Effect of wood smoke exposure on vascular function and thrombus formation in healthy fire fighters

Abstract

BackgroundMyocardial infarction is the leading cause of death in fire fighters and has been linked with exposure to air pollution and fire suppression duties. We therefore investigated the effects of wood smoke exposure on vascular vasomotor and fibrinolytic function, and thrombus formation in healthy fire fighters.MethodsIn a double-blind randomized cross-over study, 16 healthy male fire fighters were exposed to wood smoke (~1 mg/m3 particulate matter concentration) or filtered air for one hour during intermittent exercise. Arterial pressure and stiffness were measured before and immediately after exposure, and forearm blood flow was measured during intra-brachial infusion of endothelium-dependent and -independent vasodilators 4–6 hours after exposure. Thrombus formation was assessed using the ex vivo Badimon chamber at 2 hours, and platelet activation was measured using flow cytometry for up to 24 hours after the exposure.ResultsCompared to filtered air, exposure to wood smoke increased blood carboxyhaemoglobin concentrations (1.3% versus 0.8%; P < 0.001), but had no effect on arterial pressure, augmentation index or pulse wave velocity (P > 0.05 for all). Whilst there was a dose-dependent increase in forearm blood flow with each vasodilator (P < 0.01 for all), there were no differences in blood flow responses to acetylcholine, sodium nitroprusside or verapamil between exposures (P > 0.05 for all). Following exposure to wood smoke, vasodilatation to bradykinin increased (P = 0.003), but there was no effect on bradykinin-induced tissue-plasminogen activator release, thrombus area or markers of platelet activation (P > 0.05 for all).ConclusionsWood smoke exposure does not impair vascular vasomotor or fibrinolytic function, or increase thrombus formation in fire fighters. Acute cardiovascular events following fire suppression may be precipitated by exposure to other air pollutants or through other mechanisms, such as strenuous physical exertion and dehydration.Trial registrationClinicalTrials.gov Identifier: NCT01495325.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-014-0062-4) contains supplementary material, which is available to authorized users.

Associations between ambient wood smoke and other particulate pollutants and biomarkers of systemic inflammation, coagulation and thrombosis in cardiac patients

“…Our results were also consistent with two studies that measured d -Dimer (a breakdown product of fibrin that increases with coagulation) and found no association with particulate air pollutants (Delfino et al, 2008; Rückerl et al, 2006). Although we found no such association, increased P-selectin (indicator of both endothelial cell damage and platelet activation) has been previously associated with increased air pollutant concentrations (around 6–12% increases based on figures) in some (Delfino et al, 2008; Rich et al, 2012a), but not other studies (Bønløkke et al, 2014; Hunter et al, 2014). O'Toole et al (2010) reported no association between increased concentrations of PM 2.5 and PF4 (marker of platelet activation and vascular inflammation) in young adults during the winter, which is consistent with our findings.…”

“…However, these findings were not replicated in a recent study following firefighters' exposures during a fire (Jensen et al, 2014). Similarly, a recent controlled wood smoke exposure study on firefighters did not show increased thrombosis or platelet activation (Hunter et al, 2014). In contrast, our marker of wood smoke, Delta-C, showed positive but not statistically significant associations with CRP.…”

“…Cardiovascular disease, which manifests as acute coronary syndrome (ACS) or SIHD, involves a multifactorial pathophysiology including inflammation, endothelial dysfunction, coagulation and thrombosis (Brook et al, 2010). Several studies in the wood smoke literature have found no clear pattern of association between wood smoke exposure and biomarkers of inflammation and coagulation (Bønløkke et al, 2014; Hunter et al, 2014; Jensen et al, 2014). While our prior work did not find significant associations between Delta-C exposure and myocardial infarction (Evans et al, 2016), two controlled exposure studies reported increased biomarkers of inflammation and coagulation associated with wood-smoke particles (Barregard et al, 2006; Huang et al, 2003), while another reported decreased levels (Stockfelt et al, 2012).…”

Inflammatory and Vasoactive Effects of Serum Following Inhalation of Varied Complex Mixtures

“…Microvascular function assays were conducted 6 h after and blood samples were taken at 0, 6, and 20 hours after exposure for measures of oxidative stress and inflammation, with no obvious changes detected. Unosson and colleagues reported increased arterial stiffness in response to a comparable wood smoke exposure in health human subjects (Unosson et al , 2013), although in a follow-up study in firefighters, wood smoke exposure did not compromise vasodilatory capacity (Hunter et al , 2014). Utilizing filtrations systems to reduce indoor wood smoke PM levels in participating households in British Columbia, however, significantly improved vascular hyperemic response along with a 30% decrease in circulating C-reactive protein levels (Allen et al , 2011).…”

Cardiovascular health effects following exposure of human volunteers during fire extinction exercises

“…Fires in urban settings typically give rise to very complex mixtures because of the combustion of household equipment, whereas combustion of wood can be considered as a more “clean” type of smoke. Studies on controlled exposure to wood smoke have indicated little effect on microvascular vasomotor function [ 12 , 13 ], whereas HRV was decreased [ 14 ]. To the best of our knowledge, no studies have assessed biomarkers for cardiovascular disease after controlled exposure to more complex fuels than wood, such as plastic or household materials.…”