Environ Res. 2020 May;184:109292. doi: 10.1016/j.envres.2020.109292. Epub 2020 Feb 27.
Sickle cell disease (SCD) is an inherited, autosomal recessive blood disorder, among the most prevalent genetic diseases, globally. While the genetic and hemolytic dynamics of SCD have been well-characterized, the etiology of SCD-related pathophysiological processes is unclear. Although limited, observational evidence suggests that environmental factors, including urban air pollution, may play a role.
We assessed whether daily ambient air pollution concentrations are associated with corresponding emergency department (ED) visit counts for acute SCD exacerbations in Atlanta, Georgia, during a 9-year (2005-2013) period. We also examined heterogeneity in response by age and sex.
ED visit data were from 41 hospitals in the 20-county Atlanta, GA area. Associations between daily air pollution levels for 8 urban air pollutants and counts of SCD related ED visits were estimated using Poisson generalized linear models.
We observed positive associations between pollutants generally indicative of traffic emissions and corresponding SCD ED visits [e.g., rate ratio of 1.022 (95% CI: 1.002, 1.043) per interquartile range increase in carbon monoxide]. Age stratified analyses indicated stronger associations with traffic pollutants among children (0-18 years), as compared to older age strata. Associations involving other pollutants, including ozone and particulate matter and for models of individuals >18 years old, were consistent a null hypothesis of no association.
This analysis represents the first North American study to examine acute risk among individuals with SCD to urban air pollution and provide evidence of urban air pollution, especially from traffic sources, as a trigger for acute exacerbations. These findings are consistent with a hypothesis that biological pathways, including several centrally associated with oxidative stress, may contribute towards enhanced susceptibility in individuals with SCD.
镰状细胞病（SCD）是一种遗传性、常染色体隐性血液疾病，是全球最常见的遗传疾病之一。虽然 SCD 的遗传和溶血性动态已得到很好的描述，但 SCD 相关病理生理过程的病因尚不清楚。尽管有限，但观察性证据表明，环境因素，包括城市空气污染，可能起一定作用。
我们评估了在佐治亚州亚特兰大市的 9 年（2005-2013 年）期间，每日环境空气污染浓度是否与急性 SCD 加重的相应急诊就诊次数相关。我们还检查了年龄和性别差异对结果的影响。
急诊就诊数据来自亚特兰大市 20 个县的 41 家医院。使用泊松广义线性模型评估 8 种城市空气污染物的每日空气污染水平与 SCD 相关急诊就诊次数之间的关联。
我们观察到通常代表交通排放的污染物与相应的 SCD 急诊就诊次数之间存在正相关[例如，一氧化碳每增加一个四分位距，SCD 急诊就诊率的比值为 1.022（95%CI：1.002，1.043）]。分层年龄分析表明，交通污染物与儿童（0-18 岁）之间的关联更强，而与年龄较大的年龄组之间的关联较弱。涉及其他污染物（包括臭氧和颗粒物）的关联，以及年龄大于 18 岁的个体模型的关联，与无关联的零假设一致。
这是第一项研究北美的研究，调查了个体患有 SCD 对城市空气污染的急性风险，并提供了城市空气污染（特别是来自交通源的空气污染）作为急性加重的诱因的证据。这些发现与一个假设一致，即生物途径，包括与氧化应激密切相关的几种途径，可能导致 SCD 个体易感性增强。
