Risk of Chronic Obstructive Pulmonary Disease and Receipt of a Breathing Test in 26 States and the District of Columbia, 2017-2018.

We estimated the prevalence of respiratory symptoms, chronic obstructive pulmonary disease (COPD) risk level, and receipt of a breathing test among adults without reported COPD in 26 states and the District of Columbia by using 2017-2018 Behavioral Risk Factor Surveillance System data. Among adults without reported COPD, the 3 respiratory symptoms indicating COPD (chronic cough, phlegm or mucus production, shortness of breath) were common (each >10%). About 15.0% were at higher COPD risk (based on the number of symptoms, age, and smoking status); 41.4% of adults at higher risk reported receipt of a breathing test. Patient-provider recognition and communication of risk symptoms, appropriate screening, and follow-up are important for early diagnosis and treatment.

E-Cigarettes and Cardiopulmonary Health.

E-cigarettes have surged in popularity over the last few years, particularly among youth and young adults. These battery-powered devices aerosolize e-liquids, comprised of propylene glycol and vegetable glycerin, typically with nicotine, flavors, and stabilizers/humectants. Although the use of combustible cigarettes is associated with several adverse health effects including multiple pulmonary and cardiovascular diseases, the effects of e-cigarettes on both short- and long-term health have only begun to be investigated. Given the recent increase in the popularity of e-cigarettes, there is an urgent need for studies to address their potential adverse health effects, particularly as many researchers have suggested that e-cigarettes may pose less of a health risk than traditional combustible cigarettes and should be used as nicotine replacements. This report is prepared for clinicians, researchers, and other health care providers to provide the current state of knowledge on how e-cigarette use might affect cardiopulmonary health, along with research gaps to be addressed in future studies.

Chronic Obstructive Pulmonary Disease and Smoking Status - United States, 2017.

Cigarette smoking is the leading cause of chronic obstructive pulmonary disease (COPD) in the United States; however, an estimated one fourth of adults with COPD have never smoked (1). CDC analyzed state-specific Behavioral Risk Factor Surveillance System (BRFSS) data from 2017, which indicated that, overall among U.S. adults, 6.2% (age-adjusted) reported having been told by a health care professional that they had COPD. The age-adjusted prevalence of COPD was 15.2% among current cigarette smokers, 7.6% among former smokers, and 2.8% among adults who had never smoked. Higher prevalences of COPD were observed in southeastern and Appalachian states, regardless of smoking status of respondents. Whereas the strong positive correlation between state prevalence of COPD and state prevalence of current smoking was expected among current and former smokers, a similar relationship among adults who had never smoked suggests secondhand smoke exposure as a potential risk factor for COPD. Continued promotion of smoke-free environments might reduce COPD among both those who smoke and those who do not.

Critical Challenges and Compelling Questions for Chronic Obstructive Pulmonary Disease. Moving the Field Forward: A National Heart, Lung, and Blood Institute Perspective.

Although the National Heart, Lung, and Blood Institute (NHLBI) supports an active and varied portfolio of research pertaining to chronic obstructive pulmonary disease (COPD), there remain several research gaps that, when filled, could significantly help ease the burden of this disease. I use the NHLBI Strategic Vision in this article to identify opportunities for COPD research over the next decade. Filling these gaps will require collaboration between NHLBI, funded investigators, and various other stakeholders. Recent advances, including the development of powerful research technologies and the completion of the COPD National Action Plan, offer new tools that will one day improve the lives of patients with COPD and their families.

NIH electronic cigarette workshop: developing a research agenda.

BACKGROUND: Electronic cigarettes (e-cigarettes) represent an emerging public health issue. These devices deliver nicotine along with other constituents, including flavorants, via an inhalable aerosol. Their uptake is rapidly increasing in both adults and youths, primarily among current smokers. Public debate is increasing on how these devices should be regulated and used, yet only limited peer-reviewed research exists. To develop a informed policy for e-cigarettes, their effects on human behavior, physiology, and health need to be understood. PURPOSE: This paper describes proceedings from a National Institutes of Health-sponsored workshop, which was held in November 2013, to identify research needs related to the effects of e-cigarettes. Discussion topics included e-cigarette risks and abuse potential; the potential role for e-cigarettes in harm reduction and smoking cessation; unintended consequences of e-cigarette use, such as becoming a gateway to conventional cigarettes; and dual use of both e-cigarettes and conventional cigarettes. RESULTS AND CONCLUSIONS: The research needs identified by the workshop participants included the following: standards to measure the contents and emissions of e-cigarettes; biomarkers of exposure; physiological effects of e-cigarettes on tissues and organ systems, including pulmonary and cardiovascular; information on e-cigarette users, how the devices are used, and identification of the best tools to assess these measures; factors that drive use and influence patterns of use; and appropriate methods for evaluating a potential role for e-cigarettes in smoking or nicotine cessation. To understand fully the challenges and the opportunities that e-cigarettes represent, expertise will be needed in basic, behavioral, translational, and clinical sciences.

Identification of SMARCAL1 as a component of the DNA damage response.

SMARCAL1 (also known as HARP) is a SWI/SNF family protein with an ATPase activity stimulated by DNA containing both single-stranded and double-stranded regions. Mutations in SMARCAL1 are associated with the disease Schimke immuno-osseous dysplasia, a multisystem autosomal recessive disorder characterized by T cell immunodeficiency, growth inhibition, and renal dysfunction. The cellular function of SMARCAL1, however, is unknown. Here, using Xenopus egg extracts and mass spectrometry, we identify SMARCAL1 as a protein recruited to double-stranded DNA breaks. SMARCAL1 binds to double-stranded breaks and stalled replication forks in both egg extract and human cells, specifically colocalizing with the single-stranded DNA binding factor RPA. In addition, SMARCAL1 interacts physically with RPA independently of DNA. SMARCAL1 is phosphorylated in a caffeine-sensitive manner in response to double-stranded breaks and stalled replication forks. It has been suggested that stalled forks can be stabilized by a mechanism involving caffeine-sensitive kinases, or they collapse and subsequently recruit Rad51 to promote homologous recombination repair. We show that depletion of SMARCAL1 from U2OS cells leads to increased frequency of RAD51 foci upon generation of stalled replication forks, indicating that fork breakdown is more prevalent in the absence of SMARCAL1. We propose that SMARCAL1 is a novel DNA damage-binding protein involved in replication fork stabilization.