A Cohort Study of Traffic-Related Air Pollution Impacts on Birth Outcomes
Background: Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.
Objectives: We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW) , and preterm birth using spatiotemporal exposure metrics.
Methods: With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) µm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon) , and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile) , term LBW (< 2,500 g) , and preterm birth.
Results: Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI) , 1.07-1.49] and an 11% (95% CI, 1.01-1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02 ; 95% CI, 1.00-1.04 ; IDW: OR = 1.05 ; 95% CI, 1.03-1.08 per 10-µg/m increase in NO) . For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks) . No consistent patterns suggested exposure windows of greater relevance.
Conclusion: Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.
Numerous studies have indicated associations between exposure to ambient air pollution and adverse pregnancy outcomes. Such associations, if determined to be causal, are likely to result in significant public health impacts given the widespread exposure to air pollution and the fact that low birth weight (LBW) or preterm births are subsequently associated with long-term sequelae such as developmental disability and chronic lung disease (Cano et al. 2001; Dik et al. 2004). Determination of a causal relationship between air pollution and adverse pregnancy outcomes would have implications for burden of disease measures and add to the importance of strategies to mitigate the health effects of air pollution exposure.
Previous studies have been reviewed in detail. Sˇram et al. (2005) concluded that evidence is sufficient to support a causal association between ambient concentrations of particulate matter and LBW, but evidence of effects for other pollutants and for other outcomes such as preterm birth is less robust. Maisonet et al. (2004) concluded that studies to date support small effects of air pollution on preterm birth and small for gestational age birth (SGA), but not full-term LBW. In a systematic review, Glinianaia et al. (2004) suggested that evidence of associations with air pollution and fetal growth or pregnancy duration is limited and inconclusive and argued for population-based cohort designs using high-quality individual exposure estimates. These reviews highlight the difficulties in interpreting an evidence base with differences among methods and with important limitations. First, most studies are either time-series studies (Dugandzic et al. 2006; Liu et al. 2003, 2007; Mannes et al. 2005; Sagiv et al. 2005) that relate relatively short-term changes in air pollution concentrations to temporal changes in rates of adverse pregnancy outcomes or, less frequently, cohort analyses that compare outcomes between locations with differing levels of ambient air pollution (Salam et al. 2005) based on interpolated ambient monitoring network data. Between-city comparisons are subject to potential confounding because covariates may be highly correlated with air pollution, whereas time-series studies are problematic to interpret because they relate short-term changes in air pollution that are driven primarily by meteorology to outcomes. They inherently assume that the impact of air pollution on birth outcomes is acute, require knowledge of the relevant periods of pregnancy during which air pollution may have impacts, and are subject to potential confounding by seasonally varying factors. As reviewed by Glinianaia et al. (2004), a number of studies have suggested stronger relationships between birth outcomes and exposure during specific periods of pregnancy based on comparison of statistical effect sizes. However, results across studies have not consistently identified specific periods of exposure that are most closely linked to adverse pregnancy outcomes.
Increasingly, air pollution researchers have identified important spatial variability in air pollution concentrations within airsheds (Hoek et al. 2002b; Lewne et al. 2004; Zhang et al. 2004; Zhu et al. 2004). In many situations these contrasts are of greater magnitude than between-city or temporal contrasts (Jerrett et al. 2005). Such spatial contrasts, primarily related to measures of proximity to traffic corridors, have been associated with a number of health impacts including mortality (Hoek et al. 2002a; Maynard et al. 2007; Miller et al. 2007; Nafstad et al. 2004; Roemer and van Wijnen 2001), asthma and respiratory symptoms (Bayer-Oglesby et al. 2006; Brauer et al. 2002, 2007; Gauderman et al. 2005, 2007; McConnell et al. 2006; Ryan et al. 2005; Smargiassi et al. 2006), and otitis media (Brauer et al. 2006).
Application of within-airshed spatial contrasts in birth outcome studies are few (Leem et al. 2006; Parker et al. 2005; Ritz and Yu 1999; Ritz et al. 2000; Slama et al. 2007; Wilhelm and Ritz 2003, 2005). These studies, though provocative, have been limited largely to Southern California -- a metropolitan area with relatively high levels of ambient air pollution. They relied on interpolated ambient monitoring data or simple road proximity measures rather than high-resolution spatial contrasts in concentrations. We sought to assess the relationship between reproductive outcomes and spatial and temporally varying levels of air pollution in the metropolitan area of Vancouver, British Columbia, Canada, a city with relatively low levels of ambient air pollution. We estimated exposures at the individual level, for a population-based cohort using both monitor-based methods and land use regression models based on proximity to traffic sources, land use, population density, and topographic features. Even in Vancouver, an area with a dense ambient monitoring network, exposure assessment based on regulatory monitoring network data is more suited to characterizing temporal variability. Land use regression models, even those with temporal components, as in this analysis, focus on high-resolution spatial variability in air pollutant concentrations.
The literature describing associations between air pollution and birth outcomes has focused on clinically defined outcomes of LBW and preterm birth, defined in a variety of ways, which complicates comparisons. The underlying biological processes -- fetal growth restriction and inadequate gestational length -- are incompletely understood and imperfectly represented in routinely available perinatal measurements available in vital statistic records. We elected to focus on SGA births as a primary outcome measure, because birth weight as a function of gestational age has a direct effect on perinatal morbidity and mortality (Pollack and Divon 1992).
LBW may result from complex and multiple pathways of fetal growth restriction attributed to maternal, fetal, or placental factors. Three broad categories of biological factors have been suggested to play a role in inadequate fetal gestation: abnormality of the biological clock, abnormal implantation, and infection and inflammation (Mattison et al. 2003).
The current theories provide multiple sites at which environmental factors may influence biological factors to modulate fetal growth and induce preterm birth. However, specific toxicologic mechanisms including relevant timing during gestational development are not known. We explored each of these processes, fetal growth restriction and inadequate gestational length, separately, and explored the influences of exposure timing in early and late pregnancy.
Background: Evidence suggests that air pollution exposure adversely affects pregnancy outcomes. Few studies have examined individual-level intraurban exposure contrasts.
Objectives: We evaluated the impacts of air pollution on small for gestational age (SGA) birth weight, low full-term birth weight (LBW) , and preterm birth using spatiotemporal exposure metrics.
Methods: With linked administrative data, we identified 70,249 singleton births (1999-2002) with complete covariate data (sex, ethnicity, parity, birth month and year, income, education) and maternal residential history in Vancouver, British Columbia, Canada. We estimated residential exposures by month of pregnancy using nearest and inverse-distance weighting (IDW) of study area monitors [carbon monoxide, nitrogen dioxide, nitric oxide, ozone, sulfur dioxide, and particulate matter < 2.5 (PM2.5) or < 10 (PM10) µm in aerodynamic diameter], temporally adjusted land use regression (LUR) models (NO, NO2, PM2.5, black carbon) , and proximity to major roads. Using logistic regression, we estimated the risk of mean (entire pregnancy, first and last month of pregnancy, first and last 3 months) air pollution concentrations on SGA (< 10th percentile) , term LBW (< 2,500 g) , and preterm birth.
Results: Residence within 50 m of highways was associated with a 26% increase in SGA [95% confidence interval (CI) , 1.07-1.49] and an 11% (95% CI, 1.01-1.23) increase in LBW. Exposure to all air pollutants except O3 was associated with SGA, with similar odds ratios (ORs) for LUR and monitoring estimates (e.g., LUR: OR = 1.02 ; 95% CI, 1.00-1.04 ; IDW: OR = 1.05 ; 95% CI, 1.03-1.08 per 10-µg/m increase in NO) . For preterm births, associations were observed with PM2.5 for births < 37 weeks gestation (and for other pollutants at < 30 weeks) . No consistent patterns suggested exposure windows of greater relevance.
Conclusion: Associations between traffic-related air pollution and birth outcomes were observed in a population-based cohort with relatively low ambient air pollution exposure.
Numerous studies have indicated associations between exposure to ambient air pollution and adverse pregnancy outcomes. Such associations, if determined to be causal, are likely to result in significant public health impacts given the widespread exposure to air pollution and the fact that low birth weight (LBW) or preterm births are subsequently associated with long-term sequelae such as developmental disability and chronic lung disease (Cano et al. 2001; Dik et al. 2004). Determination of a causal relationship between air pollution and adverse pregnancy outcomes would have implications for burden of disease measures and add to the importance of strategies to mitigate the health effects of air pollution exposure.
Previous studies have been reviewed in detail. Sˇram et al. (2005) concluded that evidence is sufficient to support a causal association between ambient concentrations of particulate matter and LBW, but evidence of effects for other pollutants and for other outcomes such as preterm birth is less robust. Maisonet et al. (2004) concluded that studies to date support small effects of air pollution on preterm birth and small for gestational age birth (SGA), but not full-term LBW. In a systematic review, Glinianaia et al. (2004) suggested that evidence of associations with air pollution and fetal growth or pregnancy duration is limited and inconclusive and argued for population-based cohort designs using high-quality individual exposure estimates. These reviews highlight the difficulties in interpreting an evidence base with differences among methods and with important limitations. First, most studies are either time-series studies (Dugandzic et al. 2006; Liu et al. 2003, 2007; Mannes et al. 2005; Sagiv et al. 2005) that relate relatively short-term changes in air pollution concentrations to temporal changes in rates of adverse pregnancy outcomes or, less frequently, cohort analyses that compare outcomes between locations with differing levels of ambient air pollution (Salam et al. 2005) based on interpolated ambient monitoring network data. Between-city comparisons are subject to potential confounding because covariates may be highly correlated with air pollution, whereas time-series studies are problematic to interpret because they relate short-term changes in air pollution that are driven primarily by meteorology to outcomes. They inherently assume that the impact of air pollution on birth outcomes is acute, require knowledge of the relevant periods of pregnancy during which air pollution may have impacts, and are subject to potential confounding by seasonally varying factors. As reviewed by Glinianaia et al. (2004), a number of studies have suggested stronger relationships between birth outcomes and exposure during specific periods of pregnancy based on comparison of statistical effect sizes. However, results across studies have not consistently identified specific periods of exposure that are most closely linked to adverse pregnancy outcomes.
Increasingly, air pollution researchers have identified important spatial variability in air pollution concentrations within airsheds (Hoek et al. 2002b; Lewne et al. 2004; Zhang et al. 2004; Zhu et al. 2004). In many situations these contrasts are of greater magnitude than between-city or temporal contrasts (Jerrett et al. 2005). Such spatial contrasts, primarily related to measures of proximity to traffic corridors, have been associated with a number of health impacts including mortality (Hoek et al. 2002a; Maynard et al. 2007; Miller et al. 2007; Nafstad et al. 2004; Roemer and van Wijnen 2001), asthma and respiratory symptoms (Bayer-Oglesby et al. 2006; Brauer et al. 2002, 2007; Gauderman et al. 2005, 2007; McConnell et al. 2006; Ryan et al. 2005; Smargiassi et al. 2006), and otitis media (Brauer et al. 2006).
Application of within-airshed spatial contrasts in birth outcome studies are few (Leem et al. 2006; Parker et al. 2005; Ritz and Yu 1999; Ritz et al. 2000; Slama et al. 2007; Wilhelm and Ritz 2003, 2005). These studies, though provocative, have been limited largely to Southern California -- a metropolitan area with relatively high levels of ambient air pollution. They relied on interpolated ambient monitoring data or simple road proximity measures rather than high-resolution spatial contrasts in concentrations. We sought to assess the relationship between reproductive outcomes and spatial and temporally varying levels of air pollution in the metropolitan area of Vancouver, British Columbia, Canada, a city with relatively low levels of ambient air pollution. We estimated exposures at the individual level, for a population-based cohort using both monitor-based methods and land use regression models based on proximity to traffic sources, land use, population density, and topographic features. Even in Vancouver, an area with a dense ambient monitoring network, exposure assessment based on regulatory monitoring network data is more suited to characterizing temporal variability. Land use regression models, even those with temporal components, as in this analysis, focus on high-resolution spatial variability in air pollutant concentrations.
The literature describing associations between air pollution and birth outcomes has focused on clinically defined outcomes of LBW and preterm birth, defined in a variety of ways, which complicates comparisons. The underlying biological processes -- fetal growth restriction and inadequate gestational length -- are incompletely understood and imperfectly represented in routinely available perinatal measurements available in vital statistic records. We elected to focus on SGA births as a primary outcome measure, because birth weight as a function of gestational age has a direct effect on perinatal morbidity and mortality (Pollack and Divon 1992).
LBW may result from complex and multiple pathways of fetal growth restriction attributed to maternal, fetal, or placental factors. Three broad categories of biological factors have been suggested to play a role in inadequate fetal gestation: abnormality of the biological clock, abnormal implantation, and infection and inflammation (Mattison et al. 2003).
The current theories provide multiple sites at which environmental factors may influence biological factors to modulate fetal growth and induce preterm birth. However, specific toxicologic mechanisms including relevant timing during gestational development are not known. We explored each of these processes, fetal growth restriction and inadequate gestational length, separately, and explored the influences of exposure timing in early and late pregnancy.
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