Abstract
Fine particulate matter air pollution (PM2.5) is a potential cause of preterm birth. Inconsistent findings from observational studies have motivated researchers to conduct more studies, but some degree of study heterogeneity is inevitable. The consequence of this feedback is a burgeoning research effort that results in marginal gains. The aim of this study was to develop and apply a method to establish the sufficiency and stability of estimates of associations as they have been published over time. Cohort studies identified in a recent systematic review and meta-analysis on the association between preterm birth and whole-pregnancy exposure to PM2.5 were selected. The estimates of the cohort studies were pooled with cumulative meta-analysis, whereby a new meta-analysis was run for each new study published over time. The relative risks (RR) and 95% confidence interval (CI) limits needed for a new study to move the cumulative RR to 1.00 were calculated. Findings indicate that the cumulative relative risks (cRR) for PM2.5 (cRR 1.07, 95% CI 1.03, 1.12) converged in 2015 (RR 1.07, 95% CI 1.01, 1.14). To change conclusions to a null association, a new study would need to observe a protective RR of 0.93 (95% CI limit 1.02) with precision equivalent to that achieved by all past 24 cohort studies combined. Preterm birth is associated with elevated PM2.5, and it is highly unlikely that any new observational study will alter this conclusion. Consequently, establishing whether an observational association exists is now less relevant an objective for future studies than characterising risk (magnitude, impact, pathways, populations and potential bias) and interventions. Sufficiency and stability can be effectively applied in meta-analyses and have the potential to reduce research waste.
Highlights
Publisher’s Note: MDPI stays neutralIt is well-accepted that fine particulate matter air pollution (PM2.5 ) is a cause of death from stroke, heart attack, lung cancer and chronic obstructive pulmonary disease [1,2,3]
The authors of the systematic review and meta-analysis (SRMA) reported that the pooled relative risk (RR) of preterm birth was 1.07 per 10 μg/m3 increase in whole-pregnancy exposure to PM2.5
The lowest prevalence of preterm birth was 3.0%, which was reported for a study from Victoria, Australia [44], and the largest was 14.0%, which was reported for a study from Colorado, USA [27]
Summary
It is well-accepted that fine particulate matter air pollution (PM2.5 ) is a cause of death from stroke, heart attack, lung cancer and chronic obstructive pulmonary disease [1,2,3]. These particulates are derived from heavy metals, sulphates and nitrates from incomplete fuel combustion, agricultural ammonia emissions, black carbon from burning diesel and biomass, sand, mineral dust and other specific sources that vary by geographic setting [4,5]. Despite the establishment of plausible biological pathways, the scientific statement for effects of PM2.5 exposure on pregnancy and birth outcomes such as preterm birth is “suggestive, but insufficient to infer” causation, partially due to the lack of consistent observational epidemiological findings. Preterm birth, defined as birth before 37 weeks of gestation, is a major health problem and has a global incidence with regard to jurisdictional claims in published maps and institutional affiliations
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