From bench to policies: ready for a nanoparticle air quality standard?

As ambient concentrations of urban particulate matter (PM) increase, more people end up in hospital due to heart attacks, and more people suffer sudden death even prior to getting help from cardiologists. This is one of the many current conclusions from an exponentially growing transdisciplinary research agenda on air quality and health. The annual output of .2000 peerreviewed publications is now . 10 times larger than 20 years ago. This research is not just a self-serving ‘l’art pour l’art’ but it comes with a long-standing tradition to apply knowledge to policies. The success stories include the adoption of clean air standards for several markers of ambient air pollution [e.g. PM up to 10 mm (PM10) or 2.5 mm (PM2.5) in diameter, ozone, sulfur dioxide, nitrogen dioxide, and others] and the implementation of strategies to comply with the science-based standards. The underlying objective of clean air policies is the protection or improvement of health and, as can been demonstrated, these policies are indeed effective. The public health-driven research agenda that underlies clean air policies does not just go from the bench to the bedside but embraces the community. In fact, epidemiological research plays a very strong role in the assessment of air pollution-related health effects. However, like all sciences, epidemiology has its limits. For example, Peters et al. convincingly showed with a very elegant epidemiological study design that the risk of suffering a myocardial infarction increases almost 3-fold during the first hour after exposure to traffic. A recent comparison of the established triggers of myocardial infarction in fact ranked exposure to traffic as the most important trigger, with 7.4% of all events attributed to this activity. However, while the study of Peters et al. used state-of-the-art methods to estimate the risk, the findings are not easily translated into policy. Does the risk increase due to traffic-related pollutants? Is it caused by particles and, if so, by what constituents or what size fraction? What is the role of the gaseous pollutants? To answer such specific questions, the community must be carried to the bench. That is the key contribution of a series of studies carried out by the Scottish–Swedish–Dutch collaboration that has now published its newest findings. In contrast to more traditional toxicological studies where experiments are often done with unrealistically high concentrations or artificially manufactured pollutants, Mills et al. again used an exposure chamber that mimics daily life exposures encountered in street canyons of our cities during rush hour. Controlled exposure is provided by a realword diesel engine running on real-world diesel fuel. The seminal study of 2007 revealed mechanistic cardiovascular pathways that may explain the association between ambient air pollution and myocardial infarction. Men with a stable coronary heart disease were exposed to diesel exhaust and clean air. Diesel exhaust promoted myocardial ischaemia and inhibited endogenous fibrinolytic capacity. For cardiologists dedicated to counselling patients with coronary heart disease, the study poses some challenges as their patients can usually not escape exposure to air pollution if they live in traffic-jammed communities. The same research team then showed that diesel exhaust also affected thrombus formation in healthy young men. The new study of Mills et al. links the bench with the community in a further policyrelevant way. The experiment attempted to apportion the vascular effects of diesel exhaust into effects of (i) untreated diesel exhaust; (ii) the gas phase of diesel exhaust after removal of the particles; and (iii) pure nano-sized carbon particles. Only unfiltered diesel exhaust compromised the vasodilatation mediated by bradykinin, acetylcholine, and sodium nitroprusside. Filtered diesel and pure carbon particles had no effect on these outcomes. In the complementary tissue model, acetylcholineand sodium nitroprussidemediated vasorelaxation of aortic rings from rats was attenuated under exposure to diesel exhaust particles but not to pure carbon nanoparticles. These findings highlight the specific relevance of the real-world combustion-related nano-sized particles. The identity of the surface constituents of the nanoparticles that may have caused these effects cannot be determined with this experiment. This led the authors to the policy-related statement that ‘understanding of