Traffic’s soot elevates blood pressure

Legions of studies have shown that air pollution can harm the heart and blood vessels.  Identifying how has proven trickier. Scientists now have linked airborne concentrations of tiny black-carbon particles — soot — with increasing blood pressure in older men. They also showed that the genes we inherit appear to play a big role in determining our vulnerability to soot’s pressurizing impacts.

Elissa Wilker of the Harvard School of Public Health, in Boston, and her colleagues measured blood pressure in nearly 800 Massachusetts men on up to three occasions. All were around 72 years old and among participants of a long-running Veterans Affairs study. The researchers correlated those readings with black-carbon concentrations collected at an urban air-sampling station in Boston for the seven days leading up to the blood pressure measurements.

And for each roughly 0.4 microgram per cubic meter of air average increase in airborne soot, systolic pressure climbed roughly 3 millimeters of mercury and diastolic rose about 2.25 mmHg within these men.

But there was considerable heterogeneity among the participants. And to home in on why, Wilker’s team looked at genetic differences in some elements of genes, features known as single nucleotide polymorphisms, or SNPs. These are tiny patches of DNA where one of the four building blocks, known as nucleotides, has been substituted for another. Once a change occurs, it can be inherited by all of an individual’s descendants.

The change also might alter the function of that snippet of DNA. And that’s what the researchers looked for: correlations between specific SNPs within these men — which varied across the group — and how their blood-pressure responded to increases in airborne soot. They focused on SNPs that previous studies by others had linked with genes associated with “microRNA processing” and disease.

MicroRNAs, Wilker explains, are really small noncoding segments of genetic material that don’t serve as templates for the production of proteins. Instead, they have a regulatory function, she says. Their role, much of which is still being teased out, seems to be a silencing or suppression of the activity of other genes. So microRNAs are very important, she notes.

The pollution-responsive SNPs, she says, play a role in assembling the building blocks of microRNAs into mature regulatory elements. In most cases, the unusual SNPs identified in some of the men here are thought to down-regulate the production and maturation of certain microRNAs.

In an upcoming paper in Environmental Health Perspectives, published online ahead of print, Wilker’s group linked four SNPs (located in the genes DICER, GEMIN4, DGCR8 AND GEMIN3) with perturbations in the men’s responsiveness to soot. The general expectation is that any processes normally controlled by the SNP-affected microRNAs would not be dampened appropriately.

So what do the affected microRNAs do? “There are hundreds of microRNAs,” Wilker says, “and they regulate genes in many different ways.” Indeed, she notes, some can regulate more than one gene. So it’s too early to responsibly gauge what these upstream changes might all mean. Indeed, she and her coauthors note in their paper, one SNP that was linked with a reduced soot-triggered elevation in blood pressure “has been associated with higher bladder cancer rates.” Bottom line: How good or bad a SNP appears to be may depend upon which of its several functions we focus on.

The long-term goal, Wilker says, is to “better characterize the pathways that are responsible for susceptibility to pollution.” Indeed, she says, “The SNPs identified in this study could play a role contributing to the many biological and environmental factors that influence the way an individual responds to air-pollution exposures . . [and] may have implications for individual-level interventions as well as future policy recommendations” aimed at regulating specific emission levels.

People are already talking about one day being able to screen people for various SNPs, identifying those who may face a higher-than-normal risk from particular diseases or environmental exposures. Not to scare them, of course, but to find those who might benefit from counseling on lifestyle changes to reduce that risk. For instance, people with some of the SNPs highlighted in the new paper might be cautioned not to buy a home along a major roadway or to take a job as a toll-road fee collector.

They might even be cautioned to drive in ways that limit the infiltration of traffic-generated pollutants. (That’s my take, based on reading an Australian paper, also available online, ahead of press, and due to appear in Environmental Science & Technology. It shows that shutting off access to outdoor air when traffic is congested and pollutant loadings high, can dramatically lower in-car concentrations of potentially toxic ultrafine particles.)

But in terms of such prescriptions, “We’re not there yet,” Wilker cautions. Factoring in the significance of an individual’s genome to pollution vulnerability is going to prove complex. But it is coming.