by Dr. B. N. Filatov

Chemistry brought people a lot of useful things, at the same time stepping up the hazard to natural environment and public health. While the waste waters and sludge of chemical plants constitute an indirect threat, migrating from one environment into another, emissions into the atmosphere of gases, aerosols, and suspended non-soluble particles very often produce a direct effect not only on the people working at this or that chemical plant, but on the population in general.

In most cases of any transport of chemicals in environment there is man at the end of it, while the harmful effect is determined by their toxicity and the volume of intake. That is why in assessing chemicals it is expedient to take into account not only their toxicity, but also their persistency in the environment and accumulation in the mammals organisms (Fig. 1).

In case of a single short-time emission of chemicals into the environment, the greatest danger of accumulation is presented by toxicants with the half life period of months or years. Thus, regular (operational) emissions of chemicals are a great threat in view of their accumulation in the environment. In this situation even the substances with the half life period of a few days can accumulate in the organisms of mammals and cause chronic intoxication.

To establish the chronic effects and delayed aftereffects of toxic chemicals they often use the epidemiological method. But it has certain limitations. Thus, in case of a combination of chemicals or their aggregation with other hazardous factors, objective quantitative assessment of environmental pollution and the cause-effect links is practically impossible. Epidemiological studies are often limited by the necessity of having a great enough number of cases, which means sickness of a significant part of a population. And what is more important, epidemiological studies cannot prevent the spreading of a disease, as the "exposure – disease" correlation is usually determined after the detrimental effect on health has manifested itself.

Of greater value, though of less reliability, is the prognostic risk assessment method developed by US scientists.

Surely, although risk assessment is valuable in predicting the possible development of a disease and the chances of a lethal outcome, it should not be done for its own sake. Such assessments should be made to determine the sources of risks and to minimize the risks. The key element in the risk concept is human health and its protection from risks stemming from the effect of toxic chemicals in the air, water, soil of food.

Risk is the rate of occurrence of a certain hazard. Thus, carcinogenic risk may be interpreted as the rate or probability of malignant tumors formation, being the quantitative characteristic of a relative random value, used for the description of carcinogenic hazard. Risk is usually subdivided into individual and social (population).

Individual risk is the probability of a certain hazard appearing (e.g. malignant tumor formation under the exposure to a carcinogen) at a certain point in space, where the individual may be. Thus, individual risk characterizes the intensity of the hazard distribution.

Social risk is the rate of malignant tumors formation inside a certain number of people exposed to a specific hazard. Thus, social risk characterizes the scale (spread) of a specific hazard among a population living on a certain territory.

This is a comprehensive problem, so it can be disintegrated into separate fragments, starting from man as the object of exposure, to the source of hazardous chemicals.

Methodologically the simplest is the "breathing chain" assuming an outlet of chemicals into the atmospheric air in form of industrial emissions and their further penetration into human organism through the breathing organs. The key moment in such risk assessments is the admission of their dependency on numerous assumptions and judgments.

The procedure of risk assessment includes four stages:

The first stage is the identification of a hazard, including the selection of chemicals most hazardous for human health and the selection of industrial enterprises making the highest contributions from stationary emission sources.

The next stage is determining the type and levels of harmful effect on man. It is vital to determine the levels of exposure and the affected part of the population. To determine levels of exposure to atmospheric pollution indirect models were used with the calculation of diffusion variance. Chronic exposure is expressed in the chronic daily intake of a xenobiotic into human organism.

The third stage is the assessment of the "doze-response" effect and is aimed at establishing interrelations between the levels of exposure to pollutants and potentially unwelcome aftereffects.

We studied two types of such aftereffects - carcinogenic and general toxic effects. In assessing the first one we assumed no thresholds of the effect. The second was determined on assessing mortality in the result of prolonged (chronic) exposure to suspended solid (non soluble) particles less than 10 microns in diameter. We assessed only health hazards created by stationary sources of toxic emissions into the atmospheric air of Volgograd.

The main goal of the study was to demonstrate how the risk assessment methods recommended by the US Environmental Protection Agency can be adapted to the ways and methods of gathering information on pollution and the tools of atmospheric pollution modelling employed in Russia, as well as whether they are applicable to the assessment of health risks posed by stationary sources of atmospheric pollution with chemicals.

The choice of pollutants is determined, on the one hand, by the availability of an adequate methodology and, on the other, by the uneven atmospheric air pollution with these chemicals in Volgograd: industrial emissions of carcinogens are not typical for Volgograd, while big metallurgical and machine-building plants are a major source of suspended particles. Besides, suspended particles may be interpreted as indicators of pollution with accompanying chemicals - nitrogen and sulfur oxides, benzapyrene and others.

Upon analysis of gas emissions by the Volgograd industrial enterprises, in order to identify risks we chose 29 industrial enterprises with the summary volume of emissions equaling 80% of all the industrial emissions into the atmospheric air (Table 1). The emitted pollutants include 14 carcinogens.

To assess the carcinogenic risk and the risk of suspended particles, data on annual average concentrations of chemicals on the studied territory are needed. To obtain these values we used simulation methods officially recognized in Russia, such as the "Ecologist" model.

As risk assessment needs annual average values, and "Ecologist" produces results in 20-minute maximum concentrations, a special methodology was developed to convert the data into the needed format. Two factors were used. The first one was defined as the time of the plant operation during the year (as a fraction of "one"). The second factor reflecting continuity of emissions throughout the year was defined as the ratio of annual average emissions of the plant (annual total in t/year for all pollutants converted into average values in g/sec) to the maximum 20-minute specific emissions. Average annual concentrations C for each pollutant from each plant were calculated by the following formula:

C_i = a*wf1*wf2*d (1)

where:

a - is a standard 20-minute concentration in the point of the hazardous effect (according to the "Ecologist" model);

wf1 - is weight factor 1, representing the plant's operation time (as a fraction of one);

wf2 - is weight factor 2, representing continuity of the emission;

d - specific maximum emission of pollutant i.

At the next stage the exposure effect of the identified chemicals on man is determined. The primary task here is establishing the number of people exposed to toxic chemicals. We assumed this number of people for this project as equal to 1 million people. Population density varies significantly in the city: living quarters and industrial zones are sometimes located nearby.

Using the population density map we chose 20 points within the city. Each was representative of 5% of the city population, which is 50 000 people. Each point is located on the nearest cross-section of the dispersion model lines and is the center of a specific zone.

Next task was the identification of chemicals concentrations in the atmospheric air at the points of exposure (PE). Use of the dispersion models allowed us to establish the contribution of each plant into the pollution of the studied territory with account of the points of exposure.

The third stage (assessment of the "doze-effect" correlation) envisaged establishing correlation between the levels of pollutants and the probability of potential adverse effects (additional cases of malignant tumors and lethality).

Annual carcinogenic risk (K) was calculated for each PE, assuming the sum of daily average concentrations of all the registered potential carcinogens as constant throughout life, and taking into account the URF factor (mg/kg - day)^-1, which is the basis for the extrapolation on men of carcinogenic activity data (Table 2), established in experiments on animals (Table 3):

K_j = S (C_j*D*V*)UPFi/m*G (2)

K_j is the individual summary carcinogenic risk in PE;

C_j is concentration of carcinogens in PE_j;

D is the daily breathing volume (m3);

m is the body mass(kg);

G is average life span in years.

Thus we can calculate the individual average annual carcinogenic risk per one assumed inhabitant of each of the 20 PE. Multiplying the produced value by 50000 we get the average annual population carcinogenic risk for all the inhabitants of this PE. Summing up the data for all PEs, we get the annual average population carcinogenic risk (Kr) for the whole population of the city.

N Carcinogen Potential factor

1 benzene 0.029
2 benzapyrene 7.300
3 chlorobenzene 0.170
4 cadmium 6.100
5 hydrocarbon tetrachloride 0.053
6 chloroform 0.0817
7 chromium hexavalent 41.000
8 formaldehyde 0.045

9 nickel 1.190

10 vinyl chloride 0.095
11 polyvinyl chloride dust 0.095
12 benzapyrene sorbed on soot 7.300

The study suggests that the annual average population risk of tumors formation due to stationary atmospheric pollution sources in Volgograd is 13E-6. That is, if we assume that the atmospheric air pollution by carcinogens from stationary sources in Volgograd will stay at the same level as in 1995 for 70 years of life, each year we may expect 13 additional cases of tumor formation.

Soot Benzene Benzapyrene

PE C, Risk C, Risk C, Risk
mg/m3 mg/m3 mg/m3

1

7 4.696 0.035 0.661 0.0039 0.0001 0.0001
8 4.696 0.035 0.661 0.0039 0.0001 0.0001
9 4.696 0.035 0.661 0.0039 0.0001 0.0001
10 4.696 0.035 0.661 0.0039 0.0001 0.0001
11 9.393 0.070 1.322 0.0078 0.0002 0.0003
12 9.393 0.070 1.322 0.0078 0.0002 0.0003
13 9.393 0.070 1.322 0.0078 0.0002 0.0003
14 11.741 0.0875 1.653 0.0098 0.0002 0.0003
15 14.089 0.1049 1.984 0.0117 0.0002 0.0003
16 32.874 0.2449 4.628 0.0274 0.0006 0.0009
17 30.526 0.2274 4.298 0.0254 0.0005 0.0007
18 72.794 0.5422 10.249 0.0607 0.0013 0.0019
19 82.186 0.6122 11.571 0.0685 0.0014 0.0021
20 46.963 0.3498 6.612 0.0391 0.0008 0.0012

Nearest point 206.639 29.093 0.0036
Sum total 2.5188 0.2817 0.0089

According to medical statistics for 1993-1995, more than 6 thousand cases of malignant tumors were registered in Volgograd annually. The calculated 13 additional cases caused by stationary sources characterize, as expected, a comparatively low risk level. But it should be noted that the registered level was the result of accumulated dozes received by the population throughout the previous years of life with food and water, polluted with carcinogens, and the inhalation of xenobiotics in the years of worse atmospheric air pollution. In 1995, as in all other territories of Russia, the major industrial enterprises of Volgograd were in a state of industrial decline. That is why the risk assessment calculated by the 1995 emissions was surely underestimated.

With all the assumptions made, it should be noted that the new methodology, employed in Russia for the first time, allowed us to indicate the maximum risk region (Fig. 2), determine the maximum risk sources (Fig. 3) and state that the hazard from stationary sources of air pollution in Volgograd comes not from the widely acknowledged carcinogens, such as benzapyrene, nickel, chromium, but from vinyl chloride and hydrocarbon tetrachloride emitted by two big local chemical plants. Thus, industrial enterprises for the priority management of carcinogenic risk were identified.

Note: 3 - Drilling equipment plant

13 - "Chimprom" plant

27 - Volgograd aluminum works.

Solid particles, in particular, fractions less then 10 microns in diameter, were considered in this study as non-carcinogenic substances, having an expressed effect on the breathing organs and being indicators of atmospheric air pollution with associated gases (oxides of nitrogen, sulfur, hydrogen fluoride etc.) (See Table 4).

Name of substance Aluminum works Krasny Oktyabr

Aluminum oxide + -
Barium chloride + -
Vanadium pentoxide + -
Ferrous oxide + +
Manganese and its compounds + +
Sodium hydroxide + +
Soot + -
Fluorine non-organic compounds + -
Naphthalene + -
Anthracene + -
Phenanthrene + -
Pyrene + -
Stearin + -
Black oil ashes of TPP + -
Chromium hexavalent - +
Colophony - +

Non-organic dust (silicon dioxide) + +
Asbestos containing dust + -
Wood dust + +
Non differentiated dust + +

Lack of methodological tools for risk assessment in case of permanent habitation in conditions of expressed atmospheric air pollution with fine dust faced us with the task of developing principally new methods. We based our method of non carcinogenic risk assessment on the regularity found in US epidemiological studies, that is: with an increase in the concentration of the finely divided solid particles fraction by 10 mkg/m3 over the background value, lethality increases by about 1%. If we assume total population equal to 200 million people, and take into account the mortality level, the daily individual lethality risk under exposure to stable atmospheric pollution with suspended particles and accompanying toxic gases at the level of 10 mkg/m3 may be determined by the following formula:

S₁₀ = S*0.01/N*d = 2100000*0.01/250000000/365 = 2.3E^-7 (3)

N is population size;

d is period of exposure, number of days.

The individual annual ratio of lethality risk under constant atmospheric air pollution with suspended particles and accompanying toxic gases (S_PM10) at the level of 10 mkg/m3 will be:

S_PMlO = S₁₀*d = 8.4E^-5 (4)

Correspondingly, for a population of 50000 people living in any PE with such a pollution level, expected lethality value will be 4.2 a year with a linear increase in the number of lethal cases in case of higher atmospheric air pollution with solid particles. The study of hazardous effect of suspended particles in the atmospheric air and accompanying toxic gases let us determine that 85% contribution into the mortality risk in Volgograd due to the emission of toxic chemicals in 1995 was that of two industrial enterprises – "Krasny Oktyabr" and "Aluminum works" (Fig. 4). The spacial distribution of risk showed that the mortality risk due to the toxic emissions is centered round these two enterprises and makes a 60% contribution into the total risk assessment of Volgograd (fig. 5). Besides, our study determined that although the volume of solid particles emissions of "Chimprom" was in 1995 much higher than that of the aluminum works, the lethality risk was much higher with the aluminum plant emissions.

Note: 27 - Volgograd aluminum works

Thus, this methodology makes it possible to assess carcinogenic and non-carcinogenic population and individual risk from stationary sources of chemical pollutants, including those persistent in the environment. But the produced results characterize only that part of xenobiotics which enter human organisms with the direct inhalation of polluted air.

Persistent chemicals get into soil, plants, surface of buildings and structures, open water reservoirs and then enter human organism through ecological chains, accumulating within a long period of time and creating supplementary, and sometimes the main threat to human health. Thus, polychlorinated byphenils, dioxins, dibenzofurans, getting into soil, stay there for months and years, gradually fed from new sources of pollution.

Assessment of persistent chemicals transport along the ecological chains is surely based on a number of assumptions and conditions. But even a model with a large number of inderterminacies and conditions allows more or less accurate assessment of risk to human health, while nature studies (including monitoring) of pollution by persistent chemicals of different environments without mathematical modeling of the toxicant migration from environment to environment just state the momentary situation, as a rule not charting out any perspective.

Numerous mathematical models have been proposed for the assessment of chemicals migration in the environment. Most representative migration processes are produced by Makkoun Tomas E., Daniels Jeffry (1991). The assessment algorithms they produce are quite acceptable. But they view man as the final element in each analyzed chain, while intermediary links have to be clearly stated. Thus, to determine the quantity of pollutants in drinking water one may use the following algorithm:

H = C_w*F_ww (5)

where H is the total quantity of the substance consumed by man within his life time with drinking water in concentration C_w (mg/l);

F_ww is the factor of penetrating effect for the conversion of the chemical's concentration in water into the equivalent of the chronic daily doze (mg/kg-day), deduced from the equation:

F_ww = I_w / BM (6)

where I_w / BM is the consumption of drinking water per 1 kg of the body mass. The assessment of possible effects of soil pollution should be carried out with care. For example, let us take sedimentation of benzapyrene emitted into the atmosphere by local industrial enterprises of Moscow. For the city dwellers there is little danger of consuming this carcinogen with vegetables and fruit, as they are not locally grown. The situation in Volgograd is different as many people have vegetable gardens and fruit gardens within the city borders.

Thus, additional risk of health damage by persistent chemicals may and should be calculated on the basis of nature studies with the use of mathematical models.

Name N by CA 1 2 3 4 5 6 7 8 9 10

Compiled from: L. Kenworthy "A Citizen's Guide to Promotion Toxic Waste Reduction" N.Y., 1990

1 - carcinogenity 6 - chronic toxicity
2 - genetic and chromosome mutation 7 - neurotoxicity