Particulate matter
Prenatal PM2.5 linked to preterm birth in Puerto Rico
Open access · cc by · source: Europe PMC
In the PROTECT birth cohort, an IQR rise in pregnancy-average PM2.5 was associated with higher preterm-birth risk among relatively healthy Puerto Rican women.
Study at a glance
- Design
- Cohort — PROTECT pregnancy cohort with pregnancy-average PM2.5 and preterm-birth risk ratios
- N
- N=1092 · 1,092 PROTECT participants with live singleton births in 21 municipalities
- Population
- Pregnant women in the PROTECT cohort in Puerto Rico
- Outcome
- Preterm birth associated with prenatal PM2.5 (with phthalate-interaction tests)
Structured fields used in claim comparison tables when every cited study has a complete layer.
Key findings
About 9.1% of births were preterm. Mean pregnancy PM2.5 was 6.8 μg/m³. An IQR increase in prenatal PM2.5 raised preterm-birth risk (RR 1.014 individual-adjusted; RR 1.012 also municipal-adjusted). Phthalate metabolites did not modify the association.
Methodology
Authors followed 1092 PROTECT participants with live singleton births in 21 Puerto Rican municipalities (2011–2018), assigned pregnancy-average PM2.5 from nearby EPA monitors, and estimated risk ratios for preterm birth with modified Poisson models, including phthalate-interaction tests.
Limitations
Monitor-based, municipality-at-birth assignment misses residential moves and fine-scale PM2.5, so exposure error likely biases toward the null; the cohort excluded major comorbidities, and few preterm births limited effect-modification power.
How this study connects
Role on claims
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Evidence for the claim as stated.
In the PROTECT birth cohort, an IQR rise in pregnancy-average PM2.5 was associated with higher preterm-birth risk among relatively healthy Puerto Rican women.
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.
PROTECT followed 1,092 pregnancies with live singleton births in 21 Puerto Rican municipalities (2011–2018). About 9.1% of births were preterm; mean pregnancy PM₂.₅ was 6.8 μg/m³. An IQR increase raised preterm-birth risk only modestly (RR 1.014 individual-adjusted; RR 1.012 also municipal-adjusted). Phthalate metabolites did not modify the association. Monitor-based, municipality-at-birth assignment likely biases toward the null.
Evidence for the claim as stated.
Papers sharing the cohort label are not one design. Veneto is an ecological SMR for municipalities; CCHS and PROTECT assign person- or pregnancy-level exposures and model individual outcomes; MIREC maps residues without a disease endpoint; the GraMo phthalate–adipose analysis is a cross-sectional surgery sample that cannot establish temporality (WQS β = −30.089 for GSH). 'Cohort evidence that pollution kills' collapses those differences.
Evidence for the claim as stated.
PROTECT also studied preterm birth (~9.1% of 1,092 pregnancies) but with modified Poisson risk ratios, not logistic ORs. Mean pregnancy PM₂.₅ was 6.8 μg/m³; an IQR increase gave RR 1.014 (individual-adjusted) and 1.012 (also municipal-adjusted). Phthalate metabolites did not modify the association. Monitor-based municipality assignment likely biases toward the null.
Evidence for the claim as stated.
Two preterm-birth analyses both sit near a 9% outcome and do not report the same contrast. Los Angeles finds ~30% PAH odds increases (benzo(a)pyrene 13%) plus 9–13% for several PM sources, with PAH data from only two stations. PROTECT reports RR 1.014 per IQR of pregnancy PM₂.₅ at a mean of 6.8 μg/m³. Odds ratios and risk ratios are not interchangeable, and the exposure products (PAH stations versus municipality monitors) are not the same assignment.
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.
Papers sharing the cohort label are not one design. Veneto is an ecological SMR for municipalities; CCHS and PROTECT assign person- or pregnancy-level exposures and model individual outcomes; MIREC maps residues without a disease endpoint; the GraMo phthalate–adipose analysis is a cross-sectional surgery sample that cannot establish temporality (WQS β = −30.089 for GSH). 'Cohort evidence that pollution kills' collapses those differences.
Two preterm-birth analyses both sit near a 9% outcome and do not report the same contrast. Los Angeles finds ~30% PAH odds increases (benzo(a)pyrene 13%) plus 9–13% for several PM sources, with PAH data from only two stations. PROTECT reports RR 1.014 per IQR of pregnancy PM₂.₅ at a mean of 6.8 μg/m³. Odds ratios and risk ratios are not interchangeable, and the exposure products (PAH stations versus municipality monitors) are not the same assignment.
Related papers in this topic
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