Miatta A Buxton1, Wei Perng2, Martha María Tellez-Rojo3, Yanelli Rodríguez-Carmona4, Alejandra Cantoral3, Brisa N Sánchez5, Luis O Rivera-González6, Carina J Gronlund7, Nitin Shivappa8, James R Hébert8, Marie S O'Neill9, Karen E Peterson4. 1. Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA. Electronic address: mabuxton@umich.edu. 2. Department of Epidemiology, School of Public Health, University of Colorado, Aurora, CO, USA. 3. Center for Research on Nutrition and Health, National Institute of Public Health, Cuernavaca, Morelos, Mexico. 4. Department of Nutritional Sciences, School of Public Health, University of Michigan, Ann Arbor MI, USA. 5. Department of Epidemiology and Biostatistics, School of Public Health, Drexel University, Philadelphia, PA, USA. 6. Division of Community Health Investigations, Agency for Toxic Substances and Disease Registry, (CDC/ATSDR), Edison, NJ, USA. 7. Institute for Social Research, Survey Research Center, University of Michigan, Ann Arbor, MI, USA. 8. Department of Epidemiology and Biostatistics, School of Public Health, University of South Carolina, Columbia, SC, USA; Connecting Health Innovations LLC, Columbia, SC, USA. 9. Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA; Department of Environmental Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA.
Abstract
BACKGROUND: Particulate matter ≤10 μm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts. OBJECTIVES: To evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks. METHODS: PM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines. RESULTS: In adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 μg/m3) during the second trimester, while negative associations were seen during the second (≥74 μg/m3) and third trimesters (55-65 μg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth. DISCUSSION: Associations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.
BACKGROUND: Particulate matter ≤10 μm in aerodynamic diameter (PM10) and diet quality are risk factors for systemic inflammation, which is associated with preterm birth (PTB). PM10 and a pro-inflammatory diet (assessed by the Dietary Inflammatory Index [DII®]) have been individually evaluated as causes of PTB and differences by offspring sex have been reported for the DII. However, additional studies are needed to evaluate joint effects of these associations to inform intervention efforts. OBJECTIVES: To evaluate the independent and joint effects of PM10 and energy-adjusted DII (E-DII) on PTB risks. METHODS: PM10 estimates were generated from daily citywide averages for 1216 pregnant women from three subcohorts of the Early Life Exposures in Mexico to Environmental Toxicants study using data from the Mexico City Outdoor Air Monitoring Network. Among a subset of participants (N = 620), E-DII scores were calculated using a validated food frequency questionnaire. Cox Proportional Hazards models were run for select periods during pregnancy and entire pregnancy averages for E-DII and PM10. We assessed for potential non-linear associations using natural splines. RESULTS: In adjusted models, PM10 exposure was associated with increased risks of PTB for a range of values (58-72 μg/m3) during the second trimester, while negative associations were seen during the second (≥74 μg/m3) and third trimesters (55-65 μg/m3). Analyses conducted using distributed lag models for periods closer to delivery (max lag = 90) did not show negative associations between PM10 exposure and preterm birth, and indeed positive significant associations were observed (estimates and figures). E-DII was not associated with PTB and there was no evidence of effect modification by infant sex. There was no evidence of interaction between PM10 and E-DII and the risk of preterm birth. DISCUSSION: Associations between PM10 and PTB in Mexico City varied over time and across levels of PM10. Our findings of negative associations in the second and third trimesters, which are contrary to the hypothesized relationship between PM10 and PTB, may be due to a number of factors, including live birth bias and the exposure period evaluated. Differences in results for the periods evaluated suggest that PM10 from shorter exposure windows may play a more proximal role in initiating preterm labor.
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