## 3 Results and Discussion
### Cd Exposure Schemes
#### 3.2.3 Cd Exposure of Dams during Pregnancy-Lactation Period  
From 52 records included in this review, 37 described Cd exposure during pregnancy and lactation. The research articles published from 1979 to 2022 mostly report experiments in rats (29/37) than in mice (8/37).Experimental data and results summarized in Table 3 show differences in experimental features. Nevertheless, some reports mentioned identical strain, concentration/dose, exposure time, etc. Thus, they were grouped within the Table 3. Cd in drinking water was the most mentioned route of administration (23/37), followed by intragastric via (11/37), and Cd administered in food (3/37). Some authors such as [PERSON] et al. [29], [PERSON] et al. [30; 31], [PERSON] and [PERSON] [32], [PERSON] et al. [33], and [PERSON] et al. [34] reported Cd concentration in drinking water and mentioned the Cd doses estimated from daily water consumption, while [PERSON] et al. [1], [PERSON] et al. [35], [PERSON] et al. [36], [PERSON] and [PERSON] [37], and [PERSON] et al. [38] described Cd concentration in drinking water and daily water consumption but they do not mentioned the estimated dose. In this case, we calculated the Cd dose by multiplying the water consumption by the Cd concentration. On the other hand, authors such as [PERSON] et al. [39], [PERSON] et al. [14], [PERSON] et al. [40], [PERSON] et al. [41], [PERSON] et al. [42], [PERSON] et al. [43], [PERSON] et al. [44], [PERSON] et al. [45], [PERSON] et al. [46], [PERSON] and [PERSON] [47], and [PERSON] et al. [48] only reported the concentration of Cd in drinking water without estimating either dose or water consumption. The highest Cd concentration described was 100 mg/L from GD 0 to PND 21 [39] and the lowest was 0.15 \(\mu\)g/L from GD 0 to PND 11 [48] both administered in drinking water, whereas the highest dose was 68 mg Cd/kg b.w. and the lowest 1.089 ug Cd/kg b.w. both estimated from water consumption. Although, pregnancy-lactation scheme consists of administering Cd during both periods (Figure 2c), Table 3 indicates that exposure times were different. From 37 papers included in this scheme 18 reported a Cd exposure from GD 0 to PND 21, four articles mention exposed dams from GD 0 to PND 11 or 1-5 days before, seven papers described the onset of Cd exposure several DBM ending at PND 21, five begin DBM and end on PND 15, 28 or 35, and three papers reported a varied exposure time. Cross-fostering was reported by two authors, [PERSON] et al. [41] and [PERSON] et al. [43], but describing different experimental features. While [PERSON] et al. administered 50 mg Cd/L to rat dams in drinking water from 28 DBM to PND 21, [PERSON] et al. exposed mouse dams to 10 mg Cd/L from GD 0 to PND21. Effects of Cd exposure during Pregnancy-Lactation Period. Whereas Cd exposure schedules during pregnancy and lactation induce separately effects on offspring related to Cd transfer gestationally and by breast milk respectively, pregnancy-lactation scheme combines both exposures generating effects related to perinatal exposure. Probably, this scheme simulates perinatal Cd exposure in humans more closely since pregnant women can be exposed before and after pregnancy and considering that Cd presents a half-life of 17-30 years in human body [49]. The effects evaluated in pregnancy-lactation scheme includes neurotoxicity, changes in sexual maturation, alterations in biochemical parameters, and Cd transfer and retention. From 37 papers included in this exposure-scheme 15 studied neurological Cd-effects, 13 were related to changes in sexual maturation, 5 reported biochemical effects and 4 evaluated Cd transfer or retention. Analyses of brain tissue and/or behavioral tests conducted on offspring demonstrate that Cd exposure during pregnancy-lactation period altered chemical and enzyme activities in the brains of the offspring.