In utero

Environmental exposures to PCBs are significantly lower than those reported in the workplace and are therefore unlikely to cause adverse human health effects in adults. However, it is apparent from the results of several recent studies on children that there was a correlation between in utero exposure to PCBs, eg, cord blood levels, and developmental deficits (65—68) including reduced bkth weight, neonatal behavior anomaUes, and poorer recognition memories. At four years of age, there was stiU a correlation between prenatal PCB exposure levels and short-term memory function (verbal and quantitative). In these studies the children were all exposed to relatively low environmental levels of PCBs. Although these effects may be related to other contaminants, it is clear that this is an area of concern regarding the potential adverse human health impacts of PCBs. 

It is known that the brain is one of the most sensitive sites of action of steroids in utero, and recently there have been suggestions that EDs may affect normal brain development and behaviour. For example, it has been alleged that in utero exposure to polychlorinated biphenyl compounds (PCBs) resulted in adverse effects on neurologic and intellectual function (memory and attention) in young children born to women who had eaten PCB contaminated fish in the USA." It has also been speculated that exposure to environmental pollutants with steroidal activity may be infinencing human sexual development and sexually controlled behavioiir." ... 

B2 knockout embryos subjected to salt stress in utero show suppressed renin expression and an abnormal kidney phenotype and develop early postnatal hypertension. Consistently, although basal bradykinin formation is defective tissue kallikrein-null mice have normal blood pressure however suffer from cardiovascular abnormalities. However suggesting a function of kinin signaling during development. 

Gupta RC, Rech RH, Lovell KL, et al. 1985. Brain cholinergic, behavioral, and morphological development in rats exposed in utero to methyl parathion. Toxicol Appl Pharmacol 77 405-413. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to a chemical the distinguishing feature between the two terms is the stage of development during which the insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero death. 

NoUer, K.L., Blair, P.B., and Obrien, PC. et al. (1988). Increased occurrence of autoimmune-disease among women exposed in utero to diethylstilbestrol. Fertility and Sterility 49, 1080-1082. 

Lantz RC, Petrick JS, Hays AM. Altered protein expression following in utero exposure to arsenic. Society of Toxicology, 2005. 

Dlagnosable In utero (some) Dlagnosable In utero Fetal sex can be determined... 

Nadler, H. L. and Messina, A. M. "In-Utero Detection of Type-II Glycogenosis (Pompe s Disease). Lancet, (1969),... 

A more recent study at Woburn was conducted by the Massachusetts Department of Health. Investigators found that the risk of leukemia in the group exposed to TCE in utero was about 8 times higher than that found in the unexposed group (MDPH 1996). It was concluded that these results were consistently in the direction of an association and support the hypothesis that childhood leukemia in this population may be... 

Endogenous estrogens are known to be active in a number of areas of the brain. There are indications that estrogens may play a role in mood, locomotor activity, pain sensitivity, vulnerability to neurodegenerative diseases and cognition (McEwan, 1999). In humans, the blood brain barrier is not fiilly developed at birth and, for this reason, the central nervous system (CNS) may be more sensitive to phytoestrogens in utero or at birth. As ERs are expressed in the CNS, phytoestrogens may also be active in this area. 

In mart, an overlooked feature is the occurrence of mucoid-like plugs in the foetal nostrils (Schaeffer, 1910). The presence of this blockage can be confirmed by endoscopic inspection in utero these plugs seem likely to affect free amniotic flow, since they appear to be reinforced by a folded membranous gathering at the nasal vestibule (PI. 4B). A degree of restriction of fluid access to the VN aperture, which is immediately caudal to the nostril aperture, and is patent in foetal life, may be a protective feature (Jordan, 1972). The timing of the dissolution of these sealant devices prior to parturition is regrettably not known. 

Coppola D.M. and O Connell R.J. (1989). Stimulus access to olfactory and vomeronasal receptors in utero. Neuroscience Lett 106, 241-248. 

What are the effects on the developing nervous system after chronic in utero exposure Neurophysiological, neurophar-macol ogical, and neuroanatomi cal studies should be useful. 

With the increased use of PCP by young women, pediatricians have begun to identify the newborn s neurobehavioral symptoms after In utero exposure. In 1980, Golden et al. were the first to document the placental transfer of PCP in humans and to describe the resulting neurobehavioral symptoms. They reported on one infant whose mother had smoked an average of six joints per day of marijuana dusted with PCP. The behaviors emerging shortly after birth... 

Methyldopa Preferred first-line therapy on the basis of long-term follow-up studies supporting safety after exposure in utero. Surveillance data do not support an association between drug and congenital defects when the mother took the drug early in the first trimester. 

Genetic factors cannot explain the recent rapid rise in asthma prevalence. Asthma appears to require both genetic predisposition and environmental exposure. Many patients with occupational asthma develop the disease late in life upon exposure to specific allergens in the workplace. Environmental influences in utero or in infancy may contribute to the development of asthma. Maternal smoking during pregnancy or exposure to secondhand smoke after birth increases the risk of childhood asthma.3 Adult-onset asthma is not uncommon and may be related to atopy, nasal polyps, aspirin sensitivity, occupational exposure, or a recurrence of childhood asthma. 

Diagnosis of CF is based on two separate elevated sweat chloride concentrations of greater than or equal to 60 mEq/L (or mmol/L) obtained through pilocarpine iontophoresis (referred to as the sweat test ). Genetic testing (CFTR mutation analysis) may be performed to confirm the diagnosis, screen in utero, or detect carrier status. More than 70% of diagnoses are made by 12 months of age and almost all are made by age 12. 

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