We have seen some recent outbreaks of Escherichia coli O157:H7, the common pathogenic strain of the common gut bacterium, in the human food supply, most notably in spinach last fall.

Since then, it has been common to see assertions in the mainstream media (e.g. by the quite knowledgeable food industry writer Michael Pollan) that E. coli O157 is purely a product of the mega-feedlot industry, because the pathogen is not found in the guts of grass-fed cattle. It is a very attractive assertion to those of us who support a trend away from factory farms, which are demonstrably less healthy both to humans and the environment in many ways. So, I thought it would be worthwhile to investigate this further.

Buried within a forest of "green" sites promoting this idea was a link by a commenter to a brief Kansas State news release claiming that this assertion was false. Dr. David Renter, assistant professor of veterinary epidemiology at KSU, has done research himself on this important human health topic and has studied the prevalence of E. coli O157 not only in feedlot vs. range-fed cattle, but in wildlife as well.

In Renter et al., 2003, he and his colleagues found E. coli O157 in 2.48% of fecal samples from rangeland cattle in Kansas and Nebraska, similar to a rate found in previous studies of "confined" (=feedlot) cattle. They also tested several hundred samples from wildlife, including coyotes, whitetailed deer, raccoons, and possums. In wildlife, the pathogen was only found in one possum sample.

An earlier study (Renter et al., 2001) confirmed the presence of E. coli O157 in fecal samples from wild deer in Nebraska, albeit at the very low rate of 0.25% (a rate of 25 out of 10,000).

Surpirsingly, Kudva et al. (1997) found, in sheep, the opposite trend I expected to see based on media reports on cows. Animals were innoculated with E. coli O157, then fed one of two diets: grass hay, or corn and alfalfa. In this case, grass-fed sheep were shedding bacteria twice as long as corn/alfalfa-fed sheep.

So where did the grain vs. grass theory come from? It turns out it was from a Science paper in 1998 by Diez-Gonzalez et al., which did not specifically address pathogenic E. coli. As explained by Gannon et al. (2002):

A grass diet would certainly be expected to cause a change in the intestinal microflora as well as parameters such as volatile fatty acid species and concentrations and the pH of the digesta. A recent study has shown that grain feeding selects for acidresistant E. coli strains and that feeding Timothy hay rapidly reduces the numbers of these organisms shed in the faeces... While this appears to be the case, the authors of this somewhat controversial study failed to demonstrate that E. coli O157: H7 was one of the acid-resistant E. coli strains selected for by grain feeding and reduced by hay feeding. Recent studies by Hovde and colleagues ... showed that hay feeding increases rather than decreases faecal shedding of E. coli O157: H7 by beef cattle which were orally inoculated with the organism.
... In addition, naturally occurring antimicrobial substances in certain plants may play a role in faecal shedding of the organism by cattle e.g. Duncan and colleagues have shown that certain coumarins derived from plants inhibit growth of E. coli O157: H7.

So, once again, complex nuances in a biological system fail to penetrate the aura of the either-or dichotomy so loved by the media.

There is no doubt that the relationship between E. coli, domesticated animals, and husbandry methods is not simple. As Renter et al. (2003) state:

The observed number of E. coli O157 XbaIPFGE subtypes, the frequency and persistence of specific subtypes, and the presence of indistinguishable subtypes in cattle, water, and wildlife indicate that the molecular epidemiology of E. coli O157 in range cattle production environments is complex. A clear description of the complex molecular epidemiology requires explicit definition of factors related to the molecular biology and micro- and macroecology of the organism.

The "subtypes" to which they refer number, in this study alone, 70 of just the O157 strain that they were studying. Many more exist. There are lots of possible ways to address the likely growing E. coli problem. Antibiotics are one, but there are of course problems with resistance there (Flucky et al., 2007). Hopefully, environmentally friendly rearing practices will be part of the solution, but it is clear they would not be a complete solution. E. coli O157, wherever and whenever it came from, will be with us for the duration. The question is, can we use prevention to keep it to a level that was shown in the wild deer (0.25%), or are we going to try to medicate it out of the system?

It would be wonderful if mass food supply problems had simple management answers - not that conversions of half our cattle back to pasture from feedlots would be easy. There are serious problems with our food supply, and we need aggressive journalists to be informing the public about agribusiness practices that should be changed in order to avoid major public health consequences - the recent melamine pet food scandal is a prime example of where both regulation and enforcement are severely lacking.

We need Michael Pollan and others like him to be watching out for us. But they must make absolutely sure that their credibility remains intact, because we need to know that they are more trustworthy sources than government and corporate spokesmen with obvious agendas. We need someone to be telling us the truth. So either the journalists must improve their scientific literacy enough to do the appropriate research for their story, or they must hire someone who has it already.

(Mr. Pollan, if you are hiring, I am available for freelance work.)


References:

Diez-Gonzalez F, Callaway TR, Kizoulis MG, Russell JB. (1998) Grain feeding and the dissemination of acidresistant Escherichia coli from cattle. Science, 281, 1666–8.

Fluckey, W.M., Loneragan, G.H., Warner, R. & Brashears, M.M. (2007) Antimicrobial drug resistance of Salmonella and Escherichia coli isolates from cattle feces, hides, and carcasses. Journal of Food Protection, 70, 551-556.

Gannon, V.P.J., Graham, T.A., King, R., Michele, P., Read, S., Ziebell, K. & Johnson, R.P. (2002) Escherichia coli O157: H7 infection in cows and calves in a beef cattle herd in Alberta, Canada. Epidemiology and Infection, 129, 163-172.

Kudva, I.T., Hunt, C.W., Williams, C.J., Nance, U.M. & Hovde, C.J. (1997) Evaluation of dietary influences on Escherichia coli O157:H7 shedding by sheep. Applied and Environmental Microbiology, 63, 3878-3886.

Renter, D.G., Sargeant, J.M. & Hungerford, L.L. (2004) Distribution of Escherichia coli O157: H7 within and among cattle operations in pasture-based agricultural areas. American Journal of Veterinary Research, 65, 1367-1376.

Renter, D.G., Sargeant, J.M., Oberst, R.D. & Samadpour, M. (2003) Diversity, frequency, and persistence of Escherichia coli O157 strains from range cattle environments. Applied and Environmental Microbiology, 69, 542-547.

Labels: ecology, environmental toxins, health

Recent concern about apparent die-offs in bees apparently has now led to speculation that cellphone radiation is the cause for bee disappearance. Instapundit has weighed in, questioning with well deserved skepticism the validity of this claim.

Because I am a scientist, I do not try to establish validity of such reports via Google, but via Web of Science, the search engine that encompasses academic literature, both peer-reviewed and not. As far as I am concerned, until data have been published in peer-reviewed literature, any fantastic "scientific" claims are just clamors for attention.

There is no information yet in the scientific literature regarding possible causes of CCD or "colony collapse disorder" as some have tagged the syndrome of the disappearing bees. This is not too surprising, because it appears to be a fairly recent phenomenon, but I guarantee you that because the USDA supports several Bee Research Laboratories in the western U.S., this problem, if genuine, is being addressed by qualified government scientists as I write (if all the bee lab guys I used to know weren't long retired from the lab, I would call one now to get his take on it).

The mere fact that the U.S.D.A. has labs of bee scientists confirms that domesticated honey bees are indeed important to the pollination of crops in the U.S. But as I pointed out in my last post on the topic, they are by no means the only species of pollinator out there. So don't expect any food shortage panics anytime soon.

What of the cell radiation theory then? Cell radiation has been a human health concern for quite some time, and thus the literature on this topic is quite robust. Some studies (but not others) have found increased cell apoptosis (cell death that is orderly - as opposed to sudden and widespread) due to exposure to cell radiation, but even this doesn't mean we should necessarily be alarmed, because all these studies were performed on cell cultures (in vitro), not on real people using cell phones in a usual manner (in vivo). A recent paper (Valberg, P.A., van Deventer, T.E. & Repacholi, M.H. (2007) Workgroup report: Base stations and wireless networks-radiofrequency (RF) exposures and health consequences. Environmental Health Perspectives, 115, 416-424.) examines evidence that radio-frequency radiation (including cell phones) affects actual human health adversely, and concludes that there is no evidence that it does so. In fact, the authors point out (from the abstract):

The possibility of RF health effects has been investigated in epidemiology studies of cellular telephone users and workers in RT occupations, in experiments with animals exposed to cell-phone RF, and via biophysical consideration of cell-phone RF electric-field intensity and the effect of RF modulation schemes. As summarized here, these separate avenues of scientific investigation provide little support for adverse health effects arising from RF exposure at levels below current international standards. Moreover, radio and television broadcast waves have exposed populations to RF for > 50 years with little evidence of deleterious health consequences. Despite unavoidable uncertainty, current scientific data are consistent with the conclusion that public exposures to permissible RF levels from mobile telephony and base stations are not likely to adversely affect human health.

Here is a table from the paper comparing all the sources of RF we are exposed to (sorry about the low resolution):

So my advice is, chat away until further notice - with the caveat that out of caution, avoid giving cell phones to young kids because developing brains are certainly more sensitive to environmental effects than grown ones, models suggest that child heads absorb EM radiation more than adult heads (De Salles, A.A., Bulla, G. & Rodriguez, C.E.F. (2006) Electromagnetic absorption in the head of adults and children due to mobile phone operation close to the head. Electromagnetic Biology And Medicine, 25, 349-360.). Obviously, if anyone had found major health effects yet there would have been a massive response to deal with it by some country.

Back to the bees though. Different species will not necessarily be affected the same way as humans, especially such distantly related groups such as insects, but as of yet I, as an entomologist who does not specialize in bees, doubt that cell radiation is causing CCD. The article quotes some one knowledgeable about cell radiation, not insects, in asserting the likelihood that it does. Most important, bees navigate primarily via polarized light, which is in a completely different part of the EM spectrum from radio waves. How radio waves could possibly impact their use of light for navigation (any more than it does humans' use of light for navigation) is at best nonintuitive, so I would never believe it until I saw the published paper showing me the evidence. I am not holding my breath for that paper to appear.

Other references:

Erogul, O., Oztas, E., Yildirim, I., Kir, T., Aydur, E., Komesli, G., Irkilata, H.C., Irmak, M.K. & Peker, A.F. (2006) Effects of electromagnetic radiation from a cellular phone on human sperm motility: An in vitro study. Archives Of Medical Research, 37, 840-843.

Joubert, V., Leveque, P., Cueille, M., Bourthoumieu, S. & Yardin, C. (2007) No apoptosis is induced in rat cortical neurons exposed to GSM phone fields. Bioelectromagnetics, 28, 115-121.

Remondini, D., Nylund, R., Reivinen, J., de Gannes, F.P., Veyret, B., Lagroye, I., Haro, E., Trillo, M.A., Capri, M., Franceschi, C., Schlatterer, K., Gminski, R., Fitzner, R., Tauber, R., Schuderer, J., Kuster, N., Leszczynski, D., Bersani, F. & Maercker, C. (2006) Gene expression changes in human cells after exposure to mobile phone microwaves. Proteomics, 6, 4745-4754.

Thorlin, T., Rouquette, J.M., Hamnerius, Y., Hansson, E., Persson, M., Bjorklund, U., Rosengren, L., Ronnback, L. & Persson, M. (2006) Exposure of cultured astroglial and microglial brain cells to 900 MHz microwave radiation. Radiation Research, 166, 409-421.

Zhao, T.Y., Zou, S.P. & Knapp, P.E. (2007) Exposure to cell phone radiation up-regulates apoptosis genes in primary cultures of neurons and astrocytes. Neuroscience Letters, 412, 34-38.

Labels: bees, behavior, environmental toxins

The paper below is no surprise. It's basically saying that burning fireworks creates all types of nasty toxins. The human health component of this I think is fairly well known, at least to anyone who has been in China or Hawai`i during Chinese holidays. The one New Year I was in Hawaii I spent partially in Honolulu and partially back home on Kaua`i. Fireworks started going on Dec. 30, and by the time I flew home on the 31st, two apartments had already burned down and it wasn't even dark yet. I lived in a fairly rural subdivision on former pineapple fields on Kaua`i, and the air was hardly breathable that night in my house, despite the fact that I set off no fireworks of my own.

State officials were trying to rein it in by the time I left Hawai`i in 2001. There were supposedly a lot more restrictions on fireworks use, which turns out to be a good thing not only for the asthma sufferers, but for the population at large. This paper makes me wonder for the first time what the toxins released from these celebrations a couple times a year (the other biggie is Chinese New Year; July 4th in Hawai`i is not nearly such a big event) are doing to the watershed. I guess on the bright side, the fireworks are pretty much limited to low elevations where there are almost no native species left anyway, so perhaps that's why I have not heard of it referred to as a major conservation issue...

Ying Wang; Guoshun Zhuang; Chang Xu; Zhisheng An, 2007. The air pollution caused by the burning of fireworks during the lantern festival in Beijing. Atmospheric Environment 41:417-431.

The effects of the burning of fireworks on air quality in Beijing was firstly assessed from the ambient concentrations of various air pollutants (SO2, NO2, PM2.5, PM10 and chemical components in the particles) during the lantern festival in 2006. Eighteen ions, 20 elements, and black carbon were measured in PM2.5 and PM10, and the levels of organic carbon could be well estimated from the concentrations of dicarboxylic acids. Primary components of Ba, K, Sr, Cl-, Pb, Mg and secondary components of C5H6O42-, C3H2O42-, C2O42-, C4H4O42-, SO42-, NO3- were over five times higher in the lantern days than in the normal days. The firework particles were acidic and of inorganic matter mostly with less amounts of secondary components. Primary aerosols from the burning of fireworks were mainly in the fine mode, while secondary formation of acidic anions mainly took place on the coarse particles. Nitrate was mainly formed through homogeneous gas-phase reactions of NO2, while sulfate was largely from heterogeneous catalytic transformations of SO2. Fe could catalyze the formation of nitrate through the reaction of alpha-Fe2O3 with HNO3, while in the formation of sulfate, Fe is not only the catalyst, but also the oxidant. A simple method using the concentration of potassium and a modified method using the ratio of Mg/Al have been developed to quantify the source contribution of fireworks. It was found that over 90% of the total mineral aerosol and 98% of Pb, 43% of total carbon, 28% of Zn, 8% of NO3-, and 3% of SO42- in PM2.5 were from the emissions of fireworks on the lantern night.

Labels: environmental toxins