Background

Air pollution is a leading contributor to premature mortality worldwide and is often represented by particulate matter (PM), a key contributor to its harmful health effects. Concentration-response relationships are useful for quantifying the effects of air pollution in relevant populations and in considering potential effect thresholds. Controlled human exposures can provide data on acute effects and concentration–response relationships that complement epidemiological studies.

Objectives

We examined PM concentration-responses after controlled human air pollution exposures to examine exposure–response markers, assess effect modifiers, and identify potential effect thresholds.

Methods

We reviewed primary research from published controlled human exposure studies where responses were reported at multiple target PM concentrations or summarized per unit change in PM to identify concentration-dependent effects.

Results

Of the 191 publications identified through PubMed and supplementary searches, 31 were eligible. Eligible studies collectively represented four pollutant models: concentrated ambient particles, engineered carbon nanoparticles, diesel exhaust, and woodsmoke. We identified concentration-dependent effects on oxidative stress markers, inflammation, and cardiovascular function that overlapped across different pollutants. Metabolic syndrome and glutathione s-transferase mu 1 genotype were identified as potential effect modifiers.

Discussion

Improved understanding of concentration–response relationships is integral to biomonitoring and mitigation of health effects through impact assessment and policy. Although we identified potential concentration–response markers, thresholds, and modifiers, our conclusions on these relationships were limited by a dearth of eligible publications, considerable variability in methodology, and inconsistent reporting standards between studies. More research is required to validate these observations. We recommend that future studies harmonize estimate reporting to facilitate the identification of robust response markers across research and applied settings.

中文翻译：

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受控人体暴露中空气污染对浓度的健康影响

背景

空气污染是导致全球过早死亡的主要原因，并且通常以颗粒物（PM）为代表，颗粒物是其有害健康影响的关键因素。浓度-响应关系可用于量化相关人群中空气污染的影响并考虑潜在的影响阈值。受控的人类暴露可以提供补充流行病学研究的急性影响和浓度-反应关系的数据。

目标

我们检查了受控的人类空气污染暴露后的PM浓度-反应，以检查暴露-反应标记，评估效应修饰剂并确定潜在效应阈值。

方法

我们回顾了已发表的受控人体暴露研究的主要研究，该研究在多个目标PM浓度下报告了反应，或对PM的每单位变化进行了总结，以确定浓度依赖性效应。

结果

通过PubMed和补充搜索确定的191种出版物中，有31种符合条件。合格的研究共同代表了四种污染物模型：浓缩的环境颗粒，工程碳纳米颗粒，柴油机废气和烟熏。我们确定了氧化应激标记，炎症和心血管功能的浓度依赖性效应，这些效应在不同污染物之间重叠。代谢综合征和谷胱甘肽S-转移酶mu 1基因型被确定为潜在的影响修饰符。

讨论

通过影响评估和政策，对浓度-反应关系的更好理解对于生物监测和减轻健康影响是不可或缺的。尽管我们确定了潜在的浓度-反应标记，阈值和修饰语，但由于缺乏合格的出版物，方法学上的巨大差异以及研究之间的报告标准不一致，我们对这些关系的结论受到了限制。需要更多的研究来验证这些观察结果。我们建议未来的研究统一估算报告，以促进跨研究和应用环境确定可靠的响应标记。