BACKGROUND: Airway responsiveness after acute inhalation of ozone is related to the concentration and duration of ozone exposure. Using barometric whole-body plethysmography and increase in enhanced pause (Penh) as an index of airway obstruction, we measured the response of BALB/c mice to acute ozone inhalation to study the time course change of pulmonary function after ozone exposure. METHODS: Penh was measured before and after exposure to filtered air or 0.12, 0.5, 1, or 2 ppm ozone for 3 hr (n = 6/group). In addition, Penh was measured 24, 48 and 72 hr after ozone exposure. Bronchoalveolar lavage (BAL) and histopathologic examinations were performed. RESULTS: The increase in Penh after ozone exposure was significantly higher in the 0.12, 0.5, 1 and 2 ppm groups compared with the control group (all p < 0.01). Increases in Penh 24 hr after ozone exposure were significantly lower than those immediately after acute ozone exposure; however, increases in Penh 72 hr after ozone exposure were significantly higher than those in the control group (each p < 0.01). The proportion of neutrophils in BAL fluid was significantly higher in the group exposed to 2 ppm ozone than in the groups exposed to filtered air or 0.12 ppm ozone (both p < 0.01). CONCLUSION: These results indicate that airway obstruction is induced following ozone exposure in a concentration-dependent manner and persists for at least 72 hr.
BACKGROUND: Airway responsiveness after acute inhalation of ozone is related to the concentration and duration of ozone exposure. Using barometric whole-body plethysmography and increase in enhanced pause (Penh) as an index of airway obstruction, we measured the response of BALB/c mice to acute ozone inhalation to study the time course change of pulmonary function after ozone exposure. METHODS:Penh was measured before and after exposure to filtered air or 0.12, 0.5, 1, or 2 ppm ozone for 3 hr (n = 6/group). In addition, Penh was measured 24, 48 and 72 hr after ozone exposure. Bronchoalveolar lavage (BAL) and histopathologic examinations were performed. RESULTS: The increase in Penh after ozone exposure was significantly higher in the 0.12, 0.5, 1 and 2 ppm groups compared with the control group (all p < 0.01). Increases in Penh 24 hr after ozone exposure were significantly lower than those immediately after acute ozone exposure; however, increases in Penh 72 hr after ozone exposure were significantly higher than those in the control group (each p < 0.01). The proportion of neutrophils in BAL fluid was significantly higher in the group exposed to 2 ppm ozone than in the groups exposed to filtered air or 0.12 ppm ozone (both p < 0.01). CONCLUSION: These results indicate that airway obstruction is induced following ozone exposure in a concentration-dependent manner and persists for at least 72 hr.
Authors: H S Koren; R B Devlin; D E Graham; R Mann; M P McGee; D H Horstman; W J Kozumbo; S Becker; D E House; W F McDonnell Journal: Am Rev Respir Dis Date: 1989-02
Authors: E Hamelmann; J Schwarze; K Takeda; A Oshiba; G L Larsen; C G Irvin; E W Gelfand Journal: Am J Respir Crit Care Med Date: 1997-09 Impact factor: 21.405
Authors: R B Devlin; W F McDonnell; R Mann; S Becker; D E House; D Schreinemachers; H S Koren Journal: Am J Respir Cell Mol Biol Date: 1991-01 Impact factor: 6.914
Authors: Colette N Miller; Janice A Dye; Allen D Ledbetter; Mette C Schladweiler; Judy H Richards; Samantha J Snow; Charles E Wood; Andres R Henriquez; Leslie C Thompson; Aimen K Farraj; Mehdi S Hazari; Urmila P Kodavanti Journal: Environ Health Perspect Date: 2017-12-21 Impact factor: 9.031