Ozone and Pulmonary Innate Immunity

Hollingsworth, John W.; Kleeberger, Steven R.; Foster, W. Michael

doi:10.1513/pats.200701-023aw

Cited by 111 publications

(90 citation statements)

References 94 publications

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“…We also observed associations with several trafficrelated primary pollutants during the warm season. These pollutants have been found to cause asthma exacerbations and airway inflammation in observational and experimental studies (32)(33)(34)(35)(36); as supported by both the quintile analysis and the smooth estimates of dose-response, we observed evidence that associations were present at relatively low ambient concentrations.…”

Section: Discussionsupporting

confidence: 76%

Short-term Associations between Ambient Air Pollutants and Pediatric Asthma Emergency Department Visits

Strickland¹,

Darrow²,

Klein³

et al. 2010

Am J Respir Crit Care Med

319

231

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Rationale: Certain outdoor air pollutants cause asthma exacerbations in children. To advance understanding of these relationships, further characterization of the dose-response and pollutant lag effects are needed, as are investigations of pollutant species beyond the commonly measured criteria pollutants. Objectives: Investigate short-term associations between ambient air pollutant concentrations and emergency department visits for pediatric asthma. Methods: Daily counts of emergency department visits for asthma or wheeze among children aged 5 to 17 years were collected from 41 Metropolitan Atlanta hospitals during 1993-2004 (n 5 91,386 visits). Ambient concentrations of gaseous pollutants and speciated particulate matter were available from stationary monitors during this time period. Rate ratios for the warm season (May to October) and cold season (November to April) were estimated using Poisson generalized linear models in the framework of a case-crossover analysis. Measurements and Main Results: Both ozone and primary pollutants from traffic sources were associated with emergency department visits for asthma or wheeze; evidence for independent effects of ozone and primary pollutants from traffic sources were observed in multipollutant models. These associations tended to be of the highest magnitude for concentrations on the day of the emergency department visit and were present at relatively low ambient concentrations. Conclusions: Even at relatively low ambient concentrations, ozone and primary pollutants from traffic sources independently contributed to the burden of emergency department visits for pediatric asthma.Keywords: ambient particulate matter; asthma; minors; ozone A broad literature supports associations between ambient air pollutant concentrations and asthma exacerbations (1-3). Children are thought to be particularly susceptible to ambient air pollutants, because their lungs and immune systems are not fully developed, they breathe more air per unit body weight and are typically more active than adults, and their peripheral airways are anatomically smaller than adults so that inflammation results in proportionally greater airway obstruction (4-6). To help advance understanding of the relationships between ambient air pollutant concentrations and asthma exacerbations in children, further characterization of the dose-response and pollutant lag effects are needed, as are investigations of pollutant species beyond the commonly measured urban air pollutants (3, 7). Further investigation of pollutant mixtures and effect modification may also provide insights (8, 9); for example, there have been reports of stronger pollution effects during the warm season (10-15) even though pediatric asthma rates peak during the cold season (16). To lessen concerns about uncontrolled confounding, aggressive control for variables, such as meteorology and seasonal asthma trends, is required.In the present study, we analyzed data from the Study of Particles and Health in Atlanta (SOPHIA) (14,(17)(18)(19)(20)(21), one of...

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Section: Discussionsupporting

confidence: 76%

Short-term Associations between Ambient Air Pollutants and Pediatric Asthma Emergency Department Visits

Strickland¹,

Darrow²,

Klein³

et al. 2010

Am J Respir Crit Care Med

319

231

View full text Add to dashboard Cite

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“…In the lung, TNFα is thought to contribute to a variety of inflammatory conditions including acute respiratory distress syndrome, idiopathic pneumonia, chronic obstructive pulmonary disease and asthma (reviewed in Mukhopadhyay et al, 2006) Ozone is a highly reactive oxidant present in photochemical smog. Inhalation of toxic levels of ozone leads to airway inflammation and damage to the alveolar epithelium in the lower lung (Laskin et al, 2003;Uysal and Schapira, 2003;Hollingsworth et al, 2007). A number of studies have suggested that at least one mechanism underlying the toxicity of ozone involves excessive production of cytotoxic mediators including reactive oxygen and nitrogen intermediates by activated lung macrophages (reviewed in (Laskin et al, 2003)).…”

Section: Introductionmentioning

confidence: 99%

Regulation of caveolin-1 expression, nitric oxide production and tissue injury by tumor necrosis factor-α following ozone inhalation

Fakhrzadeh

Laskin²,

Laskin

2008

Toxicology and Applied Pharmacology

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Alveolar macrophages (AM) and inflammatory mediators including nitric oxide and peroxynitrite contribute to ozone-induced lung injury. The generation of these mediators is regulated, in part, by the transcription factor NF-κB. We previously demonstrated a critical role for NF-κB p50 in the ozone-induced injury. In the present studies mechanisms regulating NF-κB activation in the lung after ozone inhalation were analyzed. Treatment of wild type (WT) mice with ozone (0.8 ppm, 3 h) resulted in a rapid increase in NF-κB binding activity in AM, which persisted for at least 12 h. This was not evident in mice lacking TNFα which are protected from ozone-induced injury; there was also no evidence of nitric oxide or peroxynitrite production in lungs from these animals. These data demonstrate that TNFα plays a role in NF-κB activation and toxicity. TNFα signaling involves PI-3-kinase (PI3K)/protein kinase B (PKB), and p44/42 MAP kinase (MAPK) which are important in NF-κB activation. Ozone Inhalation resulted in rapid and transient increases in p44/42 MAPK and PI3K/PKB in AM from WT mice, which was evident immediately after exposure. Caveolin-1, a transmembrane protein that negatively regulates PI3K/PKB and p44/42 MAPK signaling, was downregulated in AM from WT mice after ozone exposure. In contrast, ozone had no effect on caveolin-1, PI3K/PKB or p44/42 MAPK expression in AM from TNFα knockout mice. These data, together with our findings that TNFα suppressed caveolin-1 in cultured AM, suggest that TNFα and downstream signaling mediate activation of NF-κB and the regulation of inflammatory genes important in ozone toxicity, and that this process is linked to caveolin-1.

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“…It has been shown that O 3 can induce inflammation in airways by affecting the innate immune signaling, impairment of antibacterial host defense and disruption of epithelial barrier [29,30]. Experimental studies results show that, epithelial cells produce increased amounts of IL-6, IL-8, or fibronectin following ozone exposure and both IL-6 and fibronectin are secreted vectorially [31].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Relation Between Air Pollution and Hepatic Encephalopathy Exacerbation

Alavinejad¹,

Mard²,

Esk³

et al. 2016

GHOA

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In this retrospective cross sectional survey, by evaluating the records of Ahvaz aerology stations and air pollution committee of Ahvaz Jundishapur University, the DATA about 4 major air AbstractBackground: To evaluate relation between air pollution and rate and duration of hospital admission due to hepatic encephalopathy as a major complication of liver cirrhosis. Methods:In this retrospective study, during a 10 months period, the number and average duration of hospitalization of patients admitted in GI ward of a referral center due to hepatic encephalopathy were recorded in an industrial capital city. Concomitantly the level of 4 major air pollutants including SO 2 , CO, NO 2 and O 3 measured and the correlation between severity of hepatic encephalopathy and air pollution determined by Pearson correlation coefficient.Results: Average number of admission was 5 to 6 patients per month (1-10). The average duration of hospitalization was 7.6 days (3-19). After comparison of average concentration of 4 major air pollutants with rate of hepatic encephalopathy, there was a relation, between O3 concentration and duration of admissions (P=0.048, correlation coefficient 0.636) and also a non-significant relation between O3 concentration and number of admissions (P=0.78, correlation coefficient 0.58). DATA analysis did not reveal any significant relation between SO 2 , NO 2 and CO and the rate and duration of admission due to hepatic encephalopathy (P > 0.05). Conclusion:It seems that O 3 as one of the major air pollutants can aggravates course of hepatic encephalopathy. This issue should further be clarified in future studies.

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Ozone and Pulmonary Innate Immunity

Cited by 111 publications

References 94 publications

Short-term Associations between Ambient Air Pollutants and Pediatric Asthma Emergency Department Visits

Short-term Associations between Ambient Air Pollutants and Pediatric Asthma Emergency Department Visits

Regulation of caveolin-1 expression, nitric oxide production and tissue injury by tumor necrosis factor-α following ozone inhalation

Evaluation of Relation Between Air Pollution and Hepatic Encephalopathy Exacerbation

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