Croft · Air quality, atmosphere, & health 2018 · observational cohort study · n=135

Do elevated blood levels of omega-3 fatty acids modify effects of particulate air pollutants on fibrinogen?

Cited 8 times in the scientific literature.

Level 3 - non-randomized controlled study

Observational cohort study examining effect modification of air pollution exposure by biomarker levels.

PubMed 30147809 · doi:10.1007/s11869-018-0586-0 · record verified 2026-08-30

What was done

Researchers measured plasma fibrinogen and omega-3 fatty acid levels (% of total identified fatty acids) in blood samples from 135 patients treated at the University of Rochester Medical Center for myocardial infarction or stable ischemic heart disease requiring cardiac catheterization. Using ambient measurements of ultrafine, accumulation mode, and fine particles (PM2.5), Delta-C, and black carbon, linear regression models with interaction terms were used to evaluate whether associations between pollutant concentrations over the preceding 1-96 hours and serum fibrinogen differed between individuals with high (>5.12%) versus low-to-medium (<=5.12%) serum omega-3 fatty acid levels.

What was found

Each 5.6 ug/m3 increase in PM2.5 concentration in the prior hour was associated with a 3.1% increase in fibrinogen (95% CI: 1.5%, 4.7%) in subjects with low-to-medium total omega-3 levels, but only a 0.9% increase (95% CI: -1.5%, 3.2%) in patients with high omega-3 levels. This pattern was observed for fish oil-derived docosahexaenoic and eicosapentaenoic acids but not plant-derived alpha-linolenic acid. A similar attenuation was observed for black carbon in the prior 24 hours, but not for other particulate matter metrics.

Why it matters

This study provides evidence that higher circulating marine omega-3 fatty acids may mitigate acute prothrombotic and inflammatory fibrinogen responses triggered by particulate air pollution in cardiac patients.

Limits

The sample size was small (135 patients) and restricted to a single medical center population with cardiac disease. Ambient monitoring was used as a proxy for individual air pollution exposure, and residual confounding cannot be ruled out in an observational design.

Cited by