nitrogen-dioxide and Ischemic-Attack--Transient

While several studies have investigated the effects of short-term air pollution on cardiovascular disease, less is known about its effects on cerebrovascular disease, including stroke and transient ischaemic attack (TIA). The aim of the study was to assess the effects of short-term variation in air pollutants on the onset of TIA and minor stroke.. We performed secondary analyses of data collected prospectively in the North West of England in a multi-centre study (NORTHSTAR) of patients with recent TIA or minor stroke. A case-crossover study was conducted to determine the association between occurrence of TIA and the concentration of ambient PM10 or gaseous pollutants.. A total of 709 cases were recruited from the Manchester (n = 335) and Liverpool (n = 374) areas. Data for the Manchester cohort showed an association between ambient nitric oxide (NO) and risk of occurrence of TIA and minor stroke with a lag of 3 days (odds ratio 1.06, 95% CI: 1.01 - 1.11), whereas negative association was found for the patients from Liverpool. Effects of similar magnitude, although not statistically significant, were generally observed with other pollutants. In a two pollutant model the effect of NO remained stronger and statistically significant when analysed in combination with CO or SO2, but was marginal in combination with NO2 or ozone and non-significant with PM10. There was evidence of effect modification by age, gender and season.. Our data suggest an association between NO and occurrence of TIA and minor stroke in Greater Manchester.

Topics: Adult; Aged; Aged, 80 and over; Air Pollutants; Carbon Monoxide; England; Female; Humans; Incidence; Ischemic Attack, Transient; Male; Middle Aged; Nitric Oxide; Nitrogen Dioxide; Particulate Matter; Stroke; Sulfur Dioxide

Case-crossover studies used to investigate associations between an environmental exposure and an acute health response, such as stroke, will often use the day an individual presents to an emergency department (ED) or is admitted to hospital to infer when the stroke occurred. Similarly, they will use patient's place of residence to assign exposure. The validity of using these two data elements, typically extracted from administrative databases or patient charts, to define the time of stroke onset and to assign exposure are critical in this field of research as air pollutant concentrations are temporally and spatially variable. Our a priori hypotheses were that date of presentation differs from the date of stroke onset for a substantial number of patients, and that assigning exposure to ambient pollution using place of residence introduces an important source of exposure measurement error. The objective of this study was to improve our understanding on how these sources of errors influence risk estimates derived using a case-crossover study design.. We sought to collect survey data from stroke patients presenting to hospital EDs in Edmonton, Canada on the date, time, location and nature of activities at onset of stroke symptoms. The daily mean ambient concentrations of NO₂ and PM(2.5) on the self-reported day of stroke onset was estimated from continuous fixed-site monitoring stations.. Of the 336 participating patients, 241 were able to recall when their stroke started and 72.6% (95% confidence interval [CI]: 66.9-78.3%) experienced stroke onset the same day they presented to the ED. For subjects whose day of stroke onset differed from the day of presentation to the ED, this difference ranged from 1 to 12 days (mean = 1.8; median = 1). In these subjects, there were no systematic differences in assigned pollution levels for either NO₂ or PM(2.5) when day of presentation rather than day of stroke onset was used. At the time of stroke onset, 89.9% (95% CI: 86.6-93.1%) reported that they were inside, while 84.5% (95% CI: 80.6 - 88.4%) reported that for most of the day they were within a 15 minute drive from home. We estimated that due to the mis-specification of the day of stroke onset, the risk of hospitalization for stroke would be understated by 15% and 20%, for NO₂ and PM(2.5), respectively.. Our data suggest that day of presentation and residential location data obtained from administrative records reasonably captures the time and location of stroke onset for most patients. Under these conditions, any associated errors are unlikely to be an important source of bias when estimating air pollution risks in this population.

Topics: Aged; Aged, 80 and over; Air Pollutants; Alberta; Cities; Cohort Studies; Cross-Over Studies; Environmental Exposure; Female; Humans; Ischemic Attack, Transient; Male; Middle Aged; Nitrogen Dioxide; Particulate Matter; Retrospective Studies; Risk Assessment; Stroke; Time Factors

To evaluate the association between air pollutants and the occurrence of acute stroke from 10-year population-based study.. The daily stroke count was obtained from Dijon Stroke Register between March 1994 and December 2004. The register recorded all first-ever strokes among residents of Dijon (150,000 inhabitants) in France, using standard diagnostic criteria. Pollutant concentrations (SO2, CO, NO2, O3 and PM10) were measured hourly. A bi-directional case-crossover design was used to examine the association between air pollutant and stroke onset. The conditional logistic regression model included the meteorological parameters (temperature, relative humidity), influenza epidemics and holidays.. The authors collected 493 large artery infarcts, 397 small artery infarcts, 530 cardio-embolic infarcts, 67 undeterminate infarcts, 371 transient ischaemic attacks and 220 haemorrhagic strokes. For single-pollutant model and for a 10 mg/m(3) increase of O3 exposure, a positive association was observed only in men, over 40 years of age, between ischaemic stroke occurrence and O3 levels with 1-day lag, (OR 1.133, 95% CI 1.052 to 1.220) and 0-day lag (OR 1.058, 95% CI 0.987 to 1.134). No significant associations were found for haemorrhagic stroke. In two-pollutant models, the effects of O3 remained significant after each of the other pollutants were included in the model, in particular with PM10. A significant association was observed for ischaemic strokes of large arteries (p = 0.02) and for transient ischaemic attacks (p = 0.01). Moreover, the authors found an exposure-response relations between O3 exposure and ischaemic stroke (test for trend, p = 0.01). An increase in association in men with several cardiovascular risk factors (smoker, dyslipidemia and hypertension) was also observed.. These observational data argue for an association between ischaemic stroke occurrence and O3 pollution levels; these results still need to be confirmed by other studies.

Topics: Acute Disease; Adult; Age Factors; Aged; Air Pollutants; Arteries; Carbon Monoxide; Climate; Epidemiologic Methods; Female; France; Holidays; Humans; Ischemic Attack, Transient; Male; Middle Aged; Nitrogen Dioxide; Ozone; Registries; Sex Factors; Stroke; Sulfur Dioxide