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Volume 8

Journal of Environmental & Analytical Toxicology

Environment and Health Congress 2018

July 11-12, 2018

July 11-12, 2018 Sydney, Australia

World Congress on

Environmental Toxicology and Health

Role of endocrine disturbing chemicals in development of autism spectrum disorders

Omar Bagasra

Claflin University, USA

A

utism Spectrum Disorder (ASD) is a set of complex developmental disorders whose etiology is unknown. Although

the symptoms may vary from person to person, they include impairment or loss of speech, lack of empathy and social

interaction deficiency. The cases of ASD have continued to increase drastically each year, with the CDC estimating 1:45 children

diagnosed, from 1 in 10,000 40 years ago. It is believed that the ASD is caused by a combination of genetic and environmental

factors, but recent studies suggest that epigenetic factors as well as exposure to endocrine disturbing environmental chemicals,

to which expecting mothers are exposed on a daily bases, may play a critical role in its pathogenesis. Although there are

no biomarkers for the disease, low levels of Oxytocin (OXY) and Arginine Vasopressin (AVP) have been reported. These

neuropeptides play a critical role in neurodevelopment of social interaction. Social interaction deficiencies are a principal sign

of ASD in children. OXY, is involved in social recognition, pair bonding and anxiety, as well as being linked to autism. Numerous

studies have shown that children with autism have plasma levels of OXY and AVP that are significantly lower than average. The

importance for normal OXY and OXY receptor function in males may explain how hormonal malfunction leads to ASD male

bias. Also, mothers of ASD children have lower levels of OXY and AVP and, in typical children, lower concentrations of OXY

in plasma are associated with lower social and cognitive functioning. There is an inexplicable bias toward males in classical

autism by a ratio of ~4:1, and ~10:1 in Asperger’s Syndrome (AS). The clinical picture is very heterogeneous and the etiology

is unknown. The heritability is high in ASD but no individual gene variants exerting a major impact on susceptibility have as

yet been identified. The mechanism for gender bias in autism is unknown although several hypotheses have been advanced

including: (1) Epigenetic mechanisms ‘the extreme male brain’ hypothesis of Baron-Cohen which postulates that elevated fetal

testosterone is a risk factor for ASD, (2) genetic mechanisms which involves X or Y chromosome inactivation and (3) recently,

Hu, et al. have shown that retinoic acid-Related Orphan Receptor Alpha (RORA) is reduced in the brain and lymphoblastoid

cell lines of multiple cohorts of individuals with ASD. This gene targets CYP19A1 (aromatase), in a gender-dependent manner

that can also lead to elevated testosterone (or male hormones-like chemicals) levels, a proposed risk factor for autism. To date,

none of these hypotheses have been either proven or disproven. Given the high clinical heterogeneity of ASD, it is possible

that each of these mechanisms for gender bias may apply to specific cohorts of individuals with ASD. We will present data on

the neuro-modifying effects of several endocrine disturbing chemicals on developing human brain neurons and their effects at

morphologic, immunologic and at molecular levels.

Biography

Omar Bagasra has completed his PhD from University of Louisville, Kentucky, USA and his MD from UACJ, Mexico. He has completed his Post-doctorate at Union

University, Albany, New York and Residency and Fellowships at Hahnemann University, Temple University, Schools of Medicine. He is the Founding Director of

South Carolina Center for Biotechnology at Claflin University, South Carolina, USA. He has published more than 140 papers in reputed journals and published over

10 books. His recent book describes the role of environmental factors in autism. He has been serving as Editorial Board Member of over 15 journals.

obagasra@claflin.edu

Omar Bagasra, J Environ Anal Toxicol 2018, Volume 8

DOI: 10.4172/2161-0525-C1-011