Maternal Smoking during Pregnancy and the Prevalence of Autism Spectrum Disorders, Using Data from the Autism and Developmental Disabilities Monitoring Network

Zilber School of Public Health, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53201-0413, USA.
Environmental Health Perspectives (Impact Factor: 7.98). 04/2012; 120(7):1042-8. DOI: 10.1289/ehp.1104556
Source: PubMed

ABSTRACT Reported associations between gestational tobacco exposure and autism spectrum disorders (ASDs) have been inconsistent.
We estimated the association between maternal smoking during pregnancy and ASDs among children 8 years of age.
This population-based case-cohort study included 633,989 children, identified using publicly available birth certificate data, born in 1992, 1994, 1996, and 1998 from parts of 11 U.S. states subsequently under ASD surveillance. Of these children, 3,315 were identified as having an ASD by the active, records-based surveillance of the Autism and Developmental Disabilities Monitoring Network. We estimated prevalence ratios (PRs) of maternal smoking from birth certificate report and ASDs using logistic regression, adjusting for maternal education, race/ethnicity, marital status, and maternal age; separately examining higher- and lower-functioning case subgroups; and correcting for assumed under-ascertainment of autism by level of maternal education.
About 13% of the source population and 11% of children with an ASD had a report of maternal smoking in pregnancy: adjusted PR (95% confidence interval) of 0.90 (0.80, 1.01). The association for the case subgroup autistic disorder (1,310 cases) was similar: 0.88 (0.72, 1.08), whereas that for ASD not otherwise specified (ASD-NOS) (375 cases) was positive, albeit including the null: 1.26 (0.91, 1.75). Unadjusted associations corrected for assumed under-ascertainment were 1.06 (0.98, 1.14) for all ASDs, 1.12 (0.97, 1.30) for autistic disorder, and 1.63 (1.30, 2.04) for ASD-NOS.
After accounting for the potential of under-ascertainment bias, we found a null association between maternal smoking in pregnancy and ASDs, generally. The possibility of an association with a higher-functioning ASD subgroup was suggested, and warrants further study.

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    • "Specifically, any factor that is not differentially related to PM during pregnancy vs. before or after pregnancy is very unlikely to confound our results. Thus, for example, while population density, choosing to take folate supplements during pregnancy, or a host of other potential confounders (Gray et al. 2013; Kalkbrenner et al. 2012) may be related to PM 2.5 exposure, they would be expected to be equally related to PM 2.5 exposure before or after pregnancy as during it. But no association with them were seen in mutually adjusted models. "
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    ABSTRACT: Autism spectrum disorder (ASD) is a developmental disorder with increasing prevalence worldwide, yet with unclear etiology. To explore the association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child. We conducted a nested case-control study of participants in the Nurses' Health Study II (NHS II), a prospective cohort of 116,430 US female nurses recruited in 1989, followed by biennial mailed questionnaires. Subjects were NHS II participants' children born 1990-2002 with ASD (n=245), and children without ASD (n=1522) randomly selected using frequency matching for birth years. ASD was based on maternal report, which was validated against the Autism Diagnostic Interview-Revised in a subset. Monthly averages of PM with diameters ≤2.5 µm (PM2.5) and 2.5-10 µm (PM10-2.5) were predicted from a spatiotemporal model for the continental US and linked to residential addresses. PM2.5 exposure during pregnancy was associated with increased odds of ASD, with an adjusted odds ratio (OR) for ASD per interquartile range higher PM2.5 (4.42 µg/m(3)) of 1.57 (95% CI: 1.22, 2.03) among women with the same address before and after pregnancy (160 cases, 986 controls). Associations with PM2.5 exposure 9 months before or after the pregnancy were weaker in independent models and null when all three time periods were included, while the association with the 9 months of pregnancy remained (OR=1.63; 95% CI: 1.08-2.47). The association between ASD and PM2.5 was stronger for exposure during the third trimester (OR=1.42 per inter-quartile range increase in PM2.5, 95% CI: 1.09, 1.86) than other trimesters (ORs 1.06 and 1.00) when mutually adjusted. There was little association between PM10-2.5 and ASD. Higher maternal exposure to PM2.5 during pregnancy, in particular the third trimester, was associated with greater odds of her child having ASD.
    Environmental Health Perspectives 12/2014; 123(3). DOI:10.1289/ehp.1408133 · 7.98 Impact Factor
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    • "However, as noted earlier, the available data on ASD sub-types are not adequate for meta-analysis: they are too few and too heterogeneous in outcome definition . It is regrettable that available data on ASD with and without intellectual disability is too limited to be amenable to meta-analysis (Lee et al. 2012; Kalkbrenner et al. 2012). This is clearly an area of interest because ASD is likely a collection of conditions with different etiologies, but whether intellectual disability is the salient distinguishing feature remains to be clarified and deserves a more in-depth treatment than the aim of our work permits. "
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    ABSTRACT: We conducted a meta-analysis of 15 studies on maternal prenatal smoking and ASD risk in offspring. Using a random-effects model, we found no evidence of an association (summary OR 1.02, 95 % CI 0.93-1.12). Stratifying by study design, birth year, type of healthcare system, and adjustment for socioeconomic status or psychiatric history did not alter the findings. There was evidence that ascertaining exposure at the time of birth produced a lower summary OR than when this information was gathered after birth. There was no evidence of publication bias. Non-differential exposure misclassification was shown to have the potential for negligible influence on the results. We found no evidence to support a measurable association between maternal prenatal smoking and ASD in offspring.
    Journal of Autism and Developmental Disorders 11/2014; 45(6). DOI:10.1007/s10803-014-2327-z · 3.34 Impact Factor
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    • "For example, pregnancy stress results in the section of corticotrophinreleasing hormone (CRH) from the hypothalamus, and increased plasma levels of CRH have been linked to preterm labor (Hobel et al., 1999). While some evidence suggests that such maternal risk factors can contribute to the development of ASD (Rizzo et al., 1997; Croen et al., 2002, 2007; Hultman et al., 2002; Glasson et al., 2004; Beversdorf et al., 2005; Larsson et al., 2005; Lauritsen et al., 2005; Leonard et al., 2006; Reichenberg et al., 2006; Dionne et al., 2008; Durkin et al., 2008; Grant and Soles, 2009; Grether et al., 2009; King et al., 2009; Li et al., 2009a,b; Burstyn et al., 2010; James et al., 2010; Kalkbrenner et al., 2012; Meguid et al., 2010; Roza et al., 2010; Shelton et al., 2010; Dodds et al., 2011; Lee et al., 2012; Parner et al., 2012; Rai et al., 2012; Sandin et al., 2012; Schmidt et al., 2012 "
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    ABSTRACT: Autism Spectrum Disorder (ASD) is the collective term for neurodevelopmental disorders characterized by qualitative impairments in social interaction, communication, and a restricted range of activities and interests. Many countries, including Australia, have reported a dramatic increase in the number of diagnoses over the past three decades, with current prevalence of ASD at 1 in every 110 individuals (~1%). The potential role for an immune-mediated mechanism in ASD has been implicated by several studies, and some evidence suggests a potential link between prenatal infection-driven inflammation and subsequent development of ASD. Furthermore, a modest number of contemporary studies have reported a markedly increased prevalence of ASD in children born preterm, who are at highest risk of exposure to perinatal inflammation. However, the mechanisms that underpin the susceptibility to infection-driven inflammation during pregnancy and risk of preterm birth, and how these intersect with the subsequent development of ASD in the offspring, is not understood. This review aims to summarize and discuss the potential mechanisms and evidence for the role of prenatal infection on the central nervous system, and how it may increase the susceptibility for ASD pathogenesis in children born preterm.
    Frontiers in Neuroscience 07/2013; 7(7):123. DOI:10.3389/fnins.2013.00123 · 3.66 Impact Factor
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