Asking about the biological effects of radiation in human body.
Well, the deterministic effects are those which can be seen in very short time after exposure because the exposure exceeded the threshold, while the stochastic effects happen after a while such as cancer and they have no threshold.
Ionizing radiation exposure causes cancer and non-cancer health effects, each of which differs greatly in the shape of the dose–response curve, latency, persistency, recurrence, curability, fatality and impact on quality of life. For dose limitation purposes, the International Commission on Radiological Protection (ICRP) has classified such diverse effects into tissue reactions (formerly termed non-stochastic and deterministic effects) and stochastic effects. Effective dose limits aim to reduce the risks of stochastic effects (cancer/heritable effects) and are based on the detriment-adjusted nominal risk coefficients, assuming a linear non-threshold (LNT) dose response and a dose and dose rate effectiveness factor (DDREF) of 2. Equivalent dose limits aim to avoid tissue reactions (vision-impairing cataracts and cosmetically unacceptable non-cancer skin changes) and are based on a threshold dose.
The following paper gives an overview as to historical changes in the definition of tissue reactions and stochastic effects.
https://www.researchgate.net/publication/262054513_Classification_of_radiation_effects_for_dose_limitation_purposes_History_current_situation_and_future_prospects?ev=srch_pub
Article Classification of radiation effects for dose limitation purp...
ICRP has defined stochastic effects as the probability of an effect occurring, and not its severity, is regarded as a function of dose without threshold. This definition remains unchanged from the first recommendations in ICRP Publication 26 issued in 1977.
In ICRP Publication 26 issued in 1977, ICRP defined "non-stochastic" effects as opposed to "stochastic" effects. "non-stochastic" here means "not of a random or statistical nature".
However, it was thought that although the initial cellular changes are random, the large number of cells involved in the initiation of a clinically observable, nonstochastic effect gives the effect a deterministic character. Therefore, in ICRP Publication 60 issued in 1990, "non-stochastic" effects was renamed "deterministic effects". "deterministic" here means "causally determined by preceding events".
It was then thought that deterministic effects are not predetermined solely at the time of irradiation and can be altered after irradiation by the use of various biological response modifiers. Thus, in ICRP Publication 103 issued in 2007, "deterministic" effects was renamed "tissue reactions".
ICRP has defined tissue reactions as injury in populations of cells characterized by a threshold dose and an increase in the severity of the reaction as the dose is increased further. Acute doses of up to 0.1 Gy were believed to produce no functional impairment of tissues. A threshold dose is defined as the amount of ionizing radiation required to cause a particular effect in only 1% of exposed individuals.
ICRP Publication 118 issued in 2012 includes the most updated list of ICRP thresholds for various early and late occurring tissue reactions. Of these, the threshold dose for vision impairing cataracts of the ocular lens is now 0.5 Gy with >20 years follow-up independent of the rate of dose delivery. The threshold of 0.5 Gy for circulatory disease (cardio- and cerebro-vascular disease) is newly recommended, again independent of the rate of dose delivery, but with >10 years follow-up.
It is about short time and long time effects. You can find the extended description in ICRP reports and especially in academic lecture notes. If you need further information, i can share my notes with you ... Good Luck !
Radiation is simply a mechanism whereby energy passes through space. It takes the form of an electromagnetic wave, with the frequency of the electromagnetic wave determining its position in the electromagnetic spectrum. Low-frequency waves such as radio waves lie at one end of the spectrum and high-energy, high-frequency X-rays/Gamma rays at the other end. These high-frequency, high-energy waves are termed “ionizing” (as opposed to non-ionizing) radiation because they contain sufficient energy to displace an electron from its orbit around a nucleus. The most important consequence of this displaced electron on human tissue is the potential damage it can inflict on DNA, which may occur directly or indirectly. Direct damage occurs when the displaced electron hits and breaks a DNA strand. Indirect damage occurs when the electron reacts with a water molecule, creating a powerful hydroxyl radical which then damages the cell’s DNA.
Damage to a cell’s DNA in either of these ways can have several consequences. A single-strand DNA break is usually repaired appropriately by the cell with no subsequent deleterious sequelae. However, a break affecting both strands of DNA allows the potential for abnormal reconnection of the strands, which likely accounts for all the adverse biological effects ionizing radiation has on humans. First, DNA may rejoin itself incorrectly, rendering the cell nonviable with cell death taking place. Second, it may rejoin as a symmetrical translocation with the potential expression of an oncogene during division (and development of subsequent malignancy) or with abnormal division in gonads, giving rise to potential hereditary disorders.
Radiosensitivity is the probability of a cell, tissue, or organ suffering an effect per unit dose of radiation. Radiosensitivity is highest in cells which are highly mitotic or undifferentiated. For this reason the basal epidermis, bone marrow, thymus, gonads, and lens cells are highly radiosensitive. Muscle, bones, and nervous system tissues have a relative low radiosensitivity.
Agrees with previous writers, Explanations given by Hamada Sir are fabulous and complete.
Just want to add that stochastic effects do not have threshold dose (as pointed by Hamada) as single cell mutation can lead to the induction of these effects.
The stochastic effects are those for what the probability of occurrence is function of the doses. In this case there is no a threshold dose. Cancer and hereditary problems are examples of these effects. The characteristic curve between the effect and dose is linear.
On the other hand, in the deterministic effects the damages caused by the radiation increase with the increase in the dose. In this specific effect there is a threshold dose. Anemia, cataract and radiodermites are examples of these effects. The characteristic curves between the effect and dose is not linear.
The biological effects can be classified as somatic and hereditary. The former is related to alterations that occur in the somatic cells and take place in the individual submitted to exposition. This effect is not transmitted for next generations. The latter can be transmitted for next generations. This effect is consequence of chromosome modifications (DNA) of the individual irradiated.
I have taken a looked at answers posted hitherto by others, and wish to discuss the following three statements. [1] The deterministic and stochastic effects occur at short time and long time after exposure, respectively. [2] The stochastic effects do not have a threshold. [3] Radiosentivity is higher in more mitotic cells.
[1] The deterministic and stochastic effects occur at short time and long time after exposure, respectively. Is this true?
For radiation protection purposes, all effects have been classified either into deterministic or stochastic effects. Deterministic effects (currently called tissue reactions) occur both at short and long time after exposure. Latency generally becomes longer after exposure to lower dose. Long time here means decades: e.g., ICRP’s latest threshold of 0.5 Gy for cataracts and circulatory disease with a follow-up of two decades and a decade after exposure. Manifestation time for stochastic effects also varies among types of cancer: e.g., leukemia arise much earlier than solid cancer after exposure.
Thus, “the deterministic and stochastic effects occur at short time and long time after exposure, respectively” is not always correct. However, it may be possible that its impression comes from the findings on normal tissue complications following the radiotherapy. In radiotherapy, tolerance dose is used where deterministic effects occur at relatively short time because of high dose. Tolerance dose is proposed in 1972 by Rubin and Casarett who defined a clinically acceptable minimum injurious tolerance dose, as a dose that causes severe complications in 1–5% of patients within 5 years post-radiotherapy. On the other hand, ICRP considers lifetime risk for radiation protection purposes.
It may also be interesting to note that historically, ICRP (more precisely, its predecessor IXRPC) used the tolerance dose concept in 1934–1950 assuming the existence of threshold doses for all radiation effects including cancer.
[2] The stochastic effects do not have a threshold. Is this true?
The shape of the dose response curve varies among types of cancer. Typical examples are leukemia (linear-quadratic) and several types of solid cancer such as non-melanoma skin cancer (the spline model with a change in slope at 1 Gy) and bone sarcoma (threshold of 0.85 Gy) in Japanese atomic bomb survivors. However, this does not contradict the LNT model because LNT is the model simplified for all types (but not each type) of cancer for radiation protection purposes.
You may be interested in the following question and answers:
https://www.researchgate.net/post/What_are_the_experimental_evidences_or_data_which_contradict_LNT_model_of_radiological_protection/1
[3] Radiosentivity is higher in more mitotic cells. Is this true?
In general, law of Bergonié-Tribondeau formulated in 1906 explains very well differences in radiosensitivity in various cell types. However, there are exceptions such as oocytes and lymphocytes (both are resting but sensitive).
Also, I do not think that the high radiosensitity of the ocular lens can be explained by law of Bergonié-Tribondeau, although historically, an attempt was made to correlate the lower mitotic index with lower sensitivity to radiation cataractogenesis in terms of species differences where the order of the spontaneous mitotic index in the lens epithelium from the highest to the lowest was mice, rats, rabbits, dogs and monkeys. For more details, please see L. von Sallmann, L. Caravaggio, C.M. Munoz, A. Drungis, Species differences in the radiosensitivity of the lens, Am. J. Ophthalmol. 43 (5) (1957) 693–704, doi: http://dx.doi.org/10.1016/0002-9394(57)91508-8.
Risk for heritable effects has been included in computation of radiation detriment on a prudent basis for radiation protection purposes. However, no human evidence is available heretofore in marked contrast to experimental evidence in animal models.
Thank you so much for your answers and good notes. According to writers notes the biological effects of ionizing radiation can be divided into two categories: stochastic effects ( genetic risks in offspring) and deterministic effects (generally occur only after a high dose acute exposure of ionizing radiation and these effects include many healthy problems. Both the stochastic and deterministic effects depend on radiation dose and time of exposure.
Thanks a lot again
I would prefer "stochastic effects (cancer risks in exposed individuals and heritable risks in their offspring) and deterministic effects (occur only after a threshold dose of ionizing radiation and these effects include many healthy problems" to "stochastic effects ( genetic risks in offspring) and deterministic effects (generally occur only after a high dose acute exposure of ionizing radiation and these effects include many healthy problems".
For some deterministic effects, the same threshold has been recommended irrespective of the rate of dose delivery, e.g., 0.5 Gy to the ocular lens, heart and brain for cataracts and circulatory effects for acute, fractionated, protracted and chronic exposures.
The latest report on the solid cancer incidence data in atomic bomb survivors has been published. https://www.ncbi.nlm.nih.gov/pubmed/28319463
The sex averaged dose response now exhibits an significant upward curvature (p = 0.03) in a linear quadratic model assuming the common curvature for males and females that was estimated to be 0.22 per Gy [95% confidence intervals (CIs): 0.01 to 0.60]. For this, the shape of the dose response was significantly different between sexes, such that the dose response was linear for females, but exhibited an significant upward curvature for males.
A threshold was not significant. For females, the estimated threshold of 0.08 Gy was not different from 0, and the upper bound of the 95% CI was 0.2 Gy. For males, the best estimate of 0.75 Gy was not different from 0, and the upper bound of the 95% CI was 0.8 Gy.
To address whether recent epidemiological studies support the linear non-threshold model for use in radiation protection, the US National Council on Radiation Protection and Measurements (NCRP) established the Scientific Committee 1-25 (SC 1-25) "Recent Epidemiologic Studies and Implications for the Linear-Nonthreshold Model" in late 2015 under Program Area Committee 1 (PAC1).
http://ncrponline.org/program-areas/sc-1-25-recent-epidemiologic-studies-and-implications-for-the-linear-nonthreshold-model/
SC 1-25 is working on the draft of a commentary, of which final form to be published late this year as NCRP Commentary. Will keep you updated.
Thank you so much Dr. Nobuyuki Hamada. Really your answers are very good and give us many information about biological effects of radiation. thanks a lot again.
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