Air Pollution Exposure Laboratory, Division of Respiratory Medicine, Department of Medicine, Vancouver Coastal Health Research Institute, The University of British Columbia, Vancouver, British Columbia, Canada.
Air Pollution Exposure Laboratory, Division of Respiratory Medicine, Department of Medicine, Vancouver Coastal Health Research Institute, The University of British Columbia, Vancouver, British Columbia, Canada.
Environ Int. 2021 May;150:106424. doi: 10.1016/j.envint.2021.106424. Epub 2021 Feb 15.
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.
We examined PM concentration-responses after controlled human air pollution exposures to examine exposure-response markers, assess effect modifiers, and identify potential effect thresholds.
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.
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.
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.
空气污染是全球范围内导致过早死亡的主要因素，通常以颗粒物 (PM) 来表示，这是其对健康产生有害影响的主要因素。浓度-反应关系可用于量化相关人群中空气污染的影响，并考虑潜在的效应阈值。人体受控暴露可以提供有关急性效应和浓度-反应关系的数据，补充流行病学研究。
我们研究了受控人体空气污染暴露后的 PM 浓度反应，以检验暴露反应标志物、评估效应修饰物，并确定潜在的效应阈值。
我们对已发表的受控人体暴露研究中的原始研究进行了回顾，这些研究报告了多个目标 PM 浓度的反应，或根据 PM 浓度变化进行了汇总，以确定浓度依赖性效应。
通过 PubMed 和补充搜索共确定了 191 篇出版物，其中 31 篇符合条件。符合条件的研究共同代表了四种污染物模型：环境浓缩颗粒、工程碳纳米颗粒、柴油废气和木烟。我们发现，氧化应激标志物、炎症和心血管功能的浓度依赖性效应在不同污染物之间存在重叠。代谢综合征和谷胱甘肽 S-转移酶 mu1 基因型被确定为潜在的效应修饰物。
改善对浓度-反应关系的理解是通过影响评估和政策进行生物监测和减轻健康影响的重要组成部分。尽管我们确定了潜在的浓度-反应标志物、阈值和修饰物，但由于符合条件的出版物数量不足、方法学差异较大以及研究之间报告标准不一致，我们对这些关系的结论受到限制。需要进一步研究来验证这些观察结果。我们建议未来的研究协调估计报告，以促进在研究和应用环境中识别稳健的反应标志物。
