Reducing indoor air pollution by air conditioning is associated with improvements in cardiovascular health among the general population.
ABSTRACT Indoor air pollution is associated with cardiovascular effects, however, little is known about the effects of improving indoor air quality on cardiovascular health. The aim of this study was to explore whether improving indoor air quality through air conditioning can improve cardiovascular health in human subjects. We recruited a panel of 300 healthy subjects from Taipei, aged 20 and over, to participate in six home visits each, to measure a variety of cardiovascular endpoints, including high sensitivity-C-reactive protein (hs-CRP), 8-hydroxy-2'-deoxyguanosine (8-OHdG), fibrinogen in plasma and heart rate variability (HRV). Indoor particles and total volatile organic compounds (VOCs) were measured simultaneously at the participant's home during each visit. Three exposure conditions were investigated in this study: participants were requested to keep their windows open during the first two visits, close their windows during the next two visits, and close the windows and turn on their air conditioners during the last two visits. We used linear mixed-effects models to associate the cardiovascular endpoints with individual indoor air pollutants. The results showed that increases in hs-CRP, 8-OHdG and fibrinogen, and decreases in HRV indices were associated with increased levels of indoor particles and total VOCs in single-pollutant and two-pollutant models. The effects of indoor particles and total VOCs on cardiovascular endpoints were greatest during visits with the windows open. During visits with the air conditioners turned on, no significant changes in cardiovascular endpoints were observed. In conclusion, indoor air pollution is associated with inflammation, oxidative stress, blood coagulation and autonomic dysfunction. Reductions in indoor air pollution and subsequent improvements in cardiovascular health can be achieved by closing windows and turning on air conditioners at home.
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ABSTRACT: During the tenth biennial examination of the Framingham Study, 1315 participants who were free of cardiovascular disease had fibrinogen levels measured. During the ensuing 12 years, cardiovascular disease developed in 165 men and 147 women. For both sexes, the risk of cardiovascular disease was correlated positively to antecedent fibrinogen values higher than the 1.3 to 7.0 g/L (126 to 696 mg/dL) range. The magnitude of the risk diminished with advancing age in women but not in men. Risk for coronary heart disease also was significantly related to fibrinogen level. Here, the magnitude of risk displayed diminishing impact with age, again only in women. Risk of stroke increased progressively with fibrinogen level in men but not in women. The impact of fibrinogen value, considered as a separate variable, on cardiovascular disease was comparable with the major risk factors, such as blood pressure, hematocrit, adiposity, cigarette smoking, and diabetes. Fibrinogen values were also significantly related to these risk factors. Taking all these into account in a multivariate analysis, fibrinogen level was still significantly related to the incidence of cardiovascular disease in men and marginally significant in women. For coronary heart disease, the fibrinogen level was significant for both men and women. Elevated fibrinogen level is a predictor of cardiovascular disease that should be added to the cardiovascular risk factor profile.JAMA The Journal of the American Medical Association 10/1987; 258(9):1183-6. · 29.98 Impact Factor
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ABSTRACT: Experimental evidence suggests that autonomic markers such as heart-rate variability and baroreflex sensitivity (BRS) may contribute to postinfarction risk stratification. There are clinical data to support this concept for heart-rate variability. The main objective of the ATRAMI study was to provide prospective data on the additional and independent prognostic value for cardiac mortality of heart-rate variability and BRS in patients after myocardial infarction in whom left-ventricular ejection fraction (LVEF) and ventricular arrhythmias were known. This multicentre international prospective study enrolled 1284 patients with a recent (<28 days) myocardial infarction. 24 h Holter recording was done to quantify heart-rate variability (measured as standard deviation of normal to normal RR intervals [SDNN]) and ventricular arrhythmias. BRS was calculated from measurement of the rate-pressure response to intravenous phenylephrine. During 21 (SD 8) months of follow-up, the primary endpoint, cardiac mortality, included 44 cardiac deaths and five non-fatal cardiac arrests. Low values of either heart-rate variability (SDNN <70 ms) or BRS (<3.0 ms per mm Hg) carried a significant multivariate risk of cardiac mortality (3.2 [95% CI 1.42-7.36] and 2.8 [1.24-6.16], respectively). The association of low SDNN and BRS further increased risk; the 2-year mortality was 17% when both were below the cut-offs and 2% (p<0.0001) when both were well preserved (SDNN >105 ms, BRS >6.1 ms per mm Hg). The association of low SDNN or BRS with LVEF below 35% carried a relative risk of 6.7 (3.1-14.6) or 8.7 (4.3-17.6), respectively, compared with patients with LVEF above 35% and less compromised SDNN (> or = 70 ms) and BRS (> or = 3 ms per mm Hg). ATRAMI provides clinical evidence that after myocardial infarction the analysis of vagal reflexes has significant prognostic value independently of LVEF and of ventricular arrhythmias and that it significantly adds to the prognostic value of heart-rate variability.The Lancet 02/1998; 351(9101):478-84. · 39.06 Impact Factor
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ABSTRACT: An important public health challenge has been the need to protect children's health. To accomplish this goal, the scientific community needs scientifically based child-specific risk assessment methods. Critical to their development is the need to understand mechanisms underlying children's sensitivity to environmental toxicants. Risk is defined as the probability of adverse outcome and when applied to environmental risk assessment is usually defined as a function of both toxicity and exposure. To adequately evaluate the potential for enhanced health risks during development, both child-specific factors affecting toxicity and exposure need to be considered. In the first section of this article, example mechanisms of susceptibility relevant for toxicity assessment are identified and discussed. In the second section, examples of exposure factors that help define children's susceptibility are presented. Examples of pesticide research from the newly funded Child Health Center at the University of Washington will be given for illustration. The final section discusses the importance of putting these considerations of children's susceptibility into an overall framework for ascertaining relevancy for human risk assessment.Environmental Health Perspectives 04/2000; 108 Suppl 1:13-21. · 7.26 Impact Factor