Fetal development causes

Successful reproduction (and sex) involves many complex chemical processes that can be disrupted at various points to reduce fertility and conception. Part of this process is under control of the endocrine system, and chemicals that affect the endocrine system are termed endocrine disruptors. In the 1950s, understanding of the endocrine system led to the development of birth control pills as a way to reduce fertility in humans. This is a desirable and planned use of endocrine disruptors. Subsequently, it was discovered that a number of chemicals released into the environment could disrupt the endocrine system and reduce fertility of wildlife. Some are concerned that exposure to these chemicals, such as DDT and dioxin (TCDD), may also affect human fertility (Table 17.1). Approximately 15% of couples of reproductive age are infertile. Endocrine disruptors may also affect fetal development, causing demasculization and feminization of the offspring, which in turn cause reduced fertility in the next generation. 

The induction of damage by influences in embryonic or fetal development, causing malformations or embryonic death, is a problem of the toxicity rather than mutagenicity of the inducing agent (Gebhart et al. 

This material is hazardous through inhalation, skin absorption, penetration through broken skin, ingestion, and produces local skin/eye impacts. It is known to mimic estrogen in the body (hyperestrogenism). In animals, it has caused feminization of male animals and interfered with conception, ovulation, and fetal development in female animals. Specific signs and symptoms of acute high-dose exposure to zearalenone have not been established or have not been published. 

Chromosomal disorders can also be caused by changes in chromosome structure. These changes are caused by the breakage and reunion of chromosome segments when an egg or sperm cell is formed or in early fetal development. Pieces of DNA can be rearranged within one chromosome, or transferred between two or more chromosomes. The effects of structural changes depend on their size and location. Many different structural changes are possible some cause medical problems, while others may have no effect on a person s health. 

Changes in chromosome structure can also cause chromosomal disorders. Some changes in chromosome structure can be inherited, while others occur as random accidents during the formation of reproductive cells or in early fetal development. Because the inheritance of these changes can be complex, people concerned about this type of chromosomal abnormality may want to talk with a genetics professional. 

In animals, chloroform causes some fetal loss and delays in fetal development when administered during gestation at levels of 100ppm or more. Teratogenic effects such as cleft palate were observed in the mouse only at doses associated with maternal toxicity. ... 

In rats, inhalation exposure to 330-1,000 ppm during gestation caused maternal weight loss and clear maternal hepatotoxicity, but no effect on conception, number of implants, or number of resorptions (Schwetz et al. 1974). There were no gross anomalies, although fetal size was somewhat decreased. These data suggest that the fetus is not preferentially sensitive to carbon tetrachloride, and effects of carbon tetrachloride on fetal development and post-natal survival are likely secondary to maternal toxicity. 

Chemicals that cross the placental barrier can act directly on the embryo/fetus, and it is likely that the majority of chemicals that cause developmental toxicity act in this way. Teratogenic chemicals are most likely to act directly on the fetus. Some chemicals cause maternal toxicity at high doses but interfere with embryonic or fetal development at lower doses, and these chemicals are of concern in reproductive toxicology. Many of the most widely recognized embiyotoxic or teratogenic chemicals are selectively active in this manner, and the dose that causes developmental toxicity can be much lower than the dose that is toxic to the mother (Khera, 1984). 

Many chemicals cause a decrease in brain size during fetal development. Changes in brain size can be caused in various ways. A decreased brain weight may be a consequence of general undernutrition caused by effects on placental functioning. Examples of other possible mechanisms are inhibition of cell multiplication or cell growth, increased cell death, disrupted trophic effects induced by changes in cell maturation and neurochemistry. 

Ethylene dichloride has also been reported to cross the placental barrier in rats, accumulate in placental and fetal tissues and to cause abnormal fetal development (ref. 29c). 

Macrolide antibiotics are contraindicated in patients with known hypersensitivity or intolerance to any macrolide. Because clarithromycin can have adverse effects on embryo-fetal development in animals, this drug should be avoided in pregnant women unless no other therapy is appropriate. Concurrent administration of the macrolides and astemizole or terfenadine can cause elected antihistamine levels, resulting in life-threatening cardiac arrhythmias, and should be avoided. 

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