Ambient air pollution and thrombosis

Sarah Robertson*, Mark R. Miller

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

54 Citations (Scopus)

Abstract

Air pollution is a growing public health concern of global significance. Acute and chronic exposure is known to impair cardiovascular function, exacerbate disease and increase cardiovascular mortality. Several plausible biological mechanisms have been proposed for these associations, however, at present, the pathways are incomplete. A seminal review by the American Heart Association (2010) concluded that the thrombotic effects of particulate air pollution likely contributed to their effects on cardiovascular mortality and morbidity. The aim of the current review is to appraise the newly accumulated scientific evidence (2009-2016) on contribution of haemostasis and thrombosis towards cardiovascular disease induced by exposure to both particulate and gaseous pollutants. Seventy four publications were reviewed in-depth. The weight of evidence suggests that acute exposure to fine particulate matter (PM2.5) induces a shift in the haemostatic balance towards a pro-thrombotic/pro-coagulative state. Insufficient data was available to ascertain if a similar relationship exists for gaseous pollutants, and very few studies have addressed long-term exposure to ambient air pollution. Platelet activation, oxidative stress, interplay between interleukin-6 and tissue factor, all appear to be potentially important mechanisms in pollution-mediated thrombosis, together with an emerging role for circulating microvesicles and epigenetic changes. Overall, the recent literature supports, and arguably strengthens, the contention that air pollution contributes to cardiovascular morbidity by promoting haemostasis. The volume and diversity of the evidence highlights the complexity of the pathophysiologic mechanisms by which air pollution promotes thrombosis; multiple pathways are plausible and it is most likely they act in concert. Future research should address the role gaseous pollutants play in the cardiovascular effects of air pollution mixture and direct comparison of potentially susceptible groups to healthy individuals.

Original languageEnglish
Article number1
JournalParticle and Fibre Toxicology
Volume15
Issue number1
DOIs
Publication statusPublished - 2018

Bibliographical note

Funding Information:
This work was partially supported by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Health Impacts of Environmental Hazards (HPRU-2012-10,030). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, the Department of Health or Public Health England. MRM is funded by a British Heart Foundation Special Project Grant (SP/15/8/31575).

Publisher Copyright:
© The Author(s). 2018.

Keywords

  • Air pollution
  • Coagulation
  • Diesel exhaust
  • Nitrogen dioxide
  • Ozone
  • Particulate matter
  • Thrombosis

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