Particulate matter
PM2.5 lowers lung function in COPD, NO2 in asthma
Open access · cc by · source: Europe PMC
In a Rome panel, fine particles reduced FVC and FEV1 among COPD patients, NO2 reduced FEV1 among asthmatics, and IHD patients showed no spirometric response.
How this study connects
Role on claims
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Evidence for the claim as stated.
In a Rome panel, fine particles reduced FVC and FEV1 among COPD patients, NO2 reduced FEV1 among asthmatics, and IHD patients showed no spirometric response.
Evidence for the claim as stated.
A 29-adult Rome panel completed 449 home or clinic spirometries paired with 24-hour PM₂.₅, coarse PM, gases and PM₂.₅ metals from two sites. COPD patients lost FVC with 24–48 h PM₂.₅/PM₁₀ and FEV₁ after 72 h; Zn, Fe and Ni tracked those decrements. Asthmatics lost FEV₁ with cumulative NO₂, not PM₂.₅. IHD patients had no pollutant-related lung-function change. Indoor and outdoor PM₂.₅ correlated strongly (ρ = 0.81). Ozone never exceeded 100 μg/m³.
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.
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
- Cohort — Repeated home/clinic spirometry paired with ambient PM and gases in Rome
- N
- N=29 · 29 adults with COPD, asthma, or IHD; 449 spirometries
- Population
- Adults with COPD, asthma, or ischemic heart disease in Rome
- Outcome
- Short-term lung-function changes related to PM2.5 metals and NO2
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
PM2.5 lowers lung function in COPD, NO2 in asthma
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
29 patients completed 449 spirometries
Overall, the 29 study subjects underwent a total of 449 spirometries.
Indoor and outdoor PM2.5 correlated at ρ=0.81
Daily indoor concentrations of PM 2.5 (averages of 24 h samples collected at the homes of three subjects per survey) were highly correlated with average ambient PM 2.5 (ρ = 0.81, p < 0.01).
Key findings
COPD patients lost FVC with 24–48 h PM2.5/PM10 and FEV1 after 72 h; Zn, Fe, and Ni tracked those decrements. Asthmatics lost FEV1 with cumulative NO2, not PM2.5. IHD patients had no pollutant-related lung-function change. Indoor and outdoor PM2.5 correlated strongly (ρ=0.81).
Methodology
Twenty-nine adults with COPD, asthma, or ischemic heart disease completed 449 home or clinic spirometries across spring and winter 1999, paired with 24-hour PM2.5, PM10–2.5, gases, and PM2.5 metals from two Rome sites, plus a small indoor PM2.5 check.
Limitations
The panel is tiny (29 people), metals were outdoor not personal, IHD patients had no pre-existing lung disease so a null lung test does not rule out cardiac effects, and ozone never exceeded 100 μg/m³.
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