Abstract:BackgroundLow birth weight (LBW) and environmental tobacco smoke (ETS) exposure are each associated with wheezing in children. This study was designed to examine the combined association of LBW and ETS with wheezing.MethodsA retrospective birth cohort analysis linked with a national survey of allergic disorders among 1,018,031 junior high school students in Taiwan (1995–1996) was analyzed. The reported incidence of wheezing (yes or no) and ETS exposure (4 categories: 0, 1–20, 21–40 and greater than or equal to… Show more
“…Indeed, it has been previously found in observational studies that lower birth weight is correlated to higher risk of asthma in both childhood and adolescence 23–27 . More, importantly, this inverse association between birth weight and childhood asthma is unlikely confounded by familial factors 28 and is also supported by large-scale meta-analyses 3,17,29,30 .…”
The association between lower birth weight and childhood asthma is well established. However, it remains unclear whether the influence of lower birth weight on asthma can persist into adulthood. We conducted a Mendelian randomization analysis to assess the causal relationship of birth weight (~140,000 individuals) on the risk of adult asthma (~62,000 individuals). We estimated the causal effect of birth weight to be 1.00 (95% CI 0.98~1.03,
p
= 0.737) using the genetic risk score method. We did not observe nonlinear relationship or gender difference for the estimated causal effect. With the inverse-variance weighted method, the causal effect of birth weight on adult asthma was estimated to be 1.02 (95% CI 0.84~1.24,
p
= 0.813). Additionally, the iMAP method provides no additional genome-wide evidence supporting the causal effects of birth weight on adult asthma. Our results were robust against various sensitivity analyses, and MR-PRESSO and MR-Egger regression showed that no instrument outliers and no horizontal pleiotropy were likely to bias the results. Overall, our study provides no evidence for the fetal origins of diseases hypothesis for adult asthma, implying that the impact of birth weight on asthma in years of children and adolescents does not persist into adult and previous findings may be biased by confounders.
“…Indeed, it has been previously found in observational studies that lower birth weight is correlated to higher risk of asthma in both childhood and adolescence 23–27 . More, importantly, this inverse association between birth weight and childhood asthma is unlikely confounded by familial factors 28 and is also supported by large-scale meta-analyses 3,17,29,30 .…”
The association between lower birth weight and childhood asthma is well established. However, it remains unclear whether the influence of lower birth weight on asthma can persist into adulthood. We conducted a Mendelian randomization analysis to assess the causal relationship of birth weight (~140,000 individuals) on the risk of adult asthma (~62,000 individuals). We estimated the causal effect of birth weight to be 1.00 (95% CI 0.98~1.03,
p
= 0.737) using the genetic risk score method. We did not observe nonlinear relationship or gender difference for the estimated causal effect. With the inverse-variance weighted method, the causal effect of birth weight on adult asthma was estimated to be 1.02 (95% CI 0.84~1.24,
p
= 0.813). Additionally, the iMAP method provides no additional genome-wide evidence supporting the causal effects of birth weight on adult asthma. Our results were robust against various sensitivity analyses, and MR-PRESSO and MR-Egger regression showed that no instrument outliers and no horizontal pleiotropy were likely to bias the results. Overall, our study provides no evidence for the fetal origins of diseases hypothesis for adult asthma, implying that the impact of birth weight on asthma in years of children and adolescents does not persist into adult and previous findings may be biased by confounders.
“…Importantly, this inverse association between birth weight and childhood asthma is not confounded by familial factors (Örtqvist et al 2009) and supported by large-scale meta-analyses (Lin et al 2014;Mebrahtu et al 2015;Mu et al 2014;Xu et al 2014).…”
The association between lower birth weight and childhood asthma is well established by observational studies. However, it remains unclear whether the influence of lower birth weight on asthma can persist into adulthood. Here, we conducted a Mendelian randomization analysis to assess the causal relationship of birth weight on the risk of adult asthma. Specifically, we carefully selected genetic instruments based on summary statistics obtained from large-scale genome-wide association meta-analyses of birth weight (up to ~160,000 individuals) and adult asthma (up to ~62,000 individuals). We performed Mendelian randomization using two separate approaches: a genetic risk score approach and a two-sample inverse-variance weighted (IVW) approach. With 37 genetic instruments for birth weight, we estimated the causal effect per one standard deviation (SD) change of birth weight to be an odds ratio (OR) of 1.00 (95% CI 0.98~1.03, p=0.737) using the genetic risk score method. We did not observe nonlinear relationship or gender difference for the estimated causal effect. In addition, with the IVW method, we estimated the causal effect of birth weight on adult asthma was observed (OR=1.02, 95% CI 0.84~1.24, p=0.813). Additionally, the iMAP method provides no additional genome-wide evidence supporting the causal effects of birth weight on adult asthma. The result of the IVW method was robust against various sensitivity analyses, and MR-PRESSO and the Egger regression showed that no instrument outliers and no horizontal pleiotropy were likely to bias the results. Overall, this Mendelian randomization study provides no evidence for the fetal origins of diseases hypothesis for adult asthma, implying that the impact of birth weight on asthma in years of children and adolescents does not persist into adult and previous findings may be biased by confounders.
To inform the clinical practice guidelines' recommendations developed by the European Academy of Allergy and Clinical Immunology systematic reviews (SR) assessed using GRADE on the impact of environmental tobacco smoke (ETS) and active smoking on the risk of new‐onset asthma/recurrent wheezing (RW)/low lung function (LF), and on asthma‐related outcomes. Only longitudinal studies were included, almost all on combustion cigarettes, only one assessing e‐cigarettes and LF. According to the first SR (67 studies), prenatal ETS increases the risk of RW (moderate certainty evidence) and may increase the risk of new‐onset asthma and of low LF (low certainty evidence). Postnatal ETS increases the risk of new‐onset asthma and of RW (moderate certainty evidence) and may impact LF (low certainty evidence). Combined in utero and postnatal ETS may increase the risk of new‐onset asthma (low certainty evidence) and increases the risk of RW (moderate certainty evidence). According to the second SR (24 studies), ETS increases the risk of severe asthma exacerbations and impairs asthma control and LF (moderate certainty evidence). According to the third SR (25 studies), active smoking increases the risk of severe asthma exacerbations and of suboptimal asthma control (moderate certainty evidence) and may impact asthma‐related quality‐of‐life and LF (low certainty evidence).
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