**3.2 PAHs in products of plant and animal origin**

Environmental pollution caused by increased industrial production has resulted in the contamination of several food products, including vegetables, milk products, fruits, tea, oils, coffee, smoked meat and cereals with PAHs. Contaminated soil, water and air are known to be the main PAH contamination sources for food. Furthermore, PAHs may also contaminate food products by means of smoke generation, grilling on charcoal, processing, improper cooking methods and the use of feed additives [3, 14]. Cereals (corn, wheat, barley and oat) in industrialised regions enhance PAH levels in comparison with more outlying regions. Grain samples from a heavily industrialised region included 10 times more PAHs than samples from areas far from industry. The growth of rye near an autobahn resulted in PAH pollution, which reduced lightly 7–25 m far off from the way [15]. PAHs disrupt the growth and development of plants, which eventually reduces the overall biological activity in the ecosystem. This reduced activity also restricts productivity. Given their lipophilic nature, PAHs are deposited particularly in the double layer of membranes in plants. Plants that grow in regions with high levels of PAHs in the soil and air also contain high levels of PAHs [6, 16–18]. Thus, plants can be used to

#### *Animal Husbandry*


#### **Table 1.**

*Polycyclic aromatic hydrocarbon compounds evaluated as priority pollutants [13].*

detect environmental pollution with PAHs. This also indicates that plants serve as a point of entry for PAHs into the food chain [17]. PAHs enter the human body either by the consumption of contaminated plants or by the consumption of products from animals fed on contaminated plants [1, 8].

Moreover, environmental factors may also cause the contamination of oilseeds with PAHs, such that these compounds pass into vegetable oils during the processing of oilseeds [19]. The European Food Safety Authority (EFSA) has pointed out to meat and meat products as another important source of the daily exposure of consumers to PAHs. The level of PAHs produced in meat and meat products varies with the fat content and oxygen concentration of meat, the type and temperature of the heat source used for processing, the distance maintained between the food product and heat source and the duration of processing. The direct contact of food with flames, extended heat treatment and high temperatures during processing particularly increase PAH levels [2, 10].

A previous study on the synergistic toxicity of PAHs with other pollutants investigated the combined effects of fly ash and sulphur dioxide (SO2) on cucumbers. It was observed that neither fly ash nor sulphur dioxide showed effect alone, but when combined, the two caused severe chlorosis, which is a plant disease that manifests as the yellowing of leaves [20]. As a result, the active organic substances found in fly ash were claimed to be PAHs [17].

#### **3.3 The effects of PAHs on human and animal health**

The significant role of environmental factors in the development of cancer, one of the major diseases of the modern day, has been well acknowledged. Chemicals originating from hazardous substances, including industrial wastes, flue gases, litter, pesticides and tobacco smoke, pollute the environment, and by contaminating

#### *Polycyclic Aromatic Hydrocarbons (PAHs) and Their Importance in Animal Nutrition DOI: http://dx.doi.org/10.5772/intechopen.101816*

air, water, soil and food, these chemicals threaten human health [4]. PAHs, including sulphur dioxide, pesticides, insecticides and nitric oxide, are carcinogenic and toxic to humans [9].

The toxicity of PAHs is not related to molecular size, but rather to the chemical structure of molecules. Generally, a carcinogenic effect is induced by the binding of PAH metabolites to deoxyribonucleic acid (DNA) [11, 12]. Once having entered the human body, PAHs cause DNA mutation. It is considered that benzo[a]anthracene and benzo[a]pyrene are particularly carcinogenic to animals and humans, respectively; thus, they are used as model compounds in cancer research [21, 22]. To exemplify, upon exposure to tobacco/cigarette smoke, benzo[a]pyrene diol epoxide adducts bind covalently to several guanine positions of the DNA p53 gene in the bronchial epithelial cells and cause cancer-inducing mutations.

Due to the potential danger posed by PAHs, food and environmental contamination risks are of high importance for human health. The fumes of fossil fuels, tobacco smoke, fruits, vegetables, bread, cereals, meat, processed and salted products and milk all contain PAHs. Moreover, the grilling or high-temperature cooking of meat and other food products increases the level of PAHs in food [4, 23]. As PAHs are generated in the form of a complex mixture of compounds, humans are most likely to be exposed to multiple PAHs at the same time. The amount of PAHs entering the human body may vary with eating, drinking, dermal contact with contaminated material and the presence of other chemical substances [24]. PAHs may enter all body tissues that contain fat. In the human body, fat is mainly deposited in the kidneys and liver. Small amounts of fat are also deposited in the spleen, ovaries and adrenal glands [4].

In order to eliminate PAHs, the human body renders them water-soluble, and this process, which involves oxidative metabolism, generates highly productive diol epoxide derivatives. These diol epoxide derivatives chemically react with DNA. Eventually, the chemical binding of PAHs to DNA causes cancer [25]. Furthermore, biological research on the placenta has shown that PAHs cause predisposition to the lung, liver, nervous system and lymphatic tissue tumours in children [3, 26]. Low IQ and childhood asthma have been reported to be associated with prenatal exposure to high levels of PAHs [27]. The Centre for Children's Environmental Health has reported that exposure to PAH pollution during pregnancy may result in adverse effects, leading to preterm labour, cardiovascular anomalies and low birth weight [12]. It is indicated that, upon PAH exposure, cancer-induced DNA damage is detected in the umbilical cord blood of babies, which may be followed by growth retardation and behavioural disorders that may increase between 6 and 8 years of age [27]. In view of these data, EFSA has stated that these compounds are potentially genotoxic and carcinogenic to humans and constitute a priority group for the assessment of health risks [12, 28].

Experimental studies on PAHs have demonstrated that animals known to have suffered from short- and long-term exposure to PAHs present with body fluid disturbances, immunity disorders and cancer of the urinary bladder, skin and lungs [4]. Following the subcutaneous and intraperitoneal injection of benzo[a]pyrene to newborn mice throughout the first 15 days after birth, it was observed that liver and lung tumours developed within a period of six months [29]. Pregnant mice exposed to very high levels of benzo[a]pyrene have been reported to display dystocia, low birth weight and other pregnancy-related problems [3, 4]. Furthermore, it is indicated that nitro-PAHs cause leukaemia and tumours of the colon and milk glands [30]. In several other research studies conducted in animals, it has been reported that exposure to PAHs, within a time frame extending from foetal development to adulthood, is highly associated with cancer development [3, 4, 26].

#### **3.4 Previous research on PAHs**

In a study conducted by Gutiérrez and Vega [1] in industrial farms located near industrial sites, the primary PAHs detected in cow's milk were reported as acenaphthene (Ace) (0.25 mg/g−1), acenaphthylene (Acy) (0.32 mg/g−1) and fluoranthene (Fla) (0.22 mg/g−1). The most probable sources of these compounds have been suggested as contaminated grass and fuel combustion. The study reported that the milk concentrations of the 16 different PAHs detected did not exceed the dietary intake level set by the United States Environmental Protection Agency (USEPA) (25 mg/g−1) and suggested that the pollutants posed a limited health risk to the animal and human populations in the study location.

Bechtel and Waldner [8] investigated the correlation between the immune functions of an annual beef cattle population, atmospheric levels of polycyclic aromatic hydrocarbons and PM10 oil and natural gas facilities. By analysing blood samples collected from beef cattle, the researchers determined the potential correlation between exposure to atmospheric fine particles (particles of 1 μm diameter or PM10), polycyclic hydrocarbons and immune system functions. They placed herds of the annual beef cattle population at various distances to the industrial facilities located in areas producing large amounts of oil and natural gas. The researchers assessed immune system sufficiency, based on levels of B-lymphocytes and subtypes of T-lymphocytes (CD4, CD8 and WC1) in peripheral blood (n=469) and systemic antibody levels produced in response to vaccination (n=469). In this study, the mean PAH levels detected in the ambient air the animals breathed were low, and those measured at the highest levels were naphthalene (geometric mean 5.6 ng/m3 ; geometric standard deviation 38) and 1-methylnaphthalene (geometric mean 2.2 ng/m3 ; geometric standard deviation 12). The researchers reported not to have detected any statistically significant correlation between exposure to any of the pollutants detected in the ambient air and the immune system functions of the animals.

In another study investigating the level of exposure of dairy cattle and fattening pigs to PAHs, samples taken inside and outside the pens, in which the animals were housed, were analysed. The results of the study showed that the exposure level of the dairy cattle to PAHs was 86 times higher than the exposure level of the fattening pigs and revealed the main source of PAHs as feed for both species. The same study reported that the share of PAH intake, by means of water consumption and inhalation, in the total PAH load was negligible (**Table 2**) [31].


#### **Table 2.**

*PAHs contamination from cows and pigs barns [31].*

*Polycyclic Aromatic Hydrocarbons (PAHs) and Their Importance in Animal Nutrition DOI: http://dx.doi.org/10.5772/intechopen.101816*

In their research investigating the presence of PAHs in the tissues and internal organs of pigs and cattle, Ciganek and Neca [32] analysed specimens taken from the liver, lungs, kidneys, eyeballs (lens and vitreous body), muscles and fat tissue. Analyses revealed the presence of PAHs in the following internal organs and tissues of pigs and cattle at the indicated levels in ng/g, respectively: liver (3.8, 2.7), lungs (4.6, 5.4), kidneys (5.4, 6.3), fat tissue (0.05, 0.11), muscle tissue (3.6, 5.1), lens (57.9, 16.3) and vitreous body (14, 6.4). The most common PAHs detected in the specimens were phenanthrene, pyrene, naphthalene and fluorenone. As a result, in this study, no statistically significant difference was observed between the PAH levels detected in the organ and tissue samples of the pigs and cattle. However, the PAH levels detected in the tissue samples of animals of the same species housed in the same pen were found to significantly differ.

In the studies carried out to reduce the contamination of PAHs in the soil, there are also results that alfafa, ryegrass and Juncus subsecundus plants reduce the concentration of pyrene and phenanthrene compounds in the soil [33–35].
