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Biology Articles » Ecology » Air pollution and lung function among susceptible adult subjects: a panel study » Discussion

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

This study suggests an effect of fine particles on lung function of COPD patients. The metallic content of PM2.5 seems to be of importance, given the observed negative effects of Zn, Fe and Ni concentrations on lung function indices. NO2 also was associated with FEV1 decrements among COPD cases. On the other hand, no effects of PM2.5 were found among asthmatics, whose respiratory function seemed to be negatively influenced by ambient NO2 concentrations. No pollutant-related lung function changes were observed among IHD subjects, with no pre-existing lung impairment.

We acknowledge several limitations of the study. Lack of personal exposure measurements is an important shortcoming. Lifestyles and housing conditions among our study subjects were not homogenous, and we cannot expect outdoor PM2.5 concentrations in our study to be a perfect indicator of personal exposure variability, as it was reported among elderly subjects residing in a retirement facility [36,37]. However, the good correlation we observed between day-to-day variations in average outdoor and indoor PM2.5 should mitigate the possibility that findings among COPD patients are entirely due to errors in estimating personal exposure variability. Moreover, despite the high number of repeated observations per subject, the reduced number of patients in each diagnostic category gives a low power to the study, thus we cannot exclude the possibility that small effects were not detected because of the reduced sample size. Last, the present study shares with other studies of air pollution related health effects the drawback of multiple statistical testing.

There are however strengths of the study that are worth underlining. They include: (i) supervised lung function tests; (ii) many repeated observations per patient, which allowed accounting for within-subject variability; (iii) a variety of measured urban pollutants, including fine particles, coarse particles and transition metals. Furthermore, in the present study no association between respiratory function indices and average ambient concentrations of any pollutants was observed among IHD cases, whereas effects of the fine fraction of ambient particulate on lung function among COPD subjects were detected, which had a strong a priori hypothesis. In the light of such results, it seem less likely that the associations observed among COPD and asthmatic patients are chance findings due to the great number of relationships examined.

After considering validity issues, it is worth noting the results of other published works. To our knowledge, only two studies have evaluated lung function by supervised spirometry in relation to daily variation in air pollution among adults with COPD. In the panel study of Pope and Kanner [25], based on 2 repeated observations of 251 smokers with mild to moderate COPD, a 10 μg/m3 increase in PM10 was associated with an average decrease in FEV1 equal to approximately 0.2%. Brauer et al. [26], in their panel study of 16 COPD cases with moderate airway obstruction (FEV1 at baseline ≥ 0.75 l) observed a non-significant 1.1% decrease of FEV1 for 10 μg/m3 increase in ambient PM2.5. In four other studies [19-22], possible pollution-related effects on pulmonary function in COPD cases were examined by unsupervised measurements of peak expiratory flow (PEF). To our knowledge, our study is the first that was able to document a specific role of fine particles on lung function of COPD patients.

PM-related exacerbation of chronic obstructive lung disease may be sustained by multiple direct and indirect mechanisms [5,38,39]. There is empirical evidence and experimental support for direct damages to the respiratory mucosa (increased permeability and reduced mucociliar activity), for oxidative damage, and for secondary toxic effects mediated by pro-inflammatory cytokines. Relative to healthy subjects, patients with moderate-to-severe airway obstruction receive an increased dose from ultra fine particle exposure [40]. Transition metals [7,8], as well as ultra fine particles [6], may induce oxidative stress and inflammatory response. We are not aware of previous panel studies of adult COPD cases examining pulmonary function changes in relation to the metallic content of airborne PM. The exploratory analyses presented in this paper suggest that metals from inhaled particulate have a biological effect on pulmonary function. The results on Zn and Fe are of specific interest. Both metals present in the fine fraction are likely to be traffic related as they originate from engine oils, brake, engine, exhaust systems and tire wear [41]. They have a high water solubility which has been directly related to oxidative damage [42].

Results from the asthmatic panel suggest a negative influence of NO2 on FEV1, but no effect of fine particles. Our finding that NO2 is related to lung function decrements both among COPD and asthma patients is of interest. It is difficult to believe that NO2 per se is responsible of the observed effects, given its low intrinsic toxicity. It has been suggested, however, that NO2 may be considered a very good marker of the combustion mixture from traffic sources, in particular of ultra fine particles [43].

No effect of O3 concentrations on the respiratory function of asthmatics was detected, even when the analysis was restricted to the spring survey. The latter finding could be explained by the relatively good clinical conditions of the asthmatics included in the study (all in the mild intermittent stage), the relatively low levels of O3 recorded during the study period, or simply lack of power. Although many panel studies of adult asthmatics have reported associations between asthma symptoms and both PM and O3 [13,14], inconsistent results were observed with regard to lung function. Moseholm and coworkers [16] found that increased levels of SO2 and NO2 corresponded synergistically to decreased peak flow at levels above 40 μg/m3. In the asthmatic panel studied by Taggart et al. [24], changes in bronchial hyper-responsiveness were significantly correlated with 24 h mean concentrations of SO2, NO2 and black smoke, none of the criteria air pollutants seemed to affect FEV1, while previous-day NO2 levels were associated with FVC decrements. Ambient PM10 concentrations negatively affected PEF readings among the asthmatics followed by Peters et al. [17], with especially strong effects due to the number of ultra fine particles. Higgins et al. [19] observed PEF decrements associated with SO2 and O3 among the methacolin-reactors in their panel, but no independent effect of ambient NO2 levels. On the other hand, among the asthmatics followed by Hiltermann et al. [18], ambient concentrations of O3, PM10, black smoke and NO2 were found to be associated with increased symptom reports, but not with decreased PEF readings.

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