Ear To The Ground

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.

 

EPA lacks authority to regulate nanomaterials, states EPA IG, even if regulations are soon issued under FIFRA and TSCA

Prior posts have noted the wide use of nanomaterials in consumer goods, and the threat to human health that particles of such size may pose.

An example of the risk posed by nanomaterials is sunscreen. Dermal penetration of some nanomaterials into the skin can potentially pose a hazard to human health. [Prior posts have noted
that particles in this size range can breach the blood-brain "barrier."] Also, by washing sunscreen off by showering, users of materials containing nanomaterials may be unknowingly releasing nanomaterials into the water supply. Furthermore, because of titanium dioxide contaminants within the product, improper disposal of sunscreen presents a risk of harm greater than previously hypothecated. The titanium dioxide in an "empty" sunscreen bottle that is disposed in a landfill may
eventually end up leaching into waterways and being ingested by humans.

Unfortunately, a report from the EPA Office of Inspector General (EPA IG) has concluded that the EPA lacks the data or ability to manage the challenges associated with nanomaterials. According to the report, the problem begins with the lack of data from manufacturers of nanomaterials and continues with EPA's lack of formal processes to handle information and lack of communication strategy to manage all nano-related data. The result of these organizational deficiencies, the report says, is that the agency "will not be able to assure that it is effectively managing nanomaterial risks" until these internal processes are improved.

Regarding the lack of data, most companies are unwilling to voluntarily provide information. As much as 90% of industry data is labeled as confidential and therefore was not accessible to EPA. According to the EPA IG's report, only 29 companies disclosed data about their use of 123 different nanomaterials. EPA also set up a program that encouraged companies to further provide information about research, development, and use of nanomaterials. However, only four companies participated.

In prior reports the EPA IG has noted that EPA has an action plan that is moving forward. The major question, of course, is will it be effective.

The EPA IG report can be found at
http://www.epa.gov/oig/reports/2012/20121229-12-P-0162.pdf

One component of the EPA action plan that is moving forward involves proposed mandatory reporting rules for nanomaterials under the FIFRA. Additionally, EPA is developing regulations under TSCA. The TSCA regulations would include four areas: premanufacture notification, a significant new use rule, an information gathering rule, and a test rule. However, as noted above, the EPA IG has questioned if EPA has sufficient information or processes to effectively manage the human health and environmental risks of nanomaterials. A primary shortcoming is the lack of environmental and human health exposure and toxicological data. The four main problems are the lack of a formal process for coordinating and disseminating mandated information; the lack of an overall message to external stakeholders about policy changes and risks; regulating nanomaterials as chemicals will be limited by the limitations of existing statutes; and, a lack of information about risks and a reliance on industry-submitted data.

The TSCA regulatory program for nanomaterials can be found at http://epa.gov/oppt/nano/.

Information on the over 1,000+ manufacturer identified products using nanomaterials can be found at http://www.nanotechproject.org/inventories/consumer/.

Colony collapse disorder, has the answer finally been found? Possibly

Prior posts have discussed the various research done and theories put forth related to colony collapse disorder (see http://en.wikipedia.org/wiki/Colony_collapse_disorder for an overview). The range of potential causes includes pesticides, global warming, disease, and habitat destruction.

The problem has been getting worse since 2006. Once again, researchers believe they may have an answer. It is intriguing, and may even be correct. As often happens with answers to scientific questions, it is multifactoral.

Researchers knew that the pesticide imidacloprid (see http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~bZTZKk:1 and http://en.wikipedia.org/wiki/Imidacloprid) adversely affected a honeybee's ability to learn; imidaclopid is a systemic neonicotinoid insecticide. They wondered if the insecticide had other adverse effects. In particular, because colonies that go on to collapse appear to have a greater and more varied load of parasites and pathogens than other honeybee colonies, they wondered if there was an impact on the bee's immune system (see, for example, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1847501/ and http://www.apimondia.com/apiacta/articles/2003/glinski_1.pdf).

To gain insight they set up an experiment using 30 hives. The bees were feed a protein food (rather than pollen, which is fed to developing larvae) that was spiked with imidacloprid. For ten of the hives the concentration of insecticide was 10 ppb; for another ten, 20 ppb. Previous experiments have demonstrated that neither dose perceptibly harms the honeybee. An additional 10 hives were given unspiked protein food, providing the necessary experimental control. When young bees emerged, they were collected and feed spores of the fungal parasite Nosema (see http://en.wikipedia.org/wiki/Nosema_apis). 12 days later the bees were killed and assessed for their infestation.

Both groups of bees that were feed the spiked protein food harbored an average of 700,000 parasite spores per bee; bees from the "control" colony, less than 200,000. Though the insecticide was at levels thought to be harmless, it was impacting the bee's immune system and causing a more significant infestation to manifest.

Whether this is the actual cause of colony collapse disorder remains to be seen. As they say, only time will tell. However, the thesis is plausible.

The study is noted at http://www.chemeurope.com/en/publications/333610/pesticide-exposure-in-honey-bees-results-in-increased-levels-of-the-gut-pathogen-nosema.html.

Statistics, a weak link in environmental, medical, & toxicological studies?

Statistics are used throughout science both by those proposing a conclusion and those opposed to said conclusion.

Statistics form the basis for a wide variety of claims made about environmental, medical, and toxicological matters.  I would even go so far as to note that they are often utilized by charlatans to give the illusion of analysis and certainty, when no such conclusions are justified.

An interesting assessment and discussion of the problem one often encounters with statistics used in various studies can be found at http://www.sciencenews.org/view/feature/id/57091/title/Odds_Are,_Its_Wrong.  I commend it to your review.  A skeptical attitude toward any expert needs to be an attorney's SOP, especially in this age of Daubert.  (See http://en.wikipedia.org/wiki/Daubert_standard for an overview of Daubert.)

Coriander oil is found to kill E. Coli, Salmonella, & MRSA

Prior posts have noted the adverse environmental effects that are being seen with some bactericides.  Prior posts have also noted the wide variety of substances that can act as selection factors affecting the evolution of various organisms.

Researchers now report that oil extracted from coriander seeds can kill a wide variety of pathogenic bacteria.  The researchers found that coriander oil was able to damage the membrane of bacterial cells, which ultimately lead to the bacterium’s demise.

Although it is always desirable to see reports that products assumed to be "natural" have useful properties and thus the potential to replace substances often viewed as toxic or potentially harmful, it is important to bear in mind that just like various chemicals noted in prior posts, coriander oil will act as a selection factor and that ultimately resistant organisms will emerge.

The study can be found at http://jmm.sgmjournals.org/content/early/2011/08/23/jmm.0.034157-0. 

New study supports association between exposure to persistent organic pollutants and Type II diabetes

Prior research has indicated that persistent organic pollutants (e.g., organochlorine pesticides; PCB's) may interfere with the body's ability to regulate blood sugar; some persistent organic pollutants have also been associated with obesity, itself a major risk factor for diabetes.  Although many persistent organic pollutants have been banned, they (well) persist and are present in many humans.

Researchers measured blood levels of several persistent organic pollutants in about 2,000 older adults.  Just over 15 percent had Type II diabetes; the risk was higher, the researchers found, among people with the highest levels of organochlorine pesticides.  Those with levels in the top 10% were about twice as likely to have diabetes as their counterparts in the bottom 10%.  But, the link appeared to be limited to people who were overweight or obese.  As such, the researchers suggest that the being overweight or obese and the presence of persistent organic pollutants could be synergistic vis-a-vis Type II diabetes.

The researchers accounted for participants' age, sex, waist size, and blood pressure levels. However, they had no information on, among other things, diet and exercise habits, which might explain away the association.  In support of their viewpoint, the researchers point out that persistent organic pollutants have been shown to be endocrine disruptors, which may support a causal relationship.

The report can be found at http://care.diabetesjournals.org/content/early/2011/07/26/dc10-2303.abstract.

Widespread use of herbicides create immunity and resistance in weedy plants

Prior posts have noted that a wide variety of substances, including hazardous substances, can act as selection factors in fostering "evolution" amongst impacted organisms.  Now, researchers have found that many weeds, including some of significant economic importance because of the crops impacted, are resistant to multiple herbicides.  This should come as no surprise to readers of this blog. 

Resistance in weeds has been a factor known to agronomists for decades.  But researchers point to the introduction of glyphosate immune crops in 1996 as a key event because it resulted in the very heavy application of glyphosate on croplands.  Today, nearly 98% of U.S. soybeans, 88% of U.S. cotton, and 70+% of U.S. corn come from cultivars resistant to glyphosate.  It should be no surprise then that such heavy application selected for resistant weed strains, accelerating their widespread presence.  Other weeds are now showing resistance to other widely used herbicides.

For example, Hybrid Goat Grass has shown signs of tolerance to the herbicide imazamox in fields planted with wheat breed to be immune to that herbicide.  However, in this case the resistance is developing not exclusively from herbicide exposure but also from the spread of resistant genes in the pollen of wheat, the weed's distant cousin, through interbreeding.  Although farmers can target the hybrid weed with other herbicides, they risk simultaneously impacting the wheat.

Not surprisingly, weeds immune to one herbicide will generally prove resistant to other herbicides that utilize the same mode of action, usually the chemical's disruption of an enzyme essential to plant (weed) function.  For example, Common Water Hemp has risen to become a major weed in Midwestern soy and corn production.  Studies have found that it is now immune or resistance to five different herbicide groups.  The result is that soy farmers are nearly out of options for herbicides.  In Australia, it has been reported that some weedy ryegrass species are resistant to seven different herbicide types.

In the 1970's, I had the honor of co-authoring with Dr. Dale Bottrell a CEQ report on Integrated Pest Management; Dr. Bottrell has gone on to write widely about IPM [for his well reasoned assessment of IPM and its failure to be truly implemented, see http://www.issues.org/16.3/ehler.htm].  We foresaw problems of this type, not because we were great prognosticators, but because the problems were already manifesting themselves with insect pests in (for example) cotton crops.  The lessons clearly have yet to be learned.  Whether the pest is a plant or an insect, the fundamentals of environmental science apply.  Exposure to any substance can act as a selection factor, yielding resistant or "evolved" strains. 

Reports and data bases on the topics noted in this blog can be found at http://www.weedscience.org/In.asp, http://pubs.acs.org/doi/abs/10.1021/jf102652y, http://pubs.acs.org/doi/abs/10.1021/jf102704x, http://pubs.acs.org/doi/abs/10.1021/jf104719k, http://pubs.acs.org/doi/abs/10.1021/jf101286h, http://onlinelibrary.wiley.com/doi/10.1002/ps.2100/abstract, http://pubs.acs.org/doi/abs/10.1021/jf103389v, and http://pubs.acs.org/doi/abs/10.1021/jf103797n.

Prenatal vitamins may help reduce the rate of autism

Genetics appear to play an important role in autism.  See, for example, http://www.ncbi.nlm.nih.gov/pubmed/18414403.  Yet, a number of alternative theories exist (most lacking in evidence) that purport to explain the origin of autism.  For example, viral infections (particularly rubella); the vaccine for measles, mumps, and rubella (MMR); thimerosal (a mercury preservative used in some vaccines); parental age; folate deficiency or other nongenetic one-carbon metabolism disturbances; hypocholesterolemia; exposure to prenatal testosterone; and, hyperactivation of the immune system.  The reason such often unsupported theses may obtain a following is the urban myth that the rate of autism is rapidly increasing.  As noted in a prior post, the so-called increase may have more to do with improved methods of assessment and changes in classification of disorders than with an actual increase.

Recently published research shows a significant statistical effect that arises from the taking of prenatal vitamins in the three-month period prior to conception and one-month period after conception.  Women who took such vitamins during this time-frame reduced the risk of autism by 40%.  The reduction was especially significant in women with genetic variants that impact folate metabolism (folate is a significant component of prenatal vitamins).

The authors note that replication of their results is important to confirm the result found in their study.  Since the results are epidemiological in nature, they also note the need for establishing a biological mechanism to explain the effect that was apparent statistically.

The study can be found at http://journals.lww.com/epidem/Abstract/2011/07000/Prenatal_Vitamins,_One_carbon_Metabolism_Gene.8.aspx.

Parkinson's may be caused by the same bacterium that causes ulcers, new animal model studies suggest

The cause of Parkinson's Disease is unknown.  To date, many experts have suggested that it may have a genetic origin; see http://www.webmd.com/parkinsons-disease/parkinsons-causes.  Other experts point to toxins that may selectively destroy the dopaminergic neurons, thereby causing Parkinson's Disease. Toxins that have allegedly been linked to Parkinson's include manganese, carbon monoxide, carbon disulfide, and some pesticides. 

Now, researchers (using an animal model) have found evidence that the cause may be Helicobacter pylori, a bacterium that lives in the stomachs of about half the people in the world and causes ulcers and stomach cancer.  [For those with long memories, you may recall that ulcers use to be associated with stress and/or stomach acid until researchers found the cause, although they were subjected to years of abuse for their "folly".  Ultimately the two researchers received the Novel Prize in medicine for their discovery.  See http://health.dailynewscentral.com/content/view/0001725/37/.]

Middle-aged mice infected with the ulcer-causing bacterium developed abnormal movement patterns over several months of infection, the researchers have noted; yet, young mice infected with the bacterium did not show any signs of movement problems.  The researchers found that Helicobacter-infected mice make less dopamine in parts of the brain that control movement, possibly indicating that dopamine-making cells are dying just as they do in Parkinson’s Disease patients.  The bacteria did not have to be alive to cause the problem.  Feeding mice killed H. pylori produced the same effect, suggesting that some biochemical component of the bacterium is responsible.  A candidate for the disease-causing molecule is modified cholesterol.  Helicobacter is unable make its own cholesterol, so it steals cholesterol from its host and then sticks a sugar molecule on it. The structure of the modified cholesterol resembles a toxin from a tropical cycad; people in Guam who have eaten the plant's seeds have developed a disease called ALS-parkinsonism dementia complex.  The researchers are now seeking to determine if the modified cholesterol alone can lead to Parkinson-like symptoms in mice or if some other factor from the bacterium is also needed.

As with all things biological, there is a problem.  Even if researchers can show that H. pylori can cause or contribute to Parkinson’s disease, it is not clear whether getting rid of the organism would be a good thing.  Although the bacterium causes ulcers and stomach cancer, it also helps protect against allergies, asthma, esophageal cancer, and other acid reflux diseases.  Where would be the balance?  No one at present knows.  As they say, stay tuned.

The study was reported this month at the 111th annual meeting of the American Society for Microbiology:  http://gm.asm.org/index.php/component/content/article/48-newsroom/211-ulcer-bacteria-may-contribute-to-development-of-parkinsons-disease.

Three new studies conclude that prenatal pesticide exposure lowers IQ

Before noting the studies, I should note that I am very skeptical about what it is that IQ tests measure, and whether they are measuring it accurately.  Personally, I find the thesis that there are many types of intelligence to be more persuasive, but then I do not hold my self out as an expert on measuring intelligence.  For a quick summary of alternative views of intelligence, see http://www.aboutintelligence.co.uk/what-intelligence.html.

Babies exposed to pesticides before birth may have significantly lower intelligence scores by age 7 than children who were not exposed, according to three separate studies published within the last 2 weeks.  In one study, a team of researchers found that every tenfold increase in prenatal exposure to organophosphate pesticides corresponded with a 5.5 point drop in overall IQ scores in children by age 7.  In the other two studies, the researchers also looked at prenatal exposure and measured IQ at age 7.  One group of researchers sampled pesticide residues in maternal urine, while the other tested umbilical cord blood levels of chlorpyrifos, part of a class of pesticides known as organophosphates that are known to be toxic to brain cells; it was widely used for residential pesticide applications until banned by EPA in 2001 (it is still used for agricultural applications).  While the methodology of each group was different, they all determined that there was a reduction in IQ.

These studies add to the body of studies that have found a variety of adverse neurological and cognitive effects upon humans from pesticides, particularly among those exposed prenatally or at a very young age.

The three studies can be found at http://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.1003185, http://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.1003183, and http://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.1003160.  Earlier studies on the same and related topics can be found at http://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.1002056, http://www.environmentalhealthnews.org/ehs/newscience/pesticides-found-in-one-fifth-of-produce-kids-eat, and http://www.google.com/url?sa=t&source=web&cd=20&ved=0CFUQFjAJOAo&url=http%3A%2F%2Fwww.fwpp.org%2Fmedia%2F%3Fid%3D14&rct=j&q=pesticides%20IN%20%22Environmental%20Health%20Perspectives%22&ei=OQC9TZPTFoe6sQPwjIHRBQ&usg=AFQjCNGrsJFLGYpnU1-52lqVxzI-z-Qe5w.  The latter is a synopsis of a multitude of studies and where they can be found.