The article contains sections titled: 1. Phthalic Acid 2. Phthalic Anhydride 2.1. Physical Properties 2.2. Chemical Properties 2.3. Resources and Raw Materials 2.4. Production 2.4.1. Gas‐Phase Oxidation 2.4.1.1. Catalyst and Reaction Mechanism 2.4.1.2. Apparatus and Important Process Steps in the Gas‐Phase Oxidation of o ‐Xylene 2.4.2. Fluidized‐Bed Oxidation 2.4.3. Liquid‐Phase Oxidation of o ‐Xylene 2.5. Environmental Protection 2.6. Quality Specifications and Analysis 2.7. Economic Aspects 2.8. Storage and Transportation 2.9. Uses 3. Phthalimide 3.1. Properties 3.2. Production 3.2.1. Production from Phthalic Anhydride and Ammonia 3.2.2. Production from Phthalic Anhydride and Urea 3.2.3. Production from o ‐Xylene 3.3. Uses 4. Phthalonitrile 4.1. Properties 4.2. Production 4.2.1. Production from o ‐Xylene 4.2.2. Production from Phthalic Acid Derivatives 4.3. Uses 5. Phthalates 5.1. Physical and Chemical Properties 5.2. Raw Materials 5.3. Production 5.4. Environmental Protection 5.5. Quality Specifications 5.6. Storage and Transportation 5.7. Uses 5.8. Economic Aspects 6. Toxicology 6.1. Use of and Exposure to Phthalic Acid and Derivatives 6.2. Toxicological Profiles 6.2.1 Phthalic Acid 6.2.2 Phthalic Anhydride 6.2.3 Phthalimide 6.2.4. Phthalonitrile 6.2.5. Phthalate Esters 6.2.5.1. Metabolism and Toxicokinetics 6.2.5.2. Acute Toxicity 6.2.5.3. Irritation and Sensitizing Potential 6.2.5.4. Repeated DEHP Dosing 6.2.5.5. Genotoxicity and Mutagenicity 6.2.5.6. Carcinogenicity 6.2.5.7. Reproductive Toxicity 6.2.5.8. Effects of Phthalate Esters by Groups 6.3 Risk Assessment 6.3.1 Biomonitoring and Human Exposure to Phthalate Esters 6.3.2 Carcinogenicity 6.3.3 Toxicity to Reproduction 6.4 Risk Management

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It has been demonstrated in several model systems that tumors arise in a multistage process. Carcinogenic aromatic amines are complete carcinogens, which usually produce tumors in typical target tissues without any additional treatment. The tissue specificity, however, cannot readily be explained by genotoxic effects, and the role of secondary effects is not well understood. Promotional pressure on initiated cells can be produced by endogenous factors but also by the chemical itself. Comparison of the effects on rat liver of 2-acetylaminofluorene (AAF) and trans4-acetylaminostilbene (AAS) provides some evidence that initiating and promoting properties of these chemicals can be separated. AAS is a strong initiator in rat liver but seems to lack promoting activity; AAF is a less efficient initiator but has tumor promoting properties. The results obtained so far indicate that promoting pressure is not produced by the acute, cytotoxic effects of AAF. It is therefore concluded that nongenotoxic, possibly receptor-mediated effects are involved.

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