Impact of London's road traffic air and noise pollution on birth weight: retrospective population based cohort study.
ABSTRACT: Objective To investigate the relation between exposure to both air and noise pollution from road traffic and birth weight outcomes.Design Retrospective population based cohort study.Setting Greater London and surrounding counties up to the M25 motorway (2317 km2), UK, from 2006 to 2010.Participants 540?365 singleton term live births.Main outcome measures Term low birth weight (LBW), small for gestational age (SGA) at term, and term birth weight.Results Average air pollutant exposures across pregnancy were 41 ?g/m3 nitrogen dioxide (NO2), 73 ?g/m3 nitrogen oxides (NOx), 14 ?g/m3 particulate matter with aerodynamic diameter <2.5 ?m (PM2.5), 23 ?g/m3 particulate matter with aerodynamic diameter <10 ?m (PM10), and 32 ?g/m3 ozone (O3). Average daytime (LAeq,16hr) and night-time (Lnight) road traffic A-weighted noise levels were 58 dB and 53 dB respectively. Interquartile range increases in NO2, NOx, PM2.5, PM10, and source specific PM2.5 from traffic exhaust (PM2.5 traffic exhaust) and traffic non-exhaust (brake or tyre wear and resuspension) (PM2.5 traffic non-exhaust) were associated with 2% to 6% increased odds of term LBW, and 1% to 3% increased odds of term SGA. Air pollutant associations were robust to adjustment for road traffic noise. Trends of decreasing birth weight across increasing road traffic noise categories were observed, but were strongly attenuated when adjusted for primary traffic related air pollutants. Only PM2.5 traffic exhaust and PM2.5 were consistently associated with increased risk of term LBW after adjustment for each of the other air pollutants. It was estimated that 3% of term LBW cases in London are directly attributable to residential exposure to PM2.5>13.8 ?g/m3during pregnancy.Conclusions The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. The results suggest little evidence for an independent exposure-response effect of traffic related noise on birth weight outcomes.
Project description:Numerous studies have linked criteria air pollutants with adverse birth outcomes, but there is less information on the importance of specific emission sources, such as traffic, and air toxics.We used three exposure data sources to examine odds of term low birth weight (LBW) in Los Angeles, California, women when exposed to high levels of traffic-related air pollutants during pregnancy.We identified term births during 1 June 2004 to 30 March 2006 to women residing within 5 miles of a South Coast Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. Pregnancy period average exposures were estimated for air toxics, including polycyclic aromatic hydrocarbons (PAHs), source-specific particulate matter < 2.5 ?m in aerodynamic diameter (PM2.5) based on a chemical mass balance model, criteria air pollutants from government monitoring data, and land use regression (LUR) model estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of term LBW (< 2,500 g) were examined using logistic regression.Odds of term LBW increased approximately 5% per interquartile range increase in entire pregnancy exposures to several correlated traffic pollutants: LUR measures of NO, NO2, and NOx, elemental carbon, and PM2.5 from diesel and gasoline combustion and paved road dust (geological PM2.5).These analyses provide additional evidence of the potential impact of traffic-related air pollution on fetal growth. Particles from traffic sources should be a focus of future studies.
Project description:BACKGROUND:Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources. OBJECTIVES:We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities. METHODS:Based on detailed emission databases, monitoring data, and high-resolution dispersion models, we calculated source contributions to PM with aerodynamic diameter ?10?m (PM10), PM with aerodynamic diameter ?2.5?m (PM2.5), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models. RESULTS:We observed 5,166 and 3,119 incident IHD and stroke cases, respectively, in 114,758 participants. Overall, few consistent associations were observed between the different air pollution measures and IHD or stroke incidence. However, same-year levels of ambient locally emitted BC (range: 0.01-4.6??g/m3) were associated with a 4.0% higher risk of incident stroke per interquartile range (IQR), 0.30??g/m3 [95% confidence interval (CI): 0.04, 7.8]. This association was primarily related to BC from traffic exhaust. PM10 (range: 4.4-52??g/m3) and PM2.5 (range: 2.9-22??g/m3) were not associated with stroke. Associations with incident IHD were observed only for PM2.5 exposure from residential heating. DISCUSSION:Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations. https://doi.org/10.1289/EHP4757.
Project description:Road traffic is a major source of urban air pollution responsible for substantial premature mortality. Until recently, attention has focussed primarily on exhaust emissions of particulate matter from traffic as a causal factor. From analysis of air quality measurement data from the UK and France, we demonstrate that road traffic exhaust has a far greater impact on concentrations of nitrogen dioxide than of PM2.5. PM2.5 and carbonaceous particle concentrations have been declining appreciably since 2010/11 due to the use of diesel particle filters, but little change is seen in nitrogen dioxide over the period from 1995 to 2015. It is shown that the effect of NO2 from road traffic upon premature mortality was ten-fold greater than that of PM2.5 even before the widespread use of diesel particle filters, and is now considerably larger. The overwhelming contribution of diesel compared to gasoline-fuelled vehicles to emissions of both PM2.5 and NO2 emphasises the importance of further controls on emissions from diesels.
Project description:INTRODUCTION:Intrauterine growth restriction has been associated with exposure to air pollution, but there is a need to clarify which sources and components are most likely responsible. This study investigated the associations between low birth weight (LBW, <2500g) in term born infants (?37 gestational weeks) and air pollution by source and composition in California, over the period 2001-2008. METHODS:Complementary exposure models were used: an empirical Bayesian kriging model for the interpolation of ambient pollutant measurements, a source-oriented chemical transport model (using California emission inventories) that estimated fine and ultrafine particulate matter (PM2.5 and PM0.1, respectively) mass concentrations (4km×4km) by source and composition, a line-source roadway dispersion model at fine resolution, and traffic index estimates. Birth weight was obtained from California birth certificate records. A case-cohort design was used. Five controls per term LBW case were randomly selected (without covariate matching or stratification) from among term births. The resulting datasets were analyzed by logistic regression with a random effect by hospital, using generalized additive mixed models adjusted for race/ethnicity, education, maternal age and household income. RESULTS:In total 72,632 singleton term LBW cases were included. Term LBW was positively and significantly associated with interpolated measurements of ozone but not total fine PM or nitrogen dioxide. No significant association was observed between term LBW and primary PM from all sources grouped together. A positive significant association was observed for secondary organic aerosols. Exposure to elemental carbon (EC), nitrates and ammonium were also positively and significantly associated with term LBW, but only for exposure during the third trimester of pregnancy. Significant positive associations were observed between term LBW risk and primary PM emitted by on-road gasoline and diesel or by commercial meat cooking sources. Primary PM from wood burning was inversely associated with term LBW. Significant positive associations were also observed between term LBW and ultrafine particle numbers modeled with the line-source roadway dispersion model, traffic density and proximity to roadways. DISCUSSION:This large study based on complementary exposure metrics suggests that not only primary pollution sources (traffic and commercial meat cooking) but also EC and secondary pollutants are risk factors for term LBW.
Project description:BACKGROUND:Air pollution exposure has been linked to coronary heart disease, although evidence on PM2.5 and myocardial infarction (MI) incidence is mixed. OBJECTIVES:This prospective cohort study aimed to investigate associations between long-term exposure to air pollution and MI incidence, adjusting for road traffic noise. METHODS:We used data from the nationwide Danish Nurse Cohort on 22,882 female nurses (>44?years of age) who, at recruitment in 1993 or 1999, reported information on cardiovascular disease risk factors. Data on MI incidence was collected from the Danish National Patient Register until the end of 2014. Annual mean concentrations of particulate matter (PM) with a diameter <2.5??g/m3 (PM2.5), PM10, nitrogen dioxide (NO2), and nitrogen oxides (NOx) at the nurses' residences since 1990 (PM10 and PM2.5) or 1970 (NO2 and NOx) were estimated using the Danish Eulerian Hemispheric Model/Urban Background Model/AirGIS (DEHM/UBM/AirGIS) dispersion model. We used time-varying Cox regression models to examine the association between 1- and 3-y running means of these pollutants, as well as 23-y running means of NO2 and NOx, with both overall and fatal incident MI. Associations were explored in three progressively adjusted models: Model 1, adjusted for age and baseline year; Model 2, with further adjustment for potential confounding by lifestyle and cardiovascular disease risk factors; and Model 3, with further adjustment for road traffic noise, modeled as the annual mean of a weighted 24-h average (Lden). RESULTS:Of the 22,882 women, 641 developed MI during a mean follow-up of 18.6 y, 121 (18.9%) of which were fatal. Reported hazard ratios (HRs) were based on interquartile range increases of 5.3, 5.5, 8.1, and 11.5??g/m3 for PM2.5, PM10, NO2, and NOx, respectively. In Model 1, we observed a positive association between a 3-y running mean of PM2.5 and an overall incident MI with an HR=?1.20 (95% CI: 1.07, 1.35), which attenuated to HR=?1.06 (95% CI: 0.92, 1.23) in Model 2. In Model 1 for incident fatal MI, we observed a strong association with a 3-y running mean of PM2.5, with an HR=?1.69 (95% CI: 1.33, 2.13), which attenuated to HR=?1.35 (95% CI: 1.01, 1.81) in Model 2. Similar associations were seen for PM10, with 3-y, Model 2 estimates for overall and fatal incident MI of HR=?1.06 (95% CI: 0.91, 1.23) and HR=?1.35 (95% CI: 1.01, 1.81), respectively. No evidence of an association was observed for NO2 or NOx. For all pollutants, associations in Model 2 were robust to further adjustment for road traffic noise in Model 3 and were similar for a 1-y running mean exposure. CONCLUSIONS:We found no association between long-term exposure to PM2.5, PM10, NO2, or NOx and overall MI incidence, but we observed positive associations for PM2.5 and PM10 with fatal MI. We present novel findings that the association between PM and MI incidence is robust to adjustment for road traffic noise. https://doi.org/10.1289/EHP5818.
Project description:Background:Low birth weight (LBW) has been associated with adverse health outcomes across the lifespan. Among ethnic/racial minority populations, few studies have examined the association between LBW (<2,500 or ?2,500 g) and prenatal exposure to air pollution, a key modifiable environmental risk factor. Methods:We examined the association between LBW and prenatal exposure to PM2.5 in a Hispanic and black population in Puerto Rico between 1999 and 2013, adjusting for individual and municipality-level confounders. We used modified Poisson regression to estimate the association and performed sensitivity analyses treating birth weight as continuous or polychotomous. In secondary analyses, we applied a 2-stage mixed effects model suitable for longitudinally measured exposures and binary outcomes. Results:Among 332,129 total and 275,814 term births, 12.2% and 6.3% of infants had LBW, respectively. Eighty-eight percent of mothers were Hispanic. Mean (SD) PM2.5 concentrations declined from 9.9 (1.7) ?g/m3 in 1999 to 6.1 (1.1) ?g/m3 in 2013. Mean birth weights dropped to 3,044 g in 2010 and rose steadily afterward. Among term births, a SD increase in PM2.5 was associated with a 3.2% (95% CI = -1.0%, 6.3%) higher risk of LBW. First (risk ratio, 1.02; 95% CI = 1.00, 1.04) and second (1.02; 95% CI = 1.01, 1.05) trimester exposures were associated with increased LBW risk. In a 2-stage approach that longitudinally modeled monthly prenatal exposure levels, a standard deviation increase in average PM2.5 was associated with higher risk of LBW (odds ratio, 1.04; 95% CI = 1.01, 1.08). Conclusions:In Puerto Rico, LBW is associated with prenatal PM2.5 exposure.
Project description:BACKGROUND: Studies on the association between traffic noise and cardiovascular diseases have rarely considered air pollution as a covariate in the analyses. Isolated systolic hypertension has not yet been in the focus of epidemiological noise research. METHODS: The association between traffic noise (road and rail) and the prevalence of hypertension was assessed in two study populations with a total of 4,166 participants 25-74 years of age. Traffic noise (weighted day-night average noise level; LDN) at the facade of the dwellings was derived from noise maps. Annual average PM2.5 mass concentrations at residential addresses were estimated by land-use regression. Hypertension was assessed by blood pressure readings, self-reported doctor-diagnosed hypertension, and antihypertensive drug intake. RESULTS: In the Greater Augsburg, Germany, study population, traffic noise and air pollution were not associated with hypertension. In the City of Augsburg population (n = 1,893), where the exposure assessment was more detailed, the adjusted odds ratio (OR) for a 10-dB(A) increase in noise was 1.16 (95% CI: 1.00, 1.35), and 1.11 (95% CI: 0.94, 1.30) after additional adjustment for PM2.5. The adjusted OR for a 1-?g/m3 increase in PM2.5 was 1.15 (95% CI: 1.02, 1.30), and 1.11 (95% CI: 0.98, 1.27) after additional adjustment for noise. For isolated systolic hypertension, the fully adjusted OR for noise was 1.43 (95% CI: 1.10, 1.86) and for PM2.5 was 1.08 (95% CI: 0.87, 1.34). CONCLUSIONS: Traffic noise and PM2.5 were both associated with a higher prevalence of hypertension. Mutually adjusted associations with hypertension were positive but no longer statistically significant.
Project description:Prenatal exposure to fine particulate matter air pollution with aerodynamic diameter ?2.5 ?m (PM2.5) has been associated with preterm delivery and low birth weight (LBW), but few studies have examined possible effect modification by oxidative potential.The aim of this study was to evaluate if regional differences in the oxidative potential of PM2.5 modify the relationship between PM2.5 and adverse birth outcomes.A retrospective cohort study was conducted using 196,171 singleton births that occurred in 31 cities in the province of Ontario, Canada, from 2006 to 2012. Daily air pollution data were collected from ground monitors, and city-level PM2.5 oxidative potential was measured. We used random-effects meta-analysis to combine the estimates of effect from regression models across cities on preterm birth, term LBW, and term birth weight and used meta-regression to evaluate the modifying effect of PM2.5 oxidative potential.An interquartile increase (2.6??g/m3) in first-trimester PM2.5 was positively associated with term LBW among women in the highest quartile of glutathione (GSH)-related oxidative potential [odds?ratio?(OR)=1.28; 95% confidence interval (CI): 1.10, 1.48], but not the lowest quartile (OR=0.99; 95% CI: 0.87, 1.14; p-interaction=0.03). PM2.5 on the day of delivery also was associated with preterm birth among women in the highest quartile of GSH-related oxidative potential [hazard?ratio?(HR)=1.02; 95% CI: 1.01, 1.04], but not the lowest quartile [HR=0.97; 95% CI: 0.95, 1.00; p-interaction=0.04]. Between-city differences in ascorbate (AA)-related oxidative potential did not significantly modify associations with PM2.5.Between-city differences in GSH-related oxidative potential may modify the impact of PM2.5 on the risk of term LBW and preterm birth. https://doi.org/10.1289/EHP2535.
Project description:Aims:Blood biochemistry may provide information on associations between road traffic noise, air pollution, and cardiovascular disease risk. We evaluated this in two large European cohorts (HUNT3, Lifelines). Methods and results:Road traffic noise exposure was modelled for 2009 using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU). Annual ambient air pollution (PM10, NO2) at residence was estimated for 2007 using a Land Use Regression model. The statistical platform DataSHIELD was used to pool data from 144?082 participants aged??20?years to enable individual-level analysis. Generalized linear models were fitted to assess cross-sectional associations between pollutants and high-sensitivity C-reactive protein (hsCRP), blood lipids and for (Lifelines only) fasting blood glucose, for samples taken during recruitment in 2006-2013. Pooling both cohorts, an inter-quartile range (IQR) higher day-time noise (5.1?dB(A)) was associated with 1.1% [95% confidence interval (95% CI: 0.02-2.2%)] higher hsCRP, 0.7% (95% CI: 0.3-1.1%) higher triglycerides, and 0.5% (95% CI: 0.3-0.7%) higher high-density lipoprotein (HDL); only the association with HDL was robust to adjustment for air pollution. An IQR higher PM10 (2.0 µg/m3) or NO2 (7.4 µg/m3) was associated with higher triglycerides (1.9%, 95% CI: 1.5-2.4% and 2.2%, 95% CI: 1.6-2.7%), independent of adjustment for noise. Additionally for NO2, a significant association with hsCRP (1.9%, 95% CI: 0.5-3.3%) was seen. In Lifelines, an IQR higher noise (4.2?dB(A)) and PM10 (2.4 µg/m3) was associated with 0.2% (95% CI: 0.1-0.3%) and 0.6% (95% CI: 0.4-0.7%) higher fasting glucose respectively, with both remaining robust to adjustment for air/noise pollution. Conclusion:Long-term exposures to road traffic noise and ambient air pollution were associated with blood biochemistry, providing a possible link between road traffic noise/air pollution and cardio-metabolic disease risk.
Project description:Few studies have examined associations of birth outcomes with toxic air pollutants (air toxics) in traffic exhaust. This study included 8,181 term low birth weight (LBW) children and 370,922 term normal-weight children born between January 1, 1995, and December 31, 2006, to women residing within 5 miles (8 km) of an air toxics monitoring station in Los Angeles County, California. Additionally, land-use-based regression (LUR)-modeled estimates of levels of nitric oxide, nitrogen dioxide, and nitrogen oxides were used to assess the influence of small-area variations in traffic pollution. The authors examined associations with term LBW (?37 weeks' completed gestation and birth weight <2,500 g) using logistic regression adjusted for maternal age, race/ethnicity, education, parity, infant gestational age, and gestational age squared. Odds of term LBW increased 2%-5% (95% confidence intervals ranged from 1.00 to 1.09) per interquartile-range increase in LUR-modeled estimates and monitoring-based air toxics exposure estimates in the entire pregnancy, the third trimester, and the last month of pregnancy. Models stratified by monitoring station (to investigate air toxics associations based solely on temporal variations) resulted in 2%-5% increased odds per interquartile-range increase in third-trimester benzene, toluene, ethyl benzene, and xylene exposures, with some confidence intervals containing the null value. This analysis highlights the importance of both spatial and temporal contributions to air pollution in epidemiologic birth outcome studies.