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.
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.
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.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
This library holds 10 empirical papers on particulate matter with measured outcomes rather than reviews.
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.
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Same topic cluster — not a recommendation engine.