Camelina can be considered a valuable crop for bio-based products and biofuels, but, to date, there are still many uninvestigated aspects concerning the optimization of its agricultural management and its environmental impact. Consequently, a low-input camelina cultivation has been realized, in northern Italy environment, through a 4-year camelina-wheat rotation in open field. In these conditions, camelina was grown as winter crop. Camelina reached, over the years, a variable (CV=28%) mean seed yield of 0.82 Mg ha-1. This notwithstanding, the oil content - 39.17% (CV=3%) - and its related quality were rather stable, reaching an oil yield of 320 kg ha-1 particularly rich in omega-3 fatty acid. The low input cultivation system here adopted implied an energy ratio (output energy/input energy) of 4 and a 30% decrease in Global Warming Potential per hectare, compared to the standard value reported by the European Renewable Energy Directive for sunflower, reducing, at the same time, other relevant environmental burdens. However, due to its relatively low oil production, the full use of all camelina co-products should be considered in order to fulfill the sustainability requirements for European jet fuel production. In fact, stability of yields and quality of oil, oilcake and straws makes low-input camelina eligible for many other novel green chemistry applications.

Neonicotinoids are effective insecticides with specificity for invertebrate nicotinic acetylcholine receptors. Neonicotinoids are chemically stable and tend to remain in the environment for long so concerns about their neurotoxicity in humans do nothing but increase. Herein, we evaluated the chronic toxic effects of acetamiprid- and imidacloprid-based insecticides over the differentiation of human neuroblastoma SH-SY5Y cells, which were exposed to these insecticides at a concentration range similar to that applied to crop fields (0.01–0.5 mM). Both insecticides did not have acute cytotoxic effects in both non-differentiated and in staurosporine-differentiated SH-SY5Y cells cytotoxicity as measured by the MTT and vital-dye exclusion tests. However, after a chronic (7-day) treatment, only imidacloprid dose-dependently decreased the viability of SH-SY5Y cells (F(4,39) = 43.05, P < 0.001), largely when administered-during cell differentiation (F(4,39) = 51.86, P < 0.001). A well-defined dose-response curve was constructed for imidacloprid on day 4 (R² = 0.945, EC₅₀ = 0.14 mM). During differentiation, either imidacloprid or acetamiprid dose-dependently caused neurite branch retraction on day 3, likely because of oxidative stress, to the extent that cells turned into spheres without neurites after 7-day treatment. Despite their apparent safety, the neurodevelopmental vulnerability of SH-SY5Y neurons to the chronic exposure to imidacloprid and to a lesser extent to acetamiprid points to a neurotoxic risk for humans.

Several studies suggest that Iron Oxide nanoparticles may arrive to central nervous system independently of the route of administration. Actually, evidences indicate that the presence iron oxide nanoparticles into nervous system are linked to several neurodegenerative diseases. In this regard, our goal was to assess in vitro PolyVinylPirrolidone coated Iron Oxide nanoparticles, diameter of 20 nm, neuro-toxicity and their mechanism of action, which was fixed over the human neuronal cell line SH-SY5Y. Inducted biological effects were evaluated after 4–48 hours at crescents doses 1–100 μg/mL using the following endpoints: (i) Membrane integrity: Nanoparticles have produced no effect over cellular membrane for every dose and time evaluated; (ii) Mitochondrial activity: Starting at 10 μg/mL with a decrease of cellular vitality of 35%, and a maximum decrease of 45% at highest dose (100 μg/mL); (iii) Cellular morphology: Cells have evidenced no alteration after 48 hours of exposure; (iv) Cellular uptake: Dose-time dependent accumulation has observed: blue spots have been found at 10 μg/mL and over. Concluding, mitochondria are apparently the target: considering that the toxic effect produced by PolyVinylPirrolidone coated Iron Oxide nanoparticles after 48 hours of exposure in a dose-time dependent manner was evident.