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Autism spectrum disorder (ASD) is a lifelong brain disorder that causes developmental disability; according to the latest statistics, 14-15 children per 1000 are diagnosed in the USA. ASD affects how people perceive the world around them and how they interact with others. Autism is a biologically based condition, and it is now accepted that genetic factors play a role. These factors are recognised as gene mutations – permanent alteration in the DNA sequence, deletions (the loss of some DNA) and copy number variants (variations in the number of repeats of sections of DNA).  However, these genetic factors account for a small fraction of total ASD cases, which suggests that preconceptional, gestational and early childhood environmental exposures are also contributing factors. There is valid evidence linking ASD with exposure in early pregnancy to drugs such as misoprostol, thalidomide and valproic acid, as well as maternal rubella infection and chlorpyrifos (an organophosphate insecticide). This evidence clearly shows that there is a feasible mechanism through which environmental exposure could cause ASD. This is further supported by studies showing that a child’s developing brain is especially sensitive to exposures to environmental toxins such as lead, ethyl alcohol and methylmercury. Pregnant women and children are surrounded by hundreds of chemicals every day, but the toxicants that have been implicated in ASD causation so far are: Solvents Pesticides Air pollutants (mercury, nickel, cadmium, trichloroethylene, nitrogen dioxide and particles) Polychlorinated biphenyls Phthalates It has also been shown that parents of children with ASD were significantly more likely to have been exposed to chemicals at work at some point in the three months preceding the pregnancy through to weaning. The chemical products included lacquer, varnish, xylene, solvents and asphalt. Children born to mothers who lived close to pesticide-treated fields when they were pregnant (high exposure) were six times more likely to give birth to a child with ASD than mothers who lived more than 1750m from such fields and therefore had a lower exposure. The exposure was measured at the stage of the pregnancy when the baby’s cranial neural tube was closing. The cranial neural tube is the beginning of the baby’s central nervous system, and this is a crucial period for the development of the brain. The particular pesticides investigated in this study were organochlorine, dicofol and endosulfan. Children with ASD had mothers with higher blood serum levels of pesticides, such as dichlorodiphenyltrichloroethane (commonly known as DDT), compared to children who did not have ASD. Some metabolites (substances that are formed within the body) can be used to monitor previous exposure to environmental pollutants, including pesticides. Studies have used one such metabolite, non-specific dialkyl-phosphate (DAP), to study the association between pesticide exposure and developmental delays in children. It was found that high levels of DAP in maternal and child urine were associated with an increased risk of the child developing a pervasive developmental disorder prior to two years of age. The impact of prenatal exposure to chlorpyrifos has also been demonstrated in a study comparing high-exposure and low-exposure individuals with regards to mental development, attention problems, attention-deficit/hyperactivity disorder problems and pervasive developmental disorders. The proportion of children with developmental delay in the high-exposure group was two to five times greater on different psychomotor and mental development indicators, including memory learning, recognition, and manipulative skills of hands and fingers, among others. Quinoline and styrene, organic compounds, have also been associated with an elevated risk of ASD in studies comparing ambient concentrations of these air pollutants in neighbourhoods where children with and without ASD were born. Children with ASD lived in more highly polluted areas compared to children without ASD. Currently, the evidence for proving a causal relationship between environmental pollutants and ASD is incomplete. While the biological mechanisms of exposure to toxins and its link to autism are not yet properly understood, statistics do show a dramatic increase in neurobehavioural disorders for individuals with a higher exposure level to toxins. It is almost impossible to predict the genetic changes that may occur with a specific individual due to the lack of scientific data. But what is clear is that the more you are exposed to pollutants and toxins, the higher is the risk of neurobehavioural disorders for you and for your children, particularly while they are still in the womb and most vulnerable.  Facts About ASDs. (2017). CDC - Facts about Autism Spectrum Disorders - NCBDDD. Retrieved 18 September 2017, from https://www.cdc.gov/ncbddd/autism/data.html  Deth, R., Muratore, C., Benzecry, J., Power-Charnitsky, V., & Waly, M. (2008). How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis. Neurotoxicology, 29(1), 190-201. http://dx.doi.org/10.1016/j.neuro.2007.09.010  Rossignol, D., Genuis, S., & Frye, R. (2014). Environmental toxicants and autism spectrum disorders: a systematic review. Translational Psychiatry, 4(2), e360. http://dx.doi.org/10.1038/tp.2014.4  McCanlies, E., Fekedulegn, D., Mnatsakanova, A., Burchfiel, C., Sanderson, W., Charles, L., & Hertz-Picciotto, I. (2012). Parental Occupational Exposures and Autism Spectrum Disorder. Journal Of Autism And Developmental Disorders, 42(11), 2323-2334. http://dx.doi.org/10.1007/s10803-012-1468-1  Roberts, E., English, P., Grether, J., Windham, G., Somberg, L., & Wolff, C. (2007). Maternal Residence Near Agricultural Pesticide Applications and Autism Spectrum Disorders Among Children in the California Central Valley. Environmental Health Perspectives. http://dx.doi.org/10.1289/ehp.10168  Cheslack-Postava, K., Rantakokko, P., Hinkka-Yli-Salomäki, S., Surcel, H., McKeague, I., & Kiviranta, H. et al. (2013). Maternal serum persistent organic pollutants in the Finnish Prenatal Study of Autism: A pilot study. Neurotoxicology And Teratology, 38, 1-5. http://dx.doi.org/10.1016/j.ntt.2013.04.001  Eskenazi, B., Marks, A., Bradman, A., Harley, K., Barr, D., & Johnson, C. et al. (2007). Organophosphate Pesticide Exposure and Neurodevelopment in Young Mexican-American Children. Environmental Health Perspectives, 115(5), 792-798. http://dx.doi.org/10.1289/ehp.9828  Rauh, V., Garfinkel, R., Perera, F., Andrews, H., Hoepner, L., & Barr, D. et al. (2006). Impact of Prenatal Chlorpyrifos Exposure on Neurodevelopment in the First 3 Years of Life Among Inner-City Children. PEDIATRICS, 118(6), e1845-e1859. http://dx.doi.org/10.1542/peds.2006-0338  Kalkbrenner, A., Daniels, J., Chen, J., Poole, C., Emch, M., & Morrissey, J. (2010). Perinatal Exposure to Hazardous Air Pollutants and Autism Spectrum Disorders at Age 8. Epidemiology, 21(5), 631-641. http://dx.doi.org/10.1097/ede.0b013e3181e65d76