EXPOSURE ACTION INDICATOR

Distortion Another problem with extrusions is caused by distortion of the section by the effect of heat and other environmental conditions such as exposure to water or chemical agents that tend to soften the plastic. These distortions are generally reversals of the profile back to the shape that it had exiting in the die. This action indicates that the post die forming operations were done at a lower than desirable temperature which results in a molded-in stress. When the stress is relieved the product distorts. In some instances these stresses cannot be eliminated by process changes so that the product is inherently deficient in performance. 

If one dose level of at least 1,000 mg/kg body weight (expected human exposure may indicate the need for a higher dose level), using the procedures described for this study, produces no observable toxic effects and if toxicity would not be expected based on data from structurally related compounds, a full study using three dose levels may not be necessary. A careful clinical examination should be made daily with appropriate actions taken to minimize the loss of animals, (e.g., by necropsy, refrigeration of animals found dead, or isolation and sacrifice of weak or moribund animals). 

A hypothetical example of the application of the methodology follows in Table 5.9. The relevant data from chemical risk assessments and socio-economic analyses are entered into three columns corresponding to hazard, exposure and social mobilisation. For each of the two substances, the first row characterises the relevant scenarios according to the regulatory action indicators from Table 5.7. The second row, which is shaded in grey, then describes the key parameters that influence the probabilities associated with each action indicator. The corresponding ratings for the action indicators and the probability of occurrence indicators are presented in bold italics. 

Where this is not reasonably practicable and the risk assessment indicates that an exposure action value is likely to be reached or exceeded, the employer shall reduce exposure as low as reasonably practicable by establishing and implementing a programme of organizational and technical measures which is appropriate. 

A disadvantage of adsorption indicators is that silver halides are sensitised to the action of light by a layer of adsorbed dyestuff. For this reason, titrations should be carried out with a minimum exposure to sunlight. When using adsorption indicators, only 2 x 10-4 to 3 x 10 3 mol of dye per mol of silver halide is added this small concentration is used so that an appreciable fraction of the added indicator is actually adsorbed on the precipitate. 

Several medical tests can determine whether you have been exposed to methyl parathion. The first medical test measures methyl parathion in your blood or measures 4-nitrophenol, which is a breakdown product of methyl parathion, in your urine. These tests are only reliable for about 24 hours after you are exposed because methyl parathion breaks down quickly and leaves your body. These tests cannot tell whether you will have harmful health effects or what those effects may be. The next medical test measures the levels of a substance called cholinesterase in your blood. If cholinesterase levels are less than half of what they should be and you have been exposed to methyl parathion, then you may get symptoms of poisoning. However, lower cholinesterase levels may also only indicate exposure and not necessarily harmful effects. The action of methyl parathion may cause lower cholinesterase levels in your red blood cells or your blood plasma. Such lowering, however, can also be caused by factors other than methyl parathion. For example, cholinesterase values may already be low in some people, because of heredity or disease. However, a lowering of cholinesterase levels can often show whether methyl parathion or similar compounds have acted on your nerves. Cholinesterase levels in red blood cells can stay low for more than a month after you have been exposed to methyl parathion or similar chemicals. For more information, see Chapters 3 and 7. 

Biological exposure indices (BEI) published by the ACGIH are given in Table 4.35. BEIs represent the levels of determinant which are most likely to be observed in specimens collected from a healthy worker who has been exposed to chemicals to the same extent as a worker with inhalation exposure to the TLV. Due to biological variability it is possible for an individual s measurements to exceed the BEI without incurring increased health risk. If, however, levels in specimens obtained from a worker on different occasions persistently exceed the BEI, or if the majority of levels in specimens obtained from a group of workers at the same workplace exceed the BEI, the cause of the excessive values must be investigated and proper action taken to reduce the exposure. 

Regulation of transmitter release does not rest solely on the frequency at which nerve impulses reach the terminals. Early experiments using stimulated sympathetic nerve/end-organ preparations in situ, or synaptosomes, indicated that release of [ HJnoradrenaline was attenuated by exposure to unlabelled, exogenous transmitter. This action was attributed to presynaptic adrenoceptors, designated a2-adrenoceptors, which were functionally distinct from either aj- or )S-adrenoceptors. Later experiments have confirmed that ai-adrenoceptors comprise a family of pharmacologically and structurally distinct adrenoceptor subtypes. 

Available information from human exposures indicates that airborne americium-containing particles are deposited in the respiratory tract, cleared to some extent via mucociliary action, and swallowed or expelled (Edvardsson and Lindgren 1976 Fry 1976 Newton et al. 1983 Sanders 1974 Toohey and Essling 1980). Descriptions of human respiratory tract models that can be used for radiation protection also include relevant information regarding biokinetics of inhaled particles (ICRP 1994b, 1995 NCRP 1997). Quantitative data are not available, however. Supporting animal studies include inhalation exposure to aerosols of americium (Buldakov et al. 1972 DOE 1978 Gillett et al. 1985 Sanders and Mahaffey 1983 Talbot et al. 1989 Thomas et al. 1972) or intratracheal instillation of americium compounds (Moushatova et al. 1996). 

Organophosphate insecticides also inhibit RBC-ACHE and PCHE. Inhibition of ACHE in erythrocytes is assumed to mirror inhibition of ACHE in the nervous system, which is the receptor of the toxic action, to some extent. Therefore, measurements of RBC-ACHE and PCHE are used for biological monitoring of exposure to OP insecticides (Maroni, 1986). Inhibitions of RBC-ACHE and PCHE activities are correlated with intensity and duration of exposure, although at different levels for each OP compound. Blood ACHE, being the same molecular target as that responsible for acute toxicity in the nervous system, is a true indicator of effect, while PCHE can only be used as an indicator of exposure. 

Even though all OP insecticides have a common mechanism of action, differences occur among individual compounds. OP insecticides can be grouped into direct and indirect ACHE inhibitors. Direct inhibitors are effective without any metabolic modification, while indirect inhibitors require biotransformation to be effective. Moreover, some OP pesticides inhibit ACHE more than PCHE, while others do the opposite. For example, malathion, diazinon, and dichlorvos are earlier inhibitors of PCHE than of ACHE. In these cases, PCHE is a more sensitive indicator of exposure, even though it is not correlated with symptoms or signs of toxicity. 

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