Dataset Information

Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study.

ABSTRACT: PURPOSE:To investigate whether prenatal exposure to indoor fine particulate matter (PM?.?) and environmental tobacco smoke (ETS) affects susceptibility to respiratory tract infections (RTIs) in infancy, to compare their effects between prenatal and postnatal exposure, and to determine whether genetic factors modify these environmental effects. METHODS:The study population consisted of 307 birth cohort infants. A diagnosis of RTIs was based on parental report of a physician's diagnosis. Indoor PM?.? and ETS levels were measured during pregnancy and infancy. TaqMan was used for genotyping of nuclear factor erythroid 2-related factor (Nrf2) (rs6726395), glutathione-S-transferase-pi (GSTP) 1 (rs1695), and glutathione-S-transferase-mu (GSTM) 1. Microarrays were used for genome-wide methylation analysis. RESULTS:Prenatal exposure to indoor PM?.? increased the susceptibility of lower RTIs (LRTIs) in infancy (adjusted odds ratio [aOR]=2.11). In terms of combined exposure to both indoor PM?.? and ETS, prenatal exposure to both pollutants increased susceptibility to LRTIs (aOR=6.56); however, this association was not found for postnatal exposure. The Nrf2 GG (aOR=23.69), GSTM1 null (aOR=8.18), and GSTP1 AG or GG (aOR=7.37) genotypes increased the combined LRTIs-promoting effects of prenatal exposure to the 2 indoor pollutants. Such effects of prenatal indoor PM?.? and ETS exposure were not found for upper RTIs. CONCLUSIONS:Prenatal exposure to both indoor PM?.? and ETS may increase susceptibility to LRTIs. This effect can be modified by polymorphisms in reactive oxygen species-related genes.

SUBMITTER: Yang SI

PROVIDER: S-EPMC4605930 | biostudies-literature | 2015 Nov

REPOSITORIES: biostudies-literature

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Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study.

Yang Song I SI Kim Byoung Ju BJ Lee So Yeon SY Kim Hyo Bin HB Lee Cheol Min CM Yu Jinho J Kang Mi Jin MJ Yu Ho Sung HS Lee Eun E Jung Young Ho YH Kim Hyung Young HY Seo Ju Hee JH Kwon Ji Won JW Song Dae Jin DJ Jang Gwangcheon G Kim Woo Kyung WK Shim Jung Yeon JY Lee Soo Young SY Yang Hyeon Jong HJ Suh Dong In DI Hong Seo Ah SA Choi Kil Yong KY Shin Youn Ho YH Ahn Kangmo K Kim Kyung Won KW Kim Eun Jin EJ Hong Soo Jong SJ

Allergy, asthma & immunology research 20150625 6

<h4>Purpose</h4>To investigate whether prenatal exposure to indoor fine particulate matter (PM₂.₅) and environmental tobacco smoke (ETS) affects susceptibility to respiratory tract infections (RTIs) in infancy, to compare their effects between prenatal and postnatal exposure, and to determine whether genetic factors modify these environmental effects.<h4>Methods</h4>The study population consisted of 307 birth cohort infants. A diagnosis of RTIs was based on parental report of a physician's diagn ...[more]

PMID: 26333704

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Project description:BackgroundExposure 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 methodsWe 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).ResultsWe 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.ConclusionsExposure 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.

Project description:BackgroundThe lung's ability to trap and clear foreign particles via the mucociliary elevator is an important mechanism for protecting the lung against respirable irritants and microorganisms. Although cigarette smoke (CS) exposure and particulate inhalation are known to alter mucociliary clearance, little is known about how CS and nanoparticles (NPs) modify cilia beating at the cytoskeletal infrastructure, or axonemal, level.MethodsWe used a cell-free model to introduce cigarette smoke extract (CSE) and NPs with variant size and surface chemistry to isolated axonemes and measured changes in ciliary motility. We hypothesized that CSE would alter cilia beating and that alterations in ciliary beat frequency (CBF) due to particulate matter would be size- and surface chemistry-dependent. Demembranated axonemes were isolated from ciliated bovine tracheas and exposed to adenosine triphosphate (ATP) to initiate motility. CBF was measured in response to 5% CSE, CSE filtrate, and carboxyl-modified (COOH), sulphate (SO(4))-modified (sulfonated), or PEG-coated polystyrene (PS) latex NPs ranging in size from 40 nm to 500 nm.ResultsCSE concentrations as low as 5% resulted in rapid, significant stimulation of CBF (p<0.05 vs. baseline control). Filtering CSE through a 0.2-μm filter attenuated this effect. Introduction of sulphate-modified PS beads ~300 nm in diameter resulted in a similar increase in CBF above baseline ATP levels. Uncharged, PEG-coated beads had no effect on CBF regardless of size. Similarly, COOH-coated particles less than 200 nm in diameter did not alter ciliary motility. However, COOH-coated PS particles larger than 300 nm increased CBF significantly and increased the number of motile points.ConclusionsThese data show that NPs, including those found in CSE, mechanically stimulate axonemes in a size- and surface chemistry-dependent manner. Alterations in ciliary motility due to physicochemical properties of NPs may be important for inhalational lung injury and efficient drug delivery of respirable particles.

Project description:BACKGROUND: Studies that have evaluated the association between exposure to gas appliances emissions at home with respiratory health in children obtained heterogeneous and limited results. The aim of this study is to analyze the association between the use of gas cooking at home during pregnancy and respiratory problems in children during their first year of life. METHODS: In the years 2003 through 2008 pregnant women were enrolled in 4 Spanish areas and visited in different age-points following a common protocol. Outcomes studied (from a questionnaire) were any episode of lower respiratory tract infection (LRTI), wheezing, persistent cough, chestiness and otitis. The association between exposure to gas cooking at home and respiratory outcomes was assessed using logistic regression and adjusting by confounding variables. Some potential effect modifiers (i.e. smoking, fruit and vegetables consumption) were examined. RESULTS: Among the 2003 children included in the study, a total of 731 (36.6%) had a LRTI episode, 693 (34.6%) experienced wheezing, 302 (15.5%) a persistent cough, 939 (47.4%) chestiness and 620 (31.2%) had an episode of otitis during their first year of life. Gas cookers were present in 45.5% of homes. Exposure to gas cooking in homes was not associated with respiratory outcomes Odds Ratios (OR) were close to 1 and not statistically significant. However, a positive association was found for otitis among infants whose mothers reported low intakes of fruit and vegetables during pregnancy [OR (95% CI) = 1.38 (1.01-1.9)] and also wheezing and chestiness were associated with gas cookers among those children whose mothers smoked during pregnancy. CONCLUSIONS: In susceptible subjects (those whose mothers smoke and consumed below average fruit and vegetables) we found an association between exposure to gas cooking during pregnancy and risk of wheezing, chestiness and otitis during the first year of life. But more research is needed regarding not only gas cooking and respiratory health but also the possible effect modifier role of diet and tobacco.

Project description:BACKGROUND:Oxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes. OBJECTIVES:We studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures. METHODS:For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV(1)), FEV(1) over forced vital capacity (FEV(1)/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF(25-75)) was regressed on interval exposure to particulate matter <10 µm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (p(interaction)<0.05). Replication was attempted for SNPs with MAF>10% in 3320 SAPALDIA participants without GWAS. RESULTS:On the SNP-level, rs2035268 in gene SNCA accelerated FEV(1)/FVC decline by 3.8% (p(interaction)?=?2.5×10(-6)), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p(interaction)?=?9.7×10(-8)) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (p(interaction)?=?3.0×10(-4)) on FEV(1)/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful. CONCLUSIONS:Consistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobacco smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challenging.

Dataset Information

Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study.

Publications

Prenatal Particulate Matter/Tobacco Smoke Increases Infants' Respiratory Infections: COCOA Study.

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