Maternal exposure to PM2.5 during pregnancy and asthma risk in early childhood: consideration of phases of fetal lung development

Marnie F Hazlehurst; Kecia N Carroll; Christine T Loftus; Adam A Szpiro; Paul E Moore; Joel D Kaufman; Kipruto Kirwa; Kaja Z LeWinn; Nicole R Bush; Sheela Sathyanarayana; Frances A Tylavsky; Emily S Barrett; Ruby H N Nguyen; Catherine J Karr

doi:10.1097/ee9.0000000000000130

Maternal exposure to PM_2.5 during pregnancy and asthma risk in early childhood: consideration of phases of fetal lung development

Environ Epidemiol. 2021 Apr;5(2):e130. doi: 10.1097/ee9.0000000000000130.

Authors

Marnie F Hazlehurst¹, Kecia N Carroll², Christine T Loftus³, Adam A Szpiro⁴, Paul E Moore⁵, Joel D Kaufman^{1

3

6}, Kipruto Kirwa³, Kaja Z LeWinn⁷, Nicole R Bush^{7

8}, Sheela Sathyanarayana^{3

9

10}, Frances A Tylavsky¹¹, Emily S Barrett¹², Ruby H N Nguyen¹³, Catherine J Karr^{1

3

10}

Affiliations

¹ Department of Epidemiology, University of Washington, Box 357236, Seattle WA, USA 98195-7236.
² Division of General Pediatrics, Department of Pediatrics, Vanderbilt University Medical Center, 2146 Belcourt Avenue, Nashville TN, USA, 37212.
³ Department of Environmental and Occupational Health Sciences, University of Washington, Box 357234, Seattle WA, USA, 98195-7234.
⁴ Department of Biostatistics, University of Washington, Box 35732, Seattle WA, USA, 98195-7232.
⁵ Division of Allergy, Immunology and Pulmonary Medicine, Department of Pediatrics, Vanderbilt University Medical Center, 2200 Children's Way, Nashville TN, USA, 37232-9500.
⁶ Department of Medicine, University of Washington, 1959 NE Pacific St, Seattle WA, USA, 98195.
⁷ Department of Psychiatry, Weill Institute for the Neurosciences, University of California San Francisco, 401 Parnassus Ave, San Francisco CA, USA, 94143.
⁸ Department of Pediatrics, University of California San Francisco, 550 16th Street, Box 0110, San Francisco CA, USA, 94143.
⁹ Seattle Children's Research Institute, 2001 8th Ave, Seattle WA, USA, 98121.
¹⁰ Department of Pediatrics, University of Washington, Box 356320, Seattle WA, USA, 98195-6320.
¹¹ Department of Preventive Medicine, University of Tennessee Health Science Center, 66 N Pauline Street, Suite 633, Memphis TN, USA, 38163.
¹² Department of Biostatistics and Epidemiology, Environmental and Occupational Health Sciences Institute, Rutgers School of Public Health, 683 Hoes Lane West, Piscataway NJ, USA, 08854.
¹³ Division of Epidemiology and Community Health, University of Minnesota School of Public Health, 1300 S 2nd Street, Suite 300, Minneapolis MN, USA 55454.

Abstract

Background: Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows.

Objective: To assess associations between prenatal fine particulate matter exposure and asthma at age 4.

Methods: This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM_2.5) exposures during the pseudoglandular (5-16 weeks gestation), canalicular (16-24 weeks gestation), saccular (24-36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors.

Results: Children (n=1469) were on average 4.3 (standard deviation 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m³ higher PM_2.5 exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma (95% CI: 1.06-1.58). A similar association was observed with current asthma (RR 1.27, 95% CI: 1.04-1.54), but not current wheeze (RR 1.11, 95% CI: 0.92-1.33). Effect estimates for associations during other developmental windows had confidence intervals that included the null.

Conclusions: Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM_2.5.

Keywords: Air pollution; Developmental Origins of Health and Disease (DOHaD); PM2.5; child asthma; particulate matter; prenatal.

Abstract

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