Clinical Epidemiology of COPD

Maselli, Diego J.; Bhatt, Surya P.; Anzueto, Antonio; Bowler, Russell P.; DeMeo, Dawn L.; Díaz, Alejandro A.; Dransfield, Mark T.; Fawzy, Ashraf; Foreman, Marilyn G.; Hanania, Nicola A.; Hersh, Craig P.; Kim, Victor; Kinney, Gregory L.; Putcha, Nirupama; Wan, Emily S.; Wells, James M.; Westney, Gloria; Young, Kendra A.; Silverman, Edwin K.; Han, Mei Lan K.; Make, Barry J.

doi:10.1016/j.chest.2019.04.135

Cited by 75 publications

(34 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, most of the effect estimates we and others report are from secondary subgroup analyses with wide confidence intervals, meriting cautious interpretation. Nonetheless, people 45-64 with COPD are less likely to be using oxygen than people 65 and over with COPD, and thus more likely to be mobile and exposed to wildfire smoke [49]. Our findings suggest that underlying respiratory health conditions may contribute to the increased risk of respiratory and COPD-related mortality in the 45-64 age group.…”

Section: Discussionmentioning

confidence: 73%

Mortality associated with wildfire smoke exposure in Washington state, 2006–2017: a case-crossover study

et al. 2020

View full text Add to dashboard Cite

Background: Wildfire events are increasing in prevalence in the western United States. Research has found mixed results on the degree to which exposure to wildfire smoke is associated with an increased risk of mortality. Methods: We tested for an association between exposure to wildfire smoke and non-traumatic mortality in Washington State, USA. We characterized wildfire smoke days as binary for grid cells based on daily average PM 2.5 concentrations, from June 1 through September 30, 2006-2017. Wildfire smoke days were defined as all days with assigned monitor concentration above a PM 2.5 value of 20.4 μg/m 3 , with an additional set of criteria applied to days between 9 and 20.4 μg/m 3. We employed a case-crossover study design using conditional logistic regression and time-stratified referent sampling, controlling for humidex. Results: The odds of all-ages non-traumatic mortality with same-day exposure was 1.0% (95% CI: − 1.0-4.0%) greater on wildfire smoke days compared to non-wildfire smoke days, and the previous day's exposure was associated with a 2.0% (95% CI: 0.0-5.0%) increase. When stratified by cause of mortality, odds of same-day respiratory mortality increased by 9.0% (95% CI: 0.0-18.0%), while the odds of same-day COPD mortality increased by 14.0% (95% CI: 2.0-26.0%). In subgroup analyses, we observed a 35.0% (95% CI: 9.0-67.0%) increase in the odds of same-day respiratory mortality for adults ages 45-64. Conclusions: This study suggests increased odds of mortality in the first few days following wildfire smoke exposure. It is the first to examine this relationship in Washington State and will help inform local and state risk communication efforts and decision-making during future wildfire smoke events.

show abstract

Section: Discussionmentioning

confidence: 73%

Mortality associated with wildfire smoke exposure in Washington state, 2006–2017: a case-crossover study

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Although highly expressed miR‐221 and miR‐92a were also measurable in bronchial epithelial cells, lung tissues and plasma of asthma and lung cancer patients, 34 , 35 , 36 the specificity of miR‐221 and miR‐92a in COPD diagnosis might not be reduced for that we focused on serum in this investigation. Despite this strength, combination with other biomarkers or association with clinical symptoms 37 , 38 might yield more desirable results in COPD diagnosis than application of miR‐221/miR‐92a alone.…”

Section: Discussionmentioning

confidence: 99%

MiR‐221‐3p and miR‐92a‐3p enhances smoking‐induced inflammation in COPD

Shen

Song

2021

Clinical Laboratory Analysis

View full text Add to dashboard Cite

Background Smoking is likely to facilitate airway inflammation and finally contributes to chronic obstructive pulmonary disease (COPD). This investigation was intended to elucidate miRNAs that were involved in smoking‐induced COPD. Methods Altogether 155 COPD patients and 77 healthy volunteers were recruited, and their serum levels of miR‐221‐3p and miR‐92a‐3p were determined. Besides, human bronchial epithelial cells (16HBECs) were purchased, and they were treated by varying concentrations of cigarette smoke extract (CSE). The 16HBECs were, additionally, transfected by miR‐221‐3p mimic, miR‐92a‐3p mimic, miR‐221‐3p inhibitor or miR‐92a‐3p inhibitor, and cytokines released by them, including TNF‐α, IL‐8, IL‐1β, and TGF‐β1, were monitored using enzyme linked immunosorbent assay (ELISA) kits. Results Chronic obstructive pulmonary disease patients possessed higher serum levels of miR‐221‐3p and miR‐92a‐3p than healthy volunteers (p < 0.05), and both miR‐221‐3p and miR‐92a‐3p were effective biomarkers in diagnosing stable COPD from acute exacerbation COPD. Moreover, viability of 16HBECs was undermined by CSE treatment (p < 0.05), and exposure to CSE facilitated 16HBECs’ release of TNF‐α, IL‐8, IL‐1β, and TGF‐β1 (p < 0.05). Furthermore, miR‐221‐3p/miR‐92a‐3p expression in 16HBECs was significantly suppressed after transfection of miR‐221‐3p/miR‐92a‐3p inhibitor (p < 0.05), which abated CSE‐triggered increase in cytokine production and decline in viability of 16HBECs (p < 0.05). Conclusion MiR‐221‐3p and miR‐92a‐3p were involved in CSE‐induced hyperinflammation of COPD, suggesting that they were favorable alternatives in diagnosing COPD patients with smoking history.

show abstract

“…As hepatic IGF1 seemed to drive body weight in the neonatal stage, body weight was negatively correlated with the methylation status of Igf1 (especially CpG-1254). Therefore, a regu- (1,15,30) and of interest is that the PSE effect on lung inflammation in adult offspring was sex specific.…”

Section: Discussionmentioning

confidence: 99%

Prenatal smoke effect on mouse offspringIgf1promoter methylation from fetal stage to adulthood is organ and sex specific

Zeng

Meyer

Lkhagvadorj

et al. 2020

American Journal of Physiology-Lung Cellular and Molecular Phys

View full text Add to dashboard Cite

Prenatal smoke exposure (PSE) is associated with reduced birth weight, impaired fetal development, and increased risk for diseases later in life. Changes in DNA methylation may be involved, as multiple large-scale epigenome-wide association studies showed that PSE is robustly associated with DNA methylation changes in blood among offspring in early life. Insulin-like growth factor-1 (IGF1) is important in growth, differentiation, and repair processes after injury. However, no studies investigated the organ-specific persistence of PSE-induced methylation change of Igf1 into adulthood. Based on our previous studies on the PSE effect on Igf1 promoter methylation in fetal and neonatal mouse offspring, we now have extended our studies to adulthood. Our data show that basal Igf1 promoter methylation generally increased in the lung but decreased in the liver (except for 2 persistent CpG sites in both organs) across three different developmental stages. PSE changed Igf1 promoter methylation in all three developmental stages, which was organ and sex specific. The PSE effect was less pronounced in adult offspring compared with the fetal and neonatal stages. In addition, the PSE effect in the adult stage was more pronounced in the lung compared with the liver. For most CpG sites, an inverse correlation was found for promoter methylation and mRNA expression when the data of all three stages were combined. This was more prominent in the liver. Our findings provide additional evidence for sex- and organ-dependent prenatal programming, which supports the developmental origins of health and disease (DOHaD) hypothesis.

show abstract

Clinical Epidemiology of COPD

Cited by 75 publications

References 44 publications

Mortality associated with wildfire smoke exposure in Washington state, 2006–2017: a case-crossover study

Mortality associated with wildfire smoke exposure in Washington state, 2006–2017: a case-crossover study

MiR‐221‐3p and miR‐92a‐3p enhances smoking‐induced inflammation in COPD

Prenatal smoke effect on mouse offspringIgf1promoter methylation from fetal stage to adulthood is organ and sex specific

Contact Info

Product

Resources

About