Publications

The California Tobacco Control Program is the longest standing, publicly funded tobacco control program in the U.S. California's adult smoking rate declined from 23.7% (1989) to 11% (2016) but California still has more than 3 million smokers dispersed over 58 counties, requiring a coordinated approach to further tobacco control. Early California Tobacco Control Program success is rooted in public health policy strategies and a statewide media campaign that shifted social norms. In 2009, concepts for a coordinated approach were introduced by the California Tobacco Control Program in the state's first tobacco quit plan. The state quit plan called for public health's tobacco control programs to engage healthcare systems and insurers to work more directly with the California Smoker's Helpline (Helpline). With California's Medicaid (Medi-Cal) program expansion and the implementation of electronic medical record systems, health care plans and providers received additional support for system changes. Simultaneous with these changes, coordinated tobacco control efforts began, including California's Medi-Cal Incentives to Quit Smoking project (2012-2015). In the Medi-Cal Incentives to Quit Smoking project, safety-net providers and Medi-Cal plans were outreached and engaged to promote incentives for Medi-Cal members to utilize Helpline services. In another effort, UC Quits (2013-2015), the five University of California health systems used electronic medical record tools to promote tobacco treatments and electronic referrals to the Helpline. Now, as tobacco prevention is increasingly prioritized for quality improvement, California Tobacco Control Program is funding CA Quits, a statewide tobacco-cessation learning collaborative and technical assistance resource to promote integration of tobacco treatment services and quality improvement activities into safety-net health systems. CA Quits, in coordination with the Helpline, will connect public health departments, Medi-Cal plans, and safety-net providers to accelerate health systems change for tobacco-cessation treatment throughout the state. SUPPLEMENT INFORMATION: This article is part of a supplement entitled Advancing Smoking Cessation in California's Medicaid Population, which is sponsored by the California Department of Public Health.

Objective- We evaluated the biological effects of low-dose methotrexate on 3 novel brachial artery grayscale ultrasound measures that may indicate subclinical arterial injury. Approach and Results- Exploratory analysis from a clinical trial of people with HIV infection at increased cardiovascular disease risk who were randomly assigned to low-dose methotrexate (target dose 15 mg/wk) or placebo. Brachial artery ultrasound grayscale median, gray level difference statistic texture-contrast (GLDS-CON), and gray level texture entropy were measured at baseline and after 24 weeks of intervention. Findings from the intention-to-treat (N=148) and adequately-dosed (N=118) populations were consistent, so the adequately-dosed population results are presented. Participants were a median (Q1, Q3) age of 54 (50, 60) years. After 24 weeks, the low-dose methotrexate intervention was associated with a 25.4% (-18.1, 58.6; P=0.007) increase in GLDS-CON compared with 1.3% (-29.1, 44.7; P=0.97) with placebo ( P=0.05) and a 0.10 u (-0.06, 0.23; P=0.026) increase in entropy compared with 0.02 u (-0.11, 0.14; P=0.54) with placebo ( P=0.14). At week 24, changes in CD4+ T cells correlated inversely with changes in GLDS-CON (ρ=-0.20; P=0.031), and entropy (ρ=-0.21; P=0.023). Changes in D-dimer levels, but no other inflammatory biomarkers, also correlated inversely with changes in GLDS-CON (ρ=-0.23; P=0.014) and entropy (ρ=-0.26; P=0.005). Conclusions- Brachial artery GLDS-CON and entropy increased after 24 weeks of low-dose methotrexate, though the latter was not significantly different from placebo. Grayscale changes were associated with decreases in CD4+ T-cell and D-dimer concentrations and may indicate favorable arterial structure changes.