Lung Function and Inflammatory Responses in Healthy Young Adults Exposed to 0.06 ppm Ozone for 6.6 Hours

Abstract

Rationale: Exposure to ozone causes a decrease in spirometric lung function and an increase in airway inflammation in healthy young adults at concentrations as low as 0.08 ppm, close to the National Ambient Air Quality Standard for ground level ozone. Objectives: To test whether airway effects occur below the current ozone standard and if they are more pronounced in potentially susceptible individuals, such as those deficient in the antioxidant gene glutathione S-transferase mu 1 (GSTM1). Methods: Pulmonary function and subjective symptoms were measured in 59 healthy young adults (19-35 yr) immediately before and after exposure to 0.0 (clean air, CA) and 0.06 ppm ozone for 6.6 hours in a chamber while undergoing intermittent moderate exercise. The polymorphonuclear neutrophil (PMN) influx was measured in 24 subjects 16 to 18 hours postexposure. Measurements and Main Results: Subjects experienced a significantly greater (P 5 0.008) change in FEV 1 (6 SE) immediately after exposure to 0.06 ppm ozone compared with CA (21.71 6 0.50% vs. 20.002 6 0.46%). The decrement in FVC was also greater (P 5 0.02) after ozone versus CA (22.32 6 0.41% vs. 21.13 6 0.34%). Similarly, changes in %PMN were greater after ozone (54.0 6 4.6%) than CA (38.3 6 3.7%) exposure (P , 0.001). Symptom scores were not different between ozone versus CA. There were no significant differences in changes in FEV 1 , FVC, and %PMN between subjects with GSTM1-positive and GSTM1-null genotypes. Conclusions: Exposure of healthy young adults to 0.06 ppm ozone for 6.6 hours causes a significant decrement of FEV 1 and an increase in neutrophilic inflammation in the airways. GSTM1 genotype alone appears to have no significant role in modifying the effects.

Tropospheric ozone and its precursors from the urban to the global scale from air quality to short-lived climate forcer

“…Studies since the 2005 global update have shown that healthy exercising human subjects showed impaired lung function at concentrations of 60 ppb for 6.6 h, relative to clean air controls (Kim et al, 2011). The report noted that the subjects were healthy adults and thus not representative of the general population, or of real-world combinations of susceptibility and exposure.…”

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

“…Schelegle et al (2009) exposed healthy young adults to varying concentrations of ozone (60, 70, 80 and 87 ppb) for 6.6 hours, with continuous exercise (V E = 40 litres per minute), and reported significant decrements at 70 ppb, but not 60 ppb. Recent studies have tended to support evidence of small, but measureable, decrements at 60 ppb (Brown, Bateson & McDonnell, 2008;Kim et al, 2011). More detailed modelling studies have provided evidence of thresholds for these transient lung function responses.…”

“…These data tended to suggest that the threshold of ozone-induced inflammation was somewhat higher than that for lung function changes. With respect to this question, Kim et al (2011) exposed 59 healthy, exercising young adults to 0.06 ppm ozone for 6.6 hours under controlled chamber conditions and reported a significant and acute decrease in FEV1 and increased neutrophilic inflammation of the airways, sampled using induced sputum. Of note, this paper found no influence of possession of the GSTM1 null genotype on the responses observed.…”

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

“…32 Healthy human subjects exposed to 0.6-ppm O 3 , a level below the current 0.8-ppm standard, had significant O 3 -induced decreases in lung function and increased neutrophilic inflammation in the airways compared to subjects exposed to clean air. 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.…”

“…64 Due to the central role of inflammation and oxidative stress in the response to air pollution, genes that modulate inflammation and antioxidant defense mechanisms are considered to contribute to interindividual variability in response to air pollution. 33 Genetically standardized animal models have been used to identify candidate genes that may convey an increased susceptibility to air pollution-induced health impacts on chromosomes 4, 11, and 17. These studies report correlations between several hallmarks of respiratory health effects, including lung hyperpermeability, injury and inflammation, and genetic differences within these chromosomes.…”