Nadya Y Rivera Rivera1, Marcela Tamayo-Ortiz2, Adriana Mercado García3, Allan C Just4, Itai Kloog5, Martha Maria Téllez-Rojo3, Robert O Wright4, Rosalind J Wright6, Maria José Rosa7. 1. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 2. National Council of Science and Technology (CONACYT) - National Institute of Public Health (INSP), Cuernavaca, Morelos, Mexico. 3. Center for Nutrition and Health Research, National Institute of Public Health, Cuernavaca, Morelos, Mexico. 4. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 5. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Department of Geography and Environmental Development, Ben-Gurion University of the Negev, P.O.B. Beer Sheva, Israel; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 6. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Kravis Children's Hospital, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, USA. 7. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: maria.rosa@mssm.edu.
Abstract
BACKGROUND: Exposure to particulate matter <2.5 μm in diameter (PM2.5) and environmental tobacco smoke (ETS) are associated with respiratory morbidity starting in utero. However, their potential synergistic effects have not been completely elucidated. Here, we examined the joint effects of prenatal and early life PM2.5 and prenatal ETS exposure on respiratory outcomes in children. MATERIAL AND METHODS: We studied 536 mother-child dyads in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study in Mexico City. Exposure to PM2.5 was estimated using residence in pregnancy and child's first year of life with a satellite-based spatio-temporal model. ETS exposure was assessed by caregiver's report of any smoker in the household during the second or third trimester. Outcomes included report of ever wheeze and wheeze in the past 12 months (current wheeze) assessed when children were 6-8 years old considered in separate models. Associations were modeled using distributed lag models (DLM) with daily PM2.5 averages for pregnancy and the first year of life, adjusting for child's sex, birth weight z-score, mother's age and education at enrollment, maternal asthma, season of conception and stratified by prenatal ETS exposure (yes/no). RESULTS: We identified a sensitive window from gestational week 14 through postnatal week 18 during which PM2.5 was associated with higher risk of ever wheeze at age 6-8 years. We also observed a critical window of PM2.5 exposure between postnatal weeks 6-39 and higher risk of current wheeze. We found significant associations between higher prenatal and early life PM2.5 exposure and higher cumulative risk ratios of ever wheeze (RR:3.76, 95%CI [1.41, 10.0] per 5 μg/m3) and current wheeze in the past year (RR:7.91, 95%CI [1.5, 41.6] per 5 μg/m3) only among children born to mothers exposed to ETS in pregnancy when compared to mothers who were not exposed. CONCLUSIONS: Exposure to prenatal ETS modified the association between prenatal and early life PM2.5 exposure and respiratory outcomes at age 6-8 years. It is important to consider concurrent chemical exposures to more comprehensively characterize children's environmental risk. Interventions aimed at decreasing passive smoking might mitigate the effects of ambient air pollution.
BACKGROUND: Exposure to particulate matter <2.5 μm in diameter (PM2.5) and environmental tobacco smoke (ETS) are associated with respiratory morbidity starting in utero. However, their potential synergistic effects have not been completely elucidated. Here, we examined the joint effects of prenatal and early life PM2.5 and prenatal ETS exposure on respiratory outcomes in children. MATERIAL AND METHODS: We studied 536 mother-child dyads in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) study in Mexico City. Exposure to PM2.5 was estimated using residence in pregnancy and child's first year of life with a satellite-based spatio-temporal model. ETS exposure was assessed by caregiver's report of any smoker in the household during the second or third trimester. Outcomes included report of ever wheeze and wheeze in the past 12 months (current wheeze) assessed when children were 6-8 years old considered in separate models. Associations were modeled using distributed lag models (DLM) with daily PM2.5 averages for pregnancy and the first year of life, adjusting for child's sex, birth weight z-score, mother's age and education at enrollment, maternal asthma, season of conception and stratified by prenatal ETS exposure (yes/no). RESULTS: We identified a sensitive window from gestational week 14 through postnatal week 18 during which PM2.5 was associated with higher risk of ever wheeze at age 6-8 years. We also observed a critical window of PM2.5 exposure between postnatal weeks 6-39 and higher risk of current wheeze. We found significant associations between higher prenatal and early life PM2.5 exposure and higher cumulative risk ratios of ever wheeze (RR:3.76, 95%CI [1.41, 10.0] per 5 μg/m3) and current wheeze in the past year (RR:7.91, 95%CI [1.5, 41.6] per 5 μg/m3) only among children born to mothers exposed to ETS in pregnancy when compared to mothers who were not exposed. CONCLUSIONS: Exposure to prenatal ETS modified the association between prenatal and early life PM2.5 exposure and respiratory outcomes at age 6-8 years. It is important to consider concurrent chemical exposures to more comprehensively characterize children's environmental risk. Interventions aimed at decreasing passive smoking might mitigate the effects of ambient air pollution.
Authors: Maria José Rosa; Kyung Hwa Jung; Matthew S Perzanowski; Elizabeth A Kelvin; Katherine W Darling; David E Camann; Steven N Chillrud; Robin M Whyatt; Patrick L Kinney; Frederica P Perera; Rachel L Miller Journal: Respir Med Date: 2010-12-15 Impact factor: 3.415
Authors: Robert Urman; Rob McConnell; Talat Islam; Edward L Avol; Frederick W Lurmann; Hita Vora; William S Linn; Edward B Rappaport; Frank D Gilliland; W James Gauderman Journal: Thorax Date: 2013-11-19 Impact factor: 9.139
Authors: Chris Carlsten; Anne Dybuncio; Allan Becker; Moira Chan-Yeung; Michael Brauer Journal: Occup Environ Med Date: 2010-10-15 Impact factor: 4.402
Authors: Lance A Wallace; Herman Mitchell; George T O'Connor; Lucas Neas; Morton Lippmann; Meyer Kattan; Jane Koenig; James W Stout; Ben J Vaughn; Dennis Wallace; Michelle Walter; Ken Adams; Lee-Jane Sally Liu Journal: Environ Health Perspect Date: 2003-07 Impact factor: 9.031
Authors: Antonio Anax Falcão de Oliveira; Tiago Franco de Oliveira; Michelle Francini Dias; Marisa Helena Gennari Medeiros; Paolo Di Mascio; Mariana Veras; Miriam Lemos; Tania Marcourakis; Paulo Hilário Nascimento Saldiva; Ana Paula Melo Loureiro Journal: Part Fibre Toxicol Date: 2018-10-19 Impact factor: 9.400
Authors: Giuliana Ferrante; Salvatore Fasola; Giovanna Cilluffo; Giorgio Piacentini; Giovanni Viegi; Stefania La Grutta Journal: Front Public Health Date: 2022-06-14
Authors: Haley von Holst; Pratibha Nayak; Zygmunt Dembek; Stephanie Buehler; Diana Echeverria; Dawn Fallacara; Lisa John Journal: Heliyon Date: 2021-10-12