BPL is a highly active molecule with numerous biological properties. The chemical reacts rapidly with nucleophilic centers such as proteins, particularly sulfur containing amino acids, and nucleic acids. The product of these reactions is an alkylated moiety which in the case of DNA results in the induction of mutations and chromosome aberrations. The predominant alkylated base in DNA exposed to BPL is 7-(2-carboxyethyl) guanine. Adenine is alkylated to a lesser extent at the 3-position [44]. Alkylation of guanine can lead to either depurination or an ionized form of the molecule capable of mis-hydrogen bonding with thymidine. Depurination can also lead to numerous transition or transversion types of base-pair substitutions. Conversely, alkylguanine-specific repair reduces the DNA-modifying effects of BPL. Anomalous base-pairing between guanine and thymine would be expected to result in GC to AT transition base-pair substitution mutations, and a substantial amount of the mutation data obtained from phage, bacteria and yeast indicate but the predominant mechanism is base-pair substitutions of the GC to AT type. In addition to base-pair substitutions, BPL was shown to produce multilocus deletions in phage, Neurospora and probably yeast. This information, plus the data showing DNA cross-linking in phage, clearly indicates the high degree of reactivity and the multiplicity of mechanisms by which mutagenic effects can be induced by BPL. The rapid and extensive binding of the active form of BPL to nucleophilic centers is also obvious from its in vivo toxicity. Administration of BPL to mice or rats does not result in either germ cell or bone marrow effects as found with other slower reacting alkylating agents (e.g., triethylene melamine). The biological half-life of BPL in vivo is probably too short for substantial quantities of the alkylating form to reach either target site. The lack of systemic neoplasia from either subcutaneous or oral exposure of animals to BPL is consistent with these data. As a result of this type of chemical reactivity, it is difficult to determine the impact of BPL on humans. Risk assessments using normal methods of exposure, such as drinking water, feed or i.p. or i.m. injection would be expected to show little or no mutagenic effects in acute or chronic studies. Yet, the potent mutagenic properties of this chemical are clearly obvious in plant, microbial or tissues exposed at the site of application but has little carcinogenic activity for systemic targets, even though DiPaolo et al. [22] reported transplacental transport and malignant transformation by BPL administered i.p. to pregnant hamsters. The significance of this finding is not clear in the light of normal human exposure to BPL. Because of the wealth of chemical, physical and biological information available on BPL, this chemical appears to be an excellent material for use in studies aimed at elucidating the mechanisms of mutagenesis and carcinogenesis and the functional relationship linking these two phenomena.