Power Melinda C, Adar Sara D, Yanosky Jeff D, Weuve Jennifer
Department of Epidemiology and Biostatistics, George Washington University Milken Institute School of Public Health, 950 New Hampshire Avenue NW, Washington, DC 20052, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205, USA.
Department of Epidemiology, University of Michigan School of Public Health, 1420 Washington Heights, Ann Arbor, MI 48109, USA.
Neurotoxicology. 2016 Sep;56:235-253. doi: 10.1016/j.neuro.2016.06.004. Epub 2016 Jun 18.
Dementia is a devastating condition typically preceded by a long prodromal phase characterized by accumulation of neuropathology and accelerated cognitive decline. A growing number of epidemiologic studies have explored the relation between air pollution exposure and dementia-related outcomes.
We undertook a systematic review, including quality assessment, to interpret the collective findings and describe methodological challenges that may limit study validity. Articles, which were identified according to a registered protocol, had to quantify the association of an air pollution exposure with cognitive function, cognitive decline, a dementia-related neuroimaging feature, or dementia.
We identified 18 eligible published articles. The quality of most studies was adequate to exemplary. Almost all reported an adverse association between at least one pollutant and one dementia-related outcome. However, relatively few studies considered outcomes that provide the strongest evidence for a causal effect, such as within-person cognitive or pathologic changes. Reassuringly, differential selection would likely bias toward a protective association in most studies, making it unlikely to account for observed adverse associations. Likewise, using a formal sensitivity analysis, we found that unmeasured confounding is also unlikely to explain reported adverse associations.
We also identified several common challenges. First, most studies of incident dementia identified cases from health system records. As dementia in the community is underdiagnosed, this could generate either non-differential or differential misclassification bias. Second, almost all studies used recent air pollution exposures as surrogate measures of long-term exposure. Although this approach may be reasonable if the measured and etiologic exposure windows are separated by a few years, its validity is unknown over longer intervals. Third, comparing the magnitude of associations may not clearly pinpoint which, if any, pollutants are the probable causal agents, because the degree of exposure misclassification differs across pollutants. The epidemiologic evidence, alongside evidence from other lines of research, provides support for a relation of air pollution exposure to dementia. Future studies with improved design, analysis and reporting would fill key evidentiary gaps and provide a solid foundation for recommendations and possible interventions.
痴呆是一种具有毁灭性的疾病，通常在漫长的前驱期之前出现，其特征是神经病理学积累和认知能力加速下降。越来越多的流行病学研究探讨了空气污染暴露与痴呆相关结局之间的关系。
我们进行了一项系统综述，包括质量评估，以解释汇总研究结果并描述可能限制研究有效性的方法学挑战。根据注册方案确定的文章必须量化空气污染暴露与认知功能、认知衰退、与痴呆相关的神经影像学特征或痴呆之间的关联。
我们确定了18篇符合条件的已发表文章。大多数研究的质量从足够到典范不等。几乎所有研究都报告了至少一种污染物与一种痴呆相关结局之间的不良关联。然而，相对较少的研究考虑了能为因果效应提供最有力证据的结局，例如个体内的认知或病理变化。令人欣慰的是，在大多数研究中，差异选择可能会偏向于保护性关联，因此不太可能解释所观察到的不良关联。同样，通过正式的敏感性分析，我们发现未测量的混杂因素也不太可能解释所报告的不良关联。
我们还确定了几个常见挑战。首先，大多数关于新发痴呆的研究是从卫生系统记录中确定病例的。由于社区中的痴呆未得到充分诊断，这可能会产生非差异性或差异性错误分类偏差。其次，几乎所有研究都将近期的空气污染暴露用作长期暴露的替代指标。虽然如果测量的暴露窗口和病因暴露窗口相隔数年，这种方法可能是合理的，但其在更长时间段内的有效性尚不清楚。第三，比较关联程度可能无法明确指出哪些污染物（如果有的话）可能是致病因素，因为不同污染物的暴露错误分类程度不同。流行病学证据以及其他研究领域的证据支持空气污染暴露与痴呆之间的关系。未来设计、分析和报告得到改进的研究将填补关键的证据空白，并为建议和可能的干预措施提供坚实基础。
