Ear To The Ground

Fracking's impacts arise from defective wells

Prior posts have noted studies showing that adverse impacts arising from fracking operations often result from defective wells and waste ponds.  A new study supports prior research with its finding that contamination of drinking water supplies arise from faulty wells.

The researchers used noble gases to trace the path of methane since these inert chemicals are not affected by microbial activity or oxidation.  By measuring the ratios of the noble materials to the methane they were able to accurately determine the distance to the likely source.  The scientists analysed results at 113 wells in the Marcellus shale in Pennsylvania and 20 in the Barnett shale in Texas. They found eight clusters of wells with problems.

The study found that "Gas geochemistry data implicate leaks through annulus cement (four cases), production casings (three cases), and underground well failure (one case) rather than gas migration induced by hydraulic [activities] deep underground."

The report can be found at:  http://www.pnas.org/content/early/2014/09/12/1322107111.

The study supports the implementation of standards and requirements directed and related to well integrity.

BEFORE YOU HIT SEND, CONSIDER -- IGNORANCE IS RISK: IMPACT OF NSA MONITORING TECHNOLOGIES ON ATTORNEY-CLIENT COMMUNICATIONS (PARTS 1&2)

Knew or should have known, a standard often applied in a myriad of legal context, could soon be the one applied to attorneys who ignore the risks associated with communicating with clients using modern technologies (i.e., text messaging, emails, telephone calls, and voice-mail) without appreciating the risk. “Ignorance is Bliss,” is a dangerous proposition in the practice of law when it comes to ignoring current technologies.  What obligations require attorneys to protect their client communications, and what practical steps can be taken to meet statutory and ethical obligations related to confidentiality? Is there a real risk, or is the risk limited to action movies?

Want to read more?  For Part 1, go to:  http://www.lexisnexis.com/legalnewsroom/litigation/b/litigation-blog/archive/2013/07/23/ignorance-is-risk-impact-of-nsa-monitoring-technologies-on-attorney-client-communications-part-1.aspx

For Part 2 go to:  http://www.lexisnexis.com/legalnewsroom/litigation/b/litigation-blog/archive/2013/07/24/ignorance-is-risk-response-options-to-nsa-monitoring-of-attorney-client-communications-part-2.aspx

OEHHA proposes to list "emissions from coal combustion" under California's Proposition 65

OEHHA, the State regulatory agency overseeing the administration of Propositon 65, has announced its intent to list "emissions from the combustion of coal" as a carcinogen.  See http://www.oehha.ca.gov/prop65/CRNR_notices/admin_listing/intent_to_list/noil060713coal.html.  The emissions at issue are both from industrial facilities and residential settings.  According to the American Lung Association, these emissions include acid gases (hydrogen chloride, hydrogen fluoride, Dioxins & Furans (e.g., 2,3,7,8-TCDD), methylmercury, metals (arsenic, beryllium, cadmium, chromium, nickel, selenium, manganese, lead), Polynuclear Aromatic Hydrocarbons (PAH's), radioisotopes (radium, uranium), and volative organic compounds (e.g., benzene, toluene, ethylbenzene, xylene, aldehydes [including formaldehyde]).  See http://www.lung.org/assets/documents/healthy-air/coal-fired-plant-hazards.pdf.

OEHHA is citing to the "authoritative bodies" listing mechanism for the listing.  [For a discussion of Prop. 65 and the various listing mechanisms, see http://www.rmkb.com/tasks/sites/rmkb/assets/image/253.pdf as well as prior posts discussing the mechanism.]  The authoritative body is IARC, as manifest in its 2010 Publication Household Use of Solid Fuels and High Temperature Frying.  See http://apps.who.int/bookorders/anglais/detart1.jsp?sesslan=1&codlan=1&codcol=72&codcch=95, pp. 225, 226, 303, and 307.  The monograph notes that "[t]here is sufficient evidence in experimental animals for the carcinogenicity of emissions from combustion of coal."

OEHHA sent out requests for information relevant to the possible listing on March 26, 2013.  Input was requested by May 14, 2013.  There were no responses. 

OEHHA is providing a second opportunity to provide relevant information on the possible listing.  Comments are due by 5 PM on July 8, 2013.  See http://www.oehha.ca.gov/prop65/CRNR_notices/admin_listing/intent_to_list/noil060713coal.html.

 

Are animal models a good analogy for humans? A recently published study of mice suggests that there may be problems

To set standards, animal models are frequently used.  Such use allows researchers to investigate disease and injury states in ways which would be considered unethical to inflict on humans.  For example, to determine some threshold injury or disease state, various groups of animals may be exposed to widely varying concentrations of the particular molecule being assessed.  It is assumed that because the animal commonly used is a mammal, as are we, that the biochemical and metabolic processes of the two different species have enough in common that useful data will be generated to, say, set standards of some sort (e.g., "no effects" levels, exposures that impact fertility or birth defects or cause cancer) or show the effectiveness of drugs.  But, is such data valid?  Recently published work on mice suggest there may be problems.

The study discussed in this blog grew out of a much larger effort to understand why nearly 150 clinical trials of drugs targeted at sepsis in humans failed.  Sepsis, a potentially deadly reaction that occurs as the body tries to fight an infection, afflicts 750,000 patients a year in the United States, kills one-fourth to one-half of them, and costs the nation $17 billion a year.  It is the leading cause of death in intensive-care units. 

These drugs were developed using mouse models and the drugs were all intended to control excessive immune responses.  Potentially deadly immune responses occur when a person’s immune system overreacts to what it perceives as danger signals, including toxic molecules from bacteria, viruses, fungi, or proteins released from cells damaged by trauma or burns.  Such immune system responses may also play a role in heart disease and cancer. 

The new study indicates that mouse models do not accurately reflect the genetic and proteomic responses to acute inflammatory stress in humans.  As noted, the research grew out of a larger project to characterize human inflammatory response to serious trauma (e.g., burns, car accidents, infection). The project was aimed at studying the multitude of genetic responses that result from these acute inflammatory stimuli in humans to ascertain the key biophysiologic response to such inflammation.  As often happens in science, serendipity intervened.

When reviewers rejected one of the group's papers because it failed to show that events in humans were reproduced in mice, the researchers began to question the relevance of mouse models.  So they decided to compare their data about human responses to that from corresponding murine (rodent) model systems.  The researchers compared changes in the expression of thousands of genes, the time course of those changes (using software designed to normalize the different time frames in which responses occur in mice and humans), and the regulation of major signaling pathways involved.

In humans, the genetic response was highly consistent even though patients were subjected to different inflammatory stimuli and different subsequent treatments, suggesting that the drugs targeting these molecular mechanisms could work for multiple inflammatory diseases. The common patterns seen in humans were not reproduced in mouse models, and the responses among the various mouse models varied widely.  The researchers also compared existing gene expression data from human patients and corresponding mouse models for several acute inflammatory diseases, including sepsis and acute respiratory distress syndrome, as well as response to injury.  Again, mouse models poorly mimicked the response among humans, which were highly consistent.  What was seen was that different conditions in mice — burns, trauma, sepsis — did not engender the same response.  Each condition used different groups of genes. In humans, though, similar genes were used in all three conditions. 

Learned commentary on the study were highly varied.  Some noted that the "commonality" alleged in various mouse models of humans was set too low, that there needs to be a higher degree to which a model reproduces human disease in terms of molecular mechanisms, rather than just phenotype (the observable physical or biochemical characteristics of an organism).  Critics noted that the research focused on one strain of mice, and that until data was in on other strains, it was too early to draw sweeping conclusions.  Other critics noted that the paper was correct insofar as the behavior of white blood cells goes, but that it was improper to draw any sweeping conclusions about other bodily organs (e.g., lungs, liver, heart, brain).

What does this mean, then, if anything, for litigators?  Now that Daubert has come to California, one has to think in terms of genes, RNA, molecular pathways etc.  It is not enough to allow an expert to waive his/her hands and say X causes Y without asking --- why is that?  Explain to me exactly how disease Z comes about in terms of genes being utilized or blocked, molecules conveying messages, modifications happening to normal pathways. 

The study can be found at http://www.pnas.org/content/110/9/3507.   

Can addressing air pollution decrease global warming? You betcha

Prior posts have noted the adverse health impacts from small particles, often referred to generally as PM10 and/or PM2.5.  Prior posts have also noted the adverse impact of soot on global warming, which because it is black and absorbs heat warms up the atmosphere and whatever it is coating (e.g., glaciers).  Yet addressing this problem can both improve public health and decrease global warming.

To date, strategies to address global warming have focused on gases that stay in the atmosphere from medium- to long-term (e.g., methane [half life, 7 years] and carbon dioxide [half life, 19 to 49 years, without getting into the complexities of the CO2 cycling between atmosphere, ocean, plants etc., which could drive the half-life to a 5-100 year "bracket"]).  [Regarding impacts of methane, see http://epa.gov/climatechange/ghgemissions/gases/ch4.html.  Regarding impacts of CO2, see http://epa.gov/climatechange/ghgemissions/gases/co2.html.] 

In contrast, soot stays in the atmosphere for a much shorter period of time.  A recent study suggests a serious re-think may be needed because soot is the second most damaging greehouse agent after CO2 and twice as bad as previously believed.

The study found that the soot that is currently present has a warming effect of 1.1 watts per square meter of the Earth's surface.  This is greater than methane (a greenhouse gas that I have noted in prior posts is often ignored or downplayed in the discussion of strategy to address global warming) and second only to CO2 at 1.7 watts per square meter.  The prior UNEP estimate for soot was 0.3-0.6.

The study argues that the warming from soot will be especially significant in the Northern latitudes (e.g., glaciers, snowpacks).  Also, it sees a potential threat to regional precipitation patterns, such as the Asian monsoons.  Now, let's turn to the other side of soot.  The UNEP attributes 2.4 million deaths per year due to the adverse effect of such particulates on lungs, an issue noted in numerous prior posts.  [See http://www.unep.org/ccac/ShortLivedClimatePollutants/tabid/101650/Default.aspx.]

As noted, CO2 lasts a long time in the atmosphere.  In contrast, soot drops out within weeks.  Controlling soot means that it goes away relatively quickly.  In Europe and America, 70% of soot comes fro diesel engines, which may be the more harmful form of such airborne particulates (see http://www.ncbi.nlm.nih.gov/pubmed/21810552).  Better exhaust controls and the scrapping of old, high pollution cars would have a major beneficial effect.  In the LDC's, the problem also includes inefficient stoves and dirty fuel; these are problems that should be easy to address if well understood and simple technologies are provided to replace the current processes. 

The benefits of reducing soot is that it has immediate, local health benefits and is cheaper than addressing CO2 emissions.  No global treaty is needed, and there are no free rides; benefits are local with improved health.  Such controls may reduce by half a degree the temperature rise projected for global warming, buying politicans and world leaders roughly two additional decades to address controls on methane and CO2.

The study can be found at:  http://onlinelibrary.wiley.com/doi/10.1002/jgrd.50171/abstract. 

Unique marine ecosystems indicate how ocean acidification will affect sea life

A number of adverse environmental impacts are projected to occur from global warming. Although several atmospherically located substances will drive temperature increases, significant levels of CO2 may acidify the oceans. Ocean acidification is the name given to the ongoing decrease in the pH (see http://en.wikipedia.org/wiki/PH) of the Earth's oceans, which will be caused by the uptake of anthropogenic CO2 from the atmosphere. About a quarter of the carbon dioxide in the atmosphere goes into the oceans, where it forms carbonic acid, which will drive down pH levels. If global warming from CO2 proceeds apace, what will the impact be on marine ecosystems? Will acidification affect sea life? Some unique marine sites provide insight to what the future might look like.

Some unique marine sites provide a clue about what these effects may be. Researchers have been collecting data from marine sites off Italy, Baja California, and Papua New Guinea, where high concentrations of CO2 percolate out of the seabed from volcanic activity below. Directly above these CO₂ seeps, pH plummets to at least 7.8, a value that is projected to occur widely by 2100 and that is substantially lower than the normal level for the area, 8.1. These sites may offer a preview of what may happen to seafloor ecosystems as CO2 levels continue to rise, causing ocean water pH to drop.

Compared with nearby "normal-pH" sites, species richness in low-pH zones was diminished by 30%. Coral and some algae, as well as sea urchins, were gone. Fish may be present, but unlike in areas with a normal pH, they did not deposit their eggs in the low pH areas. Although seagrasses appear to survive unaffected in the low-pH seawater, close inspection showed that fish had nibbled the fronds. One possible explanation for this behavior: At low pH, these grasses no longer produced the phenolic compounds (see http://en.wikipedia.org/wiki/Natural_phenolic) that deter grazing animals from eating the plants.

Researchers also transferred a host of healthy marine species to these areas to gauge the effect of these naturally acidic regions. Although many survived, once seasonal temperature increases occurred, many of the transplanted corals and mollusks died. Researchers concluded the impact of acidification plus temperature was a "double whammy." Laboratory experiments showed also that coral larvae exposed to low pH environments had their metabolism slow to 65% of normal; their ability to make energy from nutrients in the water also decreased. In essence, the coral larvae were slowly starving. Turf algae also had a decrease in the production of two key pigments that communicated to the larvae to settle on a particular spot; this impairment was confirmed in the natural sites.

Studies addressing these issues can be found at: http://phys.org/news/2012-02-british-scientist-aaas-threat-posed.html; http://www.ucar.edu/communications/Final_acidification.pdf; http://www.nature.com/nclimate/journal/vaop/ncurrent/full/nclimate1533.html; & http://www.nature.com/nclimate/journal/v1/n3/full/nclimate1122.html.

Photoelectric cells to dye for

Is it possible to efficiently harness the often dim and indirect light found inside a room (e.g., from incandescent bulbs, fluorescent tubes, compact fluorescent bulbs, and light emitting diodes). The answer would now appear to be "yes."

A Walsh firm claims to have taken the efficiency of dye-based cells from 15% to 26%, which if correct would allow its economically efficient deployment indoors. Dye-based cells were invented at the Federal Polytechnic School of Lausanne, Switzerland, in the 1990's. Tinker with the composition of the dye, and the frequency of light that can be captured can be adjusted to make dye-based cells more flexible than silicon cells.

The dye molecules are bound to titanium dioxide, a less expensive semiconductor than silicon. The assembly is immersed in an electrolyte and sandwiched between two electrodes. When a photon of light is absorbed by a dye molecule, an electron is knocked into the titanium dioxide. Thereafter the electron travels to one of the two electrodes and a current is generated. Another advantage of dye-based cells is that they are literally flexible; some are already being woven into clothing to power cell phones, IPods etc.

Another potential market is to provide photovoltaics in regions in which silicon cells are not that well suited, such as areas frequently overcast or foggy.

Further information on dye-based cells can be found at: http://www.g24i.com/news,dye-sensitized-solar-to-go,179.html; http://www.g24i.com/news,dye-sensitized-cells-break-new-record,215.html; http://www.theengineer.co.uk/sectors/energy-and-environment/news/dye-based-organic-pvs-could-remove-need-for-batteries/1012299.article; http://en.wikipedia.org/wiki/Dye-sensitized_solar_cell; and, http://www.greenmanufacturer.net/news/power-sources/2012/04/12/new-record-set-for-recycling-indoor-light-to-electricity.

U.S. Supreme Court notes that compliance orders are reviewable before action has to be taken

Until a couple of weeks ago, the lower Federal courts generally held that an entity subject to a compliance order had to implement the actions required before being in a position to challenge the order and perhaps seek reimbursement for unnecessary expenditures.  Not so anymore.

The EPA issued a compliance order which accused the landowners of depositing fill materials on a residential lot they owned, stated that the owners engaged in the discharge of pollutants into a navigable waterway without a permit, in violation of § 301 of the Clean Water Act, 33 U.S.C. Section 1311, and directed the owners to restore the site in accordance with an EPA-created restoration work plan.  The EPA denied the owners' request for a hearing, and the owners sued the EPA, claiming that the EPA acted arbitrarily and capriciously in violation of 5 U.S.C. Section 706(2)(A), and violated their right to due process of law, when it issued the compliance order.  Like most environmental laws, the penalty for not implementing the compliance order is very large under the CWA (may not "exceed [$37,500] per day for each violation."  21 U.S.C. Section 1319(d)).

The landowners sought declarative and injunctive relief, but the District Court dismissed the claims for want of subject-matter jurisdiction.  The Ninth Circuit affirmed, concluding that the Clean Water Act precluded pre-enforcement judicial review of compliance orders and that such preclusion did not violate due process.  On appeal, the U.S. Supreme Court unanimously disagreed.

The Court, at 2012 U.S. LEXIS 2320, found that the APA provides for judicial review of "final agency action for which there is no other adequate remedy in a court."  5 U.S.C. Section 704.  The compliance order here has all the hallmarks of APA finality.  Through it, the EPA determined rights or obligations, and required the landowners to restore their property according to an agency-approved plan and to give the EPA access. The Court also found that legal consequences flow from the order, which, according to the Government's litigating position, exposes the landowners to double penalties in future enforcement proceedings. The order also severely limits their ability to obtain a permit for their fill from the Army Corps of Engineers per 33 U.S.C. Section 1344 and 33 C.F.R. Section 326.3(e)(1)(iv). 

Further, the order's issuance marks the consummation of the agency's decisionmaking process for the EPA's findings in the compliance order were not subject to further agency review.  The landowners also had "no other adequate remedy in a court," as required by 5 U.S.C. Section 704.  A civil action brought by the EPA under 33 U.S.C. Section 1319 ordinarily provides judicial review in such cases, but the landowners could not initiate that process.  Each day they failed to implement the order, additional potential liability accrued.  The Court also found that applying to the Corps of Engineers for a permit and then filing suit under the APA if that permit is denied also does not provide an adequate remedy for the EPA's action.

Overturning case law that the lower courts have followed for years, the Court found that the CWA is not a statute that "preclude[s] judicial review" under the APA.  Instead, the APA was seen as creating a presumption favoring judicial review of administrative action.

 

Could the Amazon become a GHG emitter rather than a sink?

The Amazon has long been conceived of as a CO2 sink because of its mass of vegetation. Researchers are now concerned that drought and deforestation may make it a net emitter.

Because of regular measurements of about 100,000 trees, researchers estimate that the Amazon was absorbing about 1.5 billion tons of carbon dioxide (CO2) annually at the turn of the century. Plants absorb the gas during photosynthesis, storing the carbon component as leaves, wood, and roots, and injecting it into the soil. The entire rain forest is thought to contain about 100 billion tons of carbon, equivalent to 10 years of global CO₂ emissions from burning fossil fuels. However, mass tree deaths brought about by recent droughts and deforestation may be pushing the region to a point at which it will give off more of the greenhouse gas than it absorbs. That effect is seen currently at the Amazon’s southern and eastern edges in places where forests have been cleared by loggers or burned to make room for cattle and crops.

These bald patches have two adverse impacts. First, they store little carbon. Second, they threaten remaining trees by reducing the amount of moisture that is released into the air and by pulling rain away from the surrounding forest. Dry seasons in the southern and eastern fringes of the Amazon have gotten longer. When the rains do come, precipitation that would have been captured by forest runs off into rivers instead. A 2003 study found that water flowing through the Tocantins River in southeastern Amazonia increased by nearly 25% as croplands spread to encompass almost half of the land providing drainage for the river.

For now, the impact of this deforestation will probably remain confined to these peripheral parts of the Amazon. However, one computer simulation suggested that a surge in deforestation that cleared 40 percent of the Amazon basin could trigger a tipping point, a runaway conversion of forest to savanna. Critics note that the uncertainties are sufficiently large as to make such predictions of questionable merit.

Climate change, rather than direct deforestation, may ultimately be the factor that threatens the Amazon as a whole. Rising global temperatures are predicted to warm waters in the Atlantic Ocean and stimulate the El Nino weather patterns that influence how much rain falls on the Amazon, making droughts more frequent and more severe. [The same weather patterns in the Pacific Ocean influence rainfall in the Western U.S.] Trees in the Amazon’s interior are resilient against drought since their roots reach far below the surface, tapping deep water sources that provide sustenance during lean times. There are limits. In a study reported in 2010, researchers channeled away up to half of the rain falling on small plots of land in eastern Amazonia for seven years. By the third year, tree growth had slowed substantially and tree death had nearly doubled.

A severe dry spell in 2005 had a significant impact. Rainfall decreased over a third of the Amazon, by as much as 75 percent in some places. At the time, scientists estimated that the forest released more than 1.5 billion tons of carbon as trees died off, and labeled the devastation a once-in-a-century event. Then an even worse drought hit in 2010, when an even larger area lost even more carbon. An analysis of satellite images reported last April showed significant signs of adverse effects. These events may be a statistical fluke. It is also important to try to bear in mind the impacts of normal variability in contrast to longterm trends.

Prudence would suggest that deforestation should be minimized as much as possible.

Reports on this topic can be found at http://www.nature.com/nature/journal/v481/n7381/abs/nature10717.html; http://www.agu.org/pubs/crossref/2011/2011GL046824.shtml; http://onlinelibrary.wiley.com/doi/10.1111/j.1469-8137.2010.03309.x/abstract; & http://www.sciencedirect.com/science/article/pii/S0022169403002671.

Methylene chloride (dichloromethane) linked to 13 deaths since 2000 from use as paint stripper

Methylene chloride is used in a wide variety of applications: Extraction solvent for decaffeination of coffee, extraction solvent for spices and beer hops, dip-type metal cleaner, vapor degreasing of metals, carrier solvent in the textile industry, aerosol, refrigerant, low temperature heat-transfer agent, and in chemical processing (e.g., manufacture of polycarbonate plastics, insecticides and herbicides, pharmaceuticals). It is also used to fumigate grain and for oil dewaxing. See http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~OG1F60:1:use.  However, it is also used in residential settings because it is a fast, efficient paint stripper; it is available in at least 42 products sold at home improvement stores and on the Internet.  Unfortunately, if proper precautions are not taken, its use can be fatal.

Methylene chloride is rapidly absorbed through the lungs into the circulatory system.  It is also absorbed from the stomach and gut; dermal exposure results in absorption, but at a slower rate than via other routes of exposure.  Methylene chloride is quite rapidly excreted, mostly via the lungs.  It can cross the blood-brain barrier and be transferred across the placenta.  At high concentrations, most of the absorbed methylene chloride is exhaled unchanged.  The acute effects are primarily associated with the central nervous system, lungs, kidneys, and the liver.  The main toxic effects of methylene chloride are reversible CNS "depression" and carboxyhemoglobin formation (replaces oxygen in red blood cells with carbon dioxide).  

Researchers at the Univ. of Michigan recently identified two deaths from workers refinishing bathtubs; methylene chloride paint strippers were apparently being used to remove epoxy paint.  In both cases the workers were using paint stripping materials labeled for use in paint removal from aircraft.  However, in the confined space of a bathroom, they were overcome by the fumes and died.  The researchers identified 13 deaths nationwide related to methylene chloride in paint stripping materials.  A confounding factor is assessing the extent of such deaths is that the mortality can be mistaken for a heart related fatality.

Most regulation in the U.S. focuses on methylene chloride as a carcinogen; it has been listed as such under California's Prop. 65 since 1988.  Last year the EU banned methylene chloride from furniture stripping agents.  The Michigan report suggests that more aggressive warnings should be given on labels, or the U.S. should follow the EU and ban methylene chloride from stripping agents.

The report on the fatalities can be found at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6107a2.htm.