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171.
Chen Chen John Wang Jeff Kwong JinHee Kim Aaron van Donkelaar Randall V. Martin Perry Hystad Yushan Su Eric Lavigne Megan Kirby-McGregor Jay S. Kaufman Tarik Benmarhnia Hong Chen 《CMAJ》2022,194(20):E693
Background:The tremendous global health burden related to COVID-19 means that identifying determinants of COVID-19 severity is important for prevention and intervention. We aimed to explore long-term exposure to ambient air pollution as a potential contributor to COVID-19 severity, given its known impact on the respiratory system.Methods:We used a cohort of all people with confirmed SARS-CoV-2 infection, aged 20 years and older and not residing in a long-term care facility in Ontario, Canada, during 2020. We evaluated the association between long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ground-level ozone (O3), and risk of COVID-19-related hospital admission, intensive care unit (ICU) admission and death. We ascertained individuals’ long-term exposures to each air pollutant based on their residence from 2015 to 2019. We used logistic regression and adjusted for confounders and selection bias using various individual and contextual covariates obtained through data linkage.Results:Among the 151 105 people with confirmed SARS-CoV-2 infection in Ontario in 2020, we observed 8630 hospital admissions, 1912 ICU admissions and 2137 deaths related to COVID-19. For each interquartile range increase in exposure to PM2.5 (1.70 μg/m3), we estimated odds ratios of 1.06 (95% confidence interval [CI] 1.01–1.12), 1.09 (95% CI 0.98–1.21) and 1.00 (95% CI 0.90–1.11) for hospital admission, ICU admission and death, respectively. Estimates were smaller for NO2. We also estimated odds ratios of 1.15 (95% CI 1.06–1.23), 1.30 (95% CI 1.12–1.50) and 1.18 (95% CI 1.02–1.36) per interquartile range increase of 5.14 ppb in O3 for hospital admission, ICU admission and death, respectively.Interpretation:Chronic exposure to air pollution may contribute to severe outcomes after SARS-CoV-2 infection, particularly exposure to O3.By November 2021, COVID-19 had caused more than 5 million deaths globally1 and more than 29 400 in Canada.2 The clinical manifestations of SARS-CoV-2 infection range from being asymptomatic to multiple organ failure and death. Identifying risk factors for COVID-19 severity is important to better understand etiological mechanisms and identify populations to prioritize for screening, vaccination and medical treatment. Risk factors for severity of COVID-19 include male sex, older age, pre-existing medical conditions and being from racialized communities.3–5 More recently, ambient air pollution has been implicated as a potential driver of COVID-19 severity.6–10Long-term exposure to ambient air pollution, a major contributor to global disease burden,11 could increase the risk of severe COVID-19 outcomes by several mechanisms. Air pollutants can reduce individuals’ pulmonary immune responses and antimicrobial activities, boosting viral loads.8 Air pollution can also induce chronic inflammation and overexpression of the alveolar angiotensin-converting enzyme 2 (ACE) receptor,7 the key receptor that facilitates SARS-CoV-2 entry into cells.12,13 Exposure to air pollution contributes to chronic conditions, such as cardiovascular disease, that are associated with unfavourable COVID-19 prognosis, possibly owing to persistent immune activation and excessive amplification of cytokine development.10 Thus, greater exposure to long-term air pollution may lead to severe COVID-19 outcomes.Reports exist of positive associations between long-term exposure to particulate matter with diameters equal to or smaller than 2.5 or 10 μm (PM2.5 and PM10), ground-level ozone (O3) and nitrogen dioxide (NO2), and metrics of COVID-19 severity (e.g., mortality and case fatality rate).8–10 However, most studies to date have used ecological and cross-sectional designs, owing to limited access to individual data, which leads to ambiguity in interpreting the results, thus hindering their influence on policy. 6,14 Ecological designs do not allow for disentangling the relative impacts of air pollution on individual susceptibility to infection and disease severity.14 Residual confounding by factors such as population mobility and social interactions is also problematic. Therefore, a cohort study with data on individuals with SARS-CoV-2 is a more appropriate design.6,14 Studies that have used individual data were conducted in specific subpopulations15,16 or populations with few severe cases,17 or had limited data on individual exposure to air pollutants.18 In Canada, 1 ecological study found a positive association between long-term exposure to PM2.5 and COVID-19 incidence,19 but no published study has explored the association between air pollution and COVID-19 severity.We aimed to examine the associations between long-term exposure to 3 common air pollutants (PM2.5, NO2 and O3) and key indicators of COVID-19 severity, including hospital admission, intensive care unit (ICU) admission and death, using a large prospective cohort of people with confirmed SARS-CoV-2 infection in Ontario, Canada, in 2020. The air contaminants PM2.5, NO2 and O3 are regularly monitored by the Canadian government, and are key pollutants that are considered when setting air-quality policies. They originate from varying sources (NO2 is primarily emitted during combustion of fuel, O3 is primarily formed in air by chemical reactions of nitrogen oxides and volatile organic compounds, and PM2.5 can be emitted during combustion or formed by reactions of chemicals like sulphur dioxide and nitrogen oxides in air) and they may affect human health differently.20,21,22 相似文献
172.
利用化工厂污泥废水中分离到的一株耐酸脱硫弧菌(Desulfovibrio SRB7),对不同pH,温度、碳源、菌废比等条件下SRB7还原Cr(VI)能力进行研究.并从H2S还原途径、电子传递途径以及胞外聚合物(EPS)吸附途径研究SRB7菌体整体去除Cr(VI)的特性.结果表明:当Cr(VI)起始浓度为50 mg/L时,pH 7.5,培养温度36℃,碳源为乳酸钠,混合菌液和Cr(VI)溶液的菌废比为1:5(V/V)能获得很好的还原效果.在SRB7去除Cr(VI)的特性中,吸附途径对Cr(VI)的去除几乎不起作用;电子传递途径在Cr(VI)的还原过程中不占优势,24 h去除率为51.42%;而H2S途径在Cr(VI)的还原过程中占主导地位,24 h去除率为78.02%. 相似文献
173.
174.
应用Pichia pastoris酵母表达了犬冠状病毒大熊猫野毒株(CCV DXMV)S蛋白主要抗原区基因片断。用特异性引物扩增出CCV DXMV株S1基因片断,并将其克隆到pGEM-T载体中得到pTS1。用KpnI和Notl双酶切pTS1回收目的基因S1定向克隆到pPICZCαA中,构建出重组质粒pPICZCαAS1。将pPICZCαASl用SacI内切酶线性化后,电转化感受态GS115酵母细胞,用PCR法筛选阳性重组子。用1%的甲醇诱导重组酵母菌,取培养物上清进行重组蛋白的检测。结果重组酵母菌培养物上清用SDS-PAGE电泳可检测到相对分子量为106kDa大小的重组蛋白,Westem-blot证实该重组蛋白可以与CCV多克隆抗体发生特异性血清学反应。凝胶薄层扫描分析表明,3株重组酵母菌在1%甲醇诱导144h后,重组蛋白S1表达量约占培养物上清总蛋白量的6.6-8.6%左右。用重组蛋白S1免疫BALB/C小鼠3次后,小鼠血清CCV中和抗体可达1:8-1:16,表明重组S1蛋白具有一定的免疫原性。 相似文献
175.
采伐是调整林分结构的重要手段。不同林层的树木对采伐强度有着不同的响应方式。但以往考察采伐对树木生长的影响时多采用定性或简单定量的方法(如按树高等距)划分森林的垂直层次, 这就忽略了同一林层内不同树种间和不同发育阶段树木生长的差异。该研究在吉林蛟河天然阔叶红松(Pinus koraiensis)林内建立轻度(胸高断面积采伐强度17.3%)、中度(34.7%)、重度(51.9%)采伐以及对照(不采伐)样地, 跟踪调查采伐后自然恢复2、4、7年保留木的生长动态。根据不同树种每一个体所处的林层位置和生长发育阶段, 将保留木划分为3个组别: 林冠层树种的成熟个体(I)、林冠层树种的未成熟个体(II)以及林下层树种的全部个体(III), 比较不同恢复时期各组别树木的生长对于采伐强度的响应差异。结果表明, 第II组树木的平均胸径相对生长速率(0.033 cm·cm-1·a-1)显著高于第I (0.016 cm·cm-1·a-1)和III组(0.018 cm·cm-1·a-1)。总体来看, 采伐促进了大多数林冠层优势树种(第I、II组)的生长, 尤其是第II组树木的相对生长速率随采伐强度的增加而增加, 但第I组树木的相对生长速率只在重度采伐样地显著高于对照样地。然而林冠层少见种的生长速率并未受到采伐活动的显著影响。值得注意的是, 第I和II组树木生长对于采伐的响应都存在一定的时间滞后, 伐后短期内(2年)采伐样地与对照样地的生长速率没有显著差异, 而采伐对树木生长的促进效果在伐后2-4年才开始出现, 并在随后的监测期内持续存在。各组别树木的相对生长速率均随初始胸径的增大而降低, 且这种负相关关系的斜率随采伐强度增加逐渐增大, 表明随着采伐强度增加, 较小的树木个体从减弱的竞争中获益更多, 呈现出更加明显的生长释放现象。 相似文献
176.
自然条件下生物结皮是藻、藓及地衣等结皮类型以不同比例组成的混合群落,显著影响土壤养分含量,目前混合生物结皮对土壤养分的影响与其群落结构的关系尚不清楚,限制了混合生物结皮土壤养分的评估。为此,研究通过测定单一组成的藻结皮、藓结皮以及80%藻+20%藓、60%藻+40%藓、40%藻+60%藓和20%藻+80%藓4个不同藻藓比例的混合生物结皮土壤有机碳、全氮、全磷、速效磷、铵态氮和硝态氮含量,研究了混合生物结皮土壤养分与其群落结构之间的关联。结果显示:(1)藓结皮层土壤有机碳、全氮、速效磷、铵态氮和硝态氮含量显著高于藻结皮,分别高出166.4%、77.2%、55.1%、56.2%和42.2%。(2)藻藓混合生物结皮土壤有机碳、全氮、速效磷和铵态氮含量与组成和盖度等结构特征有关,可以通过单一类型生物结皮土壤养分含量与盖度加权预测混合生物结皮土壤养分储量。(3)混合生物结皮土壤有机碳、全氮、速效磷和铵态氮储量实测值(x)与预测值(y)拟合的线性函数分别为y=0.97x、y=0.96x、y=1.18x和y=0.92x。(4)混合生物结皮对全磷和硝态氮含量的影响与群落结构无关。生物结皮对下层0—5 ... 相似文献
177.
毛竹材用丰产林密度效应模型研究 总被引:9,自引:0,他引:9
应用毛竹材用丰产林234块标准地材料,研究出毛竹材用丰产林密度效应的数学模型W=0.230518N~(0.967324)D~(2.060102),并对模型进行生产弹性和边际产量分析,结果表明:毛竹材用丰产林分密度总的生产弹性值大于1,说明该地区毛竹生产力还有望进一步提高,从边际产量分析结果,如增加密度,还可提高竹林产量.该研究为毛竹材用丰产林经营活动提供科学理论的依据. 相似文献
178.
179.
目的:通过观察PQ中毒患者SOD、TNF-α、IL-6、PaO2、PaCO2、BUN和Cr水平,及血浆PQ浓度的变化,旨在探讨大黄在治疗PQ中毒中的作用。方法:36例急性百草枯中毒患者随机分为对照组(n=15)和治疗组(n=21),所有患者均给予常规治疗,对照组应用甘露醇导泻,治疗组应用生大黄混悬液导泻,采用酶联免疫吸附法(enzyme linked immunosorbent assay,ELISA)检测所有患者血清SOD、TNF-α、IL-6水平,高效液相色谱法(High Performance Liquid Chromatography,HPLC)测定患者血浆PQ浓度,并测定PaO2、PaCO2、BUN和Cr。结果:治疗组患者第1、3、7天PaO2、SOD水平显著高于对照组,PaCO2、BUN、Cr、TNF-α、IL-6水平和PQ浓度亦较对照组均显著降低(P0.05)。结论:大黄可降低PQ中毒患者血中PQ浓度,抑制TNF-α、IL-6的表达,明显升高SOD的水平,改善PQ中毒患者肺、肾功能。 相似文献
180.
北京市生态用地规划与管理对策 总被引:7,自引:0,他引:7
不合理土地开发加速了对自然生态系统的干扰和侵占,导致生态系统服务功能下降,危机区域生态安全,开展生态用地规划是构建区域生态安全格局的基础。合理规划和管理不同土地利用类型的数量和空间分布对区域可持续发展具有重要意义。目前我国广泛应用的土地利用分类体系主要以土地的社会经济属性为基础,忽视其生态属性,导致以提供生态系统服务为主、保障生态安全的土地缺乏保护机制,具有重要生态功能的土地得不到有效保护。以北京市为例,建立了北京市生态用地分类与规划的思路与程序,在明确北京市生态安全与生态系统服务功能的关系基础上分析了北京市生态系统服务功能重要性及其空间格局,并进行了北京市生态用地规划。研究规划了保障北京市生态安全的7类生态用地:地表水涵养与保护用地、地下水保护用地、生物多样性保护用地、水土保持用地、河流防护用地、公路防护用地和城市绿地,总面积5137.37km2,占北京市域面积的31.31%。最后从生态用地识别和划分、将生态用地融入土地利用分类体系、生态用地管理措施和对策3个方面探讨了生态用地规划和管理的方法与措施。研究结果为北京市土地利用规划和有效管理提供依据,也为其它地区的生态用地规划提供参考。 相似文献