Tuesday, November 30, 2010

Ecotoxicologists: heed this advice!

As my readers likely know by now, seabirds are often used as bioindicators of contaminants in aquatic ecosystems. Such studies rely on the fact that contaminants are ingested through contaminted prey so that contaminants in seabirds are reflective of the local diet - and ecosystem. But it turns out that linking contaminant exposures to diet in seabirds is more tricky then  many biologists realize.

A recent paper by Alexander Bond discusses the utility - or futility - of comparing diet and contaminant signatures within feathers of seabirds. Such studies often rely on stable carbon and nitrogen isotopes to evaluate diet.



Nitrogen isotopes increase in a predicatable stepwise fashion from prey to consumer, providing a signature of an individuals position within the food web (trophic level). Stable carbon doesn't follow the same enrichment from one trophic level to the next, but carbon signatures can differentiate prey ingested in marine/freshwater habitats or benthic/pelagic habitats.  These isotope signatures of various tissues reflect the birds diet at the time of tissue synthesis. So for flight feathers which can take about a month to grow, they isotope signatures within the feathers indicate the birds diet during that month of feather growth. Easy enough.

Contaminants on the other hand, aren't quite as predictable. Mercury for example, is ingested via prey and excreted through gauno, feathers, and eggs. But before excretion, it passes through the liver where some Hg is converted to inorganic Hg. Whatever MeHg is left remains in a body resevoir until it can be excreted through molting (feathers) or egg production. What this means is that Hg in feathers is equal to Hg ingested in the diet, less Hg detoxified in the liver and Hg eliminated into other feathers and eggs. But the time scales of isotope and contaminant integration in tissues don't exactly line up because there is also a body pool of Hg that biologists haven't determined precise excretion rates for.

So Bond makes an important point that many seabird contaminant papers using isotopes to explain how diet influences contaminant burdens, may be comparing apples and oranges. Thus it becomes critical to know which tissues do indeed reflect local diet and contaminant exposure (i.e. blood). He concludes that relationships between trophic position and contaminants are therefore not much of a relationship at all, unless the time scales are closely matched.

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