الف) Reference dose

ب) Safe Human Dose

ج) NOAEL

د) LOAEL

 The calculation of a safe human dose essentially makes an extrapolation on the basis of the size differential between humans and the test species. Usually this is a straightforward body-weight extrapolation, but a surface area scalar for dose could also be used. The calculation is similar to the following

NOAEL = threshold dose or some other no-observable-adverse-effect-level selected from the no-effect region of the dose–response curve

SHD = safe human dose

UF = the total uncertainty factor, which depends on the nature and reliability of the animal data used for the extrapolation

 N = number of milligrams consumed per day

Two methods of estimating the threshold are used. The more desirable method uses the highest reported dose or exposure level for which no toxicity was observed. adverse effect level” (NOAEL), is considered for practical purposes to represent the threshold dose. Sometimes, the available data do not include a NOAEL; that is, all of the doses tested produced some measurable toxic effect. In this situation, the lowest dose producing an adverse effect,  termed the “lowest observable adverse effect level” (LOAEL), is identified from the dose response data. The threshold dose will lie below, and hopefully near, this dose. A threshold dose is then projected from the LOAEL, usually by dividing the LOAEL by a factor of 10 (see Figure 18.3

the greater the uncertainty that the NOAEL or LOAEL from the literature actually represents the threshold dose in humans 
The purpose of dividing the NOAEL or LOAEL by uncertainty factors is to ensure that the SHD used in the risk assessment is below the actual human threshold dose for toxicity for all individuals in the exposed population, thereby avoiding any underestimation of risk. The greater the uncertainty associated with the data, ظthe larger the uncertainty factor required to insure protection.The general rationale for selecting the size of the uncertainty factor for a particul ararea of uncertainty is as follows

منابع مورد استفاده:

Phillip L. Williams, Robert C. James, Stephen M. Roberts-The Principles of Toxicology-Wiley-Interscience 

Using the measured absorbance’s, calculate the corresponding concentrations (µg/mL) of lead in the sample, Cs, and average media blank, Cb, from the calibration graph. 17. Using the solution volumes (mL) of the sample, Vs, and media blanks, Vb, calculate the concentration, C (mg/m3), of lead in the air volume sampled, V(L)1

  NIOSH Manual of Analytical Methods (NMAM) 5th Edition - Method 7082 LEAD by Flame AAS 

بررسی و تحلیل توسط دبیر انجمن در انجمن بهداشت حرفه ای ایران

مکانیسم عمل استراز توسط ارگانوفسفره و کربامات مهار استیل کولین است که مسئول علائم حاد مرتبط با این ترکیبات است. استیل کولین استراز آنزیمی است که در شکاف سیناپسی واقع شده است و عملکرد آن تقسیم استیل کولین است که انتقال دهنده عصبی در موارد ذیل است: اعصاب پاراسمپاتیک پس از انقباض، سوماتیک انتهای اعصاب حرکتی در عضله اسکلتی، فیبرهای preganglionic در اعصاب پاراسمپاتیک و سمپاتیک،و در برخی از سیناپس ها در سیستم عصبی مرکزی.

Acute Effects of Organophosphate and Carbamate Insecticides: The effects of organophosphate and carbamate insecticides can be either local (e.g., sweating from localized dermal exposure) or systemic.The clinical manifestation of overexposure to organophosphate and carbamate compounds is a result of muscarinic, nicotinic, and CNS symptoms. In systemic intoxications with organophosphate and carbamate compounds, the muscarinic effects are generally the first effects to develop.[357]Ref ,page

The development of OPIDN is not physiologically related to cholinesterase inhibition. The nerve lesion in OPIDN is that of a distal symmetric predominantly motor polyneuropathy of the long, large-diameter axons (the short, small diameter nerves appear to be spared) in the peripheral nerves.OPIDN, as its name suggests, has a  delayed onset of approximately 1–3 weeks following an acute life-threatening exposure to an organophosphate capable of causing delayed neuropathy. [358]Ref,page