Increased specific airway reactivity of persons with mild allergic asthma after 7.6 hours of exposure to 0.16 ppm ozone☆☆☆★

Kehrl, Howard; Peden, David B.; Ball, Beth A.; Folinsbee, Larry; Horstman, Donald H.

doi:10.1016/s0091-6749(99)70013-8

Cited by 97 publications

(68 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To that well-established practice, we would add the caveat that it could be informative to observe both beneficial as well as detrimental effects. Second, in both our studies (15,16) as well as in those of others (4,6,7,13), large intersubject variability has been noted. Efforts to examine reasons for such variability using molecular and genetic approaches, including the use of genetically altered animals, could prove to be most informative.…”

Section: Discussionsupporting

confidence: 63%

See 1 more Smart Citation

Interactions of allergens and irritants in susceptible populations in producing lung dysfunction: implications for future research.

Hastie

Peters

2001

Environ Health Perspect

View full text Add to dashboard Cite

Environmental agents, when applied in combination or sequentially, can induce a wide variety of adverse health effects in humans. To determine the effects of sequential allergen challenge and acid exposure on human bronchial epithelial cell function, we subjected normal, nonallergic control and ragweed-allergic individuals to bronchoscopic segmental ragweed challenge in vivo. We harvested bronchial epithelial cells by brush biopsy both before challenge and 24 hr after challenge and exposed cells to an acid stress in vitro (pH 5 for 3 hr), followed by a 1-hr recovery period at normal pH. In normal, nonallergic subjects, segmental allergen challenge produced no effects on ciliary activity; pH 5 exposure produced reduced ciliary activity (a decrease in the percent of the initially active area), with significant recovery after cells were returned to a normal pH. Ciliary activity from allergic subjects was also inhibited by pH 5 exposure; however, activity was not recovered when cells were placed in medium of normal pH. Ciliary activity in allergics who developed a stress response postantigen challenge, as determined by an induction of the 27 kDa stress (heat shock) protein, displayed no ciliary dysfunction when exposed to a pH 5 stress. In this case, a stress sufficient to provoke a heat shock (stress) protein (HSP) response (but not one that produced more severe lung injury and did not provoke an HSP response) protected cells from a subsequent acid stress. Because of our observations and recent findings reported in the literature, we suggest that in order to define the wide variety of health effects of environmental agents, control as well as at-risk populations should be studied and the ability to define potentially beneficial as well as detrimental effects should be built into the experimental design. Inclusion of different and novel end points also should be considered.

show abstract

Section: Discussionsupporting

confidence: 63%

“…Similarly, acid aerosols have been reported to produce pulmonary dysfunction (8,9). The effects of such exposures might be expected to be magnified when the exposed individual either has a degree of preexisting lung dysfunction such as asthma, and/or when multiple different exposures are performed (10)(11)(12)(13).…”

mentioning

confidence: 99%

Interactions of allergens and irritants in susceptible populations in producing lung dysfunction: implications for future research.

Hastie

Peters

2001

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…It is known that inhalation of ambient ozone can modify adaptive immune function (reviewed in Ref. 5) in both rodents (6 -9) and humans (10,11). However, COPD is characterized by increased numbers of macrophages, neutrophils, and cytotoxic CD8 lymphocytes, suggesting a role of innate immune function in pathogenesis of this disease.…”

mentioning

confidence: 99%

Ambient Ozone Primes Pulmonary Innate Immunity in Mice

Hollingsworth

Maruoka

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

Exposure to ozone in air pollution in urban environments is associated with increases in pulmonary-related hospitalizations and mortality. Because ozone also alters clearance of pulmonary bacterial pathogens, we hypothesized that inhalation of ozone modifies innate immunity in the lung. To address our hypothesis, we exposed C57BL/6J mice to either free air or ozone, and then subsequently challenged with an aerosol of Escherichia coli LPS. Pre-exposure to ozone resulted in enhanced airway hyperreactivity, higher concentrations of both total protein and proinflammatory cytokines in lung lavage fluid, enhanced LPS-mediated signaling in lung tissue, and higher concentrations of serum IL-6 following inhalation of LPS. However, pre-exposure to ozone dramatically reduced inflammatory cell accumulation to the lower airways in response to inhaled LPS. The reduced concentration of cells in the lower airways was associated with enhanced apoptosis of both lung macrophages and systemic circulating monocytes. Moreover, both flow cytometry and confocal microscopy indicate that inhaled ozone causes altered distribution of TLR4 on alveolar macrophages and enhanced functional response to endotoxin by macrophages. These observations indicate that ozone exposure increases both the pulmonary and the systemic biologic response to inhaled LPS by priming the innate immune system.

show abstract

“…Increases in ambient ozone concentration are associated with hospital admissions and reported symptoms from individuals with asthma and allergic rhinitis [1][2][3]. In challenge studies of asthmatic subjects, our research group has shown ozone induces eosinophilic infiltration in both upper and lower airways, decrements in pulmonary function, and enhances response to allergen [4][5][6]. Even in the absence of provocation with an allergen, atopic asthmatics appear to mount greater airway inflammatory responses after ozone exposure than healthy subjects [7,8].…”

Section: Introductionmentioning

confidence: 99%

Ozone enhancement of lower airway allergic inflammation is prevented by γ-tocopherol

Wagner

Jiang

Harkema

et al. 2007

Free Radical Biology and Medicine

Self Cite

View full text Add to dashboard Cite

Ozone is a commonly encountered environmental oxidant which has been linked to asthma exacerbation in epidemiological studies. Ozone induces airway inflammation and enhances response to inhaled allergen. It has been suggested that antioxidant therapy may minimize the adverse effects of ozone in asthma. We have previously shown that the antioxidant gammatocopherol (γT), an isoform of vitamin E, also has anti-inflammatory effects. We employed a Brown Norway rat model of ozone-enhanced allergic responses to test the therapeutic effects of γT on O 3 -induced airway inflammation. Ovalbumin (OVA) -sensitized rats were intranasally challenged with 0 or 0.5% OVA on Days 1 and 2, and exposed to 0 or 1 ppm ozone (8h/day) on Days 4 and 5. Rats were also given 0 or 100 mg/kg γT on Days 2 through 5. Pulmonary tissue and bronchoalveolar lavage fluid (BALF) were collected on Day 6. OVA challenge caused increased total cells (267% increase) and eosinophils (4000%) in BALF that was unaffected by ozone exposure. Morphometric evaluation of lung tissue revealed increases in intraepithelial mucosubstances (IM) (300%) and subepithelial eosinophils (400%) in main axial airways. Ozone exposure of allergic rats enhanced IM increases in proximal axial airways (200%), induced cysleukotrienes, MCP-1 and IL-6 production in BALF, and upregulated expression of IL-5 and IL-13 mRNA. γT treatment had no effect on IM increases by allergen, but blocked enhancement by ozone. γT attenuated both OVA-or ozone -stimulated eosinophilic infiltration, and increases of BALF cys-leukotrienes, MCP-1 and IL-6, as well as IL-5 and IL-13 mRNA. These data Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript demonstrate broad anti-inflammatory effects of a γT and suggest it may be an effective therapy of allergic airway inflammation.

show abstract

Increased specific airway reactivity of persons with mild allergic asthma after 7.6 hours of exposure to 0.16 ppm ozone☆☆☆★

Cited by 97 publications

References 24 publications

Interactions of allergens and irritants in susceptible populations in producing lung dysfunction: implications for future research.

Interactions of allergens and irritants in susceptible populations in producing lung dysfunction: implications for future research.

Ambient Ozone Primes Pulmonary Innate Immunity in Mice

Ozone enhancement of lower airway allergic inflammation is prevented by γ-tocopherol

Contact Info

Product

Resources

About