Chronic Exposure to Ambient Levels of Urban Particles Affects Mouse Lung Development

• Published in: American journal of respiratory and critical care medicine Vol. 178; no. 7; pp. 721 - 728
• Main Authors: Mauad, Thais, Rivero, Dolores Helena Rodriguez Ferreira, de Oliveira, Regiani Carvalho, de Faria Coimbra Lichtenfels, Ana Julia, Guimaraes, Eliane Tigre, de Andre, Paulo Afonso, Kasahara, David Itiro, de Siqueira Bueno, Heloisa Maria, Saldiva, Paulo Hilario Nascimento
• Format: Journal Article
• Language: English
• Published: New York, NY Am Thoracic Soc 01.10.2008; American Lung Association; American Thoracic Society
• Subjects: Air Pollutants - adverse effects; Air pollution; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Brazil; Carbon; Children & youth; Chronic obstructive pulmonary disease, asthma; D. Environmental and Occupational Lung Disease; Disease Models, Animal; Female; Inhalation Exposure - adverse effects; Intensive care medicine; Male; Medical sciences; Mice; Outdoor air quality; Particulate Matter - adverse effects; Pneumology; Pollutants; Pulmonary Alveoli - growth & development; Pulmonary Alveoli - pathology; Respiratory Function Tests; Urban Population; Vehicle Emissions; Brazil; Intensive care; Rodentia; Urban area; particulate matter; Vertebrata; Chronic; Mammalia; Mouse; Animal; alveolization; pressure- volume curves; Resuscitation; lung development
• ISSN: 1073-449X; 1535-4970
• DOI: 10.1164/rccm.200803-436OC

Chronic exposure to air pollution has been associated with adverse effects on children's lung growth. We analyzed the effects of chronic exposure to urban levels of particulate matter (PM) on selected phases of mouse lung development. The exposure occurred in two open-top chambers (filtered and nonfiltered) placed 20 m from a street with heavy traffic in São Paulo, 24 hours/day for 8 months. There was a significant reduction of the levels of PM(2.5) inside the filtered chamber (filtered = 2.9 +/- 3.0 microg/m(3), nonfiltered = 16.8 +/- 8.3 microg/m(3); P = 0.001). At this exposure site, vehicular sources are the major components of PM(2.5) (PM <or= 2.5 microm). Exposure of the parental generation in the two chambers occurred from the 10th to the 120th days of life. After mating and birth of offspring, a crossover of mothers and pups occurred within the chambers, resulting in four groups of pups: nonexposed, prenatal, postnatal, and pre+postnatal. Offspring were killed at the age of 15 (n = 42) and 90 (n = 35) days; lungs were analyzed by morphometry for surface to volume ratio (as an estimator of alveolization). Pressure-volume curves were performed in the older groups, using a 20-ml plethysmograph. Mice exposed to PM(2.5) pre+postnatally presented a smaller surface to volume ratio when compared with nonexposed animals (P = 0.036). The pre+postnatal group presented reduced inspiratory and expiratory volumes at higher levels of transpulmonary pressure (P = 0.001). There were no differences among prenatal and postnatal exposure and nonexposed animals. Our data provide anatomical and functional support to the concept that chronic exposure to urban PM affects lung growth.