What are the known causes of Teratogens?

The Cause No 1:Unavodable factors:- .

For instance : Drugs for epilepsy, different preexisting  infection, asthma, chronic cardiovascular disor­der antihypertensive, Aantidiabetics, anticoagulants etc ). Many of these exposures are not readily avoidable, as pregnancy is often not planned or recognized for an extended period after conception, or because there is a continuing need for maternal treatment for health conditions (e.g. epilepsy, infection, asthma, chronic cardiovascular disor­ders).

Exposure to various agents in the home or workplace, Fear of loss of job: A compromise !!! or as a conse­quence of maternal lifestyles and self-medication, is almost universal, and pre-conception planning only rarely provides an opportunity to identify exposures of concern. As a consequence, questions about the significance of such an exposure, whether stated or not, are often a source of concern to pregnant women or their care provider.

What are other developmental toxicants ?? Not all yield t in permanent adverse out­comes for the fetus or newborn. Some agents may have at least partially reversible or transient effects if recognized early, such as fetal growth restriction from tobacco smoking. It is important to recognize that struc­tural birth defects resulting from exposure to human teratogens are not the only manifestations of exposure to developmental toxicants. Fetal or postnatal growth disorders, functional developmental disorders including cognitive and behavioral deficits, abnormalities of placental function putting the fetus at increased risk, and death (embryonic, fetal, perinatal or postnatal) are all among potential manifestations of expo­

sures. Furthermore, some adverse outcomes may not become apparent until many years later (e.g. reproductive consequences and cancer from exposure to diethylstilbestrol).

Pathogenetic factors in evaluation of risk

from exposure to teratogens and other

developmental toxicants

When evaluating the likely significance of exposure to potentially hazardous agents, it is essential to consider the following issues in the context of the known or likely pathogenetic mechanisms for adverse fetal outcomes.

Dose and duration of exposure

In general, the larger the dose, the more likely an effect, and the more likely the effect will be significant.

Likewise, the longer the duration of exposure, the greater the chance that susceptible periods of organogenesis and development will be encountered.

Timing

Timing of exposure is critical: certain organ systems may have a limited period of susceptibility for damage.

Although it is commonly thought that damage can only result during the period of organogenesis, i.e. during the first trimester, this is not correct. Some organ systems (e.g. the brain) undergo developmental processes later in pregnancy and can be damaged throughout the prenatal period.

Pathogenetic mechanism(s)

Teratogens and developmental toxicants produce their adverse effect by specific mechanisms. As these mechanisms are often important in mul­tiple tissues and organs, it is not surprising that several specific types of damage may result.

Those agents that affect basic morphogenetic processes commonly are related to first trimester exposures. However, those agents which act through mechanical pressures are likely to have the greatest impact during the third trimester, and those agents that produce necrosis through inflammation and/or hemorrhage can potentially destroy nor­mally developing structures throughout pregnancy.

Host susceptibility

Variability in the genetic factors related to metabolism of drugs and chemicals may result in differential susceptibility of the host. These pharmacogenetic factors must be expressed at a relevant time in the tissue or organ system affected.

There are two potentially relevant 'hosts' to be considered. Mother and embro/fetus only share 50% of the genome. Thus, depending on the pathogenesis of the adverse outcome, maternal or fetal (or perhaps both) genotype may be more important.