329
sources from which PAHs can originate [6, 13, 14]. As they are semi-volatile in
nature and based on their molecular weights, PAHs may occur either in a particulate
or gaseous form in the environment [15]. Water and soil are predominantly contaminated due to atmospheric PAHs deposition, particularly in distant areas including
lakes located at high-altitudes [16–18], or the waste produced from industrial process which gain access to the water resources. In marine environment, noticeable
sources of PAHs are oil spills, which are deposited in sea as residues. Beside biological degradation, the fate of PAH in environment depends on various other factors, such as in air soil and water, PAH can go through photo-oxidation, photo and
chemical oxidation, respectively. Moreover, some PAHs, for example, naphthalene
and alkyl naphthalene, are moderately vanished by vaporization [19].
Exposure of Humans to ePAHs
Living organisms possibly exposed to environmental PAHs through multiple ways
result in various biological and social effects. Studies have shown relationship
between water and sediments contaminated with PAHs which induce cytochrome
P450 (CYP), elevate 7-ethoxyresorufin-O-deethylase (EROD) properties, damage
DNA, rupture lysosomal membrane, and cause endocrine and reproductive failure
in fish and invertebrates. Atmospheric and soil PAHs are also taken by the plants
which cause injuries to their leaves, reduce biomass, and various other harmful
biological and physiological effects. Moreover, soil microbial community composition is also influenced strongly by soil PAH contamination level. Humans become
exposed to ecological PAHs via PAH-contaminated diet intake including accidental
ingestion of dust and soil through hand-to-mouth behaviors, skin contact, and inhalation [20–22]. Epidemic studies have shown that from occupational environments,
PAHs heavy exposure elevates cancer development risks including skin, larynx,
lungs, and bladder cancers [23–25]. Cancer causing mechanism of PAHs is related
with their capability to produce reactive diol epoxide which is quickly catalyzed by
CYP, regulated through PAH exposure, and their consecutive binding covalently to
DNA [26–28]. PAHs in non-occupational settings have been considered as etiological agents for both cardiovascular and cardiopulmonary disorders. From both
in vitro and in vivo studies, it has been proposed that ROS (reactive oxygen species)
are associated with PAHs in ambient particulate matter, causing inflammatory
responses and oxidative stress, necessary for the occurrence and aggravation of
asthma and hypersensitive diseases. Moreover, long term exposure of low-dose
PAHs can cause immune-mediated pregnancy loss, and PAHs exposure in pregnancy affect fetal development including birth weight, size, length, and circumference of the head. It has been estimated that each gram of tobacco contains a total of
100 ng of PAHs, irrespective of the manufacturing industries [29], and from 20
cigarettes pack, a smoker inhales 0.26 lg of BaP [30]. Smokes from the vehicles and
household fire are the main sources of PAHs [11]. Barbecued, grilled, or smoked
19 Role of Polycyclic Aromatic Hydrocarbons as EDCs in Metabolic Disorders
sources from which PAHs can originate [6, 13, 14]. As they are semi-volatile in
nature and based on their molecular weights, PAHs may occur either in a particulate
or gaseous form in the environment [15]. Water and soil are predominantly contaminated due to atmospheric PAHs deposition, particularly in distant areas including
lakes located at high-altitudes [16–18], or the waste produced from industrial process which gain access to the water resources. In marine environment, noticeable
sources of PAHs are oil spills, which are deposited in sea as residues. Beside biological degradation, the fate of PAH in environment depends on various other factors, such as in air soil and water, PAH can go through photo-oxidation, photo and
chemical oxidation, respectively. Moreover, some PAHs, for example, naphthalene
and alkyl naphthalene, are moderately vanished by vaporization [19].
Exposure of Humans to ePAHs
Living organisms possibly exposed to environmental PAHs through multiple ways
result in various biological and social effects. Studies have shown relationship
between water and sediments contaminated with PAHs which induce cytochrome
P450 (CYP), elevate 7-ethoxyresorufin-O-deethylase (EROD) properties, damage
DNA, rupture lysosomal membrane, and cause endocrine and reproductive failure
in fish and invertebrates. Atmospheric and soil PAHs are also taken by the plants
which cause injuries to their leaves, reduce biomass, and various other harmful
biological and physiological effects. Moreover, soil microbial community composition is also influenced strongly by soil PAH contamination level. Humans become
exposed to ecological PAHs via PAH-contaminated diet intake including accidental
ingestion of dust and soil through hand-to-mouth behaviors, skin contact, and inhalation [20–22]. Epidemic studies have shown that from occupational environments,
PAHs heavy exposure elevates cancer development risks including skin, larynx,
lungs, and bladder cancers [23–25]. Cancer causing mechanism of PAHs is related
with their capability to produce reactive diol epoxide which is quickly catalyzed by
CYP, regulated through PAH exposure, and their consecutive binding covalently to
DNA [26–28]. PAHs in non-occupational settings have been considered as etiological agents for both cardiovascular and cardiopulmonary disorders. From both
in vitro and in vivo studies, it has been proposed that ROS (reactive oxygen species)
are associated with PAHs in ambient particulate matter, causing inflammatory
responses and oxidative stress, necessary for the occurrence and aggravation of
asthma and hypersensitive diseases. Moreover, long term exposure of low-dose
PAHs can cause immune-mediated pregnancy loss, and PAHs exposure in pregnancy affect fetal development including birth weight, size, length, and circumference of the head. It has been estimated that each gram of tobacco contains a total of
100 ng of PAHs, irrespective of the manufacturing industries [29], and from 20
cigarettes pack, a smoker inhales 0.26 lg of BaP [30]. Smokes from the vehicles and
household fire are the main sources of PAHs [11]. Barbecued, grilled, or smoked
19 Role of Polycyclic Aromatic Hydrocarbons as EDCs in Metabolic Disorders