The shape of the exposure-response curve for long-term ambient fine particulate (PM2.5) exposure and cause-specific mortality is poorly understood, especially for rural populations and underrepresented minorities. We used hybrid machine learning and Cox proportional hazard models to assess the association of long-term PM2.5 exposures on specific causes of death for 53 million U.S. Medicare beneficiaries (aged ≥65) from 2000 to 2008. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socio-economic status (SES) in our main analyses, with approximately 4 billion person-months of follow-up, and additionally for warm season average of 1-h daily maximum ozone exposures in a sensitivity analysis. The impact of non-traffic PM2.5 on mortality was examined using two stage models of PM2.5 and nitrogen dioxide (NO2). A 10 μg /m3 increase in 12-month average PM2.5 prior to death was associated with a 5% increase in all-cause mortality, as well as an 8.8, 5.6, and 2.5% increase in all cardiovascular disease (CVD)-, all respiratory-, and all cancer deaths, respectively, in age, gender, race, ZIP code, and SES-adjusted models. PM2.5 exposures, however, were not associated with lung cancer mortality. Results were not sensitive to control for ozone exposures. PM2.5-mortality associations for CVD- and respiratory-related causes were positive and significant for beneficiaries irrespective of their sex, race, age, SES and urbanicity, with no evidence of a lower threshold for response or of lower Risk Ratios (RRs) at low PM2.5 levels. Associations between PM2.5 and CVD and respiratory mortality were linear and were higher for younger, Black and urban beneficiaries, but were largely similar by SES. Risks associated with non-traffic PM2.5 were lower than that for all PM2.5 and were null for respiratory and lung cancer-related deaths. PM2.5 was associated with mortality from CVD, respiratory, and all cancer, but not lung cancer. PM2.5-associated risks of CVD and respiratory mortality were similar across PM2.5 levels, with no evidence of a threshold. Blacks, urban, and younger beneficiaries were most vulnerable to the long-term impacts of PM2.5 on mortality.

中文翻译：

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长期PM2.5暴露对特定死亡原因的影响：5300万美国医疗保险受益人的暴露-反应曲线和效应改变。

对于长期的环境细颗粒物（PM2.5）暴露和特定原因死亡率的暴露-响应曲线的形状知之甚少，尤其是对于农村人口和代表性不足的少数民族而言。我们使用混合机器学习和Cox比例风险模型评估了2000年至2008年间5300万美国Medicare受益人（≥65岁）的长期PM2.5暴露与特定死亡原因的关联。模型包括年龄，性别分层，种族和邮政编码，并在我们的主要分析中控制了邻里社会经济地位（SES），进行了大约40亿人月的随访，此外，在暖季中平均每天最多暴露1小时的臭氧敏感性分析。使用PM2.5和二氧化氮（NO2）的两个阶段模型检查了非交通PM2.5对死亡率的影响。死亡前12个月的平均PM2.5增加10μg/ m3，导致全因死亡率增加5％，所有心血管疾病（CVD）分别增加8.8、5.6和2.5％， ，年龄，性别，种族，邮政编码和SES调整后的模型分别代表所有呼吸道和所有癌症死亡。但是，PM2.5暴露与肺癌死亡率无关。结果对控制臭氧暴露不敏感。与受益人的性别，种族，年龄，SES和城市化程度无关，与CVD和呼吸有关的原因的PM2.5死亡率关联对受益人而言是积极的和重要的，没有证据表明响应阈值降低或风险比（RRs）降低在低PM2.5水平下。PM2.5和CVD与呼吸道疾病之间的相关性呈线性关系，而年轻的黑人和城市受益人的相关性更高，但在很大程度上与SES相似。与非交通型PM2.5相关的风险低于所有PM2.5，与呼吸道和肺癌相关的死亡无效。PM2.5与CVD，呼吸道疾病和所有癌症（而非肺癌）的死亡率相关。在PM2.5水平上，与PM2.5相关的CVD和呼吸道疾病的风险相似，没有阈值的证据。黑人，城市居民和年轻受益者最容易受到PM2.5对死亡率的长期影响。没有任何阈值的证据。黑人，城市居民和年轻受益者最容易受到PM2.5对死亡率的长期影响。没有任何阈值的证据。黑人，城市居民和年轻受益者最容易受到PM2.5对死亡率的长期影响。