Ozone-induced Airway Inflammation in Human Subjects as Determined by Airway Lavage and Biopsy

Abstract

Ozone (O3) is a major constituent of urban air pollution. The acute effects of the inhalation of O3 at ambient or near-ambient concentrations on bronchoalveolar lavage (BAL) end points consistent with a distal lung inflammatory response have been well documented in human subjects. Animal toxicologic studies have shown that the airway is also a major site of O3-induced injury and inflammation. To date, no studies have confirmed this finding in human subjects. Effects of O3 on the proximal airways are not adequately studied by BAL, which is primarily influenced by events occurring in the terminal bronchioles and alveoli. We hypothesized that O3 causes injury and inflammation in the airways in addition to that previously documented to occur in the distal lung. We performed isolated lavage of the left mainstem bronchus and forceps biopsy of the bronchial mucosa in a group of 14 healthy, athletic subjects 18 h after exposure to 0.20 ppm O3 for 4 h during moderate exercise in order to assess this possibility. We followed an identical protocol in a similar group of 12 subjects exposed to filtered air. The mean (SD) total cell count and the lactate dehydrogenase (LDH) concentration in the isolated airway lavage were significantly greater after O3 than after air, 13.9 (20.5) versus 4.9 (5.4) cells/ml x 10(4) and 18.9 (11.2) versus 9.6 (9.0) U/L, respectively. Morphometry (2,070 neutrophils/cm2 of tissue for O3 and 330 neutrophils/cm2 of tissue for air) demonstrated that O3 exposure induced an acute inflammatory cell influx into the airway.(ABSTRACT TRUNCATED AT 250 WORDS)

Children's health and the environment: public health issues and challenges for risk assessment.

“…Daily fluctuations in PM 10 have been associated with increased emergency room visits for childhood asthma (Rennick and Jarman 1992;Schwartz et al 1993), hospital admissions for asthma (Montealegre et al 1993), decrements in peak flow rates in normal children (Neas et al 1995), increased respiratory symptoms (Forsberg et al 1993), and increased medication use in children with asthma (Pope 1991). Ozone has been of particular concern, as it provokes airway inflammation at very low levels (Aris et al 1993). In addition, ozone increases airway reactivity (Horstman et al 1990;Kreit et al 1989), and there is evidence to suggest that ozone may potentiate the effects of allergens (Molfino et al 1991).…”

Effects of azithromycin on ozone-induced airway neutrophilia and cytokine release

“…The exposure sessions were performed in a custom-built steel and glass exposure chamber (Model No. W00327-3R; NorLake Inc., Hudson, WI, USA), which is 2.5 m62.5 m62.4 m in size, and has an average airflow rate of 170 m 3 . min ).…”

Airway function, oedema, cell infiltration and nitric oxide generation in conscious ozone‐exposed guinea‐pigs: effects of dexamethasone and rolipram

“…Anti-oxidant and scavenger enzymes normally sequester increased levels of ROS after ozone exposure, however, oxidative stress occurs if the level of ozone exceeds the capacity of the anti-oxidative mechanisms (Cardile et al, 1995). In animals and humans, inhaled ozone (O 3 ) induces AHR to various spasmogens (Schultheis, et al, 1994;Seltzer et al, 1986;Arakida et al, 2000), decreases expiratory¯ow and volume (Hazucha, 1987;Joad et al, 1994) and bronchial biopsies and lavage exhibit evidence of leukocyte in¯ux, oedema and epithelial damage (Murlas & Roum, 1985;Aris et al, 1993). Thus, oxidant stress arising after ozone inhalation shares many features associated with COPD and asthma.…”