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EC number: 238-405-1
CAS number: 14433-76-2
Table 29Thyroxine (T4) Concentrations (ng/mL)
Group 1(0 ppm)
Group 2(1000/500 ppm)
Group 3(4000/2000 ppm)
Group 4(12,500/6250 ppm)
F0 Generation – Males
F1 Unselected – Males (PND 22-24)
F1 Surplus – Females (PND 21-24)
Cohort 1A – Males
Cohort 1A – Female
F2 Generation – Males (PND 22)
Table 30Summary Group Mean Organ Weight Data – Scheduled Euthanasia F0 Males
Nominal Dietary Concentration (ppm)
No. animals per group
Absolute value (g)
% of body weight
% of brain weight
Anova & Dunnett: * = p ≤ 0.05; ** = p ≤ 0.01
Table 33Summary Test Item-related Microscopic Findings – Scheduled Euthanasia F0 Males
No. animals examined
Gland, Thyroid (No. Examined)
Hypertrophy, follicular cell, minimal
Table 31Summary Group Mean Organ Weight Data – Scheduled Euthanasia F1 Cohort 1A
Table 32Summary Group Mean Organ Weight Data – Scheduled Euthanasia F1 Cohort 1B
The objective of this study was to determine the potential toxicity of N, N‑Dimethyldecan‑1‑amide, when given by oral dietary administration to rats to assess the reproductive function in adult animals and their offspring according to OECD 443 (BASF SE 2021). This study was designed to provide an evaluation of the pre and postnatal effects of chemicals on development as well as a thorough evaluation of systemic toxicity in pregnant females, lactating females, young and adult offspring. Detailed examination of key developmental endpoints, such as offspring viability, neonatal health, developmental status at birth, and physical and functional development until adulthood, was expected to identify specific target organs in the offspring. In addition, the study provided information about the effects of the test item on the integrity and performance of the adult male and female reproductive systems.
The study design was as follows:
Text Table 1Experimental Design – F0 Animals
Formulated Dietary Concentration (ppm)a
Number of Animals
a Correction factor of 1.02 applied.b During the lactation phase, as the maternal food consumption increased, the dietary concentration for females only was lowered by 50%.
Text Table 2Experimental Design – F1 Animals Cohort 1A Post-weaning
a Correction factor of 1.02 applied.
Text Table 3Experimental Design – F1 Animals Cohort 1B Post-weaning (Reproductive)
b During the lactation phase, as the maternal food consumption increased, the dietary concentration for females only was lowered by 50%.
The following parameters and end points were evaluated in this study: clinical observations, body weights, food consumption, estrous cycles, estimated achieved doses, mating performance and fertility indices (F0 and Cohort 1B), duration of gestation and overall litter performance (F0 and Cohort 1B), F1 and F2 survival indices, litter and pup weights, pre- weaning physical development of F1 and F2 pups, assessments of sexual maturation of F1 animals (Cohorts 1A and 1B), clinical pathology parameters (haematology, coagulation, clinical chemistry and urinalysis [F0 and Cohort 1A]), thyroid stimulation hormone (TSH) and thyroxine (T4) analysis, gross necropsy findings, organ weights, immunophenotyping analysis (Cohort 1A), sperm evaluation (F0 and Cohort 1A males), ovarian follicle counts (Cohort 1A) and histopathological examinations.
Administration of the test item via the diet at 12,500/6250 ppm was associated with toxicity as evidenced by lower food consumption in males and females at 12,500/6250 ppm and in female animals only at 4000/2000 ppm. Effects on development were observed with a lower in body weight gain during lactation at the high dose group (6250 ppm). In the high dose (12,500/6250 ppm) there was also evidence of a delayed sexual maturation in the F1 generation pups (Cohort 1A and Cohort 1B pups) average time to vaginal opening was 38.5 days compared to 32.3 days (Cohort 1A) and 37.7 days compared with 33.4 days (Cohort 1B). This delay is considered to be a consequence of delayed body weight development. The body weights at the time of sexual maturity were within the historical control range. The delay in vaginal opening did not adversely affect the time to the first estrous. Due to the delay in sexual maturation, mating of Cohort 1B animals and production of an F2 generation was triggered. This evaluation demonstrated that despite the delay in sexual maturation, there were no adverse changes on the fertility and maternal performance of the Cohort 1B animals, nor was the viability and survival of the F2 generation affected.
Adaptive changes in the form of follicular cell hypertrophy, were observed in the thyroids of rats following administration of the test item in the diet.
In conclusion, administration of N,N-Dimethyldecan-1-amide by diet was tolerated in male and female rats at doses up to 12,500/6250 ppm. Toxicity was manifest through lower food consumption and lower body weight gains, including in the offspring of rats administered N,N‑Dimethyldecan-1-amide at 12,500/6250 ppm as well as delays in sexual maturation in female offspring as the consequence of lower body weights. However these delays in sexual maturation did not go on to affect the fertility or maternal performance of the animals.
The administration of N, N-dimethyldecan-1-amide was associated with effects on the thyroid gland of F0 Generation males only at 12,500 ppm, which was not considered to be adaptive and not adverse based on the minimal grade of severity and incidence.
Based on the results of this extended one generation reproductive toxicity study (Cohort 1), the following no-observed-adverse-effect level (NOAEL) of N,N-Dimethyldecan-1-amide were established:
Parental toxicity (F0 and F1): 12,500/6250 ppmReproductive NOAEL (F0 and F1): 12,500/6250 ppmPost-Natal Developmental NOAEL: 4000/2000 ppm.
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