Investigating the effects of the 2007 Texas tobacco tax increase on the smoking behavior of adults

Smoking is major cause of premature mortality and morbidity in the United States. The health consequences of tobacco usage are increasingly concentrated in minority and lower socioeconomic groups. One of the most effective means of deterring tobacco consumption and generating revenue to fund prevention activities is the levying of excise taxes. In 2007 the state of Texas increased the excise tax on cigarettes by $1.00 per pack. This study sought to determine if there was a significant effect on smoking prevalence in the state by examining Behavioral Risk Factor Surveillance System (BRFSS) data for two years leading up to the tax increase-2005 and 2006- and two years post tax increase -2007 and 2008. Results were compared against a chi square distribution and three multiple logistic regression models were created to adjust for race/ethnicity, age, education and income. Results from this study show that there was not a significant decrease in smoking prevalence for most of the groups stratified by age, income and ethnicity. There was not a significant decrease in the younger adults aged 18-34 by income, ethnicity, or education. Smoking prevalence increased for some groups, e.g., Hispanic females. In the regression models, the tax effect was not significant. While overall prevalence decreased by 9%, there were not significant reductions among non-White or Hispanic survey participants. Taxed sales dropped by approximately 17% according to the Texas Comptroller. Without BRFSS data measuring daily cigarette consumption among current smokers, now not assessed, it is impossible to determine whether the discrepancy in reported prevalence and taxes sales is attributable to consumption of fewer cigarettes among smokers or tax avoidance.^

The Influence of Immunization Route on the Adjuvant Effect of alpha-Galactosylceramide

Potent vaccine formulations ideally include adjuvants to activate innate immune responses and enhance antigen-specific adaptive immunity. The synthetic glycolipid alpha-Galactosylceramide (α-GalCer) effectively activates the innate immune mediating NKT cells to produce cytokines and activate downstream immune cells, resulting in development of humoral and cell mediated immune responses to co-administered antigens. While a single intravenous immunization of α-GalCer strongly activates NKT cells, multiple doses by this route are well documented to induce anergy in NKT cells. Anergy is defined as the deficiency in NKT proliferation and cytokine production, including IL-4 and IFNγ. However, our studies have shown that two doses of α-GalCer administered intranasally by the intranasal route leads to reactivation of NKT cells and improved adaptive immune responses after each subsequent dose. I therefore investigated the role of multiple routes of immunization in activation of NKT cells, i.e. anergy versus repeated activation. Specifically, I hypothesized that the differential capacity of NKT cells to produce IFNγ, as a result of route of immunization with α-GalCer, influences the induction of adaptive immune responses to co-administered antigen. Our experimental design utilizes the observation that intranasal immunization primarily induces immune responses in the lungs while intravenous immunization induces responses in the liver. Using intracellular cytokine staining for IFNγ production and Elispot analyses for determining NKT and T cell activation, respectively, it was determined that administering two consecutive intravenous doses resulted in anergy to NKT cells (no IFNγ production) in the liver and lack of adaptive immunity while second immunization by the intranasal route overcame anergy in the lung. The outcome in the other tissues analyzed was mixed and could be the result of tissue microenvironment among others possible reasons. When intranasal dosing preceded systemic, NKT cells were reactivated to produce IFNγ and induced positive adaptive immune responses in the responding lung tissue. These results indicate that the mechanism by which mucosal and systemic immunization routes activate NKT cells may differ in that there is a differential tissue-specific effect induced by each route. Future studies are necessary to determine the reason for these tissue-specific effects and how they relate to NKT cell activation.