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In Reply: Dr Twickler and colleagues postulate that inhaled particles (particulate matter <2.5 µm or PM_2.5) 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 PM_2.5-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 PM_2.5.¹ 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 PM_2.5 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

Finally, both scenarios . . . [Full Text of this Article]

Qinghua Sun, MD, PhD; Sanjay Rajagopalan, MD
sanjay.rajagopalan@msnyuhealth.org
The Zena and Michael A. Wiener Cardiovascular Institute
Marie-Josée and Henry R. Kravis Center for Cardiovascular Health
Mount Sinai School of Medicine
New York, NY

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