Smoke and Mirrors: Policy Solutions for Deterring Adolescent Use of Nicotine Electronic Cigarettes

In recent years, there has been a dramatic spike in the number of adolescents that regularly use nicotine electronic cigarettes. As recently as 2019, a large outbreak of e- cigarette, or vaping, product use-associated lung injuries was observed in adolescents, leading many to question the safety of these devices, particularly when use by adolescents. By way of a literature review, this thesis will examine the history of nicotine and electronic cigarettes in the United States, as well as existing data on the nature of nicotine electronic cigarettes and the ways in which they are marketed. From these findings, it is clear that adolescents are particularly susceptible to beginning nicotine use, due to the questionable marketing practices of nicotine electronic cigarette firms, as well as social and peer influences to try nicotine electronic cigarettes. It is clear that while nicotine electronic cigarettes have not proven to be uniquely harmful to a user, some of the chemical components used to produce vapour in these devices can be harmful and carcinogenic. Nevertheless, it was found that the recent outbreak of e- cigarette related lung injury cases was not directly associated with nicotine electronic cigarettes that are presently available on the market; rather, these injuries were a result of bootlegged vaping products. In order to analyse the findings of this thesis, an evaluative policy framework was used so as to create a policy solution that deters adolescent use of nicotine electronic cigarettes. This thesis proposes the use of regulation, education, and repeal of certain legislative actions in order to address this public issue

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)