**Q. I have read many papers and attended conference presentations on EDC’s. By way of an example, I mention a conference paper where someone went around collecting soil samples in a farm area. They analyzed them for nonspecific estrogens. They had no idea of the bioavailability in humans and did not even know if they might be active in humans. The results were reported as if they were important. Estrogen is ubiquitous in the environment. The notion that it would be readily found in soil sample collected in a farm area had never occurred to them. Thus they made an observation that could have been anticipated and had no way of putting it in context once it was presented. This is perhaps a dramatic example, however, to some extend there appears to be a great deal of this kind of research being presented. The need to clearly establish or refute causality when studying EDC seems to be a pressing issue. And observational studies that ignore this causality may in fact be deleterious to the research.Would you please comment?
A. Yes, indeed.  Now the high quality journals, such as the SETAC , SOT, and ACS will not publish things like that, but there are no shortage of venues that love to print that the sky is falling.  Did you see the CIIT article on the receptors?  Many EDC do bind human receptors, but very poorly.  Thus enormous quantities of them are required to have the same effect as the natural hormone.   DES was an exception and is surely a potent EDC. 

** Q. I was not aware that soy exhibits estrogenic affects and could have adverse health affects to infants fed a diet of soy formula.  I agree with the perspective of the undergrad student from the University of Pittsburgh that wouldn’t both cow’s milk-based formula and a mother’s milk also contain estrogen?  While it seems that mother’s milk would provide the safest, healthiest sustenance for a developing infant, the Dutch Children Playing study (though I found it inconclusive), raises attention to the issue that mother’s milk can also contain EDC’s and other toxicants.  It’s easy to conclude that nothing is really safe; and yet, humans continue to very effectively produce viable offspring.
A. Yes, “don’t breathe the air or drink the water.”  Estrogen and similar steroid hormones circulate in the blood in large carrier molecules and generally do not cross barriers they are not supposed to.  I would not think there was much, if any, estrogen in mother’s milk.  It can and does carry any lipophilic contaminants that are in the mother’s fat. 

Q. I was wondering about alfatoxin B1 in peanut butter.  After researching the IARC web site it says the altatoxin B1 is found primarily in peanut butter and maize.  Is there a difference in exposure risk between peanut butter and maize?  I find this quite disturbing considering corn syrup is in everything we eat.
A. I don’t know.  Generally the aflatoxin B1 is a mold in the outer cover of the seed, not inside.  I don’t know how corn oil is made, but it is probably a grind and squeeze operation followed by gravity separation as the oil floats.  That would not remove the aflatoxin, but would dilute it if it was only in a small percentage of the corn.  There are EPA and FDA guides on aflatoxin in foods.  My guess is that in the US the corn oil would be safe.  Corn syrup or sweetener is made by a different process and I doubt it has any –but I’ve never studies it.

Q. Do you know why there is Quaternium-15 in my baby’s shampoo, but not in any of the adult shampoo I own?  What is more worth preserving in baby shampoo than in regular shampoo?  Or is something worse than formaldehyde used in adult shampoo?
A. Interesting question.  I spent some time with this and could not figure out how the molecule releases the formaldehyde.  It may be that there are substances in the baby shampoo that bacteria are attracted to, or that other anti-bacterials don’t work. 

Q. I thought EDTA is used as a chelating agent (preservative) in canned food to prevent the metals that leach from the can from destroying the structure and therefore taste of the food.  If you eat expired canned food, it tastes awful, I think because all of EDTA’s ligands are used and you’re eating metal and/or spoiled food.   Anyway, would it then be difficult to get calcium out of a glass of milk if you drank it while eating canned food (unless the canned food was expired)? 
A. Never thought of that.  I don’t think there is very much EDTA in canned food relative to calcium in milk.  I believe the EDTA is destroyed in the stomach acid; it is usually given by injection in the case of metals poisoning.  It may be that spoilage of food taste is due to entropy.  The food is in a higher state and it gradually breaks down into lower states with time. 

Q. The key entity, it seems to me, is the NRC, which (as noted above) doesn't yet accept causal linkage between reproductive and breast issues with EDCs. Yet, at the same time, there seems to be growing evidence that something is going on here. The question I have is this: what is lacking in terms of animal studies and modeling (tools that seem accepted in other fields of toxicology for setting human exposure levels) that are holding us back on better knowledge and acceptance (or modification, or rejection) of the endocrine disruption hypothesis?
A. We've jumped from toxicology 101 to the cutting edge of research. I can't make a full study in order to satisfy myself. It seems clear that the receptor for the estrogen-like chemicals is not the estrogen receptor, but somewhere else. Most of those chemicals bind so poorly to the estrogen receptors, that they are unlikely to have an effect. Research was sidetracked for a while because one research group reported that combinations of those chemicals could have a dramatic effect. But later that group's research was refuted ("could not be reproduced.") So where do these chemicals bind? I don't believe that is known yet, and until it is, you can't really judge what animal model to use.

Q. Can you explain a bit more about the oxidative burst. I got that it kills invading cells but that is about it!
A. You got that the white blood cell has ingested the bacteria (or whatever), it now must kill it. The besides various digestive enzymes, the cell has the capability to make powerful oxidizing agents. Because these are dangerous to the cell itself, it only makes them on demand. It stores the enzymes and power sources to make the oxidizing agents and releases them all at once. The most important oxidative chemicals are hydrogen peroxide and hypochlorous acid.

Q. What does lymph do?
A. The lymph system drains the connective tissue.

Q.I am not sure what you mean by "The spleen is an immune filter of the blood."
A. The blood moves through the spleen and many white blood cells are there to filter out foreign materials, especially bacteria.

Q. It seems like it is not so difficult to correlate an adverse effect to a specific contaminant in the lab setting. But how can they break out the multiple contaminants (i.e. pesticide residues on fruits/vegetables, steroids/hormones in meat products, PCBs and dioxins in fish, etc.) plus natural chemicals that face humans/animals outside of the lab setting? It seems to me that they need to find out the exposure timing and the mechanisms involved for each contaminant in the lab and then take it to the field setting.
A. Very good question. You have hit upon one of the critical points in human epidemiology – you don't know to what all the subjects were exposed. Chemicals and mixtures in the environment can't be studied, even in laboratory animals, unless you know all the chemicals in question and expose the animals correspondingly. But, how do you do the dose-response testing of a mixture. If you have 5 dose levels for one chemical and 5 for the second, do you need 25 tests of the combinations? How about 3 chemicals – 125 tests? Wow. The practical answer is twofold. First, there has not been enough testing with individual chemicals, you'd want to do that first. Second, unless there is some known potentiation or synergism, the effects of traces of other chemicals are not significant. No, I can't prove that.

Q. I read an article in Time or one of those fluffy news mags about the increase of girls going through puberty earlier nowadays than in the past. One of the hypotheses was exposure to estrogen in drinking water. Have you heard about this phenomena or do you have an opinion?
A. Yes, it's an important topic. There is very little estrogen in that water, but there are small quantities in some water supplies. It gets there from the urine of females who use birth control pills. It seems to me you could do epidemiology with girls who are on city water versus those on well water. But country girls might have dietary differences etc.