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Abstract
In this study, fruit flies (Drosophila melanogaster) were exposed to an estimated daily human E171 consumption concentration for 20 generations. Exposure to E171 resulted in: a change in normal developmental and reproductive dynamics, reduced fecundity after repetitive breeding, increased genotoxicity, the appearance of aberrant phenotypes and morphologic changes to the adult fat body. Marks of adaptive evolution and directional selection were also exhibited. The larval stages were at a higher risk of sustaining damage from E171 as they had a slower elimination rate of TiO2 compared to the adults. This is particularly worrisome, since among the human population, children tend to consume higher daily concentrations of E171 than do adults. The genotoxic effect of E171 was statistically higher in each subsequent generation compared to the previous one. Aberrant phenotypes were likely caused by developmental defects induced by E171, and were not mutations, since the phenotypic features were not transferred to any progeny even after 5 generations of consecutive crossbreeding. Therefore, exposure to E171 during the early developmental period carries a higher risk of toxicity. The fact that the daily human consumption concentration of E171 interferes with and influences fruit fly physiological, ontogenetic, genotoxic, and adaptive processes certainly raises safety concerns.
Highlights
Since 1916, more than 200,000,000 metric tons of titanium dioxide (TiO2) have been produced worldwide, of which a significant amount is used as an inactive human food ingredient, E1711
Virgin E171 females had higher fecundity, usually during the first few matings, followed by a sharp decline in fecundity after 3–5 days of consecutive mating when compared to the control (RANOVA; time * treatment interaction, p < 0.001 for each generation) (Fig. 2)
If adaptation to E171 toxicity is geared toward shorter developmental time (DT) and faster growth through the generations, loss of fecundity in later generations is in agreement with the trade-off that more available energy would be allocated toward fast development/growth and less toward late reproduction[24]
Summary
Since 1916, more than 200,000,000 metric tons of titanium dioxide (TiO2) have been produced worldwide, of which a significant amount is used as an inactive human food ingredient, E1711. We showed that dietary exposure of D. melanogaster to E171 leads to a significant increase in pupation time, down-regulation of the genes involved in oxidative stress, and occasional aberrant phenotypes[17]. This was a preliminary study in which only the larvae of a single generation were fed with various concentrations of E171 in order to www.nature.com/scientificreports/. The aim of the present research is to assess the dietary exposure of 20 subsequent generations of D. melanogaster (through its entire life cycle of larvae and adults) to an estimated daily human consumption concentration of E171 TiO2. The effects of E171 on fecundity, egg to adult viability, developmental time, genotoxicity, morphology, frequency of phenotype aberrations, and breeding dynamics were monitored
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