COPD in the major nonsmoking adult: A systematic review and meta-analysis

Cunalata-Paredes, Andrea Verónica; Gea-Izquierdo, Enrique

doi:10.1080/19338244.2020.1828243

Cited by 7 publications

(14 citation statements)

References 34 publications

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“…We identified 19 reviews, studying six different risk factors [ 46 , 54 , 57 , 60 , 61 , 64 , 69 , 70 , 72 , 76 , 77 , 79 , 81 – 83 , 85 , 86 , 93 , 94 ]. P ark et al .…”

Section: Resultsmentioning

confidence: 99%

“…[ 82 ], with a 10 μg·m -3 increase in NO 2 being associated with an mHR of 1.07 (95% CI 1.00–1.16) [ 60 ] and an mRR of 1.02, respectively. Indoor air pollution caused by indoor biomass burning was found to be a risk factor for COPD in several reviews [ 54 , 57 , 61 , 69 , 70 , 72 , 76 , 77 , 79 , 81 , 83 , 85 , 86 , 93 , 94 ]. Found mORs ranged between 1.52 (95% CI 1.39–1.67), found by N joku et al .…”

Section: Resultsmentioning

confidence: 99%

“…12 reviews identified risk factors in early life [ 50 , 52 , 57 , 68 , 70 , 72 , 80 , 85 , 92 , 93 , 94 ]. Six of these focused on respiratory problems in early life and COPD risk [ 50 , 57 , 72 , 85 , 93 , 94 ], with found mORs ranging between 2.23 (95% CI 1.63–3.07) [ 50 ] and 3.44 (95% CI 1.33–8.90) [ 72 ]. Additionally, D uan et al .…”

Section: Resultsmentioning

confidence: 99%

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Identifying risk factors for COPD and adult-onset asthma: an umbrella review

et al. 2023

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BackgroundCOPD and adult-onset asthma (AOA) are the most common noncommunicable respiratory diseases. To improve early identification and prevention, an overview of risk factors is needed. We therefore aimed to systematically summarise the nongenetic (exposome) risk factors for AOA and COPD. Additionally, we aimed to compare the risk factors for COPD and AOA.MethodsIn this umbrella review, we searched PubMed for articles from inception until 1 February 2023 and screened the references of relevant articles. We included systematic reviews and meta-analyses of observational epidemiological studies in humans that assessed a minimum of one lifestyle or environmental risk factor for AOA or COPD.ResultsIn total, 75 reviews were included, of which 45 focused on risk factors for COPD, 28 on AOA and two examined both. For asthma, 43 different risk factors were identified while 45 were identified for COPD. For AOA, smoking, a high body mass index (BMI), wood dust exposure and residential chemical exposures, such as formaldehyde exposure or exposure to volatile organic compounds, were amongst the risk factors found. For COPD, smoking, ambient air pollution including nitrogen dioxide, a low BMI, indoor biomass burning, childhood asthma, occupational dust exposure and diet were amongst the risk factors found.ConclusionsMany different factors for COPD and asthma have been found, highlighting the differences and similarities. The results of this systematic review can be used to target and identify people at high risk for COPD or AOA.

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“…We identified 19 reviews, studying six different risk factors [ 46 , 54 , 57 , 60 , 61 , 64 , 69 , 70 , 72 , 76 , 77 , 79 , 81 – 83 , 85 , 86 , 93 , 94 ]. P ark et al .…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Identifying risk factors for COPD and adult-onset asthma: an umbrella review

et al. 2023

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“…A systematic review and meta-analysis that aimed at identifying risk factors for COPD in nonsmoking adults showed that second-hand smoking was the main risk factor in this population [ 1 ]. Among patients included in the analysis, 56% had active smoking as the risk factor and 44% were nonsmokers; in the latter population, 46.9% of patients had passive smoke exposure.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, smoking (active or passive) was associated with 76% of COPD cases. Patients who were exposed to smoke as passive smokers and who were healthy had a probability of developing COPD of 94.6% (pooled OR 52.97, 95% CI 44.65–62.83) [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Smoking cessation and vaccination

Laucho-Contreras

2023

Eur Respir Rev

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A significant proportion of COPD patients (∼40%) continue smoking despite knowing that they have the disease. Smokers with COPD exhibit higher levels of nicotine dependence, and have lower self-efficacy and self-esteem, which affects their ability to quit smoking. Treatment should be adapted to the needs of individual patients with different levels of tobacco dependence. The combination of counselling plus pharmacotherapy is the most effective cessation treatment for COPD. In patients with severe COPD, varenicline and bupropion have been shown to have the highest abstinence rates compared with nicotine replacement therapy. There is a lack of evidence to support that smoking cessation reduction or harm reduction strategies have benefits in COPD patients. The long-term efficacy and safety of electronic cigarettes for smoking cessation need to be evaluated in high-risk populations; therefore, it is not possible to recommend their use for smoking cessation in COPD. Future studies with the new generation of nicotine vaccines are necessary to determine their effectiveness in smokers in general and in COPD patients.

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Pacenta polypeptide injection alleviates the fibrosis and inflammation in cigarette smoke extracts‐induced BEAS‐2B cells by modulating MMP‐9/TIMP‐1 signaling

Zhu

et al. 2023

J Biochem & Molecular Tox

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Chronic obstructive pulmonary disease (COPD) has high morbidity and mortality. Here, we aimed to explore the roles and potential correlation of placenta polypeptide injection (PPI) and MMP‐9/TIMP‐1 signaling pathway in COPD. BEAS‐2B cells were treated with cigarette smoke extract (CSE) to establish a COPD cell model in vitro. The cell survival and cytotoxic effect were measured by CCK‐8, LDH release and flow cytometry assays. The inflammatory responses were determined by western blot and ELISA assay. Cell fibrosis was assessed by immunofluorescence and western blot assays. PPI treatment had no cytotoxic effect on BEAS‐2B cells until the final concentration reached to 10%. In the range of 0%–8% final concentration, PPI treatment weakened CSE‐induced the decrease of cell viability and the increase of LDH level in a concentration‐dependent manner. Four percent PPI treatment enhanced cell viability and decreased cell apoptosis of CSE‐treated cells in a time‐dependent manner. Moreover, 4% PPI treatment significantly decreased inflammatory responses and fibrosis induced by CSE, while AMPA (MMPs agonist) had opposite effects. Notably, AMPA reversed the protective roles of PPI on CSE‐induced inflammation and fibrosis. Mechanistically, 4% PPI treatment significantly suppressed MMP‐1, MMP‐2, MMP‐3, MMP‐9, MMP‐13, and MMP‐19 levels, but enhanced TIMP‐1, TIMP‐2, TIMP‐3, and TIMP‐4 levels. Among them, MMP‐9 and TIMP‐1 might be the main target of PPI. PPI effectively attenuated CSE‐induced inflammation and fibrosis in vitro by regulating MMP‐9/TIMP‐1 signaling pathway.

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COPD in the major nonsmoking adult: A systematic review and meta-analysis

Cited by 7 publications

References 34 publications

Identifying risk factors for COPD and adult-onset asthma: an umbrella review

Identifying risk factors for COPD and adult-onset asthma: an umbrella review

Smoking cessation and vaccination

Pacenta polypeptide injection alleviates the fibrosis and inflammation in cigarette smoke extracts‐induced BEAS‐2B cells by modulating MMP‐9/TIMP‐1 signaling

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