Low weight at birth is a common adverse developmental effect reported in human populations and animal toxicity studies.
Maternal infection is a cause of adverse developmental outcomes including embryonic resorption, intrauterine fetal death, and preterm labor.
Less severe food insecurity is associated with reduced quality and variety of dietary intakes [ 3, 4], possibly associated with obesity in adults [ 5], and a range of adverse developmental, psychological and health outcomes in children[ 6].
3 5 Toddlers with problem behaviours are at risk for a variety of adverse developmental outcomes including conflictual relationships with other peers or family, poor academic performance, delinquency and later maladjustment.
Second, the associated risk factors may present an additional risk of adverse developmental outcomes in the offspring of depressed mothers.
For other microbes that cause microcephaly (such as cytomegalovirus or rubella), infection occurring in the first half of the pregnancy (before 20 weeks) is usually associated with a higher likelihood of adverse developmental outcomes, not one very late like Tdap.
In utero exposure to PFCs is associated with a range of nonspecific adverse developmental outcomes in mouse, rat, and rabbit models (Lau et al. 2007; Olsen et al. 2009), including reduced fetal weight and increased neonatal mortality.
There is a concern about the potential adverse developmental and reproductive effects of PFCs due to their persistence in the environment and long serum elimination half-lives (i.e. 3.8, 5.4 and 8.5 years for PFOA, PFOS and PFHxS, respectively) (Olsen et al., 2007).
However, an important question in human studies remains whether prenatal substance use exposure has an aetiological role in pathways to adverse developmental and behavioural outcomes via teratological effects.
It was concluded that it was not possible from currently available data to determine whether there is an association between prenatal MeHg exposure and adverse developmental effects in children.
