New research in rodents has demonstrated the alarming potential of a wide range of commonly encountered chemicals, from pesticides to vehicle fuels, to cause disease not just in the individual exposed to them but in future generations - whether they are also exposed to such toxic chemicals or not - as a result of epigenetic effects.
The study was conducted by scientists at Washington State University and the results published online in the journal PLoS ONE this week. The team, led by molecular biologist Michael Skinner, were able to show in rats that a whole host of environmental pollutants caused negative health effects in threee generations of an exposed animal's offspring.
This is the first study to look at generational health effects of exposures to chemicals from a wide range of different classes. The study was funded by the US Army who wish to understand the effects of chemicals to which troops are likely to be exposed on the battlefield - in an effort one would hope - to avoid a repeat of an epidemic of Gulf War illness (GWI) type health problems following future conflicts. As such Skinner and his team looked at the effects of dioxins, the pesticides DEET and permethrin, the plastic ingredients bisphenol A and phthalates, as well as jet fuel (which is not so dissimilar to the gas/petrol you fill your car with).
Epigenetics refers to heritable changes in gene expression and physiological function caused by mechanisms that do not involve changes in the DNA itself. In the case of this study the DNA of the rats remained unchanged, but the chemical pollutants investigated changed the way genes turned on and off, which in turn caused negative changes in physiological function and disease.
Skinner's previous research had shown similar effects from a pesticide and a fungicide but the range of chemical compounds tested in the current study is unprecedented.
"We didn't expect them all to have transgenerational effects, but all of them did," he told the technology website Gizmodo. "I thought hydrocarbon [jet fuel] would be negative but it was positive too."
The negative health effects from exposure to the chemicals was wide-ranging but much centred around endocrine disrupting characteristics.
Some chemicals tested led to premature puberty among great-granddaughters, with an increased risk of disease in reproductive tissues. In some tests, the chemicals disrupted ovarian function, something that in humans could lead to infertility or premature menopause. And another chemical exposure caused premature death of sperm-forming cells in the great-grandsons - again increasing the risk of infertility if the same effects were seen in humans.
This study and the work of other scientists in the field of epigenetics provides a new perspective on the study of how diseases develop. While toxicologists primarily focus on animals directly exposed to a toxic compound, Skinner's work further demonstrates that diseases can also stem from older, ancestral exposures that are then mediated through epigenetic changes in sperm.
Such investigation may also lead to means by which to identify and diagnose exposures through the use of specific epigenetic molecular markers.
"In the future we might be able to use these epigenetic biomarkers to determine your ancestral and personal exposure early in life and to predict your susceptibility to get a disease later in life," Skinner said.
Source: Manikkam M Guerrero-Bosagna C Tracey R Haque M Skinner MK (2012) Transgenerational Actions of Environmental Compounds on Reproductive Disease and Identification of Epigenetic Biomarkers of Ancestral Exposures PLoS ONE 7 (2): e31901 DOI: 10.1371/journal.pone.0031901