• Anti allergic
• Anti bacterial
• Anti histaminic
• Anti inflammatory
• Anti pyretic
• Anti septic
• Anti spasmodic
• Anti ulcer
• Hepatoregenerative
• Pesticide

• Metabolism: PAH metabolism occurs in all tissues, usually by cytochrome P-450 and its associated enzymes. PAHs are metabolized into reactive intermediates, which include epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations. The phenols, quinones, and dihydrodiols can all be conjugated to glucuronides and sulfate esters; the quinones also form glutathione conjugates. (L10)
• Uses/Sources: PAHs are released into the environment via the combustion of fossil fuels, coke oven emissions and vehicle exhausts, as well as naturally from forest fires and vocanic eruptions. PAHs from these sources may contaminate nearly water systems. They are also found in coal tar and charbroiled food. (L10)
• Health Effects: PAHs are carcinogens and have been associated with the increased risk of skin, respiratory tract, bladder, stomach, and kidney cancers. They may also cause reproductive effects and depress the immune system. (L10)
• Symptoms: Acute exposure to PAHs causes irritation and inflammation of the skin and lung tissue. (A10)
• Treatment: There is no know antidote for PAHs. Exposure is usually handled with symptomatic treatment. (L10)
• Route of Exposure: Oral (L10) ; inhalation (L10)

• Carcinogenicity: Not listed by IARC.
• Toxicity: LD50: >4000 mg/kg (Oral, Rat) (L912) LD50: 180 mg/kg (Intraperitoneal, Rat) (L912) LD50: 520 mg/kg (Subcutaneous, Rat) (L912)

The ability of PAH's to bind to blood proteins such as albumin allows them to be transported throughout the body. Many PAH's induce the expression of cytochrome P450 enzymes, especially CYP1A1, CYP1A2, and CYP1B1, by binding to the aryl hydrocarbon receptor or glycine N-methyltransferase protein. These enzymes metabolize PAH's into their toxic intermediates. The reactive metabolites of PAHs (epoxide intermediates, dihydrodiols, phenols, quinones, and their various combinations) covalently bind to DNA and other cellular macromolecules, initiating mutagenesis and carcinogenesis. (L10, L23, A27, A32)