The Respiratory Responses of Subjects With Allergic Rhinitis To Ozone Exposure and Their Relationship To Nonspecific Airway Reactivity

McDonnell, William F.; Horstman, Donald H.; Abdul-Salaam, Sa'id; Raggio, L. J.; Green, James

doi:10.1177/074823378700300405

Cited by 40 publications

(16 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A similar study by McDonnell et al at the EPA involving 26 nonasthmatic subjects with allergic rhinitis exposed to 0.18 ppm ozone or filtered air also failed to demonstrate a markedly different response to ozone as compared to previously tested nonatopic subjects (28 (37). In the United Kingdom, asthma mortality rates have risen more rapidly than in the United States (38).…”

Section: Controlled Human Exposure Studiesmentioning

confidence: 79%

The role of ozone exposure in the epidemiology of asthma.

Balmes

1993

Environ Health Perspect

View full text Add to dashboard Cite

Asthma is a clinical condition characterized by intermittent respiratory symptoms, nonspecific airway hyperresponsiveness, and reversible airway obstruction. Although the pathogenesis of asthma is incompletely understood, it is clear that airway inflammation is a paramount feature of the condition. Because inhalation of ozone by normal, healthy subjects causes increased airway responsiveness and inflammation, it is somewhat surprising that most controlled human exposure studies that have involved asthmatic subjects have not shown them to be especially sensitive to ozone. The acute decrement in lung function that is the end point traditionally used to define sensitivity to ozone in these studies may be due more to neuromuscular mechanisms limiting deep inspiration than to bronchoconstriction. The frequency of asthma attacks following ozone exposures may be a more relevant end point. Epidemiologic studies, rather than controlled human exposure studies, are required to determine whether ozone pollution increases the risk of asthma exacerbations. Asthma affects approximately 10 million people in the United States and, thus, the answer to this question is of considerable public health importance. Both the prevalence and severity of asthma appear to be increasing in many countries. Although increased asthma morbidity and mortality are probably of multifactorial etiology, a contributory role of urban air pollution is plausible. The epidemiologic database to support an association between asthma and ozone exposure is limited, but the results of several studies suggest such an association. Some potential approaches to further investigation of the relationship between asthma and ozone, including those that would link controlled human exposures to population-based studies, are considered. -Environ Health Perspect 101 (Suppl 4): 219-224 (1993).

show abstract

Section: Controlled Human Exposure Studiesmentioning

confidence: 79%

The role of ozone exposure in the epidemiology of asthma.

Balmes

1993

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…Since inhalation of O 3 by healthy subjects increases airway responsiveness and airway inflammation, asthmatic subjects were expected to be more sensitive to the acute effects of O 3 [56]. Neurologically mediated inhibition of inspiratory effort involving C-fibres rather than bronchoconstriction has been proposed as the primary mechanism for O 3 -induced decrements in forced expiratory volume in one second (FEV1) [47,57,58].…”

Section: Ozonementioning

confidence: 99%

Outdoor air pollution, climatic changes and allergic bronchial asthma

D’Amato¹,

Liccardi²,

D’Amato³

et al. 2002

Eur Respir J

223

158

View full text Add to dashboard Cite

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.

show abstract

“…With the exception of two studies, McDonnell et al (1987) and Adams (2003a), there is limited recovery response data following exposure reducing the ability to estimate K el . McDonnell et al (1987) studied 26 healthy asymptomatic male subjects with allergic rhinitis aged 18-35 years, who inhaled 180 ppb O 3 for 2.75 h while performing heavy intermittent exercise (EVR = 35 L/min/BSA) followed by a 2.75 h recovery period during which FEV 1 was evaluated three times. The mean estimated K el for this study was 0.0400 ± 0.0346 min −1 compared to a mean value of 0.0289 ± 0.055 s −1 for all the studies from which K el was estimated.…”

Section: Discussionmentioning

confidence: 95%