International Journal of Epidemiology 2001;30:1138-1140
© International Epidemiological Association 2001
Brief Report |
Particles, and not gases, are associated with the risk of death in patients with chronic obstructive pulmonary disease
Unit of Respiratory and Environmental Research, IMIM, Barcelona, Catalonia, Spain.
Dr Jordi Sunyer, Unitat de Recerca Respiratòria i Ambiental, Institut Municipal d'Investigació Mèdica (IMIM), Doctor Aiguader 80, E-08003 Barcelona, Catalonia, Spain. E-mail: jsunyer{at}imim.es
Abstract
Objectives We aim to assess the independent association of particles, after controlling for gaseous pollutants, with the risk of death among a cohort of patients with chronic obstructive pulmonary disease (COPD).
Methods Residents of Barcelona, aged over 35 years, who attended emergency room services for COPD exacerbation from 1985 to 1989 and who died in the period 1990–1995 (n = 2305) were selected. The analysis followed a case-crossover procedure with ambidirectional controls. Air pollution exposure (particulate matter <10 µm (PM10), ozone, nitrogen dioxide and carbon monoxide) was measured at the city monitoring stations.
Results Levels of PM10 (odds ratio for the interquartile difference = 1.11, 95% CI : 1.00– 1.24), but not gaseous pollutants, were associated with mortality for all causes of death after adjusting for meteorological variables and influenza epidemics. In the two-pollutant models, the association of mortality with PM10 was not confounded by the inclusion of gases, while the association of gaseous pollutants was notably reduced after adjustment for particles. There was no interaction between particles and gaseous pollutants.
Conclusions Findings reinforce the deleterious role of urban particles as a trigger of death in COPD patients, and suggest that they are the major culprit among the air pollutants. The role of other pollutants, if any, was additive and not multiplicative.
Keywords Air pollution, lung diseases, obstructive, mortality, particles
Accepted 26 January 2001
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  J Sunyer, D Jarvis, T Gotschi, R Garcia-Esteban, B Jacquemin, I Aguilera, U Ackerman, R de Marco, B Forsberg, T Gislason, et al. Chronic bronchitis and urban air pollution in an international study Occup. Environ. Med., December 1, 2006; 63(12): 836 - 843. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Kunzli and C. Schindler A call for reporting the relevant exposure term in air pollution case-crossover studies J Epidemiol Community Health, June 1, 2005; 59(6): 527 - 530. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. F. van Eeden, A. Yeung, K. Quinlam, and J. C. Hogg Systemic Response to Ambient Particulate Matter: Relevance to Chronic Obstructive Pulmonary Disease Proceedings of the ATS, April 1, 2005; 2(1): 61 - 67. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Agopyan, J. Head, S. Yu, and S. A. Simon TRPV1 receptors mediate particulate matter-induced apoptosis Am J Physiol Lung Cell Mol Physiol, March 1, 2004; 286(3): L563 - L572. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Annesi-Maesano, N. Agabiti, R. Pistelli, M-F. Couilliot, and F. Forastiere Subpopulations at increased risk of adverse health outcomes from air pollution Eur. Respir. J., May 1, 2003; 21(40_suppl): 57S - 63s. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. L. Lambert, J. B. Mangum, M. P. DeLorme, and J. I. Everitt Ultrafine Carbon Black Particles Enhance Respiratory Syncytial Virus-Induced Airway Reactivity, Pulmonary Inflammation, and Chemokine Expression Toxicol. Sci., April 1, 2003; 72(2): 339 - 346. [Abstract] [Full Text] [PDF]
|
|