Potential exposure, polycyclic

These exposure estimates [for benzo[a]pyrene] and the determinations of the tumorigenic potential of [polycyclic aromatic hydrocarbons] in bioassays strongly suggest that [polycyclic aromatic hydrocarbons] play a significant role in the induction of respiratory tract cancer in smokers... 

A number of studies have examined the potential for airborne aluminum to induce respiratory effects in chronically exposed workers. Exposure to aluminum fumes and dust occurs in potrooms where hot aluminum metal is recovered from ore, in welding operations, and the production and use of finely powdered aluminum. Wheezing, dyspnea, and impaired lung function have been observed in potroom workers (Bast-Peetersen et al. 1994 Chan-Yeung et al. 1983 Simonsson et al. 1985). Because these workers were also exposed to a number of other toxic chemicals including sulfur dioxide, polycyclic aromatic hydrocarbons (PAHs), carbon monoxide, and hydrogen fluoride, it is difficult to ascribe the respiratory effects to aluminum. 

The primary routes of potential human exposure to coke oven emissions are inhalation and dermal contact. Occupational exposure to coke oven emissions may occur for those workers in the aluminum, steel, graphite, electrical, and construction industries. Coke oven emissions can have a deleterious effect on human health. Coke oven emissions contain literally several thousand compounds, several of which are known carcinogens and/or cocarcinogens including polycyclic organic matter from coal tar pitch volatiles, jS-naphthylamine, benzene, arsenic, beryllium, cadmium, chromate, lead, nickel subsulfide, nitric oxide, and sulfur dioxide. Most regulatory attention has been paid to coal tar pitch volatiles. 

HSPs as cellular markers of stress HSPs are involved in various aspects of cellular function and a lot is being learnt about its role in normal and pathological states. Recent studies from lower animals, especially fish, have revealed the potential use of induced fish HSPs as a biomarker of exposure to environmental stressors. Industrial effluents, polycyclic aromatic hydrocarbons, metals such as copper, zinc, mercury, pesticides, etc. have shown to induce HSP in fish. Further, the HSP response may vary with the stressor, tissue, species of fish, and the family of HSP studied. Hence it appears that a more extensive and probably a high-throughput profiling (using genomic and pro-teomic) approaches may be necessary to identify patterns of HSP modulation by various stressors. 

Low concentrations of carcinogenic polycyclic aromatic hydrocarbons (PAHs) have also been evaluated for a potential hormetic effect. Exposure of grunion embryos (Leuresthes tenuis-, a freshwater tel-eost) to 7ppb of benzo [a]pyrene resulted in significantly increased respiration rates compared with unexposed controls, whereas at higher concentrations of 24.2, 361, or 868.8 ppb, respiration rates were not... 

This statement was prepared to give you information about polycyclic aromatic hydrocarbons (PAHs) and to emphasize the human health effects that may result from exposure to them. The Environmental Protection Agency (EPA) has identified 1,408 hazardous waste sites as the most serious in the nation. These sites make up the National Priorities List (NPL) and are the sites targeted for long-term federal clean-up activities. PAHs have been found in at least 600 of the sites on the NPL. However, the number of NPL sites evaluated for PAHs is not known. As EPA evaluates more sites, the number of sites at which PAHs are found may increase. This information is important because exposure to PAHs may cause harmful health effects and because these sites are potential or actual sources of human exposure to PAHs. 

A wide variety of chemicals and drugs have been shown to affect the immune system adversely, including pesticides (A). Studies with the polycyclic aromatic hydrocarbons (PAHs) have demonstrated that most carcinogenic PAHs are immunosuppressive, whereas their noncarci-nogenic congeners are not (5) see review (6). Thus, it follows that exposure to carcinogenic pesticides could potentially result in damage to the immune system. 

The quasi-Favorskii rearrangement has been used often in the synthesis of unnatural, conplex, polycyclic structures. Indeed, this method is uniquely suited for such targets. However, undesired side reactions can occur. An exanple, discussed here within its mechanistic context, is based on a report by Ueda and coworkers. They treated the polycyclic dibrominated diketone 37 with potassium hydroxide in the expectation of obtaining cubane-l,3-dicarboiq lic acid 38. Given what was known about quasi-Favorskii reactions at the time (vide supra), the plan made perfect sense. However, exposure of 37 to 5% KOH for 15 min at 80 °C afforded not 38 but the cyclopropyl lactone 43 fScheme 7.12). A proposed mechanism for the process began with a Haller-Bauer cleavage, always a potential risk in quasi-Favorskii... 

Petroleum hydrocarbons contain a wide range of substances that are potential health hazards. These include aliphatic compounds, monocyclic aromatics, polycyclic aromatics, and heavy metals. Most petroleum products have an objectionable taste and odor well below the level that might induce chronic toxicity in humans. Thus, the most frequently reported symptoms of exposure are relatively mild and include nausea, vomiting, and diarrhea. 

Polycyclic aromatic hydrocarbons are potent immunosuppressive environmental contaminants. Immunotoxic effects of PAHs, which may contribute to their carcinogenic potential, have been established in various animal models and in human immune cells (van Grevenynghe et al., 2004). Inhibition of the production of immunocompetent cells (lymphocytes and monocytes) is likely one of the mechanisms contributing to the immunosuppression due to PAHs. Exposure to PAHs inhibits the differentiation of monocytes into dendritic cells and macrophages it also induces apoptosis of both pre-T cells in the thymus and pre-B cells in the bone marrow, which may account for thymic atrophy and decreased lymphoid cell recovery from the spleen, lymph nodes, and bone marrow in PAH-exposed mice (Lutz et al., 1998 Page et al., 2002). These toxic effects towards precursors of immune cells have been linked, at least in part, to the PAHs metabolism into toxic reactive intermediates triggering apoptosis of pre-B eells (Mann et al., 1999). 

---