Letters Section Editor: Robert M. Golub, MD, Senior Editor.
In Reply: Dr Twickler and colleagues postulate that inhaled particles (particulate matter <2.5 μm or PM2.5) in our study may have potentiated atherosclerosis by serving as a “nidus” (Trojan horse hypothesis). There are a number of issues that need to be verified before this postulate can be accepted as a potential mechanism of PM2.5-mediated atherosclerosis.
The foremost issue pertains to the fate of inhaled particles. Although there is some evidence that inhaled ultrafine particles enter the systemic circulation, this is by no means certain for PM2.5.1 Our study did include ultra-fine particles by design and this could certainly represent one mechanism, but we do not have evidence that this occurred. It is also possible that PM2.5 may potentiate humoral and cellular inflammatory mechanisms from a distance (eg, the lung interface), which would circumvent invoking a direct incursion of these particles into the systemic vasculature.2
Sun Q, Rajagopalan S. Trojan Horse Hypothesis: Inhaled Airborne Particles, Lipid Bullets, and Atherogenesis—Reply. JAMA. 2006;295(20):2354-2355. doi:10.1001/jama.295.20.2354-b