A recent article by Girouard and Zagury (doi:10.1016/j.scitotenv.2008.12.019) on the available of arsenic bound in soil highlights a recurring theme in soil environmental toxicology. Our current measurement techniques for contaminants in soil may be significantly underestimating the risk associated with a polluted soil to small children. Typically, we recommend that soils be sieved to pass a 2 mm sieve, or in other words, only particles less than 2 mm are analyzed. Sometimes we suggest that soils should be sieved to pass a 0.25 mm sieve. The reason we do this is that we know that concentrations of pollutants increase as we sieve to smaller and smaller sizes. However, what we don’t know is how ‘available’ pollutants in these smaller size classes would be to small children, or in other words, how easily can pollutants in small sized particles enter our bloodstream. The work by Girouard and Zagury indicates that the answer to this question is: more easily. Thus, the smaller the particles the more risk is posed to small children who might accidentally eat these soils. (as an aside, I’m sure you are wondering how much soil a children will eat. We estimate around 100 mg per day but in some cases, children can eat up to 13 g). As a society we need to revist how we assess risk from contaminated soils and ask the question: are we being protective enough?

Well it has been a frustrating week.  Methanol can be substituted but peaks broaden and more non-polar substances co-elute.  The Thermo guideline is a good first step but I think that the method development is going to take longer than I had initially hoped.   Hopefully the acetonitrile shortage will alleviate soon and we can go back to the original solvents.

A recent article (doi:10.1016/j.chemosphere.2007.08.035) by Budinsky et al investigated how readily dioxins and furans that contaminate soil can enter into our bloodstream.  They used two different animals to test this, a rat and a swine model. They used a rat model because the carcinogenic risk factors associated with dioxins and furans have been derived from rat toxicological data.  They also used a swine model because juvenile swine are our best available animal model for human exposure to ingested contaminated soil.

Two key findings jump out of this study. The first is that for rats around 30% of the dioxins reached the bloodstream whereas for pigs it was around 23%.  In contrast, a common chemical test meant to assess exposure to humans predicted only a 17%.  Thus, it looks like certain in vitro digestors might be underestimating exposure by around 2 fold. This should not be too surprising as currently the use of in vitro digestors for organic chemicals is not well accepted and still require substantial research and development before we begin to accept their use to predict human exposure.

The second key finding was that EROD activity varied depending on if the rats were exposed to dioxins in soil compared to oil.  This finding is very troubling.  Often we assess exposure of organic chemicals on the induction of these EROD enzymes (a subset of the P450 enzyme group).   The work by Budinsky et al. indicates that this may not be appropriate.  The reason is that typically an animal is exposed to the organic chemical in some sort of carrier, like corn oil and then this is compared to the organic chemical in soil.  What Budinksy et al. findings show is that the soil itself influences EROD activity.  Thus, if we calculate relative bioavailability through EROD activity it will be confounded by the dosing vehicle.

At the end of the day, I think that the Budinsky et al. article highlights how little we understand about pollutants in soil.  It certainly demonstrated to me that when working with pollutants in soil we need to be extra vigilant that we don’t make any assumptions until they are rigourously checked.

If you want to find this article and read about it yourself, simply open http://dx.doi.org and enter doi:10.1016/j.chemosphere.2007.08.035 in the text box provided, and then click Go