Originally posted by bobkrech
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Thanks for the reference.
None of the work has been published in a peer reviewed journal, and the evidence of brain damage is indirect at best. A juvenile large mouth bass put into a 2 1/2 gallon aquarium with 2 others, might exhibit some stress under normal circumstances when confined in this maner.
Even the investigator states that much more work has to be done before any conclusions can be drawn. This quick 2 day study seems like a quick and dirty experiment to get some data for a grant proposal.
Bob Krech
The study was published in a peer reviewed journal.
https://ehp.niehs.nih.gov/members/2004/7021/7021.pdf
What she measured has nothing to do with environmental stress. She measured significant peroxidation of brain tissues. High population density would tend to lower hyperoxides (more waste material from more animals undergoing more oxidation in the environment leaving less to inhale). Thus, her exposure control populations exposed to H2O2 were a good choice. She also had non-exposure controls similarly confined and they showed no effects. The H2O2 exposed showed peroxidation in gill and liver, sites tasked with countering hypreoxide exposure via supreoxide dismutase reactions, but not in the brain which depends on filtering of hyperoxides by the rest of the body in order to prevent damage. As proof of the latter, consider that those brain problems caused by oxidative stress are usually internally generated (i.e neuronal death mediated by MPTP/MPP+ in Parkinsonism). Her study showed that something that could cause oxidative stress problems elsewhere were not nullified by SOD and making it across the blood/brain barrier.
Her comments about it being "just the first step" is a common understated way to say "I was first", and also leading to the inevitable "more work needs to be done". No scientist worth their grant money will ever say "That's enough, we don't need any more work done here".
My work on secondary chemicals from tobacco focused on prevention of MPP+ production from MPTP by preventing oxidation via monoamine oxidase inhibition, and so prevention of damage to the substantia nigra (Parkinson's) required only 6, 12 or 18 hours of exposure to MPTP, followed immediately, 6 hours, or 12 hours by exposure to the hypothetical prevention mechanism, trimethyl naphthoquinone. Measurng cell death required up to 30 days, but measuring the changes in neuronal tissue precursor to it could be done immediately, and the both were shown to correlate. So, I think I can confidently state that I can read her work and evaluate it, and that I find nothing wrong with a two day exposure cycle. I find the fact that statistically significant results were obtained with such short exposure to make it more important, not less. My own work was on the humans, not the mice, and my tests required overnight abstinence for tobacco, testing, smoking a cigarette, and testing again within 15 minutes (the half life of tobacco blood level being 17 minutes). That's some mighty short exposure cycle. I could only test one at a time rather than a bunch at once, but my testing took less than two hours, including taking them across campus for a blood draw. I there'd been 20 of me and 20 EEGs, the data collection would have been done in two days (each subject being tested twice, on different days).
She has 14 first authorships in 6 years, plus 8 non-firsts. That's a paper every 3 months. She's doing something right. Being married to a co-researcher and daughter-in-law of another probably helps. Makes it easier, but not less valid. Reading over her other work, primarily horomonal, I suspect they handed her a project to conduct, while they were the experts in the associated biochemistry, but that doesn't make it less valid either. The primary investigator need not be the primary expert; secondary authors are frequently expert consultants that sometimes never see the apparatus. In her case she went home every night with one of them.
As is common, Wired is a horrible source for reading anything scientific. If they knew what they were doing, they would have associated her gill results with the increase in asthma in people exposed to exhaust from diesel motors, a common source of buckballs in the soot. Their comment about it being unpublished was technically correct in that it hadn't appeared yet. It was in Wired on 7 April 2004, and in Environmental Health Perspectives on 1 July 2004. It was at least "submitted; under review", but was almost certainly completed and accepted, since it was made available online by EHP the same day the Wired article came out. Perhaps the "unpublished" was accurate when the interview, article research and writing was done.
