Abstract
BackgroundStudies provide compelling evidences for particulate matter (PM) associated cardiovascular health effects. Elderly individuals, particularly those with preexisting conditions like hypertension are regarded to be vulnerable. Experimental data are warranted to reveal the molecular pathomechanism of PM related cardiovascular impairments among aged/predisposed individuals. Thus we investigated the cardiovascular effects of ultrafine carbon particles (UfCP) on aged (12–13 months) spontaneously hypertensive rats (SHRs) and compared the findings with our pervious study on adult SHRs (6–7 months) to identify age related predisposition events in cardiovascular compromised elderly individuals.MethodsAged SHRs were inhalation exposed to UfCP for 24 h (~180 μg/m3) followed by radio-telemetric assessment for blood pressure (BP) and heart rate (HR). Bronchoalveolar lavage (BAL) fluid cell differentials, interleukin 6 (IL-6) and other proinflammatory cytokines; serum C-reactive protein (CRP) and haptoglobin (HPT); and plasma fibrinogen were measured. Transcript levels of hemeoxygenase 1 (HO-1), endothelin 1 (ET1), endothelin receptors A, B (ETA, ETB), tissue factor (TF), and plasminogen activator inhibitor-1 (PAI-1) were measured in the lung and heart to assess oxidative stress, endothelial dysfunction and coagulation cascade.ResultUfCP exposed aged SHRs exhibited increased BP (4.4%) and HR (6.3%) on 1st recovery day paralleled by a 58% increase of neutrophils and 25% increase of IL-6 in the BAL fluid. Simultaneously higher CRP, HPT and fibrinogen levels in exposed SHRs indicate systemic inflammation. HO-1, ET1, ET-A, ET-B, TF and PAI-1 were induced by 1.5-2.0 folds in lungs of aged SHRs on 1st recovery day. However, in UfCP exposed adult SHRs these markers were up-regulated (2.5-6 fold) on 3rd recovery day in lung without detectable pulmonary/systemic inflammation.ConclusionsThe UfCP induced pulmonary and systemic inflammation in aged SHRs is associated with oxidative stress, endothelial dysfunction and disturbed coagulatory hemostasis. UfCP exposure increased BP and HR in aged SHRs rats which was associated with lung inflammation, and increased expression of inflammatory, vasoconstriction and coagulation markers as well as systemic changes in biomarkers of thrombosis in aged SHRs. Our study provides further evidence for potential molecular mechanisms explaining the increased risk of particle mediated cardiac health effects in cardiovascular compromised elderly individuals.
Highlights
Air pollution mediated cardiopulmonary effects are one of the major public health concerns in industrialized cities throughout the world [1,2,3,4]
Aged spontaneously hypertensive rats (SHRs) served as their own control and were exposed first to filtered air and 4 weeks later to ultrafine carbon particles (UfCP) for 24 h to assess the effect on cardiac performance using a radio telemetric system
cardiovascular diseases (CVD) related biomarkers were further analyzed at the target site and systematically in animals without telemetric implant on the 1st and 3rd recovery days following 24 h exposure to UfCP to assess inflammation, oxidative stress, endothelial dysfunction, and coagulation cascade
Summary
Air pollution mediated cardiopulmonary effects are one of the major public health concerns in industrialized cities throughout the world [1,2,3,4]. There is a growing concern about the potential health hazards caused by increased emissions of combustion derived ultrafine particles (UFPs) from motor vehicles [7,8]. Several epidemiological studies suggested that the carbonaceous UFPs emitted from diesel-powered motor vehicles and other combustion sources induce airway inflammation and reduced lung function [9,10]. The pulmonary deposition efficiency of inhaled UFPs, along with chemical constituents absorbed on their large surface area, are considered to drive the emerging health effects linked to cardiopulmonary toxicity. Studies provide compelling evidences for particulate matter (PM) associated cardiovascular health effects Individuals, those with preexisting conditions like hypertension are regarded to be vulnerable. In UfCP exposed adult SHRs these markers were up-regulated (2.5-6 fold) on 3rd recovery day in lung without detectable pulmonary/systemic inflammation
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