Emily
Editor, Senior Moderator
https://www.sciencedirect.com/science/article/abs/pii/S0048969721007774
Linchen He, Christina Norris, Xiaoxing Cui, Zhen Li, Karoline K. Barkjohn, Yanbo Teng, Lin Fang, Lili Lin, Qian Wang, Xiaojian Zhou, Jianguo Hong, Feng Li, Yinping Zhang, James J. Schauer, Marilyn Black, Michael H. Bergin, Junfeng (Jim) Zhang,
Role of endogenous melatonin in pathophysiologic and oxidative stress responses to personal air pollutant exposures in asthmatic children,
Science of The Total Environment,
Volume 773,
2021,
145709,
ISSN 0048-9697,
https://doi.org/10.1016/j.scitotenv.2021.145709.
(https://www.sciencedirect.com/science/article/pii/S0048969721007774)
Abstract: Background
Heightening oxidative stress and inflammation is an important pathophysiological mechanism underlying air pollution health effects in people with asthma. Melatonin can suppress oxidative stress and inflammation in pulmonary and circulatory systems. However, the role of melatonin in the oxidative stress and physiological responses to air pollution exposure has not been examined in children with asthma.
Methods
In this panel study of 43 asthmatic children (5–13 years old), each child had 4 clinic visits with a 2-week interval between two consecutive visits. At each visit, urine samples were collected and subsequently analyzed for 6-sulfatoxymelatonin (aMT6s) as a surrogate of circulating melatonin and for malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) as two biomarkers of systemic oxidative stress. At each clinic visit, children were measured for pulmonary function and fractional exhaled nitric oxide (FeNO, a marker of pulmonary inflammation). None of the children reported to have taking melatonin supplementation. Concentrations of indoor and ambient PM2.5 and ozone (O3) were combined with individual time-activity data to calculate personal air pollutant exposures.
Results
We found that interquartile range increases in urinary MDA and 8-OHdG concentrations were associated with significantly increased urinary aMT6s concentrations by 73.4% (95% CI: 52.6% to 97.0%) and 41.7% (22.8% to 63.4%), respectively. Increases in daily personal exposure to O3 and to PM2.5 were each associated with increased urinary aMT6s concentrations. Increasing urinary aMT6s concentrations were associated with decreased FeNO and resonant frequency, indicating improved airway inflammation and lung elasticity, respectively.
Conclusion
The results suggest that systemic oxidative stress heightened by air pollution exposure may stimulate melatonin excretion as a defense mechanism to alleviate the adverse effects.
Keywords: Air pollution; Melatonin; Pulmonary physiology; Oxidative stress; Airway mechanics; Lung function
Linchen He, Christina Norris, Xiaoxing Cui, Zhen Li, Karoline K. Barkjohn, Yanbo Teng, Lin Fang, Lili Lin, Qian Wang, Xiaojian Zhou, Jianguo Hong, Feng Li, Yinping Zhang, James J. Schauer, Marilyn Black, Michael H. Bergin, Junfeng (Jim) Zhang,
Role of endogenous melatonin in pathophysiologic and oxidative stress responses to personal air pollutant exposures in asthmatic children,
Science of The Total Environment,
Volume 773,
2021,
145709,
ISSN 0048-9697,
https://doi.org/10.1016/j.scitotenv.2021.145709.
(https://www.sciencedirect.com/science/article/pii/S0048969721007774)
Abstract: Background
Heightening oxidative stress and inflammation is an important pathophysiological mechanism underlying air pollution health effects in people with asthma. Melatonin can suppress oxidative stress and inflammation in pulmonary and circulatory systems. However, the role of melatonin in the oxidative stress and physiological responses to air pollution exposure has not been examined in children with asthma.
Methods
In this panel study of 43 asthmatic children (5–13 years old), each child had 4 clinic visits with a 2-week interval between two consecutive visits. At each visit, urine samples were collected and subsequently analyzed for 6-sulfatoxymelatonin (aMT6s) as a surrogate of circulating melatonin and for malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) as two biomarkers of systemic oxidative stress. At each clinic visit, children were measured for pulmonary function and fractional exhaled nitric oxide (FeNO, a marker of pulmonary inflammation). None of the children reported to have taking melatonin supplementation. Concentrations of indoor and ambient PM2.5 and ozone (O3) were combined with individual time-activity data to calculate personal air pollutant exposures.
Results
We found that interquartile range increases in urinary MDA and 8-OHdG concentrations were associated with significantly increased urinary aMT6s concentrations by 73.4% (95% CI: 52.6% to 97.0%) and 41.7% (22.8% to 63.4%), respectively. Increases in daily personal exposure to O3 and to PM2.5 were each associated with increased urinary aMT6s concentrations. Increasing urinary aMT6s concentrations were associated with decreased FeNO and resonant frequency, indicating improved airway inflammation and lung elasticity, respectively.
Conclusion
The results suggest that systemic oxidative stress heightened by air pollution exposure may stimulate melatonin excretion as a defense mechanism to alleviate the adverse effects.
Keywords: Air pollution; Melatonin; Pulmonary physiology; Oxidative stress; Airway mechanics; Lung function