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Rapeseed Methyl Ester Biodiesel Exhaust Exposure Causes Vascular Dysfunction in Man
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för tillämpad fysik och elektronik. (Thermochemical Energy Conversion Laboratory (TEC-Lab))
Vise andre og tillknytning
(engelsk)Manuskript (preprint) (Annet vitenskapelig)
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-96448OAI: oai:DiVA.org:umu-96448DiVA, id: diva2:764748
Tilgjengelig fra: 2014-11-20 Laget: 2014-11-20 Sist oppdatert: 2018-06-07
Inngår i avhandling
1. Acute cardiovascular effects of biofuel exhaust exposure
Åpne denne publikasjonen i ny fane eller vindu >>Acute cardiovascular effects of biofuel exhaust exposure
2014 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Background

Anthropogenic air pollution is a global health problem estimated to contribute to millions of premature deaths. Exposure to biomass smoke is common due to varying sources, such as wildfires, indoor cooking over open fires, and residential heating from wood stoves. In urban environments transportation and industry rely heavily on the combustion of fossil fuels yet environmental policies increasingly support a shift to renewable fuels such as biodiesel. It has not been investigated how either wood smoke or biodiesel exhaust affect human health in general or the cardiovascular system in particular. We hypothesized that wood smoke exposure would induce acute cardiovascular impairment via similar underlying mechanisms as have been established for petrodiesel exhaust exposure. We also hypothesized that replacing petrodiesel with biodiesel, as a blend or pure biodiesel, would generate an exhaust profile with a less harmful effect on the cardiovascular system than petrodiesel exhaust.

Methods

In four separate studies healthy non-smoking subjects were exposed to different air pollutants in controlled exposure chambers followed by clinical investigations of the cardiovascular system. All studies were performed as randomized controlled trials in a crossover fashion with each individual acting as her own control. In study I healthy volunteers were exposed to wood smoke at a target concentration of particulate matter (PM) 300 µg/mfor three hours followed by measures of blood pressure, heart rate variability and central arterial stiffness. In study II subjects were exposed to wood smoke at a target concentration of PM 1000 µg/mfor one hour followed by measures of thrombus formation using the Badimon technique and vasomotor function using forearm venous occlusion plethysmography. In study III subjects were exposed to petrodiesel exhaust and a 30% rapeseed methyl ester (RME30) biodiesel blend for one hour at a target concentration of PM 300 µg/m3. Following exposure, thrombus formation and vasomotor function were assessed as in study II. In study IV subjects were exposed to petrodiesel exhaust at a target concentration of PM 300 μg/m3for one hour and pure rapeseed methyl ester (RME100) exhaust generated at identical running conditions of the engine. Following exposure, thrombus formation and vasomotor function were assessed as in study II and III.

Results

In study I fourteen subjects (8 males) were exposed to wood smoke at P M 294±36 μg/m3. Compared to filtered air exposure, measures of central arterial stiffness were increased and heart rate variability was decreased following wood smoke exposure. No effect was seen on blood pressure. In study II sixteen males were exposed to wood smoke at PM 899±100 μg/m3. We found no evidence of increased thrombus formation or impaired vasomotor function following wood smoke exposure. In study III sixteen subjects (14 males) were exposed to petrodiesel exhaust (PM 314±27 µg/m3) and RME30 exhaust (PM 309±30 µg/m3). Thrombus formation and vasomotor function were equal following either exposure. In study IV nineteen males were exposed to petrodiesel exhaust (PM 310±34 µg/m3, 1.7±0.3 x105 particles/cm3) and RME100 exhaust (PM 165±16 µg/m3, 2.2±0.1 x10particles/cm3). As in study III, thrombus formation and vasomotor function were identical following both exposures.

Conclusions

We have for the first time demonstrated that wood smoke exposure can increase central arterial stiffness and decrease heart rate variability in healthy subjects. We did not, however find evidence of increased thrombus formation and impaired vasomotor function following wood smoke exposure at a higher concentration for a shorter time period. We have, for the first time, demonstrated that exhaust from RME biodiesel induced acute adverse cardiovascular effects of increased thrombus formation and impaired vasomotor function in man. These effects are on par with those seen following exposure to petrodiesel exhaust, despite marked physicochemical differences of the exhaust characteristics.

sted, utgiver, år, opplag, sider
Umeå: Umeå Universitet, 2014. s. 96
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1690
Emneord
Cardiovascular, air pollution, endothelial dyssfunction, arterial stiffness, wood smoke, woodsmoke, biodiesel, RME, biofuel, diesel exhaust
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-96449 (URN)978-91-7601-175-1 (ISBN)
Disputas
2014-12-12, Sal D, 9 trappor, byggnad 1D, Norrlands Universitetssjukhus, Universitetssjukhuset, Umeå, 12:56 (engelsk)
Opponent
Veileder
Forskningsfinansiär
Swedish Heart Lung FoundationAFA Insurance
Tilgjengelig fra: 2014-11-21 Laget: 2014-11-20 Sist oppdatert: 2018-06-07bibliografisk kontrollert

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