Article

Effects of air pollutants on acute stroke mortality.

Department of Occupational and Environmental Medicine, Inha University College of Medicine, 7-241, 3rd Street Shinheung-Dong, Jung-Gu, Incheon 400-103, Korea.
Environmental Health Perspectives (Impact Factor: 7.03). 03/2002; 110(2):187-91. DOI: 10.1289/ehp.02110187
Source: PubMed

ABSTRACT The relationship between stroke and air pollution has not been adequately studied. We conducted a time-series study to examine the evidence of an association between air pollutants and stroke over 4 years (January 1995-December 1998) in Seoul, Korea. We used a generalized additive model to regress daily stroke death counts for each pollutant, controlling for seasonal and long-term trends and meteorologic influences, such as temperature, relative humidity, and barometric pressure. We observed an estimated increase of 1.5% [95% confidence interval (CI), 1.3-1.8%] and 2.9% (95% CI, 0.3-5.5%) in stroke mortality for each interquartile range increase in particulate matter < 10 microm aerodynamic diameter (PM(10)) and ozone concentrations in the same day. Stroke mortality also increased 3.1% (95% CI, 1.1-5.1%) for nitrogen dioxide, 2.9% (95% CI, 0.8-5.0%) for sulfur dioxide, and 4.1% (95% CI, 1.1-7.2%) for carbon monoxide in a 2-day lag for each interquartile range increase in single-pollutant models. When we examined the associations among PM(10) levels stratified by the level of gaseous pollutants and vice versa, we found that these pollutants are interactive with respect to their effects on the risk of stroke mortality. We also observed that the effects of PM(10) on stroke mortality differ significantly in subgroups by age and sex. We conclude that PM(10) and gaseous pollutants are significant risk factors for acute stroke death and that the elderly and women are more susceptible to the effect of particulate pollutants.

1 Follower
 · 
146 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sodium metabisulfite (SMB) is most commonly used as the preservative in many food preparations and drugs. So far, few studies about its negative effects were reported. The purpose of this study was to investigate the effect of SMB on the expression of big-conductance Ca2+-activated K+ (BKCa), ATP-sensitive K+ (K-ATP), and L-type calcium (L-Ca2+) channels in rat aorta in vivo and in vitro. The results showed that the mRNA and protein levels of the BKCa channel subunits alpha and beta 1 of aorta in rats were increased by SMB in vivo and in vitro. Similarly, the expression of the K-ATP channel subunits Kir6.1, Kir6.2, and SUR2B were increased by SMB. However, SMB at the highest concentration significantly decreased the expression of the L-Ca2+ channel subunits Ca(v)1.2 and Ca(v)1.3. These results suggest that SMB can activate BKCa and K-ATP channels by increasing the expression of alpha, beta 1, and Kir6.1, Kir6.2, SUR2B respectively, while also inhibit L-Ca2+ channels by decreasing the expression of Ca(v)1.2 and Ca(v)1.3 of aorta in rats. The molecular mechanism of SMB-induced vasorelaxant effect might be related to the expression changes of BKCa, K-ATP, and L-Ca2+ channels subunits. Further work is needed to determine the relative contribution of each channel in SMB-mediated vasorelaxant effect.
    Journal of Hazardous Materials 03/2015; 284. DOI:10.1016/j.jhazmat.2014.10.053 · 4.33 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The association between particulate air pollution and high-sensitivity C-reactive protein (hs-CRP) has been well documented in epidemiological studies. Periodontitis has been linked to elevated hs-CRP levels in recent studies. It is still unknown whether patients with periodontal infections are more susceptible to particulate air pollution. The aim of this study was to investigate whether particles with aerodynamic diameters of less than 2.5μm (PM2.5) had greater effects on increasing hs-CRP among patients with periodontal infections compared to periodontally healthy individuals. We conducted a cross-sectional study on two panels of adult subjects, 100 adult patients with chronic periodontitis and 100 periodontally healthy adults, in order to evaluate the association between particulate matter (PM) and hs-CRP. We collected blood samples from each subject, measured hs-CRP and monitored average exposure to PM2.5 over 24h four times during 2010 to 2012. We used mixed-effects models to estimate the association between PM2.5 and hs-CRP and adjusted for cardiovascular risk factors. We found that a 10μg/m(3) increase in PM2.5 was associated with a 3.22% (95% confidence interval, CI: 1.21, 5.23; p<0.01) increase in hs-CRP among all adult subjects. The effect of PM2.5 in patients was significantly higher than the effect in healthy participants. In the healthy adult panel, a 10μg/m(3) increase in PM2.5 was associated with a 1.17% (95% CI: 0.54, 1.80; p<0.01) increase in hs-CRP. For adults in the patient group, a 10μg/m(3) increase in PM2.5 was associated with a 9.62% (95% CI: 7.05, 12.19; p<0.01) increase in hs-CRP. We concluded that personal exposure to PM2.5 was associated with increases in hs-CRP among adult subjects. The presence of periodontal disease led to a considerably increased effect magnitude by more than eight fold.
    Science of The Total Environment 10/2014; 502C:585-589. DOI:10.1016/j.scitotenv.2014.09.081 · 4.10 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Epidemiological investigations have revealed that sulfur dioxide (SO2) exposure is linked to cardiovascular diseases. Our previous study indicated that the vasorelaxant effect of SO2 might be partly related to ATP-sensitive K(+) (KATP), big-conductance Ca(2+)-activated K(+) (BKCa) and L-type calcium (L-Ca(2+)) channels. The present study was designed to further investigate the effects of gaseous SO2 and its derivatives on the gene and protein expression of these channels in the rat aortas in vitro. The results showed that the mRNA and protein levels of the KATP channel subunits Kir6.1, Kir6.2 and SUR2B of the rat aortas in SO2 and its derivatives groups were higher than those in control group. Similarly, the expression of the BKCa channel subunits α and β1 were increased by SO2 and its derivatives. However, SO2 and its derivatives at 1500μM significantly decreased the expression of the L-Ca(2+) channel subunits Cav1.2 and Cav1.3. Histological examination of the rat aorta tissues showed moderate injury of tunica media induced by SO2 and its derivatives at 1500μM. These results suggest that SO2 and its derivatives can activate the KATP and BKCa channels by increasing the expression of Kir6.1, Kir6.2, SUR2B and α, β1, respectively, while also inhibiting the L-Ca(2+) channels by decreasing the expression of Cav1.2 and Cav1.3 of the rat aortas. The molecular mechanism of the vasorelaxant effect of SO2 and its derivatives might be related to the expression changes of KATP, BKCa and L-Ca(2+) channel subunits, which may play a role in the pathogenesis of SO2-associated cardiovascular diseases.
    European Journal of Pharmacology 09/2014; DOI:10.1016/j.ejphar.2014.08.025 · 2.68 Impact Factor

Preview

Download
1 Download
Available from