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Few researches have been investigated on the effects of ambient air pollutants from coal combustion on acute exacerbation of chronic obstructive pulmonary disease (AECOPD) hospitalizations. The whole time series was split into heating season and non-heating season. We used a quasi-Poisson generalized linear regression model combined with distributed lag non-linear models (DLNMs) to estimate the relative cumulative risk and calculate the air pollutant hospitalization burden of AECOPD for lag 0-7 days in heating season and non-heating season. There were higher PM2.5, PM10, NO2, SO2, and CO concentrations in heating seasons than non-heating season in Shijiazhuang; however, O3 was higher in non-heating season than heating season. The AECOPD-associated relative cumulative risks for PM2.5, PM10, NO2, and SO2 for lag 0-7 days were significantly positively associated with hospitalization in heating and non-heating season; we found that the cumulative relative risk of NO2 was the greatest in every 1 unit of air pollutants during the heating season and the cumulative relative risk of SO2 was the greatest during the non-heating season. The results showed that 17.8%, 12.9%, 1.7%, 16.7%, and 10.5% of AECOPD hospitalizations could be attributable to PM2.5, PM10, SO2, NO2, and CO exposure in heating season, respectively. However, the results showed that 19.5%, 22.4%, 15%, 8.3%, and 10.4% of AECOPD hospitalizations could be attributable to PM2.5, PM10, SO2, NO2, and O3 exposure in non-heating season, respectively. The attributable burden of AECOPD hospitalization in heating season and non-heating season are different. PM2.5, PM10, NO2, and CO are the main factors of heating season, while PM10, PM2.5, SO2, and O3 are the main factors of non-heating season. In conclusions, the centralized heating can change the influence of attributable risk. When government departments formulate interventions to reduce the risk of acute hospitalization of chronic obstructive pulmonary disease (COPD), the influence of heating on disease burden should be considered.

Few studies have investigated the acute exacerbations of chronic obstructive pulmonary disease (AECOPD)-associated attributable burden under exposure to high levels of air pollution among Asians. Data on hospitalization for AECOPD, air pollution and meteorological factors from 1 January 2013 to 31 December 2016 were collected in Shijiazhuang, China. We used a Poisson generalized linear regression model combined with a distributed lag nonlinear model (DLNM) to evaluate the relative cumulative risk for a lag of 0–7 days and examined the potential effect modifications by age and sex via stratification analyses, controlling for long-term trends, seasonal patterns, meteorological factors, and other possible confounders. Then, we computed hospitalization percentages attributable to air pollutants. The AECOPD-associated relative cumulative risks for PM2.5, PM10, NO2, SO2, and CO for a lag of 0–7 days were significantly positively correlated with hospitalization. The associations were stronger in females and retired patients. The NO2 Cum RR of AECOPD admission was the greatest. A 10μg/m3 increase in daily NO2 concentration was associated with 6.7% and 5.7% increases in COPD hospitalizations in the retired and female groups, respectively. The results showed that 13%, 9.4%, 1.7%, 9.7%, and 8.8% of AECOPD hospitalizations were attributable to exposure to PM2.5, PM10, SO2, NO2, and CO, respectively. If the air pollutant concentration was reduced to the 24-h average grade II levels of NAAQS of China, the AECOPD attributable percentage for PM2.5 and PM10 would decrease by 80%. The air pollutants PM2.5, PM10, SO2, NO2, and CO were significantly relevant to AECOPD-associated hospitalization. The associations differed by individual characteristics. The retired and female populations were highly vulnerable.

Background Acute lower respiratory infections (ALRIs) have a high mortality rate. We aimed to apply a platform that rapidly detects 36 microorganisms and 49 antibiotic resistance markers in the clinical diagnosis of ALRI and drug resistance prediction. Methods Multicenter collection of clinical samples from patients with ALRIs was carried out from 2017 to 2018. Sputum culture (SC) was performed, which provided two outcomes: the detected pathogens and the resistance to different antibiotics. Additionally, each sputum sample was used to extract deoxyribonucleic acids (DNAs) followed by high-throughput sequencing. Results Eleven commonly observed pathogens were surveyed, and for all samples with positive SC results (137 cases), the overall coverage was 95.62% according to the sequencing results. The receiver operating characteristic (ROC) curve was drawn, and cutoff reads of the most frequently detected pathogens were acquired. Overall, sequencing exhibited significantly higher sensitivity in the detection of pathogens compared with the traditional SC method, with a generally satisfactory specificity. Furthermore, we investigated the correlation between antibiotic resistance gene phenotypes and the actual outcomes of the drug sensitivity test, and some significant correlations were found, especially for the resistance to Amikacin in the presence of blaOXA7. Conclusions Sequencing-based sputum metagenomics can reveal a profile of the lung pathogen microbiome. The sequencing method offers both sufficient accuracy and significantly higher sensitivity in the detection of pathogens, and can be at least a complementary approach to traditional SC reporting. The sequencing technique also revealed some novel potential correlations between the presence of different pathogens, as well as new antimicrobial-resistant genes.

Background Previous studies have found associations between asthma morbidity and air pollution especially in young population, (PLoS One 12:e0180522, 2017; Can J Public Health 103:4-8, 2012; Environ Health Perspect 118:449-57, 2010; Am J Respir Crit Care Med 182:307-16, 2010; J Allergy Clin Immunol 104:717-22, 2008; J Allergy Clin Immunol 104:717-22, 1999; Environ Res 111:1137-47, 2011) but most of them were conducted in areas with relatively low air pollutant level. Moreover, very few studies have investigated the effect and burden modification of heating season during which the ambient air pollution level is significantly different from that during non-heating season in north China. Objectives This study aimed to evaluate the effect and burden modification of heating on short-term associations between adult asthma hospitalizations and ambient air pollution in the north China city of Shijiazhuang. Methods Generalized additive models combined with penalized distributed lag nonlinear models were used to model associations between daily asthma hospitalizations and ambient air pollutants from 1 January 2013 to 16 December 2016 in Shijiazhuang city, adjusting for long-term and seasonality trend, day of week, statutory holiday, daily mean air pressure and temperature. Attributable risks were calculated to evaluate the burden of asthma hospitalizations due to air pollutants exposure. The effect of pollutants on hospitalization and the attributable measures were estimated in heating and non-heating season separately and the comparisons between the two seasons were conducted. Results All pollutants demonstrated positive and significant impacts on asthma hospitalizations both in heating season and non-heating season, except for O3 in heating season where a negative association was observed. However, the differences of the pollutant-specific effects between the two seasons were not significant. SO2 and NO2 exposure were associated with the heaviest burden among all pollutants in heating season; meanwhile, PM10 and PM2.5 were associated with the heaviest burden in heating season. Conclusions In conclusion, we found evidence of the effect of ambient air pollutants on asthma hospitalizations in Shijiazhuang. The central heating period could modify the effects in terms of attributable risks. The disease burden modification of heating should be taken into consideration when planning intervention measures to reduce the risk of asthma hospitalization.

Background Ambient fine particulate matter (PM2.5) could induce lung injury. Aryl hydrocarbon receptor (AhR) is involved in the molecular mechanisms of prooxidative and pro-inflammatory effect of PM2.5. Molecular hydrogen has antioxidant properties. The protective effect and mechanism of hydrogen on PM2.5-induced lung injury remain unclear. Objectives This study aimed to determine whether hydrogen could alleviate lung injury in a rat model of subacute exposure to concentrated ambient PM2.5, and explore the mechanism related to AhR. Methods Male Wastar rats were exposed to either concentrated ambient particles (CAPs) (diameter: ≤2.5 μm, average concentration: 1328 ± 730 μg/m3) or filtered air (FA) by nose-only inhalation (5 h/day, 5 days/week for 4 weeks). Hydrogen-treated rats inhaled 66.7% hydrogen from water electrolysis for 2 h after each exposure to CAPs or FA. Results CAPs inhalation induced lung injury, as demonstrated by pulmonary function decrease, histopathological damage, mucus hypersecretion [Periodic acid-Schiff (PAS) staining for mucins, immunohistochemistry and quantitative real-time PCR (RT-qPCR) for mucin 5AC (MUC5AC) expression], increased pro-inflammatory cytokines (TNF-α, IL-8 and IL-1β) and oxidative damage indexes [malondialdehyde (MDA) and 8-isoprostane F2α (8-iso-PG)]. While, hydrogen inhalation significantly alleviated the damages mentioned above. In addition, low expression of AhR in lung tissues determined by Western Blot was found after CAPs exposure, whereas hydrogen inhibited AhR decline induced by CAPs. Conclusions High concentrations of hydrogen could ameliorate pulmonary dysfunction, airway mucus hypersecretion, oxidation damage, and inflammation response in rats exposed to concentrated ambient PM2.5. Additionally, hydrogen alleviates lung injury induced by PM2.5 possibly through AhR-dependent mechanisms.