OBJECTIVE

Carbon monoxide (CO) is an odorless, colorless gas produced by fossil fuel combustion. On October 29, 2012, Hurricane Sandy moved ashore near Atlantic City, New Jersey, causing widespread morbidity and mortality, $30 to $50 billion in economic damage, and 8.5 million households to be without power. The combination of power outages and unusually low temperatures led people to use alternate power sources, placing many at risk for CO exposure.

METHODS

We examined Hurricane Sandy-related CO exposures from multiple perspectives to help identify risk factors and develop strategies to prevent future exposures. This report combined data from 3 separate sources (health departments, poison centers via the National Poison Data System, and state and local public information officers).

RESULTS

Results indicated that the number of CO exposures in the wake of Hurricane Sandy was significantly greater than in previous years. The persons affected were mostly females and those in younger age categories and, despite messaging, most CO exposures occurred from improper generator use.

CONCLUSIONS

Our findings emphasize the continued importance of CO-related communication and ongoing surveillance of CO exposures to support public health response and prevention during and after disasters. Additionally, regional poison centers can be a critical resource for potential on-site management, public health promotion, and disaster-related CO exposure surveillance. (Disaster Med Public Health Preparedness. 2017;11:562-567).

BACKGROUND

The antiretroviral medication, tenofovir disoproxil fumarate (TDF), is used by most human immunodeficiency virus-infected persons in the United States despite higher risks of chronic kidney disease. Although chronic kidney disease is a strong risk factor for heart failure (HF), the association of TDF with incident HF is unclear.

METHODS AND RESULTS

We identified 21 435 human immunodeficiency virus-infected patients in the United States Veterans Health Administration actively using antiretrovirals between 2002 and 2011. We excluded patients with a prior diagnosis of HF. TDF was analyzed categorically (current, past, or never use) and continuously (per year of use). Proportional hazards regression and fully adjusted marginal structural models were used to determine the association of TDF exposure with risk of incident HF after adjustment for demographic, human immunodeficiency virus-related, and cardiovascular risk factors. During follow-up, 438 incident HF events occurred. Unadjusted 5-year event rates for current, past, and never users of TDF were 0.9 (95%CI 0.7-1.1), 1.7 (1.4-2.2), and 4.5 (3.9-5.0), respectively. In fully adjusted analyses, HF risk was markedly lower in current TDF users (HR=0.68; 95%CI 0.53-0.86) compared with never users. Among current TDF users, each additional year of TDF exposure was associated with a 21% lower risk of incident HF (95%CI: 0.68-0.92). When limited to antiretroviral-naive patients, HF risk remained lower in current TDF users (HR=0.53; 95%CI 0.36-0.78) compared to never users.

CONCLUSIONS

Among a large national cohort of human immunodeficiency virus-infected patients, TDF use was strongly associated with lower risk of incident HF. These findings warrant confirmation in other populations, both with TDF and the recently approved tenofovir alafenamide fumarate.

Atrial fibrillation affects more than 33 million people worldwide and increases the risk of stroke, heart failure, and death. Fourteen genetic loci have been associated with atrial fibrillation in European and Asian ancestry groups. To further define the genetic basis of atrial fibrillation, we performed large-scale, trans-ancestry meta-analyses of common and rare variant association studies. The genome-wide association studies (GWAS) included 17,931 individuals with atrial fibrillation and 115,142 referents; the exome-wide association studies (ExWAS) and rare variant association studies (RVAS) involved 22,346 cases and 132,086 referents. We identified 12 new genetic loci that exceeded genome-wide significance, implicating genes involved in cardiac electrical and structural remodeling. Our results nearly double the number of known genetic loci for atrial fibrillation, provide insights into the molecular basis of atrial fibrillation, and may facilitate the identification of new potential targets for drug discovery.