Rachel B Smith1, Sean D Beevers2, John Gulliver3, David Dajnak2, Daniela Fecht4, Marta Blangiardo5, Margaret Douglass4, Anna L Hansell6, H Ross Anderson7, Frank J Kelly8, Mireille B Toledano9. 1. MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK; NIHR HPRU in Health Impact of Environmental Hazards, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK. 2. MRC-PHE Centre for Environment and Health, Environmental Research Group, Faculty of Life Sciences & Medicine, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK. 3. MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK; Centre for Environmental Health and Sustainability, University of Leicester, Leicester, UK. 4. UK Small Area Health Statistics Unit, MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, W2 1PG, UK. 5. MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK. 6. NIHR HPRU in Health Impact of Environmental Hazards, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK; Centre for Environmental Health and Sustainability, University of Leicester, Leicester, UK; UK Small Area Health Statistics Unit, MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, W2 1PG, UK. 7. MRC-PHE Centre for Environment and Health, Environmental Research Group, Faculty of Life Sciences & Medicine, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK; Population Health Research Institute, St George's, University of London, Cranmer Terrace, London SW17 0RE, UK. 8. NIHR HPRU in Health Impact of Environmental Hazards, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK; MRC-PHE Centre for Environment and Health, Environmental Research Group, Faculty of Life Sciences & Medicine, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK. 9. MRC-PHE Centre for Environment and Health, Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK; NIHR HPRU in Health Impact of Environmental Hazards, King's College London, Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK. Electronic address: m.toledano@imperial.ac.uk.
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.
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.
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