Air pollutants and respiratory hypersensitivity

Devalia, Jagdish L.; Rusznák, C.; Wang, Jiahua; Khair, Omer; Abdelaziz, Muntasir M.; Calderón, Moisés A.; Davies, Robert J.

doi:10.1016/0378-4274(96)03687-9

Cited by 41 publications

(15 citation statements)

References 38 publications

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“…In their unique location at the interface between the air space and the submucosal regions, the epithelial cells of the upper and lower respiratory tract serve as common targets for airborne pollutants and several viral pathogens, including the rhinoviruses (7)(8)(9). A pathophysiologic consequence shared by rhinovirus infection and exposure to oxidant pollutants is an inflammatory response involving the influx of neutrophils and other cells into the airway tissues and air spaces.…”

Section: Synergism Between Rhinovirus Infection and Oxidant Pollutantmentioning

confidence: 99%

Synergism between rhinovirus infection and oxidant pollutant exposure enhances airway epithelial cell cytokine production.

Spannhake

Reddy

Jacoby

et al. 2002

Environ Health Perspect

103

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Of the several factors believed to exacerbate asthmatic symptoms, air pollution and viral infections are considered to be particularly important. Although evidence indicates that each of these respiratory insults individually can increase asthma severity in susceptible individuals, we know little about the extent to which exposure to environmental oxidant pollutants can influence the course of respiratory viral infection and its associated inflammation. To investigate the interaction of these two stimuli within their common epithelial cell targets in the upper and lower respiratory tracks, we infected primary human nasal epithelial cells and cells of the BEAS-2B line grown at the air-liquid interface with human rhinovirus type 16 (RV16) and exposed them to NO2 (2.0 ppm) or O3 (0.2 ppm) for 3 hr. Independently, RV16, NO2, and O3 rapidly increased release of the inflammatory cytokine interleukin-8 through oxidant-dependent mechanisms. The combined effect of RV16 and oxidant ranged from 42% to 250% greater than additive for NO2 and from 41% to 67% for O3. We abrogated these effects by treating the cells with the antioxidant N-acetylcysteine. Surface expression of intercellular adhesion molecule 1 (ICAM-1) underwent additive enhancement in response to combined stimulation. These data indicate that oxidant pollutants can amplify the generation of proinflammatory cytokines by RV16-infected cells and suggest that virus-induced inflammation in upper and lower airways may be exacerbated by concurrent exposure to ambient levels of oxidants commonly encountered the indoor and outdoor environments.

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Section: Synergism Between Rhinovirus Infection and Oxidant Pollutantmentioning

confidence: 99%

Synergism between rhinovirus infection and oxidant pollutant exposure enhances airway epithelial cell cytokine production.

Spannhake

Reddy

Jacoby

et al. 2002

Environ Health Perspect

103

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“…Intratracheal instillation of DEP with OVA enhanced airway responsiveness, infiltration of eosinophils, and hyperplasia of goblet cells in mice [5]. NO 2 exposure alone or combined exposure of NO 2 and SO 2 enhanced airway response to inhaled allergens in asthmatics [11, 12]. It is impossible to divide the effects of DEP and gaseous components in this study.…”

Section: Discussionmentioning

confidence: 99%

Diesel Exhaust Inhalation Enhances Airway Hyperresponsiveness in Mice

Miyabara

Ichinose

Takano

et al. 1998

Int Arch Allergy Immunol

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Background: Repeated intratracheal instillation of diesel exhaust particles and ovalbumin-induced airway hyperresponsiveness and airway inflammation in mice. However, the effects of daily inhalation of diesel exhaust may differ from the effects of direct instillation. Methods: Therefore, mice were exposed to diesel exhaust by inhalation 12 h per day for 3 months. Before the diesel exhaust exposure, ovalbumin was injected intraperitoneally as a sensitization. After 3 weeks of diesel exhaust exposure, these mice were challenged with ovalbumin every 3 week thereafter. Results: Diesel exhaust exposure with antigen challenge induced airway hyperresponsiveness and airway inflammation which was characterized by increased numbers of eosinophils and mast cells in lung tissue. The recruitment of inflammatory cells was accompanied by an increment in goblet cells on bronchial epithelium. Diesel exhaust exposure alone also enhanced airway hyperresponsiveness, but did not induce eosinophilic infiltration and/or an increment in goblet cells. Conclusion: Diesel exhaust inhalation enhanced airway hyperresponsiveness and airway inflammation caused by ovalbumin sensitization in mice.

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“…SO 2 has been shown to have a synergistic effect with the allergic reaction and other pollutants, e.g. SO 2 (200 ppb) and NO 2 (400 ppb) in combination have been shown to decrease the allergen dose (house dust mite) required to produce a 20% drop in FEV1 by 60% (Devalia et al, 1996). However, high SO 2 concentrations have also been shown to reduce the allergen release from pollen (Behrendt et al, 1997;Santra et al, 1991).…”

Section: Co-exposure To Pollen and Other Pollutantsmentioning

confidence: 99%