Chronic exposure to high levels of particulate air pollution and small airway remodeling.

Abstract

Recent evidence suggests that chronic exposure to high levels of ambient particulate matter (PM) is associated with decreased pulmonary function and the development of chronic airflow obstruction. To investigate the possible role of PM-induced abnormalities in the small airways in these functional changes, we examined histologic sections from the lungs of 20 women from Mexico City, a high PM locale. All subjects were lifelong residents of Mexico City, were never-smokers, never had occupational dust exposure, and never used biomass fuel for cooking. Twenty neversmoking, non-dust-exposed subjects from Vancouver, British Columbia, Canada, a low PM region, were used as a control. By light microscopy, abnormal small airways with fibrotic walls and excess muscle, many containing visible dust, were present in the Mexico City lungs. Formal grading analysis confirmed the presence of significantly greater amounts of fibrous tissue and muscle in the walls of the airways in the Mexico City compared with the Vancouver lungs. Electron microscopic particle burden measurements on four cases from Mexico City showed that carbonaceous aggregates of ultrafine particles, aggregates likely to be combustion products, were present in the airway mucosa. We conclude that PM penetrates into and is retained in the walls of small airways, and that, even in nonsmokers, long-term exposure to high levels of ambient particulate pollutants is associated with small airway remodeling. This process may produce chronic airflow obstruction.

Relative Effects of Air Pollution on Lungs and Heart

“…These new findings should not be misinterpreted to indicate that high levels of air pollution have little or no effect on the lungs of never smokers. In never smokers, there is clear evidence that high levels of air pollution cause structural damage in the lung periphery 6,7,16 and accelerate decline in lung function. 17 Nonsmokers exposed to high levels of air pollution will probably not die of COPD, but they may develop a higher-than-normal risk of death from pneumonia or influenza consistent with the present data.…”

Health Effects of Fine Particulate Air Pollution: Lines that Connect

“…347 There is evidence, even in nonsmokers, that long-term exposure to PM air pollution results in pulmonary retention of fine particles and small airway remodeling and contributes to COPD. 348,349 Epidemiologic evidence that supports this hypothesis includes various studies that have observed that longterm PM exposures are associated with deficits in lung function 350 -354 and increased symptoms of obstructive airway disease, such as chronic cough, bronchitis, and chest illness. 25,[355][356][357][358][359] Recently published results from the Southern California Children's Health Study indicate that exposure to PM 2.5 and other combustion-related air pollutants were significantly associated with deficits in the rate of lung function growth in children (see Figure 2d).…”

Pollution atmosphérique et maladies respiratoires

“…Néanmoins, on ne peut exclure que les particules les plus fines aient un effet direct sur les tissus voisins par transcytose, au travers des épithéliums [17]. Une exacerbation et/ou un dérèglement des fonctions épithéliales associés à une exposition répétée aux polluants environnementaux, ozone et PM, peuvent être à l'origine d'une inflammation chronique et d'un remodelage bronchique caractérisé par l'épaississement du tissu musculaire lisse, une métaplasie muqueuse et une fibrose péribronchique [18]. Ces modifications s'observent aussi chez des patients atteints de BPCO et d'asthme.…”

“…La cascade proapoptotique est alors déclenchée par la chute du potentiel transmembranaire de la mitochondrie et la libération cytosolique du cytochrome c. Les macrophages, sans doute parce qu'ils ont une plus grande capacité de phagocytose, sont plus sensibles que les cellules épithéliales à l'induction de l'apoptose [19]. Cette constatation est importante pour expliquer la persistance des particules dans le poumon profond (zones alvéolaires) associée à l'inflammation chronique et au remodelage bronchique [18]. La découverte récente que les PDi à faible concentration pouvaient, par contre, inhiber l'apoptose dans la lignée alvéolaire humaine A549 en provoquant la baisse d'expression de la protéine p21, particulièrement importante dans le contrôle du cycle cellulaire, pose la question de leur rôle à long terme sur la prolifération cellulaire et l'hyperplasie [20].…”