Air pollution is often linked to adverse effects on respiratory health but it can have even stronger ties to cardiovascular health issues. In the first SOCAAR Seminar of 2013, Drs. Krystal Godri Pollitt and Bruce Urch discuss their findings from a number of recent human exposure studies looking at the effects of particulate matter (PM) exposure on cardiovascular health.
A number of studies over the last 10-20 years have found pollutant exposure has led to increases in cardiovascular related illness or death. But the mechanisms of the body’s response to exposure is still unclear. The research presented aims to improve the understanding of the response pathways to PM exposure, information which could ultimately be used to improve the air quality policies that are implemented.
In setting out to answer how pollutants affect cardiovascular health, blood pressure changes and signs of endothelial impairment with exposure were investigated. Inhaled pollutants can elevate blood pressure from two pathways. The first occurs within minutes of exposure because of an imbalance in the autonomic nervous system that causes artery constrictions. The second can occur within hours or days, resulting from vascular oxidative stress and inflammation. The endothelium is the tissue that lines the inner surface of blood vessels which helps regulates blood flow and structure. Changes in the brachial artery diameter may indicate signs of endothelial impairment.
Three studies were carried out to compare the outcomes of exposure to various size fractions and constituents of particles, as well as exposure to ozone. Exposures to filtered air and medical air were used as the controls. Measurements such as blood pressure, brachial artery diameter or flow mediated dilation were taken before, during, and after participants were subjected to periods of two-hour exposures.
In one study, exposure to concentrated ambient fine (0.1-2.5 µm in diameter) PM (150 µg/m3) and ozone (0.12 ppm) resulted in a 0.09 mm brachial artery diameter decrease which corresponds to a 4.7% reduction in blood flow. While the changes are not considered significant for a healthy person, it may be a significant issue for someone with hypertension or cardiovascular disease says Urch.
“This was the first controlled human exposure study with PM to show vascular changes using flow mediated dilation,” says Urch. “No one else had shown that before in the vasculature, previous results were mainly focused on respiratory or inflammatory changes.”
Other outcomes of exposure include: increase in diastolic blood pressure during the 2 hour concentrated PM exposure period and decrease in flow mediated dilation 20 hours after exposure. These changes were linked to the total PM concentration and the constituents of PM (including elemental and organic carbon).
A question that was raised in these studies was the importance of PM composition in relation to health effects. A parallel study was conducted in Michigan, evaluating the outcomes of pollutants (concentrated ambient fine PM and ozone) on cardiovascular health. The Michigan study found similar increases in diastolic blood pressure but saw no changes in flow mediated dilation with exposure. Urch believes the compositional differences in the pollutants (PM) studied in Michigan and Toronto may be reason for the different outcomes. According to Urch, Michigan is more of a rural site with less traffic than Toronto and he and his colleagues are now going over the compositional data to see if that explains the different outcomes.
Future studies include investigating strategies for reducing cardiovascular effects of air pollution and examining the effects of pollutants on the brain, which is also impacted by vascular changes.