Low physical activity (PA) levels have a negative impact on the health status of patients with Chronic Obstructive Pulmonary Disease (COPD). Smartphone applications (apps) focused on PA promotion may mitigate this problem; however, their effectiveness depends on patient adherence, which can be influenced by the technological features of the apps. This systematic review identified the technological features of smartphone apps aiming to promote PA in patients with COPD.

A literature search was performed in the databases ACM Digital Library, IEEE Xplore, PubMed, Scopus and Web of Science. Papers including the description of a smartphone app for PA promotion in patients with COPD were included. Two researchers independently selected studies and scored the apps features based on a previously developed framework (38 possible features).

Twenty-three studies were included and 19 apps identified, with an average of 10 technological features implemented. Eight apps could be connected to wearables to collect data. The categories 'Measuring and monitoring' and 'Support and Feedback' were present in all apps. Overall, the most implemented features were 'progress in visual format' (n = 13), 'advice on PA' (n = 14) and 'data in visual format' (n = 10). Only three apps included social features, and two included a web-based version of the app.

The existing smartphone apps include a relatively small number of features to promote PA, which are mostly related to monitoring and providing feedback. Further research is warranted to explore the relationship between the presence/absence of specific features and the impact of interventions on patients' PA levels.

Evidence suggests that ozone is associated with an increased risk of hypertension, diabetes, or chronic kidney disease (CKD). However, the associations of ozone exposure with the dynamic progression of these diseases among Asian population remain unknown. This study included 9,256,945 participants from Taiwan's National Health Insurance Research Database between 2006 and 2021. Multimorbidity was defined as the coexistence of CKD and either hypertension or diabetes. The ordinary kriging method was used to estimate daily concentrations of ozone, sulfur dioxide, carbon monoxide, nitrogen dioxide, suspended fine particles, and suspended particles. Then, five-year average concentrations of pollutants were calculated. We performed multi-state survival models to analyze the association between ozone and dynamic progression of these diseases. During follow-up, 3,555,498 participants experienced hypertension, diabetes, or CKD; 656,515 experienced multimorbidity; and 792,555 died. Ozone exposure was significantly associated with incidence of the results in all transitions. The hazard ratios of each IQR (3.57 ppb) increment in ozone for the transition to incident disease were 1.016 [95 % confidence interval (CI): 1.014, 1.017], for the transition to death were 1.04 [95 % CI: 1.036, 1.043], for the transition to multimorbidity were 1.015 [95 % CI: 1.012, 1.017]. Furthermore, with each IQR increase of ozone, the hazard ratios for transition from the disease incidence to death and from multimorbidity to death were 1.03 [95 % CI: 1.026, 1.033] and 1.007 [95 % CI: 1.002, 1.013], respectively. Our results suggest long-term exposure to ozone might be an important determinant for the incidence and dynamic progression of hypertension, diabetes, and CKD in Taiwan.

Air pollution is an environmental risk factor associated with lung and cardiovascular disease that may be mediated by physiological pathways such as oxidative stress. Previous studies have identified associations between air pollution and biomarkers of oxidative stress (8-OHdG, 4-HNE, and fluorescent oxidation products (FOPs)), as well as lung health marker CC16, in younger and asthmatic populations. The objective of this study of a large population-based sample of non-smoking adults was to explore the relationship between long-term and short-term atmospheric pollution exposures and plasma or urine levels of these biomarkers. Our study was a post-hoc analysis of the cross-sectional ELISABET study from 2011 to 2013. We included non-smoking inhabitants of Lille, France from the ELISABET study. We assessed mean pluri-annual residential and short-term exposures to atmospheric pollution components (PM10, NO2, and O3) and collected several biomarkers (CC16, 8-OHdG, 4-HNE, and fluorescent oxidation products (FOPs)). We searched for associations between pollutants and biomarkers using log-linear robust multivariate regressions. Our work did not show any association between short- or long-term exposure to air pollution components and CC16, 8-OHdG, 4-HNE or FOP in a large (980 subjects) sample of Lille's general population, despite having sufficient statistical power to replicate previous findings of associations between air pollution and these biomarkers found in younger or asthmatic populations.

This systematic review examines how extreme temperatures impact Chronic Obstructive Pulmonary Disease (COPD) morbidity and mortality, focusing on identifying vulnerable subpopulations.

We conducted a systematic literature search from January 1, 2000, to November 6, 2024, across databases like PubMed, MEDLINE and EMBASE, Web of Science, and Scopus, focusing on observational studies that quantitatively defined extreme temperatures and their impacts on COPD morbidity and mortality. Out of 3140 records, 25 studies met the inclusion criteria. We extracted data on study characteristics, effect estimates, and confounders, employing methods to assess the risk of bias and synthesize results.

We observed that extreme heat increased the relative risk (RR) for COPD morbimortality by 1.19-fold (95 % CI: 1.09-1.29; p < 0.05), and extreme cold increased the RR by 1.35-fold (95 % CI: 1.22-1.50; p < 0.05). Extreme heat was associated with a 1.23-fold (95 % CI: 1.11-1.35; p < 0.05) increase in COPD mortality. In contrast, extreme cold was associated with both COPD morbidity and mortality, with morbidity increasing by 1.47-fold (95 % CI: 1.26-1.71; p < 0.05) and mortality by 1.28-fold (95 % CI: 1.12-1.45; p < 0.05). Extreme heat poses a higher risk for female COPD patients compared to males. Moreover, extreme heat and cold were associated with morbimortality risk among older adults. Asian populations were sensitive to both temperature extremes, whereas Europeans were predominantly susceptible to extreme cold.

This variability in response to extreme temperatures affects COPD morbidity and mortality, emphasizing the need for tailored medical and emergency responses to effectively mitigate health risks during extreme weather events.

Air pollutants and meteorological conditions have shown significant adverse effects on human health; however, their impact on mental health remains inconclusive and underexplored. Thus, this study aimed to investigate the association between long-term exposure to air pollutants (PM2.5 and PM10), meteorological factors, and depression and anxiety.

We selected 10,076 participants aged 15-49 from the Nepal Demographic and Health Survey (NDHS) 2022, who had lived in their current domiciles for over five years. The Patient Health Questionnaire-9 (PHQ-9) and the Generalized Anxiety Disorder (GAD-7) scale were used to quantify the presence of depression and anxiety. The mean levels of air pollutants (PM2.5 and PM10), temperature, and relative humidity between August 2021 and July 2022 were obtained from the national air quality monitoring center and the meteorological department. Adjusted linear and polynomial logistic regression models were used to estimate the risk of depression and anxiety.

The prevalence of depression and anxiety among participants was 3.8% and 16.9%, respectively. Increased PM2.5 and PM10 concentrations were significantly associated with increased PHQ-9 (PM2.5: β, 0.015; PM10: β, 0.011) and GAD-7 (PM2.5: β, 0.024; PM10: β, 0.011) scores. Exposure to higher PM2.5 and PM10 concentrations increased the risk of depression {OR, 95% CI (PM2.5: 1.05, 1.03-1.08); (PM10: 1.04, 1.01-1.05)} and anxiety {OR, 95% CI (PM2.5: 1.06, 1.04-1.10); (PM10: 1.03, 1.01-1.04)}, whereas higher temperatures and higher humidity showed a protective effect (p < 0.05).

This study demonstrates the substantial impact of air pollutants and meteorological factors on mental health status. Findings suggest that exposure to air pollutants may serve as an independent risk factor for depression and anxiety. Therefore, further robust investigations including large epidemiological cohorts and longitudinal observational studies are needed to elucidate these associations.

Not applicable.

Recovery from chronic obstructive pulmonary disease (COPD) exacerbations is heterogeneous and has a profound impact on disease trajectories. Resolution of airway inflammation is an active process which may be driven by Specialized Pro-resolving Mediators (SPMs).

To characterize the temporal change in SPMs in the sputum of COPD patients during COPD exacerbations, their association with exacerbation triggers and exacerbation recovery.

Participants were recruited from the London COPD Exacerbation Cohort between 01/11/2016 and 01/04/2018. Participants were reviewed at baseline, exacerbation onset, 1 week, 2 weeks and 6 weeks during their exacerbation recovery. Sputum, nasopharyngeal swabs, phlebotomy, quality of life questionnaires and spirometry were performed at each visit. SPMs were measured in sputum by liquid chromatography tandem mass spectrometry. Respiratory viruses were measured by quantitative PCR and bacteria by microbiological culture.

There were 68 exacerbations during the study period. Median time to symptomatic recovery was 21 days for viral exacerbations compared to 13 days in non-viral exacerbations (P<0.001). There was a significant increase in Resolvin D1 (RvD1) at exacerbation onset in bacterial exacerbations but not viral exacerbations. Lower levels of RvD1 were associated with prolonged respiratory symptoms during the 1-week and 2-week recovery time points. Exogenous RvD1 significantly reduced IL-6 and CXCL8 response to rhinovirus infection in COPD bronchial epithelial cells.

There is a dynamic temporal change in airway SPMs during COPD exacerbations. Reduced levels of RvD1 were associated with prolonged respiratory symptoms. SPMs may be a potential therapeutic approach to promote exacerbation recovery.

Cystic fibrosis is a genetic disease in which phenotypic variability is still poorly understood. Our hypothesis is that the exposome, and more specifically exposure to air pollution and/or anxiety, could play a role in this phenomenon. In this context, we have developed an experimental study in which cystic fibrosis mice were exposed to stress (anxiety) and then to complex realistic atmospheres. Our results should provide mechanistic elements for a better understanding of the phenotypic variability observed in cystic fibrosis patients and thus be able to propose new avenues for better management of these patients.

Health effects of ultrafine particles (UFPs) and their interactions with temperature are less studied. We investigated the risks of UFPs concentrations and extreme temperatures on hospitalizations for high-burden diseases (HBDs) in New York State (NYS).

This case-crossover study included hospitalizations for HBDs that contain ischemic heart diseases, diabetes, stroke, kidney diseases, and depression using NYS Hospital Discharge Data (2013-2018). Daily pollutants and temperature data were obtained from a chemical transport model validated by multiple prior studies. UFP changes were measured using interquartile range increase, and extreme heat and cold were defined as temperatures >= 90th% and <=10th% respectively by month and location. Conditional logistic regression was applied controlling for criteria pollutants, relative humidity, and time-varying variables.

Among 1,308,518 cases, significant risk ratios (RR) were observed for UFPs (RRs ranged: 1.009-1.012) and extreme heat (RRs ranged: 1.024-1.028) on overall HBDs, but extreme cold had protective effects on HBDs. The adverse effect of UFPs had significant interactions with extreme cold and was higher in winter and fall. UFPs affected all HBD subtypes except kidney diseases, and extreme heat increased the risks of ischemic heart disease and kidney disease. There were disparities across demographics in exposures-HBDs associations although they were not statistically significant. Elevated UFP concentrations were associated with four clinical indicators (hospital stays, charges etc.).

We observe positive associations between elevated UFP concentrations or extreme heat and HBD hospitalizations, but negative associations with extreme cold. The UFPs' risks were higher in children and during cold seasons.

Little is known about the association between air pollution and self-perceived health (including both health-related quality of life [HRQoL] and self-rated health [SRH]). The aim of this study was therefore to explore whether long-term air pollution exposure is associated with worse self-perceived health, as measured by different tools.

We used a land-use regression model to determine the annual average levels of particulate matter with a diameter <10 μm (PM10), coarse particles (PMcoarse), fine particles (PM2.5), fine particle absorbances (PM2.5abs), particle number concentration (PNC), ozone (O3), nitrogen dioxide (NO2), and nitrogen oxide (NOX) for geocoded residential addresses (2014-2015). Questionnaires and face-to-face interviews were used to collect HRQoL (measured using the European Quality of Life 5 Dimensions [EQ-5D] index and the European Quality of Life Visual Analogue Scale [EQ-VAS]) and SRH indicators (measured through two survey questions) (2018-2019) from participants of the Cooperative Health Research in the Region of Augsburg (KORA)-Fit study in Germany. We explored associations via generalized additive models, multinomial logistic regression, and logistic regression.

We included 2610 participants with a mean age of 64.0 years in this cross-sectional study, of which 1428 (54.7%) were female. Each interquartile range (IQR) increase in O3 was associated with a reduced EQ-5D index value (% change of mean points and 95% confidence interval: -0.91% [-1.76; -0.06]). The average EQ-VAS score declined between -1.57% and -0.96% with each IQR increase in PM10, PMcoarse, PM2.5abs, PNC, NO2, and NOX. These pollutants were associated with increased occurrence of poor SRH, with odds ratios ranging from 1.24 to 2.67. PM2.5abs was linked to a higher likelihood of reporting a worse comparative SRH (2.59 [1.12; 5.99]). Body mass index and self-perceived stress modified these associations.

Long-term air pollution exposure was associated with poor self-perceived health, presenting as lower HRQoL and higher odds of poor SRH. Single-item indicators measuring self-perceived health status may work better than multi-dimensional indicators.

Particulate matter less than 2.5 microns in aerodynamic diameter (PM2.5) is a significant air pollutant known to adversely affect respiratory health and increase the incidence of chronic obstructive pulmonary disease (COPD). Furthermore, climate change exacerbates these impacts, as extreme temperatures and relative humidity (RH) levels can intensify the effects of PM2.5. This study aims to examine the joint effects of PM2.5, temperature, and RH on the risk of COPD.

A case-control study was conducted among 1,828 participants from 2017 to 2022 (995 COPD patients and 833 controls). The radial basis function interpolation was utilized to estimate participants' individual mean and differences in PM2.5, temperature, and RH in 1-day, 7-day, and 1-month periods. Logistic regression models examined the associations of environmental exposures with the risk of COPD adjusting for confounders. Joint effects of PM2.5 by quartiles of temperature and RH were also examined.

We observed that a 1 µg/m3 increase in PM2.5 7-day and 1-month mean was associated with a 1.05-fold and 1.06-fold increase in OR of COPD (p < 0.05). For temperature and RH, we observed U-shaped effects on OR for COPD with optimal temperatures identified as 21.2 °C, 23.8 °C, and 23.8 °C for 1-day, 7-day, and 1-month mean temperature, respectively, and optimal RH levels identified as 73.8%, 76.7%, and 75.4% for 1-day, 7-day, and 1-month mean RH, respectively (p < 0.05). The joint effect models show that high temperatures (> 23.5 °C) and both extremely low (69.3%) and high (80.9%) RH levels generally exacerbate the effects of PM2.5 on OR for COPD, especially over longer exposure durations.

The joint effects of PM2.5, temperature, and RH on the risk of COPD underscore the importance of air pollution control and comprehensive research to mitigate COPD risk in the context of climate change.

Sarcoidosis is a granulomatous disease with varying courses of disease progression. Environmental exposures are thought to be contributors to disease onset. Exposure to air pollutants such as fine particulate matter of 2.5 μm diameter or smaller (PM2.5) and nitrogen dioxide (NO2) have been identified as contributors to health disparities in lung diseases; little is known about these environmental exposures' associations with disease outcomes in sarcoidosis.

Is higher exposure to PM2.5 and NO2 associated with worse lung function in sarcoidosis?

We conducted a retrospective, cross-sectional study of individuals with pulmonary sarcoidosis seen from 2005 to 2015. Home addresses at the year of enrollment were geocoded, and exposure to PM2.5 and NO2 was modeled using high-resolution 1 km × 1 km annual surface exposure data during the year of enrollment. Racial and sex differences in exposure were determined. Multivariable linear regression models were used to examine the associations between PM2.5 and NO2 and the pulmonary function test measures FVC, FEV1, and diffusing capacity of the lungs for carbon monoxide (Dlco).

Among the 415 individuals in the analysis, Black individuals had significantly higher exposure to PM2.5 and NO2 compared with non-Hispanic White individuals, 12.2 μg/m3 (SD 2.4) vs 11 μg/m3 (SD 2.2) and 6.3 parts per billion (ppb) (SD 1.9) vs 5.0 ppb (SD 2.0), respectively. Every 1 μg/m3 higher exposure to PM2.5 was associated with 1.12% lower Dlco% predicted (95% CI, -1.83 to -0.41; P < .05). Every 1 ppb higher exposure to NO2 was associated with 1.04% lower Dlco% predicted (95% CI, -1.91 to -0.18; P < .05) in fully adjusted models. There were no significant associations between these pollutants and either FVC or FEV1% predicted.

Higher exposure to PM2.5 and NO2 was associated with worse Dlco% predicted. Black individuals with sarcoidosis were exposed to higher PM2.5 and NO2 than non-Hispanic White individuals. Air pollution exposure may be a contributor to reported health disparities in sarcoidosis.

Chronic Obstructive Pulmonary Disease (COPD) mortality rates and global warming have been in the focus of scientists and policymakers in the past decade. The long-term shifts in temperature and weather patterns, commonly referred to as climate change, is an important public health issue, especially with regard to COPD.

Using the most recent county-level age-adjusted COPD mortality rates among adults older than 25 years, this study aimed to investigate the spatial trajectory of COPD in the United States between 2001 and 2020. Global Moran's I was used to investigate spatial relationships utilising data from Terra satellite for night-time land surface temperatures (LSTnt), which served as an indicator of warming within the same time period across the United States. The forest-based classification and regression model (FCR) was applied to predict mortality rates.

It was found that COPD mortality over the 20-year period was spatially clustered in certain counties. Moran's I statistic (I=0.18) showed that the COPD mortality rates increased with LSTnt, with the strongest spatial association in the eastern and south-eastern counties. The FCR model was able to predict mortality rates based on LSTnt values in the study area with a R2 value of 0.68.

Policymakers in the United States could use the findings of this study to develop long-term spatial and health-related strategies to reduce the vulnerability to global warming of patients with acute respiratory symptoms.

This systematic review examines how extreme temperatures impact chronic obstructive pulmonary disease (COPD) morbidity and mortality, focusing on identifying vulnerable subpopulations.

We conducted a systematic literature search from January 1, 2000, to November 6, 2024, across databases like PubMed, MEDLINE and EMBASE, Web of Science, and Scopus, focusing on observational studies that quantitatively defined extreme temperatures and their impacts on COPD morbidity and mortality. Out of 3140 records, 25 studies met the inclusion criteria. We extracted data on study characteristics, effect estimates, and confounders, employing methods to assess the risk of bias and synthesize results.

We observed that extreme heat increased the relative risk (RR) for COPD morbimortality by 1.16-fold (95 % CI: 1.08-1.26; p < 0.05), and extreme cold increased the RR by 1.32-fold (95 % CI: 1.20-1.46;). Extreme heat was associated with a 1.19-fold (95 % CI: 1.09-1.30; p < 0.05) increase in COPD mortality. In contrast, extreme cold was associated with both COPD morbidity and mortality, with morbidity increasing by 1.47-fold (95 % CI: 1.26-1.71; p < 0.05) and mortality by 1.23-fold (95 % CI: 1.10-1.38; p < 0.05). Extreme heat poses a higher risk for female COPD patients compared to males. Moreover, extreme heat and cold were associated with morbimortality risk among older adults. Asian populations were sensitive to both temperature extremes, whereas Europeans were predominantly susceptible to extreme cold.

This variability in response to extreme temperatures affects COPD morbidity and mortality, emphasizing the need for tailored medical and emergency responses to effectively mitigate health risks during extreme weather events.

Ambient pollution and non-optimal temperature are major risk factors for respiratory health. However, the relationships between short-term exposure to these factors and bronchiectasis mortality remain unknown.

A nationwide, time-stratified case-crossover study across Mainland China was conducted from 2013 to 2019. Records of bronchiectasis deaths were extracted from the National Death Registration Reporting Information System. Daily concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), ozone (O3), and daily temperature were obtained from high-resolution prediction models. We utilized conditional logistic regression model and distributed lag nonlinear model to explore the associations of these exposures with bronchiectasis mortality.

We included a total of 19,320 bronchiectasis deaths. Air pollutant was associated with bronchiectasis mortality within the first 3 days after exposure and the exposure-response relationships were almost linear. An interquartile range increase in PM2.5, PM2.5-10, and O3 was associated with increments of 3.18%, 4.14%, and 4.36% in bronchiectasis mortality at lag 02 d, respectively. Additionally, lower temperature was associated with higher odds of bronchiectasis mortality. Compared to referent temperature (23.6 °C), the odds ratio for bronchiectasis mortality associated with extremely low temperature (P1: -13.4 °C) was 1.54 (95% CI: 1.05, 2.25).

This national study provides compelling evidence, and highlights the necessity and importance of reducing air pollution exposures and keeping warm for susceptible populations.

National Natural Science Foundation of China (81925001; 82330070); Innovation Program of Shanghai Municipal Education Commission (202101070007-E00097); Program of Shanghai Municipal Science and Technology Commission (21DZ2201800); Program of Shanghai Shenkang Development Center (SHDC12023110); and Major Project of National Health Commission of China.

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory condition characterized by persistent inflammation and oxidative stress, which ultimately leads to progressive restriction of airflow. Extensive research findings have cogently suggested that the dysregulation of essential transition metal ions, notably iron, copper, and zinc, stands as a critical nexus in the perpetuation of inflammatory processes and oxidative damage within the lungs of COPD patients. Unraveling the intricate interplay between metal homeostasis, oxidative stress, and inflammatory signaling is of paramount importance in unraveling the intricacies of COPD pathogenesis. This comprehensive review aims to examine the current literature on the sources, regulation, and mechanisms by which metal dyshomeostasis contributes to COPD progression. We specifically focus on iron, copper, and zinc, given their well-characterized roles in orchestrating cytokine production, immune cell function, antioxidant depletion, and matrix remodeling. Despite the limited number of clinical trials investigating metal modulation in COPD, the advent of emerging methodologies tailored to monitor metal fluxes and gauge responses to chelation and supplementation hold great promise in unlocking the potential of metal-based interventions. We conclude that targeted restoration of metal homeostasis represents a promising frontier for ameliorating pathological processes driving COPD progression.

To estimate the burden of chronic obstructive pulmonary disease (COPD) and lower respiratory tract infections (LRIs) stratified by geographic location, and social-demographic status for 21 regions across the world from 1990 to 2019.

The analysis utilized data from the Global Burden of Disease (GBD) Study, focusing on mortality and disability-adjusted life years (DALYs) as measures of COPD and LRI burden. Trend analyses using the Joinpoint model were conducted across five socio-demographic index (SDI) quintiles.

We investigated the burden of COPD and LRIs employing restricted cubic splines to flexibly identify relationships between DALY rates and SDI. This method allowed for detailed examination of trends over time across different regions and socio-demographic contexts.

From 1990 to 2019, the ASMR of COPD attributed to PM for global and five SDI quintiles decreased 61.80 %, 53.41 %, 63.04 %, 63.00 %, 40.98 %, 12.14 % respectively. In terms of PM Pollution, there was an inverted U-shaped association between the DALY and SDI for COPD, the DALY rate associated with LRIs due to PM pollution exhibited a progressive decline as SDI increased.

Even though the trend in mortality and DALY of COPD and LRIs decreased globally, the COPD and LRI burden attributed to PM pollution remains high, particularly in lower SDI quintiles.

The concurrence of chronic obstructive pulmonary disease (COPD) and lung cancer has been widely reported and extensively addressed by pulmonologists and oncologists. However, most studies have focused on shared risk factors, DNA damage pathways, immune microenvironments, inflammation, and imbalanced proteases/antiproteases. In the present review, we explore the association between COPD and lung cancer in terms of airway pluripotent cell fate determination and discuss the various cell types and signaling pathways involved in the maintenance of lung epithelium homeostasis and their involvement in the pathogenesis of co-occurring COPD and lung cancer.

Ambient air pollution is recognized as a major risk factor for chronic obstructive pulmonary disease (COPD) which is the third leading cause of death worldwide. We examined whether variations in daily outdoor air pollutants levels were associated with excess hospital emergency room visits (ERV) for acute exacerbation of COPD (AECOPD).

This two-center ecological cohort study was conducted in Amiens, France. We collected all consecutive ERV for AECOPD throughout 2017 and developed single pollutant models to assess the association between AECOPD and nitrogen dioxide (NO2), ozone (O3), or particulate matter (PM2.5 and PM10) levels, while adjusting for temperature, hygrometry, influenza circulation and pollen allergy risk. For a subgroup of patients, we also applied geographical modeling to analyze annual exposure to outdoor air pollutants.

We recorded 240 ERV among 168 COPD patients in 2017 and identified 9 peaks of ERV. There was a statistically significant positive correlation between the daily ERV for AECOPD and the daily average concentrations of PM2.5 (RR = 1.06 (95%CI = [1.00-1.11]), p = 0.049), but no correlation with NO2, O3 or PM10 (p = 0.073, p = 0.114 and p = 0.119, respectively). Our geographical modeling study revealed that long-term exposure to any of the four outdoor air pollutants was not associated with more frequent AECOPD.

Even though the pollution levels measured generally remained below or near the 2021 short-term air quality guidelines issued by the World Health Organization, significant aggregate-level associations were found between severe AECOPD leading to ERV and daily concentrations of PM2.5.

NCT03079661.

As a result of climate change, exposure to high temperatures is becoming more common, even in countries with temperate climates. For patients with chronic diseases, heat poses significant health risks. Empowering patients is a crucial element in protecting the population from the adverse effects of heat. In this context, self-reports of protective behavior are often used to gain a mutual understanding of patients' issues. However, the extent to which self-reported behavior is associated with health complaints remains unclear.

This study aims to describe the association between light to moderate heat and health complaints in everyday life, and to analyze whether self-reported protective behavior and related psychosocial factors are linked to these complaints.

We conducted a pilot cohort study using internet climate data merged with an online survey of patients with chronic diseases recruited through general practitioner practices. Patients were eligible if they were 18 years or older and had at least one chronic disease. The heat was modeled using temperature and humidity data. Health complaints were assessed through up to 7 follow-up evaluations on the hottest day of each week during the observation period. Data were analyzed using 3 nested models with mixed effects multivariable linear regression, adjusting for random effects at the climate measuring station and participant levels. Model 1 included heat exposure, sociodemographic data, and chronic diseases. Model 2 added protective behavior and health literacy, while model 3 incorporated self-efficacy and somatosensory amplification (ie, the tendency to catastrophize normal bodily sensations such as insect bites).

Of the 291 eligible patients, 61 (21.0%) participated in the study, providing 294 observations. On average, participants were 61 (SD 14) years old, and 31 (51%) were men. The most prevalent conditions were cardiovascular diseases (n=23, 38%) and diabetes mellitus (n=20, 33%). The most commonly reported symptoms were tiredness/fatigue (232/294 observations, 78.9%) and shortness of breath (142/294 observations, 48.3%). Compared with temperatures of 27°C or lower, a heat index between over 27°C and 32°C (β=1.02, 95% CI 0.08-1.96, P=.03) and over 32°C (β=1.35, 95% CI 0.35-2.35, P=.008) were associated with a higher symptom burden. Lower health literacy (β=-0.25, 95% CI -0.49 to -0.01, P=.04) and better self-reported protective behavior (β=0.65, 95% CI 0.29-1.00, P<.001) were also linked to increased symptom burden but lost statistical significance in model 3. Instead, lower self-efficacy (β=-0.39, 95% CI -0.54 to -0.23, P<.001) and higher somatosensory amplification (β=0.18, 95% CI 0.07-0.28, P=.001) were associated with a higher symptom burden.

Compared with colder weather, light and moderate heat were associated with more severe health complaints. Symptom burden was lower in participants with higher self-efficacy and less somatosensory amplification. Self-reported protective behavior was not linked to a lower symptom burden. Instead, we found that patients who tended to catastrophize normal bodily sensations reported both better protective behavior and a higher symptom burden simultaneously.

ClinicalTrials.gov NCT05961163; https://clinicaltrials.gov/ct2/show/NCT05961163.

Previous studies linked higher daily ambient air temperature and pollution with increased cardiorespiratory morbidity, but immediate effects of personal, hourly exposures on resting heart rate remained unclear. We followed 30 older former smokers with chronic obstructive pulmonary disease (COPD) in Massachusetts for four nonconsecutive 30-day periods over 12 months, collecting 54,487 hourly observations of personal air temperature, fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and resting heart rate. We explored the single lag effects (0-71 h) and cumulative effects (0-5 h, the significant lag windows) of air temperature and pollution on resting heart rate using generalized additive mixed models with distributed lag nonlinear models. Single lag effects of higher air temperature and pollutants on higher resting heart rate were most pronounced at lag 0 to 5 h. Cumulative effects of higher air temperature, PM2.5, O3, and NO2 (each interquartile range increment) on higher resting heart rate at lag 0-5 h, show differences of (beats per minute [bpm], 95% CI) 1.46 (1.31-1.62), 0.35 (0.32-0.39), 2.32 (2.19-2.45), and 1.79 (1.66-1.92), respectively. In conclusion, higher personal hourly air temperature, PM2.5, O3, and NO2 exposures at lag 0-5 h are associated with higher resting heart rate in COPD patients.

Rationale: It is unknown whether air pollution is associated with radiographic features of interstitial lung disease in individuals with chronic obstructive pulmonary disease (COPD). Objectives: To determine whether air pollution increases the prevalence of interstitial lung abnormalities (ILA) or percent high-attenuation areas (HAA) on computed tomography (CT) in individuals with a heavy smoking history and COPD. Methods: We performed a cross-sectional study of SPIROMICS (Subpopulations and Intermediate Outcome Measures in COPD Study), focused on current or former smokers with COPD. Ten-year exposure to particulate matter ⩽2.5 μm in aerodynamic diameter (PM2.5), nitrogen oxides (NOx), nitrogen dioxide (NO2), and ozone before enrollment CT (completed between 2010 and 2015) were estimated with validated spatiotemporal models at residential addresses. We applied adjusted multivariable modified Poisson regression and linear regression to investigate associations between pollution exposure and relative risk (RR) of ILA or increased percent HAA (between -600 and -250 Hounsfield units), respectively. We assessed for effect modification by MUC5B-promoter polymorphism (variant allele carriers GT or TT vs. GG at rs3705950), smoking status, sex, and percent emphysema. Results: Among 1,272 participants with COPD assessed for HAA, 424 were current smokers, and 249 were carriers of the variant MUC5B allele. A total of 519 participants were assessed for ILA. We found no association between pollution exposure and ILA or HAA. Associations between pollutant exposures and risk of ILA were modified by the presence of MUC5B polymorphism (P value interaction term for NOx = 0.04 and PM2.5 = 0.05) and smoking status (P value interaction term for NOx = 0.05; NO2 = 0.01; and ozone = 0.05). With higher exposure to NOx and PM2.5, MUC5B variant carriers had an increased risk of ILA (RR per 26 ppb NOx, 2.41; 95% confidence interval [CI], 0.97-6.0; and RR per 4 μg ⋅ m-3 PM2.5, 1.43; 95% CI, 0.93-2.2, respectively). With higher exposure to NO2, former smokers had an increased risk of ILA (RR per 10 ppb, 1.64; 95% CI, 1.0-2.7). Conclusions: Exposure to ambient air pollution was not associated with interstitial features on CT in this population of heavy smokers with COPD. MUC5B modified the association between pollution and ILA, suggesting that gene-environment interactions may influence prevalence of interstitial lung features in COPD.

Chronic obstructive pulmonary disease (COPD) and lung cancer represent formidable challenges in global health, characterized by intricate pathophysiological mechanisms and multifaceted disease progression. This comprehensive review integrates insights from diverse perspectives to elucidate the intricate roles of long non-coding RNAs (lncRNAs) in the pathogenesis of COPD and lung cancer, focusing on their diagnostic, prognostic, and therapeutic implications. In the context of COPD, dysregulated lncRNAs, such as NEAT1, TUG1, MALAT1, HOTAIR, and GAS5, emerge as pivotal regulators of genes involved in the disease pathogenesis and progression. Their identification, profiling, and correlation with the disease severity present promising avenues for prognostic and diagnostic applications, thereby shaping personalized disease interventions. These lncRNAs are also implicated in lung cancer, underscoring their multifaceted roles and therapeutic potential across both diseases. In the domain of lung cancer, lncRNAs play intricate modulatory roles in disease progression, offering avenues for innovative therapeutic approaches and prognostic indicators. LncRNA-mediated immune responses have been shown to drive lung cancer progression by modulating the tumor microenvironment, influencing immune cell infiltration, and altering cytokine production. Their dysregulation significantly contributes to tumor growth, metastasis, and chemo-resistance, thereby emphasizing their significance as therapeutic targets and prognostic markers. This review summarizes the transformative potential of lncRNA-based diagnostics and therapeutics for COPD and lung cancer, offering valuable insights into future research directions for clinical translation and therapeutic development.

Rationale: Exposure to particulate matter is associated with various adverse health outcomes. Ultrafine particles (UFPs; diameter <0.1 μm) are a unique public health challenge because of their size. However, limited studies have examined their impacts on human health, especially across seasons and demographic characteristics. Objectives: To evaluate the effect of UFP exposure on the risk of visiting the emergency department (ED) for a chronic lower respiratory disease (CLRD) in New York State in 2013-2018. Methods: We used a case-crossover design and conditional logistic regression to estimate how UFP exposure led to CLRD-related ED visits. GEOS-Chem Advanced Particle Microphysics, a state-of-the-art chemical transport model with a size-resolved particle microphysics model, generated air pollution simulation data. We then matched UFP exposure estimates to geocoded health records for asthma, bronchiectasis, chronic bronchitis, emphysema, unspecified bronchitis, and other chronic airway obstructions in New York State from 2013 through 2018. In addition, we assessed interactions with age, ethnicity, race, sex, meteorological factors, and season. Results: Each 1-(interquartile range [IQR]) increase in UFP exposure led to a 0.37% increased risk of a respiratory-related ED visit on lag 0-0, or the day of the ED visits, (95% confidence interval [CI], 0.23-0.52%) and a 1.81% increase on lag 0-6, or 6 days before the ED visit, (95% CI, 1.58-2.03%). The highest risk was in the emphysema subtype (lag 0-5, 4.18%; 95% CI, 0.16-8.37%), followed by asthma (lag 0-6, 2.00%), chronic bronchitis (lag 0-6, 1.78%), other chronic airway obstructions (lag 0-6, 1.60%), and unspecified bronchitis (lag 0-6, 1.49%). We also found significant interactions between UFP health impacts and season (Fall, 3.29%), temperature (<90th percentile, 2.27%), relative humidity (>90th percentile, 4.63%), age (children aged <18 yr, 3.19%), and sex (men, 2.06%) on lag 0-6. Conclusions: In this study, UFP exposure increased CLRD-related ED visits across all seasons and demographic characteristics, yet these associations varied according to various factors, which requires more research.

Few studies have compared the associations between long-term exposures to particulate matters (aerodynamic diameter ≤1, ≤2.5 and ≤10 µm: PM1, PM2.5 and PM10, respectively) and asthma and asthma-related respiratory symptoms. The objective of the present study was to compare the strength of the aforementioned associations in middle-aged and elderly adults.

We calculated the mean 722-day personal exposure estimates of PM1, PM2.5 and PM10 at 1 km×1 km spatial resolution between 2013 and 2019 at individual levels from China High Air Pollutants (CHAP) datasets. Using logistic regression models, we presented the associations as odds ratios and 95% confidence intervals, for each interquartile range (IQR) increase in PM1/PM2.5/PM10 concentration. Asthma denoted a self-reported history of physician-diagnosed asthma or wheezing in the preceding 12 months.

We included 7371 participants in COPD surveillance from Guangdong, China. Each IQR increase in PM1, PM2.5 and PM10 was associated with a greater odds (OR (95% CI)) of asthma (PM1: 1.22 (1.02-1.45); PM2.5: 1.24 (1.04-1.48); PM10: 1.30 (1.07-1.57)), wheeze (PM1: 1.27 (1.11-1.44); PM2.5: 1.30 (1.14-1.48); PM10: 1.34 (1.17-1.55)), persistent cough (PM1: 1.33 (1.06-1.66); PM2.5: 1.36 (1.09-1.71); PM10: 1.31 (1.02-1.68)) and dyspnoea (PM1: 2.10 (1.84-2.41); PM2.5: 2.17 (1.90-2.48); PM10: 2.29 (1.96-2.66)). Sensitivity analysis results were robust after excluding individuals with a family history of allergy. Associations of PM1, PM2.5 and PM10 with asthma and asthma-related respiratory symptoms were slightly stronger in males.

Long-term exposure to PM is associated with increased risks of asthma and asthma-related respiratory symptoms.

This study investigated the correlation between the individual chemical constituents of particulate matter 2.5 μm (PM2.5) and respiratory parameters as well as the living environment and daily behaviors in patients with chronic obstructive pulmonary disease (COPD). Data were obtained from prospective COPD panel conducted in South Korea. Following collection via a microPEM, 18 metallic elements were determined using energy-dispersive X-ray fluorescence spectroscopy. All participants completed detailed questionnaires on living environments and lifestyle practices. Eighty-nine stable COPD patients (mean age 68.1 years; 94.4% male) were analyzed. Several constituents (titanium, aluminum, bromine, and silicone) were significantly associated with respiratory outcomes. Copper and manganese concentrations were significantly associated with the living environment. Increased ventilation time and air purifier operation were associated with lower concentrations of copper, silicone, barium, and titanium. These findings suggest varying relationships between PM2.5 constituents and clinical parameters in COPD patients, providing a basis for personalized interventions and future research.

Little is known about the relationship between long-term joint exposure to mixtures of air pollutants and the prevalence of chronic obstructive pulmonary disease (COPD). We aimed to assess the joint impact of long-term exposure to ambient air pollution on the prevalence of COPD in Korea, especially in areas with high levels of air pollution.

We included 22,387 participants who underwent spirometry tests in 2010-2019. The community multiscale air quality model was used to estimate the levels of ambient air pollution at residential addresses. The average exposure over the 5 years before the examination date was used to calculate the concentrations of air pollution. Forced expiratory volume in 1 s and forced vital capacity were used to define restrictive lung disease, COPD, and moderate-to-severe COPD. Quantile-based g-computation models were used to assess the joint impact of air pollution on COPD prevalence.

A total of 2535 cases of restrictive lung disease, 2787 cases of COPD, and 1399 cases of moderate-to-severe COPD were identified. In the individual pollutant model, long-term exposure was significantly associated with both restrictive lung disease and COPD. In the mixture pollutant model, the odds ratios (ORs, 95% confidence intervals) for restrictive lung disease increased with each quartile increment in the 1- to 5-year average mixtures: 1.14 (1.02-1.28, 1 year), 1.25 (1.11-1.41, 2 years), 1.26 (1.11-1.42, 3 years), 1.32 (1.16-1.51, 4 years), and 1.37 (1.19-1.58, 5 years), respectively. The increase in ORs of restrictive lung disease accelerated over time. By contrast, the ORs of COPD showed a decreasing trend over time.

Long-term exposure to air pollutants, both individually and jointly, was associated with an increased risk of developing COPD, particularly restrictive lung disease. Our findings highlight the importance of comprehensively assessing exposure to various air pollutants in relation to COPD.

Environmental pollutants injure the mucociliary elevator, thereby provoking disease progression in chronic obstructive pulmonary disease (COPD). Epithelial resilience mechanisms to environmental nanoparticles in health and disease are poorly characterised.

We delineated the impact of prevalent pollutants such as carbon and zinc oxide nanoparticles, on cellular function and progeny in primary human bronchial epithelial cells (pHBECs) from end-stage COPD (COPD-IV, n=4), early disease (COPD-II, n=3) and pulmonary healthy individuals (n=4). After nanoparticle exposure of pHBECs at air-liquid interface, cell cultures were characterised by functional assays, transcriptome and protein analysis, complemented by single-cell analysis in serial samples of pHBEC cultures focusing on basal cell differentiation.

COPD-IV was characterised by a prosecretory phenotype (twofold increase in MUC5AC+) at the expense of the multiciliated epithelium (threefold reduction in Ac-Tub+), resulting in an increased resilience towards particle-induced cell damage (fivefold reduction in transepithelial electrical resistance), as exemplified by environmentally abundant doses of zinc oxide nanoparticles. Exposure of COPD-II cultures to cigarette smoke extract provoked the COPD-IV characteristic, prosecretory phenotype. Time-resolved single-cell transcriptomics revealed an underlying COPD-IV unique basal cell state characterised by a twofold increase in KRT5+ (P=0.018) and LAMB3+ (P=0.050) expression, as well as a significant activation of Wnt-specific (P=0.014) and Notch-specific (P=0.021) genes, especially in precursors of suprabasal and secretory cells.

We identified COPD stage-specific gene alterations in basal cells that affect the cellular composition of the bronchial elevator and may control disease-specific epithelial resilience mechanisms in response to environmental nanoparticles. The identified phenomena likely inform treatment and prevention strategies.

No prior studies have linked long-term air pollution exposure to incident sudden cardiac arrest (SCA) or its possible development trajectories. We aimed to investigate the association between long-term exposure to air pollution and SCA, as well as possible intermediate diseases. Based on the UK Biobank cohort, Cox proportional hazard model was applied to explore associations between air pollutants and SCA. Chronic obstructive pulmonary disease (COPD) and major adverse cardiovascular events (MACE) were selected as intermediate conditions, and multistate model was fitted for trajectory analysis. During a median follow-up of 13.7 years, 2884 participants developed SCA among 458 237 individuals. The hazard ratios (HRs) for SCA were 1.04-1.12 per interquartile range increment in concentrations of fine particulate matter, inhalable particulate matter, nitrogen dioxide, and nitrogen oxides. Most prominently, air pollutants could induce SCA through promoting transitions from baseline health to COPD (HRs: 1.06-1.24) and then to SCA (HRs: 1.16-1.27). Less importantly, SCA could be developed through transitions from baseline health to MACE (HRs: 1.02-1.07) and further to SCA (HRs: 1.12-1.16). This study provides novel and compelling evidence that long-term exposure to air pollution could promote the development of SCA, with COPD serving as a more important intermediate condition than MACE.

Previous studies have found associations between polymorphisms in some candidate genes and chronic obstructive pulmonary disease (COPD) risk. However, the association between TLR2 and TLR9 polymorphisms and COPD risk remains uncertain.

Four variants (rs352140, rs3804099, rs3804100, and rs5743705) of the TLR2 and TLR9 genes in 540 COPD patients and 507 healthy controls were genotyped using the Agena MassARRAY system. Odds ratio (OR) and 95% confidence interval (CI) were calculated to assess the association of TLR2 and TLR9 polymorphisms with COPD risk by logistic regression analysis.

TLR9-rs352140, TLR2-rs3804100, and TLR2-rs5743705 were related to a lower risk of COPD among Chinese people and the significance still existed after Bonferroni correction. Additionally, rs3804099, rs3804100, and rs352140 were found to be associated with COPD development in different subgroups (males, age ≤ 68 years, smokers, BMI < 24 kg/m2, and acute exacerbation).

Our findings indicated that TLR9 and TLR2 polymorphisms had protective effects on the development of COPD among Chinese people.

There is mounting evidence that climate change is having a significant influence on exacerbations of airway disease. We herein explore the physical factors of carbon dioxide, temperature increases, and humidity on intensifying allergen and fungal growth, and worsening air quality. The direct influence of these factors on promoting allergic rhinitis, chronic rhinosinusitis, and allergic fungal rhinosinusitis is reviewed.

Pollution and climate change constitute a combined, grave and pervasive threat to humans and to the life-support systems on which they depend. Evidence shows a strong association between pollution and climate change on cardiovascular and respiratory diseases, and pulmonary vascular disease (PVD) is no exception. An increasing number of studies has documented the impact of environmental pollution and extreme temperatures on pulmonary circulation and the right heart, on the severity and outcomes of patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension (PH), on the incidence of pulmonary embolism, and the prevalence and severity of diseases associated with PH. Furthermore, the downstream consequences of climate change impair health care systems' accessibility, which could pose unique obstacles in the case of PVD patients, who require a complex and sophisticated network of health interventions. Patients, caretakers and health care professionals should thus be included in the design of policies aimed at adaptation to and mitigation of current challenges, and prevention of further climate change. The purpose of this review is to summarize the available evidence concerning the impact of environmental pollution and climate change on the pulmonary circulation, and to propose measures at the individual, healthcare and community levels directed at protecting patients with PVD.

This study analyzed the burden of chronic obstructive pulmonary disease (COPD) in China, the United States, and India from 1990 to 2019 and projected the trends for the next decade.

This study utilized the GBD 2019 to compare the age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR), age-standardized disability-adjusted life years (DALYs) rate, and the proportion attributed to different risk factors in China, the United States, and India. Joinpoint models and autoregressive integrated moving average (ARIMA) models were employed to capture the changing trends in disease burden and forecast outcomes.

From 1990 to 2019, China's age-standardized COPD incidence and mortality rates decreased by 29% and 70%, respectively. In the same period, India's rates decreased by 8% and 33%, while the United States saw an increase of 9% in COPD incidence and a 22% rise in mortality rates. Smoking and ambient particulate matter pollution are the two most significant risk factors for COPD, while household air pollution from solid fuels and low temperatures are the least impactful factors in the United States and India, respectively. The proportion of risk from household air pollution from solid fuels is higher in India than in China and the United States. Predictions for 2030 suggest that the age-standardized DALY rates, ASIR, and ASMR in the United States and India are expected to remain stable or decrease, while China's age-standardized incidence rate is projected to rise.

Over the past three decades, the incidence of COPD has been decreasing in China and India, while showing a slight increase in the United States. Smoking and ambient particulate matter pollution are the primary risk factors for men and women, respectively. The risk of household air pollution from solid fuels in India needs attention.