Exposure limits toxins

Although the 0SHA/NI0SH air sampling scheme has not been applied to acute hazards, it would be useful to illustrate the implications of doing so. Consider exposures to the acute toxin, hydrogen cyanide (HCN). Let us assume that the current exposure limit recommended by NIOSH of 5.0 mg/m3 (18) is used as the PEL and that the AL is one half of this value (2.5 mg/m3). The air concentration of HCN required to produce death in man in 10 min is V lOO mg/m3 (18 >19) or 20 times the PEL. 

Performance of Schemes Based upon Tolerance Sets and Limiting Distributions for Evaluating Acute Exposures to Lethal Toxins. [Exposure Limit = 10.0]... 

International occupational exposure limits (OELs) for NMP generally range between 5 and 50 ppm as an 8h time-weighted average (TWA). The American Conference of Governmental Industrial Hygienists has not established an 8 h TWA OEL for NMP. Several countries have established a short-term excursion limit of 75 ppm. The California Office of Environmental Health Hazard Assessment has identified NMP as a reproductive toxin and established maximum allowable daily limits for exposure of 3200 pg day (via inhalation) and 17 000pgday ... 

In earlier generations when the primary concern was survival, time considerations were limited to the immediate event. Delayed effects or the consequence of repeated exposure was of little concern. In time, we became more concerned about the effects of repeated exposure to levels which were not an immediate threat to survival but may eventually become a threat to life - still of the individual exposed. As we became more aware of long-range effects of overexposure, we learned that exposure to toxins can affect us later and even in future generations. Thus, the focus of concern has extended from an immediate effect on the exposed person, to an effect on the exposed person at a later time, to a possible effect on some member of a future generation completely removed from the toxin in question. 

A disease or illness is nontraumatic physiological harm or loss of capacity produced by systemic, continued, or repeated stress or strain exposure to toxins, poisons, fumes, and so on or other continued and repeated exposures to conditions of the environment over a long period of time. For practical purposes, an occupational illness or disease is any reported condition that does not meet the definition of injury (from a mishap). Illness includes both acute and chronic illnesses, such as, but not limited to, a skin disease, respiratory disorder, or poisoning. 

Immediately dangerous to life or health (IDLH) levels are the ceiling limit for respirators other than SCBAs. However, IDLH levels have not been established for toxins. Therefore, any potential exposure to aerosols of these agents should be regarded with extreme caution and the use of SCBAs for respiratory protection should be considered. 

Medical Management Victims may have a feverish respiratory syndrome without chest x-ray abnormalities, and diagnosis is usually clinical. Medical and emergency medical services personnel should be aware of and should report any number of victims showing up within a limited amount of time presenting typical symptoms and instances of SEB pulmonary exposure as being indicative of being an intentional attack with SEB toxin. 

Phycotoxins accumulate in fish and shellfish because of the natural feeding habits of the respective organisms, rather than because of food handling or processing practices. The toxins causing the diseases discussed in this chapter are heat stable (Australia New Zealand Food Authority, 2001 Committee on Evaluation of the Safety of Fishery Products, 1991). Complete inactivation of saxitoxin (associated with PSP) requires at least ten minutes of exposure to 260°C dry heat. Brevetoxins (associated with NSP) were inactivated (i.e., to levels below the limit of assay detection using Japanese medaka [Oryzias latipes]) by exposure to 500°C heat for 10 to 15 minutes (Poli, 1988). Complete inactivation required 10 minutes exposure to 2760°C dry heat (Wannamacher, 2000). 

Because wholesale bans of this type will not occur, then another approach to achieving safety, at least for pollutants, might be suggested. Why not seek the goal of no detectable chemicals in the media of human exposure If automobiles emit various nitrogen oxides, simply ensure that emission rates are sufficiently low so that these noxious chemicals cannot be found in air. If PCBs are migrating from a hazardous waste site, impose limits on that migration so that no detectable PCBs are found in the off-site environment. Control afla-toxin contamination of raw food commodities to ensure none can be found in finished foods. Why not apply this approach to all pollutants (it obviously is not applicable to products) ... 

When the duration of exposure to GT-4 was limited to 10 minutes and the percent inhibition for an agonist concentration equivalent to the 50% control response was measured at 90 minutes as a function of toxin concentration, a linear response was obtained (Figure 5). Figure 5 shows that the exposure of the preparation to 2.8 ng/ml, 7.0 ng/ml and 70 ng/ml for 10 minutes resulted in inhibitions of 30, 36, and 66% of the contractile response from control levels, respectively. In addition, exposure of the preparation to 2.8, 7.0 and 70 ng/ml for 15 minutes resulted in 45, 55, and 98% inhibition of the contractile response, respectively. We can express the effects of GT-3 by stating both the dose and time to achieve a 50% inhibition from the control or a DCI50 value. 

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