Nociceptive mechanisms modulate ozone-induced  human lung function decrements

Passannante, Anthony N.; Hazucha, Milan J.; Bromberg, Philip A.; Seal, Elston; Folinsbee, Larry; Koch, Gary G.

doi:10.1152/jappl.1998.85.5.1863

Cited by 46 publications

(36 citation statements)

References 21 publications

(21 reference statements)

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“…46,47 A third mechanism is modulation of the autonomic nervous system via nerve endings in the lung, which then affects cardiac and vascular function. Ozone-induced lung-function changes are also known to be mediated by C nerve fibers in the lung of humans 48 via the selective stimulation of transient receptor potential cation channel, subfamily A, member 1 ion channels, 49 and it is likely that the autonomic nervous system HRV and repolarization changes reported here are also mediated via nerve fibers that terminate in the lung. Recent rodent studies show a significant role for autonomic mediation of HRV and arrhythmia after exposure to ozone.…”

Section: Devlin Et Al Ozone Induces Cardiovascular Changes 109mentioning

confidence: 72%

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

et al. 2012

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Background— Recent epidemiology studies have reported associations between short-term ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution and mortality, and support for a causal relationship has come from controlled-exposure studies that describe pathophysiological mechanisms by which particulate matter could induce acute mortality. In contrast, for ozone, almost no controlled-human-exposure studies have tested whether ozone exposure can modulate the cardiovascular system. Methods and Results— Twenty-three young healthy individuals were exposed in a randomized crossover fashion to clean air and to 0.3-ppm ozone for 2 hours while intermittently exercising. Blood was obtained immediately before exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately before exposure and continued for 24 hours. Lung function was performed immediately before and immediately after exposure, and bronchoalveolar lavage was performed 24 hours after exposure. Immediately after ozone exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator inhibitor-1, a 51.3% decrease in the high-frequency component of heart rate variability, and a 1.2% increase in QT duration. Changes in interleukin-1B and plasminogen activator inhibitor-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation. Conclusions— This controlled-human-exposure study shows that ozone can cause an increase in vascular markers of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control of heart rate and repolarization. We believe that these findings provide biological plausibility for the epidemiology studies that associate ozone exposure with mortality. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01492517.

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Section: Devlin Et Al Ozone Induces Cardiovascular Changes 109mentioning

confidence: 72%

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

et al. 2012

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“…Ozone-induced decrements in lung function are thought to be mediated via interaction of the pollutant with C-fibers innervating the lung in humans and dogs (Bromberg and Koren 1995;Coleridge et al 1993;Passannante et al 1998). Administration of β-adrenergic receptor and muscarinic receptor antagonists effectively blocked PM-induced cardiac oxidative stress in rats (Rhoden et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Exposure to Concentrated Coarse Air Pollution Particles Causes Mild Cardiopulmonary Effects in Healthy Young Adults

Graff¹,

Cascio²,

Rappold³

et al. 2009

Environ Health Perspect

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“…In the present study, O 3 -induced changes in sGaw during cumulative MCh aerosol challenge did not correlate with delayed recovery in the FEV 1 or FEF . It has been suggested that changes in lung function during and immediately postexposure to O 3 are related to irritant and neural mechanisms (19,27), whereas the delayed changes in the FEV 1 and FEF 25-75 1 day postexposure may represent epithelial injury, receptor dysfunction, and inflammation at distal airway sites (14,25).…”

Section: Discussionmentioning

confidence: 99%

Bronchial reactivity of healthy subjects: 18–20 h postexposure to ozone

Foster

Brown

Macri

et al. 2000

Journal of Applied Physiology

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Exposure of humans to ambient levels of ozone (O3) causes inflammatory changes within lung tissues. These changes have been reported for the “initial” (1- to 3-h) and “late” (18- to 20-h) postexposure periods. We hypothesized that at the late period, when protein and cellular markers of inflammation at the airway surface remain abnormal and the integrity of the epithelial barrier is compromised, bronchial reactivity would be increased. To test this, we measured airway responsiveness to cumulative doses of methacholine (MCh) aerosol in healthy subjects 19 ± 1 h after a single exposure to O3 (130 min at ambient levels between 120 and 240 parts/billion and alternate periods of rest and moderate exercise) or filtered air. Exposures were conducted at two temperatures: mild (22°C) and moderate (30°C). At the late period, bronchial reactivity to MCh increased, i.e., interpolated dose of MCh leading to a 50% fall in specific airway conductance (PC50) was less after O3 than after filtered air. PC50 for O3 at 22°C was 27 mg/ml (20% less than the PC50 after filtered air), and for O3 at 30°C it was 19 mg/ml (70% less than the PC50 after filtered air). The forced expiratory volume in 1 s (FEV1) at the late time point after O3 was slightly but significantly reduced (2.3%) from the preexposure level. There was no relationship found between the functional changes observed early after exposure to O3 and subsequent changes in bronchial reactivity or FEV1 at the late time point. These results suggest that bronchial reactivity is significantly altered ∼1 day after O3; this injury may contribute to the respiratory morbidity that is observed 1–2 days after an episode of ambient air pollution.

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Nociceptive mechanisms modulate ozone-induced human lung function decrements

Cited by 46 publications

References 21 publications

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

Exposure to Concentrated Coarse Air Pollution Particles Causes Mild Cardiopulmonary Effects in Healthy Young Adults

Bronchial reactivity of healthy subjects: 18–20 h postexposure to ozone

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