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Laura
McGuinn
Author
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
Spring 2018
2018
Epidemiology
air pollution, autism spectrum disorder, fine particulate matter, neurodevelopment, socioeconomic status
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Epidemiology
Julie
Daniels
Thesis advisor
Marilie
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
Laura
McGuinn
Author
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
Spring 2018
2018
Epidemiology
air pollution, autism spectrum disorder, fine particulate matter, neurodevelopment, socioeconomic status
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Epidemiology
Julie
Daniels
Thesis advisor
Marilie
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
Laura
McGuinn
Author
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
Spring 2018
2018
Epidemiology
air pollution, autism spectrum disorder, fine particulate matter, neurodevelopment, socioeconomic status
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Epidemiology
Julie
Daniels
Thesis advisor
Marilie
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
Laura
McGuinn
Author
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
Spring 2018
2018
Epidemiology
air pollution, autism spectrum disorder, fine particulate matter, neurodevelopment, socioeconomic status
eng
Doctor of Philosophy
Dissertation
Epidemiology
Julie
Daniels
Thesis advisor
Marilie D.
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
University of North Carolina at Chapel Hill
Degree granting institution
Laura
McGuinn
Creator
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
Epidemiology
air pollution; autism spectrum disorder; fine particulate matter; neurodevelopment; socioeconomic status
eng
Doctor of Philosophy
Dissertation
Epidemiology
Julie
Daniels
Thesis advisor
Marilie D.
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
University of North Carolina at Chapel Hill
Degree granting institution
2018
2018-05
Laura
McGuinn
Author
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
Spring 2018
2018
Epidemiology
air pollution, autism spectrum disorder, fine particulate matter, neurodevelopment, socioeconomic status
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Epidemiology
Julie
Daniels
Thesis advisor
Marilie D.
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
Laura
McGuinn
Creator
Department of Epidemiology
Gillings School of Global Public Health
Early Life Exposure to Air Pollution and Autism Spectrum Disorder: Susceptible Time Windows and Populations
Autism Spectrum Disorder (ASD) is a highly heterogeneous disease, with multiple underlying causes, including genetic and environmental factors. Early life air pollution exposure has been implicated as a risk factor for ASD, potentially working through an inflammatory pathway. Previous air pollution and ASD studies have been limited by several factors, including spatial and exposure variability, consideration of area-level socioeconomic status, and evaluation of associations by ASD severity. To address these limitations, this dissertation assessed the association between pre- and postnatal air pollution exposure during critical windows of neurodevelopment using data from the Study to Explore Early Development, a population-based case-control study with six different sites located throughout the United States.
Specific Aim 1 assessed the association between particulate matter ≤2.5 µm in diameter (PM2.5) and ozone exposure during three months prior to pregnancy, over the entire pregnancy period, as well as more refined periods of exposure reflecting each trimester of pregnancy and the first year of life. Specific Aim 2 evaluated the modifying role of neighborhood deprivation on the association between pregnancy and first year of life roadway proximity and PM2.5 exposure and ASD. For both of these aims, important confounders were considered and several sensitivity analyses were conducted to assess the robustness of the study findings. In Specific Aim 1, a potential critical window of susceptibility was identified during the late prenatal and early postnatal period, including associations for PM2.5 exposure during the first year of life [OR=1.26 per 1.6 µg/m3 (95% CI: 1.02, 1.57)] and ozone exposure during the third trimester [OR=1.22 per 6.6 ppb (95% CI:1.05, 1.42)]. Associations varied by geographic location, potentially due to different exposure levels and composition of PM2.5. In Specific Aim 2, the association between first year of life PM2.5 exposure and ASD varied by neighborhood deprivation level, with the strongest observed association for those in the highest deprivation level. The findings from this study may aid in setting air pollution standards for regulatory action for susceptible populations and suggests that economically deprived regions may be of greatest risk.
2018-05
2018
Epidemiology
air pollution; autism spectrum disorder; fine particulate matter; neurodevelopment; socioeconomic status
eng
Doctor of Philosophy
Dissertation
University of North Carolina at Chapel Hill Graduate School
Degree granting institution
Julie
Daniels
Thesis advisor
Marilie D.
Gammon
Thesis advisor
David
Richardson
Thesis advisor
Lucas
Neas
Thesis advisor
Ana
Rappold
Thesis advisor
text
McGuinn_unc_0153D_17532.pdf
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