LEVELS OF POLYCYCLIC AROMATIC HYDROCARBONS IN FRESH WATER FISH DRIED UNDER DIFFERENT DRYING REGIME

Source and Emission of PAHs

PAHs are mainly derived from anthropogenic activities related to pyrolysis and incomplete combustion of organic matter. Sources of PAHs affect their characterization and distribution, as well as their toxicity. Major sources of PAH emissions may be divided into four classes: stationary sources (including domestic and industrial sources), mobile emission, agriculture activities, and natural sources (Wania et al, 1996).

1.3. Stationary Sources

Some PAHs are emitted from point sources and this is hardly shifted (moved) for a long period of time. Stationary sources are further subdivided into two main sources: domestic and industrial.

1.3.1. Domestic Sources

Heating and cooking are dominant domestic sources of PAHs. The burning and pyrolysis of coal, oil, gas, garbage, wood, or other substances are the main domestic sources. Domestic sources are important contributors to the total PAHs emitted into the environment. Difference in climate patterns and domestic heating systems produce large geographic variations in domestic emission. PAH emissions from these sources may be a major health concern because of their prevalence in indoor environments (Ravindra et al., 2008). According to a recent World Health Organization (WHO) report, more than 75% of people in China, India, and South East Asia and 50-75% of people in parts of South America and Africa use combustion of solid fuel, such as wood, charcoal for daily cooking.

Main indoor PAH sources are cooking and heating and infiltration from outdoors. PAH emissions from cooking account for 32.8% of total indoor PAHs (Zhu et al., 2009). LMW PAHs which originate from indoor sources are the predominant proportion of the total PAHs identified in residential non-smoking air. Toxicity of PAH mixtures from indoor sources is lower than mixtures which contain large amounts of high molecular weight PAHs. Cigarette smoke is also a dominant sources of PAHs in indoor environments. In many studies, PAHs in the indoor air of smoking residences tend to be higher than those of non-smoking residences.

1.3.2. Industrial Sources

Sources of PAHs include emission from industrial activities, such as primary aluminum and coke production, petrochemical industries, rubber tire and cement manufacturing, bitumen and asphalt industries, wood preservation, commercial heat and power generation, and waste incineration (Fabbri and Vassura , 2006).

1.3.3. Mobile Sources

Mobile sources are major causes of PAHs emissions in urban areas. PAHs are mainly emitted from exhaust fumes of vehicles, including automobile, railways, ships, aircrafts, and other motor vehicles. PAHs emissions from mobile sources are associated with use of diesel, coal, gasoline, oils, and lubricant oil. Exhaust emissions of PAHs from motor vehicles are formed by three mechanisms: (1) synthesis from smaller molecules and aromatic compounds in fuel; (2) storage in engine deposits and in fuel; (3) pyrolysis of lubricants (Baek et al., 1991). One of the major influences on the production of PAHs from gasoline automobiles is the air-to-fuel ratio. It has been reported that the amount of PAHs in engine exhaust decreases with leaner mixtures (Ravindra et al., 2006b). A main contribution to PAH concentrations in road dust as well as urban areas is vehicle exhaust. Abrantes et al., (2009) reported that the total emissions and toxicities of PAHs released from light-duty vehicles using ethanol fuels are less than those using gasohol. Low molecular weight PAHs are the dominant PAHs emitted from light duty vehicles and helicopter engines.

1.3.4 Agricultural Sources

Open burning of bush wood, straw, moorland heather, and stubble are agricultural sources of PAHs. All of those activities involve burning organic materials under suboptimum combustion conditions. Thus it is expected that a significant amount of PAHs are produced from the open burning of biomass. PAH concentrations released from wood combustion depend on wood type, kiln type, and combustion temperature. Between 80 – 90% of PAHs emitted from biomass burning are low molecular weight PAHs, including naphthalene acenaphthylene, phenanthene, fluoranthene and pyrene. Lu et al., (2009) reported that PAHs emitted from the open burning of rice and bean straw are influenced by combustion parameters. Total emissions of 16 PAHs from the burning of rice and bean straw varied from 9.29 to 23.6µg/g and from 3.13 to 49.9µg/g respectively. PAH emissions increased with increasing temperature from 200 to 700⁰c.

Maximum  emissions  of  PAHs  were  observed  at  40%  O2  content  in  supplied  air.  However,

emission of PAHs released from the open burning of rice straw negatively correlate with the moisture content in the straw (Lu et al., 2009).

1.3.5. Natural Sources

Accidental burning of forests, woodland, and moorland due to lightning strikes are natural sources of PAHs. Furthermore, volcanic eruptions and decaying organic matter are also important natural sources, contributing to the levels of PAHs in the atmosphere. The degree of PAH production depends on meteorological conditions such as wind, temperature, humidity, and fuel characteristics and type; such as moisture content, green wood, and seasonal wood (Wild and Jones, 1995).

1.3.6 Uses of PAHs

PAHs are not synthesized chemically for industrial purposes. Rather than industrial sources, the major source of PAH is the incomplete combustion of organic material such as coal, oil, and wood. However, 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. Acenaphthene, Anthracene, Fluoranthene, Fluorene, Phenanthrene and Pyrene are used in the manufacture of dyes, plastics, pigments, pharmaceutical and agrochemicals such as pesticides, wood preservatives resins and so on.

Other PAHs may be contained in asphalt used for the construction of roads, as well as roofing tar. Precise PAHs, specific refined products, are used also in the field of electronics, functional plastics, and liquid crystals. (Katarina, 2011).

1.4 Routes of Exposure for PAHs

PAH exposure through air, water, soil, and food sources occurs on a regular basis. The routes of exposure include ingestion, inhalation, and dermal contact in both occupational and non-occupational settings. Some exposure may involve more than one route simultaneously, affecting the total absorbed dose (such as dermal and inhalation exposure from contaminated air). All non-workplace source of exposure such as diet, smoking, and burning of coal and wood should be taken into consideration (ATSDR, 1995).

1.4.1 Air

PAHs concentrations in air can vary from less than 5 to 200,000 (ng/m³) (Cherng et al., 1996; Georgiadis and Kyrtopoulos, 1999). Although environmental air levels are lower than those associated with specific occupational exposure, they are of public health concern when spread over large urban populations (Zmirou et al., 2000).

The background levels of the Agency for Toxic Substances and Disease Registry’s toxicological priority for PAHs in ambient air have been reported to be 0.02 – 1.2 ng/m³ in rural areas and 0.15 – 19.3 ng/m³ in urban areas (ATSDR, 1995).

Cigarette smoking and environmental tobacco are other sources of air exposure. Smoking one cigarette can yield an intake of 20-40ng of benzo (a) pyrene (Philips, 1996; O’Neill et al., 1997). Smoking one pack of unfiltered cigarette per day yields 0.7µg/day benzo (a) pyrene exposure. Smoking a pack of filtered cigarette per day yields 0.4 µg/day (Sullivan and Krieger 2001).

Environmental tobacco smoke contains a variety of PAHs, such as benzo (a) pyrene, and more than 40 known or suspected human carcinogens. Side-stream smoke (smoke emitted from a burning cigarette between puffs) contains PAHs and other cytotoxic substances in quantities much higher than those found in mainstream smoke (exhaled smoke of smoker) (Jinot and Bayard, 1996; Nelson, 2001).

1.4.2. Water

PAHs can leach from soil into ground water. Water contamination also occurs from industrial effluents and accidental spills during oil shipment at sea. Concentrations of benzo (a) pyrene in drinking water are generally lower than those in untreated water and about 100 fold lower than the US Environmental Protection Agency’s (EPA) drinking water standard. (EPA’s maximum contaminant level (MCL) for benzo (a) pyrene in drinking water is 0.2 parts per billion {ppb}(US EPA, 1995).

1.4.3 Soil

Soil contains measurable amounts of PAHs primarily from airborne fallout. Documented level of PAHs in soil near oil refineries have been as high as 200,000 micrograms per kilogram (µg/kg) of dried soil. Levels in soil samples obtained near cities and areas with heavy traffic were typically less than 2,000 µg/kg (IARC, 1973).

1.4.4 Food Stuffs

In non-occupational settings, up to 70% of PAH exposure for non-smoking person can be associated with diet (Skupinska et al., 2004). PAH concentrations in foodstuffs vary. Charring meat or barbecuing food over a charcoal, wood, or other type of fire greatly increase the concentration of PAHs. For example, the PAH level for charring meat can be as high as 10-20 µg/kg (Philips, 1999). Charbroiled and smoked meats and fish contain more PAHs than do uncooked products, with up to 2.0 µg/kg of benzo (a) pyrene detected in smoked fish. Tea, roasted peanuts, coffee, refined vegetable oil, cereals, spinach, and many other foodstuffs contain PAHs. Some crops such as wheat, rye and lentils, may synthesize PAHs or absorb them via water, air, or soil (Grimmer, 1968; Shabad and Cohan 1972; IARC, 1973).

1.4.5 Other Sources of Exposure

PAHs are found in prescription and non-prescription coal tar products used to treat dermatologic disorders such as psoriasis and dandruff (Van Schooten, 1996). PAHs and their metabolites are excreted in breastmilk, and they readily cross the placenta.

Antracene laxative use has been associated with melanosis of the colon and rectum (Badiali et al., 1985).

1.5 Individuals at Risk of Exposure

Workers in industries or trades using or producing coal or coal products are at highest risk for PAHs exposure. Those workers include, but are not limited to Aluminum workers, Asphalt workers, Carbon black workers, Chimney sweeps, Coal-gas workers, Fishermen (coal tar on nets), Graphite electrode workers, Machinists, Mechanics (auto and disel engine), Printers, Road (pavement) workers, Roofers, Steel foundry workers, Tire and rubber manufacturing workers, and Workers exposed to creosote, such as Carpenters, Farmers, railroad workers, Tunnel construction workers, and Utility workers

Exposure is almost always to mixtures that pose a challenge in developing conclusions (Samet, 1995). Fetuses may be at risk for PAH exposure. PAH and its metabolites have been shown to cross the placenta in various animal studies (ATSDR, 1995). Because PAH are excreted in breast milk, nursing infants of exposed mothers can be easily exposed.

1.6 Standard and Regulations of PAHs Exposure.

The United States Government Agencies have established standards that are relevant to PAHs exposure in the workplace and the environment. There is a standard relating to PAHs in the workplace, and also a standard for PAHs in drinking water.

Occupational safety and health administrations (OSHA) have not established a substance-specific standard for occupational exposure to PAHs. Exposures are regulated under OSHA’s Air contaminants standard for substances termed coal tar pitch volatiles (CTPVs) and coke oven emission. Employees exposed to CTPVs in the coke oven industry are covered by the coke oven emissions standard.

The OSHA coke oven emission standard required employers to control employee exposure to coke oven emissions by the use of engineering controls and work practices.

Whenever the engineering and work practices control that can be instituted are not sufficient to reduce employee exposure to or below the permissible exposure limit (PEL), the employer shall nonetheless use them to reduce exposure to the lowest level achievable by these controls and shall supplement them by the use of respiratory protection. The OSHA standards also include elements of medical surveillance for workers exposed to coke oven emissions (ATSDR, 1995).

Air

The OSHA PEL for PAHs in the workplace is 0.2miligram/cubic meter (mg/m³). The OSHA – mandated PAH workroom air standard is an 8-hour time-weighted average (TWA) permissible

exposure limit (PEL) of 0.2 mg/m³, measured as the benzene-solube fraction of coal tar pitch

volatiles. The OSHA standard for coke oven emissions is 0.15 mg/m³. The National Institute for Occupational Safety and Health (NIOSH) has recommended that the workplace exposure limit for PAHs be set at the lowest detectable concentration which was 0.1 mg/m³ for coal tar pitch volatile agents at the time of the recommendation (ATSDR, 1995).

Table 2: Levels of PAHs Exposures from Workplace

(ATSDR, 1995).

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•       TLV: threshold limit value.

•       TWA (time – weighted average), concentration for a normal 8-hour workday and a 40-hour workweek to which nearly all workers may be repeatedly exposed.

•       REL (recommended exposure limit): recommended airborne exposure limit for coal pitch volatiles (cyclohexane – extractable fraction) averaged over a 10 – hour work shift.

•       PEL (permissible exposure limit): the legal airborne permissible exposure limit (PEL) for coal tar pitch volatiles (Benezene soluble fraction) averaged over an 8 – hour work shift.

•       MCL: maximum contaminant level. (ATSDR, 1995).

Water

The maximum contaminant level goal for benzo (a) pyrene in drinking water is 0.2 parts per billions (ppb). In 1980, EPA developed ambient water quality criteria to protect human health from the carcinogenic effects of PAH exposure. The recommendation was a goal of zero (non-detectable level for carcinogenic PAHs in ambient water). EPA, as a regulatory agency, sets a maximum contaminant level (MCL) for benzo (a) pyrene, the most carcinogenic PAH at 0.2ppb. EPA also sets MCLs for five other carcinogenic PAHs (see table 2) (ATSDR, 1995).

Food

The U.S. Food and Drug Administration has not established standard governing the PAH content of foodstuffs but the Food and Agricultural Organization (FAO) and World Health Organization (WHO) have set a maximum permissible level for total polycyclic aromatic hydrocarbons and benzo (a) pyrene in certain foods. Recently the maximum permissible level of health hazard dietary intake of the PAHs in cooked and processed food are not defined accurately and varies from one country to another. Janoszka et al., (2004) reported that the health hazard level of the PAHs daily ingested in diet was found to be 3.7µg/kg in Great Britain, 5.17µg/kg in Germany, 1.2 µg/kg in New Zealand and 3 µg/kg in Italy. Generally it is known that the maximum permissible level (MPLs) of total PAHs and BaP are 10 and 1µg/kg wet cooked or processed meat and fishery products respectively as reported by FAO/WHO and Stolyhow and Sikorski (2005). The above and the Health hazard level of 5.7µg/day as reported by Janoszka et al., (2004) are the accepted reference standards even in Nigeria.

1.7 Metabolism of PAHs

Once PAHs enter the body they are metabolized in a number of organs (including liver, kidney, lungs), excreted in bile, urine or breast milk and stored to a limited degree in adipose tissue. The principal routes of exposure are: inhalation, ingestion, and dermal contact. The lipophilicity of PAHs enables them to readily penetrate cellular membranes (Yu, 2005). Subsequently metabolism renders them more water-soluble making them easier for the body to remove. However, PAHs can also be converted to more toxic or carcinogenic metabolites.

Phase I metabolism of PAHs

There are three main pathways for activation of PAHs: the formation of PAH radical cation in a metabolic oxidation process involving cytochrome P450 peroxidase, the formation of PAH-o-quinones by dihydrodiol dehydrogenase-catalysed oxidation and finally the creation of dihydrodiol epoxides, catalysed by cytochome P450 (CYP) enzymes (Guengerich, 2000). The most common mechanism of metabolic activation of PAHs, such as Benzo (a) pyrene (B(a)P), is via the formation of bay-region dihydrodiol epoxides eg. Benzo (a)pyrene-7, 8-dihydrodiol-9,10-epoxide (BPDE), via CYP450 and epoxide hydrolase (EH) as seen in figure 1 below.