Effects of malathion and carbendazim on Amazonian freshwater organisms: comparison of tropical and temperate species sensitivity distributions

The risk assessment of pesticides for freshwater ecosystems in the Amazon has relied on the use of toxicity data and water quality criteria derived for temperate regions due to a lack of ecotoxicological studies performed with indigenous species. This leaves an unknown margin of uncertainty for the protection of Amazonian ecosystems, as differences in environmental conditions and species sensitivity are not taken into account. To address this issue, the acute toxic effects of malathion (an organophosphorus insecticide) and carbendazim (a benzimidazole fungicide) were assessed on five fish and five freshwater invertebrates endemic to the Amazonian region. Subsequently, the intrinsic sensitivity of Amazonian and temperate freshwater species was compared using the species sensitivity distribution (SSD) concept. Amazonian species sensitivity to malathion was found to be similar to that of their temperate counterparts, with LC50 values ranging between 111 and 1507 μg/l for fish species and 2.1–426 μg/l for arthropod species. However, Amazonian fish appeared to be slightly less sensitive for carbendazim than temperate fish with LC50 values ranging between 1648 and 4238 μg/l, and Amazonian invertebrates were found to be significantly more resistant than their temperate counterparts, with LC50 values higher than 16000 μg/l. The results of this study suggest that for these compounds, the use of water quality criteria derived with laboratory toxicity data for temperate species will result in a sufficient protection level for Amazonian freshwater organisms. Recommendations for further research include the validation of threshold concentrations derived with temperate standard test species and with the SSD model with semi-field experiments considering larger assemblages of indigenous species under local environmental conditions

Pathogenesis of adolescent idiopathic scoliosis in girls - a double neuro-osseous theory involving disharmony between two nervous systems, somatic and autonomic expressed in the spine and trunk: possible dependency on sympathetic nervous system and hormones with implications for medical therapy

Anthropometric data from three groups of adolescent girls - preoperative adolescent idiopathic scoliosis (AIS), screened for scoliosis and normals were analysed by comparing skeletal data between higher and lower body mass index subsets. Unexpected findings for each of skeletal maturation, asymmetries and overgrowth are not explained by prevailing theories of AIS pathogenesis. A speculative pathogenetic theory for girls is formulated after surveying evidence including: (1) the thoracospinal concept for right thoracic AIS in girls; (2) the new neuroskeletal biology relating the sympathetic nervous system to bone formation/resorption and bone growth; (3) white adipose tissue storing triglycerides and the adiposity hormone leptin which functions as satiety hormone and sentinel of energy balance to the hypothalamus for long-term adiposity; and (4) central leptin resistance in obesity and possibly in healthy females. The new theory states that AIS in girls results from developmental disharmony expressed in spine and trunk between autonomic and somatic nervous systems. The autonomic component of this double neuro-osseous theory for AIS pathogenesis in girls involves selectively increased sensitivity of the hypothalamus to circulating leptin (genetically-determined up-regulation possibly involving inhibitory or sensitizing intracellular molecules, such as SOC3, PTP-1B and SH2B1 respectively), with asymmetry as an adverse response (hormesis); this asymmetry is routed bilaterally via the sympathetic nervous system to the growing axial skeleton where it may initiate the scoliosis deformity (leptin-hypothalamic-sympathetic nervous system concept = LHS concept). In some younger preoperative AIS girls, the hypothalamic up-regulation to circulating leptin also involves the somatotropic (growth hormone/IGF) axis which exaggerates the sympathetically-induced asymmetric skeletal effects and contributes to curve progression, a concept with therapeutic implications. In the somatic nervous system, dysfunction of a postural mechanism involving the CNS body schema fails to control, or may induce, the spinal deformity of AIS in girls (escalator concept). Biomechanical factors affecting ribs and/or vertebrae and spinal cord during growth may localize AIS to the thoracic spine and contribute to sagittal spinal shape alterations. The developmental disharmony in spine and trunk is compounded by any osteopenia, biomechanical spinal growth modulation, disc degeneration and platelet calmodulin dysfunction. Methods for testing the theory are outlined. Implications are discussed for neuroendocrine dysfunctions, osteopontin, sympathoactivation, medical therapy, Rett and Prader-Willi syndromes, infantile idiopathic scoliosis, and human evolution. AIS pathogenesis in girls is predicated on two putative normal mechanisms involved in trunk growth, each acquired in evolution and unique to humans