Introduction
Polycyclic aromatic hydrocarbons (PAHs) are organic compounds that are mostly colorless, white, or pale yellow solids. The term polycyclic aromatic hydrocarbon (PAH) refers to a ubiquitous group of several hundred chemically-related, environmentally persistent organic compounds having various structures and varied toxicity. Most of them are formed by a process of thermal decomposition (pyrolysis) and subsequent recombination (pyro synthesis) of organic molecules. PAHs enter the environment through various routes and are usually found as a mixture containing two or more of these compounds, e.g., soot. However, some PAHs are manufactured, and these pure PAHs usually exist as colorless, white or pale yellow solids. PAHs affect organisms through various toxic actions.
SOURCES
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous environmental pollutants generated primarily during the incomplete combustion of organic materials (e.g. coal, oil, petrol, and wood). Emissions from anthropogenic activities predominate; nevertheless, some PAHs in the environment originate from natural sources such as open burning, natural losses or seepage of petroleum or coal deposits, and volcanic activities. Major anthropogenic sources of PAHs include residential heating, coal gasification and liquefying plants, carbon black, coal-tar pitch and asphalt production, coke and aluminum production, catalytic cracking towers and related activities in petroleum refineries as well as and motor vehicle exhaust. PAHs are found in the ambient air in gas-phase and as sorbet to aerosols. Atmospheric partitioning of PAH compounds between the particulate and the gaseous phases strongly influences their fate and transport in the atmosphere and the way they enter into the human body. The removal of PAHs from the atmosphere by dry and wet deposition processes are strongly influenced by their gas/particle partitioning. Atmospheric deposition is a major source for PAHs in soil. Many PAHs have toxic, mutagenic and/or carcinogenic properties. PAHs are highly lipid soluble and thus readily absorbed from the gastrointestinal tract of mammals. They are rapidly distributed in a wide variety of tissues with a marked tendency for localization in body fat.
TYPES:
The following three types: pyrogenic, petrogenic, and biological are the major PAH sources to the environment. In petroleum hydrocarbons, and
decomposition of vegetative liter fall. Examples of anthropogenic sources of PAHs range from: Large point sources include incomplete combustion (such as incinerators and some industrial processes. Smaller point sources include, dispersed sources (such as automotive emissions, smoke from wood-burning stoves, jet aircraft exhausts, cigarette and cigar smoke, and backyard barbecues). Other anthropogenic sources of PAHs include petroleum product spills, sewage sludge, and tarry or creosote waste materials. It is important to mention that the incomplete combustion, either naturally or anthropogenically derived, has been identified as the single largest contributor of PAHs to the environment.
Uses:
PAHs are not synthesized chemically for industrial purposes. Nevertheless, there are a few commercial uses for many PAHs. They are mostly used as intermediaries in pharmaceuticals, agricultural products, photographic products, thermosetting plastics, lubricating materials, and other chemical industries. However, the general uses of some PAHs are:
Other PAHs may be contained in asphalt used for the construction of roads, in addition to roofing tar. Furthermore, specific refined products, of
precise PAHs, are used also in the field of electronics, functional plastics, and liquid crystals.
Transport and Fate of PAHs in the environment
Atmospheric emission and deposition of PAHs: The atmosphere is the most important means of PAH dispersal, it receives the bulk of the PAH environmental load resulting in PAHs being ubiquitous in the environment. PAHs are emitted to the atmosphere primarily from the incomplete combustion of organic matter. Once released to the atmosphere, PAHs are found in two separate phases, a vapor phase and a solid phase in which the PAHs are sorbet onto particulate matter. Hydrophobic organic chemicals with low vapor pressures, such as PAHs, are sorbet to atmospheric particulates more readily than chemicals with higher vapor pressures, such as benzene. The variability in vapor pressures of different PAH compounds cause the individual PAHs to distribute in different concentrations in the vapor and other sorbe phases.
PAHs in surface soils:
Atmospheric PAHs are continuously deposited to the earth by dry or wet deposition processes. Some of these PAHs are from nearby sources, such as automotive exhaust from adjacent roadways. Other PAHs are from more distant sources and have been carried
various distances through the air. In the meantime, PAHs can be added to soils if fill materials contain PAHs. When PAHs are deposited onto the earth’s surface, they can become mobile. Since the majority of PAHs in the soil will be bound to soil particles, the most important factors influencing PAH mobility of particulates in the subsurface will be sorbent particle size and the pore throat size of the soils. Such pore throat can be defined as the smallest opening found between individual grains of soil.
PAHs in sediments: PAHs are deposited to the sedimentary environment by similar processes that govern the deposition to surface soils. In rural areas, the PAHs sorbet to atmospheric particles can settle on the surface of lakes, streams, and oceans by dry or wet deposition. There they are dispersed by currents and eventually become integrated with the sediment. On the other hand, sediments near urban centers are influenced by atmospheric deposition of PAHs. They also receive inputs of PAHs from storm and sanitary sewer effluents as well as roadway runoff. Eventually, some of the PAHs will be sorbet to particles, settle, and become part of the sedimentary record.
Occurrence of PAH in foods: Raw foods should usually not contain high levels of PAH. In areas remote from urban or industrial activities, levels of PAH found in unprocessed foods reflect the background contamination. Processing of food (such as drying and smoking) and
cooking of foods at high temperatures (grilling, roasting, frying) are major sources generating PAH. Levels as high as 200lg/kg of PAH have been found in smoked fish and meat. In barbecued meat, 130lg/kg of PAH has been reported (Standing Committee on Foodstuffs, 2001). Generally, the average background values are in the range of 0.01–1lg/kg in uncooked foods. Contamination of vegetable oils (including olive residue oils) with PAH usually occurs during technological processes like direct fire drying. In this respect, the combustion products may come into contact with the oil seeds or oil. The occurrence of PAH in foods is governed mainly by the same physicochemical factors that determine their absorption and distribution in man. These factors are the relative solubility of PAH in water and organic solvents. Such solubility determines their capacity for transport and distribution between different environmental compartments and their uptake and accumulation by living organisms.
Effect on human health
17 PAHs have been identified as being of greatest concern with regard to potential exposure and adverse health effects on humans and are thus considered as a group. Biological monitoring of exposure to PAHs is of primary interest, due to the widespread diffusion of these compounds and to their toxicological relevance. Some PAHs are well known as carcinogens, mutagens, and teratogens and therefore pose a serious threat to the health and the well-being of humans. The most significanthealth effect to be expected from inhalation exposure to PAHs isan excess risk of lung cancer.
Short-term health effects (acute): The impact of PAHs on human health depend mainly on the length and route of exposure, the amount or concentration of PAHs one is exposed to, as well as the relative toxicity of the PAHs. Occupational exposures to high levels of pollutant mixtures containing PAHs have resulted in symptoms such as eye irritation, nausea, vomiting, diarrhoea and confusion. Nevertheless, it is not
known which components of the mixture were responsible for these effects and other compounds commonly found with PAHs may be the cause of these symptoms. Mixtures of PAHs are also known to cause skin irritation and inflammation. Anthracene, benzopyrene and naphthalene are direct skin irritants. But, anthracene and benzopyrene are reported to be skin sensitizers, i.e. cause an allergic reaction in skin in animals and humans.
Long-term health effects (chronic): Health effects from long-term or chronic exposure to PAHsmay include decreased immune function, cataracts, kidneyand liver damage (e.g. jaundice), and breathing problems,asthma-like symptoms, and lung function abnormalities.Meanwhile, repeated contact with skin may induce rednessand skin inflammation. Naphthalene, a specific PAH, can cause the breakdown of red blood cells if inhaled or ingestedin large amounts. If Man is exposed to PAHs, the harmfuleffects that may occur largely depend on the way of exposure.
Carcinogenicity: Although unmetabolized PAHs can have toxic effects, amajor concern is the ability of the reactive metabolites, suchas epoxides and dihydrodiols, of some PAHs to bind to cellular proteins and DNA. Biochemical disruptions and celldamage occurrence lead to mutations, developmental malformations, tumors, and cancer. Evidence indicates that mixtures of PAHs are carcinogenic to humans. Meanwhile, some PAH-rich mixtures are also classified as carcinogenic to humans. The EPA has classified the following seven PAH compounds: benzoanthracene, benzopyrene, benzofluoranthene, benzofluoranthene, chrysene, dibenzanthracene, and indeno (1,2,3-cd)pyrene as probable human carcinogens.
Effects of PAH on the immune system: It has been reported that the PAHs induce suppress immune reaction in rodents. The precise mechanisms of PAH induced immune-toxicity are still not clear. It was concluded that the immune-suppression may be involved in the mechanisms by which PAH induce cancer. The immune-toxic effects of PAH have been investigated for many years. Whatever the route of exposure, the resulting effects have been considered mostly at the systemic level. Furthermore, it has been reported that some PAH when taken into the diet may induce DNA adducts in the lungs. In addition, translocations from one organ to another may result in ‘‘at distance” effects. It is worth mentioning that most of the immune-toxic effects that are reported for PAH are not Review on polycyclic aromatic hydrocarbons thought to be due to parent compounds but it refers to their reactive epoxide metabolites.
Genotoxicity of PAHs: Geno-toxic effects for some PAH have been demonstrated both in rodents and in vitro tests using mammalian (including human) cell lines. Most of the PAHs are not geno-toxic by themselves and they need to be metabolised to the diol epoxides which react with DNA, thus inducing geno-toxic damage. Geno-toxicity plays important role in the carcinogenicity process and could be also in some forms of developmental toxicity, PAHs undergo multiple metabolic transformations which may lead to the formation of electrophilic derivatives (e.g. diolepoxides, quinones, conjugated hydroxyalkyl derivatives) capable of covalent interaction with nucleophilic centers of macromolecules. Molecular analysis of p53 mutations in lung cancers of smokers shows a similar prevalence of G > T transversions, possibly
reflecting the contribution of PAH to tobacco smoke carcinogenesis. In addition to base pair substitutions, bulky adducts of PAH to DNA bases can induce frameshift mutations, deletions, S-phase arrest, strand breakage and a variety of chromosomal alterations.
Teratogenicity: Embryotoxic effects of PAHs have been described in experimental animals exposed to PAH such as benzoanthracene, benzopyrene, and naphthalene.Laboratory studies conducted on mice have demonstratedthat ingestion of high levels of benzopyrene during pregnancy resulted in birth defects and decreased body weightin the offspring. It is not known whether these effectscan occur in humans. Nevertheless, it was reported anddemonstratedthat exposure to PAH pollution during pregnancy is related to adverse birth outcomes including lowbirth weight, premature delivery, and heart malformations. High prenatal exposure to PAH is also associated withlower IQ at age three, increased behavior problems at agessix and eight, and childhood asthma. Cord blood ofexposed babies shows DNA damage that has been linkedto cancer.
Conclusion
PAHs enter the environment mainly through the air as a result of industrial and natural thermal processes. Consumers come into contact with PAHs in the form of contaminated rubber or plastic products and abrasion from rubber products, floorings, or wood preservatives. PAHs are
absorbed via the air, tobacco smoke, and consumption of specific contaminated foodstuffs, such as smoked foods. Many PAHs are carcinogenic, mutagenic, or toxic for reproduction. Due to their chemical and biological stability and their potential for bioaccumulation, they are persistent in the environment and accumulate in organisms. So, its high time to us, to raise awareness about PAHs effects on environment, also we have to less burn fossil fuel until or unless it’s too late.
References:
[1] B.G. Armstrong, E. Hutchinson, J. Unwin, T. Fletcher, Environ Health Perspect 112 (9) (2004) 970–978.
[2] CCME (Canadian Council of Ministers of the Environment). Canadian soil quality guidelines for potentially carcinogenic and other PAHs: scientific criteria document. CCME: Winnipeg: 2010.
[3] A. Baklanov, O. Ha¨nninen, L.H. Slørdal, J. Kukkonen, N.Bjergene, B. Fay, Atmos Chem Phys 7 (2007) 855–874.
[4] J. Latimer, J. Zheng, The sources, transport, and fate of PAH in the marine environment, in: P.E.T. Douben (Ed.), PAHs: an ecotoxicological perspective, John Wiley and Sons Ltd, New York, 2003.
[5] A.C. Menzie, B.B. Potocki, J. Santodonato, Environ Sci Technol 26 (1992) 1278–1284.
[6] Inomata Y, Kajino M, Sato K, Ohara T, Kurokawa JI, Ueda H, et al. Emission and atmospheric transport of particulate PAHs in Northeast Asia.Environ Sci Technol 2012; 46: 4941-4949.
[7] Lee BK, Vu VT. Sources, distribution and toxicity of polyaromatic hydrocarbons (PAHs) in particulate matter. In: Villanyi V, editor. Air pollution. Rijeka: Sciyo; 2010.
[8] Estrellan CR, Iino F. Toxic emissions from open burning. Chemosphere 2010; 80: 193-207.
[9] Chiang KC, Chio CP, Chiang YH, Liao CM. Assessing hazardous risks of human exposure to temple airborne polycyclic aromatic hydrocarbons. J Hazard Mater 2009; 166(2-3): 676-685.
[10] Mu L, Peng L, Cao J, He Q, Li F, Zhang J, et al. Emissions of polycyclic aromatic hydrocarbons from coking industries in China. Particuology 2013; 11(1): 86-93.
Research Scholar, Department of Environmental Science, Burdwan University