## 1 Introduction
Exposure may derive from four major routes, namely, ingestion (mainly with respect to PAE plasticizing; sources can be food contamination during the preparation or packaging process, drugs and nutritional preparations, baby toys), inhalation (mainly DEP and DEHP, although they show low volatility; they can originate from medical devices, e.g., bags or pipes, or be present in indoor dust, e.g., furniture, clothes, building materials, plastic components), intravenous (from medical PVC devices transporting intravenous fluids, nutritional formulas, blood; DEHP migration varies according to some parameters such as lipid content, temperature, and duration time), and dermal (mainly DEP;contamination through clothes, footwear, gloves, cosmetics, sunscreen, insecticides, hygiene products, paints, toys) [19; 20; 21; 22; 23; 24]. Phthalates have a low acute toxicity, with an LD\({}_{50}\) between 1 and 30 g of body weight [25; 26]. It should be noted that the exposure risk decreases with individual age [22]. PAEs do not show mutagenic and/or genotoxic activity [27], although a recent study shows potentially surprising mutagenic activity by DEHP [28], whereas the carcinogenic aspect is more complex [29]. DEP activity is questionable, there are no carcinogenicity data available for DiNP, DBP appears to be associated with tumor promotion activity, and DEHP exposure produces hepatocellular carcinoma in rodents along with a variety of other hepatocellular effects [30]. In addition, the European Food Safety Authority (EFSA) has established the maximum daily limit of human intake for some PAEs (DBP 0.01, BBP 0.5, DEHP 0.05, DNP 0.15, DDP 0.15 mg kg\({}^{-1}\) per day per body weight) [31]. The International Agency for Research on Cancer (IARC) has recently evaluated DEHP and modified its classification from \"possibly carcinogenic to humans (Group 2B)\" to \"not classifiable as to its carcinogenicity to humans (Group 3)\". The PAE residues in food and beverages are internationally regulated; in many countries, phthalates are banned as food substances. On the other hand, BPA, belonging to the group of diphenylmethane and bisphenol derivatives, is a pseudo-persistent chemical and, despite its short duration, is omnipresent in the environment due to its release [32]. The presence of hydroxyl groups results in good reactivity. Similar to other phenols, BPA can be converted into ethers, esters, and salts, showing good solubility in fats but less in water. The presence of BPA in the natural environment is linked exclusively to activities of anthropic origin; it is a starting material for the synthesis of plastics [33]. The release can take place during the production, transport, or processing phases. BPA has acute toxicity towards vertebrates. The LD\({}_{50}\) values in rats are 3250 mg kg\({}^{-1}\) body weight for oral intake, 841 mg kg\({}^{-1}\) intraperitoneal. and 35.26 mg kg\({}^{-1}\) intravenously [34]. Since 1988, the U.S. Environmental Protection Agency (US EPA) has estimated a reference dose for oral ingestion of 50 \(\mu\)g kg\({}^{-1}\) body weight [35], whereas the European Food Safety Authority (EFSA) recently set the tolerable daily intake (TDI) at 4 \(\mu\)g kg\({}^{-1}\) body weight (i.e., twelve and a half times lower than the previous level) [18] and a new revision is planned for 2020. In recent years. the study on BPA's toxic, teratogenic, carcinogenic, and estrogenic effects has considerably intensified, also considering its widespread use. BPA is a xenoestrogen, a compound that disturbs the functions of the endocrine system [36; 37; 38; 39]. A recent study by [PERSON] et al. (2013) [40] suggested that BPA taken from mice in does comparable to those taken by humans behaves like a carcinogen for the mammary gland. Finally, numerous investigations have shown that BPA, by exerting an action on the endocrine system, can contribute to the development of obesity [41; 42].