Proximity to point sources of environmental mercury release as a predictor of autism prevalence

University of Texas Health Science Center, San Antonio Department of Family and Community Medicine, 7703 Floyd Curl Drive, San Antonio Texas, Mail Code 7794, TX 78229-3900, USA.
Health & Place (Impact Factor: 2.81). 02/2008; 15(1):18-24. DOI: 10.1016/j.healthplace.2008.02.001
Source: PubMed

ABSTRACT The objective of this study was to determine if proximity to sources of mercury pollution in 1998 were related to autism prevalence in 2002. Autism count data from the Texas Educational Agency and environmental mercury release data from the Environmental Protection Agency were used. We found that for every 1000 pounds of industrial release, there was a corresponding 2.6% increase in autism rates (p<.05) and a 3.7% increase associated with power plant emissions(P<.05). Distances to these sources were independent predictors after adjustment for relevant covariates. For every 10 miles from industrial or power plant sources, there was an associated decreased autism Incident Risk of 2.0% and 1.4%, respectively (p<.05). While design limitations preclude interpretation of individual risk, further investigations of environmental risks to child development issues are warranted.

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Available from: Raymond F Palmer, Sep 26, 2015
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    • "Several of these studies have demonstrated associations between ASD and prenatal or perinatal air concentrations of various air pollutants, including particulate matter (Becerra et al., 2013; Kalkbrenner et al., 2010, 2014; Roberts et al., 2013; Talbott et al., 2015; Windham et al., 2006). Additionally, proximity to sources of airborne pollutants, including industrial facilities (Palmer et al., 2009), agricultural pesticides (Shelton et al., 2014), and high-traffic roadways (Volk et al., 2011), have been associated with ASD diagnosis and school-reported administrative prevalence , respectively. Based on results from these studies, observed relationships should be further investigated on a larger scale using highly reliable data. "
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    ABSTRACT: Prenatal and perinatal exposures to air pollutants have been shown to adversely affect birth outcomes in offspring and may contribute to prevalence of autism spectrum disorder (ASD). For this ecologic study, we evaluated the association between ASD prevalence, at the census tract level, and proximity of tract centroids to the closest industrial facilities releasing arsenic, lead or mercury during the 1990s. We used 2000 to 2008 surveillance data from five sites of the Autism and Developmental Disabilities Monitoring (ADDM) network and 2000 census data to estimate prevalence. Multi-level negative binomial regression models were used to test associations between ASD prevalence and proximity to industrial facilities in existence from 1991 to 1999 according to the US Environmental Protection Agency Toxics Release Inventory (USEPA-TRI). Data for 2489 census tracts showed that after adjustment for demographic and socio-economic area-based characteristics, ASD prevalence was higher in census tracts located in the closest 10th percentile compared of distance to those in the furthest 50th percentile (adjusted RR=1.27, 95% CI: (1.00, 1.61), P=0.049). The findings observed in this study are suggestive of the association between urban residential proximity to industrial facilities emitting air pollutants and higher ASD prevalence. Copyright © 2015 Elsevier B.V. All rights reserved.
    Science of The Total Environment 07/2015; 536:245-251. DOI:10.1016/j.scitotenv.2015.07.024 · 4.10 Impact Factor
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    • "Exposure to maternal infections during critical periods of development, such as prenatal and perinatal periods, has also gained attention in the search for the etiology of autism [16] [17]. The increased incidence of autism in certain regions has suggested that there is a link between geography and the genetic predisposition to autism [18] [19] [20]. Bisphenol A (4,4 -dihydroxy-2,2-diphenylpropane; BPA) is one of the environmental toxins that has recently received increased attention. "
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    ABSTRACT: Developmental disorders such as autism and attention deficit hyperactivity disorder (ADHD) appear to have a complex etiology implicating both genetic and environmental factors. Bisphenol A (BPA), a widely used chemical in the plastic containers and in the linings of food and beverage cans, has been suggested to play a possible causative role in some developmental disorders. Here, we report behavioral modifications in Drosophila melanogaster following early exposure to BPA, which may suggest BPA as an environmental risk factor for the behavioral impairments that are the basis of diagnosis of autism and ADHD. In an open field assay with perinatally BPA-exposed and vehicle-treated control Drosophila, different parameters of locomotion (distance travelled, walking speed, spatial movement, mobility, turn angle, angular velocity and meander) were analyzed using the ethovision software. We also examined the repetitive and social interaction behaviors in these flies. In an open field assay, we identified disturbances in the locomotion patterns of BPA-exposed Drosophila that may relate to the decision-making and the motivational state of the animal. An increase in repetitive behavior was observed as an increase in the grooming behavior of Drosophila following BPA exposure. Furthermore, we also observed abnormal social interaction by the BPA-exposed flies in a social setting. These results demonstrate the effect of the environmentally prevalent risk agent BPA on the behavior of Drosophila, and suggest the practicability and the ease of using Drosophila as a model in the studies of neurobehavioral developmental disorders. Copyright © 2015. Published by Elsevier B.V.
    Behavioural Brain Research 02/2015; 284. DOI:10.1016/j.bbr.2015.02.001 · 3.03 Impact Factor
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    • "These results suggest that amygdala dysfunction may contribute to core social impairment in ASD (Todd and Anderson, 2009). Exposures to environmental toxicants that activate the immune system have been implicated in ASD (Windham et al., 2006; Roberts et al., 2007; Palmer et al., 2009). Rats with gestational exposure to lipopolysaccharide, an endotoxin that activates the immune system, have been established as a prenatal infection model for developmental neuropsychiatric disorders (Baharnoori et al., 2012). "
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    ABSTRACT: Autism-like phenotypes in male valproate (VPA)-exposed offspring have been linked to high glutamatergic neurotransmission in the thalamic-amygdala pathway. Glial cystine/glutamate exchange (system Xc(-)), which exchanges extracellular cystine for intracellular glutamate, plays a significant role in the maintenance of extracellular glutamate. N-acetylcysteine (NAC) is a cystine prodrug that restores extracellular glutamate by stimulating system Xc(-). In this study, we examined the effects of NAC on autism-like phenotypes and neurotransmission in the thalamic-amygdala synapses, as well as the involvement of metabotropic glutamate receptors 2/3 (mGluR2/3). Valproate-treated rats received a single intraperitoneal injection of 500 mg/kg NaVPA on E12.5. On postnatal day 21 (P21), NAC or saline was administered once daily for 10 days. From day 8 to 10, NAC was given 1/2 h prior to behavioral testing. Chronic administration of NAC restored the duration and frequency of social interaction and ameliorated anxiety-like behaviors in VPA-exposed offspring. In amygdala slices, NAC treatment normalized the increased frequency of mEPSCs and decreased the paired pulse facilitation (PPF) induced by VPA exposure. The effects of NAC on social interaction and anxiety-like behavior in the VPA-exposed offspring were blocked after intra-amygdala infusion of mGluR2/3 antagonist LY341495. The expressions of mGluR2/3 protein and mGluR2 mRNA were significantly lower in the VPA-exposed offspring. In contrast, the mGluR3 mRNA level did not differ between the saline- and VPA-exposed offspring. These results provide the first evidence that the disruption of social interaction and enhanced presynaptic excitatory transmission in VPA-exposed offspring could be rescued by NAC, which depends on the activation of mGluR2/3.
    Frontiers in Behavioral Neuroscience 06/2014; 8:219. DOI:10.3389/fnbeh.2014.00219 · 3.27 Impact Factor
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