Bronchoalveolar Lavage Neutrophilia in Asthmatic and Healthy Volunteers After Controlled Exposure to Ozone and Filtered Purified Air

Basha, Michael A.; Gross, Kenneth B.; Gwizdala, Charles J.; Haidar, Ali H.; Popovich, John

doi:10.1378/chest.106.6.1757

Cited by 114 publications

(71 citation statements)

References 21 publications

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“…A number of laboratories have reported inter-individual variation in pulmonary function responses to O 3 in otherwise normal, healthy human subjects [35][36][37]. Inter-individual variation in the inflammatory response to O 3 has also been described [38][39][40][41][42]. A second line of evidence is the demonstration that specific gene polymorphisms associate with response phenotypes in exposed human subjects.…”

Section: Candidate Genes For Susceptibility To Air Pollutantsmentioning

confidence: 98%

Genetic aspects of susceptibility to air pollution

Kleeberger¹

2003

European Respiratory Journal

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Section: Candidate Genes For Susceptibility To Air Pollutantsmentioning

confidence: 98%

Genetic aspects of susceptibility to air pollution

Kleeberger¹

2003

European Respiratory Journal

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“…O 3 significantly increases levels of inflammatory mediators, such as IL-6, IL-8, granulocyte-macrophage colonystimulating factor (GM-CSF) and fibronectin, in bronchoalveolar lavage fluid (BALF) [64,65]. Moreover, BASHA et al [66] and SCANNEL et al [67] found increased neutrophils, cytokine levels, and evidence of epithelial permeability in BALF 18 h after short-term O 3 exposure, in subjects with mild asthma versus healthy subjects. In addition to increased neutrophils, PEDEN et al [68] also found increased eosinophils in BALF 18 h after O 3 exposure.…”

Section: Ozonementioning

confidence: 99%

Outdoor air pollution, climatic changes and allergic bronchial asthma

D’Amato¹,

Liccardi²,

D’Amato³

et al. 2002

European Respiratory Journal

222

158

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Both the prevalence and severity of respiratory allergic diseases such as bronchial asthma have increased in recent years. Among the factors implicated in this "epidemic" are indoor and outdoor airborne pollutants. Urbanisation with its high levels of vehicle emissions and Westernised lifestyle parallels the increase in respiratory allergy in most industrialised countries, and people who live in urban areas tend to be more affected by the disease than those of rural areas. In atopic subjects, exposure to air pollution increases airway responsiveness to aeroallergens. Pollen is a good model with which to study the interrelationship between air pollution and respiratory allergic diseases. Biological aerosols carrying antigenic proteins, such as pollen grains or plantderived paucimicronic components, can produce allergic symptoms. By adhering to the surface of these airborne allergenic agents, air pollutants could modify their antigenic properties. Several factors influence this interaction, i.e., type of air pollutant, plant species, nutrient balance, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the airway mucosal damage and the impaired mucociliary clearance induced by air pollution may facilitate the penetration and the access of inhaled allergens to the cells of the immune system, and so promote airway sensitisation. As a consequence, an enhanced immunoglobulin E-mediated response to aeroallergens and enhanced airway inflammation favoured by air pollution could account for the increasing prevalence of allergic respiratory diseases in urban areas.

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“…Acute ozone exposure is known to decrease pulmonary function, increase airway responsiveness, and induce airway inflammation in dogs [2], guinea pigs [3], and humans [4, 5, 6]. Ozone imposes an oxidative burden on the lung in two ways: as a consequence of its oxidizing character during exposure and by engendering inflammation.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant Responsiveness in BALB/c Mice Exposed to Ozone

Jang

Choi²,

Yang³

et al. 2005

Respiration

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Background: A single, acute exposure to ozone has been shown to modify the antioxidant defense mechanism in the respiratory tract. Objective: The aim of this study was to evaluate the effects of ozone exposure on antioxidant response in BALB/c mice. Methods: We measured enhanced pause of breathing (Penh) as a marker of airway obstruction using barometric whole-body plethysmography before and after ozone exposure [groups (n = 6): filtered air, 0.12 ppm, 0.5 ppm, 1 ppm, 2 ppm] for 3 h. Antioxidant levels were measured using high-performance liquid chromatography with electrochemical detection in bronchoalveolar lavage (BAL) fluid and lung tissue homogenates. Results: Malondialdehyde concentrations in lung tissue homogenates were significantly increased in the group exposed to 2-ppm ozone compared to the filtered air group. Uric acid and γ-tocopherol concentrations in BAL fluid were significantly increased in the ozone exposure group compared to the filtered air group (p < 0.01). Uric acid concentrations were increased in a concentration-dependent manner according to ozone concentration to which the animals were exposed. Increases in Penh after ozone exposure were significantly higher in an ozone concentration-dependent manner. The proportion of neutrophils in BAL fluid was significantly higher in the group exposed to 2 ppm than in the filtered air and the group exposed to 0.12 ppm (p < 0.01, respectively). The level of ascorbate correlated with the level of γ-tocopherol. Conclusion: These findings suggest that antioxidant responses may serve as a protective mechanism against a range of oxidants in BALB/c mice exposed to ozone.

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Bronchoalveolar Lavage Neutrophilia in Asthmatic and Healthy Volunteers After Controlled Exposure to Ozone and Filtered Purified Air

Cited by 114 publications

References 21 publications

Genetic aspects of susceptibility to air pollution

Genetic aspects of susceptibility to air pollution

Outdoor air pollution, climatic changes and allergic bronchial asthma

Antioxidant Responsiveness in BALB/c Mice Exposed to Ozone

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