Imagine that the weather report came with a description of how your genes would respond to the conditions outside. While this sounds like something out of science fiction, it has become undeniable that the environment exerts significant control over how and when our DNA is transcribed. While your environment may not change your genetic coding, new research, in a field of biology called “epigenetics”, suggests the environment can alter the way your genes are expressed. The term epigenetics has only recently entered the public parlance, but research is rapidly populating this new frontier of biology to find out how gene expression is changed by environmental factors.
The technological advances of the last century and a half have been accompanied by levels of air pollution that the human species had never been exposed to before. It begs the question: how is this affecting our species?
Smoke billowing forth from a large fire in a field – could forest fires affect your gene expression?
A recent paper out of Quebec, which investigated the effects of air pollution on gene expression, begins to answer this question. As part of a joint effort from Awadalla lab at the University of Toronto and the Canadian Partnership for Tomorrow Project, scientists gathered blood samples and data on hundreds of variables from over 300,000 Quebecois adults.
From this collection of data, the Awadalla lab chose about a thousand people to focus on. All of them lived within one of three major loci – Montreal, a highly urban center; Saguenay-Lac-Saint-Jean, a far less densely populated region; and Quebec City, which falls somewhere in the middle. The founding population of French Canadians arrived in Quebec in the 1600’s and steadily grew, with subsets breaking off occasionally to settle in new areas.
These well-documented migrations generated useful population bottlenecks that meant that the residents whose families had been in the area for more time tended to be more genetically similar. By sequencing the genomes of the individuals in the study, researchers were able to classify each one as a “local” or a “migrant” to the area.
The researchers focused on four kinds of pollutants while gathering the other half of their raw data – nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and particulate matter (PM2.5). The first three are unpleasant-smelling — and toxic — gases and the fourth is a category of airborne solid and liquid particles smaller than 2.5 micrometers in diameter. All four are known to be detrimental to human health at high levels, and all are generated by heavy industrial activity and combustion. The researchers used satellite- and land-based sources to determine the levels of pollution that had been present in the environment in the time and place when each blood sample had been collected.
In addition to containing an individual’s genome, these blood samples carried messenger RNA transcripts, sequences copied from the genome that tell the cell what parts it should be making. Analysis of these transcripts allowed the scientists to read out how the cells of different individuals were responding to pollutant levels.
The researchers saw several patterns in the data. Unsurprisingly, genes responsible for the inflammatory response and handling intake of outside gases were more highly expressed in individuals living in areas with high air pollution. This translated into cardiac and respiratory problems like asthma and even strokes.
Strikingly, factors such as socio-economic status, smoking, and even preexisting diseases had no correlation to what genes were expressed. Moreover, genetic background didn’t seem to be predisposing the individuals towards particular symptoms. In other words, the RNA expression patterns of a “local” and a “migrant” living in Montreal were more similar than two Montreal “locals” living in different areas.
So how can air pollution overpower the influences of genetic history? The answer is probably complicated, but the researchers found a handful of sites in the genome where variation in DNA sequence strongly correlated to large-scale symptoms. A few of these regions were coding sites for proteins that interact with chromatin, the structure that wraps DNA and controls whether or not it’s expressed. These proteins, among others, are likely responsible for launching the response to pollution, but untangling how they do this will be no easy feat.
Still, scientists have never been better equipped to rise to such a challenge. Genomic and epigenomic technologies are evolving at breakneck speed, and population studies such as the one used in this paper are expanding in both breadth and depth. It seems likely that every place we call home over the course of our lives leaves a mark on our DNA, annotating the genome of our ancestors with our individual histories.
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