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维基百科,自由的百科全书

參考書目

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  • (英文)Morison, Samuel Eliot, History of United States naval operations in World War II: The Battle of the Atlantic, September 1939-May 1943, University of Illinois Press,線上電子版, 2001, ISBN 0252-069-633 
Jsjsjs1111/沙盒
化学信息
  • InChI=bbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbb
  • Key:OYVAGSVQBOHSSS-QRQYLRPSSA-O
Jsjsjs1111/沙盒
IUPAC名
aaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaaa
若非注明,所有数据均出自标准状态(25 ℃,100 kPa)下。

2011年统计用区划代码和城乡划分代码:石洞街道. 中华人民共和国国家统计局. 2011. 

此用户关注或感兴趣於化学

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60.251.107.200

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The hazard symbol for carcinogenic chemicals in the Globally Harmonized System.

致癌物可以是任何化学物质、放射性同位素,或者辐射,它们直接参与癌症的恶化或者促进癌细胞的增殖的。致癌物质的致癌性可能是因为它们有对细胞代谢过程或基因组的破坏能力。许多仿色性物质被认为是致癌物,但他们的致癌性来源于它们发出来的辐射,如γ-射线或α-粒子。 Common examples of carcinogens are inhaled asbestos, certain dioxins, and tobacco smoke.

Carcinogens may increase the risk of getting cancer by altering cellular metabolism or damaging DNA directly in cells, which interferes with biological processes, and induces the uncontrolled, malignant division, ultimately leading to the formation of tumors. Usually DNA damage, if too severe to repair, leads to programmed cell death, but if the programmed cell death pathway is damaged, then the cell cannot prevent itself from becoming a cancer cell.

There are many natural carcinogens. Aflatoxin B1, which is produced by the fungus Aspergillus flavus growing on stored grains, nuts and peanut butter, is an example of a potent, naturally-occurring microbial carcinogen. Certain viruses such as Hepatitis B and human papilloma viruses have been found to cause cancer in humans. The first one shown to cause cancer in animals is Rous sarcoma virus, discovered in 1910 by Peyton Rous.

Benzene, kepone, EDB, asbestos, and the waste rock of oil shale mining have all been classified as carcinogenic.[1] As far back as the 1930s, industrial smoke and tobacco smoke were identified as sources of dozens of carcinogens, including benzo[a]pyrene, tobacco-specific nitrosamines such as nitrosonornicotine, and reactive aldehydes such as formaldehyde—which is also a hazard in embalming and making plastics. Vinyl chloride, from which PVC is manufactured, is a carcinogen and thus a hazard in PVC production.

Co-carcinogens are chemicals that do not necessarily cause cancer on their own, but promote the activity of other carcinogens in causing cancer.

After the carcinogen enters the body, the body makes an attempt to eliminate it through a process called biotransformation. The purpose of these reactions is to make the carcinogen more water-soluble so that it can be removed from the body. But these reactions can also convert a less toxic carcinogen into a more toxic one.

DNA is nucleophilic, therefore soluble carbon electrophiles are carcinogenic, because DNA attacks them. For example, some alkenes are toxicated by human enzymes to produce an electrophilic epoxide. DNA attacks the epoxide, and is bound permanently to it. This is the mechanism behind the carcinogenity of benzo[a]pyrene in tobacco smoke, other aromatics, aflatoxin and mustard gas.

Radiation

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CERCLA identifies all radionuclides as carcinogens, although the nature of the emitted radiation (alpha, beta, gamma, or neutron and the radioactive strength), its consequent capacity to cause ionization in tissues, and the magnitude of radiation exposure, determine the potential hazard. Carcinogenity of radiation depends of the type of radiation, type of exposure and penetration. For example, alpha radiation has low penetration and is not a hazard outside the body, but are carcinogenic when inhaled or ingested.

For example, Thorotrast, a (incidentally-radioactive) suspension previously used as a contrast medium in x-ray diagnostics, is a potent human carcinogen known because of its retention within various organs and persistent emission of alpha particles. Marie Curie, one of the pioneers of radioactivity, died of cancer caused by radiation exposure during her experiments.

Not all types of electromagnetic radiation are in fact carcinogenic. Low-energy waves on the electromagnetic spectrum are generally not, including radio waves, microwave radiation, infrared radiation and visible light. Higher-energy radiation, including ultraviolet radiation (present in sunlight), x-rays, and gamma radiation, generally is carcinogenic, if received in sufficient doses.

Several published studies suggest a link between exposure to light at night and risk of breast cancer, due to suppression of the normal nocturnal production of melatonin.[2][3] In 1978 Cohen et al. proposed that reduced production of the hormone melatonin might increase the risk of breast cancer and citing "environmental lighting" as a possible causal factor.[4] Researchers at the National Cancer Institute (NCI) and National Institute of Environmental Health Sciences have concluded a study that suggests that artificial light during the night can be a factor for breast cancer.[5] A good review of current knowledge of the health consequences of exposure to artificial light at night and an explanation of the causal mechanisms has been published in the Journal of Pineal Research in 2007.[6]

Substances or foods irradiated with electrons or electromagnetic radiation (such as microwave, X-ray or gamma) are not carcinogenic.citation needed No "radiation" remains, just like no light remains in room after you turn out the light. (In contrast, non-electromagnetic neutron radiation produced inside nuclear reactors can produce secondary radiation by making bombarded substances radioactive.)

In other words, there is no possibility of getting cancer from consuming the irradiated food.citation needed

Carcinogens in prepared food

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Cooking food at high temperatures, for example grilling or barbecuing meats, can lead to the formation of minute quantities of many potent carcinogens that are comparable to those found in cigarette smoke (i.e., benzo[a]pyrene).[7] Charring of food resembles coking and tobacco pyrolysis, and produces similar carcinogens. There are several carcinogenic pyrolysis products, such as polynuclear aromatic hydrocarbons, which are converted by human enzymes into epoxides, which attach permanently to DNA. Pre-cooking meats in a microwave oven for 2–3 minutes before grilling shortens the time on the hot pan, and removes heterocyclic amine (HCA) precursors, which can help minimize the formation of these carcinogens.[8]

Reports from the Food Standards Agency have found that the known animal carcinogen acrylamide is generated in fried or overheated carbohydrate foods (such as french fries and potato chips).[9] Studies are underway at the FDA and European regulatory agencies to assess its potential risk to humans.

Dr. T. Colin Campbell argues in The China Study that the milk protein casein, found in milk and many prepared foods, is also a carcinogen.[10] However, independent studies report that casein and other milk proteins protect against cancer.[11]

Carcinogens in cigarettes

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Tobacco smoke contains over 4000 chemical compounds, many of which are carcinogenic or otherwise toxic.[12]

Circadian disruption

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"Shiftwork that involves circadian disruption" was listed, in 2007, as a probable carcinogen by the World Health Organization's International Agency for Research on Cancer. (IARC Press release No. 180).[13] Multiple studies have documented a link between night shift work and the increased incidence of breast cancer.[14][15][16][17] Circadian disruption by exposure to light at night suppresses the production of the hormone melatonin which leads to reduction in cellular immune defense and surveillance necessary for protection from development of cancers. Melatonin also seems to have a direct protective effect against cancer possibly in part because of its strong anti oxidant properties.[18]

Mechanisms of carcinogenicity

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Carcinogens can be classified as genotoxic or nongenotoxic. Genotoxins cause irreversible genetic damage or mutations by binding to DNA. Genotoxins include chemical agents like N-nitroso-N-methylurea (MNU) or non-chemical agents such as ultraviolet light and ionizing radiation. Certain viruses can also act as carcinogens by interacting with DNA.

Nongenotoxins do not directly affect DNA but act in other ways to promote growth. These include hormones and some organic compounds.[19]

Classification of carcinogens

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Approximate equivalences
between classification schemes
IARC GHS NTP ACGIH EU
Group 1 Cat. 1A Known A1 Cat. 1
Group 2A Cat. 1B Reasonably
suspected
A2 Cat. 2
Group 2B
Cat. 2   A3 Cat. 3
Group 3
  A4  
Group 4 A5

International Agency for Research on Cancer

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The International Agency for Research on Cancer (IARC) is an intergovernmental agency established in 1965, which forms part of the World Health Organization of the United Nations. It is based in Lyon, France. Since 1971 it has published a series of Monographs on the Evaluation of Carcinogenic Risks to Humans[20] that have been highly influential in the classification of possible carcinogens.

  • Group 1: the agent (mixture) is definitely carcinogenic to humans. The exposure circumstance entails exposures that are carcinogenic to humans.
  • Group 2A: the agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans.
  • Group 2B: the agent (mixture) is possibly carcinogenic to humans. The exposure circumstance entails exposures that are possibly carcinogenic to humans.
  • Group 3: the agent (mixture or exposure circumstance) is not classifiable as to its carcinogenicity to humans.
  • Group 4: the agent (mixture) is probably not carcinogenic to humans.

Globally Harmonized System

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The Globally Harmonized System of Classification and Labelling of Chemicals (GHS) is a United Nations initiative to attempt to harmonize the different systems of assessing chemical risk which currently exist (as of March 2009) around the world. It classifies carcinogens into two categories, of which the first may be divided again into subcategories if so desired by the competent regulatory authority:

  • Category 1: known or presumed to have carcinogenic potential for humans
    • Category 1A: the assessment is based primarily on human evidence
    • Category 1B: the assessment is based primarily on animal evidence
  • Category 2: suspected human carcinogens

U.S. National Toxicology Program

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The National Toxicology Program of the U.S. Department of Health and Human Services is mandated to produce a biennial Report on Carcinogens.[21] As of March 2009, the latest edition was the 11th report (2005).[1] It classifies carcinogens into two groups:

  • Known to be a human carcinogen
  • Reasonably anticipated to be a human carcinogen

American Conference of Governmental Industrial Hygienists

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The American Conference of Governmental Industrial Hygienists (ACGIH) is a private organization best known for its publication of threshold limit values (TLVs) for occupational exposure and monographs on workplace chemical hazards. It assesses carcinogenicity as part of wider assessment of the occupational hazards of chemicals.

  • Group A1: Confirmed human carcinogen
  • Group A2: Suspected human carcinogen
  • Group A3: Confirmed animal carcinogen with unknown relevance to humans
  • Group A4: Not classifiable as a human carcinogen
  • Group A5: Not suspected as a human carcinogen

European Union

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The European Union classification of carcinogens is contained in the Dangerous Substances Directive and the Dangerous Preparations Directive. It consists of three categories:

  • Category 1: Substances known to be carcinogenic to humans.
  • Category 2: Substances which should be regarded as if they are carcinogenic to humans.
  • Category 3: Substances which cause concern for humans, owing to possible carcinogenic effects but in respect of which the available information is not adequate for making a satisfactory assessment.

This assessment scheme is being phased out in favor of the GHS scheme (see above), to which it is very close in category definitions.

Procarcinogen

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A procarcinogen is a precursor to a carcinogen. One example is nitrites when taken in by the diet. They are not carcinogenic themselves, but turn into nitrosamines in the body, which are carcinogenic.[22]

Common carcinogens

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Occupational carcinogens

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Occupational carcinogens are agents that pose a risk of cancer in several specific work-locations:

Carcinogen Associated cancer sites or types Occupational uses or sources
Arsenic and its compounds
Asbestos

Not in use, but still found in:

  • Constructions
  • Roofing papers
  • Floor tiles
  • Fire-resistant textiles
  • Friction linings
Benzene
Beryllium and its compounds
  • Lung
  • Missile fuel
  • Lightweight alloys
  • Aerospace applications
  • Nuclear reactors
Cadmium and its compounds
  • Prostate
  • Yellow pigments
  • Phosphors
  • Solders
  • Batteries
  • Metal paintings and coatings
Hexavalent chromium(VI) compounds
  • Lung
  • Paints
  • Pigments
  • Preservatives
Ethylene oxide
  • Leukemia
  • Ripening agent for fruits and nuts
  • Rocket propellant
  • Fumigant for foodstuffs and textiles
  • Sterilant for hospital equipment
Nickel
  • Nose
  • Lung
  • Nickel plating
  • Ferrous alloys
  • Ceramics
  • Batteries
  • Stainless-steel welding byproduct
Radon and its decay products
  • Lung
  • Uranium decay
  • Quarries and mines
  • Cellars and poorly ventilated places
Vinyl chloride
  • Hemangiosarcoma
  • Liver
Shiftwork that involves

circadian disruption[13]

  • Breast
Involuntary smoking (Passive smoking)[23]
Unless else specified in boxes, then ref is: [24]

Others

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See also

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RE:唔好意思

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您还是说普通话吧(因为我觉得打广州话很麻烦)…… 作为一个新人(按照注册账号时间来说),对于这个我刚注册就参与的投票讨论,我认为主要问题是这几点:

  1. Msuker肯定是有错的,他不应该以咄咄逼人的语气讨论,不应讽刺别人,同时他也似乎没能做到WP:善意推定(不过您作为一个老维基人应该知道他一直说话都是这样的)。当然,他在讨论时尽管“可怕”,但他没有违反WP:CIV(可能是因为他比较喜欢说别人人身攻击因而自己也比较注意吧)。严格上来说,他尽管有错,但并没有违反任何成文条款(WP:AGF只是指引)。这里也引用费勒姆兄的原话:“人身攻擊的定義很廣泛,如果你認定我部份內容是有人身攻擊的話,那麼你會不會認為是假定惡意?”
  2. Msuker说话很强硬、辛辣,让人很难受(用广州话说就是“好窜”),这点我承认,他以前也因此招了不少麻烦——他与某S君华德禹JackycheungClitheringWs227的大量冲突,看他的封禁纪录也是“罪行累累”[1]。但在我看来,他在讨论中或许有“攻击别人”,但没有脏话,而且也是有理有据(这不是我个人的观点,其他人也这样说过[2])。
  3. Msuker之所以在这个投票中又一次如此激动,不能仅仅怪罪于他,主要问题还是在某S君身上。某S君从一开始在这个投票中就不断“玩弄规则”,先是在投票时使用“全体票数”来拖,然后又说Msuker拉票要封禁,最后又在投票结束后说“对大家不公平”,被Msuker驳倒又转移话题说这个投票应该留给香港人自己投(作为发起人的他自己都不是香港人),这几点你应该也看得到。像我作为一个使用粤语的广州人,本来也想投选项2,但看到他的无理取闹,迫使我改变了主意(就像Shizhao罢免案里那些看不惯支持者“政治审查”的理由而改票的人一样)。输打赢要,从某种程度上来说,一切问题都是他引起的。
  4. 这次投票的讨论中大家都比较激动,而我特别欣赏的是LUFC。在这个讨论中,尽管他支持香港译名,但他一直很理性,而且在某S同学耍赖之时也劝说了他[3]
  5. 最后总结这次讨论:不论Msuker的所作所为有多不妥,投票结果出来了,这就是事实,无法否认,我们不能够因噎废食。唉,也希望这次争论能尽快结束,大家能够尽快回到正常的条目编写中,而不是在这些无谓地方上争论如此长的时间(现在投票结果迟迟不出导致的又是冲突——见Talk:洛达·安塔尔Talk:伊戈·古斯域治)。

以上就是我作为一个新人对此次讨论的意见,如有不当,还请费勒姆兄海涵。PS:请问您为什么找我问这个问题,是不明白我为什么一直支持Msuker吗?如果是的话,理由见上面2、3条。
另外还有,Msuker这段话真的说得很有道理:

什么样的人做什么样的事,不多说了。我只想说,诸位管理员、行政员,难道真的就为了怕惹事,怕某些人惦记,默不作声,视方针、共识、投票、讨论结果于不顾?这是你们申请做管理员、行政员时候的初衷?

不知道您是否也这样认为呢?—CHEM.is.TRY 2010年5月28日 (五) 12:44 (UTC)

Notes

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  1. ^ 1.0 1.1 Report on Carcinogens, Eleventh Edition; U.S. Department of Health and Human Services, Public Health Service, National Toxicology Program (2005).
  2. ^ Scott Davis; Dana K. Mirick; Richard G. Stevens. Night Shift Work, Light at Night, and Risk of Breast Cancer. Journal of the National Cancer Institute. 2001, 93 (20): 1557–1562. PMID 11604479. doi:10.1093/jnci/93.20.1557.  已忽略未知参数|author-separator= (帮助)
  3. ^ Eva S. Schernhammer; Francine Laden; Frank E. Speizer; Walter C. Willett; David J. Hunter; Ichiro Kawachi; Graham A. Colditz. Rotating Night Shifts and Risk of Breast Cancer in Women Participating in the Nurses' Health Study. Journal of the National Cancer Institute. 2001, 93 (20): 1563–1568. PMID 11604480. doi:10.1093/jnci/93.20.1563.  已忽略未知参数|author-separator= (帮助)
  4. ^ Cohen M, Lippman M, Chabner B. Role of pineal gland in aetiology and treatment of breast cancer. Lancet 1978;2:14–16.
  5. ^ The Independent Avoid breast cancer. Sleep in the dark...
  6. ^ Navara KJ, Nelson RJ (2007) The dark side of light light at night: physiological, epidemiological, and ecological consequences. J. Pineal Res. 2007; 43:215–224
  7. ^ Wei Zheng, Deborah R Gustafson, Rashmi Sinha, James R Cerhan, et al. "Well-done meat intake and the risk of breast cancer." Journal of the National Cancer Institute. Oxford: Nov 18, 1998.Vol. 90, Iss. 22; pg. 1724, 6 pgs.
  8. ^ National Cancer Institute, 2004 analysis and recommendations
  9. ^ Acrylamide. 
  10. ^ Thomas M., II Campbell; Campbell, Thomas M.; Colin T., PH D. Campbell. The China study: the most comprehensive study of nutrition ever conducted and the startling implications for diet, weight loss and long-term health. Benbella Books. 2005. ISBN 1-932100-38-5. 
  11. ^ Parodi PW. A role for milk proteins and their peptides in cancer prevention. Current Pharmaceutical Design. 2007, 13 (8): 813–28. PMID 17430183. doi:10.2174/138161207780363059. 
  12. ^ http://quitsmoking.about.com/cs/nicotineinhaler/g/carbonmonoxide.htm
  13. ^ 13.0 13.1 IARC Monographs Programme finds cancer hazards associated with shiftwork, painting and firefighting, International Agency for Research on Cancer (PDF), [2009-01-24] 
  14. ^ Schernhammer E, Schulmeister K. Melatonin and cancer risk: does light at night compromise physiologic cancer protection by lowering serum melatonin levels? Br J Cancer 2004;90:941–943.
  15. ^ Hansen J. Increased breast cancer risk among women who work predominantly at night. Epidemiology 2001; 12:74–77.
  16. ^ Hansen J. Light at night, shiftwork, and breast cancer risk.J Natl Cancer Inst 2001; 93:1513–1515.
  17. ^ Schernhammer E, Laden F, Speizer FE et al. Rotating night shifts and risk of breast cancer in women participating in the nurses' health study. J Natl Cancer Inst 2001; 93:1563–1568.
  18. ^ Navara KJ, Nelson RJ (2007) The dark side of light light at night: physiological, epidemiological, and ecological consequences. J. Pineal Res. 2007; 43:215–224
  19. ^ The Gale Encyclopedia of Cancer: A guide to Cancer and its Treatments, Second Edition. Page no. 137. 
  20. ^ IARC Monographs
  21. ^ Section 301(b)(4) of the Public Health Service Act, as amended by Section 262, Pub. L. 95–622.
  22. ^ Web definitions for Procarcinogen
  23. ^ Tobacco Smoke and Involuntary Smoking, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 83 (2004).
  24. ^ Table 6-2 in: Mitchell, Richard Sheppard; Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic Pathology. Philadelphia: Saunders. 2007. ISBN 1-4160-2973-7.  8th edition.
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