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Exposure continued permissible

The radiological hazard of tritium to operating personnel and the general population is controlled by limiting the rates of exposure and release of material. Maximum permissible concentrations (MPC) of radionucHdes were specified in 1959 by the International Commission on Radiological Protection (79). For purposes of control all tritium is assumed to be tritiated water, the most readily assimilated form. The MPC of tritium ia breathing air (continuous exposure for 40 h/wk) is specified as 185 kBq/mL (5 p.Ci/mL) and the MPC for tritium in drinking water is set at 3.7 GBq/mL (0.1 Ci/mL) (79). The maximum permitted body burden is 37 MBq (one millicurie). Whenever bioassay indicates this value has been exceeded, the individual is withdrawn from further work with tritium until the level of tritium is reduced. [Pg.16]

Estimation of Permissible Concentrations of Pollutants for Continuous Exposure," Report 600/2-76-155. U.S. Environmental Protection Agency, Research Triangle Park, NC, 1976. [Pg.458]

Ozone, O3, is the triatomic allotrope of oxygen. It is an unstable, blue diamagnetic gas with a characteristic pungent odour indeed, it was first detected by means of its smell, as reflected by its name (Greek o eiv, ozein, to smell) coined by C. F. Schonbein in 1840. Ozone can be detected by its smell in concentrations as low as 0.01 ppm the maximum permissible concentration for continuous exposure is 0.1 ppm but levels as high as 1 ppm are considered non-toxic if breathed for less than 10 min. [Pg.607]

Fig. 4.9 Schematic illustration of the electrosynthesis procedure using a sulfur-modified gold electrode and alternating exposure to indium- and sulfide ion containing aqueous baths, (a) A polycrystalline gold surface is first modified with a sulfur layer, (b) Indium is plated onto this layer forming indium sulfide, (c) Indium continues to deposit atop the indium sulfide layer, (d) Transfer back to a sulfide ion containing bath results in the suMdization of the residual indium sites. (Reprinted from [95], Copyright 2009, with permission from Elsevier)... Fig. 4.9 Schematic illustration of the electrosynthesis procedure using a sulfur-modified gold electrode and alternating exposure to indium- and sulfide ion containing aqueous baths, (a) A polycrystalline gold surface is first modified with a sulfur layer, (b) Indium is plated onto this layer forming indium sulfide, (c) Indium continues to deposit atop the indium sulfide layer, (d) Transfer back to a sulfide ion containing bath results in the suMdization of the residual indium sites. (Reprinted from [95], Copyright 2009, with permission from Elsevier)...
Figure 20.6 Schematic representation of the effects of 5-HT reuptake inhibitors on serotonergic neurons, (a) 5-HT is released at the somatodendritic level and by proximal segments of serotonergic axons within the Raphe nuclei and taken up by the 5-HT transporter. In these conditions there is little tonic activation of somatodendritic 5-HTia autoreceptors. At nerve terminals 5-HTib receptors control the 5-HT synthesis and release in a local manner, (b) The blockade of the 5-HT transporter at the level of the Raphe nuclei elevates the concentration of extraneuronal 5-HT to an extent that activates somatodendritic autoreceptors (5-HTia). This leads to neuronal hyperpolarisation, reduction of the discharge rate and reduction of 5-HT release by forebrain terminals, (c) The exposure to an enhanced extracellular 5-HT concentration produced by continuous treatment with SSRIs desensitises Raphe 5-HTia autoreceptors. The reduced 5-HTia function enables serotonergic neurons to recover cell firing and terminal release. Under these conditions, the SSRI-induced blockade of the 5-HT transporter in forebrain nerve terminals results in extracellular 5-HT increases larger than those observed after a single treatment with SSRIs. (Figure and legend taken from Hervas et al. 1999 with permission)... Figure 20.6 Schematic representation of the effects of 5-HT reuptake inhibitors on serotonergic neurons, (a) 5-HT is released at the somatodendritic level and by proximal segments of serotonergic axons within the Raphe nuclei and taken up by the 5-HT transporter. In these conditions there is little tonic activation of somatodendritic 5-HTia autoreceptors. At nerve terminals 5-HTib receptors control the 5-HT synthesis and release in a local manner, (b) The blockade of the 5-HT transporter at the level of the Raphe nuclei elevates the concentration of extraneuronal 5-HT to an extent that activates somatodendritic autoreceptors (5-HTia). This leads to neuronal hyperpolarisation, reduction of the discharge rate and reduction of 5-HT release by forebrain terminals, (c) The exposure to an enhanced extracellular 5-HT concentration produced by continuous treatment with SSRIs desensitises Raphe 5-HTia autoreceptors. The reduced 5-HTia function enables serotonergic neurons to recover cell firing and terminal release. Under these conditions, the SSRI-induced blockade of the 5-HT transporter in forebrain nerve terminals results in extracellular 5-HT increases larger than those observed after a single treatment with SSRIs. (Figure and legend taken from Hervas et al. 1999 with permission)...
Figure 9. DMTA curves of TEGDA + 3.4 DMPA, measured after various exposure times. Intensity 0.2 mW.cm 2. Upper curves log E. Lower curves tan 6. Frequency IHz. (Thin line for t = 5s repeat.) (Reproduced with permission from Ref. 9 Copyright 198 Polymer.) (Continued on next page.)... Figure 9. DMTA curves of TEGDA + 3.4 DMPA, measured after various exposure times. Intensity 0.2 mW.cm 2. Upper curves log E. Lower curves tan 6. Frequency IHz. (Thin line for t = 5s repeat.) (Reproduced with permission from Ref. 9 Copyright 198 Polymer.) (Continued on next page.)...
Fig. 3. Schematic of teratogenicity screening assay. Fertilized eggs are collected within a few hours of spawning. The chorions can be removed by gentle enzymatic treatment with manual removal as needed. The embryos are then cultured for the desired period of time. When embryos are incubated in 1 ml of medium, continuous exposure (without medium changes) is possible for at least 5 days. Embryos are exposed to the test substance in the culture medium. At the desired timepoint(s) (e.g., 5 dpt), larvae can be evaluated for viability and developmental parameters. (Reprinted from Brannen et al. (4), by permission of John Wiley and Sons.). Fig. 3. Schematic of teratogenicity screening assay. Fertilized eggs are collected within a few hours of spawning. The chorions can be removed by gentle enzymatic treatment with manual removal as needed. The embryos are then cultured for the desired period of time. When embryos are incubated in 1 ml of medium, continuous exposure (without medium changes) is possible for at least 5 days. Embryos are exposed to the test substance in the culture medium. At the desired timepoint(s) (e.g., 5 dpt), larvae can be evaluated for viability and developmental parameters. (Reprinted from Brannen et al. (4), by permission of John Wiley and Sons.).
FIGURE 7. Bitter response plateaus while astringency (drying) response continually increases on repeated exposure to tannic acid. [Reproduced from ref. 40 by permission of Oxford University Press]... [Pg.18]

Values tabulated denote calculated probabilities of an individual s developing cancer at some time during life following continuous annual occupational exposure for an entire working lifetime at the maximum permissible level... [Pg.124]

Figure 3. Birefringence (An) versus incident exposure in (J/cm2) for polarized UV(A) and polarized pulsed laser ( ) exposure. The continuous 325 nm power density was 0.2 W/citp, while the 575 nm pulsed laser intensity (8 ns pulses at 10 Hz) was 1.6 GW/cm2. (Reproduced with permission from Ref. 8. Figure 3. Birefringence (An) versus incident exposure in (J/cm2) for polarized UV(A) and polarized pulsed laser ( ) exposure. The continuous 325 nm power density was 0.2 W/citp, while the 575 nm pulsed laser intensity (8 ns pulses at 10 Hz) was 1.6 GW/cm2. (Reproduced with permission from Ref. 8.
In 1955, the International Commission on Radiological Protection set a maximum permissible occupational concentration of 3.7 x 103 Bq m-3 (10-10 Ci l-1), for continuous exposure, equivalent to 1.1 x 104 Bq m-3 (3 x 10-10 pCi P1) for a 40-h working week. Subsequently, when it was realised that the critical dose to the lung was from inhalation of decay products, not radon itself, the permissible concentration was defined in terms of the concentration of decay products. The current recommended limit (ICRP, 1986) for a working period of 2000 h per year is 1.5 x 103 Bq m 3 equilibrium equivalent radon concentration (a term defined in Section 1.8 below). [Pg.14]

Long-term AA-EQSs are intended to protect against long-term continuous exposure, and MAC-EQSs are intended to protect against short-term episodic events. It should be noted that the use of acute toxicity data for deriving AA-EQSs is considered permissible by some jurisdictions, for example, when suitable chronic toxicity data are not available (e.g., CCME, 2007), although the use of chronic data for this purpose is always preferable. [Pg.68]

OSHA requires employers of workers who are occupationally exposed to dinitrocresols to institute engineering controls and work practices to reduce and maintain employee exposure at or below permissible exposure limits (PEL). The employer must use engineering and work practice controls, if feasible, to reduce exposure to or below an 8-hour time-weighted average (TWA) of 0.2 ppm. Respirators must be provided and used during the time period necessary to install or implement feasible engineering and work practice controls (OSHA 1993). In 1989, the TWA was promulgated at 0.25 mg/m. However, that limits and limits over 400 other chemicals were revoked based on a 1992 Court of Appeals Decision, and the pre-1989 limit of 0.2mg/m was reinstated. Approximately 13 states continue to enforce the 0.25 mg/m limit. [Pg.131]

Table 35.1 Permissible Exposure Levels (PEL) and Air Odor Thresholds (AOT) (in ppm) for Volatile Organic Compounds120,211 (Continued)... Table 35.1 Permissible Exposure Levels (PEL) and Air Odor Thresholds (AOT) (in ppm) for Volatile Organic Compounds120,211 (Continued)...
One more complicating factor must now be considered the effect of duration of exposure. Consider the data shown in Table 20. In each of the rows, the Ct product = 100 mg min m-3. In the rows (c), (d) and (e), one might feel reasonably confident that the mortality likely to occur would be about 50%, i.e. an LCtso exposure. At the outer rows, one becomes distinctly less confident and it is unlikely that continuous exposure of a person to 0.0001 mg m 3 GB for 1.9 years would have the same effect as exposure to 10 mg m 3 for 10 min. Interestingly, the US permissible exposure limit for GB (expressed as an 8-h time-weighted average (TWA), is 0.0001 mg m 3 such an exposure, on a daily, life-long basis, would be regarded as safe. [Pg.55]

C. F. Schonbein in 1840. Ozone can be detected by its smell in concentrations as low as 0.01 ppm the maximum permissible concentration for continuous exposure is 0.1 ppm but levels as high as 1 ppm are considered non-toxic if breathed for less than 10 min. [Pg.607]


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Permissiveness

Permissives

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