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

TY - JOUR

T1 - Impacts of air pollution and noise on risk of preterm birth and stillbirth in London

AU - Smith, Rachel B.

AU - Beevers, Sean D.

AU - Gulliver, John

AU - Dajnak, David

AU - Fecht, Daniela

AU - Blangiardo, Marta

AU - Douglass, Margaret

AU - Hansell, Anna L.

AU - Anderson, H. Ross

AU - Kelly, Frank J.

AU - Toledano, Mireille B.

PY - 2020/1/1

Y1 - 2020/1/1

N2 - 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.

AB - 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.

KW - Nitrogen dioxide

KW - Nitrogen oxides

KW - Ozone

KW - Particulate matter

KW - Pregnancy

KW - Traffic

KW - Vehicle exhaust

UR - https://www.scopus.com/pages/publications/85075501815

U2 - 10.1016/j.envint.2019.105290

DO - 10.1016/j.envint.2019.105290

M3 - Article

AN - SCOPUS:85075501815

SN - 0160-4120

VL - 134

JO - Environment International

JF - Environment International

M1 - 105290

ER -