Introduction

Electronic cigarettes or e-cigarettes are marketed as tobacco-free nicotine delivery devices that have received little laboratory evaluation. In this study, the smoking properties of conventional and e-cigarettes were compared by examining the vacuum required to produce smoke (conventional cigarettes) or aerosol (e-cigarettes) and the density of the smoke/aerosol over time.

Methods

Vacuum was measured using a manometer coupled to a smoking machine. The density of aerosol or smoke was measured spectrophotometrically. E-cigarettes were subjected to smoke-out experiments in which vacuum and aerosol density were measured until each cartridge was exhausted.

Results

The vacuum required to smoke conventional cigarettes varied among the eight brands tested. Lights and ultra-light brands required stronger vacuums to smoke than unfiltered and regular filtered brands. Except for one brand, higher vacuums were required to smoke e-cigarettes than conventional brands. Smoke/aerosol density was stable for conventional brands and for e-cigarettes over the first 10 puffs; however, aerosol density of e-cigarettes dropped during subsequent smoking, and higher vacuums were required to produce aerosol as the puff number increased. While conventional cigarettes were uniform in their smoking behavior within brands, vacuum and density varied within brands of e-cigarettes.

Discussion

Generally, e-cigarettes required stronger vacuums (suction) to smoke than conventional brands, and the effects of this on human health could be adverse. The amount of aerosol produced by e-cigarettes decreased during smoking, which necessitated increasing puff strength to produce aerosol. The decreased efficiency of aerosol production during e-cigarette smoking makes dosing nonuniform over time and calls into question their usefulness as nicotine delivery devices.

Objective

A high plasma level of inflammasome mediator interleukin-18 was associated with mortality in observational acute respiratory distress syndrome cohorts. Statin exposure increases both inflammasome activation and lung injury in mouse models. We tested whether randomization to statin therapy correlated with increased interleukin-18 in the ARDS Network Statins for Acutely Injured Lungs from Sepsis trial.

Design

Retrospective analysis of randomized controlled clinical trial.

Setting

Multicenter North American clinical trial, the ARDS Network Statins for Acutely Injured Lungs from Sepsis.

Patients

Six hundred eighty-three subjects with infection-related acute respiratory distress syndrome, representing 92% of the original trial population.

Interventions

Random assignment of rosuvastatin or placebo for up to 28 days or 3 days after ICU discharge.

Measurements and main results

We measured plasma interleukin-18 levels in all Statins for Acutely Injured Lungs from Sepsis patients with sample available at day 0 (baseline, n = 683) and day 3 (after randomization, n = 588). We tested the association among interleukin-18 level at baseline, rising interleukin-18, and the impact of statin therapy on 60-day mortality, adjusting for severity of illness. Baseline plasma interleukin-18 level greater than or equal to 800 pg/mL was highly associated with 60-day mortality, with a hazard of death of 2.3 (95% CI, 1.7-3.1). Rising plasma interleukin-18 was also associated with increased mortality. For each unit increase in log2 (interleukin-18) at day 3 compared with baseline, the hazard of death increased by 2.3 (95% CI, 1.5-3.5). Subjects randomized to statin were significantly more likely to experience a rise in plasma interleukin-18 levels. Subjects with acute kidney injury, shock, low baseline interleukin-18, and those not receiving systemic corticosteroids were more likely to experience rising interleukin-18. Randomization to statin therapy was associated with rising in interleukin-18 in all of those subsets, however.

Conclusions

Elevated baseline plasma interleukin-18 was associated with higher mortality in sepsis-induced acute respiratory distress syndrome. A rise in plasma interleukin-18 was also associated with increased mortality and was more common in subjects randomized to statin therapy in this clinical trial.