Polycyclic Aromatic Hydrocarbons
Polycyclic aromatic hydrocarbons (PAHs) are a class of organic, persistent pollutants. Their structure is compromised of multiple single or fused aromatic rings, which are rings of hydrogen atoms, carbon atoms, and delocalized electrons; electrons that are not bound to a single atom or covalent bond. This results in a stable structure and therefore, PAHs have high melting and boiling points. Consequently, they are found as a colorless, white, or pale yellow solid. Additionally, their persistent nature is a result of PAHs being lipophilic and having a low aqueous solubility.
PAHs can be traced back to one of two sources- natural sources or human sources. Examples of a natural source include volcanic eruptions, forest fires, and certain plant and bacterial processes. Examples of human sources include oil spills, fossil fuel emissions, cigarette smoke, grilled meats, and asphalt roads. Additionally, all PAHs manufactured within the commercial market to be used as an additive or diluent in preservatives, dyes, pigments, resins, and pharmaceuticals fall under this category. All of these sources can be divided into three categories; pyrogenic, petrogenic, and biological. A pyrogenic source is any source involving the high-temperature burning of organic substances with little or no oxygen. Sources that fall under this category include coal distillation, which is the turning of coal into coal tar and/or coke, the incomplete combustion of wood and coal in heating systems, and the incomplete combustion of vehicular motor fuel. Chrysene, a by-product of coal distillation consisting of four fused benzene rings, is an example of a pyrogenic PAH. A petrogenic source is a source that has to do with crude oil or crude oil products. Examples of this would be oil spills in freshwater or Oceanic ecosystems and underground tank spills. Benzokfluoranthene is an example of a petrogenic PAH. Lastly, a biological source includes PAHs that are released from vegetative decay from a plant or bacterial process. The fungus strain Muscodor Albus produces PAH Naphthalene as well as other volatile compounds for decomposition.
The number of PAH sources is especially concerning once noting that PAHs often lead numerous to health risks including cancer and poor fetal development. Since PAHs are lipophilic and are persistent pollutants, they can survive in lipid-based biological tissue, such as fat tissue, and accumulate. Combining this with the fact that a number of PAHs are carcinogenic; cancer-causing, mutagenic; causing an abnormal amount of DNA mutations, and genotoxic; causing damage to genetic information, PAHs can pose numerous health concerns.
Once a PAH enters the human body by either ingestion, inhalation, or dermal contact, its carcinogenicity and mutagenicity can only be activated by its metabolism. Cytochrome P450s (CYP) and epoxide hydrolase are two critical enzymes in the metabolic system of a PAH. CYPs activate the PAHs into optically active oxides and then the epoxide hydrolase turns the oxides into optically active dihydrodiols (diols). The CYPs then turn the diols into four optically active isoforms of diol-epoxides. These diol-epoxides are highly reactive towards DNA and form a series of stable DNA adducts, which are segments that connect DNA to a cancer-causing chemical. This process turns the PAH carcinogenic and mutagenic by introducing the adduct.
The site of induction is especially important when determining the toxicity of a PAH. High metabolic rates decrease the PAH levels in surrounding tissues. The body’s highest metabolic rate is found in the liver, and then the lungs, intestinal mucosa, skin, and kidneys. Consequently, inhalation and dermal contact are the most toxic routes of PAHs because they directly avoid the liver and instead go to the lungs and skin which have lower metabolic rates. This is why sources of PAHs that are ingested, such as grilled meats, are not as much of a health concern as PAH sources that can be inhaled such as fossil fuel emissions.
The number of health risks associated with PAHs increases with newborns. Since PAHs can pass the placental barrier, if a pregnant woman were to come in contact with PAHs, it could compromise the development of the fetus. This could cause stillborn births, cognitive impairment, decreased birth weight and fetal growth. Furthermore, this could still impact the fetus over the long run by having long-term health conditions during infancy, such as increased risk for infant mortality, asthma, obesity, respiratory diseases, and symptomatic bronchial inflammation, and even during adulthood, such as increased risk for cancer, high blood pressure, diabetes, and heart disease.
Although there are many preventative options and ways to identify PAHs, there are no treatment options for the increased health risks associated with contacting PAHs.
Polycyclic Aromatic Hydrocarbons