1. Ashwood P, Schauer J, Pessah IN, de Water JV. {{Preliminary evidence of the in vitro effects of BDE-47 on innate immune responses in children with autism spectrum disorders}}. {J Neuroimmunol};2009 (Feb 9)

Autism spectrum disorders (ASD) are complex neurodevelopmental disorders that manifest in childhood. Immune dysregulation and autoimmune reactivity may contribute to the etiology of ASD and are likely the result of both genetic and environmental susceptibilities. A common environmental contaminant, 2,2′,4,4′-tetrabrominated biphenyl (BDE-47), was tested for differential effects on the immune response of peripheral blood mononuclear cells (PBMC) isolated from children with ASD (n=19) and age-matched typically developing controls (TD, n=18). PBMC were exposed in vitro to either 100 nM or 500 nM BDE-47, before challenge with bacterial lipopolysaccharide (LPS), an innate immune activator, with resultant cytokine production measured using the Luminex multiplex platform. The cytokine responses of LPS stimulated PBMC from ASD and TD subjects diverged in the presence of 100 nM BDE. For example, cells cultured from the TD group demonstrated significantly decreased levels of the cytokines IL-12p40, GM-CSF, IL-6, TNFalpha, and the chemokines MIP-1alpha and MIP-1beta following LPS stimulation of PBMC pretreated with 100 nM BDE-47 compared with samples treated with vehicle control (p<0.05). In contrast, cells cultured from subjects with ASD demonstrated an increased IL-1beta response to LPS (p=0.033) when pretreated with 100 nM BDE-47 compared with vehicle control. Preincubation with 500 nM BDE-47 significantly increased the stimulated release of the inflammatory chemokine IL-8 (p<0.04) in cells cultured from subjects with ASD but not in cells from TD controls. These data suggest that in vitro exposure of PBMC to BDE-47 affects cell cytokine production in a pediatric population. Moreover, PBMC from the ASD subjects were differentially affected when compared with the TD controls suggesting a biological basis for altered sensitivity to BDE-47 in the ASD population.

2. Besag FM. {{The relationship between epilepsy and autism: a continuing debate}}. {Acta Paediatr};2009 (Feb 4)

3. Bouder JN, Spielman S, Mandell DS. {{Brief Report: Quantifying the Impact of Autism Coverage on Private Insurance Premiums}}. {J Autism Dev Disord};2009 (Feb 13)

Many states are considering legislation requiring private insurance companies to pay for autism-related services. Arguments against mandates include that they will result in higher premiums. Using Pennsylvania legislation as an example, which proposed covering services up to $36,000 per year for individuals less than 21 years of age, this paper estimates potential premium increases. The estimate relies on autism treated prevalence, the number of individuals insured by affected plans, mean annual autism expenditures, administrative costs, medical loss ratio, and total insurer revenue. Current treated prevalence and expenditures suggests that premium increases would approximate 1%, with a lower bound of 0.19% and an upper bound of 2.31%. Policy makers can use these results to assess the cost-effectiveness of similar legislation.

4. t Hart-Kerkhoffs LA, Jansen LM, Doreleijers TA, Vermeiren R, Minderaa RB, Hartman CA. {{Autism spectrum disorder symptoms injuvenile suspects of sex offenses}}.{ J Clin Psychiatry};2009 (Feb 10)

OBJECTIVE: To investigate autism spectrum disorder (ASD) symptoms in juvenile suspects of sex offenses. METHOD: A group of 175 juvenile suspected sex offenders (all males, mean +/- SD age = 14.9 +/- 1.4 years) was compared with a matched healthy control group (N = 500, mean +/- SD age = 14.0 +/- 1.4 years) and a group of children with DSM-IV-diagnosed ASD (N = 114, mean +/- SD age = 14.2 +/- 1.9 years) with respect to autistic symptoms as measured by means of a standardized questionnaire, the Children’s Social Behavior Questionnaire. Furthermore, specific subgroups of sexual offenders, i.e., child molesters, solo peer offenders, and group offenders, were compared with regard to levels of ASD symptoms. The study was conducted from May 2003 to December 2006. RESULTS: Significantly higher levels of ASD symptoms were found in juvenile sex offenders than in healthy controls, while levels were lower than in the ASD group (F = 148.259, p < .05). Solo peer offenders and child molesters scored higher on several subscales as well as on core autistic symptoms than group offenders (F = 5.127, p < .05). CONCLUSIONS: Levels of ASD symptoms are higher in juvenile suspects of sex offenses as compared to the healthy population, which argues for considering specific diagnostic assessment in this population, especially in solo offenders and child molesters.