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autism Other factors associated with

Skyli
16.05.2018

Content:

  • autism Other factors associated with
  • Genetic and Environmental Factors in Autism
  • Review ARTICLE
  • None of the environmental factors is sufficient to yield autism, but rather a associated with increased risk of autism in their offspring; however, in other studies. The search strategy was adapted appropriately to the other databases, PsycINFO and Chemical factors studied from – in association with autism. During the prenatal period, the factors associated with autism risk were are likely to be resulted from other factors, such as prenatal, perinatal.

    autism Other factors associated with

    Prevalence of autism in a United States population: Genetic heritability and shared environmental factors among twin pairs with autism. Arch Gen Psychiatry ; Prenatal and perinatal risk factors in a twin study of autism spectrum disorders.

    J Psychiatr Res ; Perinatal and neonatal risk factors for autism: Curr Opin Pediatr ; Prenatal and perinatal risk factors for autism: Arch Pediatr Adolesc Med ; Advancing paternal age and autism.

    Arch General Psychiatry ; Prenatal and perinatal risk factors for autism. J Perinat Med ; J Autism Dev Disord ; Pre- and perinatal factors in high-functioning females and males with autism. Obstetrical suboptimality in autistic children. Pre-, peri-, and neonatal factors and infantile autism. J Child Psychol Psychiatry ; Epidemiology of autistic disorder and other pervasive developmental disorders.

    J Clin Psychiatry ; 66 suppl A qualitative and quantitative review of obstetric complications and autistic disorder. J Dev Phys Disabil ; A case-control study of obstetric complications and later autistic disorder. Pre-, peri- and neonatal risk factors for autism. Acta Obstet Gynecol Scand ; Preferred reporting items for systematic reviews and meta-analyses: Ann Intern Med ; Beyond the Basics Measuring inconsistency in meta-analyses. Meta-analysis in clinical trials.

    Control Clin Trials ; 7: Statistical aspects of the analysis of data from retrospective studies of disease. J Natl Cancer Inst ; Operating characteristics of a rank correlation test for publication bias. Bias in meta-analysis detected by a simple, graphical test. Prenatal, perinatal and postnatal factors associated with autism spectrum disorder. J Pediatr Rio J ; Perinatal risk factors for infantile autism.

    Prenatal and perinatal risk factors for autism in China. Perinatal factors and the development of autism: Pre-eclampsia, birth weight, and autism spectrum disorders. The role of prenatal, obstetric and neonatal factors in the development of autism. Perinatal and maternal risk factors for autism spectrum disorders in New South Wales, Australia. Child Care Health Dev ; Pediatr Int ; Prenatal, perinatal, and neonatal factors associated with autism spectrum disorders. Autism spectrum disorders, maternal characteristics and obstetric complications among singletons born in Alberta, Canada.

    Chronic Dis Can ; Birth defects in children with autism spectrum disorders: Am J Epidemiol ; Advanced parental age and the risk of autism spectrum disorder. Risk of autism and increasing maternal and paternal age in a large north American population. Risk factors for autism and Asperger syndrome. Perinatal factors and migration. Independent and dependent contributions of advanced maternal and paternal ages to autism risk.

    Autism Res ; 3: Maternal and paternal age and risk of autism spectrum disorders. Paternal age increases the risk for autism in an Iranian population sample. Mol Autism ; 1: Advancing maternal age is associated with increasing risk for autism: Parental age and autism spectrum disorders. Ann Epidemiol ; Obstetric risk factors and autism spectrum disorders in Finland.

    J Pediatr ; Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children years of age. Acta Paediatr ; Many studies have explored the association between optimality scores composite measures of compromised prenatal, perinatal and neonatal health overall and ASD. Systematic reviews , have found that reduced prenatal and neonatal optimality is more evident than perinatal suboptimality in ASD cases.

    However, since those reviews, a prospective cohort study has found that having at least four obstetric suboptimality factors mainly prenatal and perinatal in the first birth were significantly correlated with ASD. Systematic reviews , have implicated fetal hypoxia intrauterine deprivation of oxygen in ASD etiology, based on several perinatal factors that may serve as markers of hypoxia, including low Apgar score, caesarean section and growth retardation.

    However, fetal hypoxia has been weakly associated with ASD according to a population- based cohort study. Multiple births have been associated with ASD according to a meta-analysis as well as a cohort study, whereas an ecological study did not find an association. According to a review of research trends, immune dysregulation has been widely studied and possesses the strongest evidence base of the physiological abnormalities in ASD.

    Several studies have examined the role of autoimmunity in ASD. Three case-control studies have consistently demonstrated that antibody reactivity to human fetal brain protein is more prevalent in mothers of children with ASD or specifically autism than in mothers of children who do not have ASD or specifically autism. Two cohort studies and a case-control study found an association between maternal or family history of autoimmune diseases and ASD , or autistic regression, whereas another case-control study found no association.

    Reviews have discussed growing evidence for the role of autoimmunity in ASD, stemming mostly from animal models and human clinical studies, but have indicated a need to identify the functions of the autoantibodies that might be affecting neurodevelopment. Brain inflammation has also been implicated in the etiology of ASD. According to the reviews based mainly on animal and human clinical studies, early-life immune insults such as toxic substances, food additives or stress may result in a cascade of excitotoxicity in the brain, - and may be related to dysregulation of glutamate neurotransmission.

    Emerging evidence, mostly from case-control studies, has shown that increased proinflammatory cytokine production is found in the serum or cerebrospinal fluid of ASD children or the amniotic fluid of their mothers, - although a decreased neonatal level of cytokines has also been observed.

    Infections may trigger the chronic inflammation of the CNS, affecting brain development and maturation, which has been implicated in ASD etiology. A systematic review indicated that more research is required to explore this association. Neonatal jaundice, a result of elevated serum bilirubin levels hyperbilirubinemia , has been a concern because unconjugated bilirubin can be toxic to the developing CNS.

    Five studies , , - and two systematic reviews 13 , investigated this risk factor. According to the systematic reviews, hyperbilirubinemia was associated with an increased risk of autism 13 , with a summary effect estimate of 1. While a meta-analysis indicated no significant relationship between neonatal seizures and ASD, four small studies have provided some evidence for a possible association. According to a review of research trends, oxidative stress was one of the most-studied physiological abnormalities in ASD, with one of the strongest evidence bases, mainly consisting of clinical and animal studies.

    Biomarkers included altered levels of oxidative stress defence systems, including metallothioneins and antioxidant enzymes. Deficiencies in minerals and levels of trace elements were the most-studied of the nutritional factors in association with ASD, followed by vitamin D deficiency Table 6. Evidence for mineral deficiencies and levels of trace elements in children with ASD or specifically, autism, comes mainly from case-control studies examining hair samples and remains inconclusive.

    Studies looking at associations between levels of zinc, 37 , 95 , , - iron, 37 , , , , - magnesium, 37 , , , , copper, 37 , , , , , , , , molybdenum, 37 , , , , nickel, , , , , and selenium 37 , , , , and ASD have had conflicting results.

    Calcium deficiencies have also been documented in association with ASD or autism in children, , , , with some inconsistencies. Vitamin D plays a crucial role in various functions, such as neurodevelopment, the anti-inflammatory response and the detoxification pathway.

    It has been suggested that migration may play a role in the etiology of ASD, because of increased autism prevalence rates among immigrants in northern European countries, and because immigrants with dark skin are more prone to vitamin D deficiency due to their skin pigmentation.

    Furthermore, a systematic review concluded that there was inadequate support for an association, and that more population-based longitudinal studies are needed, given the plausible biological evidence. We found few studies on infant feeding methods in relation to ASD, although two case-control studies found that the absence or late initiation of breastfeeding was significantly associated with ASD or autism, , in contrast to findings of an ecological study. Evidence supporting an association between folic acid intake and ASD is very sparse, although a recent prospective cohort study found maternal folic acid intake to be protective against ASD, in contrast to an ecological study that found positive correlations between the percentages of prescription prenatal vitamins and pediatric vitamins containing folic acid and ASD incidence.

    Socioeconomic status SES , ethnicity, immigrant status and stress were recurring social factors examined in association with ASD Table 7. The importance of SES emerged as a predictor of ASD risk in nine studies, , , , - but findings were mixed.

    However, other studies had different results. Most studies that examined the relationship between maternal ethnicity and ASD found a significant association, , , , , , with the exception of one study in the United Kingdom. In contrast, another American study found that Black race was associated with increased odds of ASD, particularly with ID, but case ascertainment was more likely from school sources.

    Maternal immigrant status is another social factor that emerged in eight studies , , , - and two systematic reviews 13 , supporting an association with ASD or ASD subtype. For example, a decline in autism rates among Hispanic children in the United States was attributed to undocumented immigrant parents' reluctance to seek diagnostic services due to fears of being reported to the authorities and having to face deportation when threatened by anti-immigrant policy enforcement.

    Prenatal exposure to environmental stressors, including stress-related immunological and neuroinflammatory abnormalities and placental dysfunction that can affect fetal neurodevelopment, may play a role in ASD etiology. In addition to the chemical, physiological, nutritional and social dimensions, several other factors emerged that were investigated for association with ASD.

    Two studies showed that autism births occur in geographical clusters, which could indicate that local factors are involved in the prevalence. Most of the research on the environmental contribution to ASD etiology focussed on physiological or chemical risk factors, and less on social and nutritional factors. Within these dimensions, however, the vast literature is riddled with inconsistent findings. Biomarkers of heavy metal exposure, particularly mercury, from levels measured in biological specimens such as hair, blood and urine have been studied intensely, but its association with ASD remains uncertain due to conflicting findings.

    Because most of these studies only measure biomarkers of heavy metal, and do not ascertain actual exposure sources, temporality of association is unknown. Furthermore, many of the biomarker studies had small sample sizes. These findings are consistent with a recent systematic review by Rossignol and colleagues 11 published in , after the completion of our review , who examined the association between environmental toxicant exposure and ASD.

    In contrast, emerging evidence for the association between traffic-related air pollutants and ASD or autism has been relatively consistent, although further research is required to establish specificity of association and improve external validity beyond the American landscape. Despite numerous studies exploring the relationship between MMR or thimerosalcontaining vaccines and ASD, there is a lack of convincing support for this association.

    Additionally, evidence of an association between fetal or childhood exposure to various medications and ASD is limited to a few studies. A lack of association between tobacco smoke exposure and ASD is also apparent, although some studies have indicated a possible link with PDD-NOS, warranting further study on ASD subgroups separately if causal relationships are to be elucidated. Moreover, studies on exposure to occupational chemicals, pesticides and alcohol were limited.

    The most widely and consistently implicated physiological factors in ASD onset include advanced parental age, low birth weight, prematurity and clustering of pregnancy complications. A consistent association between hyperbilirubinemia and ASD has been demonstrated as well. More research is warranted on the effects of advanced grandparental age on ASD, based on preliminary findings.

    Emerging epidemiological evidence for immune abnormalities related to autoimmunity and brain inflammation have also been reported in children with ASD or their mothers. However, further work is required to establish temporality of association and to elucidate their possible role in ASD etiology.

    More research is also needed to understand other physiological factors such as birth characteristics, maternal chronic conditions, hormones and child conditions in relation to ASD. Studies have indicated a potential relationship between chronic conditions such as pregnancy weight gain or maternal diabetes and ASD.

    However, due to heterogeneity and lack of specificity of exposures, further research is warranted. Evidence for a link between earlier birth order, greater parity and short interpregnancy intervals and ASD exists, although the etiological contribution is not clear.

    The association between oxidative stress and ASD has been demonstrated by a limited number of small epidemiological studies. The relationship between nutritional factors and ASD has not been well studied compared to that with chemical and physiological factors.

    The current literature suggests that associations between social factors such as SES and ethnicity and ASD may vary across countries, depending on possible case ascertainment biases.

    However, maternal immigrant status has been consistently correlated with ASD. Whether this may relate to SES, adaptation to a new environment, stress or changes in vitamin D exposure as suggested by some studies requires further investigation. Overall, the lack of consistency, temporality and specificity of the associations observed in many studies precludes the establishment of causality. Longitudinal studies may be helpful in establishing temporality to identify possible causal relationships.

    Consistent methods of measuring exposure and case ascertainment and consideration for potential confounders could reduce heterogeneity. Underlying mechanisms of some of these associations need to be investigated through further biological research. Of the reviews that have explored possible risk factors of ASD to date, none have examined the entire scope of the environmental contribution to ASD. We conducted a comprehensive, systematic search of the literature. Although all relevant articles may not have been retrieved in this review, a large number of potentially contributing factors were identified that can provide an adequate picture of the breadth of environmental contribution to ASD etiology.

    Although the search strategy to retrieve relevant ASD articles aimed for comprehensiveness, key scientific journals were not hand-searched and no searches were performed on citations referenced in included studies and grey literature. Furthermore, more information on environmental factors may have been missed if articles covering them also dealt with animal models or genetic studies, which were excluded.

    This is evident for research in immune abnormalities and oxidative stress, because articles retrieved were fewer in number although reviews have indicated a vast amount of research, likely from clinical and animal studies. Because the aim of this scoping review was to assess the current state of knowledge of environmental risk factors of ASD, quality assessment of these studies was not performed to assess the strength of evidence. Our scoping review examined research conducted between and on environmental factors potentially associated with ASD, grouped into four categories: We found that physiological factors including advanced parental age, low birth weight, prematurity, hyperbilirubinemia and clustering of pregnancy complications have been consistently reported as risk factors for ASD.

    While evidence for an association with traffic-related air pollutants is emerging, research on nutritional factors associated with ASD is limited. Of the factors in the social dimension, immigrant status has been consistently associated with ASD, which warrants further research.

    Large prospective studies, adjusting for sociodemographic confounders, are needed to resolve inconsistencies, especially in the area of heavy metal exposure, where evidence for an association with ASD is still inconclusive. Because there are a variety of associations with ASD, the etiology is likely multifactorial. Future studies should continue exploring how these different factors may be interrelated.

    Overall, the lack of consistency, temporality and specificity of associations between environmental factors and ASD remains the largest barrier to establishing causal relationships. National Center for Biotechnology Information , U. Author information Copyright and License information Disclaimer. This article has been cited by other articles in PMC. ASD, autism spectrum disorder, autism, environmental exposure, etiology.

    Highlights The environmental factors most commonly studied in association with ASD were physiological and chemical factors. Research on nutritional and social factors is limited. Older parental age, low birth weight, premature birth, neonatal jaundice and clustering of pregnancy complications were consistently reported to be associated with ASD. Introduction Autism spectrum disorder ASD is a group of neurodevelopmental disorders with varying levels of severity in impairment in social communication and interaction, and restricted repetitive behaviours, interests and activities.

    Open in a separate window. Process for searching and screening research on autism spectrum disorders found in three electronic databases, published between and Results The literature encompassed a wide scope of research investigating potential environmental risk factors associated with ASD.

    TABLE 1 Final selection of research articles on associations between environmental factors and autism spectrum disorder, by dimension and article type.

    Final selection of articlesa on associations between environmental factors and autism spectrum disorder, by subject and article type. Final selection of articles on associations between environmental factors and autism spectrum disorder, by subject and time period, — and — TABLE 2 Chemical factors studied from — in association with autism spectrum disorder, by article type and subtheme.

    TABLE 4 Associations of prenatal, perinatal or postnatal exposure to air pollutants in children with autism spectrum disorder or autism, found in studies published — TABLE 5 Physiological factors studied from — in association with autism spectrum disorder, by article type and subtheme. TABLE 6 Nutritional factors studied from — in association with autism spectrum disorder, by article type and subtheme.

    TABLE 7 Social factors studied from — in association with autism spectrum disorder, by article type and subtheme. Discussion Most of the research on the environmental contribution to ASD etiology focussed on physiological or chemical risk factors, and less on social and nutritional factors.

    Strengths and limitations Of the reviews that have explored possible risk factors of ASD to date, none have examined the entire scope of the environmental contribution to ASD. Conclusion Our scoping review examined research conducted between and on environmental factors potentially associated with ASD, grouped into four categories: Diagnostic and Statistical Manual of Mental Disorders: Trends in the prevalence of developmental disabilities in US children, — Prevalence of autism spectrum disorder among children aged 8 years — Autism and Developmental Disabilities Monitoring Network, 11 sites, United States, Estimated prevalence of autism spectrum disorders among children 2—14 years of age in three Canadian regions — [Internet].

    Incidence of autism spectrum disorders: Diagnostic change and the increased prevalence of autism. The rise in autism and the role of age at diagnosis. Genetic heritability and shared environmental factors among twin pairs with autism. Understanding and determining the etiology of autism. Environmental toxicants and autism spectrum disorders: A review of research trends in physiological abnormalities in autism spectrum disorders: Pre-, peri- and neonatal risk factors for autism. Acta Obstet Gynecol Scand.

    Exploring the environmental contribution. Nutritional and environmental approaches to preventing and treating autism and attention deficit hyperactivity disorder ADHD: J Altern Complement Med. Enhancing the scoping study methodology: Use of birth certificates to examine maternal occupational exposures and autism spectrum disorders in offspring. Parental occupational exposures and autism spectrum disorder. J Autism Dev Disord. Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley.

    Tipping the balance of autism risk: Urinary porphyrin profiles as a biomarker of mercury exposure: J Toxicol Environ Health. Porphyrinuria in childhood autistic disorder: A prospective assessment of porphyrins in autistic disorders: Urinary porphyrin excretion in neurotypical and autistic children. An investigation of porphyrinuria in Australian children with autism. J Toxicol Environ Health A.

    Porphyrinuria in Korean children with autism: Biomarkers of environmental toxicity and susceptibility in autism. A biomarker of mercury body-burden correlated with diagnostic domain specific clinical symptoms of autism spectrum disorder. Environmental mercury release, special education rates, and autism disorder: Proximity to point sources of environmental mercury release as a predictor of autism prevalence. Reduced levels of mercury in first baby haircuts of autistic children.

    A prospective study of prenatal mercury exposure from maternal dental amalgams and autism severity. Acta Neurobiol Exp Wars ; 69 2: Seafood consumption and blood mercury concentrations in Jamaican children with and without autism spectrum disorders. Heavy metals and trace elements in hair and urine of a sample of Arab children with autistic spectrum disorder.

    Maedica Buchar ; 6 4: Low-level chronic mercury exposure in children and adolescents: Toxicological profile for mercury [Internet]. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: Pediatric neurobehavioral diseases in Nevada counties with respect to perchlorate in drinking water: An ecological study on childhood autism.

    Int J Health Geogr. Ambient air pollution and autism in Los Angeles County, California. Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8.

    Traffic-related air pollution, particulate matter, and autism. Autism spectrum disorders in relation to distribution of hazardous air pollutants in the San Francisco Bay area. Ambient air pollution and the progression of atherosclerosis in adults. Ileal-lymphoid-nodular hyperplasia, non-specific colitis, and pervasive developmental disorder in children.

    MMR vaccination and pervasive developmental disorders: Maternal smoking during entire pregnancy associated with PDD; no association with first trimester smoking.

    Adjusted for maternal age, SES and psychiatric diagnosis. Maternally-reported smoking collected on medical records could be inaccurate. Some indication for an association with high-functioning ASD. All studies relied on self-reported smoking, often from birth records, which can be inaccurate.

    Few studies considered environmental cigarette smoke exposure, and those that did had other limitations. Further studies investigating high-functioning ASD and potential gene x environment interactions, and utilizing objective markers of cigarette smoking i. Subject to potential inaccuracies of self-reported use. Cases not clinically confirmed. No increased risk from light to moderate maternal alcohol consumption.

    ASD case parents reported significantly lower alcohol use than control parents same for autism and PDD. Clinically-confirmed cases and controls screened for ASD. No adjustment for confounders. One study observed high OR for methylene chloride in urban areas, but unlike all other air pollution studies, used speech- and language-impaired as control group.

    Associations not consistent across studies for lead and vinyl chloride. Available studies used same exposure database, which represents only select years of modelling. A problematic discrepancy is with tobacco smoke, which contains many of the same constitutents [e.

    Large study, objective measure of a wide range of a priori-selected pollutants. Used semi-Bayes analysis to adjust simultaneously for all pollutants. Control group had speech or language impairments, may not represent exposures of population; hence results could be biased, not comparable with other studies. Exposure estimated for periods 0 to 4 years after delivery. Two distinct studies implicate criteria pollutants including NO 2 , PM 2.

    A single study examined ozone and found consistent associations across various models adjusted for a second pollutant. Although all studies adjusted for multiple socioeconomic and demographic factors, possible residual confounding cannot be precluded.

    Additionally, the lack of consistent evidence for an association with tobacco smoke, which contains metals, NO 2 , PM 2. Similarly for ozone and PM 2. Maternal report of household flooring material via questionnaire when children were years of age.

    Association of ASD with vinyl flooring in bedrooms, a major indoor contributor to phthalates. Unbiased, population-based sampling; exposure reporting unlikely to be influenced by case status.

    Suggestive risk for ASD, but further studies needed, with appropriate attention to timing of exposure information. Need to consider the possibility that different phthalates may have different effects, and hence multiple sources for human exposures. Low molecular weight phthalate metabolite concentrations associated with poorer Social Responsiveness Scale scores Social Cognition, Communication, Awareness domains.

    Measurement of phthalates during pregnancy, which thereby accounts for multiple sources of the low molecular weight compounds. Single measure-ments of phthalates may not be representative of long-term exposures. Insufficient to draw conclusions on risk for ASD. Error in studies to date likely to be nondifferential. However, use of one or two isolated measurements may not provide valid surrogates for overall prenatal or infant exposures.

    Genetic heritability and shared environmental factors among twin pairs with autism. Brain asymmetries in autism and developmental language disorder: Risk factors for autism: Embryological origin for autism: Maternal influenza infection causes marked behavioral and pharmacological changes in the offspring.

    Association of autistic spectrum disorder with season of birth and conception in a UK cohort. Effects of season of birth on autism spectrum disorders: Closely spaced pregnancies are associated with increased odds of autism in California sibling births. The role of prenatal, obstetric and neonatal factors in the development of autism. Short interpregnancy intervals and unfavourable pregnancy outcome: Association between short interpregnancy intervals and term birth weight: Declining levels of erythrocyte folate during the postpartum period among Hispanic women living on the Texas-Mexico border.

    Sex differences in prevalence of congenital neural defects after periconceptional famine exposure. Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation. Effects of vitamin B12 and folate deficiency on brain development in children. Prenatal vitamins, one-carbon metabolism gene variants, and risk for autism. Food and Nutrition Board. Association between maternal use of folic acid supplements and risk of autism spectrum disorders in children.

    Maternal use of folic acid supplements during pregnancy and four-year-old neurodevelopment in a population-based birth cohort. Prevention of neural tube defects: Maternal folic acid supplement use in early pregnancy and child behavioural problems: The Generation R Study.

    Lower maternal folate status in early pregnancy is associated with childhood hyperactivity and peer problems in offspring. Folic acid supplements in pregnancy and severe language delay in children.

    A functional polymorphism in the reduced folate carrier gene and DNA hypomethylation in mothers of children with autism. Maternal dietary fat intake in association with autism spectrum disorders.

    Role of omega-3 fatty acids in brain development and function: Fetal and neonatal levels of omega Epidemiologic evidence supporting the role of maternal vitamin D deficiency as a risk factor for the development of infantile autism. Prevalence of autism according to maternal immigrant status and ethnic origin.

    Serum levels of hydroxyvitamin D in mothers of Swedish and of Somali origin who have children with and without autism. Risk of autism spectrum disorders in children born after assisted conception: Associations between indoor environmental factors and parental-reported autistic spectrum disorders in children years of age.

    Autism spectrum disorders, maternal characteristics and obstetric complications among singletons born in Alberta, Canada. Maternal smoking during pregnancy and the prevalence of autism spectrum disorders, using data from the autism and developmental disabilities monitoring network.

    Narrowly versus broadly defined autism spectrum disorders: Who underreports smoking on birth records: Smoking during pregnancy and risk of autism spectrum disorder in a Finnish National Birth Cohort. Influence of maternal tobacco smoking during pregnancy on uterine, umbilical and fetal cerebral artery blood flows.

    Extent of nicotine and cotinine transfer to the human fetus, placenta and amniotic fluid of smoking mothers. Maternal cigarette smoking and child psychiatric morbidity: Nicotine exposure during pregnancy is a factor which influences serotonin transporter density in the rat brain.

    Potential explanation of the reported association between maternal smoking and autism. Maternal smoking during pregnancy and psychiatric adjustment in late adolescence. The relationship of maternal smoking to psychological problems in the offspring.

    Family history, maternal smoking, and clubfoot: Smoking, genetic polymorphisms in biotransformation enzymes, and nonsyndromic oral clefting: Prenatal alcohol exposure and autistic spectrum disorders—a populatio n-based prospective study of 80, children and their mothers.

    A longitudinal study of the long-term consequences of drinking during pregnancy: Molecular substrates of social avoidance seen following prenatal ethanol exposure and its reversal by social enrichment.

    Parental psychiatric disorders associated with autism spectrum disorders in the offspring. Autism, affective and other psychiatric disorders: Correlation of family history with specific autistic subgroups: Asperger's syndrome and bipolar affective disease.

    Substance exposure in utero and developmental consequences in adolescence: Neurobiological consequences of maternal cannabis on human fetal development and its neuropsychiatric outcome. Regional brain morphometry and impulsivity in adolescents following prenatal exposure to cocaine and tobacco. Prenatal valproate exposure and risk of autism spectrum disorders and childhood autism. Antidepressant use during pregnancy and childhood autism spectrum disorders.

    Association of autism with induced or augmented childbirth in north Carolina birth record and education research databases. Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8. Proximity to point sources of environmental mercury release as a predictor of autism prevalence. Autism spectrum disorders in relation to distribution of hazardous air pollutants in the San Francisco bay area.

    Concentration and size distribution of ultrafine particles near a major highway. Diesel exhaust particles induce oxidative stress, proinflammatory signaling, and P-glycoprotein up-regulation at the blood-brain barrier. Effects of lactational exposure to benzo[alpha]pyrene B[alpha]P on postnatal neurodevelopment, neuronal receptor gene expression and behaviour in mice.

    Down-regulation of early ionotrophic glutamate receptor subunit developmental expression as a mechanism for observed plasticity deficits following gestational exposure to benzo a pyrene. Maternal serum persistent organic pollutants in the Finnish Prenatal Study of Autism: Are thyroid hormone concentrations at birth associated with subsequent autism diagnosis?

    Disrupting effects of hydroxy-polychlorinated biphenyl PCB congeners on neuronal development of cerebellar Purkinje cells: Is retinoic acid-related orphan receptor-alpha RORA a target for gene-environment interactions contributing to autism? Polychlorinated biphenyls, organochlorine pesticides and neurodevelopment. Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley.

    Organophosphate pesticide exposure and neurodevelopment in young Mexican-American children. Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first 3 years of life among inner-city children. Neurobehavioral deficits and increased blood pressure in school-age children prenatally exposed to pesticides. Prenatal exposure to organophosphates, paraoxonase 1, and cognitive development in childhood.

    Brain anomalies in children exposed prenatally to a common organophosphate pesticide. Changes in pest infestation levels, self-reported pesticide use, and permethrin exposure during pregnancy after the U. Environmental Protection Agency restriction of organophosphates. Urinary concentrations of metabolites of pyrethroid insecticides in the general U. National Health and Nutrition Examination Survey Tipping the balance of autism risk: Stereospecific action of pyrethroid insecticides on the gamma-aminobutyric acid receptor-ionophore complex.

    Perinatal effects of two pyrethroid insecticides on brain neurotransmitter function in the neonatal rat. Associations between phthalate metabolite urinary concentrations and body size measures in New York City children. Prenatal phthalate exposure is associated with childhood behavior and executive functioning.

    Relationship between urinary phthalate and bisphenol A concentrations and serum thyroid measures in U. Analysis of PCB congeners related to cognitive functioning in adolescents. Exposure to hydroxylated polychlorinated biphenyls OH-PCBs in the prenatal period and subsequent neurodevelopment in eastern Slovakia. Assessment of the binding of hydroxylated polybrominated diphenyl ethers to thyroid hormone transport proteins using a site-specific fluorescence probe.

    Acute postnatal exposure to brominated diphenylether 47 delays neuromotor ontogeny and alters motor activity in mice. Perinatal exposure to low-dose BDE, an emergent environmental contaminant, causes hyperactivity in rat offspring. PBDEs in year-old children from California and associations with diet and indoor environment.

    Association between urinary bisphenol A concentration and obesity prevalence in children and adolescents. Urinary bisphenol A and type-2 diabetes in U. Maternal metabolic conditions and risk for autism and other neurodevelopmental disorders.

    Association of hospitalization for infection in childhood with diagnosis of autism spectrum disorders: Immune involvement in schizophrenia and autism: Is maternal influenza or fever during pregnancy associated with autism or developmental delays?

    Genetic and Environmental Factors in Autism

    The role of environmental factors in the development of autism is a crucial area of study. thalidomide and valproic acid has been linked to increased risk of autism. Scientists use the term "environmental" to refer to influences other than . Likewise, no correlation was observed between the severity of ASD and different factors. After logistic regression, the risk factors retained for autism in the final. Environmental factors associated with autism spectrum disorder: a . adapted appropriately to the other data- bases . ASD or autism, although another time-.

    Review ARTICLE



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