Impacts of air pollution and noise on risk of preterm birth and stillbirth in London

Rachel B. Smith, Sean D. Beevers, John Gulliver, David Dajnak, Daniela Fecht, Marta Blangiardo, Margaret Douglass, Anna L. Hansell, H. Ross Anderson, Frank J. Kelly, Mireille B. Toledano*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

Background: Evidence for associations between ambient air pollution and preterm birth and stillbirth is inconsistent. Road traffic produces both air pollutants and noise, but few studies have examined these co-exposures together and none to date with all-cause or cause-specific stillbirths. Objectives: To analyse the relationship between long-term exposure to air pollution and noise at address level during pregnancy and risk of preterm birth and stillbirth. Methods: The study population comprised 581,774 live and still births in the Greater London area, 2006–2010. Outcomes were preterm birth (<37 completed weeks gestation), all-cause stillbirth and cause-specific stillbirth. Exposures during pregnancy to particulate matter with diameter <2.5 μm (PM2.5) and <10 μm (PM10), ozone (O3), primary traffic air pollutants (nitrogen dioxide, nitrogen oxides, PM2.5 from traffic exhaust and traffic non-exhaust), and road traffic noise were estimated based on maternal address at birth. Results: An interquartile range increase in O3 exposure was associated with elevated risk of preterm birth (OR 1.15 95% CI: 1.11, 1.18, for both Trimester 1 and 2), all-cause stillbirth (Trimester 1 OR 1.17 95% CI: 1.07, 1.27; Trimester 2 OR 1.20 95% CI: 1.09, 1.32) and asphyxia-related stillbirth (Trimester 1 OR 1.22 95% CI: 1.01, 1.49). Odds ratios with the other air pollutant exposures examined were null or <1, except for primary traffic non-exhaust related PM2.5, which was associated with 3% increased odds of preterm birth (Trimester 1) and 7% increased odds stillbirth (Trimester 1 and 2) when adjusted for O3. Elevated risk of preterm birth was associated with increasing road traffic noise, but only after adjustment for certain air pollutant exposures. Discussion: Our findings suggest that exposure to higher levels of O3 and primary traffic non-exhaust related PM2.5 during pregnancy may increase risk of preterm birth and stillbirth; and a possible relationship between long-term traffic-related noise and risk of preterm birth. These findings extend and strengthen the evidence base for important public health impacts of ambient ozone, particulate matter and noise in early life.

Original languageEnglish
Article number105290
JournalEnvironment International
Volume134
DOIs
Publication statusPublished - Jan 2020
Externally publishedYes

Bibliographical note

Funding Information:
We thank Peter Hambly of the SAHSU database team for technical support and the TRAFFIC study group for their constructive comments. CACI tobacco expenditure data is © Copyright 1996-2014 CACI Limited. We attest that we have obtained appropriate permissions and paid any required fees for use of copyright protected materials. Funding: This work was funded by the UK Natural Environment Research Council , Medical Research Council , Economic and Social Research Council , Department of Environment, Food and Rural Affairs , and Department of Health ( NE/I00789X/1 , NE/I008039/1 ) through the cross-research council Environmental Exposures & Health Initiative. The research was part funded by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Health Impact of Environmental Hazards at King’s College London in partnership with Public Health England (PHE). The work of the UK Small Area Health Statistics Unit (SAHSU) is funded by Public Health England as part of the MRC-PHE Centre for Environment and Health, funded also by the UK Medical Research Council (MR/L01341X/1). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, Public Health England or the Department of Health. The funders had no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication. Author contributions: MBT, JG, HRA, SDB, FJK contributed to study conception and design; DF, JG, SDB, DD, HRA and FJK to exposure assessment; and MD, DF and ALH to acquisition of health and confounder data. RBS contributed to study design, wrote the statistical analysis plan, conducted the data analyses, and drafted the report. MBT contributed to the statistical analysis plan and the data analyses. MB contributed to the study design and statistical analysis plan. All authors contributed to interpreting the analyses and critically revising the article, approved the final manuscript. Data sharing: Health data are available from the data providers on application with appropriate ethics and governance permissions, but we do not hold data provider, ethics, or governance permissions to share the dataset with third parties.

Funding Information:
We thank Peter Hambly of the SAHSU database team for technical support and the TRAFFIC study group for their constructive comments. CACI tobacco expenditure data is ? Copyright 1996-2014 CACI Limited. We attest that we have obtained appropriate permissions and paid any required fees for use of copyright protected materials. Funding: This work was funded by the UK Natural Environment Research Council, Medical Research Council, Economic and Social Research Council, Department of Environment, Food and Rural Affairs, and Department of Health (NE/I00789X/1, NE/I008039/1) through the cross-research council Environmental Exposures & Health Initiative. The research was part funded by the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Health Impact of Environmental Hazards at King's College London in partnership with Public Health England (PHE). The work of the UK Small Area Health Statistics Unit (SAHSU) is funded by Public Health England as part of the MRC-PHE Centre for Environment and Health, funded also by the UK Medical Research Council (MR/L01341X/1). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, Public Health England or the Department of Health. The funders had no role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the article for publication. Author contributions: MBT, JG, HRA, SDB, FJK contributed to study conception and design; DF, JG, SDB, DD, HRA and FJK to exposure assessment; and MD, DF and ALH to acquisition of health and confounder data. RBS contributed to study design, wrote the statistical analysis plan, conducted the data analyses, and drafted the report. MBT contributed to the statistical analysis plan and the data analyses. MB contributed to the study design and statistical analysis plan. All authors contributed to interpreting the analyses and critically revising the article, approved the final manuscript. Data sharing: Health data are available from the data providers on application with appropriate ethics and governance permissions, but we do not hold data provider, ethics, or governance permissions to share the dataset with third parties. None.

Publisher Copyright:
© 2019 The Authors

Keywords

  • Nitrogen dioxide
  • Nitrogen oxides
  • Ozone
  • Particulate matter
  • Pregnancy
  • Traffic
  • Vehicle exhaust

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