Electronic Letters are short, timely responses to selected articles published in Science. Recently published E-Letters appear below. To submit an E-Letter on one of our articles, go to the article and follow the "Submit an E-Letter" link in the "Article Tools" area.

E-Letter responses published in the past 60 days:

Read E-Letter responses published in the last 1, 2, 3, 4, 5, 6, 7, 14, 21 days

13 E-Letter responses published for 9 different topic sources.

Articles			E-Letter Responses
	n-focus: From Burning Dung to Global Warming and Back Again Kerr (16 October 2009) [Full text] [PDF]		Burn Less Dung Lawrence R. Zeitlin   (11 November 2009) Read every E-Letter response to this article
	p-forum: Looming Global-Scale Failures and Missing Institutions Walker et al. (11 September 2009) [Full text] [PDF]		Missing Formal Institutions? P K Rao   (3 November 2009) Read every E-Letter response to this article
	letters: Teaching and Learning Strategies That Work Hoffmann and McGuire (4 September 2009) [Full text] [PDF]		One More Classroom Strategy for Increasing Learning Lawrence R. Zeitlin   (3 November 2009) Read every E-Letter response to this article
	n-focus: On the Origin of Cooperation Pennisi (4 September 2009) [Full text] [PDF]		Cultural Group Selection Overlooked Timothy M. Waring   (13 October 2009) Read every E-Letter response to this article
	reports: Motile Cilia of Human Airway Epithelia Are Chemosensory Shah et al. (28 August 2009) [Abstract] [Full text] [PDF]		Response to A. Pronin's E-Letter Michael J. Welsh, et al.   (28 October 2009) Denatonium Curse Alexey Pronin   (28 October 2009) Read every E-Letter response to this article
	reports: Functional Characterization of the Antibiotic Resistance Reservoir in the Human Microflora Sommer et al. (28 August 2009) [Abstract] [Full text] [PDF]		Are Human Microflora Influenced by Environmental Exposure to Antibiotics? Peter Oelschlaeger, et al.   (13 October 2009) Read every E-Letter response to this article
	books: Selling Science Coyne (7 August 2009) [Full text] [PDF]		A Path to Selling Science Donald M. Marcus   (16 October 2009) Correcting the Record on Unscientific America Chris Mooney, et al.   (16 October 2009) Read every E-Letter response to this article
	p-forum: Nutrient Imbalances in Agricultural Development Vitousek et al. (19 June 2009) [Full text] [PDF]		Response to E. Ongley and Y. Tao's E-Letter Peter M. Vitousek   (3 November 2009) Agricultural N and P Runoff: A Major Pollutant of NCP Surface Water? Edwin Ongley, et al.   (3 November 2009) Read every E-Letter response to this article
	perspective: OCEANS: Limits to Marine Life Brewer and Peltzer (17 April 2009) [Full text] [PDF]		Response to B. Seibel et al's. E-Letter Peter G. Brewer, et al.   (13 November 2009) Critique of the Respiration Index Brad A. Seibel, et al.   (13 November 2009) Read every E-Letter response to this article

n-focus: From Burning Dung to Global Warming and Back Again Kerr (16 October 2009) [Full text] [PDF] From Burning Dung to Global Warming and Back Again Burn Less Dung 11 November 2009 Lawrence R. Zeitlin, Professor Emeritus City University of New York, New York, NY 10010, USA Respond to this E-Letter: Re: Burn Less Dung The News Focus story ("From burning dung to global warming and back again," R. A. Kerr, 16 October 2009, p. 362) reminds me of my visiting professorship to India 25 years ago, where I observed that the typical rural household was burning dung patties in a very inefficient way. The typical patty, a dried pancake-like disk of dung, was ignited on the outside and burned on its ever-decreasing surface. The fire started out hot and then decreased in intensity as the burning surface area became smaller. Additional patties were added to maintain the heat. Facing a thermodynamically similar problem in the design of solid-state rocket motors, NASA engineers worked out constant area shapes for the burning of solid fuel propellants. These usually had thick cross-like or hollow cylinder cross-sections that would maintain the same surface area as they burned and kept rocket thrust constant. The same logic could be applied to dung patties. A simple wood or plastic mold would let the Indian householder shape patties to burn at constant heat for greater cooking efficiency. Since half of the cooking fires in rural Asia use dung for fuel, the fuel saving is obvious, not to mention minimization of the brown cloud that hangs over the subcontinent. Lawrence R. Zeitlin City University of New York, New York, NY 10010, USA.

p-forum: Looming Global-Scale Failures and Missing Institutions Walker et al. (11 September 2009) [Full text] [PDF] Looming Global-Scale Failures and Missing Institutions Missing Formal Institutions? 3 November 2009 P K Rao, Development Economist Respond to this E-Letter: Re: Missing Formal Institutions? The Policy Forum "Looming global-scale failures and missing institutions" (B. Walker et al., 11 September 2009, p. 1345) is an interesting contribution offered by several well-known experts. However, I believe that the emphasis on the role of formal organizational arrangements and of institutions, should these organizations rise to that status, is founded on assumptions that (i) negligible transaction costs accompany formation of global-scale entities; (ii) these entities function efficiently; and (iii) top-down mechanisms can correct market failures. The idea that we need additional institutions to address the many environmental crises may not be justified. It is more useful to examine the problem in terms of bottom-up approaches and agent-principal models. In the former approach, the roles of consumers and producers are better recognized and influenced. For example, differential taxation can induce less red meat consumption (which alone can offset about 50% of greenhouse gas emissions at negligible cost), and incentives can lead to the production of less carbon-intensive products, reliance on renewable energy, and technical innovations. P. K. Rao Princeton, NJ, USA.

letters: Teaching and Learning Strategies That Work Hoffmann and McGuire (4 September 2009) [Full text] [PDF] Teaching and Learning Strategies That Work One More Classroom Strategy for Increasing Learning 3 November 2009 Lawrence R. Zeitlin, Professor Emeritus City University of New York, New York, NY 10016, USA Respond to this E-Letter: Re: One More Classroom Strategy for Increasing Learning R. Hoffman and S. Y. McGuire present a useful guide for increasing learning ("Teaching and learning strategies that work," Letters, 4 September 2009, p. 1203). Here is another strategy that I employed with great success at the City University of New York Graduate Center. Most graduate courses, at least those not heavy with specific facts or mathematical equations, can be broken down into a number of key concepts. A month before the final exam, on which the bulk of the grade would depend, I prepared a list of 20 essay-type questions, each covering a main concept and its integration with other concepts. Thus, a question in industrial engineering might be: "Explain how the Black Death and the Napoleonic Wars fostered the development of the factory system of production." The list of questions was distributed to the class well before the final exam. Students were able to prepare answers to all the questions in advance, but by doing so, they mastered the material taught in the lectures and readings. On the day of the final exam 5 of the 20 questions were drawn at random from a paper bag in the classroom. Since there was no way of knowing which questions would be drawn, astute students would prepare answers for all of them. This approach had the dual purpose of ensuring that the students learned the key concepts of the course and relieving students' anxiety before the exam. Lawrence Zeitlin City University of New York, New York, NY 10016, USA.

n-focus: On the Origin of Cooperation Pennisi (4 September 2009) [Full text] [PDF] On the Origin of Cooperation Cultural Group Selection Overlooked 13 October 2009 Timothy M. Waring, PhD Candidate University of California, Davis, CA 95616, USA Respond to this E-Letter: Re: Cultural Group Selection Overlooked E. Pennisi's recent News Focus story ("On the origin of cooperation," 4 September 2009, p. 1196), like the rest of her work, is refreshingly deep, crisp, and insightful. I found, however, that when speaking of the evolution of human cooperation she left out a very important mechanism: cultural group selection. Pennisi mentions group selection but refers only to Samuel Bowles' work on the genetic group selection of the human lineage. This is no doubt valuable; if humans were the result of genetic group selection then human cooperation is certainly easier to explain. The group selection of cultural variation becomes possible because mechanisms of imitation reduce cultural variation within groups and tend to increase it between groups. Cultural group selection not only produces a selection of cultural variants but may easily implicate the fitness of the individuals carrying those cultural variants (1–3). Just as genetic variation may have fitness consequences, so too, does cultural variation. The importance of the group selection of cultural variation for human genetic evolution is almost always overlooked, and is likely a more powerful force than simple genetic group selection, which remains an extremely rare phenomenon. Timothy M. Waring University of California, Davis, CA 95616, USA. References 1. L. L. Cavalli-Sforza, M. W. Feldman, Theor. Popul. Biol. 4, 42 (1973). 2. R. Boyd, P. J. Richerson, Culture and the Evolutionary Process (Univ. of Chicago Press, Chicago, IL, 1985), pp. 227–240. 3. J. Soltis, R. Boyd, P. J. Richerson, Curr. Anthropol. 36, 473(1995).

reports: Motile Cilia of Human Airway Epithelia Are Chemosensory Shah et al. (28 August 2009) [Abstract] [Full text] [PDF] Motile Cilia of Human Airway Epithelia Are Chemosensory Response to A. Pronin's E-Letter 28 October 2009 Michael J. Welsh Department of Internal Medicine, Howard Hughes Medical Institute, University of Iowa, Iowa City, IA, Alok S. Shah, Yehuda Ben-Shahar Respond to this E-Letter: Re: Response to A. Pronin's E-Letter The goal of our Report was to test the hypothesis that mammalian motile cilia could act as a chemosensory organelle, and we used the bitter signal transduction system as a test ("Motile cilia of human airway epithelia are chemosensory," 28 August 2009, p. 1131, published online 23 July 2009). A. Pronin indicates that correlations between T2R alleles and individuals' sensitivity to bitter tastants has been the most compelling evidence that T2R receptors detect bitter compounds and mediate the sense of taste. He goes on to say that we should do the corresponding study in airway epithelia. We agree that his work (1) and that of others (2–4) correlating T2R alleles and bitter taste sensitivity has been important. But many other discoveries indicated that T2Rs are receptors for bitter compounds [for examples see (5–10)], and a narrow focus on correlating T2R alleles and bitter taste sensitivity misses the contribution of that work, as well as important points in our Report. Although the experiment that Pronin proposes could be interesting, our current data support the conclusions of our Report. In our Report, multiple experiments revealed that T2Rs and their signal transduction machinery are located in ciliated epithelial cells and that bitter compounds elicit a cellular response. Pronin emphasizes denatonium. However, we also discovered that [Ca2+]i increased in response to salicin (100 micromolar/200 micromolar/70 micromolar), thujone (10 micromolar/-/3–30 micromolar), quinine (100 micromolar/1 micromolar/300 micromolar), and nicotine (100 micromolar/19 micromolar/100 micromolar) (parentheses indicate: concentration we tested/taste sensitivity in vivo/concentrations raising [Ca2+]i in our in vitro assays) (4, 9, 11–13). We applied denatonium at 100 micromolar, which is greater than the concentration detectable by humans. Although Pronin says that mM denatonium can cause artifacts, studies indicating that mM concentrations of denatonium stimulated hT2R4 and mT2R8 contained controls indicating that the response was not an artifact (6). Moreover, we found that denatonium only increased [Ca2+]i in epithelial cells that were ciliated (fig. S8 of our Report). More important, there need not be a close correlation between a psychophysical gustatory response in humans and a physiologic response in airway epithelia. The relationship between concentration and response could differ substantially for the perceived taste of a compound and for its stimulation of airway epithelial cells. Our findings that various T2Rs show distinct localization patterns along the cilia also raise the possibility that different T2Rs may vary in their coupling to signaling pathways. Thus, Pronin's comments about denatonium concentration might not hold for physiological or biochemical studies in lung cells. Indeed, using a biochemical assay, Pronin previously reported that 10 to 30 micromolar denatonium was required to activate T2R44 (14) and said, "Although the concentration of denatonium needed for detectable activation of hT2R44 in the GTPγS binding assay is still significantly higher than the reported 'bitter threshold' in humans, we do not expect it to match precisely human taste sensitivity. The 'bitter threshold' is a concentration at which humans begin to differentiate between water alone and water plus a compound (i.e., 'barely detectable'). Sensory detection thresholds are often much lower than observed in heterologous assays." Pronin says that we should determine whether variations in individuals' sensitivity to tasting phenylthiocarbamide (PTC) correlate with the response of ciliated airway epithelia to PTC. We have not tested PTC on airway epithelia. Although we agree that this could be an interesting study, testing for such a correlation would be technically difficult. We used primary cultures of differentiated human airway epithelial cells derived from trachea and bronchi obtained from lungs rejected for organ transplant. Obtaining cultures from individuals who were screened for PTC sensitivity would not be a trivial undertaking. In addition, interpretations can be complicated because most bitter compounds activate multiple T2Rs (4, 6, 9, 12, 15). We thank Dr. Pronin for the suggestion. Michael J. Welsh, Alok S. Shah, and Yehuda Ben-Shahar Department of Internal Medicine, Howard Hughes Medical Institute, University of Iowa, Iowa City, IA 52242, USA. References 1. A. N. Pronin et al., Curr. Biol. 17, 1403 (2007). 2. U. K. Kim et al., Science 299,1221 (2003). 3. B. Bufe et al., Curr. Biol. 15, 322 (2005). 4. B. Bufe, T. Hofmann, D. Krautwurst, J. D. Raguse, W. Meyerhof, Nat. Genet. 32, 397 (2002). 5. E. Adler et al., Cell 100, 693 (2000). 6. J. Chandrashekar et al., Cell 100, 703 (2000). 7. H. Matsunami, J. P. Montmayeur, L. B. Buck, Nature 404, 601 (2000). 8. J. Chandrashekar, M. A. Hoon, N. J. Ryba, C. S. Zuker, Nature 444, 288 (2006). 9. W. Meyerhof, Rev. Physiol. Biochem. Pharmacol. 154, 37 (2005). 10. K. L. Mueller et al., Nature 434, 225 (2005). 11. M. Behrens et al., Biochem. Biophys. Res. Commun. 319, 479 (2004). 12. A. Caicedo, E. Pereira, R. F. Margolskee, S. D. Roper, J. Neurosci. 23, 9947 (2003). 13. L. Liu, S. A. Simon, Chem. Senses 23, 125 (1998). 14. A. N. Pronin, H. Tang, J. Connor, W. Keung, Chem. Senses 29, 583 (2004). 15. M. Behrens, C. Reichling, C. Batram, A. Brockhoff, W. Meyerhof, Ann. N. Y. Acad. Sci. 1170, 111 (2009). Motile Cilia of Human Airway Epithelia Are Chemosensory Denatonium Curse 28 October 2009 Alexey Pronin, Principal Scientist Senomyx, Inc., 4767 Nexus Centre Drive, San Diego, CA 92121, USA Respond to this E-Letter: Re: Denatonium Curse In their Report ("Motile cilia of human airway epithelia are chemosensory," 28 August 2009, p. 1131, published online 23 July 2009), A. S. Shah et al. claim that the motile cilia emerging from human airway epithelial cells propel harmful inhaled material out of the lung due to activation of bitter taste receptors (T2Rs) in cilia. Because gene manipulations cannot be done in humans, the most compelling evidence that T2Rs expressed in taste buds indeed mediate bitter taste in humans came from correlating individuals' taste sensitivity with specific T2R alleles (1, 2) and/or bitter compound effects in heterologous assays (2–4). This correlation between compound taste and effects on airway epithelial cells is lacking in Shah et al.'s Report. The authors used salicin at 100 micromolar, which is below the bitter taste threshold (0.2 mM) for most people (4). In contrast, they used denatonium at 1 mM, which is 50,000 times as high as the bitter taste threshold (20 nM). But the effects on calcium concentration in airway cells were the same. The authors showed that 1 mM denatonium caused airway epithelial cell cilia to beat 10 to 25% faster, whereas at 100 micromolar it had no effect. However, even at 10 micromolar, denatonium is already so bitter to humans that people cannot distinguish between 10 and 100 micromolar solutions (5). The authors mentioned that denatonium was shown to activate hT2R4 in mM range (6). We now know that hT2R4 response is not relevant to denatonium taste, and other receptors (hT2R47) are activated by denatonium at much lower (nM to micromolar) concentrations in vitro. Physiologically active compound concentrations are largely determined by the compound's affinity to its receptor. Signaling machinery downstream from the receptor, which can vary among cell types, can have only a small effect on a cell’s sensitivity to a stimulus. If bitter taste and effects on the beat rate of the airway epithelial cell cilia were mediated by the same receptors (hT2Rs), they should be observed at similar compound concentrations, which they are not. Denatonium has been routinely used in experiments as a prototypical bitter compound. However, when used in vitro at concentrations of 1 mM or higher it causes numerous artifacts. Attributing observed effects to denatonium taste would be equivalent to attributing the effects of 1M sulfuric acid to the acid's sour taste rather than the harsh, low pH of the solution. Widespread use of this compound at such high concentrations does not make it acceptable, and more relevant compounds and/or concentrations should be used. If Shah et al. want to confirm that T2Rs mediate airway epithelial cell responses to bitter compounds, they should collect airway cells from phenylthiocarbamide (PTC)–sensitive and –insensitive individuals and demonstrate that PTC (0.1 to 0.5 mM) causes responses in cells from PTC-tasters but not from PTC-nontasters, thereby providing a correlation with bitter taste. Alexey Pronin Senomyx, Inc., 4767 Nexus Centre Drive, San Diego, CA 92121, USA. References 1. U.-K. Kim et al., Science 299, 1221 (2003). 2. A. N. Pronin et al., Curr. Biol. 17, 1403 (2007). 3. B. Bufe et al., Curr. Biol. 15, 322 (2005). 4. B. Bufe et al., Nat. Genet. 32, 397 (2002). 5. R. S. J. Keast, M. M. E. Bournazel, P. A. S. Breslin, Chem. Senses 28, 301(2003). 6. J. Chandrashekar et al., Cell 100, 703 (2000).

reports: Functional Characterization of the Antibiotic Resistance Reservoir in the Human Microflora Sommer et al. (28 August 2009) [Abstract] [Full text] [PDF] Functional Characterization of the Antibiotic Resistance Reservoir in the Human... Are Human Microflora Influenced by Environmental Exposure to Antibiotics? 13 October 2009 Peter Oelschlaeger, Assistant Professor Department of Chemistry, California State Polytechnic University, Pomona, CA 91768, USA, Jeffrey H. Toney Respond to this E-Letter: Re: Are Human Microflora Influenced by Environmental Exposure to Antibiotics? The Report by M. O. Sommer et al. describes an extensive array of antibiotic resistance genes found in the human microflora ("Functional characterization of the antibiotic resistance reservoir in the human microflora," 28 August 2009, p. 1128), including the discovery of 95 unique inserts containing functional antibiotic resistance genes. More than one out of four of these genes encode beta-lactamases that inactivate beta-lactams, such as penicillin and amoxicillin, by hydrolysis—consistent with the wide use of these antibiotics. On average, an adult in the United States makes two outpatient visits per year and 15.3% of these visits result in the prescription of an antibiotic (1). To avoid potential influence of antibiotics on the study of human microfloral genes, these investigators chose two unrelated healthy subjects who had not been exposed to antibiotics for at least one year. This would allow sufficient time for the elimination of bacterial subpopulations that may have been exposed to antibiotics while the individual was undergoing treatment. However, it is highly unlikely that an individual living in a developed country could escape any exposure to antibiotics; detectable levels can be found in water, agricultural products and meat. In the United States, an estimated 8,600 to 13,000 tons of antibiotics (about half of the total consumption) are used for nontherapeutic purposes, including agriculture and animal husbandry (2). A host of antibiotics have been detected in wastewater at levels of 1.7 to 1.9 micrograms/liter (3). A clearer picture of the reported "immense diversity of antibiotic resistance machinery in the human microbiome" will emerge if comparative studies can be done with individuals from environments naïve to industrial exposure. Peter Oelschlaeger Department of Chemistry, California State Polytechnic University, Pomona, CA 91768, USA. Jeffrey H. Toney College of Natural, Applied and Health Sciences, Kean University, Union, NJ 07083, USA. References 1. C. L. Roumie et al., J. Gen. Intern. Med. 20, 697 (2005). 2. K. Kuemmerer, in Pharmaceuticals in the Environment: Sources, Fate, Effects and Risks, K. Kuemmerer, Ed. (Springer, Berlin - Heidelberg, 2004), pp. 27–44. 3. A. Alder et al., in Pharmaceuticals in the Environment: Sources, Fate, Effects and Risks, K. Kuemmerer, Ed. (Springer, Heidelberg - Berlin, 2004), pp. 55–66.

books: Selling Science Coyne (7 August 2009) [Full text] [PDF] Selling Science A Path to Selling Science 16 October 2009 Donald M. Marcus Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA Respond to this E-Letter: Re: A Path to Selling Science J. Coyne's Book Review of Unscientific America by C. Mooney and S. Kirshenbaum ("Selling science," 7 August 2009, p. 678) doesn’t serve the basic function of describing the scope and contents of a book. His review is a dismissive rant that misrepresents the text. For example, Coyne claims that the authors attribute the scientific illiteracy of Americans to "two failings of scientists themselves: their vociferous atheism and their ham-handed and ineffectual efforts to communicate the importance of science to the public." In fact, in a chapter on religion, the authors maintain that the contemptuous dismissal of religious believers by a few writers, such as Richard Dawkins, interferes with communication to the public by needlessly insulting believers, and serves only to elicit vitriolic responses from the religious right. The book's thesis is that science should be an integral part of popular culture. They quote the late Carl Sagan: "We've arranged a global civilization in which most crucial elements profoundly depend on science and technology. We have also arranged things so that almost no one understands science and technology. This is a prescription for disaster." In addition to the assault on religion, Mooney and Kirshenbaum cite other factors that limit public understanding of science, including the lack of ongoing relationships with politicians, and the drastic decrease in in-depth coverage of science by newspapers, television, and the Internet. Driven by consolidation of the media into large conglomerates that emphasize the bottom line, the number of newspapers that contain regular science-related sections shrank from 95 to 34 between 1989 and 2005. Only one minute of every 300 minutes of cable news is devoted to science. The authors encourage the scientific community to engage in more outreach, and they recommend training some scientists to function primarily as "communicators." The book is clear and lively, and it includes 66 pages of notes containing references and citations. In addition to providing little information about the book, the review is an example of an intemperate style that is an obstacle to civil discourse. It is unworthy of Science. Donald M. Marcus Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA. Selling Science Correcting the Record on Unscientific America 16 October 2009 Chris Mooney , Sheril Kirshenbaum Respond to this E-Letter: Re: Correcting the Record on Unscientific America The late New York Senator Daniel Patrick Moynihan once remarked that "Everyone is entitled to his own opinions, but not his own facts." A similar rule applies to book reviews: Every reviewer is entitled to dislike a particular book, but not to misrepresent its arguments and contents. Unfortunately, J. Coyne has taken the latter course with our book Unscientific America ("Selling science," Book Reviews, 7 August 2009, p. 678). He calls our work "shallow and unreflective," but virtually every time he tries to describe it he makes an error—either attributing to us views and positions we do not hold, or claiming the book lacks content that it actually does contain. The problem is apparent from Coyne's opening sentence, in which he asserts that Unscientific America argues that the problem of American scientific illiteracy "derives from two failings of scientists themselves: their vociferous atheism and their ham-handed and ineffectual efforts to communicate the importance of science to the public." This would be a very foolish position; thankfully, it isn't ours. On the contrary, as we describe it, scientific illiteracy—really, the gap between science and society—is a complex, multifaceted, multidecadal problem. It is hardly something that can be blamed exclusively on the failings of scientists, although surely scientists have contributed to the divide. Coyne's misrepresentations continue as he asserts that we "claim that scientific illiteracy once was ameliorated by people like Carl Sagan and Stephen Gould but is now exacerbated by the 'new atheists.'" Our views are nowhere near so simplistic. The same goes for this assertion: "Other data contradict Mooney and Kirshenbaum's claim that American ignorance of scientific issues reveals a failure of outreach." In a complex society and world, in which citizens' views of scientific issues are influenced by the educational system, the news media (new and old), the entertainment media, interpersonal communications, political predilections, religious commitments, and much else, how could anyone hold the naive positions that Coyne attributes to us? We certainly don't. To give just one example, consider our observation about where vaccine skeptics get their "science": "From the Internet, celebrities, other parents, and a few non-mainstream researchers and doctors who continue to challenge the scientific consensus, all of which forms a self-reinforcing echo chamber of misinformation." The actual task undertaken in Unscientific America is to update C. P. Snow's famous "two cultures" analysis, originally written for mid-20th century Britain, for 21st century America. Accordingly, we repeatedly depict a "two cultures" divide between scientists and other parts of our society. Neither side understands the other adequately, and both sides are responsible for communication failures and disconnects. Relating none of this, Coyne instead poses the following rhetorical question: "Do [Mooney and Kirshenbaum] really think that if Dawkins had not written The God Delusion, Americans would wholeheartedly embrace evolution and vaccination and finally recognize the threat of global warming?" Here are the facts: Anti-evolutionism is over 100 years old. The latest outgrowth of anti-vaccine activism, over the mercury-containing preservative thimerosal, is about a decade old, but distrust of vaccination also goes back well over a century. Finally, global warming denial goes back decades. With all of these preexisting factors in place, Dawkins' The God Delusion was then published in 2006—and it isn't even about global warming or vaccination. So, no: We are quite confident that these instances of anti-science sentiment would be with us no matter what Richard Dawkins did. Yet this admission does nothing to weaken our argument that the confrontational tactics of Dawkins and the New Atheists (including Coyne), in the present moment, are counterproductive. Perhaps the most revealing aspect of Coyne's review is his use of our own arguments to attack the positions he incorrectly attributes to us. For instance, take Coyne's observation that "The public's reluctance to accept scientific facts may reflect not just a lack of exposure but a willful evasion of facts due to conflicting economic agendas (e.g., the case of global warming) personal agendas (vaccines), or religious agendas." Yes, but how is this a strike against our book? We deal with such factors from the outset; Coyne even quotes our observation that "college-educated Democrats are now more than twice as likely as college-educated Republicans to believe that global warming is real and is caused by human activities." Coyne writes that "the problem of an 'unscientific America' may be far more complex than the authors let on," but in truth, we describe the problem with far more complexity than Coyne lets on. Much more might be said, but allow us to rebut one final claim: Coyne's repeated accusation that we want anti-religion scientists to "keep quiet." This is simply not the case. In fact, as we observe in an endnote: "We want to emphasize that New Atheists enjoy freedom of speech. No one is asking them to be quiet. However, we have every right to point out the consequences of the divisiveness they are fueling over science and religion." We welcome vigorous debate over our book's arguments and suggestions, and have been regular participants in that discussion on the Internet. Unfortunately, readers of Science have no way of knowing that several of the errors we note above were already corrected in that earlier discussion after Coyne reviewed our book on his blog—though no note of those corrections is reflected in Coyne's Science review (1, 2). The failure to mention this previous interaction does readers a disservice, depriving them of valuable context about the reviewer's willingness to accurately represent our book. Chris Mooney and Sheril Kirshenbaum References 1. E. Scott, C. Mooney, "Unscientific Unscientific America. Part 1," 14 July 2009; http://whyevolutionistrue.wordpress.com/2009/07/14/unscientific-unscientific-america-part-1/. 2. C. Mooney, S. Kirshenbaum, "Some More Words to the New Atheist Blogosphere on Unscientific America," 27 July 2009; http://blogs.discovermagazine.com/intersection/2009/07/27/some-more-words-to-the-new-atheist-blogosphere-on-unscientific-america/.

p-forum: Nutrient Imbalances in Agricultural Development Vitousek et al. (19 June 2009) [Full text] [PDF] Nutrient Imbalances in Agricultural Development Response to E. Ongley and Y. Tao's E-Letter 3 November 2009 Peter M. Vitousek Department of Biology, Stanford University, Stanford, CA 94305, USA Respond to this E-Letter: Re: Response to E. Ongley and Y. Tao's E-Letter E. Ongley and Y. Tao do not disagree with our point, based on thorough experimental research summarized by X.-T. Ju et al. (1), that additions of N and P to double-cropped fields in the North China Plain (NCP) and elsewhere are both excessive and environmentally damaging (2). Their disagreement is with unreferenced analyses by "Chinese scientists" concluding that the majority of N and P in surface water in a particular catchment of the NCP derives from agricultural systems. Ongley and Tao suggest that excessive fertilizer use there pollutes groundwater rather than surface water, and that excessive withdrawals of that polluted groundwater have broken the connection between groundwater and base flow in regional rivers. We agree that understanding the distribution of excessive nutrient additions in particular sites and regions requires knowledge of local conditions; as Ju et al. demonstrate (1), the fates of these nutrients differ substantially in double-cropped systems in North versus South China. However, regardless of this variation in loss, agri-environmental policies must focus on the fundamental problem—additions of nutrients in excess of crop requirements. Where farmers add more than 200 kg ha-1 year-1 and 50 kg ha-1 year-1 of N and P, respectively, in excess of what can be used by crops (1), environmental degradation is inevitable. That degradation may be experienced in soils, groundwater, surface water, regional air quality, and/or greenhouse gas accumulation; the answer will typically be "all of the above, but to differing extents depending on site conditions and management practices" (3). We doubt that surface waters in the NCP are largely free of agricultural influence. The volatilization and atmospheric deposition documented by Ju et al. (1) and base flow from groundwater (however reduced by withdrawals), as well as the runoff from animal systems and occasional storms mentioned by Ongley and Tao, are all likely to cause elevated N and P concentrations in surface waters. However, the larger point is that we should focus on the source of excessive nutrients in agricultural systems, not on just one of their several fates. Peter M. Vitousek Department of Biology, Stanford University, Stanford, CA 94305, USA. References 1. X.-T. Ju et al., Proc. Natl. Acad. Sci. U.S.A. 106, 3041 (2009). 2. P. M. Vitousek et al., Science 324, 1519 (2009). 3. J.-W. Erisman, M. A. Sutton, J. Galloway, Z. Klimont, W. Winiwarter, Nat. Geosci. 1, 636 (2008). Nutrient Imbalances in Agricultural Development Agricultural N and P Runoff: A Major Pollutant of NCP Surface Water? 3 November 2009 Edwin Ongley , Yu Tao Respond to this E-Letter: Re: Agricultural N and P Runoff: A Major Pollutant of NCP Surface Water? P. M. Vitousek et al's. Policy Forum on fertilizer use and potential environmental impacts, at least for the North China Plain (NCP) ("Nutrient imbalances in agricultural development," 19 June 2009, p. 1519), has the potential to skew policy priorities by misidentifying causes and effects. Chinese scientists claim that agricultural N and P contribute a substantial component of total river pollution loads (1). We believe that methodological problems result in substantial overestimation (1). Increasing aridity and capture of surface water on the fields means that during many years there is little or no runoff. N pollutes groundwater, but without runoff, there can be no fertilizer contributing to surface water pollution. It is not known whether decadal rainfall events that produce major runoff from fields are significant for receiving waters, whether these respond more to smaller but more frequent events, or whether frequent runoff events are important relative to the large loadings on a continuous basis from urban and industrial sources. If the first is true, then agricultural impact must consider nutrient accumulation on the field; if the second or third is true, then there may be little effect on receiving waters. The only clear link between agriculture and surface water quality on an annual basis is that of farm and village feedlot operations that are located on banks of canals to facilitate cleaning of (mainly) liquid wastes. The N levels in groundwater have no effect on surface water, given that NCP rivers receive little to no base flow due to excessive draw-down of the groundwater table. Chinese non-point source investigations routinely ignore atmospheric N input that may amount to as much as 25% of the total N in fertilizer (2). For lakes throughout China, point-source and non-point source nutrient loads remain poorly quantified, with large degrees of uncertainty (3). Edwin Ongley Environment Canada (retired), Montreal, Canada. Yu Tao Chinese Research Academy of Environmental Sciences, Beijing, China. References 1. E. D. Ongley, Y. Tao, in The Management of Water Quality and Irrigation Technologies, J. Albiac, A. Dinar, Eds. (Earthscan Publications UK, 2009), pp. 7–39. 2. J. L. Shen et al., Environ. Pollut. (2009). 3. Y. Wang, in The Management of Water Quality and Irrigation Technologies, J. Albiac, A. Dinar, Eds. (Earthscan Publications UK, 2009), pp. 117–134.

perspective: OCEANS: Limits to Marine Life Brewer and Peltzer (17 April 2009) [Full text] [PDF] OCEANS: Limits to Marine Life Response to B. Seibel et al's. E-Letter 13 November 2009 Peter G. Brewer Montgomery Bay Aquarium Research Institute, 7700 Sandholt Road, Moss Landing, CA 95039, USA, Edward T. Peltzer Respond to this E-Letter: Re: Response to B. Seibel et al's. E-Letter The comments of B.Seibel et al. precisely illustrate the problem policy-makers face when they are confronted with such basic questions as "Is there a dangerous threshold for climate change and CO2 levels?" and "What are the impacts of elevated CO2 levels and climate change on marine life?" The approach by Seibel et al. does not help to provide quantitative answers to these questions. Climate change is complex but nonetheless scientists have made great strides in providing realistic answers as illustrated by the IPCC series of reports. Unfortunately, the translation of the physiological processes supporting marine life into a simple and robust numerical system compatible with climate change models still presents a substantial challenge. Without this we are not able to make useful predictions about the future of life in the ocean. Furthermore, Seibel et al. suggest that thermodynamic rules do not apply and that physical limits to aerobic life do not exist. We disagree. In our Perspective (1), we explicitly stated that "Actual limits will be species dependent and remain to be determined (see the figure for some hypothetical limits)." We thus anticipated many of the species-specific issues raised here. The additional question of whether the extreme life forms cited as tolerant of a high CO2, low O2 ocean world are considered to be a desirable outcome is another matter. As one of us has noted (2): "There will be ecological losers on a very large scale. We may also find winners along the way as animals that can tolerate a high-CO2 ocean will expand their range, but we cannot say whether any of these species will be those valued by mankind." This comment remains true today. Thermodynamic rules are very commonly used to describe challenges to marine life. For example, the thermodynamic property of aragonite saturation state is used in the now rapidly growing body of ocean acidification literature to quantify the challenges to coral reefs (3, 4). These too are open systems, so why is this problem different from respiration limits? There is plenty of carbonate and calcium out there, so why bother with a thermodynamic calculation? We bother because experience has taught us that the thermodynamic conditions impose limits. Although the impact varies according to the species, the aragonite saturation state provides an essential index for quantifying those limits and observing trends both spatially and temporally. Although there are many species well adapted to forming aragonitic shells at low pH—there are even fresh water oysters forming pearls and happily growing at pH < 7—scientists cannot in good conscience point this out as an acceptable outcome for the ocean or tell those concerned with coral reefs that there are plenty of examples of evolutionary adaptation to calcification at lower pH. Thus the thermodynamic limit of aragonite saturation has become an important benchmark for scientists and policy-makers alike. The limits to aerobic life are indeed bounded by the external fluid. All surfaces in the ocean, including those involved in respiration, are linked to the bulk fluid through a diffusive boundary layer. This is a fundamental principle of all air-sea gas exchange models (5), of mineral dissolution rates (6), and in setting limits to phytoplankton growth rates (7). More recently, detailed observations of the physical boundary layer surrounding marine animals in motion (8) have been presented clearly showing restricted mixing in a boundary layer extending well beyond the molecular diffusion layer. The limiting rate of transport of O2 in, and CO2 out, of a respiratory system is that of molecular diffusion in the boundary layer. The limit is set when there is no gradient; that is, for a diffusive boundary layer of thickness z the external partial pressure of oxygen (pO2) and/or partial pressure of carbon dioxide (pCO2) is equal to the internal state and diffusive chemical transport will not occur. At that point the animal will either sense the limit and vacate the space, or adapt to the challenge by either altering body chemistry to change the pO2:pCO2 ratio, or increasing water velocity over its surface to thin the boundary layer. This kinetic option will increase the rates of exchange, but not change the molecular ratio. Both strategies take work (meaning an expenditure of energy), which will impose stress on the organism that must somehow be accounted for, and thus some numerical formalism is required. The ratio of the gas fugacities we provide offers the most practical and general approach for this assessment. A few animals are already adapted to chemically stressed environments as noted by Seibel et al.; we may consider these as poised at some point on the pO2/pCO2 scale. In a changing world they must respond to this condition as above to maintain their status; they too are driven by this constraint. Even the hydrothermal vent worms now living at respiration index (RI) ≤ 0 which possess the chemical option and "maintain an arterial pH well above that of the CO2-enriched seawater in which they live" must expend additional resources when their external conditions change for the worse, and our discussion relates to evaluating a world of global change. The record of geochemical description of ocean sub-oxic conditions is very clear. The classic chapter by A. C. Redfield et al. (9) defined the series of chemical events occurring when dissolved O2 levels fall below a critical value, typically about 5 to 10 micromoles/kg. At that point dissolved O2 levels become limiting, most aerobic microbes turn to alternate electron acceptors, and iodate, nitrate, etc. are reduced. This limit has been cited in virtually all ocean geochemical textbooks for over 40 years. While the equivalent CO2 side of the classic Redfield equation as written was always present, to our knowledge it was not used. We have simply included that term as a newly changing constraint since it is the rapidly changing term and the impact of this is of world-wide interest. We show that it can indeed exert a significant influence in chemically stressed regions of the ocean today; our calculations show that previously unanticipated very high pCO2 levels will be reached in the mid-waters of the future ocean. Widely cited reviews of ocean hypoxia (10, 11) are absent any mention of the pCO2 condition, and show such reluctance to quantification that "concept" graphs are used for illustration (10) making it difficult to place this within the framework of a changing CO2 world. Yet we all know from the basic respiration equation that the changing CO2 chemistry will have an impact. Elegant models predicting the future O2 status of the ocean are now available (12) showing a large expansion of low O2 conditions. Adding the changing CO2 condition and finding clear and robust ways to relate these combined effects to the challenges faced by marine life is an important task. Our Perspective (1) is a simple plea for "a precise, universally accepted definition that would allow a common limit to be used when mapping changing conditions." We do not have that at present. For example, simply presenting a dissolved O2 number without the accompanying temperature and salinity does not allow pO2 to be calculated. And equally, without presenting pCO2 data we are missing an essential component. The complexity of global change is so huge that it is wise to have some clear examples to guide us. After publication of our Perspective (1), we came across the classic paper on the respiration and asphyxiation of the squid Loligo pealei (13). Those data show that the animal expired at a pO2:pCO2 ratio of about 25:1, or a RI of 1.4; the clarity is much appreciated. The common squid is a high-performance animal not representative of all marine species, but calamari is highly prized as a human delicacy and it would surely be missed if displaced from the region it occupies today. We could do worse to find an iconic example of the challenge faced by marine life in the quickly developing growth of low pO2-high pCO2 zones. Peter G. Brewer and Edward T. Peltzer Monterey Bay Aquarium Research Institute, 7700 Sandholdt Road, Moss Landing, CA 95039, USA. References 1. P. G. Brewer, E. T. Peltzer, Science 324, 347 (2009). 2. R. J. Cicerone et al., Eos 85, 351 (2004). 3. J. C. Orr et al., Nature 437, 681 (2005). 4. Royal Society, Ocean Acidification due to Increasing Carbon Dioxide (R. Soc., London, 2005). 5. W. S. Broecker, T.-H. Peng, Tracers in the Sea (Eldigio Press, Lamont Doherty Geological Observatory, 1982). 6. P. H. Santschi et al., J. Geophys. Res. 96, 10,641 (1991). 7. D. Wolf-Gladrow, U. Riebesell, Mar. Chem. 59, 17 (1997). 8. K. Katija, J. O. Dabiri, Nature 460, 624 (2009). 9. A. C. Redfield et al., The Sea (Wiley-Interscience, New York, 1963), vol. 2. 10. R. J. Diaz, R. Rosenberg, Science 321, 926 (2008). 11. J. S. Gray et al., Mar. Ecol. Prog. Ser. 238, 249 (2002). 12. G. Shaffer et al., Nature Geosci. 2, 105 (2009). 13. A. C. Redfield, R. Goodkind, J. Exp. Biol. 6, 340 (1929). OCEANS: Limits to Marine Life Critique of the Respiration Index 13 November 2009 Brad A. Seibel Department of Biological Sciences, University of Rhode Island, Kingston, RI 02891, USA, Peter R. Girguis, James J. Childress Respond to this E-Letter: Re: Critique of the Respiration Index The respiration index (RI = Log10{PO2/PCO2}), proposed by P. G. Brewer and E. T. Peltzer ("Limits to marine life," Perspectives, 17 April 2009, p. 347), is theoretically invalid as a metric to define the operational limits of marine life and results in dangerous predictions regarding the tolerance of marine organisms to ocean acidification and expanding oxygen mininum zones. Human emissions of carbon dioxide will affect marine ecosystems directly through ocean acidification (1) and indirectly through expanding oxygen minimum zones (2). Understanding the extent and severity of the impact on organisms requires knowledge of both oxygen and carbon dioxide levels. Such critical levels represent species-specific adaptations in oxygen uptake and acid-base regulation that have evolved for each species within their specific habitats. One cannot set a single index for tolerance of these parameters because individual species have evolved unique tolerances to their habitats, and these limits are usually far from the ultimate limits that can evolve in extreme habitats. An RI < 0.4 is proposed as an approximate limit for prokaryotes, while an RI < 1.0 is supposedly limiting to metazoans. This fails to consider organismal physiology (3), assuming that the energy obtainable (free energy, ∆G) from oxidation of organic carbon (Corg) in cellular respiration is linearly related to the ambient partial pressures (P) of reactants and products, as if in a closed system moving toward equilibrium. Brewer and Peltzer further assume that the gas partial pressures inside the cell, where aerobic respiration occurs, are equivalent to those in the environment. Both of these assumptions are incorrect and, as a result, the RI is inconsistent with the available physiological data on oxygen and carbon dioxide tolerances of organisms. Intracellular concentrations of oxygen and carbon dioxide are regulated independently by kinetic and physiological mechanisms. Critical thresholds for oxygen and carbon dioxide are independent of each other and result, not from reductions in free energy of Corg oxidation, but from limits to oxygen supply and acid-base regulation, which vary widely among species (7). Brewer and Peltzer suggest that the oxidation of Corg to CO2 and H2O during cellular respiration may be expressed as a Gibbs function: ∆G = ∆G° - RT * ln([PCO2]/[Corg][PO2]) where ∆G° is the free energy under standard conditions in vitro, R is the universal gas constant, and T is temperature. Thermodynamics is the driving force for all chemical reactions, including those mediated by organisms. However, the Gibbs function as used by Brewer and Peltzer is descriptive only of closed systems, in which the substrates for the reaction are consumed and the products accumulate. In such cases, the ratio of the concentrations of reactants influences the tendency of the reaction to progress in either a net forward or reverse direction until equilibrium is reached, at which point no net flux occurs and ∆G is zero. In contrast, living organisms are open systems that acquire free energy from their surroundings and operate at an approximate steady state (4). The concentrations of substrates and products in living systems are actively maintained at disequilibrium to ensure a constant ∆G and thus, thermodynamic drive, for forward flux through the pathways of energy metabolism (5, 6). The RI is further flawed because it fails to distinguish intracellular from environmental gas partial pressures. This distinction is especially important within the marine oxygen minimum zones discussed by Brewer and Peltzer, where the total quantity of oxygen is not limiting, just its availability (7). This means that resident organisms can, through physiological adaptations, obtain sufficient oxygen despite an environmental RI well below 1. Oxygen is extracted by active ventilation of the seawater and rapid circulation of blood across gills of large surface area (7). It is concentrated and transported through high-affinity respiratory proteins in extra- and intracellular circulatory systems (8). The local acid-base balance can be adjusted actively to enhance oxygen off-loading at the respiring tissues. Even in organisms without extracellular circulatory systems, the enzyme complexes in metabolic pathways contribute to oxygen flux through adapted oxygen affinities [such as the Michaelis constant for O2 of cytochrome C oxidase in electron transport (9)]. Thus, the effective concentration of oxygen at the energy metabolism site may be higher than in the environment and, above a critical level, is independent of environmental oxygen concentration and rates of oxygen demand (8). It is this capacity for oxygen uptake, relative to energy demand, that determines hypoxia tolerance in organisms (9). The effect of increasing PCO2 (hypercapnia) on metabolism is complex, but often includes pH effects on protein function. Hypercapnia can lead to oxygen limitation among organisms with respiratory proteins because oxygen-binding affinity is adaptively pH-sensitive. Furthermore, hypercapnia can adversely affect cellular function by reducing cytoplasmic pH. However, most organisms are well adapted to control vascular and intracellular pH and PCO2 by passive chemical buffering, catalytic conversion (to bicarbonate) and active transport (10). For example, siboglinid worms living at hydrothermal vents are capable of extruding proton equivalents at an extremely high rate to maintain an arterial pH well above that of the CO2-enriched seawater in which they live (11). Accordingly, they are capable of carrying out aerobic respiration at an environmental RI well below zero (12). Another example of organismal adaptations is found in Gnathophausia ingens, a midwater crustacean living at hypoxic depths off California (13). This species' ability to extract oxygen from the ambient water is enhanced at low pH (7.1). In light of such adaptations to regulate internal gas partial pressures, ocean scientists "typically ignore the CO2 side of the respiration equation," not on the "unspoken assumption that PCO2 levels are low" as stated by Brewer and Peltzer, but because the equilibrium state of the overall reaction is not influenced by gas partial pressures. Dead zones do not typically result from absolute limits to biological function, but rather from the evolved performance limitations among individual marine species within each habitat. We know that the evolved limits correlate with the minimum oxygen level experienced by individual species and very different limits are found among marine organisms living in different marine environments (7). Dead zones will likely be exacerbated by expanding hypoxia, and may be influenced by ocean acidification under some circumstances. However, adaptation to specific environments cannot be accommodated by the RI, which leads to dangerously wrong predictions. The authors state, for example, that normal aerobic function will not be affected by ocean acidification in well-oxygenated waters. However, the deleterious influence of carbon dioxide on oxygen transport may be most pronounced in well-oxygenated surface waters where high temperature and activity levels drive oxygen demand toward the limits of transport capacity (14). Furthermore, the RI may lead readers to conclude that most marine animals are oxygen limited only at very low PO2 (RI < 1). In contrast, most marine organisms are not adapted to hypoxic conditions and become limited at much higher oxygen partial pressures (for instance, at an RI ~ 2; 15). Thus, regions where oxygen-minimum zones expand onto otherwise oxygenated shelves stand to be most dramatically affected. This may be seen off the coast of Oregon, where water from the oxygen-minimum layer containing a rich and abundant fauna adapted to low oxygen creates a dead zone when it enters shallower depths and encompasses animals that have not evolved adaptations to low PO2 levels (16, 17). No general predictive index for oxygen and CO2 tolerance is possible because tolerances to these parameters have evolved in individual species due to selection by their particular environmental conditions. Tolerance of hypoxia and hypercapnia is species specific and reflects their evolutionary adaptation to regional variation in environmental gas levels over long periods of time. Brad A. Seibel Department of Biological Sciences, University of Rhode Island, Kingston, RI 02891, USA. Peter R. Girguis Department of Organismal and Evolutionary Biology, Harvard University, Cambridge, MA 02138, USA. James J. 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