Background Heated tobacco products (also called ‘heat-not-burn’ products) heat tobacco at temperatures below that of combustion, causing nicotine and other compounds to aerosolise. One such product, IQOS from Philip Morris International, is being marketed internationally with claims of harm reduction. We sought to determine whether exposure to IQOS aerosol impairs arterial flow-mediated dilation (FMD), a measure of vascular endothelial function that is impaired by tobacco smoke.
Methods We exposed anaesthetised rats (n=8/group) via nose cone to IQOS aerosol from single HeatSticks, mainstream smoke from single Marlboro Red cigarettes or clean air for a series of consecutive 30 s cycles over 1.5–5 min. Each cycle consisted of 15 or 5 s of exposure followed by removal from the nose cone. We measured pre-exposure and postexposure FMD, and postexposure serum nicotine and cotinine.
Results FMD was impaired comparably by ten 15 s exposures and ten 5 s exposures to IQOS aerosol and to cigarette smoke, but not by clean air. Serum nicotine levels were similar to plasma levels after humans have smoked one cigarette, confirming that exposure conditions had real-world relevance. Postexposure nicotine levels were ~4.5-fold higher in rats exposed to IQOS than to cigarettes, despite nicotine being measured in the IQOS aerosol at ~63% the amount measured in smoke. When IQOS exposure was briefer, leading to comparable serum nicotine levels to the cigarette group, FMD was still comparably impaired.
Conclusions Acute exposures to IQOS aerosol impairs FMD in rats. IQOS use does not necessarily avoid the adverse cardiovascular effects of smoking cigarettes.
- non-cigarette tobacco products
- electronic nicotine delivery devices
- harm reduction
- smoking caused disease
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Contributors PN, JL, CMH, SI and RD performed experiments and collected/analysed data. PN, CMH, PJ and MLS designed experiments, PN and MLS conceived of the project and wrote the paper.
Funding This work was supported by grant R01HL120062 from the National Heart, Lung, and Blood Institute at the National Institutes of Health (NIH) and the US Food and Drug Administration Center for Tobacco Products (FDA CTP), grant 25IR-0030 from the California Tobacco-Related Disease Research Program, and grant P50CA180890 from the National Cancer Institute at the NIH and FDA CTP. Laboratory resources for analytical chemistry were supported by grant P30 DA012393 from the National Institute on Drug Abuse at the NIH.
Disclaimer The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH or the FDA.
Competing interests None declared.
Patient consent Not required.
Ethics approval All animal procedures were approved by the University of California, San Francisco Institutional Animal Care and Use Committee.
Provenance and peer review Not commissioned; externally peer reviewed.
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