Toxicology of soot

In this article the toxicological effect of soot exposure on man is explored with emphasis on the role that soot may play in the induction of cancer and respiratory diseases. Soot may be defined as the product of the incomplete combustion of fossil fuels and other organic matter; the resultant soot particulate consists of finely divided carbon particles, hydrocarbons, and tars. Animal studies will also be cited in which the data is suggestive of a potential risk to man. General sources of soot will be identified and their polycyclic aromatic hydrocarbon (PAH) content given, since it is believed that the PAH and PAH derivatives of soot are responsible for most of its carcinogenic and mutagenic effects. However, the reader should not consider this article to be an exhaustive review of the biology of PAH. The relatively new area of genetic toxicology and recent data derived from the mutagenicity testing of various organic extracts of soot and particulate matter will also be reviewed including a discussion of how these studies may indicate a genetic risk to man. This review of the toxicological effects of soot is broken down into six main sections. Each section deals with a particular topic concerning the health, genetic effects or composition and sources of various soots. Section 1 provides an overview of the early studies on the chemistry and biology of soot. It is intended to lay the ground work for the following sections and indicate that much of today's current interest in the study of environmentally important complex mixtures stems from the pioneering research into the medical and compositional aspects of soot. Section 2 provides a general discussion of the sources of soot based on data collected in the United States. This section also deals with the composition of organically extractable material from soots produced by different sources such as general air pollution, coal, coke and automotive exhaust. Emphasis is placed upon the polycyclic aromatic hydrocarbon (PAH) fractions and their derivatives, due to their well documented biological activity. An introduction to the various analytical methods employed to determine the PAH composition of organic soot extracts is also provided which allows the reader an access to the technical methodological literature. In addition, this section lays the ground work for the discussion of determining what chemical fractions and/or individual components of organically extractable soot material is responsible for the mutagenic/carcinogenic activity of soot. Section 3 applies some of the knowledge gained in Section 2 to determine what chemical fractions and individual components of organic soot extracts are responsible for the carcinogenic nature of soot based on animal biossays. In addition, this section deals with the development of the various animal models used in evaluating the carcinogenic potential of organic soot extracts and individual PAH components. Section 3 also discusses the carcinogenic potency of different soot extracts in animal bioassays which is useful in developing human health risk assessments. This section presents data which suggest that organic extracts and various individual components of soot induce tumors in experimental animal models and in turn leads to the discussion presented in the next section (Section 4) which explores the possibility that exposure to soot increases the incidence of cancer in man. The role of human epidemiology and its use to determine whether exposure to soot results in an increased cancer incidence in man is discussed in Section 4. Urban vs rural differences are cited which suggest that living in areas with a higher burden of air pollution may be involved with a higher incidence of lung cancer. The effect of smoking upon the perceived urban vs rural differences is also discussed. Studies are also cited in which the actual amount of particulate air pollution is known. Such studies suggest that the level of soot is positively correlated with lung cancer incidence. Occupational exposure to soot and cancer incidence is also explored because the exposure conditions are more controlled and consistent. In additions, measurement of exposure is made more practical and relevant to the epidemiological data gathered. Therefore, the strongest case for soot exposure resulting in an increased incidence of cancer in man can be made based on these occupational studies. Finally, Section 4 deals with epidemiological studies correlating soot exposure, nonrespiratory cancer and nonmalignant diseases. Such studies are cited to indicate that soot exposure is a health risk to man independent from its perceived ability to increase the risk of lung cancer. Section 4 is presented to make the reader aware that a health risk is apparently associated with exposure to soot. This leads to the discussion of the development and utilization of various short-term in vitro genotoxicity bioassays in the screening of soot extracts and derived fractions for their mutagenic/carcinogenic potential in Section 5. Section 5 presents a summary of the various short-term genotoxicity assays that have been employed to study the genetic effects of various organic soot extracts and fractions. The use of short-term genotoxicity assays allows for the rapid screening of many samples and the requirement of only small sample amounts. Therefore, a complex chemical fractionation of organic soot extracts can be performed with the resulting fractions being tested for their genotoxicity in these short-term bioassays. With the identification of the genotoxic fractions, these fractions can then be further chemically analyzed for their individual component composition. Individual compounds can then be selected for further genotoxicity testing. Following this scheme of chemical/biological analysis it may be possible to identify the individual compounds or groups of compounds that are responsible for the genotoxicity of the whole organic extract of the particular soot under study. With such knowledge at hand it may be possible to design control techniques to reduce the level of these genotoxic components produced during the combustion process. However, it is necessary to realize that these genotoxicity assays may not represent the true genetic or metabolic functions of man. Therefore, soot fractions and individual component compounds that are highly mutagenic in bacterial assay systems, may not be as genotoxic in more advanced mammalian cell bioassay tests. The final section of this review (Section 6) provides a brief discussion of the metabolism of PAH, the DNA binding properties of the reactive metabolites, mechanisms of PAH induced mutagenesis and DNA repair. Such processes are ultimately connected with the mutagenic/carcinogenic potential of the PAHs which play a significant role in the mutagenic/carcinogenic nature of soot particles.