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| Blacktail shiner, C. venusta Source: Futurity.org |
1. Dose - The authors of a 2012 Endocrine Reviews article on low-dose endocrine disruptors point out (p. 18) that the EPA extrapolated reference dose for BPA in humans = 50 ug / kg body weight (Update, 7/12/12 - Check the comments for a more applicable animal toxicity value). That means, according to them, that you could eat a few specks of it with dinner every day for the rest of your life, and suffer no ill effects.
So what does this have to do with the fish paper? Note the dose (p.3): 1280 ug / L. Do the math: 1L of water = 1000 mL, density of water (room temp) = 1 g / mL, thus 1L = 1 kg. How much does a fish weigh, a few grams at most? This study overdoses them by at least a few orders of magnitude. Pardon the pun, but these little guys are literally swimming in BPA. Furthermore, the scientists change out the tank water every 24 hours, so the fish are certainly overexposed relative to their control brethren.
2. Cosolvent Effects - BPA has relatively low water solubility, so the authors dissolve it into their mixture with a cosolvent, triethylene glycol. Well, that's fine, as long as they run the control - water with triethylene glycol and no BPA - which they have. So, what happened? The female fish studied show no appreciable difference (Table 1) between straight H2O and cosolvent-H2O mixtures. Pity the poor blacktail shiner (C. venusta) males, though: they show marked dropoffs in all courtship metrics from cosolvent control water alone! (No BPA added). This data point does not merit discussion in the paper, however.
3. Standard Environment - Coloration and mating behavior definitely both suffer when we lock fish in tanks bombarded with BPA. But what about in the wild? How much BPA do these fish encounter in their native river habitats? Anywhere near these concentrations? Do wild fish caught on-site exhibit these same color losses? Is BPA exposure the sole factor influencing interspecies hybridization?
Readers, I'm no evolutionary biologist, so please set me straight on a few of these points. To clarify, I don't deny that xenobiotics (atrazine, estradiol) can affect marine life, but this particular study seems somewhat subject to interpretation - a scientific 'fish story.'
Perhaps pertinent to this is the problem with Colony Collapse Disorder (CCD), which has nearly wiped out the honey bee in North America.
ReplyDeleteThey were blaming it on mites, on diseases, on global warming, even cell phones. (Actually, the cell phones in an odd way were a hint to the actual cause.) The one thing that everyone accepted could not be the cause was pesticide use, because the pesticides in use were harmless to bees.
So they thought.
The latest research (May 2012) showed that a class of pesticides assumed to be harmless to honey bees actually isn't. While individual bees could survive an accidental application, the pesticide was being collected in pollen and nectar and thereby being stored and concentrated in the hives. There, the pesticide began to have a long term effect. Where the stored pesticides did not outright kill individual bees, it weakened them and left them vulnerable to diseases and parasites, and led to the rapid collapse of many beehives.
The cellphone correlation? Most commercial farming operations and bee-keeping is in areas where cellphones are in prevalent use. Wild hives in rural areas away from modern farming systems, were less likely to be exposed to pesticides. Hence, why hives near populated areas (and thereby, cellphones) were more affected than wild hives in isolated areas.
Bioaccumulation, the concentration up through the food chain you mention, is certainly cause for concern with endocrine disruptors. However, in the present study (14 days long), I doubt there's enough time to prove persistent effects.
DeleteAs to your first point on dose, you're right that the little guys are literally swimming in BPA, but your comparison with a human reference dose isn't quite the right way to get there. A better way is to compare with the fish equivalent called a predicted-no-effect-concentration (PNEC), which in Europe has recently been set at 1.5 micrograms/L (other estimtes are higher). Like a reference dose for humans, the PNEC is a conservative value with safety factors built in. Multi-generation studies on fish indicate no effects at concentrations in the range of 16 micrograms/L (the NOEC), with effects being observed at higher concentrations. So, the 1,280 micrograms/L test concentration is >800 times above the PNEC and 80 times above the NOEC. As you say, they're literally swiminng in BPA, at a level that would be expected to cause effects.
ReplyDeleteOn your third point, and more importantly, the median concentration of BPA detected in North American freshwater is 0.081 micrograms/L with 95th %ile at 0.47 micrograms/L (see http://dx.doi.org/10.1021/es900598e). Levels in Europe look to be a bit lower. The test concentration was >15,000 times higher than the median actually in North American freshwater and >2,700 above the 95th %ile.
Unfortunately the researchers only tested one very high concentration so difficult to know if their results are of any environmental significance.
Wow, thanks for that! This might be the most technically replete comment I've ever received...
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