Polycyclic aromatic hydrocarbons in water. Polycyclic aromatic hydrocarbons: chemical structure, formation processes and effects on the human body

These hazardous compounds are among the most important priority air pollutants (water and soil). They enter the atmospheric air during various combustion processes and with the exhaust gases of motor vehicles (anthracene and benzo[a]pyrene) were contained in more than three-quarters of the surveyed houses.

4. PAH expertise for the environment

On the environmental hazard scale from 0 to 3 shown in Figure 3 above, polycyclic aromatic hydrocarbons score 1.5. Level 3 represents a very high environmental hazard, and level 0 represents a minor hazard. Factors to be considered include assessing the degree of toxicity or non-toxicity of a substance, measuring its ability to remain active in the environment, and its ability to accumulate in living organisms. The release of the substance is not taken into account. It is reflected in the level of NPI for that substance. One of the substances rated as high hazard to the environment is nitric oxide (3) and one of the substances rated as low hazard is carbon monoxide (0.8).

5. Toxicity of PAHs for humans

The toxicity of PAHs is very dependent on the structure, even isomers can be both non-toxic and extremely toxic. Thus, highly carcinogenic PAHs can be small (less than 3 rings) or large (more than 4 rings). One PAH, benzo[a]pyrene, is the first known carcinogen and is one of the many carcinogens found in cigarettes. Seven PAHs have been classified as probable human carcinogens: benzo[a]anthracene, benzo[a]pyrene, benzo[b]fluoranthene, benzo[k]fluoranthene, chrisen, dibenz[a,h]anthracene, and indenopyrene.

PAHs known for their carcinogenic, mutagenic, and teratogenic properties: benz[a]anthracene and chrysene, benzo[b]fluoranthene, benzo[j]fluoranthene, benzo[k]fluoranthene, benzo[a]pyrene, benzopyrylene, coronene, dibenzanthracene, indenopyrene and oval (Fetzer, D.K. (2000), Lach, A (2005)).

Due to the lack of representative mixtures of PAHs for research purposes, the impact of biological and non-biological modifiers on PAH toxicity and metabolism is not yet well understood.

The following safety criteria have been proposed for total PAHs, carcinogenic PAHs and benzo(a)pyrene for drinking water and air and for total PAHs and benzo(a)pyrene in food: 0.01 to<0,2 мкг общих ПАУ/л, <0,002 мкг канцерогенных ПАУ/л и 0,0006 мкг бензо(а)пирена /л; воздух: < 0,01 мкг общих ПАУ/м 3 , <0,002 мкг канцерогенных ПАУ/м 3 и 0,0005 мкг бензо(а)пирена/м 3 ; пища: 1,6 до < 16,0 мкг общих ПАУ ежедневно и 0,16 до < 1,6 мкг бензо(а)пирена ежедневно.

6. Application of PAHs

Many PAHs are not used in principle. But some are used in medicine, for the production of paints, plastics and pesticides. Naphthalene, also known as mothballs, is used in the manufacture of dyes, explosives, plastics, lubricants, and mothkillers. Anthracene is used in paints, insecticides, and wood preservatives.

Conclusion

From the above review, it is obvious that, despite some usefulness of PAHs, their environmental and toxicological hazard is a matter of acute concern and their concentration in the environment should be greatly reduced, and in the best case, they should be completely eliminated from it.

List of sources used

1.https://ru.wikipedia.org

2. Edwards N.T. 1983. Polycyclic aromatic hydrocarbons (PAHs) in the terrestrial environment - a review. Environmental Quality Journal 12.427-441.

3. Isman G. A., Davani B., and Dodson D. A. 1984. Hydrostatic testing of gas pipelines as a source of PAHs in the aquatic environment. International Journal of Environmental Chemical Analysis. 19:27-39.

4. http://jurnal.org/articles/2009/ekol2.html

5. Isler R (1987) Effects of polycyclic aromatic hydrocarbons on fish, wildlife and invertebrates: A synoptic review.

6. US Fish and Wildlife Service, Patuxent Wildlife Research Center. Laurel. EPA. 1980. Water quality in terms of polycyclic aromatic hydrocarbon content. US Environmental Protection Agency. 440/5-80-069.193.

7. Fetzer DK (2000) Chemistry and analysis of heavy polycyclic aromatic hydrocarbons. New York. Willey.

8. Lee SD, Grant L. 1981. Health and environmental assessment of polycyclic aromatic hydrocarbons. Publishing house Patoteks. Forest South Park, Illinois. 364 p.

9. Lach A. (2005). Carcinogenic effect of polycyclic aromatic hydrocarbons. London: Imperial College Press, ISBN 1-86094-417-5.

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Currently, polycyclic aromatic hydrocarbons (PAHs) have more than 200 representatives that are strong carcinogens and, including their derivatives, belong to the largest group of known carcinogens, numbering more than 1,000 compounds.

The most active carcinogens include 3,4-benz(a)pyrene, which was identified in 1933 as a carcinogenic component of soot and tar, as well as cholanthrene, perylene, dibenz(a)pyrene, and dibenz(a,p)anthracene. Below are the structural formulas of the most carcinogenic PAHs.

Benz(p)fluoranthene is classified as a moderately active carcinogen. Less active are benz (e) pyrene, benzo (a) anthracene, dibenz (a, c) anthracene, chrysene, in-deno (1,2,3-cc1) pyrene, etc. Low-toxic PAHs include anthracene, phenan-tren , pyrene, fluoranthene, the structural formulas of which are presented below.

Some of the PAHs are mutagenic, for example, fluoranthene, perylene.

It is interesting that all these compounds have a "deepening" in the structure of the molecule, the so-called "Bay" - an area characteristic of many carcinogenic substances.

The main mechanism of their carcinogenic action is the formation of compounds with DNA molecules. There is an idea of ​​a multi-stage process of carcinogenesis involving polycyclic aromatic hydrocarbons, during which the initialization of the process of carcinogenesis occurs first, and then the initialized cells turn into malignant ones.

PAHs are widely distributed in the environment. Carcinogenic PAHs are formed in nature by abiogenic processes; Thousands of tons of benzo(a)pyrene of natural origin enter the biosphere every year. Even more - due to man-made sources. PAHs are formed in the combustion of petroleum products, coal, wood, garbage, food, tobacco, and the lower the temperature, the more PAHs are formed. Representatives of this group of compounds are found in engine exhaust gases, tobacco and smoke smoke.

Carcinogenic activity of real combinations of polycyclic aromatic hydrocarbons is 70...80% due to benzo(a)pyrene. Therefore, the presence of benzo(a)pyrene in food products and other objects can be used to judge the level of their contamination with PAHs and the degree of oncogenic danger to humans.

PAHs are extremely stable in any environment, and if they are systematically formed, there is a danger of their accumulation in natural objects. Benz(a)pyrene accumulated in the soil can pass through the roots into plants, that is, plants are polluted not only by dust settling from the air, but also through the soil. Its concentration in the soil of different countries varies from 0.5 to 1,000,000 µg/kg. The accumulation of PAHs in soils is associated with the processes of transformation of organic substances and their transfer from technogenic sources.

Different concentrations of benzo(a)pyrene were found in water depending on pollution: in groundwater - 1...10 µg/m3, in river and lake waters 10...25 µg/m3, in surface water - 25...100 µg/m3. m.

MPC of benzo(a)pyrene in the atmospheric air is 0.1 μg/100 m3, in the water of reservoirs - 0.005 mg/l, in the soil - 0.2 mg/kg.

Benz(a)peren enters the human body not only from the external environment, but also with food products in which the existence of carcinogenic hydrocarbons was not expected. It is found in bread, vegetables, fruits, vegetable oils, as well as roasted coffee, smoked meats and meat products roasted on charcoal. Its content significantly depends on the method of technological or culinary processing of raw materials and food products and the degree of environmental pollution.

In food raw materials obtained from environmentally friendly plants, the concentration of benzo (a) pyrene is 0.03 ... 1.0 μg / kg. Thus, grain samples in areas remote from industrial enterprises contain, on average, 0.73 µg/kg of benzo(a)pyrene, and grain samples in industrial areas contain 22.2 µg/kg. Apples from non-industrial areas contain 0.2 ... 0.5 μg / kg of benzo (a) pyrene, near roads with heavy traffic - up to 10 μg / kg.

Heat treatment significantly increases its content: up to 50 mcg/kg and more. Polymeric packaging materials can play an important role in food contamination with PAHs. So, milk fat extracts up to 95% of benzo (a) pyrene from paraffin paper bags or cups.

Table 3.16. The content of benzo(a)pyrene (in µg/kg) in various foods

The formation of carcinogenic hydrocarbons can be reduced by proper heat treatment. With proper roasting of coffee beans, 0.3--0.5 μg / kg of benzo (a) pyrene is formed, and in coffee surrogates - 0.9 ... 1 μg / kg, along with other polycyclic compounds. In a burnt crust of bread, the content of benzo(a)pyrene rises to 0.5 μg/kg, and in a burnt biscuit, to 0.75 μg/kg. When meat is fried, the content of benzo(a)pyrene also increases, but only slightly. Strong contamination of products with polycyclic aromatic hydrocarbons is observed when processing them with smoke. About 30 different representatives of PAHs have been identified in smoke smoke.

Fruits and vegetables contain benz (a) pyrene on average 0.2 ... 150 μg / kg of dry matter. Washing removes together with dust up to 20% of polycyclic aromatic hydrocarbons. A small part of hydrocarbons can be found inside fruits.

With food, an adult receives 0.006 mg/year of benzo(a)pyrene. In heavily polluted areas, this dose increases by 5 or more times. The content of benzo(a)pyrene (in μg/kg) in various food products is presented in Table. 3.16.

To minimize the content of carcinogens in food, the main efforts should be directed to the creation of such technological methods of storage and processing of food raw materials that would prevent the formation of carcinogens in food or exclude contamination by them.

INTRODUCTION

Polycyclic aromatic hydrocarbons (PAHs) belong to the group of persistent organic pollutants. They have pronounced carcinogenic properties. One of the most dangerous representatives of PAHs is benzo(a)pyrene (BP).

Benz (a) pyrene was discovered in 1933, later, in 1935, studies were carried out confirming its carcinogenicity. Today, benzo(a)pyrene is classified as a carcinogen of the 1st hazard class. It has mutagenic properties. Even a small concentration of BP negatively affects the human body. The concentration of BP in the air exceeding the maximum allowable concentration (MAC) with prolonged exposure can cause lung cancer. Therefore, the problem of its detection and definition is acute. Based on its physicochemical properties, a number of similar methods for its determination were developed, differing only in the stages of sampling and sample preparation. The purpose of my work was to get acquainted with the properties of PAHs and BP, to study methods for separating PAHs and methods for determining BP.

LITERATURE REVIEW

Polycyclic aromatic hydrocarbons (PAHs)

General information

PAHs are high-molecular organic compounds of the benzene series, numbering more than 200 representatives. They contain from 2 to 7 benzene rings. PAHs are widely distributed in nature and are stable over time. They have carcinogenic and mutagenic activity. Due to their toxicity and carcinogenic properties, they are classified as priority pollutants. The determination of PAHs is used in ecological and geochemical studies. The most toxic of them are 3, 4-benz(a)pyrene and 1, 12-benzperylene, which are especially often determined in environmental objects.

This class of organic compounds is one of the most active carcinogens in tobacco smoke. Polycyclic aromatic hydrocarbons cause DNA damage and destroy its structure. DNA repair processes play a decisive role in maintaining the genetic homeostasis of cells, causing their normal growth and reproduction. Hereditary differences in DNA repair systems may determine different individual susceptibility to tobacco smoke carcinogens, although this assumption still lacks a sufficient evidence base. However, it has been established that the genetic polymorphism of enzyme systems that activate and detoxify the chemical ingredients of tobacco smoke determines the degree of sensitivity of the body to carcinogenic effects.

DNA damage induced by polycyclic aromatic hydrocarbons results in mutations leading to malignant transformation of cells and the development of tumors. At present, DNA adducts with these chemical compounds have been found in many somatic cells of the human body exposed to tobacco smoke. At the molecular level, it has been proven that polycyclic aromatic hydrocarbons cause mutations in the p53 gene, which plays a key role in tobacco carcinogenesis in the lungs. The mutant P53 protein, in contrast to the wild-type P53 (wt P53), exhibits the properties of an oncogene product. It does not have the ability to block cell division with damaged DNA in the G 1 phase of the cell cycle. As a result, cells begin DNA replication on a damaged template, which leads to genome instability and increases the likelihood of malignant transformation.

Long-term smoking stimulates not only the expression of mutant P53, but also the production of insulin-like growth factor-1 (IGF-1), in particular, due to enhanced hydrolysis of its binding proteins. Activated IGF receptors are known to be involved in anti-apoptotic signal transduction. Cells lacking wt P53 are resistant to apoptosis induction. Enhancement of signal transduction triggers the process of malignant transformation of cells, contributing to both the initiation and promotion of tumor growth.

However, the potentially carcinogenic ingredients in tobacco smoke affect not the entire population, but only that part of it that is predisposed to mutations. After hydroxylation with arylhydrocarbon hydroxylase, polycyclic aromatic hydrocarbons of tobacco smoke form active epoxides, which are powerful mutagens and carcinogens. Their carcinogenicity depends, on the one hand, on the activity of epoxide-forming enzymes (arylhydrocarbon hydroxylase, etc.), on the other hand, on the activity of enzyme systems that decompose epoxides. Humans are characterized by wide variability in the induction of arylhydrocarbon hydroxylase synthesis. According to the rate of hydroxylation of polycyclic aromatic hydrocarbons in the body, three phenotypes: homozygotes with a high level of the enzyme, homozygotes with a low level of the enzyme and heterozygotes (intermediate type) with an average level of the enzyme. Determined that up to 30% of lung cancer patients have high levels of arylhydrocarbon hydroxylase although it is very rare in the general population. Given the association of this phenotype with lung carcinogenesis, smokers with a high level of induction of arylhydrocarbon hydroxylase synthesis are advised to stop smoking immediately. They are among those who have an extremely high risk of developing lung cancer due to smoking.

Women who smoke are more sensitive to induce DNA damage than male smokers. Thus, the risk of developing lung cancer in women who smoke, who received estrogen replacement therapy in menopause, is 2-2.5 times higher than in women of the same age who did not take sex hormones. The genotoxic effect of the combination of estrogens and tobacco smoke is also thought to be responsible for the higher incidence of bladder cancer in female smokers compared to male smokers with the same number of cigarettes smoked.

Modern molecular genetic methods have made it possible to establish have a genetic predisposition to bladder cancer. It is associated with mutations at the liver N-acetyltransferase locus. Under the action of this enzyme, chemical compounds foreign to the body are acetylated and excreted from the body. According to the rate of acetylation, three phenotypes are also distinguished: fast(homozygotes for normal allele) slow(homozygotes for the mutant allele) and intermediate(heterozygotes) acetylators. Bladder cancer often develops in slow acetylators. But for the manifestation of a gene mutation, the participation of an external environmental factor is necessary. Such a resolving factor that determines the implementation of a genetic predisposition to bladder cancer is smoking. It significantly increases the risk of developing bladder cancer in smokers of both sexes. One of the components of tobacco tar is 4-aminobiphenyl recognized as an organ-specific bladder carcinogen. DNA adducts with this chemical compound have been found in the bladder cells of smokers.

Benzopyrene and other polycyclic aromatic hydrocarbons ( benzanthracene, benzfluorentene, benzpyrylene, benzphenanthrene etc.) cause cancer of the oral cavity, upper respiratory tract, lungs, organs of the genitourinary system. Benzopyrene metabolites and the corresponding DNA adducts were found in the cells of the mucous membrane of the cervix of the uterus of smoking women.

The implementation of the action of carcinogens and the development of malignant tumors also contribute to many components of tobacco smoke with cocarcinogenic activity. These include hydrogen sulfide, sulfur dioxide, carbon sulphide, nitrogen oxides, formaldehyde, hydrogen cyanide, furan, phenolic solids tobacco smoke, especially pyrocatechins, as well as pyrene, fluoranthene and others. Some phenols ( catechol, cresol, guaiacol, hydroquinone, naphthol) are carcinogenic and cocarcinogenic. Tobacco smoke also contains a human carcinogen vinyl chloride and animal carcinogens hydrazine, urethane, formaldehyde.