Particulate matter
PM2.5 oxidative potential modifies heart-attack risk
Open access · cc by · source: Europe PMC
Same-day PM2.5 raises myocardial-infarction visits more where particles deplete glutathione, and NOx–ozone oxidant capacity adds further risk.
How this study connects
Role on claims
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Evidence for the claim as stated.
Same-day PM2.5 raises myocardial-infarction visits more where particles deplete glutathione, and NOx–ozone oxidant capacity adds further risk.
Evidence for the claim as stated.
A time-series in one city or a prenatal cohort is not a global mortality function.
Evidence for the claim as stated.
Among 30,101 MI emergency visits in 16 Canadian cities, mean PM₂.₅ was only 6.91 μg/m³. Glutathione oxidative burden fit better than mass alone (AIC 87,710 vs 87,718). OPGSH modified the PM₂.₅–MI association (p = 0.026); ascorbate OP (OPAA) did not (p = 0.164). Combined Ox stayed associated after adjusting for glutathione burden. Oxidative potential was a 2012–2013 regional average, not day-specific chemistry.
Evidence for the claim as stated.
Assigned 'PM₂.₅' does not predict one health number. North Carolina fused surfaces give a 3.1 g birth-weight decrement per IQR beside a 187.5 g racial gap; Rome's tiny panel finds COPD sensitive to PM₂.₅/metals but asthmatics to NO₂; Canadian MI visits at mean 6.91 μg/m³ are modified by glutathione oxidative potential, not ascorbate OP. Dust days change coarse-PM cardiac effects (9.73% vs 0.86%) with no fine-PM interaction. Mass from a monitor is not a portable toxicity.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
A time-series in one city or a prenatal cohort is not a global mortality function.
Assigned 'PM₂.₅' does not predict one health number. North Carolina fused surfaces give a 3.1 g birth-weight decrement per IQR beside a 187.5 g racial gap; Rome's tiny panel finds COPD sensitive to PM₂.₅/metals but asthmatics to NO₂; Canadian MI visits at mean 6.91 μg/m³ are modified by glutathione oxidative potential, not ascorbate OP. Dust days change coarse-PM cardiac effects (9.73% vs 0.86%) with no fine-PM interaction. Mass from a monitor is not a portable toxicity.
Study at a glance
- Design
- Case-control — Case-crossover of MI ED visits vs daily PM2.5 weighted by city oxidative potential
- N
- N=30101 · 30,101 myocardial infarction emergency visits in 16 Canadian cities
- Population
- MI emergency visits across 16 Canadian cities
- Outcome
- MI visit risk per PM2.5 and redox-weighted PM2.5
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
PM2.5 oxidative potential modifies heart-attack risk
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
30,101 myocardial infarction cases were included
In total, 30,101 cases of myocardial infarction were included in the analyses.
How was oxidative burden defined?
oxidative burden metrics were generated by multiplying ambient PM 2.5 mass concentrations by regional estimates of glutathione (OP GSH ) and ascorbate-related (OP AA ) oxidative potential.
Key findings
Mean PM2.5 was only 6.91 μg/m³. Glutathione oxidative burden fit better than mass alone (AIC 87,710 vs 87,718). OPGSH modified the PM2.5–MI association (p=0.026); OPAA did not (p=0.164). Combined Ox stayed associated after adjusting for glutathione burden.
Methodology
A case-crossover of 30,101 MI emergency visits in 16 Canadian cities related daily PM2.5 (per 5 μg/m³) to visits, then reweighted mass by city-level glutathione and ascorbate oxidative potential (OPGSH, OPAA) and tested interactions with redox-weighted NOx+ozone (Ox).
Limitations
Oxidative potential was a 2012–2013 regional average, not day-specific particle chemistry. Effect estimates live mainly in figures/tables, and ascorbate OP’s null is unexplained.
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