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Outdoor fine particles and nonfatal strokes: systematic review and meta-analysis.

Shin HH, Fann N, Burnett RT, Cohen A, Hubbell BJ - Epidemiology (2014)

Bottom Line: The frequentist meta-analysis produced pooled risk ratios of 1.06 (95% confidence interval = 1.00-1.13) and 1.007 (1.003-1.010) for long- and short-term effects, respectively.The Bayesian meta-analysis found a posterior mean risk ratio of 1.08 (95% posterior interval = 0.96-1.26) and 1.008 (1.003-1.013) from a normal prior, and of 1.05 (1.02-1.10) and 1.008 (1.004-1.013) from a gamma prior, for long- and short-term effects, respectively, per 10 μg/m PM2.5.The evidence for short-term PM2.5-related ischemic stroke is especially strong.

View Article: PubMed Central - PubMed

Affiliation: From the aEnvironmental Health Science and Research Bureau, Health Canada, Ottawa, ON, Canada; bDepartment of Mathematics and Statistics, Queen's University, Kingston, ON, Canada; cHealth and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, NC; and dHealth Effects Institute, Boston, MA.

ABSTRACT

Background: Epidemiologic studies find that long- and short-term exposure to fine particles (PM2.5) is associated with adverse cardiovascular outcomes, including ischemic and hemorrhagic strokes. However, few systematic reviews or meta-analyses have synthesized these results.

Methods: We reviewed epidemiologic studies that estimated the risks of nonfatal strokes attributable to ambient PM2.5. To pool risks among studies we used a random-effects model and 2 Bayesian approaches. The first Bayesian approach assumes a normal prior that allows risks to be zero, positive or negative. The second assumes a gamma prior, where risks can only be positive. This second approach is proposed when the number of studies pooled is small, and there is toxicological or clinical literature to support a causal relation.

Results: We identified 20 studies suitable for quantitative meta-analysis. Evidence for publication bias is limited. The frequentist meta-analysis produced pooled risk ratios of 1.06 (95% confidence interval = 1.00-1.13) and 1.007 (1.003-1.010) for long- and short-term effects, respectively. The Bayesian meta-analysis found a posterior mean risk ratio of 1.08 (95% posterior interval = 0.96-1.26) and 1.008 (1.003-1.013) from a normal prior, and of 1.05 (1.02-1.10) and 1.008 (1.004-1.013) from a gamma prior, for long- and short-term effects, respectively, per 10 μg/m PM2.5.

Conclusions: Sufficient evidence exists to develop a concentration-response relation for short- and long-term exposures to PM2.5 and stroke incidence. Long-term exposures to PM2.5 result in a higher risk ratio than short-term exposures, regardless of the pooling method. The evidence for short-term PM2.5-related ischemic stroke is especially strong.

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Related in: MedlinePlus

Plausible mode of action for PM2.5-related cardiovascular effects (adapted from US EPA).5
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Figure 1: Plausible mode of action for PM2.5-related cardiovascular effects (adapted from US EPA).5

Mentions: Pulmonary oxidative stress and systemic inflammation offer a plausible biological pathway describing the relation between long- and short-term PM exposure and stroke (Figure 1).12,13 PM2.5 may initiate a systemic inflammatory response even in the case of mild pulmonary inflammation.5 The recent Integrated Science Assessment by the US EPA finds that a number of other biological responses can mediate the pathway from systemic inflammation to the onset of stroke, including atherosclerosis, plaque rupture, pro-coagulation effects, and thrombosis.5 Determining whether PM and stroke are causally related should account for clinical and toxicological evidence, but developing quantitative risk functions requires epidemiologic literature. The effects of short- and long-term exposures to PM2.5 may be complementary, with longer-term exposures exacerbating susceptibility to shorter term PM2.5 elevations.23


Outdoor fine particles and nonfatal strokes: systematic review and meta-analysis.

Shin HH, Fann N, Burnett RT, Cohen A, Hubbell BJ - Epidemiology (2014)

Plausible mode of action for PM2.5-related cardiovascular effects (adapted from US EPA).5
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4222795&req=5

Figure 1: Plausible mode of action for PM2.5-related cardiovascular effects (adapted from US EPA).5
Mentions: Pulmonary oxidative stress and systemic inflammation offer a plausible biological pathway describing the relation between long- and short-term PM exposure and stroke (Figure 1).12,13 PM2.5 may initiate a systemic inflammatory response even in the case of mild pulmonary inflammation.5 The recent Integrated Science Assessment by the US EPA finds that a number of other biological responses can mediate the pathway from systemic inflammation to the onset of stroke, including atherosclerosis, plaque rupture, pro-coagulation effects, and thrombosis.5 Determining whether PM and stroke are causally related should account for clinical and toxicological evidence, but developing quantitative risk functions requires epidemiologic literature. The effects of short- and long-term exposures to PM2.5 may be complementary, with longer-term exposures exacerbating susceptibility to shorter term PM2.5 elevations.23

Bottom Line: The frequentist meta-analysis produced pooled risk ratios of 1.06 (95% confidence interval = 1.00-1.13) and 1.007 (1.003-1.010) for long- and short-term effects, respectively.The Bayesian meta-analysis found a posterior mean risk ratio of 1.08 (95% posterior interval = 0.96-1.26) and 1.008 (1.003-1.013) from a normal prior, and of 1.05 (1.02-1.10) and 1.008 (1.004-1.013) from a gamma prior, for long- and short-term effects, respectively, per 10 μg/m PM2.5.The evidence for short-term PM2.5-related ischemic stroke is especially strong.

View Article: PubMed Central - PubMed

Affiliation: From the aEnvironmental Health Science and Research Bureau, Health Canada, Ottawa, ON, Canada; bDepartment of Mathematics and Statistics, Queen's University, Kingston, ON, Canada; cHealth and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, NC; and dHealth Effects Institute, Boston, MA.

ABSTRACT

Background: Epidemiologic studies find that long- and short-term exposure to fine particles (PM2.5) is associated with adverse cardiovascular outcomes, including ischemic and hemorrhagic strokes. However, few systematic reviews or meta-analyses have synthesized these results.

Methods: We reviewed epidemiologic studies that estimated the risks of nonfatal strokes attributable to ambient PM2.5. To pool risks among studies we used a random-effects model and 2 Bayesian approaches. The first Bayesian approach assumes a normal prior that allows risks to be zero, positive or negative. The second assumes a gamma prior, where risks can only be positive. This second approach is proposed when the number of studies pooled is small, and there is toxicological or clinical literature to support a causal relation.

Results: We identified 20 studies suitable for quantitative meta-analysis. Evidence for publication bias is limited. The frequentist meta-analysis produced pooled risk ratios of 1.06 (95% confidence interval = 1.00-1.13) and 1.007 (1.003-1.010) for long- and short-term effects, respectively. The Bayesian meta-analysis found a posterior mean risk ratio of 1.08 (95% posterior interval = 0.96-1.26) and 1.008 (1.003-1.013) from a normal prior, and of 1.05 (1.02-1.10) and 1.008 (1.004-1.013) from a gamma prior, for long- and short-term effects, respectively, per 10 μg/m PM2.5.

Conclusions: Sufficient evidence exists to develop a concentration-response relation for short- and long-term exposures to PM2.5 and stroke incidence. Long-term exposures to PM2.5 result in a higher risk ratio than short-term exposures, regardless of the pooling method. The evidence for short-term PM2.5-related ischemic stroke is especially strong.

Show MeSH
Related in: MedlinePlus