Association of Ambient Ozone Exposure with Airway Inflammation and Allergy in Adults with Asthma

Khatri, Sumita; Holguín, Fernando; Ryan, P. Barry; Mannino, David M.; Erzurum, Serpil C.; Teague, W. Gerald

doi:10.3109/02770900902779284

Cited by 39 publications

(13 citation statements)

References 45 publications

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“…Several studies have found stronger associations in individuals with asthma or COPD (6,9,13,35,36), although many have found associations between air pollution and lung function in normal subjects (5)(6)(7)(8). Only 20% of our study population met our definition of asthma/COPD, and thus our power to detect susceptibility in this subgroup was limited.…”

Section: Discussionmentioning

confidence: 70%

Short-Term Exposure to Air Pollution and Lung Function in the Framingham Heart Study

Rice

Ljungman²,

Wilker³

et al. 2013

Am J Respir Crit Care Med

172

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Rationale: Short-term exposure to ambient air pollution has been associated with lower lung function. Few studies have examined whether these associations are detectable at relatively low levels of pollution within current U.S. Environmental Protection Agency (EPA) standards. Objectives: To examine exposure to ambient air pollutants within EPA standards and lung function in a large cohort study. Methods: We included 3,262 participants of the Framingham Offspring and Third Generation cohorts living within 40 km of the Harvard Supersite monitor in Boston, Massachusetts (5,358 examinations, 1995Massachusetts (5,358 examinations, -2011) who were not current smokers, with previousday pollutant levels in compliance with EPA standards. We compared lung function (FEV 1 and FVC) after previous-day exposure to particulate matter less than 2.5 mm in diameter (PM 2.5 ), nitrogen dioxide (NO 2 ), and ozone (O 3 ) in the "moderate" range of the EPA Air Quality Index to exposure in the "good" range. We also examined linear relationships between moving averages of pollutant concentrations 1, 2, 3, 5, and 7 days before spirometry and lung function. Measurements and Main Results: Exposure to pollutant concentrations in the "moderate" range of the EPA Air Quality Index was associated with a 20.1-ml lower FEV 1 for PM 2.5 (95% confidence interval [CI], 233.4, 26.9), a 30.6-ml lower FEV 1 for NO 2 (95% CI, 260.9, 20.2), and a 55.7-ml lower FEV 1 for O 3 (95% CI, 2100.7, 210.8) compared with the "good" range. The 1-and 2-day moving averages of PM 2.5 , NO 2 , and O 3 before testing were negatively associated with FEV 1 and FVC.Conclusions: Short-term exposure to PM 2.5 , NO 2 , and O 3 within current EPA standards was associated with lower lung function in this cohort of adults.Keywords: chronic obstructive pulmonary disease; asthma; air pollutants; U.S. Environmental Protection Agency A substantial body of evidence has shown that modest shortterm increases in ambient air pollution, especially PM 2.5 (particles with an aerodynamic diameter < 2.5 mm) and ground level ozone (O 3 ), but also nitrogen dioxide (NO 2 ), increase risk of hospitalization for chronic obstructive pulmonary disease (COPD) and respiratory mortality (1-4). Several studies have found that short-term (1-3 d) increases in PM 2.5 , NO 2 , and O 3 are associated with decreases in FEV 1 , FVC, and/or peak expiratory flow rate in healthy subjects (5-11) and in those with preexisting COPD or asthma (12)(13)(14)(15).Air quality has improved substantially since the 1980s and 1990s, when many epidemiologic investigations of lung function and air pollution were completed (16). To protect public health and in accordance with its mandate, the EPA has continued to review the latest evidence and reevaluate air quality standards. Recently, the EPA lowered the annual standard for PM 2.5 from 15 to 12 mg/m 3 and reduced the daily Air Quality Index (AQI) cut-off for "moderate" PM 2.5 from 15.4 to 12 mg/m 3 . It remains unclear whether acute effects of criteria air pollutants (inclu...

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Section: Discussionmentioning

confidence: 70%

Short-Term Exposure to Air Pollution and Lung Function in the Framingham Heart Study

Rice

Ljungman²,

Wilker³

et al. 2013

Am J Respir Crit Care Med

172

View full text Add to dashboard Cite

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“…This result was similar to the results of a previous study. 15 On the other hand, Modig et al recently reported that the effect of NO 2 on FeNO was stronger than the effect of O 3 in subjects with asthma. 36 …”

Section: Discussionmentioning

confidence: 97%

“…14 In addition, elevated O 3 levels were reported to be associated with airway inflammation in atopic participants, both with and without asthma. 15 While some findings have shown the acute effects of O 3 on respiratory symptoms, the pathophysiological mechanisms for the effects of O 3 are not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Acute Effects of Summer Air Pollution on Pulmonary Function and Airway Inflammation in Healthy Young Women

Yoda

Otani

Sakurai

et al. 2014

Journal of Epidemiology

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BackgroundExposure to air pollution has been reported to be associated with asthma exacerbation. However, little is known about the effects of air pollutant exposure in healthy people. A panel study was conducted to evaluate the acute effects of air pollutants on pulmonary function and airway inflammation in healthy subjects.MethodsExhaled breath condensate (EBC) pH, fractional concentration of exhaled nitric oxide (FeNO), and pulmonary function were measured in 21 healthy young women repeatedly for two weeks in the summer in Tokyo, Japan. The concentrations of air pollutants were obtained from the monitoring stations in the neighborhoods where the subjects lived. Statistical analyses were performed using generalized estimating equations.ResultsEBC pH decreased significantly with a 10-ppb increase in the 4-day average ozone (O3) concentration and a 10-µg/m3 increase in the 4-day average suspended particulate matter (SPM) concentration (−0.07 [95% confidence interval {CI} −0.11 to −0.03] and −0.08 [95% CI −0.12 to −0.03], respectively). Subjects with a history of rhinitis showed marked decreases in EBC pH associated with increases in O3 and SPM. The changes in forced expiratory volume in 1 second (FEV1) were also significantly associated with a 10-µg/m3 increase in the 3-day average concentration of SPM (−0.09 L [95% CI −0.17 to −0.01]). FeNO increased significantly in relation to the increase in O3 and SPM among only subjects with a history of asthma.ConclusionsOver the course of the study, EBC became significantly acidic with increases in O3 and SPM concentrations. Furthermore, higher SPM concentrations were associated with decreased FEV1. Subjects with a history of rhinitis or asthma are considered to be more susceptible to air pollutants.

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“…33 Other investigators report that atopic individuals, even those without asthma, had enhanced inflammatory responses to inhaled O 3 compared to healthy subjects at O 3 levels within current NAAQS standards. 34,35 associations between clinical and subclinical manifestations of adverse pulmonary health effects and exposure to ambient air pollutants while providing some indication of potential mechanisms involved.…”

Section: Ambient Air Pollutionmentioning

confidence: 99%

Impact of air pollution on lung inflammation and the role of Toll-like receptors

Plummer¹,

Smiley‐Jewell²,

Pinkerton³

2012

IJICMR

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Abstract:The link between air pollution and adverse pulmonary health effects is well established. The National Ambient Air Quality Standards were formulated to protect human health. These standards are strictly enforced based on strong associations between elevated air pollution levels and increased emergency room visits and hospitalizations due to respiratory conditions. Impacts of air pollution on lung health occur due to the direct interaction between the external environment and internal biological systems and processes. The innate immune system is one of the first lines of defense against inhaled air contaminants and is characterized by activation of key signaling pathways and inflammatory cell recruitment to the lung. Numerous independent and often redundant pathways participate in innate and adaptive immune responses. Given the impact of air pollution on human health, extensive research efforts have aimed to characterize the mechanisms of response to various air pollutants and evaluate risk factors contributing to individual susceptibility. A significant body of evidence exists to document air pollution-induced alterations in proinflammatory or oxidative signaling molecules. However, the role of specific pathways participating in the propagation of the inflammatory effects remains unclear. One hypothesis for interindividual susceptibility to inhaled air pollutants is that genetic polymorphisms in inflammatory or oxidative stress pathways may contribute to the diverse range of the inflammatory response. Activation of numerous receptors associated with airway cells culminates in the translocation of nuclear factor-kappa B and other transcription factors to the nucleus, and therefore initiation of altered signaling of proinflammatory mediators. Alterations in the transcription and expression of inflammatory mediators following exposure to air pollution are well documented. However, the interaction between specific air pollutants and specific cell surface and intracellular receptors has not been clearly defined. Involvement of specific pathways in the innate immune response may be dependent on differential physical and chemical characteristics of air pollution. One pathway implicated in the response to inhaled air pollutants is initiated by the activation of Toll-like receptors (TLRs). TLRs and downstream proinflammatory mediators are well studied for their role in pathogen response, yet gaps in the understanding of TLR response to nonpathogenic agents, such as air pollution, exist. TLRs are associated with inflammation and allergy, and emerging evidence suggests they may also play a role in the response and susceptibility to air pollution. However, the specific component, exogenous or endogenous, responsible for the association between air pollution and TLR activation has yet to be clearly identified. Improved understanding of pulmonary response mechanisms and potential mediators of susceptibility to air pollution, including the role of TLRs, may contribute to a reduction of the health burden of air pollutio...

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Association of Ambient Ozone Exposure with Airway Inflammation and Allergy in Adults with Asthma

Cited by 39 publications

References 45 publications

Short-Term Exposure to Air Pollution and Lung Function in the Framingham Heart Study

Short-Term Exposure to Air Pollution and Lung Function in the Framingham Heart Study

Acute Effects of Summer Air Pollution on Pulmonary Function and Airway Inflammation in Healthy Young Women

Impact of air pollution on lung inflammation and the role of Toll-like receptors

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