Air Pollution

Abstract

Background and Purpose-Air pollution is known to be associated with cardiovascular disease, but little is known about the occurrence of stroke in relation to air pollution. We investigated the association between acute stroke mortality and air pollution over a 7-year period (January 1991 through December 1997) in Seoul, Korea. Methods-A generalized additive model was used to regress daily stroke death counts for each air pollutant, controlling for time trends, day of the week, and meteorological influences such as temperature, relative humidity, and atmospheric pressure. Ischemic and hemorrhagic stroke deaths were examined separately. Results-The effects of air pollutants on ischemic stroke mortality were statistically significant, whereas this was not the case for hemorrhagic stroke mortality. We observed estimated relative risks of 1.03 (95% CI, 1.00 to 1.06) and 1.04 (95% CI, 1.01 to 1.08) for ischemic stroke mortality for each interquartile range increase in total suspended particulates and sulfur dioxide concentrations on the same day. We also found significantly increased relative risks of 1.04 (95% CI, 1.01 to 1.07) for nitrogen dioxide with a 1-day lag, of 1.06 (95% CI, 1.02 to 1.09) for carbon monoxide with a 1-day lag, and of 1.06 (95% CI, 1.02 to 1.10) for ozone with a 3-day lag for each interquartile range increase. Conclusions-These findings indicate that air pollutants are significantly associated with ischemic stroke mortality, which suggests an acute pathogenetic process in the cerebrovascular system induced by air pollution.

Urbanization and Stroke Prevalence in Taiwan: Analysis of a Nationwide Survey

“…Other prior studies have also reported that higher air pollution levels and greater levels of depression can lead to a correspondingly higher prevalence of strokes. [31][32][33][34][35][36][37] Furthermore, it is also possible that those study subjects in the upper income group would be more likely to reside in the less urbanized areas and more likely to receive regular health check-ups, possibly from private health care facilities which tend to be better equipped; thus, they would be at a lower risk of suffering a stroke attack. In contrast, the study subjects in the lower income group may well work and live in the inner city areas, and for various reasons, may be exposed to a higher risk of disease and a corresponding increase in the risk of a stroke attack.…”

Ultrastructural changes in atherosclerotic plaques following the instillation of airborne particulate matter into the lungs of rabbits

“…Research at the Lovelace Respiratory Research Institute (New Mexico, USA) in ApoE -/-mice has shown vascular remodelling and altered atherosclerotic plaque composition following PM 10 exposure and diesel emission exposure (29)(30)(31). The present study was designed to determine whether and how PM 10 exposure affected the architecture of existing atherosclerotic plaques and to determine whether the observed ultrastructure was consistent with the characteristics of a more vulnerable atherosclerotic plaque.…”

“…Urban PM 10 The urban PM 10 (ambient particulates) used in the present study, designated as Environmental Health Centre -1993 (EHC-93), were obtained from Environment Canada; EHC-93 had been collected from the troposphere in Ottawa (Ontario) in 1993 using a single-pass, videlon bag-house filtration system located at the Environmental Health Centre. The complete size distribution and composition of EHC-93 was described by Vincent et al (33) in 1997 and compared with eight other urban particulates.…”

“…The authors acknowledge that while these exposure levels are considered to be high, they are still biologically relevant exposure levels (eg, the exposure of humans during the Southeast Asian forest fires of 1997 [51]). We also acknowledge that this delivery mechanism results in high sporadic doses compared with continuous inhalation from the environment; however, epidemiologically, the connection between PM 10 exposure and increased cardiovascular morbidity and mortality resulted from sporadic increases in human exposure to PM 10 . Therefore, we believe that these observations are relevant to the further understanding of how PM 10 exposure leads to cardiovascular morbidity and mortality.…”

“…Suwa et al (26) provided light microscopic evidence that PM 10 exposure leads to increased plaque size, lipid deposition and inflammatory cell recruitment into atherosclerotic plaques in Watanabe heritable hyperlipidemic (WHHL) rabbits. Sun et al (27,28) used an apolipoprotein E knockout (ApoE -/-) mouse model to show that long-term exposure to low concentrations of PM 2.5 (particles smaller than 2.5 µm in diameter) altered vasomotor tone, and increased tissue-factor expression, vascular inflammation and atherosclerotic burden in these animals.…”