7
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Live-Birth Bias and Observed Associations Between Air Pollution and Autism

      1 , 2 , 3 , 4
      American Journal of Epidemiology
      Oxford University Press (OUP)

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          <p id="d202310e163">A recent analysis found that exposure to air pollution during specific weeks of pregnancy was negatively associated with risk of autism spectrum disorder (ASD) when mutually adjusted for postnatal air-pollution exposure. In this commentary, we describe 2 possible selection-bias processes that might lead to such results, both related to live-birth bias (i.e., the inevitable restriction of the analyzed sample to live births). The first mechanism is described using a directed acyclic graph and relates to the chance of live birth being a common consequence of both exposure to air pollution and another risk factor of ASD. The second mechanism involves preferential depletion of fetuses susceptible to ASD in the higher air-pollution exposure group. We further discuss the assumptions underlying these processes and their causal structures, their plausibility, and other studies where similar phenomena might have occurred. </p>

          Related collections

          Most cited references39

          • Record: found
          • Abstract: found
          • Article: not found

          Timing of prenatal stressors and autism.

          Recent evidence supports a role for genetics in autism, but other findings are difficult to reconcile with a purely genetic cause. Pathological changes in the cerebellum in autism are thought to correspond to an event before 30-32 weeks gestation. Our purpose was to determine whether there is an increased incidence of stressors in autism before this time period. Surveys regarding incidence and timing of prenatal stressors were distributed to specialized schools and clinics for autism and Down syndrome, and to mothers of children without neurodevelopmental diagnoses in walk-in clinics. Incidence of stressors during each 4-week block of pregnancy was recorded. Incidence of stressors in the blocks prior to and including the predicted time period (21-32 weeks gestation) in each group of surveys was compared to the other prenatal blocks. A higher incidence of prenatal stressors was found in autism at 21-32 weeks gestation, with a peak at 25-28 weeks. This does support the possibility of prenatal stressors as a potential contributor to autism, with the timing of stressors consistent with the embryological age suggested by neuroanatomical findings seen in the cerebellum in autism. Future prospective studies would be needed to confirm this finding.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder

            Background Exposure to ambient air pollution is widespread and may be detrimental to human brain development and a potential risk factor for Autism Spectrum Disorder (ASD). We conducted a systematic review of the human evidence on the relationship between ASD and exposure to all airborne pollutants, including particulate matter air pollutants and others (e.g. pesticides and metals). Objective To answer the question: “is developmental exposure to air pollution associated with ASD?” Methods We conducted a comprehensive search of the literature, identified relevant studies using inclusion/exclusion criteria pre-specified in our protocol (registered in PROSPERO, CRD # 42015017890), evaluated the potential risk of bias for each included study and identified an appropriate subset of studies to combine in a meta-analysis. We then rated the overall quality and strength of the evidence collectively across all air pollutants. Results Of 1,158 total references identified, 23 human studies met our inclusion criteria (17 case-control, 4 ecological, 2 cohort). Risk of bias was generally low across studies for most domains; study limitations were related to potential confounding and accuracy of exposure assessment methods. We rated the quality of the body of evidence across all air pollutants as “moderate.” From our meta-analysis, we found statistically significant summary odds ratios (ORs) of 1.07 (95% CI: 1.06, 1.08) per 10-μg/m3 increase in PM10 exposure (n = 6 studies) and 2.32 (95% CI: 2.15, 2.51) per 10-μg/m3 increase in PM2.5 exposure (n = 3 studies). For pollutants not included in a meta-analysis, we collectively evaluated evidence from each study in rating the strength and quality of overall evidence considering factors such as inconsistency, imprecision, and evidence of dose-response. All included studies generally showed increased risk of ASD with increasing exposure to air pollution, although not consistently across all chemical components. Conclusion After considering strengths and limitations of the body of research, we concluded that there is “limited evidence of toxicity” for the association between early life exposure to air pollution as a whole and diagnosis of ASD. The strongest evidence was between prenatal exposure to particulate matter and ASD. However, the small number of studies in the meta-analysis and unexplained statistical heterogeneity across the individual study estimates means that the effect could be larger or smaller (including not significant) than these studies estimate. Our research supports the need for health protective public policy to reduce exposures to harmful airborne contaminants among pregnant women and children and suggests opportunities for optimizing future research.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Autism prevalence following prenatal exposure to hurricanes and tropical storms in Louisiana.

              Hurricanes and tropical storms served as natural experiments for investigating whether autism is associated with exposure to stressful events during sensitive periods of gestation. Weather service data identified severe storms in Louisiana from 1980 to 1995 and parishes hit by storm centers during this period. Autism prevalences in different cohorts were calculated using anonymous data on birth dates and parishes of children diagnosed with autism in the state mental health system, together with corresponding census data on all live births in Louisiana. Prevalence increased in dose-response fashion with severity of prenatal storm exposure, especially for cohorts exposed near the middle or end of gestation (p < 0.001). Results complement other evidence that factors disrupting development during sensitive gestational periods may contribute to autism.
                Bookmark

                Author and article information

                Journal
                American Journal of Epidemiology
                Oxford University Press (OUP)
                0002-9262
                1476-6256
                November 2018
                November 01 2018
                August 07 2018
                November 2018
                November 01 2018
                August 07 2018
                : 187
                : 11
                : 2292-2296
                Affiliations
                [1 ]Braun School of Public Health and Community Medicine, the Hebrew University of Jerusalem, Jerusalem, Israel
                [2 ]Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York City, New York
                [3 ]Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
                [4 ]Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
                Article
                10.1093/aje/kwy172
                6211245
                30099488
                35358b11-d4fe-483e-a6b2-6410ba685f52
                © 2018

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

                History

                Comments

                Comment on this article