Abstract
BackgroundPolychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) are assumed to act as endocrine disruptor chemicals. Prenatal exposure to these pollutants might influence fetal steroid hormone levels, which are thought to be related to sex-typical development and autistic traits.ObjectivesWe examined associations of prenatal levels of PCDD/Fs and PCBs with autism traits and sex-typical behaviour in childhood.MethodsWe measured levels of PCDD/Fs and PCBs in maternal blood samples during pregnancy using gas chromatography/high-resolution mass spectrometry. Sex-typical behaviour was assessed at 9 years of age (n = 96) and autistic traits at 10 years of age using the Social Responsiveness Scale (SRS; n = 100). Multiple regression analyses were conducted to estimate the associations between prenatal exposure and outcome variables.ResultsBlood concentrations (WHO2005-TEq) of ƩPCDD/Fs ranged from 2.93–46.45 pg/g lipid base (median = 12.91 pg/g lipid base) and concentrations of ƩPCBs were in the range of 1.24–25.47 pg/g lipid base (median = 6.85 pg/g lipid base) which is within the range of German background exposure. We found significant negative associations between PCDD/F levels in maternal blood and SRS scores in the whole group (β = -6.66, p < .05), in girls (β = -10.98, p < .05) and, in one SRS subscale, in boys (β = -6.86, p < .05). For PCB levels, associations with one SRS subscale were significant for the whole study group as were associations with two subscales in girls. We did not find significant associations between PCDD/F or PCB levels and sex-typical behaviour for either sex.ConclusionsIn an earlier part of this study, prenatal exposure to PCDD/Fs and PCBs was found to be associated with lower testosterone levels, therefore, our findings are consistent with the idea that autism spectrum conditions are related to fetal androgen levels. Several possible mechanisms, through which PCDD/Fs and PCBs might influence autistic behaviour, are discussed.
Highlights
Autism spectrum conditions (ASC) are defined by a triad of core symptoms from an early age: Abnormal social development and communication as well as restricted interests or stereotypical behaviour [1]
Blood concentrations (WHO2005-toxicity equivalents (TEq)) of ƩPCDD/Fs ranged from 2.93–46.45 pg/g lipid base and concentrations of ƩPCBs were in the range of 1.24– 25.47 pg/g lipid base which is within the range of German background exposure
We found significant negative associations between PCDD/F levels in maternal blood and Social Responsiveness Scale (SRS) scores in the whole group (β = -6.66, p < .05), in girls (β = -10.98, p < .05) and, in one SRS subscale, in boys (β = -6.86, p < .05)
Summary
Autism spectrum conditions (ASC) are defined by a triad of core symptoms from an early age: Abnormal social development and communication as well as restricted interests or stereotypical behaviour [1]. Causal mechanisms in the development of ASC are unclear. Genetic factors such as copy-number variations, gene mutations or gene deletions are considered [5], as indicated by high concordance rates among twins and families. Two other, closely related groups of persistent organic pollutants (POPs), namely polychlorinated biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), have recently come into focus of autism research. Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polychlorinated biphenyls (PCBs) are assumed to act as endocrine disruptor chemicals. Prenatal exposure to these pollutants might influence fetal steroid hormone levels, which are thought to be related to sex-typical development and autistic traits
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