

CBC News

Traces of painkillers and other drugs can be found in the drinking water of 15 southern Ontario municipalities, a new study reports.

"This work demonstrates the potential of Ontario source waters, particularly river water sources, to contain trace levels of selected pharmaceuticals and personal-care products," says the study led by University of Waterloo biology professor Mark Servos, published in the March issue of the Water Quality Research Journal of Canada.

Researchers looked for eight types of pharmaceuticals — including ibuprofen — and the antibacterial agent triclosan in raw and treated water at 20 drinking-water treatment plants in southern Ontario.

The testing sites are not identified but all are said to be within easy reach of Environment Canada's National Water Research Institute in Burlington.

Scant trace of drugs in treated water

The researchers found that river-water samples taken downstream of sewage outfalls were the most contaminated, while raw water taken from large lakes also had low but detectable levels of several of the drugs. The study said this suggests "that these chemicals are widespread in the environment."

They did not find levels of the drugs in samples from wells.

"Most of the acidic drugs were not detectable in finished waters," the study said. It said that levels of the painkiller Naxproxen and triclosan "were detectable in finished water but were significantly reduced in concentration relative to the raw water."

Servos said the amounts of the drugs found were small, with most compounds reduced to trace or non-detectable levels after passing through water treatment plants.

"Our best scientific judgment right now is that they represent a minimal risk," he told CBC News.

Servos said people dumping medications down the toilet is only part of the problem.

"The majority of the drugs are taken by people and they're basically excreted into the toilet and they end up in the sewage treatment plant," he explained, adding the antibiotics are also leaching into the water from livestock manure.

Treatment plants not designed to remove drugs

He said sewage treatment plants are good at removing things like bacteria, but were never designed to get rid of compounds such as drugs.

He said a number of methods for removing the drugs are being explored, and that UV light, with peroxide, ozone and different kinds of carbon, can help reduce the presence.

Servos said two Ontario companies, in London and Mississauga, are on the verge of developing the technology to remove the drugs.

The study said further research is needed.

"There is a need to complete a more comprehensive assessment of these compounds in source waters and of the factors influencing their treatment and removal from finished drinking water."

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I suggest this NNPP patented development as a possible solution to this drug pollution of our drinking water:

United States Patent	7,300,634
Yaniv , et al.	November 27, 2007

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Photocatalytic process

Abstract

A photocatalytic cleaner for air or water includes a photocatalytic material coating a substrate. An anode, positioned a predetermined distance from the substrate, includes a phosphor that emits ultraviolet light in response to bombardment by electrons from a field emission cathode emitting electrons in response to an electric field. The field emission cathode may be a carbon based field emitter material including incorporating carbon nanotubes.

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Inventors:	Yaniv; Zvi (Austin, TX), Fink; Richard Lee (Austin, TX)
Assignee:	Nano-Proprietary, Inc. (Austin, TX)

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Polluting nanoparticles and CNPs - Questions

Study shows how ultrafine particles in air pollution may cause heart disease

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Nice post. I wonder if this finding hurts the claims of Nanobac?
The questions that come to mind are:
Does Nanobac need to prove that the CNP we are studying are alive?
Doesn't the claim you referenced seem to contradict that the plaque buildup in the arteries is primarily the CNPs which we believe are our living little creatures?
Does our IP cover the possible eradication processes if the nanoparticles are pollution based and not alive as we believe?
Many questions but you seem to be of better overall understanding than I so any answer or opinion would be appreciated. Thanks C

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It IS surprisingly similar!!

Nanoparticles from this recent study seem to cause problems. Are calcifying nanoparticles involved? They do not say the are not - perhaps they have never heard of CNPs!! It would be prudent, IMO, to get both research groups together to analyze ALL their findings and determine EXACTLY what is going on to cause this disease process.

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Air pollution may cause heart disease

By

Rachel Champeau 1/17/2008 1:00:00 PM

Patients prone to heart disease may one day be told by physicians to avoid not only fatty foods and smoking but air pollution too.

A new academic study led by UCLA researchers has revealed that the smallest particles from vehicle emissions may be the most damaging components of air pollution in triggering plaque buildup in the arteries, which can lead to heart attack and stroke. The findings appear in the Jan. 17 online edition of the journal Circulation Research.

The scientists identified a way in which pollutant particles may promote hardening of the arteries — by inactivating the protective qualities of high density lipoprotein (HDL) cholesterol, known as "good" cholesterol.

A multicampus team from UCLA, the University of Southern California, the University of California, Irvine, and Michigan State University contributed to the research, which was led by Dr. Andre Nel, UCLA's chief of nanomedicine. The study was primarily funded by the National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency (EPA).

"It appears that the smallest air pollutant particles, which are the most abundant in an urban environment, are the most toxic," said first author Dr. Jesus Araujo, assistant professor of medicine and director of environmental cardiology at the David Geffen School of Medicine at UCLA. "This is the first study that demonstrates the ability of nano-sized air pollutants to promote atherosclerosis in an animal model."

Nanoparticles are the size of a virus or molecule — less than 0.18 micrometers, or about one-thousandth the size of a human hair. The EPA currently regulates fine particles, which are the next size up, at 2.5 micrometers, but doesn't monitor particles in the nano or ultrafine range. These particles are too small to capture in a filter, so new technology must be developed to track their contribution to adverse health effects.

"We hope our findings offer insight into the impact of nano-sized air pollutant particles and help explore ways for stricter air quality regulatory guidelines," said Nel, principal investigator and a researcher at UCLA's California NanoSystems Institute.

Nel added that the consequences of air pollution on cardiovascular health may be similar to the hazards of secondhand smoke.

Pollution particles emitted by vehicles and other combustion sources contain a high concentration of organic chemicals that could be released deep into the lungs or even spill over into the systemic circulation.

The UCLA research team previously reported that diesel exhaust particles interact with artery-clogging fats in low-density lipoprotein (LDL) cholesterol to activate genes that cause the blood-vessel inflammation that can lead to heart disease.

In the current study, researchers exposed mice with high cholesterol to one of two sizes of air pollutant particles from downtown Los Angeles freeway emissions and compared them with mice that received filtered air that contained very few particles.

The study, conducted over a five-week period, required a complex exposure design that was developed by teams led by Dr. Michael Kleinman, professor of community and environmental medicine at UC Irvine, and Dr. Constantinos Sioutas, professor of civil and environmental engineering at USC.

Researchers found that mice exposed to ultrafine particles exhibited 55 percent greater atherosclerotic-plaque development than animals breathing filtered air and 25 percent greater plaque development than mice exposed to fine-sized particles.

"This suggests that ultrafine particles are the more toxic air pollutants in promoting events leading to cardiovascular disease," Araujo said.

Pollutant particles are coated in chemicals sensitive to free radicals, which cause the cell and tissue damage known as oxidation. Oxidation leads to the inflammation that causes clogged arteries. Samples from polluted air revealed that ultrafine particles have a larger concentration of these chemicals and a larger surface area where these chemicals thrive, compared with larger particles, Sioutas noted.

"Ultrafine particles may deliver a much higher effective dose of injurious components, compared with larger pollutant particles," Nel said.

Scientists also identified a key mechanism behind how these air pollutants are able to affect the atherosclerotic process. Using a test developed by Dr. Mohamad Navab, study co-author and a UCLA professor of medicine, researchers found that exposure to air pollutant particles reduced the anti-inflammatory protective properties of HDL cholesterol.

"HDL normally helps reduce the vascular inflammation that is part of the atherosclerotic process," said Dr. Jake Lusis, study co-author and a UCLA professor of cardiology, human genetics and microbiology, immunology and molecular genetics. "Surprisingly, we found that exposure to air pollutant particles, and especially the ultrafine size, significantly decreased the positive effects of HDL."

To explore if air particle exposure caused oxidative stress throughout the body — which is an early process triggering the inflammation that causes clogged arteries — researchers checked for an increase in genes that would have been activated to combat this inflammatory progression.

"We found greater levels of gene activation in mice exposed to ultrafine particles, compared to the other groups," Lusis said. "Our next step will be to develop a biomarker that could enable physicians to assess the degree of cardiovascular damage caused by air pollutants or measure the level of risk encountered by an exposed person."

Researchers added that previous studies assessing the cardiovascular impact of air pollution have taken place over longer periods of exposure time, such as five to six months. The current study demonstrated that ill effects can occur more quickly, in just five weeks.

"Further study will pinpoint critical chemical and toxic properties of ultrafine particles that may affect humans," Nel said.

The research team included investigators from the fields of nanomedicine, cardiology and genetics. Additional co-authors included Berenice Barajas, Xuping Wang, Brian J. Bennett and Ke Wei Gong of the David Geffen School of Medicine at UCLA, and Jack Harkema from the department of pathobiology and diagnostic investigation at Michigan State University.

Additional grant support was provided by the National Institute of Allergy and Infectious Diseases; the National Heart, Lung and Blood Institute; and the Robert Wood Johnson Foundation.

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