Air Pollution May Cause Heart Disease

Nano-Sized Particles Most Damaging – Ultrafines worse than PM2.5s.

A new Univ. of California study compares PM2.5 with ultrafine particles and finds the latter are – as long hypothesised – the most damaging to health. The study is based on exposing mice to particulate pollution and measuring signs of oxidative stress and pre-artherosclerosis changes. It shows that ultrafine ‘nanoparticles’ trigger plaque build-up in the arteries that can lead to heart attack and stroke. The study also identified a way in which pollutant particles may promote hardening of the arteries – by inactivating the protective qualities of HDL cholesterol, known as the “good cholesterol.”

The ultrafine particles are urban pollutants and a large fraction are carbonaceous particles. But they also contain metallic and elemental carbon particles produced from high temperature combustion, as incinerators. This is further evidence that the ultrafine particles ignored in the new UK and EU plans are worse than the PM2.5 fraction that is to be monitored.

The politicians and policy-makers overseeing the European Air Quality review (“Clean Air for Europe” CAFE and revision of the Air Quality Directive) decided to cover PM2.5s only and cut the ultrafine particle issue out of general documentation.

Earlier information on the health hazard from nanoparticles is given in the Annexed response to the UK Air Quality review, citing information from the WHO and a review Air Pollution: a threat to the health of our children for the EU PINCHE project. The Abstract of the new article in the American Heart Association’s journal “Circulation Research” is given below.

Ambient Particulate Pollutants in the Ultrafine Range Promote Early Atherosclerosis and Systemic Oxidative Stress

J.A. Araujo et al. Circulation Research. 2008 pre-print online DOI: 10.1161/CIRCRESAHA.107.164970

Abstract—Air pollution is associated with significant adverse health effects, including increased cardiovascular morbidity and mortality. Exposure to particulate matter with an aerodynamic diameter of < 2.5 µm (PM2.5) increases ischemic cardiovascular events and promotes atherosclerosis. Moreover, there is increasing evidence that the smallest pollutant particles pose the greatest danger because of their high content of organic chemicals and prooxidative potential. To test this hypothesis, we compared the proatherogenic effects of ambient particles of < 0.18 µm (ultrafine particles) with particles of <2.5 µm in genetically susceptible (apolipoprotein E–deficient) mice. These animals were exposed to concentrated ultrafine particles, concentrated particles of < 2.5 µm, or filtered air in a mobile animal facility close to a Los Angeles freeway. Ultrafine particle– exposed mice exhibited significantly larger early atherosclerotic lesions than mice exposed to PM2.5 or filtered air. Exposure to ultrafine particles also resulted in an inhibition of the antiinflammatory capacity of plasma high-density lipoprotein and greater systemic oxidative stress as evidenced by a significant increase in hepatic malondialdehyde levels and upregulation of Nrf2-regulated antioxidant genes. We conclude that ultrafine particles concentrate the proatherogenic effects of ambient PM and may constitute a significant cardiovascular risk factor.

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