Air pollution and lung function among susceptible adult subjects: a panel study

Susanna Lagorio,Francesco Forastiere,Paola Michelozzi,Ivano Iavarone,Valeria Fano,Bart D Ostro,Giovanni Ziemacki,Achille Marconi,Riccardo Pistelli

doi:10.1186/1476-069x-5-11

Abstract

BackgroundAdverse health effects at relatively low levels of ambient air pollution have consistently been reported in the last years. We conducted a time-series panel study of subjects with chronic obstructive pulmonary disease (COPD), asthma, and ischemic heart disease (IHD) to evaluate whether daily levels of air pollutants have a measurable impact on the lung function of adult subjects with pre-existing lung or heart diseases.MethodsTwenty-nine patients with COPD, asthma, or IHD underwent repeated lung function tests by supervised spirometry in two one-month surveys. Daily samples of coarse (PM10–2.5) and fine (PM2.5) particulate matter were collected by means of dichotomous samplers, and the dust was gravimetrically analyzed. The particulate content of selected metals (cadmium, chrome, iron, nickel, lead, platinum, vanadium, and zinc) was determined by atomic absorption spectrometry. Ambient concentrations of nitrogen dioxide (NO2), carbon monoxide (CO), ozone (O3), and sulphur dioxide (SO2) were obtained from the regional air-quality monitoring network. The relationships between concentrations of air pollutants and lung function parameters were analyzed by generalized estimating equations (GEE) for panel data.ResultsDecrements in lung function indices (FVC and/or FEV1) associated with increasing concentrations of PM2.5, NO2 and some metals (especially zinc and iron) were observed in COPD cases. Among the asthmatics, NO2 was associated with a decrease in FEV1. No association between average ambient concentrations of any air pollutant and lung function was observed among IHD cases.ConclusionThis study suggests that the short-term negative impact of exposure to air pollutants on respiratory volume and flow is limited to individuals with already impaired respiratory function. The fine fraction of ambient PM seems responsible for the observed effects among COPD cases, with zinc and iron having a potential role via oxidative stress. The respiratory function of the relatively young and mild asthmatics included in this study seems to worsen when ambient levels of NO2 increase.

Highlights

Adverse health effects at relatively low levels of ambient air pollution have consistently been reported in the last years
We considered the possibility of a non-linear effect of temperature by introducing a temperature-squared term in the regression models; since no evidence of model improvement was found in any of the panel-specific analyses, only a linear term was left
This study suggests an effect of fine particles on lung function of chronic obstructive pulmonary disease (COPD) patients

Summary

Introduction

Adverse health effects at relatively low levels of ambient air pollution have consistently been reported in the last years. We conducted a time-series panel study of subjects with chronic obstructive pulmonary disease (COPD), asthma, and ischemic heart disease (IHD) to evaluate whether daily levels of air pollutants have a measurable impact on the lung function of adult subjects with pre-existing lung or heart diseases. Throughout the 1990s, many epidemiological studies consistently reported adverse health effects at unexpectedly low levels of ambient air pollution [1]. Several chronic clinical conditions are good candidates to define the "frail" population susceptible to the acute effects of PM pollution: chronic obstructive pulmonary disease (COPD) including asthma, ischemic heart diseases (IHD), congestive heart failure, heart rhythm disorders, and diabetes [4]. The ability of particulate matter to induce oxidative stress in the airways has been proposed as an important biological mechanism [6]. Oxidative stress might up-regulate redox sensitive transcription factors (via nuclear factor kappa B, NF-kB) in airway epithelial cells, increasing the synthesis of proinflammatory cytokines and resulting in cell and tissue injury [8]

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Results

Conclusion