Acute effects of ozone exposure on lung function in mice sensitized to ovalbumin

Chiba University, Tiba, Chiba, Japan
Toxicology (Impact Factor: 3.62). 04/2002; 172(1):69-78. DOI: 10.1016/S0300-483X(01)00588-1
Source: PubMed


Pulmonary responses to ozone exposure (1.0 ppm) were investigated in mice sensitized to ovalbumin compared with control mice receiving saline. Pulmonary function parameters were measured by pneumotachography. Arterial blood gases and the concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and tumor necrosis factor-alpha (TNF-alpha) in bronchoalveolar lavage fluid were analyzed. Ozone exposure, when compared with filtered air exposure, caused significantly larger decreases in dynamic compliance (P<0.05) and minute ventilation (P<0.05) in ovalbumin-sensitized mice but not in control mice. Moreover, the decrease in minute ventilation in response to ozone exposure was significantly greater (P<0.01) in ovalbumin-sensitized mice than in control mice. Ozone exposure caused a significant decrease in PaO2 in ovalbumin-sensitized mice but not in control mice. PaO2 after ozone exposure tended to be smaller in ovalbumin-sensitized mice than in control mice. The concentration of sICAM-1 in bronchoalveolar lavage fluid increased in ovalbumin-sensitized mice, but effects of ozone exposure were not observed. These results indicated that sensitization of the immune system to ovalbumin might be a risk factor which aggravates the effects of ozone exposure on the respiratory system.

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Available from: Tomoyuki Kuwaki
    • "Ozone is also a residual compound of the reaction mixture. The adverse effects of O 3 exposure have been widely studied and include airway irritation (Nielsen et al., 1999), airway inflammation (Schelegle et al., 1991; Backus et al., 2010; Seltzer et al., 1986; Bhalla, 1999), exacerbation of asthma (Yamauchi et al., 2002; Funabashi et al., 2004; Larsen et al., 2010), and enhancement of antibody responses to inhaled aeroallergens (Sumitomo et al., 1990; Osebold et al., 1988; Neuhaus-Steinmetz et al., 2000). Ozone may thus be associated with the development of airway allergy. "
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    ABSTRACT: Inhalation of ozone (O3), a highly toxic environmental pollutant, produces airway inflammation and exacerbates asthma. However, in indoor air, O3 reacts with terpenes (cyclic alkenes), leading to formation of airway irritating pollutants. The aim of the study was to examine whether inhalation of the reaction products of O3 and the terpene, limonene, as well as limonene and low-level O3 by themselves, induced allergic sensitization (formation of specific immunoglobulin [Ig] E) and airway inflammation in a subchronic mouse inhalation model in combination with the model allergen ovalbumin (OVA). BALB/cJ mice were exposed exclusively by inhalation for 5 d/wk for 2 wk and thereafter once weekly for 12 wk. Exposures were low-dose OVA in combination with O3, limonene, or limonene/O3 reaction products. OVA alone and OVA + Al(OH)3 served as control groups. Subsequently, all groups were exposed to a high-dose OVA solution on three consecutive days. Serum and bronchoalveolar lavage fluid were collected 24 h later. Limonene by itself did not promote neither OVA-specific IgE nor leukocyte inflammation. Low-level O3 promoted eosinophilic airway inflammation, but not OVA-specific IgE formation. The reaction products of limonene/O3 promoted allergic (OVA-specific IgE) sensitization, but lung inflammation, which is a characteristic of allergic asthma, was not observed. In conclusion, the study does not support an allergic inflammatory effect attributed to O3-initiated limonene reaction products in the indoor environment.
    No preview · Article · Oct 2013 · Journal of Toxicology and Environmental Health Part A
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    • "Our sensitization protocol was similar to a study by Yamauchi et al. (2002), which has been confirmed to be sufficiently effective because OA-sensitized mice had demonstrated accelerated bronchial hyper-reactivity to methacoline compared with non-sensitized mice. At baseline, respiratory resistance was slightly larger in OA-sensitized groups and slightly lower in the two groups undergoing repeated ozone exposure, but there was no significant difference. "
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    ABSTRACT: We examined the effect of repeated ozone exposure on the respiratory system in mice, sensitized with ovalbumin (OA). OA-sensitized mice and saline-treated control mice were exposed to 1.0 ppm ozone or clean air for 6 h daily and five days weekly for five weeks. Subsequently, these mice were exposed to 1.0 ppm ozone for 1 h, and pulmonary function was evaluated by pneumotachography during ozone exposure and arterial blood gas analysis and histopathological examination were performed. OA sensitization or repeated ozone exposure did not affect baseline pulmonary function. In OA-sensitized mice receiving repeated ozone exposure, acute ozone exposure increased respiratory resistance and decreased dynamic compliance, with significant differences in both parameters compared with, after repeated ozone exposure without OA sensitization. In mice without repeated exposure, there was no difference in the effect of acute ozone exposure according to the use of OA sensitization. After 1-h exposure, arterial blood gas analysis showed a significant decrease in PaO2 in mice undergoing OA sensitization alone, with no significant reduction of this parameter in mice receiving repeated exposure. Histopathologically, alveolar epithelial hyperplasia occurred in repeatedly exposed mice. These results indicated that respiratory allergy might be a risk factor, which aggravates the effects of repeated ozone exposure.
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    ABSTRACT: Ozone (O3) is an air pollutant produced by sunlight-driven reactions involving the oxides of nitrogen and volatile organic compounds. The population of many large metropolitan areas in the US is exposed to high levels of O3, particularly in the summer months. Individuals exposed to O3 levels in human experiments at higher than common ambient levels develop reversible reductions in lung function often associated with symptoms, such as airway hyperreactivity and lung inflammation. Animal models have helped characterize potential mechanisms of lung injury from O3 exposure. Defining the adverse effects of chronic exposure to ambient levels of O3 on lung function and disease have been challenging, in part due to the presence of co-pollutants, such as particulate matter. The US Environmental Protection Agency's 1997 revised standard for O3 (0.08 ppm averaged over 8 hours) is designed to provide better protection to susceptible individuals. The revised standard is being implemented following the failure of court challenges.
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