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Open Access Research article

Estimating alcohol-related premature mortality in san francisco: use of population-attributable fractions from the global burden of disease study

Brian S Katcher12*, Randy B Reiter1 and Tomás J Aragón134

Author Affiliations

1 Community Health Epidemiology, San Francisco Department of Public Health, San Francisco, California, USA

2 Department of Clinical Pharmacy, School of Pharmacy, University of California, San Francisco, California, USA

3 Division of Epidemiology, School of Public Health, University of California, Berkeley, California, USA

4 Division of Preventive Medicine and Public Health, University of California, San Francisco, California, USA

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BMC Public Health 2010, 10:682  doi:10.1186/1471-2458-10-682

Published: 9 November 2010

Abstract

Background

In recent years, national and global mortality data have been characterized in terms of well-established risk factors. In this regard, alcohol consumption has been called the third leading "actual cause of death" (modifiable behavioral risk factor) in the United States, after tobacco use and the combination of poor diet and physical inactivity. Globally and in various regions of the world, alcohol use has been established as a leading contributor to the overall burden of disease and as a major determinant of health disparities, but, to our knowledge, no one has characterized alcohol-related harm in such broad terms at the local level. We asked how alcohol-related premature mortality in San Francisco, measured in years of life lost (YLLs), compares with other well-known causes of premature mortality, such as ischemic heart disease or HIV/AIDS.

Methods

We applied sex- and cause-specific population-attributable fractions (PAFs) of years of life lost (YLLs) from the Global Burden of Disease Study to 17 comparable outcomes among San Francisco males and females during 2004-2007. We did this in three ways: Method 1 assumed that all San Franciscans drink like populations in developed economies. These estimates were limited to alcohol-related harm. Method 2 modified these estimates by including several beneficial effects. Method 3 assumed that Latino and Asian San Franciscans drink alcohol like populations in the global regions related to their ethnicity.

Results

By any of these three methods, alcohol-related premature mortality accounts for roughly a tenth of all YLLs among males. Alcohol-related YLLs among males are comparable to YLLs for leading causes such as ischemic heart disease and HIV/AIDS, in some instances exceeding them. Latino and black males bear a disproportionate burden of harm. Among females, for whom estimates differed more by method and were smaller than those for males, alcohol-related YLLs are comparable to leading causes which rank somewhere between fifth and fourteenth.

Conclusions

Alcohol consumption is a major contributor to premature mortality in San Francisco, especially among males. Interventions to avert alcohol-related harm in San Francisco should be taken at the population level and deserve the same attention that is given to other major risk factors, such as smoking or obesity.