Harmful chemicals can enter the environment through various natural and/or anthropogenic activities, causing adverse effects on human health and the environment. There have been gradual changes in the composition of the atmosphere due to increased combustion of fossil fuels in the last century. Air pollutants such as carbon monoxide (CO), sulfur dioxide (SO2), nitrogen oxides (NOx), volatile organic compounds (VOCs), ozone (O3), heavy metals and respirable particulates (PM2.5 and PM10) differ in their chemical composition, Reactives differ in properties, emissions, decay times, and ability to spread over long or short distances. Air pollution has both acute and long-term effects on human health, affecting various systems and organs. These range from mild irritation of the upper respiratory tract to chronic respiratory and cardiovascular diseases, lung cancer, acute respiratory infections in children, chronic bronchitis in adults, exacerbation of existing cardiovascular and pulmonary diseases, and asthma attacks. Furthermore, short-term and long-term exposure is also associated with premature death and reduced life expectancy. A brief review of the effects of air pollutants on human health and their mechanisms of action is provided.
Although many physical activities (volcanoes, fires, etc.) can release various pollutants into the environment, the main cause of air pollution is anthropogenic activity. While harmful chemicals can be accidentally released into the environment, many air pollutants are released from industrial facilities and other activities and can have adverse effects on human health and the environment. By definition, an air pollutant is any substance that can harm people, animals, plants, or materials. With respect to humans, air pollutants can increase or contribute to mortality or serious illness, or pose a present or potential threat to human health. Determining whether a substance poses a health risk to humans is based on clinical, epidemiological, and/or animal studies that demonstrate that exposure to the substance has health effects. In the context of human health, “risk” refers to the probability that an adverse health effect will occur.
The main changes in the composition of the atmosphere are caused by the combustion of fossil fuels, which are mainly used for energy production and transportation. A wide variety of air pollutants have been reported, varying in chemical structure, reactivity properties, emissions, persistence in the environment, ability to be transported over long or short distances, and potential effects on human and/or animal health. However, they have some similarities and can be classified into four categories:
1. Gaseous pollutants (such as SO2, NOx, CO, ozone and volatile organic compounds).
2. Persistent organic pollutants (such as dioxin).
3. Heavy metals (lead, mercury, etc.).
4. Particulate matter.
Gaseous pollutants contribute significantly to atmospheric compositional variations and are mainly caused by the combustion of fossil fuels (Katsouyani, 2003). Nitrogen oxides are released as NO, which readily reacts with atmospheric ozone or radicals to form NO2. The most important anthropogenic sources are mobile and stationary combustion sources. Additionally, ozone is formed in the lower layers of the atmosphere through a series of reactions involving NO2 and volatile organic compounds, a process driven by sunlight. CO2, on the other hand, is a product of incomplete combustion. Its main source is also road traffic. Anthropogenic SO2 is produced by the burning of sulfur-containing fossil fuels (mainly coal and heavy oil) and the smelting of sulfur-containing ores, while its main natural sources are volcanoes and the oceans. The latter accounts for only 2% of total emissions. Finally, so-called volatile organic compounds (VOCs) are an important type of compounds derived from fuel combustion, combustion processes being the main emission source, especially for energy production and road transport. It is a class of compounds that includes organic species such as benzene. Most gaseous pollutants enter the body through breathing and mainly affect the respiratory system, but can also cause blood problems (CO, benzene) and cancer.
Persistent organic pollutants form a group of toxic chemicals. They persist in the environment for a long time, their effects increasing as they move up the food chain (bioaccumulation). These include pesticides as well as dioxins, furans, and PCBs. Generally, the collective term “dioxins” is used to cover polychlorinated dibenzodioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs), while polychlorinated biphenyls (PCBs) are called “dioxin-like compounds” and their toxicity. behave similarly to dioxins (Schecter et al., 2006). Dioxins are produced during complete combustion and whenever any material containing chlorine (such as plastic) is burned. Dioxins are released into the air and usually accumulate in the ground or water. However, they do not contaminate groundwater because they are insoluble in water.
Most dioxins in plants originate from air, dust, or pesticides, enter the food chain, and bioaccumulate due to their ability to bind stably to lipids. Heavy metals include simple metals such as lead, mercury, cadmium, silver, nickel, vanadium, chromium and manganese. These are natural components of the earth’s crust. They cannot be broken down or destroyed, can spread through the air, and eventually enter water and the human food supply. Furthermore, they enter the environment from a variety of sources such as combustion, wastewater discharge, and manufacturing facilities. Although in small quantities, they enter the human body, where they act as trace elements and are necessary to maintain normal metabolic reactions. However, at high concentrations (although relatively low), they can be toxic (Jarup, 2003). Most heavy metals are dangerous because they accumulate in the human body. Bioaccumulation means that the concentration of a chemical inside an organism increases over time compared to the concentration of the chemical in the environment. Compounds accumulate in an organism when their absorption and storage occurs more rapidly than their breakdown (metabolism) or excretion.
Particulate matter (PM) is a general term for a type of air pollutant consisting of a complex and diverse mixture of airborne particles of different sizes and structures, caused by various natural and anthropogenic activities (Poschl, 2005). The main sources of particle pollution are factories, power plants, waste incinerators, motor vehicles, construction activities, fires and, of course, wind-blown dust. Particles vary in size (PM 2.5 for aerodynamic diameter less than 2.5 mm and PM 10 for aerodynamic diameter less than 10 mm, respectively) and different categories are defined: ultrafine particles with aerodynamic diameter less than 0.1 mm, Fine particles with aerodynamic diameter less than 1 mm and coarse particles with diameter greater than 1 mm. Particle size determines where PM10 particles deposit in the airways: PM10 particles deposit primarily in the upper airways, while finer and ultrafine particles can reach the alveoli. To date, no single component has been identified that can explain the majority of PM effects. Parameters that play an important role in causing health effects include particle size and surface area, particle number and composition. PM can absorb and transmit different pollutants, so its composition varies. However, its main components are metals, organic compounds, substances of biological origin, ions, reactive gases and the carbon core of the particle. There is strong evidence that ultrafine and fine particles are more dangerous than larger (coarse) particles in terms of mortality, cardiovascular and respiratory effects. Furthermore, the presence of other organic components such as metal content, PAHs and endotoxins are the main causes of PM toxicity.
Humans are exposed to various air pollutants primarily through inhalation and swallowing, with skin contact being only a minor source of exposure. Since air pollution is the primary source of contamination of food and water, the primary intake of pollutants is often through ingestion (Throne, 1996). Harmful substances are absorbed through the gastrointestinal tract and respiratory tract, while many toxins are present in the systemic circulation and can accumulate in various tissues. Emission occurs to some extent through emissions (Madden and Fowler, 2000).
Sporadic air pollution events, such as the historic London Fog of 1952, and numerous short-term and long-term epidemiological studies have examined the effects of changes in air quality on human health. This is a consistent finding that air pollutants contribute to increased mortality and hospitalization (Bruncrieff and Holgate, 2002). Differences in the composition of air pollutants, the amount and duration of exposure, as well as the fact that people are usually exposed to mixtures of pollutants rather than individual substances, can have different effects on human health. Human health effects include nausea and difficulty breathing, skin irritation to cancer. These include birth defects, severe developmental delays in children, and reduced immune system activity, resulting in a variety of diseases. In addition, there are several susceptibility factors, such as age, nutritional status, and susceptibility to diseases. Health effects can be classified as acute, chronic (non-cancerous) and cancer effects. Epidemiological data and data from animal models indicate that primarily the cardiovascular and respiratory systems are affected. However, the function of many other organs may also be affected (Cohen et al., 2005; Huang and Ghio, 2006; Kunjali and Tager, 2005; Sharma and Aggarwal, 2005).
1. Respiratory system
Many studies have shown that high concentrations of any type of air pollution can affect the respiratory system. However, similar effects are seen after prolonged exposure to low concentrations of pollutants. Symptoms such as bronchoconstriction and dyspnea following irritation of the nose and throat, especially in asthma patients, are usually caused by sulfur dioxide (Balmes et al., 1987), nitrogen oxides (Kagawa, 1985) and some heavy metals such as arsenic, nickel or vanadium. Occur after exposure to high concentrations of metals. In addition, particles penetrating the alveolar epithelium (Ghio and Huang, 2004) and ozone can cause pneumonia (Uysal and Shapira, 2003). In patients with lung lesions or diseases, inflammation caused by pollutants worsens the condition. Furthermore, air pollutants such as nitrogen oxides increase susceptibility to respiratory infections (Cauhan et al., 1998). Finally, chronic exposure to ozone and some heavy metals reduces lung function (Rastogi et al., 1991; Tager et al., 2005), resulting in asthma, emphysema, and even lung cancer. Cancer may also occur (Kuo et al., 2006; Tager et al., 2005; Nowrot et al., 2006). Emphysema-like lesions have also been observed in rats exposed to nitrogen dioxide (Wegman et al., 2005).
2. Cardiovascular system
Carbon monoxide binds with hemoglobin, changing its structure and reducing its ability to carry oxygen (Badman and Jaffe, 1996). This reduced availability of oxygen can affect the function of various organs (especially organs with high oxygen consumption like the brain and heart), leading to decreased concentration, poor reflexes, and confusion. In addition to pneumonia, particulate matter also induce systemic inflammatory changes, which affect blood clotting (Rediker et al., 2004). Air pollution, which produces pulmonary inflammation and changes in blood clotting, can block blood vessels and cause angina and heart attacks (Vermilne et al., 2005). As a result of heavy metal pollution (particularly mercury, nickel and arsenic), symptoms such as tachycardia, hypertension and anemia due to hematopoietic inhibition have been observed (Huang and Ghio, 2006). Finally, epidemiological studies have linked dioxin exposure to increased mortality from ischemic heart disease, while heavy metals have also been shown to increase triglyceride levels in rats (Dalton et al., 2001).
3. Nervous system
The nervous system is mainly affected by heavy metals (lead, mercury, arsenic) and dioxin. Neurotoxicity has been observed following exposure to arsenic, lead, and mercury, resulting in neurological disorders with symptoms such as memory loss, sleep disorders, anger, fatigue, hand tremors, blurred vision, and slurred speech (Evan and Pamphlet , 1996; Ratnaik, 2003). Specifically, lead exposure causes damage to the dopamine system, glutamate system, and N-methyl-D-aspartate (NMDA) receptor complexes, which play important roles in memory function (Lasley and Gilbert, 2000; Lasley et al. al., 2001). Mercury also contributes to some nervous system cancers. Dioxins reduce nerve conduction velocity and impair intellectual development in children (Thomke et al., 1999; Walkowiak et al., 2001).
4. Urinary System
Heavy metals can damage the kidneys, including: B. Early tubular dysfunction manifested by increased secretion of low molecular weight proteins, leading to decreased glomerular filtration rate (GFR). In addition, they are associated with stone formation or nephrocalcinosis (Demek-Poprava and Savica-Kapusta, 2003; Jarup, 2003; Logman-Edham, 1997) and kidney cancer (Boffetta et al., 1993; Vamvakas et al., 1993). Are connected.
5. Digestive system
Dioxins cause hepatocellular damage (see discussion below on underlying cellular mechanisms of action) as well as gastrointestinal and liver cancers (Mandal, 2005), as evidenced by increases in certain enzymes in the blood (Kimbro et al., 1977).
It is very important to mention that air pollutants can also affect the developing fetus (Shell et al., 2006). Exposure to heavy metals, especially lead, increases the risk of miscarriage and poor fetal growth (premature birth, low birth weight). There is also evidence that parental lead exposure can cause congenital malformations (Bellinger, 2005) and damage to the developing nervous system, resulting in significant reductions in motor and cognitive abilities of the newborn (Garza et al., 2006). Dioxins have also been found to be transmitted from mother to fetus through the placenta. They act as endocrine disruptors and affect the growth and development of the fetal central nervous system (Wang et al., 2004). In this regard, TCDD is considered a developmental toxicant in all species studied.
The general cellular mechanism by which most air pollutants exert their harmful effects is their ability to act directly as pro-oxidants of lipids and proteins or as generators of free radicals, thereby inducing oxidative stress and inflammatory responses. (Menzel, 1994; Rahman and McEnany, 2000). Free radicals (reactive oxygen and nitrogen species) are harmful to cellular lipids, proteins, and nuclear or mitochondrial DNA, disrupting their normal function (Valkow et al., 2006). Furthermore, they can disrupt signaling pathways within the cell (Valkow et al., 2006). In eukaryotic aerobic organisms, including humans, free radicals are continuously generated during normal metabolism and in response to external environmental influences (radiation, cigarette smoke, metals, ozone, etc.). When the concentration of free radicals increases due to overload of the body’s defenses, a state of oxidative stress occurs. This oxidative state is associated with various degenerative diseases, such as: arteriosclerosis, heart attack, stroke, chronic inflammatory diseases (rheumatoid arthritis), cataracts, diseases of the central nervous system (Parkinson’s and Alzheimer’s), age-related diseases and finally cancer.
The toxic effects of heavy metals, in addition to causing oxidative stress, may also be due to their ability to replace various multivalent cations (calcium, zinc, magnesium), which act as charge carriers, mediators of catalytic reactions or structurally in protein maintenance forms. Act as elements. In fact, metals accumulate in cellular organelles and impair their functioning. For example, it has been observed that lead accumulation in mitochondria causes various changes such as inhibition of Ca2+ absorption, reduction of transmembrane potential, oxidation of pyridine nucleotides, and rapid release of accumulated Ca2+ (Chavez et al., 1987). . In addition, metals bind to proteins (Goering, 1993) and inhibit many enzymes, including mitochondrial enzymes (Rossi et al., 1993). Nucleic acid binding proteins are also involved, and it has been demonstrated that metals also bind to DNA and affect gene expression. For example, nickel enters the cell nucleus, interacts with chromatin, and represses the expression of genes such as tumor suppressor genes, thereby leading to carcinogenesis (Costa et al., 2003). Finally, some metals disrupt various voltage-gated and ligand-gated ion channels, resulting in neurotoxic effects. For example, lead N-methyl-D-aspartate (NMDA) receptors, subtypes of voltage- and calcium-gated potassium channels, cholinergic receptors, and voltage-gated calcium channels (Garza et al., 2006; Toscano and Gilarte, 2005).
Dioxins have a wide range of harmful effects (Birnbaum, 1994): they alter metabolism through the induction of various metabolic enzymes (e.g., CYP, glutathione transferase, tyrosine kinases, etc.), they interfere with hormonal regulation (e.g., estrogen , androgens, glucocorticoids, insulin, etc.), they alter homeostasis through growth factors (e.g., thyroid hormones) and Their receptors, as well as growth factors (e.g., EGF, TGFa, TNFa) and alter development and differentiation through disruption of their receptors. At the cellular level, dioxins interact with the aryl hydrocarbon receptor (AhR) (Schwartz et al., 2000). AhR contains a basic helix-loop-helix domain and functions as a transcription factor after nuclear translocation, thus facilitating the interaction of dioxin with DNA. The receptor-ligand complex binds to specific sites on DNA and alters the expression of a large number of genes. As far as cancer is concerned, it is clear from the above data that most of the pollutants play a vital role in the initiation, promotion and growth of cancer cells.
We come in contact with many types of pollutants in our daily life. As mentioned above, health effects vary depending on the type of pollutant, its concentration, duration of exposure, other pollutants present at the same time, and individual sensitivity.
As a result of increasing industrialization and the need for energy and automobiles, the burden on people living in cities is increasing. Work stress is also an important factor to consider. In the past decade, developed countries have come under increasing scrutiny of the health effects of air pollution, and more and better environmental monitoring data are needed to determine limit values. Furthermore, there is a need to strengthen efforts through appropriate measures to reduce people’s exposure to pollutants. To protect itself from potentially harmful effects from the environment, the human body is equipped with drug metabolizing enzymes or xenobiotic metabolizing enzymes (DME or XME). These enzymes play a central role in the biotransformation, metabolism, and/or detoxification of xenobiotics, which are a variety of pollutants. XME includes several enzymes such as cytochrome P450 (P450 or CYP), epoxide hydrolase, glutathione transferase, UDP-glucuronosyltransferase, sulfotransferase, NAD(P)H-quinone oxidoreductase 1, and aldo-ketoreductase. These enzymes are primarily involved in converting xenobiotics into more polar, water-soluble metabolites that can be easily excreted from the body. Finally, it should be noted that chemically reactive metabolites formed during metabolism are often just as harmful and therefore undergo additional metabolism to form inactive products. Thus, the end result of a compound modulating the detoxification enzyme system is a result of its effects on various metabolic pathways.
Many substances found in food are beneficial and protective, supporting health and the body’s own natural chelation mechanisms. These include nutrients with natural chelating properties, such as antioxidants, herbs, minerals, essential amino acids, other detoxification and protective agents, and fiber, which help detoxify the body (Kelly, 2004). Among them, dietary antioxidants contribute to the antioxidant defense system of the organism, including a variety of antioxidant enzyme-based compounds (e.g., peroxidases) and non-enzymatic compounds (e.g., food-derived compounds such as glutathione, vitamin E, and polyphenols). Contain, and protect and repair enzymes from damage.
Some natural compounds, such as vitamins C, E, A and polyphenols, found in most plant foods, destroy or remove intracellular ROS concentrations, thereby protecting the organism from the adverse effects of oxidative stress. In fact, our group has demonstrated that plasma antioxidant activity is increased in people consuming a diet rich in vegetables, fruits, and olive oil compared to a normal diet (Kampa et al., 2002). This increase is primarily due to polyphenols, which exhibit multiple biological activities, including antitumor, antimutagenic, anti-inflammatory, and antiviral activities (Bravo, 1998; Hertog and Hallman, 1996). They act by affecting basic cellular functions and have inhibitory effects. In fact, the positive role of polyphenols in cancer prevention can be partially attributed to their ability to modify enzymes that activate or detoxify environmental carcinogens.
In this brief overview, we present the adverse effects of several (air) pollutants on human health. As shown, significant damage was observed in various organs. The main conclusion is that, given increased human exposure to various pollutants, a diet rich in plant foods may protect or reduce the effects on various organs. This conclusion is supported by numerous epidemiological studies on the positive effects of the Mediterranean diet on human health.
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