adj.

有毒な、毒性のある、中毒性の

関: intoxicated、poisonous、toxicity、venomous、virulence、virulent

WordNet

of or relating to or caused by a toxin or poison; "suffering from exposure to toxic substances"
not safe to eat
having the qualities or effects of a poison (同)toxicant
marked by deep ill will; deliberately harmful; "poisonous hate"; "venomous criticism"; "vicious gossip" (同)venomous, vicious
infectious; having the ability to cause disease
the degree to which something is poisonous

PrepTutorEJDIC

毒性の,有毒な / 毒による
『有毒な』,毒を含む / 有害な;(精神的に)人を害する / 悪意のある,意地の悪い / 不快な,いやな
有毒な,毒性の / 憎悪に満ちた,敵意に満ちた
(動物が)毒液を出す / 毒のある,有毒な / (言葉・行為などが)悪意に満ちた,陰険な / 《時におどけて》いやな,不快な
毒性,有毒性

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/06/17 18:54:32」(JST)

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The skull and crossbones is a common symbol for toxicity.

Toxicity is the degree to which a substance can damage an organism.^[1] Toxicity can refer to the effect on a whole organism, such as an animal, bacterium, or plant, as well as the effect on a substructure of the organism, such as a cell (cytotoxicity) or an organ such as the liver (hepatotoxicity). By extension, the word may be metaphorically used to describe toxic effects on larger and more complex groups, such as the family unit or society at large.

A central concept of toxicology is that effects are dose-dependent; even water can lead to water intoxication when taken in too high a dose, whereas for even a very toxic substance such as snake venom there is a dose below which there is no detectable toxic effect. Toxicity is species-specific, making cross-species analysis problematic. Newer paradigms and metrics are evolving to bypass animal testing, while maintaining the concept of toxicity endpoints.^[2]

1 Types of toxicity
2 Measuring toxicity
3 Global classifications of toxicity
- 3.1 Health hazards
  - 3.1.1 Acute toxicity
  - 3.1.2 Other methods of exposure and severity
  - 3.1.3 Other categories of toxicity
- 3.2 Environmental hazards
  - 3.2.1 Mapping environmental hazards
  - 3.2.2 Aquatic toxicity
4 Factors influencing toxicity
5 Etymology
6 See also
7 References
8 External links

Types of toxicity

There are generally three types of toxic entities; chemical, biological, and physical:

Chemical toxicants include inorganic substances such as, lead, mercury, hydrofluoric acid, and chlorine gas, and organic compounds such as methyl alcohol, most medications, and poisons from living things. While some radioactive substances are also chemical toxicants, many are not: radiation poisoning results from exposure to the ionizing radiation produced by a radioactive substance rather than chemical interactions with the substance itself.
Biological toxicants include bacteria and viruses that can induce disease in living organisms. Biological toxicity can be difficult to measure because the "threshold dose" may be a single organism. Theoretically one virus, bacterium or worm can reproduce to cause a serious infection. However, in a host with an intact immune system the inherent toxicity of the organism is balanced by the host's ability to fight back; the effective toxicity is then a combination of both parts of the relationship. A similar situation is also present with other types of toxic agents.
Physical toxicants are substances that, due to their physical nature, interfere with biological processes. Examples include coal dust, asbestos fibers or finely divided silicon dioxide, all of which can ultimately be fatal if inhaled. Corrosive chemicals possess physical toxicity because they destroy tissues, but they're not directly poisonous unless they interfere directly with biological activity. Water can act as a physical toxicant if taken in extremely high doses because the concentration of vital ions decreases dramatically if there's too much water in the body. Asphyxiant gases can be considered physical toxicants because they act by displacing oxygen in the environment but they are inert, not toxic gases.

Measuring toxicity

Toxicity can be measured by its effects on the target (organism, organ, tissue or cell). Because individuals typically have different levels of response to the same dose of a toxic substance, a population-level measure of toxicity is often used which relates the probabilities of an outcome for a given individual in a population. One such measure is the LD₅₀. When such data does not exist, estimates are made by comparison to known similar toxic things, or to similar exposures in similar organisms. Then, "safety factors" are added to account for uncertainties in data and evaluation processes. For example, if a dose of a toxic substance is safe for a laboratory rat, one might assume that one tenth that dose would be safe for a human, allowing a safety factor of 10 to allow for interspecies differences between two mammals; if the data are from fish, one might use a factor of 100 to account for the greater difference between two chordate classes (fish and mammals). Similarly, an extra protection factor may be used for individuals believed to be more susceptible to toxic effects such as in pregnancy or with certain diseases. Or, a newly synthesized and previously unstudied chemical that is believed to be very similar in effect to another compound could be assigned an additional protection factor of 10 to account for possible differences in effects that are probably much smaller. Obviously, this approach is very approximate; but such protection factors are deliberately very conservative, and the method has been found to be useful in a deep variety of applications.

Assessing all aspects of the toxicity of cancer-causing agents involves additional issues, since it is not certain if there is a minimal effective dose for carcinogens, or whether the risk is just too small to see. In addition, it is possible that a single cell transformed into a cancer cell is all it takes to develop the full effect (the "one hit" theory).

It is more difficult to determine the toxicity of chemical mixtures than a pure chemical, because each component displays its own toxicity, and components may interact to produce enhanced or diminished effects. Common mixtures include gasoline, cigarette smoke, and industrial waste. Even more complex are situations with more than one type of toxic entity, such as the discharge from a malfunctioning sewage treatment plant, with both chemical and biological agents.

The preclinical toxicity testing on various biological systems reveals the species-, organ- and dose- specific toxic effects of an investigational product. The toxicity of substances can be observed by (a) studying the accidental exposures to a substance (b) in vitro studies using cells/ cell lines (c) in vivo exposure on experimental animals. Toxicity tests are mostly used to examine specific adverse events or specific end points such as cancer, cardiotoxicity, and skin/eye irritation. Toxicity testing also helps calculate the No Observed Adverse Effect Level (NOAEL) dose and is helpful for clinical studies.^[3]

Global classifications of toxicity

The international pictogram for toxic chemicals.

For substances to be regulated and handled appropriately they must be properly classified and labelled. Classification is determined by approved testing measures or calculations and have determined cut off levels set by governments and scientists. While currently many countries have different regulations regarding the types of tests, amounts of tests and cut off levels, the implementation of Global Harmonization will begin unifying these countries as early as 2008.^[4]^[5]

Global Classification looks at three areas: Physical Hazards (explosions and pyrotechnics),^[6] Health Hazards^[7] and Environmental Hazards.^[8]

Health hazards

The types of toxicities where substances may cause lethality to the entire body, lethality to specific organs, major/minor damage, or cause cancer. These are globally accepted definitions of what toxicity is.^[7] Anything falling outside of the definition cannot be classified as that type of toxicant.

Acute toxicity

Acute toxicity looks at lethal effects following oral, dermal or inhalation exposure. It is split into five categories of severity where Category 1 requires the least amount of exposure to be lethal and Category 5 requires the most exposure to be lethal. The table below shows the upper limits for each category.

Method of administration	Category 1	Category 2	Category 3	Category 4	Category 5
Oral: LD₅₀ measured in mg/kg of bodyweight	5	50	300	2 000	5 000
Dermal: LD₅₀ measured in mg/kg of bodyweight	50	200	1 000	2 000	5 000
Gas Inhalation: LC₅₀ measured in ppmV	100	500	2 500	20 000	Undefined
Vapour Inhalation: LC₅₀ measured in mg/L	0.5	2.0	10	20	Undefined
Dust and Mist Inhalation: LC₅₀ measured in mg/L	0.05	0.5	1.0	5.0	Undefined

Note: The undefined values are expected to be roughly equivalent to the category 5 values for oral and dermal administration.^{[citation needed]}

Other methods of exposure and severity

Patch test

Skin corrosion and irritation are determined though a skin patch test analysis. This examines the severity of the damage done; when it is incurred and how long it remains; whether it is reversible and how many test subjects were affected.

Skin corrosion from a substance must penetrate through the epidermis into the dermis within four hours of application and must not reverse the damage within 14 days. Skin irritation shows damage less severe than corrosion if: the damage occurs within 72 hours of application; or for three consecutive days after application within a 14-day period; or causes inflammation which lasts for 14 days in two test subjects. Mild skin irritation minor damage (less severe than irritation) within 72 hours of application or for three consecutive days after application.

Serious eye damage involves tissue damage or degradation of vision which does not fully reverse in 21 days. Eye irritation involves changes to the eye which do fully reverse within 21 days.

Other categories of toxicity

Respiratory sensitizers cause breathing hypersensitivity when the substance is inhaled.
A substance which is a skin sensitizer causes an allergic response from a dermal application.
Carcinogens induce cancer, or increase the likelihood of cancer occurring.
Reproductively toxic substances cause adverse effects in either sexual function or fertility to either a parent or the offspring.
Specific-target organ toxins damage only specific organs.
Aspiration hazards are solids or liquids which can cause damage through inhalation.

Environmental hazards

Environmental hazards tend to focus on degradability, bioaccumulation and aquatic toxicity.^[8]

Mapping environmental hazards

There are many environmental health mapping tools. TOXMAP is a Geographic Information System (GIS) from the Division of Specialized Information Services^[9] of the United States National Library of Medicine (NLM) that uses maps of the United States to help users visually explore data from the United States Environmental Protection Agency's (EPA) Toxics Release Inventory and Superfund programs. TOXMAP is a resource funded by the US Federal Government. TOXMAP's chemical and environmental health information is taken from NLM's Toxicology Data Network (TOXNET)^[10] and PubMed, and from other authoritative sources.

Aquatic toxicity

Aquatic toxicity testing subjects key indicator species of fish or crustacea to certain concentrations of a substance in their environment to determine the lethality level. Fish are exposed for 96 hours while crustacea are exposed for 48 hours. While GHS does not define toxicity past 100 mg/l, the EPA currently lists aquatic toxicity as “practically non-toxic” in concentrations greater than 100 ppm.^[11]

Exposure	Category 1	Category 2	Category 3
Acute	≤ 1.0 mg/L	≤ 10 mg/L	≤ 100 mg/L
Chronic	≤ 1.0 mg/L	≤ 10 mg/L	≤ 100 mg/L

Note: A category 4 is established for chronic exposure, but simply contains any toxic substance which is mostly insoluble, or has no data for acute toxicity.

Factors influencing toxicity

Toxicity of a substance can be affected by many different factors, such as the pathway of administration (whether the toxin is applied to the skin, ingested, inhaled, injected), the time of exposure (a brief encounter or long term), the number of exposures (a single dose or multiple doses over time), the physical form of the toxin (solid, liquid, gas), the genetic makeup of an individual, an individual's overall health, and many others. Several of the terms used to describe these factors have been included here.

Acute exposure: A single exposure to a toxic substance which may result in severe biological harm or death; acute exposures are usually characterized as lasting no longer than a day.
Chronic exposure: Continuous exposure to a toxin over an extended period of time, often measured in months or years; it can cause irreversible side effects.

Etymology

"Toxic" and similar words came from Greek τοξον = "bow (weapon)" via "poisoned arrow", which came to be used for "poison" in scientific language, as the usual Classical Greek word ('ιον) for "poison" would transcribe as "io-", which is not distinctive enough. In some biological names, "toxo-" still means "bow", as in Toxodon = "bow-toothed" from the shape.

References

^ http://www.merriam-webster.com/dictionary/toxicity
^ "Toxicity Endpoints & Tests". AltTox.org. Retrieved 25 February 2012.
^ Parasuraman S. Toxicological screening. J Pharmacol Pharmacother [serial online] 2011 [cited 2013 Oct 12];2:74-9. Available from: http://www.jpharmacol.com/text.asp?2011/2/2/74/81895
^ United Nations Economic Commission for Europe Globally Harmonized System of Classification and Labelling of Chemicals
^ EPA implementation of Global Harmonization
^ Globally Harmonized System of Classification and Labelling of Chemicals – Part 2, Physical Hazards
^ ^a ^b Globally Harmonized System of Classification and Labelling of Chemicals – Part 3, Health Hazards
^ ^a ^b Globally Harmonized System of Classification and Labelling of Chemicals – Part 4, Environmental Hazards
^ SIS.nlm.nih.gov
^ Toxnet.nlm.nih.gov
^ EPA: Ecological risk assessment

External links

Agency for Toxic Substances and Disease Registry
Whole Effluent, Aquatic Toxicity Testing FAQ
TOXMAP Environmental Health e-Maps from the United States National Library of Medicine
Toxseek: meta-search engine in toxicology and environmental health

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English Journal

Silver nanoparticle-specific mitotoxicity in Daphnia magna.

Stensberg MC, Madangopal R, Yale G, Wei Q, Ochoa-Acuña H, Wei A, McLamore ES, Rickus J, Porterfield DM, Sepúlveda MS.Author information Department of Agriculture and Biological Engineering, Purdue University , West Lafayette, IN , USA.AbstractAbstract Silver nanoparticles (Ag NPs) are gaining popularity as bactericidal agents in commercial products; however, the mechanisms of toxicity (MOT) of Ag NPs to other organisms are not fully understood. It is the goal of this research to determine differences in MOT induced by ionic Ag(+) and Ag NPs in Daphnia magna, by incorporating a battery of traditional and novel methods. Daphnia embryos were exposed to sublethal concentrations of AgNO3 and Ag NPs (130-650 ng/L), with uptake of the latter confirmed by confocal reflectance microscopy. Mitochondrial function was non-invasively monitored by measuring proton flux using self-referencing microsensors. Proton flux measurements revealed that while both forms of silver significantly affected proton efflux, the change induced by Ag NPs was greater than that of Ag(+). This could be correlated with the effects of Ag NPs on mitochondrial dysfunction, as determined by confocal fluorescence microscopy and JC-1, an indicator of mitochondrial permeability. However, Ag(+) was more efficient than Ag NPs at displacing Na(+) within embryonic Daphnia, based on inductively coupled plasma-mass spectroscopy (ICP-MS) analysis. The abnormalities in mitochondrial activity for Ag NP-exposed organisms suggest a nanoparticle-specific MOT, distinct from that induced by Ag ions. We propose that the MOT of each form of silver are complementary, and can act in synergy to produce a greater toxic response overall.
Nanotoxicology.Nanotoxicology.2014 Dec;8:833-42. doi: 10.3109/17435390.2013.832430. Epub 2013 Sep 2.
Abstract Silver nanoparticles (Ag NPs) are gaining popularity as bactericidal agents in commercial products; however, the mechanisms of toxicity (MOT) of Ag NPs to other organisms are not fully understood. It is the goal of this research to determine differences in MOT induced by ionic Ag(+) and Ag
PMID 23927462

Systematic analysis of silver nanoparticle ionic dissolution by tangential flow filtration: toxicological implications.

Maurer EI, Sharma M, Schlager JJ, Hussain SM.Author information 711 Human Performance Wing/RHDJ, Human Effectiveness Directorate, Air Force Research Laboratory, Wright-Patterson Air Force Base , Dayton, Ohio , USA.AbstractAbstract In the field of toxicology of nanomaterials, scientists have not clearly determined if the observed toxicological events are due to the nanoparticles (NPs) themselves or the dissolution of ions released into the biophysiological environment or both phenomenon participate in combination based upon their bioregional and temporal occurrence during exposure conditions. Consequently, research involving the toxicological analysis of silver NPs (Ag-NPs) has shifted towards assessment of 'nanosized' silver in comparison to its solvated 'ionic' counterpart. Current literature suggests that dissolution of ions from Ag-NPs may play a key role in toxicity; however, the present assessment methodology to separate ions from NPs still requires improvement before a definitive cause of toxicity can be determined. Recently, centrifugation-based techniques have been employed to obtain solvated ions from the NP solution, but this approach leads to NP agglomeration, making further toxicological analysis difficult to assess. Additionally, extremely small NPs are retained in the supernatant even after ultracentrifugation, leading to incomplete separation of ions from their respective NPs. To address these complex toxicology issues we applied enhanced separation techniques with the aim to study levels of ions originating from the Ag-NP using separation by a recirculating tangential flow filtration system. This system uses a unique diffusion-driven filtration method that retains large particles within the continuous flow path, while allowing the solution (ions) to pass through molecular filters by lateral diffusion separation. Use of this technique provides reproducible NP separation from their solvated ions which permits for further quantification using an inductively coupled plasma mass spectrometry or comparison use in bioassay exposures to biological systems. In this study, we thoroughly characterised NPs in biologically relevant solutions to understand the dissolution of Ag-NPs (10 and 50 nm) over time. Our results suggest that the ion dissolution from Ag-NPs is dependent on parameters such as exposure time, chemical composition and temperature of the exposure solution. Further, the well-characterised separated ionic and NP solutions were exposed to a lung epithelial cell line (A549) to evaluate the toxicity of each fraction. Results suggest that although Ag-NPs (unseparated) show concentration-dependent toxicity, dissolution of ions appears to exacerbate the toxicological effect. This finding adds data to the set of probable toxic exposure mechanisms elicited by metallic nanomaterials and provides important consideration when assessing findings of key cell function modulation.
Nanotoxicology.Nanotoxicology.2014 Nov;8:718-27. doi: 10.3109/17435390.2013.824127. Epub 2013 Aug 1.
Abstract In the field of toxicology of nanomaterials, scientists have not clearly determined if the observed toxicological events are due to the nanoparticles (NPs) themselves or the dissolution of ions released into the biophysiological environment or both phenomenon participate in combination base
PMID 23848466

In vitro toxicological screening of nanoparticles on primary human endothelial cells and the role of flow in modulating cell response.

Ucciferri N, Collnot EM, Gaiser BK, Tirella A, Stone V, Domenici C, Lehr CM, Ahluwalia A.Author information Interdepartmental Research Center "E. Piaggio", University of Pisa , Pisa , Italy.AbstractAbstract After passage through biological barriers, nanomaterials inevitably end up in contact with the vascular endothelium and can induce cardiovascular damage. In this study the toxicity and sub-lethal effects of six types of nanoparticle, including four of industrial and biomedical importance, on human endothelial cells were investigated using different in vitro assays. The results show that all the particles investigated induce some level of damage to the cells and that silver particles were most toxic, followed by titanium dioxide. Furthermore, endothelial cells were shown to be more susceptible when exposed to silver nanoparticles under flow conditions in a bioreactor. The study underlines that although simple in vitro tests are useful to screen compounds and to identify the type of effect induced on cells, they may not be sufficient to define safe exposure limits. Therefore, once initial toxicity screening has been conducted on nanomaterials, it is necessary to develop more physiologically relevant in vitro models to better understand how nanomaterials can impact on human health.
Nanotoxicology.Nanotoxicology.2014 Sep;8:697-708. doi: 10.3109/17435390.2013.831500. Epub 2013 Sep 3.
Abstract After passage through biological barriers, nanomaterials inevitably end up in contact with the vascular endothelium and can induce cardiovascular damage. In this study the toxicity and sub-lethal effects of six types of nanoparticle, including four of industrial and biomedical importance, o
PMID 23909703

Using gold nanorods core/silver shell nanostructures as model material to probe biodistribution and toxic effects of silver nanoparticles in mice.

Meng J, Ji Y, Liu J, Cheng X, Guo H, Zhang W, Wu X, Xu H.Author information Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College , Beijing , P. R. China.AbstractAbstract The aim of this work was to probe the biodistribution and toxic effects of silver nanoparticles (NPs) with powerful anti-bacterial and anti-virus activities. For this purpose, novel silver NPs with gold nanorod (NR) core and silver shell (Au@Ag NRs) were developed and employed as a model material. The inner gold core provided an excellent internal reference for tracking the NRs in vivo. After subcutaneous injection of Au@Ag NRs, silver and gold contents in the subcutis and organs were examined by inductively coupled plasma mass spectrometry at different time points within 28 days. Histological analysis, physiological function and complement faction 3 (C3) and 5a (C5a) measurement were performed over time to reveal the toxic effect of Au@Ag NRs in vivo. Experimental results showed that majority of the Au@Ag NRs remained in the injection site except for a small amount migrating into the lymph nodes. The silver shell was dissolved in the subcutaneous tissue and released silver ions rapidly, which resulted in detectable silver accumulation in most of the organs. The accumulated silver ions in the kidney not only interacted with the kidney cells membrane but also induced a rapid increase of complement fraction C3 followed by a significant consumption and C3a and C5a production significantly in the serum, which resulted in kidney oxidative damage and eventually led to the morphological changes and filtration function impairment of the glomerulus. The released silver ions also caused oxidative injury of subcutaneous tissue in the injection site.
Nanotoxicology.Nanotoxicology.2014 Sep;8:686-96. doi: 10.3109/17435390.2013.822593. Epub 2013 Jul 29.
Abstract The aim of this work was to probe the biodistribution and toxic effects of silver nanoparticles (NPs) with powerful anti-bacterial and anti-virus activities. For this purpose, novel silver NPs with gold nanorod (NR) core and silver shell (Au@Ag NRs) were developed and employed as a model ma
PMID 23837638

Japanese Journal

Decontamination of spent iron-oxide coated sand from filters used in arsenic removal

Rahman Ismail M. M.,Begum Zinnat A.,Sawai Hikaru,Maki Teruya,Hasegawa Hiroshi
Chemosphere 92(2), 196-200, 2013-06-00
… The approach offers superior performance in removing arsenic while the spent sludge from the sand filters is an issue of concern due to the possibility of toxic releases after being discarded. …
NAID 120005254066

M12-Tet-Off pTRE2pur FLAG mTRAF3細胞株の樹立

田邊香野,坂本瞳,乾誠治,タナベカノ,サカモトヒトミ,イヌイセイジ,Tanabe Kano,Sakamoto Hitomi,Inui Seiji
熊本大学医学部保健学科紀要 9, 27-38, 2013-03-30
… To elucidate the mechanism of the TRAF3 degradation, we prepared Tet-Off gene expression system in M12 to inducibly express TRAF3 which was toxic when overexpressed in cells. …
NAID 120005254899

ボツリヌス毒素複合体の構造と機能

大山徹
東京農業大学農学集報 57(4), 223-232, 2013-03-18
ボツリヌス神経毒素(BoNT)は,自然界最強の毒素であり,コリン作動性シナプスからの神経伝達物質放出の阻害によって,ヒトや動物のボツリヌス症として知られる致死的な疾病を引き起こす。ボツリヌス菌株は,BoNT の抗原性の違いにより,A から G 型の血清型に分類され,A,B,E および F 型はヒトに対して,一方 C および D 型は動物や鳥類のボツリヌス症の原因物質とされている。全ての血清型の B …
NAID 110009558067

オオミジンコ急性遊泳試験による無機化学物質の生態影響評価

高橋峻,阿部達雄,タカハシシュン,アベタツオ,TAKAHASHI Shun,ABE Tatsuo
鶴岡工業高等専門学校研究紀要 = Research Reports of Tsuruoka National College of Technology (47), 65-68, 2013-03-00
… Therefore, the toxic strength of inorganic chemicals is investigated by Daphnia magna immobilization assay. …
NAID 120005263117