Am. J. Respir. Crit. Care Med.,
Volume 159, Number 6, June 1999, 1780-1785
Docosahexaenoic Acid and Smoking-Related
Chronic Obstructive Pulmonary Disease
EYAL
SHAHAR,
LORI L.
BOLAND,
AARON R.
FOLSOM,
MELVYN S.
TOCKMAN,
PAUL G.
MCGOVERN,
and
JOHN H.
ECKFELDT, for the Atherosclerosis Risk in
Communities Study Investigators
Division of Epidemiology, School of Public Health, and Department of Laboratory Medicine and Pathology, University
of Minnesota, Minneapolis, Minnesota; and H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida
If the inflammatory response to inhalation of cigarette smoke causes chronic obstructive pulmonary
disease (COPD), suppression of that natural response might be beneficial. We hypothesized that a
smoker's risk of developing COPD is inversely related to physiologic levels of two fatty acids that have
antiinflammatory properties: eicosapentaenoic acid (EPA, C20:5) and docosahexaenoic acid (DHA,
C22:6). The proportion of each fatty acid in plasma lipids was measured in 2,349 current or former
smokers. COPD was identified and defined by clinical symptoms and/or spirometry. After adjustment
for smoking exposure and other possible confounders, the prevalence odds of COPD were inversely
related to the DHA (but not to the EPA) content of plasma lipid components in most of the models.
For example, as compared with the first quartile of the DHA distribution, the prevalence odds ratios
(ORs) for chronic bronchitis were 0.98, 0.88, and 0.69 for the second, third, and fourth quartiles, respectively (p for linear trend = 0.09). The corresponding ORs for COPD as defined spirometrically,
were 0.65, 0.51, and 0.48 (p < 0.001). Among 543 current heavy smokers, adjusted mean values of
FEV1 (lowest to highest DHA quartile) were 2,706, 2,785, 2,801, and 2,854 ml. DHA may have a role in preventing or treating COPD and other chronic inflammatory conditions of the lung. Pilot testing of
that hypothesis in experimental models seems warranted.
