Andrew D Williams1, Jenna Kanner2, Katherine L Grantz3, Marion Ouidir3, Shanshan Sheehy4, Seth Sherman5, Candace Robledo6, Pauline Mendola7. 1. Public Health Program, Department of Population Health, School of Medicine and Health Sciences, University of North Dakota, Room E162, 1301 North Columbia Road Stop 9037, Grand Forks, ND, 58202, USA. Electronic address: andrew.d.williams@und.edu. 2. School of Medicine, University of Maryland, Baltimore, 655 W. Baltimore Stree, Baltimore, MD, 21201, USA. 3. Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6710B Rockledge Drive, Bethesda, MD, 20892, USA. 4. Slone Epidemiology Center, Boston University School of Medicine, 72 E Concord Street, Boston, MA, 02118, USA. 5. The Emmes Company, 401 North Washington Street #700, Rockville, MD, 20850, USA. 6. Department of Population Health and Biostatistics, University of Texas Rio Grande Valley School of Medicine, 2102 Treasure Hill Blvd, Harlingen, TX, 78550, USA. 7. Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6710B Rockledge Drive, Bethesda, MD, 20892, USA; Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, 401 Kimball Tower, Buffalo, NY, 14214, USA.
Abstract
AIMS/HYPOTHESIS: Women with type 1 diabetes have increased risk for poor obstetric outcomes. Prenatal air pollution exposure is also associated with adverse outcomes for women and infants. We examined whether women with type 1 diabetes are more vulnerable than other women to pollution-associated risks during pregnancy. METHODS: In singleton deliveries from the Consortium on Safe Labor (2002-2008), obstetric and neonatal outcomes were compared for women with type 1 diabetes (n = 507) and women without autoimmune disease (n = 204,384). Preconception, trimester, and whole pregnancy average air pollutant exposure (ozone (O3), carbon monoxide (CO), particulate matter >10 μm (PM10), PM > 2.5 μm (PM2.5), sulfur dioxide (SO2), nitrogen oxides (NOx)) were estimated using modified Community Multiscale Air Quality models. Poisson regression models with diabetes*pollutant interaction terms estimated relative risks and 95% confidence intervals for adverse outcomes, adjusted for maternal characteristics and geographic region. RESULTS: For whole pregnancy exposure to SO2, women with type 1 diabetes had 15% increased risk (RR:1.15 95%CI:1.01,1.31) and women without autoimmune disease had 5% increased risk (RR:1.05 95%CI:1.05,1.06) for small for gestational age birth (pinteraction = 0.09). Additionally, whole pregnancy O3 exposure was associated with 10% increased risk (RR:1.10 95%CI:1.02,1.17) among women with type 1 diabetes and 2% increased risk (RR:1.02 95%CI:1.00,1.04) among women without autoimmune disease for perinatal mortality (pinteraction = 0.08). Similar patterns were observed between PM2.5 exposure and spontaneous preterm birth. CONCLUSIONS: Pregnant women with type 1 diabetes may be at greater risk for adverse outcomes when exposed to air pollution than women without autoimmune disease.
AIMS/HYPOTHESIS: Women with type 1 diabetes have increased risk for poor obstetric outcomes. Prenatal air pollution exposure is also associated with adverse outcomes for women and infants. We examined whether women with type 1 diabetes are more vulnerable than other women to pollution-associated risks during pregnancy. METHODS: In singleton deliveries from the Consortium on Safe Labor (2002-2008), obstetric and neonatal outcomes were compared for women with type 1 diabetes (n = 507) and women without autoimmune disease (n = 204,384). Preconception, trimester, and whole pregnancy average air pollutant exposure (ozone (O3), carbon monoxide (CO), particulate matter >10 μm (PM10), PM > 2.5 μm (PM2.5), sulfur dioxide (SO2), nitrogen oxides (NOx)) were estimated using modified Community Multiscale Air Quality models. Poisson regression models with diabetes*pollutant interaction terms estimated relative risks and 95% confidence intervals for adverse outcomes, adjusted for maternal characteristics and geographic region. RESULTS: For whole pregnancy exposure to SO2, women with type 1 diabetes had 15% increased risk (RR:1.15 95%CI:1.01,1.31) and women without autoimmune disease had 5% increased risk (RR:1.05 95%CI:1.05,1.06) for small for gestational age birth (pinteraction = 0.09). Additionally, whole pregnancy O3 exposure was associated with 10% increased risk (RR:1.10 95%CI:1.02,1.17) among women with type 1 diabetes and 2% increased risk (RR:1.02 95%CI:1.00,1.04) among women without autoimmune disease for perinatal mortality (pinteraction = 0.08). Similar patterns were observed between PM2.5 exposure and spontaneous preterm birth. CONCLUSIONS: Pregnant women with type 1 diabetes may be at greater risk for adverse outcomes when exposed to air pollution than women without autoimmune disease.
Authors: Tobias A J Nijman; Elvira O G van Vliet; Manon J N Benders; Ben Willem J Mol; Arie Franx; Peter G J Nikkels; Martijn A Oudijk Journal: Placenta Date: 2016-10-12 Impact factor: 3.481
Authors: Jun Zhang; James Troendle; Uma M Reddy; S Katherine Laughon; D Ware Branch; Ronald Burkman; Helain J Landy; Judith U Hibbard; Shoshana Haberman; Mildred M Ramirez; Jennifer L Bailit; Matthew K Hoffman; Kimberly D Gregory; Victor H Gonzalez-Quintero; Michelle Kominiarek; Lee A Learman; Christos G Hatjis; Paul van Veldhuisen Journal: Am J Obstet Gynecol Date: 2010-08-12 Impact factor: 8.661