Long-term nitrogen dioxide exposure and cause-specific mortality in the U.S. Medicare population.

Long-term nitrogen dioxide exposure and cause-specific mortality in the U.S. Medicare population.
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DOI:
10.1016/j.envres.2021.112154
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发表时间:
2022-05-01
影响因子:
8.3
通讯作者:
Suh H
Suh H
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Eum KD;Honda TJ;Wang B;Kazemiparkouhi F;Manjourides J;Pun VC;Pavlu V;Suh H

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自1971年以来,每年的国家环境空气质量标准(NAAQS)的二氧化氮(NO2)一直保持在53 ppb,长期NO2暴露对死亡率的影响知之甚少。我们研究了长期NO2暴露与(NO2的12个月移动平均值)低于美国老年人的年度NAAQS和原因特异性死亡率。考克斯比例风险模型用于估计与长期NO2暴露相关的原因特异性死亡率的风险比(HR),该风险比(HR)来自2001年至2010年居住在美国境内的约5000万医疗保险受益人。2008. NO2增加10 ppb与全因死亡率增加相关(HR:1.06; 95% CI:1.05-1.06),心血管(HR:1.10; 95% CI:1.10-1.11),呼吸系统疾病(HR:1.09; 95% CI:1.08-1.11)和癌症(HR:1.01; 95% CI:1.00-1.02)调整年龄、性别、种族、邮政编码作为分层邮政编码和州一级社会经济地位(SES)作为协变量,和PM2.5暴露使用2阶段方法。NO2还与缺血性心脏病、脑血管病、充血性心力衰竭、慢性阻塞性肺病、肺炎和肺癌的死亡率升高有关。我们没有发现阈值的证据,在NO2暴露的范围内,所有死亡原因的HR都是正的和显著的。全因暴露量-反应曲线呈线性,心血管相关死亡率呈超线性,心脏病相关死亡率呈亚线性。在黑人受益人中,人权率一直最高。长期NO2暴露与多种原因导致的死亡风险升高相关,没有阈值反应的证据。我们的研究结果引起了人们对NO2年度NAAQS是否充分的关注。
Since 1971, the annual National Ambient Air Quality Standard (NAAQS) for nitrogen dioxide (NO2) has remained at 53 ppb, the impact of long-term NO2 exposure on mortality is poorly understood. We examined associations between long-term NO2 exposure (12-month moving average of NO2) below the annual NAAQS and cause-specific mortality among the older adults in the U.S. Cox proportional-hazard models were used to estimate Hazard Ratio (HR) for cause-specific mortality associated with long-term NO2 exposures among about 50 million Medicare beneficiaries living within the conterminous U.S. from 2001–2008. A 10 ppb increase in NO2 was associated with increased mortality from all-cause (HR: 1.06; 95% CI: 1.05–1.06), cardiovascular (HR: 1.10; 95% CI: 1.10–1.11), respiratory disease (HR: 1.09; 95% CI: 1.08–1.11), and cancer (HR: 1.01; 95% CI: 1.00–1.02) adjusting for age, sex, race, ZIP code as strata ZIP code- and state-level socio-economic status (SES) as covariates, and PM2.5 exposure using a 2-stage approach. NO2 was also associated with elevated mortality from ischemic heart disease, cerebrovascular disease, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, and lung cancer. We found no evidence of a threshold, with positive and significant HRs across the range of NO2 exposures for all causes of death examined. Exposure-response curves were linear for all-cause, supra-linear for cardiovascular-, and sub-linear for respiratory-related mortality. HRs were highest consistently among Black beneficiaries. Long-term NO2 exposure is associated with elevated risks of death by multiple causes, without evidence of a threshold response. Our findings raise concerns about the sufficiency of the annual NAAQS for NO2.
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