Do diesel fumes raise heart risk?
The Daily Mail reported today that "diesel fumes increase the risk of heart attacks". The news story is of a small trial in 16 healthy young men. The men did exercise in a purpose-built chamber while they were exposed to one of three different pollutants: dilute diesel exhaust, filtered diesel exhaust (the same but with particles removed), or pure carbon nanoparticulate (not produced as a result of combustion) or pure filtered air.
After each session, the men’s vasodilation response (widening of the blood vessels) was tested when different vasodilator chemicals were administered. This showed that of the three pollutants, only exposure to dilute exhaust caused significantly less vasodilation compared to exposure to filtered air.
The trial has important limitations including its small, select sample population sample. Also, the natural environment is very different from the precise experimental scenario used here, as it is filled with different chemicals and other pollutants at different levels of concentration. No health outcomes were assessed in this study, and it cannot be assumed from these findings that exposure to diesel exhaust directly increases the risk of heart attacks. However, environmental pollutants and their potential health effects are undoubtedly an important public health concern; despite limitations, the findings that nanoparticle emissions of diesel exhaust may have effects on vascular function is worthy of further study.
Where did the story come from?
The study was carried out by researchers from Edinburgh University and was funded by the British Heart Foundation. The study was published in the peer-reviewed European Heart Journal.
The news stories do not discuss the limitation of this trial, in particular its small sample of young, healthy male volunteers and the fact that it used an artificial experimental scenario. Most importantly, the claims from BBC News and the Daily Mail that diesel fumes raise heart attack risk have not been demonstrated by this study.
What kind of research was this?
The researchers say that air pollution may be a trigger of heart attack, but the individual pollutants responsible for this effect have not been established. This randomised cross-over study investigated whether different ‘combustion-derived-nanoparticles’ were associated with any adverse cardiovascular effects.
The researchers say they focused on diesel exhaust as their previous studies had demonstrated that inhalation of dilute diesel exhaust impairs vascular function and has pro-thrombotic (clotting) effects. As diesel contains a complex mix of gases, particles and volatiles, they wanted to understand which components are mediating cardiovascular risk.
This study compared the effects of breathing in dilute diesel exhaust, filtered diesel exhaust and pure carbon nanoparticulate with that of breathing in pure filtered air. Participants were exposed to each of these three chemicals and the filtered air in a random order.
Though a randomised trial is the best method for examining the effects of an intervention, the trial was small and only conducted in a select sample of young, healthy male volunteers. It provides limited information and is unable to tell us the effects on different population groups. It is also an unrealistic representation of what people would be exposed to in the natural environment, which is filled with different chemicals and other pollutants at different levels of concentration. Furthermore, the study cannot tell us the effect of exposure over different time periods as well as in the longer term.
What did the research involve?
The researchers recruited 16 healthy males aged 18-32. On four separate occasions, two weeks apart, the volunteers attended the research centre. They were randomly assigned on each occasion to be exposed for two-hour periods in a specifically built chamber to either:
- pure filtered air
- dilute diesel exhaust (90% of the exhaust from a diesel engine was shunted away while the remaining part was diluted with air)
- filtered diesel exhaust (the same method as above but with the exhaust passed through a Teflon filter to remove particles of combustion)
- pure carbon nanoparticulate (generated from graphite electrodes and the output mixed with filtered air, i.e. not produced from combustion in an engine)
While in the chamber, the participants performed moderate exercise on a bicycle with rest periods at 15 minute intervals. Six to eight hours after each exposure, vascular assessments were performed while the participant lay on a bed in a quiet, temperature-controlled room. These tests involved intravenous infusion of three different vasodilator chemicals in random order, each separated by a 20-minute interval during which time an inactive saline infusion was given to flush out the previous chemical. The participants’ heart rate and blood pressure were then tested.
The researchers then looked at whether they could replicate these findings in a laboratory study using sections taken from the aorta (the large blood vessel leaving the heart) of rats. They exposed the aortic samples to either pure carbon nanoparticulate, diesel exhaust particles or a control, and then looked at the effects of applying the vasodilator chemicals.
What were the basic results?
The researchers found that, compared with exposure to filtered air, exposure to dilute diesel exhaust reduced the extent of vasodilation that occurred with administration of each of the three vasodilator chemicals. It also caused higher systolic blood pressure (145mmHg with dilute diesel vs. 133mmHg with filtered air; systolic BP being the arterial pressure as the heart contracts and pumps blood into the arteries). Filtered diesel exhaust also caused higher systolic BP compared to filtered air (144 mmHg with filtered diesel). However, there was no difference in the response to the vasodilator chemicals when the person had been exposed to filtered air, filtered diesel exhaust, or to pure carbon nanoparticulate.
When conducting their complementary laboratory study using rat aorta, they found that, compared to control, diesel exhaust particulate again reduced the response to vasodilator chemicals, but pure carbon nanoparticulate did not.
How did the researchers interpret the results?
The researchers conclude that it is the combustion-derived nanoparticles of diesel exhaust that appear to be predominantly responsible for the adverse vascular effects of diesel exhaust inhalation.
This small trial indicates that it is the combustion-derived particles of diesel fuel that have a direct effect on blood vessels. Only exposure to diluted exhaust reduced vasodilation; exposure to filtered exhaust with the particles removed, or pure particles not produced as a result of combustion in an engine, did not have an effect.
The researchers say their study suggests that environmental health interventions should aim to reduce traffic-derived particulate emissions. Environmental pollutants and their potential health effects are undoubtedly an important public health concern, but there are important limitations to bear in mind when making any conclusions from this individual study alone:
- Though the study benefited from its randomised crossover design, it was still very small and in a select population of only 16 healthy young men. The effect on other population samples including females, children or middle aged or elderly people, or those with existing cardiovascular problems is not known.
- This was a very artificial scenario. The participants all cycled in an exposure chamber for two hours while exposed to very specific concentrations of chemicals. It does not tell us about the effects of exposure in a natural outdoor environment filled with different chemicals and other pollutants at different levels of concentration. Likewise, exposure for different brief time periods or in the longer term is not known, or whether there is any difference if the person is less physically active while exposed.
- The study has predominantly examined vasodilator response following direct administration of three vasodilator chemicals that occur naturally in the body. The fact that blood pressure was reduced less when the person had been exposed to unfiltered diesel exhaust can tell us little about whether this would have any implications for cardiovascular health. Most importantly, it cannot be assumed from these findings that exposure to diesel exhaust directly increases the risk of heart attacks.
The findings that nanoparticle emissions of diesel exhaust may have effects on vascular function is nevertheless an area worthy of further study, and provides insight into ways of mediating environmental pollutants.
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