Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles
Department of Mechanical and Aerospace Engineering, University of California, Davis, CA 95616, USA.Inhalation Toxicology (Impact Factor: 2.26). 08/2011; 23(9):520-31. DOI: 10.3109/08958378.2011.591447
This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 ppm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.
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ABSTRACT: Models of the lung airways of a rat were developed from complete measurements of the tracheobronchial airways. A silicone rubber cast of the tracheobronchial airways of a rat lung was prepared and all individual airway segments down to and including the terminal bronchioles were measured to obtain the segment diameters, lengths, branching angles and angles of inclination to gravity. Models of the rat tracheobronchial airways were constructed based on the original measurements and the subsequent analysis. Some mathematical assumptions about acinar anatomy distal to terminal bronchioles were made to extend the models to include pulmonary regions. Emphasis was placed on the "Typical Path Lung Model" which used one typical pathway to represent either a whole lung or a lobe of the lung. The models are simple and can be applied in calculation of physiologic variables or particle deposition during inhalation in various lobes of the lung.The Anatomical Record 11/1979; 195(3):483-92. DOI:10.1002/ar.1091950308
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ABSTRACT: This study examines the effects of an ambient concentration of aged and diluted sidestream cigarette smoke (ADSS) on bronchiolar epithelial cell development and the expression of cytochrome P450 isozyme 1A1 protein in the postnatal rat lung. In control animals, the labeling indices for epithelial cells in proximal bronchi and terminal bronchioles at 7 days of age were 2.3 and 4.9%, respectively, and decreased to 0.1 and 0%, by 100 days of age. With exposure to ADSS from birth, the labeling index of epithelial cells in distal airways of rats was significantly reduced at 7 and 14 days of age, but not in epithelial cells of proximal bronchi. The expression of P450 isozyme 1A1 antigen in bronchiolar epithelial cells of control rats reached the maximal level observed at 21 days of age and subsequently decreased to low levels at 50 and 100 days of age. In contrast, exposure to ADSS significantly increased the distribution and intensity of staining for 1A1 antigen in bronchiolar epithelial cells of proximal and distal airways as early as 7 days of age and maintained elevated levels of 1A1 protein in these cells through 100 days of age. At 21 and 50 days of age, NADPH reductase protein expression was higher in the airway epithelium of rats exposed from birth to ADSS than that noted in the airways of controls. In contrast, cytochrome P450 isozyme 2B and Clara cell secretory protein expression were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)American Journal of Respiratory Cell and Molecular Biology 10/1994; 11(3):312-20. DOI:10.1165/ajrcmb.11.3.8086168 · 3.99 Impact Factor
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ABSTRACT: Human health effects due to chronic exposure to ozone (O3) have not been established due to problems with exposure assignment and the use of measures of lung function which may not reflect the site of O3 toxicity in the lung. We investigated the feasibility of retrospective assessment of O3 exposure-relevant covariates and derived lifetime "effective exposure" to ozone. Mid- and end-expiratory flows (FEF25-75%, FEF75%) were regressed against effective exposure and ecological lifetime exposure. A convenience sample of 130 UC Berkeley freshmen, ages 17-21, participated twice in the same tests (residential history, questionnaire, pulmonary function), 5-7 days apart. Students had to be lifelong residents of Northern (SF) or Southern (LA) California. Monthly ambient O3 concentrations (OZ) were assigned based on the lifetime residential history. An "effective time" (T) spent in OZ environments was derived for each residence and age stratum (0-2, 3-5, 6-11, 12+) with the use of questions about "total time spent outdoors" and time spent in "moderate" and/or "heavy" activity. Effective exposure was calculated over the lifetime (OZ x T) of each subject. Ozone metrics used were 8-hr averages (10 AM-6 PM) and "hours above 60 ppb." FEF25-75% and FEF75% decreased with both effective exposure and ecologic assignment of O3 exposure. For a 20 ppb increase (interquartile range) in 8-hr O3, FEF75% decreased 334 ml/sec (95%Cl:11-657 ml/sec), which corresponds to 14% (1.0-28.3%) of the population mean FEF75%. The corresponding effect on FEF25-75% was -420 ml/sec (95%Cl: +46 to -886, P = 0.08) or 7.2% of the mean. Use of time-activity data to define exposure had no impact on estimates. Negative confounding factors were region (SF vs LA), gender, and ethnicity. Lifetime 8-hr average O3 concentrations ranged from 16 to 74 ppb with little overlap between regions. There was no evidence for different O3 effects across regions. Effects were independent of lifetime mean PM10, NO2, temperature, or humidity. Effects on FEV1 tended to be negative whereas those for FVC, although negative in some models, where inconsistent and small. The strong relationship of lifetime ambient O3 on mid- and end-expiratory flows of college freshmen and the lack of association with FEV1 and FVC are consistent with biologic models of chronic effects of O3 in the small airways. Since the present study was designed as a pilot study, these findings have to be confirmed in a larger sample that is representative of the target population.Environmental Research 02/1997; 72(1):8-23. DOI:10.1006/enrs.1996.3687 · 4.37 Impact Factor
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