Introduction to ENVIRONMENTAL TOXICOLOGY Impacts of Chemicals Upon Ecological Systems - CHAPTER 6

CHAPTER 6 Factors Modifying the Activity of Toxicants Just as there are a large number of pollutants in our environment, so are there many factors that affect the toxicity of these pollutants. The major factors affecting pollutant toxicity include physicochemical properties of pollutants, exposure time, environmental factors, interaction, biological factors, and nutritional factors. The parameters that modify the toxic action of a compound are examined in this chapter. PHYSICOCHEMICAL PROPERTIES OF POLLUTANTS Characteristics such as whether a pollutant is solid, liquid, or gas; whether the pollutant is soluble in water or in lipid; organic or inorganic material; ionized or nonionized, etc., can affect the ultimate toxicity of the pollutant. For example, since membranes are more permeable to a nonionized than an ionized substance, a non-ionized substance will generally have a higher toxicity than an ionized substance. One of the most important factors affecting pollutant toxicity is the concentration of the pollutant in question. Even a generally highly toxic substance may not be very injurious to a living organism if its concentrations remain very low. On the other hand, a common pollutant such as carbon monoxide can become extremely dangerous if its concentrations in the environment are high. As mentioned earlier, exposure to high levels of pollutants often results in acute effects, while exposure to low concentrations may result in chronic effects. Once a pollutant gains entry into a living organism and reaches a certain target site, it may exhibit an action. The effect of the pollutant, then, is a function of its concentration at the locus of its action. For this reason, any factors capable of modifying internal concentration of the chemical agent can alter the toxicity. TIME AND MODE OF EXPOSURE Exposure time is another important determinant of toxic effects. Normally, one can expect that for the same pollutant the longer the exposure time the more detrimental the effects. Also, continuous exposure is more injurious than intermittent exposure, with other factors being the same. For example, continuous exposure of rats to ozone for a sufficient period of time may result in pulmonary edema. But when the animals were exposed to ozone at the same concentration intermittently, no pulmonary edema may be observed. The mode of exposure, i.e., continuous or intermittent, is important in influencing pollutant toxicity because living organisms often can recover homeostatic balance during an “off” phase of intermittent exposure than if they are exposed to the same level of toxicant continuously. In addition, organisms may be able to develop tolerance after an intermittent dose. ENVIRONMENTAL FACTORS Environmental factors such as temperature, humidity, and light intensity also influence the toxicity of pollutants. Temperature Numerous effects of temperature changes on living organisms have been reported in the literature (Krenkel and Parker 1969). Thermal pollution has been a concern in many industries, particularly with power plants. Thermal pollution is the release of effluent that is at a higher temperature than the body of water it is released in. Vast amounts of water are used for cooling purposes by steam-electric power plants. Cooling water is often discharged at an elevated temperature causing river water temperatures to be raised to such an extent that the water may be incompatible for fish life. Temperature changes in a volume of water affect the amount of dissolved oxygen (DO). The amount of DO present at saturation in water decreases with increasing temperature. On the other hand, the rate at which most chemical reactions occur increases with increased temperatures. Many enzymes have a peak temperature range. Above and below that range they are much more inefficient at catalyzing reactions. An elevated temperature leads to faster assimilation of waste and therefore faster depletion of oxygen. This depletion also adversely affects the ability of fish and other animals to survive in these heated waters. Additionally, subtle behavior changes in fish are known to result from temperature changes too small to cause injury or death. Temperature also affects the response of vegetation to air pollution. Generally, plant sensitivity to oxidants increases with increasing temperature up to 30°C. Soybeans are more sensitive to ozone when grown at 28°C than at 20°C, regardless of exposure temperature or ozone doses (Dunning et al. 1974). The response of pinto bean to a 20 and 28°C growth temperature was found to be dependent on both exposure temperature and ozone dose. Humidity Generally, the sensitivity of plants to air pollutants increases as relative humidity increases. However, the relative humidity differential may have to be greater than 20% before differences are shown. MacLean et al. (1973) found gladioli to be more sensitive to fluoride as relative humidity increased from 50 to 80%. Light Intensity The effect of light intensity on plant response to air pollutants is difficult to generalize because of several variables involved. For example, light intensity during growth affects the sensitivity of pinto bean and tobacco to a subsequent ozone exposure. Sensitivity increased with decreasing light intensities within the range of 900 to 4000 foot-candles (fc) (Dunning and Heck 1973). In contrast, the sensitivity of pinto bean to PAN (peroxyacyl nitrate), a gaseous pollutant, increased with increasing light intensity. Plants exposed to pollutants in the dark are generally not sensitive. At low light intensities, plant response is closely correlated with stomatal opening. However, since full stomatal opening occurs at about 1000 fc, light intensity must have an effect on plant response beyond its effect on stomatal opening. INTERACTION OF POLLUTANTS Seldom are living organisms exposed to a single pollutant. Instead, they are exposed to combinations of pollutants simultaneously. In addition, the effect of pollutants is dependent on many factors including portals of entry, action mode, metabolism, and others previously described above. Exposure to combinations of pollutants may lead to manifestation of effects different from those that would be expected from exposure to each pollutant separately. The combined effects may be synergistic, potentiative, or antagonistic, depending on the chemicals and the phys-iological condition of the organism involved. Synergism and Potentiation These terms have been variously used and defined but, nevertheless, refer to toxicity greater than would be expected from the toxicities of the compounds admin-istered separately. It is generally considered that, in the case of potentiation, one compound has little or no intrinsic toxicity when administered alone, while in the case of synergism both compounds have appreciable toxicity when administered alone. For example, smoking and exposure to air pollution may have synergistic effect, resulting in increased lung cancer incidence. The presence of particulate matter such as sodium chloride (NaCl) and sulfur dioxide (SO2), or SO2 and sulfuric acid mist simultaneously, would have potentiative or synergistic effects on animals. Similarly, exposure of plants to both O3 and SO2 simultaneously is more injurious than exposure to either of these gases alone. For example, laboratory work indicated that a single 2-h or 4-h exposure to O3 at 0.03 ppm and to SO2 at 0.24 ppm did not injure tobacco plants. Exposure for 2 h to a mixture of 0.031 ppm of O3 and 0.24 ppm of SO2, however, produced moderate (38%) injury to the older leaves of Tobacco Bel W3 (Menser and Heggestad 1966) (Table 6.1). Table 6.1 Synergistic Effect of Ozone and Sulfur Dioxide on Tobacco Bel W3 Plants Toxicants, ppm Duration, h 2 2 2 O3 SO2 0.03 — — 0.24 0.031 +0.24 Leaf damage, % 0 0 38 Many insecticides have been known to exhibit synergism or potentiation. The potentiation of the insecticide malathion by a large number of other organophosphate compounds is an example. Antagonism Antagonism may be defined as that situation in which the toxicity of two or more compounds present or administered together, or sequentially, is less than would be expected when administered separately. Antagonism may be due to chemical or physical characteristics of the xenobiotics, or it may be due to the biological actions of the chemicals involved. For example, the highly toxic metal cadmium (Cd) is known to induce anemia and nephrogenic hypertension as well as teratogenesis in animals. Zinc (Zn) and selenium (Se) act to antagonize the action of Cd. Physical means of antagonism can also exist. For example, oil mists have been shown to decrease the toxic effects of O3 and NO2 or certain hydrocarbons in experimental mice. This may be due to the oil dissolving the gas and holding it in solution, or the oil containing neutralizing antioxidants. TOXICITY OF MIXTURES Evaluating the toxicity of chemical mixtures is an arduous task and direct measurement through toxicity testing is the best method for making these determi-nations. However, the ability to predict toxicity by investigating the individual components and predicting the type of interaction and response to be encountered is tantamount. These mathematical models are used in combination with toxicity testing to predict the toxicity of mixtures (Brown 1968, Calamari and Marchetti 1973, Calamari and Alabaster 1980, Herbert and VanDyke 1964, Marking and Dawson 1975, Marking and Mauck 1975). Elaborate mathematical models have been used extensively in pharmacology to determine quantal responses of joint actions of drugs (Ashford and Cobby 1974, Hewlett and Plackett 1959). Calculations are based on knowing the “site of dosage”, “site of action”, and the “physiological system” which are well documented in the pharmacological literature. Additionally, numerous models exist for predicting mix-ture toxicity but require prior knowledge of pair-wise interactions for the mixture (Christensen and Chen 1991). Such an extensive database does not exist for most organisms used in environmental toxicity testing, precluding the use of these models. Simpler models exist for evaluating environmental toxicity resulting from chem-ical mixtures. Using these models, toxic effects of chemical mixtures are determined by evaluating the toxicity of individual components. These include the Toxic Units, Additive (Marking 1977), and the Multiple Toxicity Indices (Konemann 1981). These models, working in combination, will be most useful for the amount of data that is available for determining toxicity of hazardous waste site soil to standard test organisms. The most basic model is the Toxic Unit model which involves determining the toxic strength of an individual compound, expressed as a “toxic unit”. The toxicity of the mixture is determined by summing the strengths of the individual compounds (Herbert and Vandyke 1964) using the following model: = PS + QS (6.1) 50 50 where S represents the actual concentration of the chemical in solution and T50 represents the lethal threshold concentration. If the number is greater than 1.0, less than 50% of the exposed population will survive; if it is less than 1.0, greater than 50% will survive.A toxic unit of 1.0 = incipient LC50 (Marking 1985). Building on this simple model, Marking and Dawson devised a more refined system to determine toxicity based on the formula: Am + Bm = S (6.2) i i where A and B are chemicals, i and m are the toxicities (LC50s) of A and B individually and in a mixture, and S is the sum of activity. If the sum of toxicity is additive, S = 1; sums that are less than 1.0 indicate greater than additive toxicity, and sums greater than 1.0 indicate less than additive toxicity. However, values greater than 1.0 are not linear with values less than 1.0. To improve this system and establish linearity, Marking and Dawson developed a system in which the index represents additive, greater than additive, and less than additive effects by zero, positive, and negative values, respectively. Linearity was established by using the reciprocal of the values of S that were less than 1.0, and a zero reference point was achieved by subtracting 1.0 (the expected sum for simple additive toxicity) from the reciprocal [(1/S) – 1]. In this way greater than additive toxicity is represented by index values greater than 1.0. Index values representing less than additive toxicity were obtained by multiplying the value of S that were greater than 1.0 by –1 to make them negative, and a zero reference point was determined by adding 1.0 to this negative value [S(–1)+1]. Therefore, less than additive toxicity is represented by negative index values (Figure 6.1). A summary of this procedure is as follows: ... - tailieumienphi.vn