## 1 Introduction  
Xenobiotics of both, natural and synthetic sources can influence organisms in many different ways. Since more and more chemicals are released into the environment toxicological investigations about how these xenobiotics act on organisms become increasingly important. Up to 360 \(\upmu\)g/g dry weights of organic halogens have been found in Swedish forests [1] and up to 35 \(\upmu\)g/L of adsorbable organic bromine in Berlin lakes [2]. The amount found in industrial waste water has increased almost by factor 100 [3]. These figures clearly show the increasingly importance of realistic ecotoxicological investigations on how these xenobiotics act on organisms. In many past corresponding investigations, two important issues were often not well considered: on the one hand unrealistically high concentrations were usually used while screening for the toxic potential, on the other hand most tests were restricted to determining the LD\({}_{50}\) and changes in lifespan. Only a few analyses have been conducted on neurological effects, although the nervous system is one of the primary targets for environmental chemicals and pollutions [4]. This aspect is gaining increasing significance, since many invertebrates lack real livers and even well-known hepatotoxins display major adverse neurotoxic actions, as recently exemplified with microcystin-LR in _Caenorhabditis elegans_ (_C. elegans_) [5]. One of the main reasons, why neurological examination is often omitted, is that standardized neurotoxicity screening methods devolved by the WHO and US EPA use vertebrates like rats or mice. Thus, these tests are expensive, time-consuming, complex and not least ethically questionable. We have recently developed a protocol which allows the transfer of neurotoxicity screening methods to the invertebrate model organism _C. elegans_[6]. This allows integration of neurological content issues to toxicological screenings. Recently, we investigated the impact of two organohalogens, namely 2,2',6,6'-tetrabromo-4,4'-isopropylidendiphenol (tetrabromobisphenol-A, TBBP-A) and dibromoacetic acid (DBAA), on the lifespan, growth and offspring of _C. elegans_ in natural occurring concentrations [7]. The synthetic xenobiotic, TBBP-A, is used as flame retardant and was found in marine sediments and muscles [8]. It acts as an endocrine disruptor [9]; in particular, due to its structural similarity to thyroxin, also as immunosuppressive [10,11]. Changes in neuronal behavior in mice have also been reported by [PERSON] _et al._[12]. With _C. elegans_, TBBP-A acted in a hormetic way as low concentrations extended lifespan while higher concentration decreased it [7]. Dibromoacetic acid has both sources, artificial and natural ones. It is produced by marine algae, such as _Asparagopsis_ sp. [13], but is also a by-product of freshwater disinfection [14,15]. It is a toxic, carcinogen and also neurotoxic character has been shown [16,17]. More recently, DBAA was found in considerable concentrations in freshwater, for instance in the Berlin waterways [2]. Therefore, it was of particular interest to identify a toxic potential. Interestingly, [PERSON] _et al._[7] demonstrated a stimulating effect of environmental realistic concentrations of DBAA to the lifespan of _C. elegans_. This underlines the importance to refer to environmental realistic concentrations when evaluating the interaction of chemicals with organisms. In this study, we found a stimulating effect for 0.1 \(\upmu\)M TBBP-A and 50 \(\upmu\)MDBAA, while 50 uM TBBP-A had a toxic effect. Furthermore, a microarray analysis revealed that both organobromines modulated different signaling and neurological processes. The aim of this study was to determine if changes in lifespan and growth are caused by differences in neuronal behavior and if microarray findings are also reflected in phenotypic life traits.