Aim: To date, PM2.5-associated vascular damage in metabolic abnormalities has remained controversial. We knew little about the vascular damage of PM2.5 constituents. Thus, this study aimed to investigate the relationship between long-term exposure to PM2.5 and its constituents and vascular damage in metabolic abnormalities.
Methods: A total of 124,387 participants with metabolic abnormalities (defined as at least one metabolic disorder, such as obesity, elevated blood pressure, elevated triglyceride level, elevated fasting glucose level, or low HDL cholesterol level) were recruited in this study from 11 representative centers in China between January 2011 and December 2017. PM2.5 and its constituents (black carbon [BC], organic matter [OM], sulfate [SO4 2− ], nitrate [NO3 − ], and ammonium salts [NH4 + ]) were extracted. Elevated brachial-ankle pulse wave velocity (baPWV) (≥ 1,400 cm/s) and declined ankle-brachial index (ABI) (<0.9) indicated vascular damage. Multivariable logistic regression and Quantile g-Computation models were utilized to explore the impact on outcomes.Results: Of the 124,387 participants (median age, 49 years), 87,870 (70.64%) were men. One-year lag exposure to PM2.5 and its constituents was significantly associated with vascular damage in single pollutant models. The adjusted odds ratios (OR) for each 1-μg/m 3 increase in PM2.5 was 1.013 (95% CI, 1.012-1.015) and 1.031 (95% CI, 1.025-1.037) for elevated baPWV and decreased ABI, respectively. PM2.5 constituents were also associated with vascular damage in multi-pollutant models. Among the PM2.5 constituents, BC (47.17%), SO4 2− (33.59%), and NH4 + (19.23%) have the highest contribution to elevated baPWV and NO3 − (47.89%) and BC (23.50%) to declined ABI.
Conclusion:Chronic exposure to PM2.5 and PM2.5 constituents was related to vascular damage in the abnormal metabolic population in China. The heterogeneous contribution of different PM2.5 constituents to vessel bed damage is worthy of attention when developing targeted strategies.
Background Since December 2019, COVID-19 has emerged in Wuhan, China and spread globally. As of now, there is still no explicit therapeutic regimen and the use of corticosteroid is also controversial. We aimed to explore the effectiveness of corticosteroid and provide evidence for the rational use of corticosteroid in different patients with COVID-19.Methods In this multi-centered, retrospective study, we extracted the clinical data of 649 cases with COVID-19 with definite outcome (discharged or dead) from 14 hospitals in Hubei province, and evaluated the clinical characteristics, treatment regimens, and their association with outcomes.Results Ninety-five of 649 patients had died. Older male patients with comorbidities had an increased risk of death and more obvious abnormalities in clinical indicators. Corticosteroid, γ-globulin treatment and invasive ventilation were more frequently used in non-survivors. Survivors with corticosteroid treatment had a prolonged hospitalization. The median time duration for temperature restore for non-survivors after corticosteroid treatment was longer than that of both survivors. The lymphocyte count on admission was lower in the patients treated with corticosteroids compared to those without corticosteroid treatment. Lymphocyte count recovered significantly after corticosteroid treatment in survivors, but not in non-survivors.Conclusions The responses to corticosteroid treatment were different in COVID-19 patients with different outcomes. The surviving patients with relatively lower lymphocyte count were more likely to be given corticosteroids. For non-survivors, the lymphocyte count was too low and the effect of corticosteroids was poor. Survivors under corticosteroid treatment had a prolonged hospitalization, but had a recovery of lymphocytes. The recovery of lymphocyte count and temperature after corticosteroid treatment may be used as predictors of prognosis of patients with COVID-19.
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