Exposure : Inhalation. Most rapid and direct route of exposure.

Action : Tobacco can have adverse effects on anyone’s health especially on pregnant woman. When a pregnant woman uses these substances, her baby is also exposed to them, for all substances cross the placenta through umbilical cord and enter into the baby’s bloodstream. In this case, tobacco is a teratogen agent that can disturb the development of the embryo or fetus. Teratogens halt the pregnancy or produce a congenital malformation. Other complications that may occur  includes stillbirth, premature delivery and low birth weight. These complications are the result of the fact that nicotine and carbon monoxide in tobacco (cigarette) work together to reduce the baby’s supply of oxygen.  Nicotine chokes off oxygen by narrowing blood vessels throughout your body, including the ones in the umbilical cord. It's a little like forcing the baby to breathe through a narrow straw. To make matters worse, the red blood cells that carry oxygen start to pick up molecules of carbon monoxide instead. 

Agent : Lead

Exposure : Ingestion or inhalation lead acid batteries.

Action: Ingested and inhaled lead toxic will cause neurotoxin to the nervous system.Lead chemical will accumulate in cell tissues or bone of nervous system.Excessive exposure will cause blood disorder disease or brain cancer.

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Teratogen

Agent : Cocaine & Nicotine

Exposure : Inhalation by pregnant mother

Action : 

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Agent: Heparin 

Exposure: Heparin is given parenterally because it is not absorbed from the gut, due to its high negative charge and large size. It can be injected intravenously or subcutaneously (under the skin); intramuscular injections (into muscle) are avoided because of the potential for forming hematomas

Action: The mechanism by which such high affinity heparin acts when antithrombin III is the inhibitor is promotion of the formation of an intermediate proteinase-heparin-antithrombin complex. Heparin promotion of thrombin inactivation by heparin cofactor II may occur by a similar mechanism. The requirement for a specific oligosaccharide sequence within the heparin molecule does not, however, exist for heparin cofactor II. Binding of heparin to both thrombin and antithrombin III interferes with thrombin inactivation. This binding is very dependent on the ionic strength of the reaction mixture. Low ionic strength in in vitro reactions also results in cleavage of antithrombin III by thrombin in the presence of heparin and effectively converts antithrombin III from an inhibitor to a substrate.

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Neurotoxin

1. Agent : Ammonia

2. Exposure :  Ammonia toxicity is often seen through two routes of administration, either through consumption or through endogenous ailments such as liver failure.

3. Action : cause response to cirrhosis of the liver which results in hepatic encephalopathy, and can result in cerebral edema . This cerebral edema can be the result of nervous cell remodeling. As a consequence of increased concentrations, ammonia activity in-vivo has been shown to induce swelling of astrocytes in the brain through increased production of cGMP (Cyclic Guanosine Monophosphate) within the cells which leads to Protein Kinase G-mediated(PKG) cytoskeletal modifications. The resultant effect of this toxicity can be reduced brain energy metabolism and function. Importantly, the toxic effects of ammonia on astrocyte remodling can be reduced through administration of L-carnitine. This astrocyte remodeling appears to be mediated through ammonia-induced mitochondrial permeability transition. This mitochondrial transition is a direct result of glutamine activity a compound which forms from ammonia in-vivo. Administration of antioxidants or glutaminase inhibitor can reduce this mitochondrial transition, and potentially also astrocyte remodeling.