Polycyclic and Heterocyclic Aromatic Hydrocarbons

Abstract

Aromatic hydrocarbons are the class of chemicals that include multi‐ring aromatic compounds. Smaller aromatic hydrocarbons, one to two rings, are of considerable economic importance as industrial raw materials, solvents, and components of innumerable commercial and consumer products. However, aromatics differ vastly in chemical, physical, and biological characteristics from the aliphatic and alicyclic hydrocarbons. In addition, aromatics are more toxic to humans and other mammals. Of prime importance are the carcinogenicity of styrene and the polycyclic aromatic hydrocarbons. Chemically, aromatic hydrocarbons can be divided into three groups: (a) alkyl‐, aryl‐, and alicyclic‐substituted benzene derivatives, (b) di‐ and polyphenyls, and (c) polycyclic compounds composed of two or more fused benzene ring systems. The basic chemical entity is the benzene nucleus, which occurs alone, substituted, joined, or fused. Aromatics are moderately reactive and undergo photochemical degradation in the atmosphere. Aromatic compounds occur in liquid, vapor, or solid form. The lower molecular weight derivatives possess higher vapor pressures, volatility, absorbability, and solubility in aqueous media than the comparable aliphatic or alicyclic compounds. These properties contribute to their biological activities. They are characterized also by miscibility or conversion to compounds soluble in aqueous body fluids, high lipid solubility, and donor–acceptor and polar interaction. Because of their low surface tension and viscosity, aromatics may be aspirated into the lungs during ingestion, where they can cause chemical pneumonitis. Aromatics are primary skin irritants, and repeated or prolonged skin contact may cause dermatitis, dehydrating, and defatting of the skin. Eye contact with aromatic liquids may cause lacrimation, irritation, severe burns from prolonged contact. Naphthalene causes cataracts in the eyes of experimental animals. Its vapors are respiratory and mucous membrane irritants and may cause severe systemic injury. Direct aerosol deposition or contact from ingestion and subsequent aspiration can cause severe pulmonary edema, pneumonitis, and hemorrhage. Alkylbenzenes that have C 1 to C 4 side chains are readily aspirated and can produce instant death via cardiac arrest and respiratory paralysis. For example, in hexylbenzene exposure, death occured in 18 min, during which extensive pulmonary edema occured, resulting in a considerable increase in lung weight. The higher alkylbenzenes showed few or no effects. The unique effects of benzene on bone marrow and blood‐forming mechanisms are of major importance. In general, the acute toxicity of alkylbenzenes is higher for toluene than for benzene and decreases further with increasing chain length of the substituent, except for highly branched C 8 to C 18 derivatives. The toxicity increases again for vinyl derivatives. Pharmacologically, the alkylbenzenes are CNS depressants, since they exhibit a particular affinity to nerve tissues. Aromatic hydrocarbons cause local irritation and changes in endothelial cell permeability and are absorbed rapidly. Secondary effects have been observed in the liver, kidney, spleen, bladder, thymus, brain, and spinal cord in animals. Aromatic hydrocarbons, even from a single dose, exhibit a special affinity to nerve tissue. Animals dosed with alkylbenzenes exhibit signs of CNS depression, sluggishness, stupor, anesthesia, and coma. This is in sharp contrast with benzene, which is a neuroconvulsant and produces tremors and convulsions. The CNS depressant potency of the alkylbenzenes depends on branching or side‐chain length. It diminishes with increasing numbers of substituents or side‐chain carbon number up to dodecylbenzene, which has practically no CNS depressant activity. Aromatic hydrocarbons accumulate in marine animals to a greater extent and are retained longer than alkanes. In all species tested, the accumulation of aromatic hydrocarbons depended primarily on the octanol/water partition coefficient. Once absorbed, higher molecular weight hydrocarbons are released more slowly. Polycyclic aromatic hydrocarbons are mainly solid materials that are soluble in fats, oils, and organic solvents. The mutagenic or carcinogenic properties of PAHs have been linked to physicochemical properties, such as electronegativity or K‐ and L‐region reactivity, electrophilic potency, dipole moment, intramolecular and subcellular binding, hydrophobicity, and others. However, these characteristics alone are inadequate for specific predictions. Polynuclear aromatics are practically nontoxic for acute ingestion and acute dermal application. Enzyme systems, such as aryl hydrocarbon hydroxylase (AHH), are present in almost all human and animal cell tissues and are inducible by noncarcinogenic and potentially carcinogenic hydrocarbons. The stability of cytochrome P450 epoxidase may depend on immunologic competence, as does the epoxide hydrase. BaP is both teratogenic and mutagenic in rodents. Four‐ and five‐ring PAHs are carcinogenic. They include the benz(a)anthracenes, benzofluoranthracenes, benzo(a)pyrenes, chrysenes, and dibenz(a,h)anthracene. The OSHA and ACGIH ceiling for coal tar pitch volatiles that contain one or more PAHs is 0.2 ppm with a cancer notation. Sampling techniques include collecting air particles using an absorbent glass sampler, desorption with pentane, and quantification using spectral analysis. Collection on acrylonitrile‐PVC filters is also recommended. Analytic quantification is also achieved by using gas chromatography high‐resolution mass spectrometry or chemiluminescence. Methods for cleanup from waste water are also available.

Mutagenicity of selected polycyclic aromatic hydrocarbons (PAHs)

“…Benzo[a]pyrene is the most common PAH with established mutagenicity (Stiborova et al, 2016) while phenazine is a NPAH recently identified as a disinfectant-by-product (DBP) in drinking water (Zhao et al, 2008) and there is no information; its mutagenic activity is limited. Similarly, 2methylnaphthalene has been detected in appreciable quantity in emissions from cigarettes, coal tar pitch, petroleum refineries, emission engines, and diesel exhaust fumes (HSDB, 2002;Warshawsky, 2001;ASTDR, 2005). 2-methylnaphthalene is absorbed rapidly post-ingestion, distributed and metabolised among tissues lungs and liver in less than 6 h (Melanon et al, 1982;Teshima et al, 1983;Ding et al, 2005;Fang et al, 2006).…”