Cultural Adaptation and Psychometric Validation of a Thai Version of the Turnover Intention Scale (T-TIS) for Thai Nursing Professionals.

Autism spectrum disorder (ASD) is a clinically heterogeneous neurodevelopmental disorder (NDD) diagnosed based on deficits across two core symptom domains: social communication and interaction, and restricted, repetitive patterns of behavior, interests, or activities., ASD is frequently accompanied by comorbidities such as intellectual disability, attention deficit hyperactivity disorder (ADHD), and olfactory impairments., According to the US Centers for Disease Control (CDC), based on 2022 data, the prevalence of ASD has increased fivefold since 2000 and currently affects 1 in 31 children, with a disproportionately male bias (male‐to‐female ratio 3.4:1). This epidemic‐like rise in ASD prevalence cannot be entirely explained by changes in diagnostic criteria and improved detection and awareness. While ASD has strong genetic underpinnings, genetic factors only contribute an estimated 40%–80% of ASD heritability. Moreover, findings from monozygotic twin studies show that genetics alone cannot account for ASD risk, suggesting a role for environmental factors. Thus, the etiology of ASD is hypothesized to involve gene–environment (G × E) interactions, with environmental factors exacerbating genetic susceptibility; however, the complex interactions between toxicants and genetic factors remain understudied, highlighting a critical gap in understanding their contribution to ASD risk. Mounting evidence shows significant associations between early‐life exposure to certain endocrine‐disrupting chemicals (EDCs) and NDD risk., This includes polybrominated diphenyl ethers (PBDEs), a class of persistent organic pollutants (POPs) used in a wide range of consumer products including building materials, electronics, textiles, plastics, and foams. PBDEs have been detected in human serum, placenta, and breastmilk and are readily transferred to the developing fetus, contributing to their neurodevelopmental toxicity. PBDEs have been banned or voluntarily phased out, leading to slow but measurable declines in the concentration of some congeners in environmental and biota samples., However, PBDEs continue to leach into ecosystems due to their lipophilicity and poor degradation and bioaccumulate in human and wildlife tissues via inhalation, oral and dermal exposure., , PBDE contamination is predicted to remain an ongoing health problem for decades to come due to their long half‐lives, persistence in e‐waste, and their inadvertent reappearance into the environment and consumer products via recycling and microplastic vectoring. Findings in humans and animals have raised concerns about PBDE exposure in the framework of the developmental origins of health and disease (DOHaD) hypothesis, suggesting that PBDE exposure during early developmental windows of biological plasticity may disproportionately disrupt neurobehavioral outcomes., Epidemiological studies have found that developmental PBDE exposure is associated with poor executive function, lower IQ, attention difficulties, and disrupted behavioral regulation, reported as impulsivity and reduced social competence, suggesting that PBDEs may negatively impact children's social development., , , , Recently, findings from the HOME study also revealed that male adolescents whose mothers had an increased gestational serum ∑BDE concentration exhibited decreased social competence. Postnatal BDE‐47 exposure was associated with a significantly higher risk of poor social competence symptoms in a cohort of 4 year olds from Spain. Similarly, in the EARLI study, elevated maternal BDE‐47 was associated with reduced social reciprocity scores (SRS) in their children. However, data from the HOME longitudinal cohort provide inconclusive evidence for ASD risk by PBDEs since serum levels of PBDEs in pregnant mothers (2003–2006) have been associated with both greater (BDE‐28) and fewer (BDE‐85) autistic behaviors in their toddlers.