Exposure to wood smoke increases arterial stiffness and decreases heart rate variability in humans

Abstract

BackgroundEmissions from biomass combustion are a major source of indoor and outdoor air pollution, and are estimated to cause millions of premature deaths worldwide annually. Whilst adverse respiratory health effects of biomass exposure are well established, less is known about its effects on the cardiovascular system. In this study we assessed the effect of exposure to wood smoke on heart rate, blood pressure, central arterial stiffness and heart rate variability in otherwise healthy persons.MethodsFourteen healthy non-smoking subjects participated in a randomized, double-blind crossover study. Subjects were exposed to dilute wood smoke (mean particle concentration of 314±38 μg/m3) or filtered air for three hours during intermittent exercise. Heart rate, blood pressure, central arterial stiffness and heart rate variability were measured at baseline and for one hour post-exposure.ResultsCentral arterial stiffness, measured as augmentation index, augmentation pressure and pulse wave velocity, was higher after wood smoke exposure as compared to filtered air (p < 0.01 for all), and heart rate was increased (p < 0.01) although there was no effect on blood pressure. Heart rate variability (SDNN, RMSSD and pNN50; p = 0.003, p < 0.001 and p < 0.001 respectively) was decreased one hour following exposure to wood smoke compared to filtered air.ConclusionsAcute exposure to wood smoke as a model of exposure to biomass combustion is associated with an immediate increase in central arterial stiffness and a simultaneous reduction in heart rate variability. As biomass is used for cooking and heating by a large fraction of the global population and is currently advocated as a sustainable alternative energy source, further studies are required to establish its likely impact on cardiovascular disease.Trial registrationClinicalTrials.gov, NCT01488500

Carbonaceous aerosol source apportionment using the Aethalometer model – evaluation by radiocarbon and levoglucosan analysis at a rural background site in southern Sweden

“…Carbonaceous aerosols derived from wood burning have been shown to be hazardous to humans (Barregard et al, 2006;Eriksson et al, 2014;Jalava et al, 2010;Naeher et al, 2007;Sehlstedt et al, 2010;Unosson et al, 2013). Additionally, diesel and gasoline vehicles emit large quantities of BC and associated compounds (e.g., polycyclic aromatic hydrocarbons, PAHs), which have been suggested as one of the most health-damaging particle types (Benbrahim-Tallaa et al, 2012;Hoek et al, 2002;Salvi et al, 1999).…”

Ambient and household air pollution: complex triggers of disease

“…The authors demonstrated that increased high-sensitivity C-reactive protein (a marker of inflammation), 8-hydroxy-2=-deoxyguanosine (demonstrative of oxidative stress), and fibrinogen (present in high concentration in the inflammatory response) levels and a decrease in heart rate variability (reduced heart rate variability has been shown to be a predictor of MI) were associated with increased levels of indoor air pollutant particles. These data reveal that exposure to indoor air pollution is positively correlated with inflammation, oxidative stress, and cardiac dysfunction (79). Another study (79) demonstrated that exposure to wood smoke increases arterial stiffness and decreases heart rate variability.…”

“…These data reveal that exposure to indoor air pollution is positively correlated with inflammation, oxidative stress, and cardiac dysfunction (79). Another study (79) demonstrated that exposure to wood smoke increases arterial stiffness and decreases heart rate variability. Positive associations exist between the use of solid fuel, chronic obstructive pulmonary disease (OR: 2.80, 95% CI: 1.85-4.0), and chronic bronchitis (OR: 2.32, 95% CI: 1.92-2.80) (44).…”

“…CO, carbon monoxide; NOx, nitrite/nitrate; PM10, respirable PM. Yourifuji and Kashima (89) Japan Outdoor There was a risk ratio of 10-g/m 3 increase in PM of 1.014 for hemorrhagic stroke and 1.016 for ischemic stroke Maheswaran et al (50) London, England Outdoor A 10-g/m 3 increase in PM and NO2 resuted in 52% and 28% increased stroke mortality, respectively Cesaroni et al (9) Rome, Italy Outdoor The hazard ratio for mortality was 1.03 for a 10-g/m 3 increase NO2 and 1.04 for a 10-g/m 3 increase PM2.5 Silverman et al (63) New York, NY Outdoor The relative risk of an OHCA after a 10-g/m 3 increase in PM2.5 was 1.06 Ensor et al (16) Houston, TX Outdoor The relative risk of an OHCA after a 6-g/m 3 increase in PM was 1.046 Link et al (48) Outdoor Increased odds of atrial fibrillation of 26% after a 6-g/m 3 increase in PM2.5 Koton et al (42) Israel Outdoor There was an adjusted hazard ratio of 1.3 for death and 1.5 for myocardial infaction after a 10-g/m 3 increase in PM2.5 Wichmann et al (83) Copenhagen, Denmark Outdoor Increased percent chance of an OHCA of 4% after PM2.5 exposure and 5% after PM10 exposure Unosson et al (79) Helsinki, Finland Indoor Wood smoke exposure resulted in arterial stiffness and decreased heart rate variability Kurmi et al (44) Multiple countries Indoor ORs after biomass smoke exposure of 2.80 for chronic obstructive pulmonary disease and 2.32 for chronic bronchitis Baumgartner et al (5) Yannen, China Indoor Systolic blood pressure was 2.2 mmHg higher after a 1-log g/m 3 increase in PM2.5 and diastolic blood pressure was 0.5 mmHg Smith-Sivertsen et al (64) Guatemala Indoor The relative risk was 0.42 for wheezing after a 61.6% CO exposure reduction Mondal et al (53) India Indoor Biomass smoke exposure resulted in an increased incidence of micronucleation…”

Indoor pollution and burning practices in wood stove management

“…Several studies have shown high exposure to pollutants emitted by wood-fired boilers, mainly in rural areas, where the high availability of wood encourages its use (Gaeggeler et al, 2008;Galbally et al, 2009;Ward and Lange, 2010), whereas epidemiological and controlled-exposure studies have highlighted associations between wood smoke exposure and adverse human health effects in the respiratory system (Naeher et al, 2007;Po et al, 2011;Ghio et al, 2012) and in the cardiovascular system (McGowan et al, 2002;Rappold et al, 2011, Unosson et al, 2013.…”