Local Traffic-Generated Air Pollution and Preeclampsia and Preterm Delivery
Local Traffic-Generated Air Pollution and Preeclampsia and Preterm Delivery
Background: Preeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.
Objectives: We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).
Methods: We identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NOx) and particulate matter < 2.5 µm in aerodynamic diameter (PM2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).
Results: We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NOx and PM2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NOx and PM2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NOx and PM2.5 exposure quartiles, respectively.
Conclusion: Exposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.
Preeclampsia is a multisystem disorder in pregnant women, which is characterized by elevated blood pressure, edema, and protein in the urine. Preeclampsia complicates an estimated 2–8% of pregnancies and is a major cause of maternal mortality and morbidities, perinatal deaths, preterm birth, and intrauterine growth restriction (Duley 1992; Sibai et al. 2005). Because the only cure is delivery of the baby and placenta, preeclampsia is the most frequent primary reason for elective nonspontaneous preterm birth, accounting for 30–35% of total preterm deliveries (PTD) (Goldenberg et al. 2008; Meis et al. 1998). Preeclampsia does not necessarily lead to spontaneous PTD, and the association between preeclampsia and spontaneous PTD depends on PTD subtypes defined by gestational age (e.g., very or moderately preterm) and pathway (e.g., membrane rupture or spontaneous onset of labor before membrane rupture) (Ananth et al. 1997).
More than half a million infants are born prematurely each year in theUnited States (Hamilton et al. 2006). Preterm birth is associated with 70% of neonatal deaths and up to 75% of neonatal morbidity (Challis et al. 2001). Extremely preterm infants who survive the neonatal period face an elevated risk of serious life-long health problems, including learning disabilities and other chronic conditions (Doyle 1995, 2008). A growing body of research has linked elevated air pollutant exposures to PTD at pollution levels typical of many U.S. cities (Maroziene and Grazuleviciene 2002; Perera et al. 2003; Ritz et al. 2000, 2007; Šrám et al. 2005; Wilhelm and Ritz 2005). So far, preeclampsia has been associated with air pollution in only two recent U.S. studies (Rudra and Williams 2006; Woodruff et al. 2008).
There is also a growing body of evidence linking pollutants found in traffic exhaust specifically to respiratory and cardiovascular diseases (Adar and Kaufman 2007; Delfino 2002; Heinrich and Wichmann 2004; Sarnat and Holguin 2007). Although data are limited to date (de Kok et al. 2006), evidence is emerging that fresh vehicle emissions contain more toxic compounds per unit of particle mass than do aged aerosols, in part because of the contribution of ultrafine particles (UFPs; < 0.1 µm in aerodynamic diameter), which are found in higher concentration closer to emission sources (Zhu et al. 2002). Fresh traffic emissions' toxicity may originate from a high concentration of organic components because particle number concentrations are orders of magnitude higher, increasing the surface area to which volatile and semivolatile pollutants such as polycyclic aromatic hydrocarbons (PAHs) and carbonyl compounds can adhere.
There is indirect evidence for adverse impacts of traffic-generated PAHs on birth outcomes from studies in the United States (Choi et al. 2006, 2008; Perera et al. 2003, 2004), Poland (Choi et al. 2006), and the Czech Republic (Dejmek et al. 2000). However, most previous birth outcome studies relied solely on data from air monitors operated by government agencies, which are usually sited to assess regional ambient pollution and are thus unlikely to adequately capture the high spatial heterogeneity of air pollutants directly emitted from traffic (Hitchins et al. 2000; Zhu et al. 2002). Two studies examined the impact of local traffic emissions specifically on PTD (Wilhelm and Ritz 2003; Yang et al. 2003), but both assigned exposures based on the distance to and/or level of traffic on major roadways near residences, a relatively crude measure of traffic exhaust that does not consider vehicle emission rates or meteorology (Jerrett et al. 2005). Two recent birth outcome studies (Brauer et al. 2008; Slama et al. 2007), however, employed more sophisticated techniques to model traffic-related air pollution based on land use regression (LUR) that yielded quantitative estimates for specific pollutants.
Because of population and economic growth and the lack of effective public transportation in the Los Angeles area, the amount of passenger traffic and of goods being moved through this region is projected to increase substantially in the next decade (California Environmental Protection Agency 2006). Such rapid growth in traffic-related fossil fuel use is expected to occur worldwide (Energy Information Administration 2008), adding urgency to research evaluating the impact of increased vehicle emissions on reproductive health outcomes. To address this issue, in the present study we investigated the effects of local traffic-generated air pollution on preterm birth and preeclampsia based on the CALINE4 line-source dispersion model (Benson 1989), which is specifically designed for the assessment of traffic emissions from roads. We obtained health outcomes data from a perinatal database with detailed clinical data from a four-hospital network in southern Los Angeles County and Orange County, California, from 1997 to 2006.
Abstract and Introduction
Abstract
Background: Preeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.
Objectives: We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).
Methods: We identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NOx) and particulate matter < 2.5 µm in aerodynamic diameter (PM2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).
Results: We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NOx and PM2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NOx and PM2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NOx and PM2.5 exposure quartiles, respectively.
Conclusion: Exposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.
Introduction
Preeclampsia is a multisystem disorder in pregnant women, which is characterized by elevated blood pressure, edema, and protein in the urine. Preeclampsia complicates an estimated 2–8% of pregnancies and is a major cause of maternal mortality and morbidities, perinatal deaths, preterm birth, and intrauterine growth restriction (Duley 1992; Sibai et al. 2005). Because the only cure is delivery of the baby and placenta, preeclampsia is the most frequent primary reason for elective nonspontaneous preterm birth, accounting for 30–35% of total preterm deliveries (PTD) (Goldenberg et al. 2008; Meis et al. 1998). Preeclampsia does not necessarily lead to spontaneous PTD, and the association between preeclampsia and spontaneous PTD depends on PTD subtypes defined by gestational age (e.g., very or moderately preterm) and pathway (e.g., membrane rupture or spontaneous onset of labor before membrane rupture) (Ananth et al. 1997).
More than half a million infants are born prematurely each year in theUnited States (Hamilton et al. 2006). Preterm birth is associated with 70% of neonatal deaths and up to 75% of neonatal morbidity (Challis et al. 2001). Extremely preterm infants who survive the neonatal period face an elevated risk of serious life-long health problems, including learning disabilities and other chronic conditions (Doyle 1995, 2008). A growing body of research has linked elevated air pollutant exposures to PTD at pollution levels typical of many U.S. cities (Maroziene and Grazuleviciene 2002; Perera et al. 2003; Ritz et al. 2000, 2007; Šrám et al. 2005; Wilhelm and Ritz 2005). So far, preeclampsia has been associated with air pollution in only two recent U.S. studies (Rudra and Williams 2006; Woodruff et al. 2008).
There is also a growing body of evidence linking pollutants found in traffic exhaust specifically to respiratory and cardiovascular diseases (Adar and Kaufman 2007; Delfino 2002; Heinrich and Wichmann 2004; Sarnat and Holguin 2007). Although data are limited to date (de Kok et al. 2006), evidence is emerging that fresh vehicle emissions contain more toxic compounds per unit of particle mass than do aged aerosols, in part because of the contribution of ultrafine particles (UFPs; < 0.1 µm in aerodynamic diameter), which are found in higher concentration closer to emission sources (Zhu et al. 2002). Fresh traffic emissions' toxicity may originate from a high concentration of organic components because particle number concentrations are orders of magnitude higher, increasing the surface area to which volatile and semivolatile pollutants such as polycyclic aromatic hydrocarbons (PAHs) and carbonyl compounds can adhere.
There is indirect evidence for adverse impacts of traffic-generated PAHs on birth outcomes from studies in the United States (Choi et al. 2006, 2008; Perera et al. 2003, 2004), Poland (Choi et al. 2006), and the Czech Republic (Dejmek et al. 2000). However, most previous birth outcome studies relied solely on data from air monitors operated by government agencies, which are usually sited to assess regional ambient pollution and are thus unlikely to adequately capture the high spatial heterogeneity of air pollutants directly emitted from traffic (Hitchins et al. 2000; Zhu et al. 2002). Two studies examined the impact of local traffic emissions specifically on PTD (Wilhelm and Ritz 2003; Yang et al. 2003), but both assigned exposures based on the distance to and/or level of traffic on major roadways near residences, a relatively crude measure of traffic exhaust that does not consider vehicle emission rates or meteorology (Jerrett et al. 2005). Two recent birth outcome studies (Brauer et al. 2008; Slama et al. 2007), however, employed more sophisticated techniques to model traffic-related air pollution based on land use regression (LUR) that yielded quantitative estimates for specific pollutants.
Because of population and economic growth and the lack of effective public transportation in the Los Angeles area, the amount of passenger traffic and of goods being moved through this region is projected to increase substantially in the next decade (California Environmental Protection Agency 2006). Such rapid growth in traffic-related fossil fuel use is expected to occur worldwide (Energy Information Administration 2008), adding urgency to research evaluating the impact of increased vehicle emissions on reproductive health outcomes. To address this issue, in the present study we investigated the effects of local traffic-generated air pollution on preterm birth and preeclampsia based on the CALINE4 line-source dispersion model (Benson 1989), which is specifically designed for the assessment of traffic emissions from roads. We obtained health outcomes data from a perinatal database with detailed clinical data from a four-hospital network in southern Los Angeles County and Orange County, California, from 1997 to 2006.