Parental COPD as a Risk Factor for the Development of COPD and Disease Severity in Offspring: A Systematic Scoping Review

Sikjær, Melina Gade; Klitgaard, Allan; Hilberg, Ole; Løkke, Anders

doi:10.2147/copd.s364899

Cited by 4 publications

(3 citation statements)

References 43 publications

(98 reference statements)

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“…For instance, a high prevalence of smoking and low cessation rates were found in non-Hispanic black,22 and family history of COPD was shown to be more common in non-Hispanic whites (37.1%). Prenatal COPD could increase the risk of COPD and exacerbations in the offspring 23. In addition, it is somewhat surprising that self-reported asthma was not shown to be a risk factor for young COPD in the present study.…”

Section: Discussioncontrasting

confidence: 59%

“…Prenatal COPD could increase the risk of COPD and exacerbations in the offspring. 23 In addition, it is somewhat surprising that self-reported asthma was not shown to be a risk factor for young COPD in the present study. This might be explained by the difference between self-reported asthma and medically diagnosed asthma because the latter determined by symptoms and examinations would be more scientific and credible than self-reported asthma.…”

Section: Discussionmentioning

confidence: 52%

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Prevalence, risk factors, and mortality of COPD in young people in the USA: results from a population-based retrospective cohort

Wang

Lin

et al. 2023

BMJ Open Resp Res

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BackgroundChronic obstructive pulmonary disease (COPD) has been considered a disease of the elderly, but it could also occur in young people aged 20–50 years. However, the characteristics and prognosis of COPD in such young people remain unclear.MethodsOur retrospective cohort study was based on the National Health and Nutrition Examination Survey (NHANES). Participants who 20–50 years old at baseline and completed the pulmonary function test were enrolled in our study cohort. These participants were followed up to 31 December 2019. The sample weight and Taylor Linearization Procedures were adapted to make representative estimations of prevalence and baseline characteristics. The weighted logistic regression model was used to assess the risk factors. The propensity score method and Cox proportional hazard models were applied to calculate the risk of mortality.ResultsThe weighted prevalence of COPD in young people in the USA was 1.64% and it increased with age, with a higher prevalence in males than females (2.59% vs 0.72%, p<0.001). The proportion of Global Initiative for COPD 1–2 was 96.7%. Males (OR=4.56, 95% CI: 2.74 to 7.61), non-Hispanic black (OR=2.77; 95% CI: 1.14 to 6.75), non-Hispanic white (OR=4.93; 95% CI: 2.16 to 11.28) and smoking (current smoking, OR=2.36; 95% CI: 1.40 to 3.98; ever smoking, OR=1.92; 95% CI: 1.05 to 3.51; passive smoking, OR=2.12; 95% CI: 1.41 to 3.20) were shown to be independent risk factors for COPD in young people. Compared with those matched by sex, age and race, the young people with COPD had a higher risk of all-cause death (HR=3.314, p<0.001).ConclusionCOPD in young people has a low prevalence in the USA and its independent risk factors included male, race (non-Hispanic black and non-Hispanic white) and smoking. Young COPD has a higher risk of all-cause mortality than the matched non-COPD.

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Section: Discussioncontrasting

confidence: 59%

Section: Discussionmentioning

confidence: 52%

Prevalence, risk factors, and mortality of COPD in young people in the USA: results from a population-based retrospective cohort

Wang

Lin

et al. 2023

BMJ Open Resp Res

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“…COPD is mainly triggered by the inhalation of toxic particles, especially tobacco smoke and polluted air [ 3 ]. Some COPD patients are caused by genetic factors, lung infection and malformation of lung growth and development [ 4 , 5 ]. In terms of pathogenesis, oxidative stress and inflammatory activation are two well-recognized factors that induce chronic airway inflammation and lung parenchyma destruction [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Nrf2/HO-1 signaling activation alleviates cigarette smoke-induced inflammation in chronic obstructive pulmonary disease by suppressing NLRP3-mediated pyroptosis

Zhang,

Wang,

Wang

et al. 2024

J Cardiothorac Surg

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Background This study examined the effect of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway on chronic obstructive pulmonary disease (COPD) and the potential molecular mechanism. Methods A COPD mouse model was established by cigarette smoke exposure and administered with either ML385 or dimethyl fumarate (DMF). Airway resistance of mice was detected. IL-1β and IL-6 levels in mice alveolar lavage fluid were examined by enzyme-linked immunosorbent assay. Hematoxylin and eosin staining and immunohistochemical of lung tissues were utilized to detect lung injury and NLRP3 expression. DMF was used to treat COPD cell model constructed by exposing normal human bronchial epithelial (NHBE) cells to cigarette smoke extract. NHBE cells were transfected by NLRP3-expression vectors. Expression of proteins was detected by Western blot. Results COPD mice showed the enhanced airway resistance, the inactivated Nrf2/HO-1 pathway and the overexpressed NLRP3, Caspase-1 and GSDMD-N proteins in lung tissues, and the increased IL-1β and IL-6 levels in alveolar lavage fluid. ML385 treatment augmented these indicators and lung injury in COPD mice. However, DMF intervention attenuated these indicators and lung injury in COPD mice. Nrf2/HO-1 pathway inactivation and overexpression of NLRP3, Caspase-1 and GSDMD-N proteins were observed in COPD cells. DMF intervention activated Nrf2/HO-1 pathway and down-regulated NLRP3, Caspase-1 and GSDMD-N proteins in COPD cells. However, NLRP3 overexpression abolished the effect of DMF on COPD cells. Conclusion Nrf2/HO-1 pathway activation may alleviate inflammation in COPD by suppressing the NLRP3-related pyroptosis. Activating the Nrf2/HO-1 pathway may be an effective method to treat COPD.

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Prevalence, mortality and risk factors for self-reported COPD among smokers and never smokers, NHANES 1999-2018

Li,

Xue,

et al. 2024

Tob. Induc. Dis.

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INTRODUCTION Cigarette smoke is the main risk factor for chronic obstructive pulmonary disease (COPD), but 25% to 50% of cases occur in non-smokers. In the US, limited recent national data compare COPD prevalence between smokers and never smokers. Furthermore, our study seeks to explore the prevalence and mortality of self-reported COPD among smokers (including current smokers and ex-smokers) and never smokers in the US from 1999 to 2018, and to identify the risk factors and differences. METHODS This cross-sectional analysis used data from the National Health and Nutrition Examination Survey (NHANES) 1999–2018. Age-standardized prevalence of self-reported COPD among current smokers, ex-smokers, and never smokers was calculated using sample weights and 2010 US Census estimates. Risk factors were evaluated through weighted logistic regression models. Subsequently, participants who enrolled in the study cohort were followed until 31 December 2019, to determine all-cause mortality rates. RESULTS Between 1999 and 2018, the weighted prevalence of COPD among current smokers, ex-smokers, and never smokers in the U.S. was 12.6%, 9.6%, and 4.1%, respectively. The mortality rates observed were 21.1% among current smokers with COPD, 29% among ex-smokers with COPD, and 12% among never smokers with COPD. Over this period, among the general population in the U.S., the proportion of current smokers has declined, the proportion of never smokers has increased, and the proportion of ex-smokers has remained relatively stable. From 1999 to 2018, COPD prevalence rose from 13.7% to 21.9% among current smokers, stayed at 10.1% among ex-smokers, and dropped from 4.9% to 3.3% among never smokers. Independent risk factors for COPD across all groups included being female, older, and lower income. In particular, US citizens and non-Hispanic Whites (among ex-smokers and never smokers) were at higher risk compared to their counterparts. CONCLUSIONS The prevalence and all-cause mortality of COPD among current smokers and ex-smokers remain elevated. Although the prevalence of COPD among never smokers is gradually declining, it continues to be significant, thereby maintaining a substantial burden of disease. Furthermore, common independent risk factors for COPD across current smokers, ex-smokers, and never smokers include female gender, advanced age, lower income, and deviations from normal body weight whether overweight or underweight.

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Parental COPD as a Risk Factor for the Development of COPD and Disease Severity in Offspring: A Systematic Scoping Review

Cited by 4 publications

References 43 publications

Prevalence, risk factors, and mortality of COPD in young people in the USA: results from a population-based retrospective cohort

Prevalence, risk factors, and mortality of COPD in young people in the USA: results from a population-based retrospective cohort

Nrf2/HO-1 signaling activation alleviates cigarette smoke-induced inflammation in chronic obstructive pulmonary disease by suppressing NLRP3-mediated pyroptosis

Prevalence, mortality and risk factors for self-reported COPD among smokers and never smokers, NHANES 1999-2018

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