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Interaction effects of temperature and ozone on lung function and markers of systemic inflammation, coagulation, and fibrinolysis: a crossover study of healthy young volunteers.

Kahle JJ, Neas LM, Devlin RB, Case MW, Schmitt MT, Madden MC, Diaz-Sanchez D - Environ. Health Perspect. (2014)

Bottom Line: Ozone exposure at 22°C resulted in a decrease in markers of fibrinolysis the next day.These significantly differed from the response at 32.5°C, where there was a 44.9% (p = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.042) decrease in D-dimer.Ozone-induced systemic but not respiratory effects varied according to temperature.

View Article: PubMed Central - PubMed

Affiliation: Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.

ABSTRACT

Background: Trends in climate suggest that extreme weather events such as heat waves will become more common. High levels of the gaseous pollutant ozone are associated with elevated temperatures. Ozone has been associated with respiratory diseases as well as cardiovascular morbidity and mortality and can reduce lung function and alter systemic markers of fibrinolysis. The interaction between ozone and temperature is unclear.

Methods: Sixteen healthy volunteers were exposed in a randomized crossover study to 0.3 ppm ozone and clean air for 2 hr at moderate (22°C) temperature and again at an elevated temperature (32.5°C). In each case lung function was performed and blood taken before and immediately after exposure and the next morning.

Results: Ozone exposure at 22°C resulted in a decrease in markers of fibrinolysis the next day. There was a 51.8% net decrease in PAI-1 (plasminogen activator inhibitor-1), a 12.1% net decrease in plasminogen, and a 17.8% net increase in D-dimer. These significantly differed from the response at 32.5°C, where there was a 44.9% (p = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.042) decrease in D-dimer. In contrast, decrements in lung function following ozone exposure were comparable at both moderate and elevated temperatures (forced expiratory volume in 1 sec, -12.4% vs. -7.5%, p > 0.05). No changes in systemic markers of inflammation were observed for either temperature.

Conclusion: Ozone-induced systemic but not respiratory effects varied according to temperature. Our study suggests that at moderate temperature ozone may activate the fibrinolytic pathway, while at elevated temperature ozone may impair it. These findings provide a biological basis for the interaction between temperature and ozone on mortality observed in some epidemiologic studies.

No MeSH data available.


Related in: MedlinePlus

Markers of inflammation after 2 hr ozone exposure at 0.3 ppm, with effects for moderate (22°C) and high (32.5°C) temperatures; the effect of ozone on systemic inflammation markers on the late time point is shown. The mean (effect size) and 95% CIs for 16 subjects are shown. p-Values are for ozone–temperature interaction.
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f2: Markers of inflammation after 2 hr ozone exposure at 0.3 ppm, with effects for moderate (22°C) and high (32.5°C) temperatures; the effect of ozone on systemic inflammation markers on the late time point is shown. The mean (effect size) and 95% CIs for 16 subjects are shown. p-Values are for ozone–temperature interaction.

Mentions: Effect of ozone on vascular markers of inflammation. Several epidemiologic studies have suggested that ozone can alter vascular inflammation (Bind et al. 2012; Chuang et al. 2007; Thompson et al. 2010). Accordingly, we measured blood concentrations of several factors identified as markers of systemic inflammation. Table 3 shows the 24-hr/preexposure changes in these markers for clean air and ozone exposure under the two temperature conditions. No significant changes in 24-hr/preexposure values at either temperature or any temperature–ozone interactions were observed for IL-6, IL-8, and TNFα (Figure 2). We had previously reported an increase in IL-1β after ozone at moderate temperature at this timepoint (Devlin et al. 2012). Here with a smaller sample size, we could not find a similar rise because of the very large heterogeneity in responses and the corresponding large CIs at either moderate (95% CI: –100.8%, 685.0%) or elevated (95% CI: –438.2%, 346.5%) temperatures. Similarly, for CRP there were very large CIs at moderate (95% CI: –97.5%, 205.1%) and high (95% CI: –188.4%, 113.8%) temperatures, which were driven predominantly by three individuals. For the 1-hr-post time point, there was a trend for all the inflammatory markers to be elevated following ozone exposure at moderate temperature, but none reached statistical significance (data not shown). There was no significant ozone–temperature interaction observed for any of the end points at this time point.


Interaction effects of temperature and ozone on lung function and markers of systemic inflammation, coagulation, and fibrinolysis: a crossover study of healthy young volunteers.

Kahle JJ, Neas LM, Devlin RB, Case MW, Schmitt MT, Madden MC, Diaz-Sanchez D - Environ. Health Perspect. (2014)

Markers of inflammation after 2 hr ozone exposure at 0.3 ppm, with effects for moderate (22°C) and high (32.5°C) temperatures; the effect of ozone on systemic inflammation markers on the late time point is shown. The mean (effect size) and 95% CIs for 16 subjects are shown. p-Values are for ozone–temperature interaction.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4384199&req=5

f2: Markers of inflammation after 2 hr ozone exposure at 0.3 ppm, with effects for moderate (22°C) and high (32.5°C) temperatures; the effect of ozone on systemic inflammation markers on the late time point is shown. The mean (effect size) and 95% CIs for 16 subjects are shown. p-Values are for ozone–temperature interaction.
Mentions: Effect of ozone on vascular markers of inflammation. Several epidemiologic studies have suggested that ozone can alter vascular inflammation (Bind et al. 2012; Chuang et al. 2007; Thompson et al. 2010). Accordingly, we measured blood concentrations of several factors identified as markers of systemic inflammation. Table 3 shows the 24-hr/preexposure changes in these markers for clean air and ozone exposure under the two temperature conditions. No significant changes in 24-hr/preexposure values at either temperature or any temperature–ozone interactions were observed for IL-6, IL-8, and TNFα (Figure 2). We had previously reported an increase in IL-1β after ozone at moderate temperature at this timepoint (Devlin et al. 2012). Here with a smaller sample size, we could not find a similar rise because of the very large heterogeneity in responses and the corresponding large CIs at either moderate (95% CI: –100.8%, 685.0%) or elevated (95% CI: –438.2%, 346.5%) temperatures. Similarly, for CRP there were very large CIs at moderate (95% CI: –97.5%, 205.1%) and high (95% CI: –188.4%, 113.8%) temperatures, which were driven predominantly by three individuals. For the 1-hr-post time point, there was a trend for all the inflammatory markers to be elevated following ozone exposure at moderate temperature, but none reached statistical significance (data not shown). There was no significant ozone–temperature interaction observed for any of the end points at this time point.

Bottom Line: Ozone exposure at 22°C resulted in a decrease in markers of fibrinolysis the next day.These significantly differed from the response at 32.5°C, where there was a 44.9% (p = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.042) decrease in D-dimer.Ozone-induced systemic but not respiratory effects varied according to temperature.

View Article: PubMed Central - PubMed

Affiliation: Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA.

ABSTRACT

Background: Trends in climate suggest that extreme weather events such as heat waves will become more common. High levels of the gaseous pollutant ozone are associated with elevated temperatures. Ozone has been associated with respiratory diseases as well as cardiovascular morbidity and mortality and can reduce lung function and alter systemic markers of fibrinolysis. The interaction between ozone and temperature is unclear.

Methods: Sixteen healthy volunteers were exposed in a randomized crossover study to 0.3 ppm ozone and clean air for 2 hr at moderate (22°C) temperature and again at an elevated temperature (32.5°C). In each case lung function was performed and blood taken before and immediately after exposure and the next morning.

Results: Ozone exposure at 22°C resulted in a decrease in markers of fibrinolysis the next day. There was a 51.8% net decrease in PAI-1 (plasminogen activator inhibitor-1), a 12.1% net decrease in plasminogen, and a 17.8% net increase in D-dimer. These significantly differed from the response at 32.5°C, where there was a 44.9% (p = 0.002) and a 27.9% (p = 0.001) increase in PAI-1 and plasminogen, respectively, and a 12.5% (p = 0.042) decrease in D-dimer. In contrast, decrements in lung function following ozone exposure were comparable at both moderate and elevated temperatures (forced expiratory volume in 1 sec, -12.4% vs. -7.5%, p > 0.05). No changes in systemic markers of inflammation were observed for either temperature.

Conclusion: Ozone-induced systemic but not respiratory effects varied according to temperature. Our study suggests that at moderate temperature ozone may activate the fibrinolytic pathway, while at elevated temperature ozone may impair it. These findings provide a biological basis for the interaction between temperature and ozone on mortality observed in some epidemiologic studies.

No MeSH data available.


Related in: MedlinePlus