Ambient air pollution and the risk of ischaemic and haemorrhagic stroke
- PMID: 34390672
- DOI: 10.1016/S2542-5196(21)00145-5
Ambient air pollution and the risk of ischaemic and haemorrhagic stroke
Abstract
Stroke is a leading cause of disability and the second most common cause of death worldwide. Increasing evidence suggests that air pollution is an emerging risk factor for stroke. Over the past decades, air pollution levels have continuously increased and are now estimated to be responsible for 14% of all stroke-associated deaths. Interpretation of previous literature is difficult because stroke was usually not distinguished as ischaemic or haemorrhagic, nor by cause. This Review summarises the evidence on the association between air pollution and the different causes of ischaemic stroke and haemorrhagic stroke, to clarify which people are most at risk. The risk for ischaemic stroke is increased after short-term or long-term exposure to air pollution. This effect is most pronounced in people with cardiovascular burden and stroke due to large artery disease or small vessel disease. Short-term exposure to air pollution increases the risk of intracerebral haemorrhage, a subtype of haemorrhagic stroke, whereas the effects of long-term exposure are less clear. Limitations of the current evidence are that studies are prone to misclassification of exposure, often rely on administrative data, and have insufficient clinical detail. In this Review, we provide an outlook on new research opportunities, such as those provided by the decreased levels of air pollution due to the current COVID-19 pandemic.
Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.
Conflict of interest statement
Declaration of interests CJMK is supported by a clinical established investigator grant of the Dutch Heart Foundation (grant 2012T077) and an Aspasia grant from The Netherlands Organisation for Health Research and Development (ZonMW grant 015008048). F-EdL is supported by a clinical established investigator grant of the Dutch Heart Foundation (grant number 2014 T060), by a Vidi innovational grant from The Netherlands Organisation for Health Research and Development (ZonMW grant 016.126.351). All other authors declared no competing interests.
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