Prior posts have discussed the interplay between DNA, the various forms of RNA, and proteins regarding gene "expression"; prior posts have also noted the process of methylation of genes [see Wikipedia - Methylation], which often reflects the interface between life's experiences and genetic expression (it is also the reason why the genes of "identical twins" become, in terms of expression, less and less similar as the twins grow older). Another component to gene expression is epigenesis (how heritable changes in genome function occur without a change in DNA sequence). [See What is Epigenetics.] An epigenetic change in a gene adds chemical tags that influence the manner in which a gene is regulated, often locking a gene in the "on" or "off" position.
In one sense, epigenetic changes to gene expression have not been a major concern with regard to pollutants because the accepted wisdom was that, early in development, a fetus erases any epigenetic changes acquired during its parents' lifetimes, resetting those genes back to their "healthy," default programming. Now, a study indicates that such is not the case.
In a study with rats, researchers looked at a variety of pollutants. Because the study was funded by the military, the study focused on pollutants to which soldiers were likely to be exposed (dioxins, DEET, permethrin, bisphenol A (BPA), phthalates, and jet fuel). As is SOP with many animal experiments, the rat exposures used were relatively high; however, these exposures were not high enough to cause fetal deaths or signs of toxicity in either exposed rat moms or their pups. Yet all promoted epigenetic transgenerational changes; in other words, the tags were not deleted, but existed across generations.
This was a major surprise to the researchers. Because all the pollutants resulted in epigenetic changes that went from one generation to the next and the next, it suggested to the researchers that epigenetic changes that get passed down through the generations are not some unique quirk of any one chemical; the researchers now suspect that most pollutants have the potential to do this (though it must be remembered that the experiment dealt solely with the pollutants listed above).
Each group of pollutants caused a different constellation of epigenetic changes that were linked with various reproductive problems in subsequent generations, although there was some overlap. The researchers note that this suggests that there may be a means in the future to use epigenetic biomarkers to assess what you or your ancestors were exposed to earlier in life, and perhaps apply that knowledge to predict disease and limit risk.
This also means that there is a whole new field of adverse impacts from pollutants that are not encompassed by today's risk assessment methods. It is also important to remember that there is no such thing as all-bad pollutants and all-good "natural" substances. As noted in prior posts, many so-called natural substances can be quite harmful. Until more studies are done, we will not know if the researchers have uncovered a general rule applicable to the huge variety of chemicals to which humans are exposed, including through food and the environment, or if the conclusion is limited to particular classes of substances.
In toxic torts, as noted in prior posts, we are use to thinking of cause and effect, and not transgenerational manifestations of harm. Like the field of risk assessment, that accepted mode of analysis may be in need of reformation.
The report can be found at http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0031901.