title: Effects of concentrated ambient particles on airway responsiveness and pulmonary inflammation in pulmonary hypertensive rats.
abstract: Epidemiological studies have associated particulate air pollution with exacerbation of lung function in human populations. However, the relationship between ambient particles and lung function in animal studies has been inconsistent. In order to investigate the effects of concentrated ambient particles (CAPs) on airway responsiveness, we exposed pulmonary hypertensive rats to CAPs using particle concentrator at an EPA of Taiwan supersite, located at a traffic busy urban area nearing Taipei city. The exposure group (n = 5) was exposed to CAPs for 6 h each day for 3 consecutive days (mean mass concentration = 371.7 microg/m(3)), while a control group (n = 6) was exposed to HEPA-filtered air. Whole-body barometric plethysmography was used to measure respiratory frequency, tidal volume, and airway responsiveness before and after exposure. Enhanced pause (Penh) was used as an indicator of airway responsiveness. To improve the accuracy of airway responsiveness measurement, we controlled temperature and humidity. Further, airway responsiveness was determined 5 h after particle exposure to overcome the stress effect in nose-only exposure chambers. After CAPs exposure, we found decreased respiratory frequency and increased tidal volume (p < .05). Using the methacholine challenge test, a significant difference of Penh measured before and after experiment was observed in the CAPs group (p < .05), but not in the filtered air group. Further analysis showed that the Penh difference before and after exposure in the CAPs group was significantly greater than that in the filtered air group (p < .05). We conclude that CAPs could induce airway hyperresponsiveness in pulmonary hypertensive rats.
authors.affiliation: Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei, Taiwan.
authors.forename: Yu-Chen
authors.initials: YC
authors.lastname: Lei
authors.forename: Ming-Chih
authors.initials: MC
authors.lastname: Chen
authors.forename: Chang-Chuan
authors.initials: CC
authors.lastname: Chan
authors.forename: Peng-Yau
authors.initials: PY
authors.lastname: Wang
authors.forename: Chung-Te
authors.initials: CT
authors.lastname: Lee
authors.forename: Tsun-Jen
authors.initials: TJ
authors.lastname: Cheng
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000403:Airway Resistance / Q000502:physiology; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D016085:Bronchoconstrictor Agents / Q000494:pharmacology; D002452:Cell Count; D016207:Cytokines / Q000378:metabolism; D006976:Hypertension, Pulmonary / Q000473:pathology / Q000503:physiopathology*; D008168:Lung / Q000473:pathology; D008297:Male; D016210:Methacholine Chloride; D010991:Plethysmography; D010993:Plethysmography, Whole Body; D011014:Pneumonia / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015656:Respiratory Mechanics / Q000187:drug effects*; D013990:Tidal Volume / Q000502:physiology
chemical_list: D000393:Air Pollutants; D016085:Bronchoconstrictor Agents; D016207:Cytokines; D016210:Methacholine Chloride