Association between exposure to ambient particulate matter and chronic obstructive pulmonary disease: results from a cross-sectional study in China
TL;DR: Exposure to higher PM concentrations was strongly associated with increased COPD prevalence and declined respiratory function and the associations of COPD with PM10 were consistent with PM2.5 but slightly weaker.
Abstract: Objective The association between exposure to ambient particles with a median aerodynamic diameter less than 10/2.5 µm (particulate matter, PM 10 / 2.5 ) and COPD remains unclear. Our study objective was to examine the association between ambient PM 10 / 2.5 concentrations and lung functions in adults. Methods A cross-sectional study was conducted in southern China. Seven clusters were randomly selected from four cities across Guangdong province. Residents aged ≥20 years in the participating clusters were randomly recruited; all eligible participants were examined with a standardised questionnaire and spirometry. COPD was defined as a post-bronchodilator FEV 1 /FVC less than 70%. Atmosphere PM sampling was conducted across the clusters along with our survey. Results Of the subjects initially recruited, 84.4% (n=5993) were included for analysis. COPD prevalence and atmosphere PM concentration varied significantly among the seven clusters. COPD prevalence was significantly associated with elevated PM concentration levels: adjusted OR 2.416 (95% CI 1.417 to 4.118) for >35 and ≤75 µg/m 3 and 2.530 (1.280 to 5.001) for >75 µg/m 3 compared with the level of ≤35 µg/m 3 for PM 2.5 ; adjusted OR 2.442 (95% CI 1.449 to 4.117) for >50 and ≤150 µg/m 3 compared with the level of ≤50 µg/m 3 for PM 1 . A 10 µg/m 3 increase in PM 2.5 concentrations was associated with a 26 mL (95% CI −43 to −9) decrease in FEV 1 , a 28 mL (−49 to −8) decrease in FVC and a 0.09% decrease (−0.170 to −0.010) in FEV 1 /FVC ratio. The associations of COPD with PM 10 were consistent with PM 2.5 but slightly weaker. Conclusions Exposure to higher PM concentrations was strongly associated with increased COPD prevalence and declined respiratory function. Trial registration number ChiCTR-OO-14004264; Post-results.
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Xi'an Jiaotong University1, Huazhong University of Science and Technology2, Fudan University3, China Medical University (PRC)4, Guangzhou Medical University5, Zhejiang University6, Sichuan University7, Capital Medical University8, Peking University9, Peking Union Medical College10, China-Japan Friendship Hospital11, Beijing Jishuitan Hospital12, Tulane University13
TL;DR: Prevalence of spirometry-defined COPD is highly prevalent in the Chinese adult population and prevention and early detection of COPD using spirometry should be a public health priority in China to reduce COPD-related morbidity and mortality.
811 citations
TL;DR: PM exposure enhanced the airway inflammatory response significantly through ROS-mediated activation of MAPK (ERK, JNK, p38 MAPK) and downstream NF-κB signaling pathways and appeared to be the key regulator for PM-induced lung inflammation.
Abstract: Background: Particulate matter (PM) is a high risk factor for various respiratory diseases and triggers an inflammatory response in lung tissues. However, the molecular mechanism of the PM-induced inflammatory response is incompletely understood. Methods: Human bronchial epithelial cells (HBECs) were treated with the urban PM 1649b for assessment of the inflammatory response. The intracellular level of reactive oxygen species (ROS) was measured by flow cytometry. PM-activated signaling pathways were addressed with specific inhibitors. In vivo, the C57 mice model of PM-induced acute lung inflammation was established with intratracheal instillation of PM for 2 consecutive days. The oxidant stress in lung tissues was assessed with dihydroethidium (DHE) staining, and malondialdehyde (MDA) activity and hydrogen peroxide (H2O2) assays. The histopathologic changes in lung tissues and number of inflammatory cells in bronchoalveolar lavage fluid (BALF) were examined. Expression of pro-inflammatory cytokines in BALF was measured by ELISA. Results: PM increased the expression of interleukin (IL)-1β, IL-6, IL-8, matrix metalloproteinase (MMP)- 9 and cyclooxygenase (COX)-2 in a dose-dependent manner. ROS generation and activation of MAPK (ERK, JNK, p38 MAPK) and NF-κB pathways were detected in PM-exposed HBECs. Pretreatment with N-acetylcysteine (NAC) led to the inflammatory response, ROS level and activation of the MAPK and NF-κB pathways to be attenuated. Blockade of ERK, JNK or p38 MAPK pathway with specific inhibitor prevented the release of pro-inflammatory cytokines and activation of the NF-κB pathway. Inhibition of the NF-κB pathway reduced the expression of pro-inflammatory cytokines. In vivo, PM exposure increased oxidant stress in lung tissues, infiltration of inflammatory cells around PM in lung tissues, the number of total cells and inflammatory cells in BALF, and the concentrations of IL-1β, IL-6, IL-8 and MMP-9 in BALF, all of which were reversed partially upon NAC treatment. Conclusions: PM exposure enhanced the airway inflammatory response significantly through ROSmediated activation of MAPK (ERK, JNK, p38 MAPK) and downstream NF-κB signaling pathways. Oxidative stress appeared to be the key regulator for PM-induced lung inflammation. These results suggested the molecular mechanism of lung inflammation caused by PM.
143 citations
Cites background from "Association between exposure to amb..."
...Epidemiologic data have shown that PM exposure has a high correlation with bronchial asthma (3), chronic obstructive pulmonary disease (4,5), lung cancer (6), atherosclerosis (7), ischemic stroke (8), congestive heart failure (9), myocardial ischemia (10) and birth defects (11)....
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TL;DR: The recent literature supports the contention that air pollution might contribute to transmission of epimutations from gametes to zygotes by involving mitochondrial DNA, parental allele imprinting, histone withholding and non-coding RNAs, and larger prospective studies using innovative, integrated epigenome-wide metabolomic strategy are highly warranted.
90 citations
TL;DR: It is demonstrated that altered gut microbiota in COPD patients is associated with disease progression in mice model and was characterized by a distinct overall microbial diversity and composition, a Prevotella-dominated gut enterotype and lower levels of short-chain fatty acids.
Abstract: Dysbiosis of the gut microbiome is involved in the pathogenesis of various diseases, but the contribution of gut microbes to the progression of chronic obstructive pulmonary disease (COPD) is still poorly understood. We carried out 16S rRNA gene sequencing and short-chain fatty acid analyses in stool samples from a cohort of 73 healthy controls, 67 patients with COPD of GOLD stages I and II severity, and 32 patients with COPD of GOLD stages III and IV severity. Fecal microbiota from the three groups were then inoculated into recipient mice for a total of 14 times in 28 days to induce pulmonary changes. Furthermore, fecal microbiota from the three groups were inoculated into mice exposed to smoke from biomass fuel to induce COPD-like changes. We observed that the gut microbiome of COPD patients varied from that of healthy controls and was characterized by a distinct overall microbial diversity and composition, a Prevotella-dominated gut enterotype and lower levels of short-chain fatty acids. After 28 days of fecal transplantation from COPD patients, recipient mice exhibited elevated lung inflammation. Moreover, when mice were under both fecal transplantation and biomass fuel smoke exposure for a total of 20 weeks, accelerated declines in lung function, severe emphysematous changes, airway remodeling and mucus hypersecretion were observed. These data demonstrate that altered gut microbiota in COPD patients is associated with disease progression in mice model.
73 citations
TL;DR: Accumulating evidence supporting the role of immune dysfunction, the lung microbiome, extracellular vesicles and underlying genetic susceptibility in the development of COPD and lung cancer, and epigenetic factors, involving DNA methylation and microRNA expression, have been implicated in both diseases.
Abstract: Chronic obstructive pulmonary disease (COPD) and lung cancer comprise the leading causes of lung disease-related mortality worldwide. Exposure to tobacco smoke is a mutual aetiology underlying the two diseases, accounting for almost 90% of cases. There is accumulating evidence supporting the role of immune dysfunction, the lung microbiome, extracellular vesicles and underlying genetic susceptibility in the development of COPD and lung cancer. Further, epigenetic factors, involving DNA methylation and microRNA expression, have been implicated in both diseases. Chronic inflammation is a key feature of COPD and could be a potential driver of lung cancer development. Using next generation technologies, further studies investigating the genomics, epigenetics and gene-environment interaction in key molecular pathways will continue to elucidate the pathogenic mechanisms underlying the development of COPD and lung cancer, and contribute to the development of novel diagnostic and prognostic tools for early intervention and personalised therapeutic strategies.
70 citations
Cites background from "Association between exposure to amb..."
...revealed a strong association between COPD prevalence and urban particulate matter (27)....
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References
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University of Manchester1, University of Barcelona2, St George's Hospital3, University of Marburg4, University of Texas Health Science Center at San Antonio5, Imperial College London6, University of Modena and Reggio Emilia7, University of Michigan8, Hokkaido University9, University of British Columbia10
TL;DR: It is recommended that spirometry is required for the clinical diagnosis of COPD to avoid misdiagnosis and to ensure proper evaluation of severity of airflow limitation.
Abstract: Chronic obstructive pulmonary disease (COPD) remains a major public health problem. It is the fourth leading cause of chronic morbidity and mortality in the United States, and is projected to rank fifth in 2020 in burden of disease worldwide, according to a study published by the World Bank/World Health Organization. Yet, COPD remains relatively unknown or ignored by the public as well as public health and government officials. In 1998, in an effort to bring more attention to COPD, its management, and its prevention, a committed group of scientists encouraged the U.S. National Heart, Lung, and Blood Institute and the World Health Organization to form the Global Initiative for Chronic Obstructive Lung Disease (GOLD). Among the important objectives of GOLD are to increase awareness of COPD and to help the millions of people who suffer from this disease and die prematurely of it or its complications. The first step in the GOLD program was to prepare a consensus report, Global Strategy for the Diagnosis, Management, and Prevention of COPD, published in 2001. The present, newly revised document follows the same format as the original consensus report, but has been updated to reflect the many publications on COPD that have appeared. GOLD national leaders, a network of international experts, have initiated investigations of the causes and prevalence of COPD in their countries, and developed innovative approaches for the dissemination and implementation of COPD management guidelines. We appreciate the enormous amount of work the GOLD national leaders have done on behalf of their patients with COPD. Despite the achievements in the 5 years since the GOLD report was originally published, considerable additional work is ahead of us if we are to control this major public health problem. The GOLD initiative will continue to bring COPD to the attention of governments, public health officials, health care workers, and the general public, but a concerted effort by all involved in health care will be necessary.
17,023 citations
TL;DR: This research presents a novel and scalable approach called “Standardation of LUNG FUNCTION TESTing” that combines “situational awareness” and “machine learning” to solve the challenge of integrating nanofiltration into the energy system.
Abstract: [⇓][1]
SERIES “ATS/ERS TASK FORCE: STANDARDISATION OF LUNG FUNCTION TESTING”
Edited by V. Brusasco, R. Crapo and G. Viegi
Number 2 in this Series
[1]: #F13
13,426 citations
TL;DR: A reduction in exposure to ambient fine-particulate air pollution contributed to significant and measurable improvements in life expectancy in the United States during the 1980s and 1990s.
Abstract: Background Exposure to fine-particulate air pollution has been associated with increased morbidity and mortality, suggesting that sustained reductions in pollution exposure should result in improved life expectancy. This study directly evaluated the changes in life expectancy associated with differential changes in fine particulate air pollution that occurred in the United States during the 1980s and 1990s. Methods We compiled data on life expectancy, socioeconomic status, and demographic characteristics for 211 county units in the 51 U.S. metropolitan areas with matching data on fine-particulate air pollution for the late 1970s and early 1980s and the late 1990s and early 2000s. Regression models were used to estimate the association between reductions in pollution and changes in life expectancy, with adjustment for changes in socioeconomic and demographic variables and in proxy indicators for the prevalence of cigarette smoking. Results A decrease of 10 μg per cubic meter in the concentration of fine particulate matter was associated with an estimated increase in mean (±SE) life expectancy of 0.61±0.20 year (P = 0.004). The estimated effect of reduced exposure to pollution on life expectancy was not highly sensitive to adjustment for changes in socioeconomic, demographic, or proxy variables for the prevalence of smoking or to the restriction of observations to relatively large counties. Reductions in air pollution accounted for as much as 15% of the overall increase in life expectancy in the study areas. Conclusions A reduction in exposure to ambient fine-particulate air pollution contributed to significant and measurable improvements in life expectancy in the United States.
1,874 citations
TL;DR: The evidence for the association of COPD with biomass fuel, occupational exposure to dusts and gases, history of pulmonary tuberculosis, chronic asthma, respiratory-tract infections during childhood, outdoor air pollution, and poor socioeconomic status is reviewed.
1,055 citations