***Q. Toxicology: regarding biotransformation: Detoxification:  metabolites of lower toxicity Bioactivation: metabolites more toxic than parent substance.  ToxTutorII gives the example of vinyl chloride to vinyl chloride epoxide, which covalently bonds to DNA.  Question:  Do scientists identify chemical traits that would likely result in bioactivation, is there a rule of thumb?  For example, two electrons in the outer shell leads to bioactivation, or hydrophilic compounds generally bioactivate. 
A. The buzz word is “structure-activity relationship.”  Some bioactivation can be predicted from chemistry and others determined in biochemical tests.  The Ames test for mutagenicity uses “microsomes” which are little chunks of the cell that do the bioactivation.  The chemical is then incubated with the microsomes and the mutagenicity tested. 

**Q.I’m a bit confused with the Level I models we did in module 4. We were considering the distribution of “our” chemical in different environmental sites. When I described the contribution of “my” chemical to the different sites I looked at the percentages of the chemical in each environment. But I have been reading further with these models and they say that the percentages in these models is not a result of the concentration but only of the mass, so if we include the volume of each media we will get a different result – sometimes the total opposite. Is this right?
A. Yes, the level I model is just to get you started with the concept of partitioning.  It has two flaws, one is it assumes the air is a constant volume, when if it a volatile substance the air will wash it away.  The other flaw is that it does not say anything about the rate of transfer, it only addresses equilibrium.  But Level I is a good start on the concept of partitioning.  So, your question, other than the air, you could estimate the volumes of the compartments in a real world problem, and then run the model.  If you choose a larger compartment, the concentrations computed by the model would be smaller.

**Q. As described in the material the Kow coefficients given by RAIS are different depending on the experimental and the estimated value. The values are: Experimental Log (L/Kg) = 4.74e+0 and Estimated Log (L/Kg) = 5.12e+0. Why is the different so big? And if we would apply the data to a Level I model which value would then be most reliable to use?  
A. It turns out that for the heavy PAHs, it is difficult to measure the Kow, and you will find different values from reliable sources.  In many cases they only test one or two chemicals in a homologous series, then use a model technique to predict the other Kow.  How, the difference between 4.74 and 5.12, as a practical matter, is small, since both indicate a very lipophilic substance that will rapidly partition out of water into fat or organic carbon. 

**Q. It seems like whenever I read medical info, they use “risk factors” to describe diseases.  The media tends to use “cancer causing”.  I know there are more precise definitions for each of these ideas, but is it just more scientifically conservative to talk about “risk factors” since everything is really just a explanation of probabilities?  For example, not all smokers get lung cancer [and some get cancer who do not smoke].  .  Is there a defined line between “increased risk” and “causes cancer” in the scientific community? 
A. In that sense in pathology, there are no “causes” of cancer, only risk factors. 

*Q. What leads to a “Ecological Risk Assessment” vs a “regular” risk assessment (as you described as “effect of chemicals in the environment on humans”).  Isn’t any outdoor contamination an “ecological” risk, or do all other organisms become a lesser concern if they are not a pathway to human exposure?
A. That’s really a question of administration, who’s paying for what.  But in general, human health risks are driven by current contamination and their likely effects for various levels of cleanup effort and cost – superfund cleanup.   Ecological risks are more often driven by desire to know what might be the effects from future contamination – permitting questions. 

*Q. Concerning Ghost Road Lake:  Let’s say the environmental consultant conducted his studies, PCP was found, and the contractor decides to walk away from the deal.  At that time, does the contractor have a legal obligation to report contaminated site to the city, or attach the findings to the property deed?  I understand exact laws differ from state to state, but I wonder if the next buyer would have knowledge of the chemical in the soil.  Would an environmental engineer be obligated to make the findings public record?
A. In general, if the levels were high enough so that there was a “real” threat to human health and safety, an ethical environmental engineer would be obliged to tell the appropriate authorities.  Often, however, the levels are “significant,” such that they are near or above some regulatory threshold, but unlikely to be a serious threat to human health.  That is a more complex problem.  Also, the consultant is hired by the contractor and would need her permission to do anything.  I don’t know of any laws that would require the contractor to report what she found, if she plans to walk away from the deal.  If she plans to buy it despite the contamination, that kicks off all kinds of problems for her and the bank.  We will discuss some of these in a later module and “site assessments.” You might look on Wikipedia about "brownfields" for one take on that.

*Q. I was wondering why DNA, RNA and ATP were group together in Toxicology tutor III. It is written that “Nucleic acids are large organic compounds which store and process information at the molecular level inside virtually all body cells” and that these 3 compounds are examples of nucleic acids, but how are ATP consistent with the structures of DNA and RNA?  
A. ATP is quite different than DNA and RNA and serves a very different role in the cell.  The nitrogenous base is common, and perhaps that is why they have it there. ??