STUXNET(new dangour for modren world)

Stuxnet is a Windows-specific computer worm first discovered in July 2010 by VirusBlokAda, a security firm based in Belarus. While it is not the first time that hackers have targeted industrial systems, it is the first discovered worm that spies on and reprograms industrial systems, and the first to include a programmable logic controller (PLC) rootkit. It was specifically written to attack Supervisory Control And Data Acquisition (SCADA) systems used to control and monitor industrial processes. Stuxnet includes the capability to reprogram the PLCs and hide its changes.
The worm's probable target is said to have been high value infrastructures in Iran using Siemens control systems. According to news reports the infestation by this worm might have damaged Iran's nuclear facilities in Natanz and eventually delayed the start up of Iran's Bushehr Nuclear Power Plant. Although Siemens has stated that the worm has not caused any damage, on November 29, Iran confirmed that its nuclear program had indeed been damaged by Stuxnet.
Russian digital security company Kaspersky Labs released a statement that described Stuxnet as "a working and fearsome prototype of a cyber-weapon that will lead to the creation of a new arms race in the world." Kevin Hogan, Senior Director of Security Response at Symantec, noted that 60% of the infected computers worldwide were in Iran, suggesting its industrial plants were the target. Kaspersky Labs concluded that the attacks could only have been conducted "with nation-state support", making Iran the first target of real cyberwarfare.
History
The worm was first reported by the security company VirusBlokAda in mid-June 2010, and roots of it have been traced back to June 2009. It contains a component with a build time stamp from 3 February 2010. In the United Kingdom on 25 November 2010, Sky News reported that it had received information that the Stuxnet worm, or a variation of the virus, had been traded on the black market. The name is derived from some keywords discovered in the software.
Affected countries
A study of the spread of Stuxnet by Symantec showed that the main affected countries as of August 6, 2010 were:
Country Infected computers
China 6,000,000 (unconfirmed) (October 1)
Iran 62,867
Indonesia 13,336
India 6,552
United States 2,913
Australia 2,436
United Kingdom 1,038
Malaysia 1,013
Pakistan 993
Finland 7
Germany 5 (September)
Operation
The complexity of the software is very unusual for malware, and consists of attacks against three different systems:
1. The Windows operating system,
2. An industrial software application that runs on Windows, and
3. A Siemens programmable logic controller (PLC).
The attack requires in-depth knowledge of industrial processes and an interest in attacking industrial infrastructure. These capabilities would have required a team of people to program, as well as check that the malware would not crash the PLCs. Eric Byres, who has years of experience maintaining and troubleshooting Siemens systems, told Wired that writing the code would have taken many man-months, if not years.
Windows infection
Stuxnet attacked Windows systems using four zero-day attacks (plus the CPLINK vulnerability and a vulnerability used by the Conficker worm). It is initially spread using infected removable drives such as USB flash drives, and then uses other exploits and techniques such as peer-to-peer RPC to infect and update other computers inside private networks that are not directly connected to the Internet. The number of zero-day Windows exploits used is unusual, as zero-day Windows exploits are valued, and hackers do not normally waste the use of four different ones in the same worm. Stuxnet is unusually large at half a megabyte in size, and written in different programming languages (including C and C++) which is also irregular for malware. The Windows component of the malware is promiscuous in that it spreads relatively quickly and indiscriminately.
The malware has both user-mode and kernel-mode rootkit capability under Windows, and its device drivers have been digitally signed with the private keys of two certificates that were stolen from separate companies, JMicron and Realtek, that are both located at Hsinchu Science Park in Taiwan. The driver signing helped it install kernel-mode drivers successfully and remain undetected for a relatively long period of time. Both compromised certificates have been revoked by VeriSign.
Two websites were configured as command and control servers for the malware, allowing it to be updated, and for industrial espionage to be conducted by uploading information. Both of these websites have subsequently been taken down as part of a global effort to disable the malware.
Step 7 software infection

Overview of normal communications between Step 7 and a Siemens PLC

Overview of Stuxnet hijacking communication between Step 7 software and a Siemens PLC
Once installed on a Windows system, Stuxnet infects project files belonging to Siemens' WinCC/PCS 7 SCADA control software (Step 7), and subverts a key communication library of WinCC called s7otbxbx.dll. The purpose of this subversion is to intercept communications between the WinCC software running under Windows and the target Siemens PLC devices that the software is able to configure and program when the two are connected via a data cable. In this way, the malware is able to install itself on PLC devices unnoticed, and subsequently to mask its presence from WinCC if the control software attempts to read an infected block of memory from the PLC system.

The malware furthermore used a zero-day exploit in the WinCC/SCADA database software in the form of a hard-coded database password.
PLC infection
Siemens Simatic S7-300 PLC CPU with three modules attached, each of which can control 31 slave variable-frequency drives
The entirety of the Stuxnet code has not yet been understood, but among its peculiar capabilities is a fingerprinting technology which allows it to precisely identify the systems it infects. Stuxnet requires specific slave variable-frequency drives (frequency converter drives) to be attached to the targeted Siemens S7-300 system and its associated modules. It only attacks those PLC systems with variable-frequency drives from two specific vendors: Vacon based in Finland and Fararo Paya based in Iran. Furthermore, it monitors the frequency of the attached motors, and only attacks systems that spin between 807Hz and 1210 Hz. The industrial applications of motors with these parameters are diverse, and may include pumps or centrifuges.
Stuxnet installs malware into memory block DB890 of the PLC that monitors the Profibus messaging bus of the system. When certain criteria are met, it periodically modifies the frequency to 1410 Hz and then to 2 Hz and then to 1064 Hz, and thus affects the operation of the connected motors by changing their rotational speed. It also installs a rootkit that hides the malware on the system—the first such documented case on this platform.
Removal
Siemens has released a detection and removal tool for Stuxnet. Siemens recommends contacting customer support if an infection is detected and advises installing Microsoft patches for security vulnerabilities and prohibiting the use of third-party USB flash drives Siemens also advises immediately upgrading password access codes.
The worm's ability to reprogram external programmable logic controllers (PLCs) may complicate the removal procedure. Symantec's Liam O'Murchu warns that fixing Windows systems may not completely solve the infection; a thorough audit of PLCs is recommended. Despite speculation that incorrect removal of the worm could cause damage, Siemens reports that in the first four months since discovery, the malware was successfully removed from the systems of twenty-two customers without any adverse impact.
Control system security
Main article: Control system security
Prevention of control system security incidentssuch as from viral infections like Stuxnet, is a topic that is being addressed in both the public and the private sector.
The U.S. Department of Homeland Security National Cyber Security Division operates the Control System Security Program (CSSP). The program operates a specialized Computer Emergency Response Team (ICS-CERT), conducts a biannual conference (ICSJWG), provides training, publishes recommended practices, and provides a self-assessment tool.
Several industry organizations and professional societies have published standards and best practice guidelines providing direction and guidance for control system end-users on how to establish a Control System Security management program. The basic premise that all of these documents share is that prevention requires a multi-layered approach, often referred to as "defense-in-depth". The layers include policies & procedures, awareness & training, network segmentation, access control measures, physical security measures, system hardening, e.g., patch management, and system monitoring, anti-virus and IPS. The standards and best practices also all recommend starting with a risk analysis and a control system security assessment. The purpose is to assess the current level of risk and the size of the gap between that risk and what is tolerable. The other purpose of an assessment is to identify the vulnerabilities and develop a prioritized program to eliminate or minimize them.
In response to these concerns, cyber security standards and certifications programs such as ISA 99 and SASecure have been developed to evaluate and certify the security of industrial automation products.
Automation, SCADA and control system developers often use off-the-shelf equipment, software and protocols, integrating and configuring these in different ways for a variety of applications. This "common" approach can make it easier for malware to bring down some vulnerable systems. However, proprietary automation, SCADA and control system developers are able to provide a completely bespoke solution, using new protocols and hardware/software/firmware solutions yet unknown to developers of malware.
Speculations about the target and origin
Symantec estimates that the group developing Stuxnet would have been well-funded, consisting of five to ten people, and would have taken six months to prepare. The Guardian, the BBC and The New York Times all reported that experts studying Stuxnet considered that the complexity of the code indicates that only a nation state would have the capabilities to produce it.
Israel, perhaps through Unit 8200, has been speculated to be the country behind Stuxnet in many media reports and by experts such as Richard Falkenrath, former Senior Director for Policy and Plans within the United States Department of Homeland Security. Some have also referred to several clues in the code such as a concealed reference to the word "MYRTUS", believed to refer to the Myrtle tree, or Hadassah in Hebrew. Hadassah was the birth name of the former Jewish queen of Persia, Queen Esther. However, it may be that the "MYRTUS" reference is simply a misinterpreted reference to SCADA components known as RTUs (Remote Terminal Units) and that this reference is actually "My RTUs"–a management feature of SCADA. Also, the number 19790509 appears once in the code and might refer to the date "1979 May 09", the day Habib Elghanian, a Persian Jew, was executed in Tehran. "Symantec cautions readers on drawing any attribution conclusions. Attackers would have the natural desire to implicate another party." According to the New York Times, a former member of the United States intelligence community speculated that the attack may have been the work of Unit 8200. Yossi Melman, who covers intelligence for the Israeli daily newspaper Haaretz and is at work on a book about Israeli intelligence, also suspected that Israel was involved. He noted that Meir Dagan, head of the national intelligence agency Mossad, had his term extended in 2009 because he was said to be involved in important projects. Additionally, in the past year Israeli estimates of when Iran will have a nuclear weapon had been extended to 2014. "They seem to know something, that they have more time than originally thought”, he added.
Additionally, in 2009, a year before Stuxnet was discovered, Scott Borg of the United States Cyber-Consequences Unit (US-CCU) had suggested that Israel might prefer to mount a cyber-attack rather than a military strike on Iran's nuclear facilities. According to Borg this kind of attack could involve disrupting sensitive equipment such as centrifuges using malware introduced via infected memory sticks: "Since the autumn of 2002, I have regularly predicted that this sort of cyber-attack tool would eventually be developed ... Israel certainly has the ability to create Stuxnet and there is little downside to such an attack, because it would be virtually impossible to prove who did it. So a tool like Stuxnet is Israel's obvious weapon of choice." There has also been speculation on the involvement of NATO, the United States and other Western nations. It has been reported that the United States, under one of its most secret programs, initiated by the Bush administration and accelerated by the Obama administration, has sought to destroy Iran's nuclear program by novel methods such as undermining Iranian computer systems. However, solid evidence pointing to Western (and specifically American) involvement has been scarce.
Though Israel has not publicly commented on the Stuxnet attack, it has since confirmed that cyberwarfare is now among the pillars of its defense doctrine, with a military intelligence unit set up to pursue both defensive and offensive options.
Symantec has reported that the majority of infected systems were in Iran (about 60%),which has led to speculation that it may have been deliberately targeting "high-value infrastructure" in Iran including either the Bushehr Nuclear Power Plant or the Natanz nuclear facility. Ralph Langner, a German cyber-security researcher, called the malware "a one-shot weapon" and said that the intended target was probably hit, although he admitted this was speculation.
There are reports that Iran's uranium enrichment facility at Natanz was the target of Stuxnet and the site sustained damage because of it, causing a sudden 15% reduction in its production capabilities. There was also a previous report by WikiLeaks disclosing a "serious nuclear accident" at the site in 2009. According to statistics published by the Federation of American Scientists (FAS) the number of enriched centrifuges operational in Iran mysteriously declined from about 4,700 to about 3,900 beginning around the time the nuclear incident WikiLeaks mentioned would have occurred. On November 23 it was announced that uranium production at Natanz in Iran temporarily ceased altogether because of a series of major technical problems. According to a report by the Institute for Science and International Security (ISIS) Stuxnet is "a reasonable explanation for the apparent damage" at Natanz and may have destroyed up to 1000 centrifuges (10 percent) in the months before January 2010. The authors conclude:
"The attacks seem designed to force a change in the centrifuge’s rotor speed, first raising the speed and then lowering it, likely with the intention of inducing excessive vibrations or distortions that would destroy the centrifuge. If its goal was to quickly destroy all the centrifuges in the FEP, Stuxnet failed. But if the goal was to destroy a more limited number of centrifuges and set back Iran’s progress in operating the FEP, while making detection difficult, it may have succeeded, at least temporarily."
The ISIS report further notes that Iranian authorities have attempted to conceal the breakdown by installing new centrifuges on a large scale.
Iranian reaction
The Associated Press reported that the semi-official Iranian Students News Agency released a statement on 24 September 2010 stating that experts from the Atomic Energy Organization of Iran met in the previous week to discuss how Stuxnet could be removed from their systems. According to analysts, Western intelligence agencies have been attempting to sabotage the Iranian nuclear program for some time.
The head of the Bushehr Nuclear Power Plant told Reuters that only the personal computers of staff at the plant had been infected by Stuxnet and the state-run newspaper Iran Daily quoted Reza Taghipour, Iran's telecommunications minister, as saying that it had not caused "serious damage to government systems". The Director of Information Technology Council at the Iranian Ministry of Industries and Mines, Mahmud Liaii, has said that: "An electronic war has been launched against Iran... This computer worm is designed to transfer data about production lines from our industrial plants to locations outside Iran."
It is believed that infection originated from Russian laptops belonging to Russian contractors at the site of Bushehr power plant and spreading from there with the aim of targeting the power plant control systems. In response to the infection, Iran has assembled a team to combat it. With more than 30,000 IP addresses affected in Iran, an official has said that the infection is fast spreading in Iran and the problem has been compounded by the ability of Stuxnet to mutate. Iran has set up its own systems to clean up infections and has advised against using the Siemens SCADA antivirus since it is suspected that the antivirus is actually embedded with codes which update Stuxnet instead of eradicating it.
According to Hamid Alipour, deputy head of Iran's government Information Technology Company, "The attack is still ongoing and new versions of this virus are spreading." He reports that his company had begun the cleanup process at Iran's "sensitive centres and organizations. We had anticipated that we could root out the virus within one to two months, but the virus is not stable, and since we started the cleanup process three new versions of it have been spreading," he told the Islamic Republic News Agency.
Although he did not mention Stuxnet by name, on Monday November 29, 2010, Iranian President Mahmoud Ahmadinejad for the first time admitted that malicious software code had damaged Iran's centrifuge facilities. "They succeeded in creating problems for a limited number of our centrifuges with the software they had installed in electronic parts," Mr. Ahmadinejad told reporters at a news conference, Reuters reported. "They did a bad thing. Fortunately our experts discovered that and today they are not able [to do that] anymore.
On the same day two Iranian nuclear scientists were assassinated when bombs were attached to their cars in Tehran. Wired speculated that the assassinations could indicate that whoever was behind Stuxnet felt that it was not sufficient to stop the nuclear program.

HIV AND AIDS

What Is It?

AIDS is one of the most serious, deadly diseases in human history.

More than 20 years ago, doctors in the United States identified the first cases of AIDS in San Francisco and New York. Now there are an estimated 42 million people living with HIV or AIDS worldwide, and more than 3 million die every year from AIDS-related illnesses.

AIDS is caused by the human immunodeficiency virus (HIV). HIV destroys a type of defense cell in the body called a CD4 helper lymphocyte (pronounced: lim-fuh-site). These lymphocytes are part of the body's immune system, the defense system that fights infectious diseases. But as HIV destroys these lymphocytes, people with the virus begin to get serious infections that they normally wouldn't — that is, they become immune deficient. The name for this condition is acquired immunodeficiency syndrome(AIDS).

As the medical community learns more about how HIV works, they've been able to develop drugs to inhibit it (meaning they interfere with its growth). These drugs have been successful in slowing the progress of the disease, and people with the disease now live much longer. But there is still no cure for HIV and AIDS.

Hundreds of U.S. teens become infected with HIV each year. HIV can be transmitted from an infected person to another person through blood, semen (also known as "cum," the fluid released from the penis when a male ejaculates), vaginal fluids, and breast milk.

The virus is spread through high-risk behaviors including:

· unprotected oral, vaginal, or anal sexual intercourse ("unprotected" means not using a condom)

· sharing needles, such as needles used to inject drugs (including needles used for injecting steroids) and those used for tattooing

People who have another sexually transmitted disease, such as syphilis, genital herpes, chlamydia, gonorrhea, or bacterial vaginosis are at greater risk for getting HIV during sex with infected partners.

If a woman with HIV is pregnant, her newborn baby can catch the virus from her before birth, during the birthing process, or from breastfeeding. If doctors know an expectant mother has HIV, they can usually prevent the spread of the virus from mother to baby. All pregnant teens and women should be tested for HIV so they can begin treatment if necessary.

How Does HIV Affect the Body?

A healthy body is equipped with CD4 helper lymphocyte cells (CD4 cells). These cells help the immune system function normally and fight off certain kinds of infections. They do this by acting as messengers to other types of immune system cells, telling them to become active and fight against an invading germ.

HIV attaches to these CD4 cells, infects them, and uses them as a place to multiply. In doing so, the virus destroys the ability of the infected cells to do their job in the immune system. The body then loses the ability to fight many infections.

Because their immune systems are weakened, people who have AIDS are unable to fight off many infections, particularly tuberculosis and other kinds of otherwise rare infections of the lung (such as Pneumocystis carinii pneumonia), the surface covering of the brain (meningitis), or the brain itself (encephalitis). People who have AIDS tend to keep getting sicker, especially if they are not taking antiviral medications properly.

AIDS can affect every body system. The immune defect caused by having too few CD4 cells also permits some cancers that are stimulated by viral illness to occur — some people with AIDS get forms of lymphoma and a rare tumor of blood vessels in the skin called Kaposi's sarcoma. Because AIDS is fatal, it's important that doctors detect HIV infection as early as possible so a person can take medication to delay the onset of AIDS.

How Do People Know They Have HIV?

Once a person's blood lacks the number of CD4 cells required to fight infections, or the person has signs of specific illnesses or diseases that occur in people with HIV infection, doctors make a diagnosis of AIDS.

Severe symptoms of HIV infection and AIDS may not appear for 10 years. And for years leading up to that, a person may not have symptoms of AIDS. The amount of time it takes for symptoms of AIDS to appear varies from person to person. Some people may feel and look healthy for years while they are infected with HIV. It is still possible to infect others with HIV, even if the person with the virus has absolutely no symptoms. You cannot tell simply by looking at someone whether he or she is infected.

When a person's immune system is overwhelmed by AIDS, the symptoms can include:

· extreme weakness or fatigue

· rapid weight loss

· frequent fevers that last for several weeks with no explanation

· heavy sweating at night

· swollen lymph glands

· minor infections that cause skin rashes and mouth, genital, and anal sores

· white spots in the mouth or throat

· chronic diarrhea

· a cough that won't go away

· trouble remembering things

Girls may also experience severe vaginal yeast infections that don't respond to usual treatment, as well as pelvic inflammatory disease (PID).

How Can It Be Prevented?

One of the reasons that HIV is so dangerous is that a person can have the virus for a long time without knowing it. That person can then spread the virus to others through high-risk behaviors. HIV transmission can be prevented by:

· abstaining from sex (not having oral, vaginal, or anal sex)

· always using latex condoms for all types of sexual intercourse

· avoiding contact with the bodily fluids through which HIV is transmitted

· never sharing needles

How Do Doctors Test for and Treat HIV?

If you think that you may have HIV or AIDS or if you have had a partner who may have HIV or AIDS, see your family doctor, adolescent doctor, or gynecologist. He or she will talk with you and perform tests. The doctor may do a blood test or a swab of the inside of your cheek. Depending on what type of test is done, results may take from a few hours to several days. Let the doctor know the best way to reach you confidentially with any test results.

People can also get tested for HIV/AIDS at special AIDS clinics around the country. Clinics offer both anonymous (meaning the clinic doesn't know a person's name) and confidential (meaning they know who a person is but keep it private) testing. Most AIDS testing centers will ask you to follow up for counseling to get your results, whether the test is negative or positive.

If you're not sure how to find a doctor or get an AIDS test, you can contact the National AIDS Hotlines at (800) 342-AIDS (English) or (800) 344-7432 (Spanish). A specialist there will explain what you should do next.

There is no cure for AIDS, which makes prevention so important. Combinations of antiviral drugs and drugs that boost the immune system have allowed many people with HIV to resist infections, stay healthy, and prolong their lives, but these medications are not a cure. Right now there is no vaccine to prevent HIV and AIDS, although researchers are working on developing one.

DIABETES MELLITUS

DIABETES MELLITUS

Diabetes mellitus, often simply referred to as diabetes—is a group of metabolic diseases in which a person has high blood sugar, either because the body does not produce enough insulin, or because cells do not respond to the insulin that is produced. This high blood sugar produces the classical symptoms of polyuria (frequent urination), polydipsia (increased thirst) andpolyphagia (increased hunger).
There are three main types of diabetes:
 Type 1 diabetes: results from the body's failure to produce insulin, and presently requires the person to inject insulin. (Also referred to as insulin-dependent diabetes mellitus, IDDM for short, and juvenile diabetes.)
 Type 2 diabetes: results from insulin resistance, a condition in which cells fail to use insulin properly, sometimes combined with an absolute insulin deficiency.
 Gestational diabetes: is when pregnant women, who have never had diabetes before, have a high blood glucose level during pregnancy. It may precede development of type 2 DM.
Other forms of diabetes mellitus include congenital diabetes, which is due to genetic defects of insulin secretion, cystic fibrosis-related diabetes, steroid diabetes induced by high doses of glucocorticoids, and several forms of monogenic diabetes.
All forms of diabetes have been treatable since insulin became available in 1921, and type 2 diabetes may be controlled with medications. Both type 1 and 2 are chronic conditions that usually cannot be cured. Pancreas transplants have been tried with limited success in type 1 DM; gastric bypass surgery has been successful in many with morbid obesity and type 2 DM. Gestational diabetes usually resolves after delivery. Diabetes without proper treatments can cause many complications. Acute complications include hypoglycemia, diabetic ketoacidosis, or nonketotic hyperosmolar coma. Serious long-term complications include cardiovascular disease, chronic renal failure, retinal damage. Adequate treatment of diabetes is thus important, as well as blood pressure control and lifestyle factors such as smoking cessation and maintaining a healthy body weight.
As of 2000 at least 171 million people worldwide suffer from diabetes, or 2.8% of the population. Type 2 diabetes is by far the most common, affecting 90 to 95% of the U.S. diabetes population.
Definition
The term diabetes, without qualification, usually refers to diabetes mellitus, which roughly translates to excessive sweet urine (known as "glycosuria"). Several rare conditions are also named diabetes. The most common of these is diabetes insipidus in which large amounts of urine are produced (polyuria), which is not sweet (insipidus meaning "without taste" in Latin).
The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and non-insulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. Various sources have defined "type 3 diabetes" as: gestational diabetes, insulin-resistant type 1 diabetes (or "double diabetes"), type 2 diabetes which has progressed to require injected insulin, and latent autoimmune diabetes of adults (or LADA or "type 1.5" diabetes)
Classification
Most cases of diabetes mellitus fall into three broad categories: type 1, type 2, and gestational diabetes. A few other types are described.
Type 1 diabetes
Type 1 diabetes mellitus is characterized by loss of the insulin-producing beta cells of the islets of Langerhans in the pancreas leading to insulin deficiency. This type of diabetes can be further classified as immune-mediated or idiopathic. The majority of type 1 diabetes is of the immune-mediated nature, where beta cell loss is a T-cell mediated autoimmune attack. There is no known preventive measure against type 1 diabetes, which causes approximately 10% of diabetes mellitus cases in North America and Europe. Most affected people are otherwise healthy and of a healthy weight when onset occurs. Sensitivity and responsiveness to insulin are usually normal, especially in the early stages. Type 1 diabetes can affect children or adults but was traditionally termed "juvenile diabetes" because it represents a majority of the diabetes cases in children.
Type 2 diabetes
Type 2 diabetes mellitus is characterized by insulin resistance which may be combined with relatively reduced insulin secretion. The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor. However, the specific defects are not known. Diabetes mellitus due to a known defect are classified separately. Type 2 diabetes is the most common type.
In the early stage of type 2 diabetes, the predominant abnormality is reduced insulin sensitivity. At this stage hyperglycemia can be reversed by a variety of measures and medications that improve insulin sensitivity or reduce glucose production by the liver.
Gestational diabetes
Gestational diabetes mellitus (GDM) resembles type 2 diabetes in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2%–5% of all pregnancies and may improve or disappear after delivery. Gestational diabetes is fully treatable but requires careful medical supervision throughout the pregnancy. About 20%–50% of affected women develop type 2 diabetes later in life.
Even though it may be transient, untreated gestational diabetes can damage the health of the fetus or mother. Risks to the baby include macrosomia (high birth weight), congenital cardiac and central nervous system anomalies, and skeletal muscle malformations. Increased fetal insulin may inhibit fetal surfactant production and cause respiratory distress syndrome. Hyperbilirubinemia may result from red blood cell destruction. In severe cases, perinatal death may occur, most commonly as a result of poor placental perfusion due to vascular impairment. Labor may be indicated with decreased placental function. A cesarean section may be performed if there is marked fetal distress or an increased risk of injury associated with macrosomia, such as shoulder dystocia.
A 2008 study completed in the U.S. found that the number of American women entering pregnancy with preexisting diabetes is increasing. In fact the rate of diabetes in expectant mothers has more than doubled in the past 6 years. This is particularly problematic as diabetes raises the risk of complications during pregnancy, as well as increasing the potential that the children of diabetic mothers will also become diabetic in the future.
Other types
Pre-diabetes indicates a condition that occurs when a person's blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 diabetes. Many people destined to develop type 2 diabetes spend many years in a state of pre-diabetes which has been termed "America's largest healthcare epidemic.
Some cases of diabetes are caused by the body's tissue receptors not responding to insulin (even when insulin levels are normal, which is what separates it from type 2 diabetes); this form is very uncommon. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function. Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis). Diseases associated with excessive secretion of insulin-antagonistic hormones can cause diabetes (which is typically resolved once the hormone excess is removed). Many drugs impair insulin secretion and some toxins damage pancreatic beta cells. The ICD-10 (1992) diagnostic entity, malnutrition-related diabetes mellitus (MRDM or MMDM, ICD-10 code E12), was deprecated by the World Health Organization when the current taxonomy was introduced in 1999.
Following is a comprehensive list of other causes of diabetes:
 Genetic defects of β-cell Function
 Maturity onset diabetes of the young (MODY)
 Mitochondrial DNA mutations
 Genetic defects in insulin processing or insulin action
 Defects in proinsulin conversion
 Insulin gene mutations
 Insulin receptor mutations
 Exocrine Pancreatic Defects
 Chronic pancreatitis
 Pancreatectomy
 Pancreatic neoplasia
 Cystic fibrosis
 Hemochromatosis
 Fibrocalculous pancreatopathy
 Endocrinopathies
 Growth hormone excess (acromegaly)
 Cushing syndrome
 Hyperthyroidism
 Pheochromocytoma
 Glucagonoma
 Infections
 Cytomegalovirus infection
 Coxsackievirus B
 Drugs
 Glucocorticoids
 Thyroid hormone
 β-adrenergic agonists

Signs and symptoms

Overview of the most significant symptoms of diabetes.
The classical symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst) and polyphagia (increased hunger). Symptoms may develop rapidly (weeks or months) in type 1 diabetes while in type 2 diabetes they usually develop much more slowly and may be subtle or absent.
Prolonged high blood glucose causes glucose absorption, which leads to changes in the shape of the lenses of the eyes, resulting in vision changes; sustained sensible glucose control usually returns the lens to its original shape. Blurred vision is a common complaint leading to a diabetes diagnosis; type 1 should always be suspected in cases of rapid vision change, whereas with type 2 change is generally more gradual, but should still be suspected.
People (usually with type 1 diabetes) may also present with diabetic ketoacidosis, a state of metabolic dysregulation characterized by the smell of acetone; a rapid, deep breathing known as Kussmaul breathing; nausea; vomiting and abdominal pain; and an altered states of consciousness.
A rarer but equally severe possibility is hyperosmolar nonketotic state, which is more common in type 2 diabetes and is mainly the result of dehydration. Often, the patient has been drinking extreme amounts of sugar-containing drinks, leading to a vicious circle in regard to the water loss.
A number of skin rashes can occur in diabetes that are collectively known as diabetic dermadromes.
Causes
The cause of diabetes depends on the type. Type 2 diabetes is due primarily to lifestyle factors and genetics.
Type 1 diabetes is also partly inherited and then triggered by certain infections, with some evidence pointing at Coxsackie B4 virus. There is a genetic element in individual susceptibility to some of these triggers which has been traced to particular HLA genotypes (i.e., the genetic "self" identifiers relied upon by the immune system). However, even in those who have inherited the susceptibility, type 1 diabetes mellitus seems to require an environmental trigger.
Pathophysiology


The fluctuation of blood sugar (red) and the sugar-lowering hormone insulin (blue) in humans during the course of a day with three meals. One of the effects of a sugar-rich vs a starch-rich meal is highlighted.


Mechanism of insulin release in normal pancreatic beta cells. Insulin production is more or less constant within the beta cells, irrespective of blood glucose levels. It is stored within vacuoles pending release, via exocytosis, which is primarily triggered by food, chiefly food containing absorbable glucose. The chief trigger is a rise in blood glucose levels after eating
Insulin is the principal hormone that regulates uptake of glucose from the blood into most cells (primarily muscle and fat cells, but not central nervous system cells). Therefore deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.
Humans are capable of digesting some carbohydrates, in particular those most common in food; starch, and some disaccharides such as sucrose, are converted within a few hours to simpler forms most notably the monosaccharide glucose, the principal carbohydrate energy source used by the body. The rest are passed on for processing by gut flora largely in the colon. Insulin is released into the blood by beta cells (β-cells), found in the Islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage.
Insulin is also the principal control signal for conversion of glucose to glycogen for internal storage in liver and muscle cells. Lowered glucose levels result both in the reduced release of insulin from the beta cells and in the reverse conversion of glycogen to glucose when glucose levels fall. This is mainly controlled by the hormone glucagon which acts in the opposite manner to insulin. Glucose thus forcibly produced from internal liver cell stores (as glycogen) re-enters the bloodstream; muscle cells lack the necessary export mechanism. Normally liver cells do this when the level of insulin is low (which normally correlates with low levels of blood glucose).
Higher insulin levels increase some anabolic ("building up") processes such as cell growth and duplication, protein synthesis, and fat storage. Insulin (or its lack) is the principal signal in converting many of the bidirectional processes of metabolism from a catabolic to an anabolic direction, and vice versa. In particular, a low insulin level is the trigger for entering or leaving ketosis (the fat burning metabolic phase).
If the amount of insulin available is insufficient, if cells respond poorly to the effects of insulin (insulin insensitivity or resistance), or if the insulin itself is defective, then glucose will not have its usual effect so that glucose will not be absorbed properly by those body cells that require it nor will it be stored appropriately in the liver and muscles. The net effect is persistent high levels of blood glucose, poor protein synthesis, and other metabolic derangements, such as acidosis.
When the glucose concentration in the blood is raised beyond its renal threshold (about 10 mmol/L, although this may be altered in certain conditions, such as pregnancy), reabsorption of glucose in the proximal renal tubuli is incomplete, and part of the glucose remains in the urine (glycosuria). This increases the osmotic pressure of the urine and inhibits reabsorption of water by the kidney, resulting in increased urine production (polyuria) and increased fluid loss. Lost blood volume will be replaced osmotically from water held in body cells and other body compartments, causing dehydration and increased thirst.
Diagnosis
2006 WHO Diabetes criteria edit

Condition 2 hour glucose Fasting glucose
mmol/l(mg/dl) mmol/l(mg/dl)
Normal <7.8 (<140) <6.1 (<110)
Impaired fasting glycaemia <7.8 (<140) ≥ 6.1(≥110) & <7.0(<126)
Impaired glucose tolerance ≥7.8 (≥140) <7.0 (<126)
Diabetes mellitus ≥11.1 (≥200) ≥7.0 (≥126)
Diabetes mellitus is characterized by recurrent or persistent hyperglycemia, and is diagnosed by demonstrating any one of the following:
 Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL).
 Plasma glucose ≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral glucose load as in aglucose tolerance test.
 Symptoms of hyperglycemia and casual plasma glucose ≥ 11.1 mmol/L (200 mg/dL).
 Glycated hemoglobin (Hb A1C) ≥ 6.5%.
A positive result, in the absence of unequivocal hyperglycemia, should be confirmed by a repeat of any of the above-listed methods on a different day. It is preferable to measure a fasting glucose level because of the ease of measurement and the considerable time commitment of formal glucose tolerance testing, which takes two hours to complete and offers no prognostic advantage over the fasting test. According to the current definition, two fasting glucose measurements above 126 mg/dL (7.0 mmol/L) are considered diagnostic for diabetes mellitus.
People with fasting glucose levels from 100 to 125 mg/dL (5.6 to 6.9 mmol/L) are considered to have impaired fasting glucose. Patients with plasma glucose at or above 140 mg/dL (7.8 mmol/L), but not over 200 mg/dL (11.1 mmol/L), two hours after a 75 g oral glucose load are considered to have impaired glucose tolerance. Of these two pre-diabetic states, the latter in particular is a major risk factor for progression to full-blown diabetes mellitus as well as cardiovascular disease.
Management
Diabetes mellitus is a chronic disease which is difficult to cure. Management concentrates on keeping blood sugar levels as close to normal ("euglycemia") as possible without presenting undue patient danger. This can usually be with close dietary management, exercise, and use of appropriate medications (insulin only in the case of type 1 diabetes mellitus. Oral medications may be used in the case of type 2 diabetes, as well as insulin).
Patient education, understanding, and participation is vital since the complications of diabetes are far less common and less severe in people who have well-managed blood sugar levels. Wider health problems may accelerate the deleterious effects of diabetes. These includesmoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise.
Lifestyle modifications
There are roles for patient education, dietetic support, sensible exercise, with the goal of keeping both short-term and long-term blood glucose levels within acceptable bounds. In addition, given the associated higher risks of cardiovascular disease, lifestyle modifications are recommended to control blood pressure.
Medications
Oral medications
Routine use of aspirin has not been found to improve outcomes in uncomplicated diabetes.
Insulin
Main article: Insulin therapy
Type 1 treatments usually include combinations of regular or NPH insulin, and/or synthetic insulin analogs.
Support
In countries using a general practitioner system, such as the United Kingdom, care may take place mainly outside hospitals, with hospital-based specialist care used only in case of complications, difficult blood sugar control, or research projects. In other circumstances, general practitioners and specialists share care of a patient in a team approach. Optometrists, podiatrists/chiropodists, dietitians, physiotherapists, nursing specialists (e.g., DSNs (Diabetic Specialist Nurse)), nurse practitioners, or Certified Diabetes Educators, may jointly provide multidisciplinary expertise. In countries where patients must provide for their own health care (e.g. in the US, and in much of the undeveloped world).
Peer support links people living with diabetes. Within peer support, people with a common illness share knowledge and experience that others, including many health workers, do not have. Peer support is frequent, ongoing, accessible and flexible and can take many forms—phone calls, text messaging, group meetings, home visits, and even grocery shopping. It complements and enhances other health care services by creating the emotional, social and practical assistance necessary for managing disease and staying healthy.
Prognosis
Diabetes doubles the risk of vascular problems, including cardiovascular disease.
According to one study, women with high blood pressure (hypertension) were three times more likely to develop type 2 diabetes as compared with women with optimal BP after adjusting for various factors such as age, ethnicity, smoking, alcohol intake, body mass index (BMI), exercise, family history of diabetes, etc. The study was conducted by researchers from the Brigham and Women’s Hospital, Harvard Medical School and the Harvard School of Public Health, USA, who followed over 38,000 female health professionals for ten years.
Except in the case of type 1 diabetes, which always requires insulin replacement, the way type 2 diabetes is managed may change with age. Insulin production decreases because of age-related impairment of pancreatic beta cells. Additionally, insulin resistance increases because of the loss of lean tissue and the accumulation of fat, particularly intra-abdominal fat, and the decreased tissue sensitivity to insulin. Glucose tolerance progressively declines with age, leading to a high prevalence of type 2 diabetes and postchallenge hyperglycemia in the older population. Age-related glucose intolerance in humans is often accompanied by insulin resistance, but circulating insulin levels are similar to those of younger people. Treatment goals for older patients with diabetes vary with the individual, and take into account health status, as well as life expectancy, level of dependence, and willingness to adhere to a treatment regimen. Glycated hemoglobin is better than fasting glucose for determining risks of cardiovascular disease and death from any cause.
Epidemiology


Prevalence of diabetes worldwide in 2000 (per 1000 inhabitants). World average was 2.8%.
no data ≤ 7.5 7.5–15 15–22.5 22.5–30 30–37.5 37.5–45 45–52.5 52.5–60 60–67.5 67.5–75 75–82.5 ≥ 82.5


Disability-adjusted life year for diabetes mellitus per 100,000 inhabitants in 2002.
no data ≤ 100 100-200 200-300 300-400 400-500 500-600 600-700 700-800 800-900 900-1000 1000-1500 ≥ 1500
In 2000, according to the World Health Organization, at least 171 million people worldwide suffer from diabetes, or 2.8% of the population. Its incidence is increasing rapidly, and it is estimated that by 2030, this number will almost double. Diabetes mellitus occurs throughout the world, but is more common (especially type 2) in the more developed countries. The greatest increase in prevalence is, however, expected to occur in Asia and Africa, where most patients will probably be found by 2030. The increase in incidence of diabetes in developing countries follows the trend of urbanization and lifestyle changes, perhaps most importantly a "Western-style" diet. This has suggested an environmental (i.e., dietary) effect, but there is little understanding of the mechanism(s) at present, though there is much speculation, some of it most compellingly presented.
For at least 20 years, diabetes rates in North America have been increasing substantially. In 2008 there were about 24 million people with diabetes in the United States alone, from those 5.7 million people remain undiagnosed. Other 57 million people are estimated to have pre-diabetes.
The Centers for Disease Control has termed the change an epidemic. The National Diabetes Information Clearinghouse estimates that diabetes costs $132 billion in the United States alone every year. About 5%–10% of diabetes cases in North America are type 1, with the rest being type 2. The fraction of type 1 in other parts of the world differs. Most of this difference is not currently understood. The American Diabetes Association cite the 2003 assessment of the National Center for Chronic Disease Prevention and Health Promotion (Centers for Disease Control and Prevention) that 1 in 3 Americans born after 2000 will develop diabetes in their lifetime.
According to the American Diabetes Association, approximately 18.3% (8.6 million) of Americans age 60 and older have diabetes. Diabetes mellitus prevalence increases with age, and the numbers of older persons with diabetes are expected to grow as the elderly population increases in number. The National Health and Nutrition Examination Survey (NHANES III) demonstrated that, in the population over 65 years old, 18% to 20% have diabetes, with 40% having either diabetes or its precursor form of impaired glucose tolerance.
Indigenous populations in first world countries have a higher prevalence and increasing incidence of diabetes than their corresponding non-indigenous populations. In Australia the age-standardised prevalence of self-reported diabetes in Indigenous Australians is almost 4 times that of non-indigenous Australians. Preventative community health programs such as Sugar Man (diabetes education) are showing some success in tackling this problem.
History
(pronounced /ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɨs/;/mɨˈlaɪtəs/ or /ˈmɛlɨtəs/) was coined by Aretaeus of Cappadocia. It was derived from the Greek verb διαβαίνειν, diabaínein, itself formed from the prefix dia-, "across, apart," and the verb bainein, "to walk, stand." The verb diabeinein meant "to stride, walk, or stand with legs asunder"; hence, its derivative diabētēs meant "one that straddles," or specifically "a compass, siphon." The sense "siphon" gave rise to the use of diabētēs as the name for a disease involving the discharge of excessive amounts of urine. Diabetes is first recorded in English, in the form diabete, in a medical text written around 1425. In 1675, Thomas Willis added the word mellitus, from the Latinmeaning "honey", a reference to the sweet taste of the urine. This sweet taste had been noticed in urine by the ancient Greeks, Chinese, Egyptians, Indians, and Persians. In 1776, Matthew Dobson confirmed that the sweet taste was because of an excess of a kind of sugar in the urine and blood of people with diabetes.
Diabetes mellitus appears to have been a death sentence in the ancient era. Hippocrates makes no mention of it, which may indicate that he felt the disease was incurable. Aretaeus did attempt to treat it but could not give a good prognosis; he commented that "life (with diabetes) is short, disgusting and painful."
Sushruta (6th century BCE) identified diabetes and classified it as Medhumeha. He further identified it with obesity and sedentary lifestyle, advising exercises to help "cure" it. The ancient Indians tested for diabetes by observing whether ants were attracted to a person's urine, and called the ailment "sweet urine disease" (Madhumeha). The Chinese, Japanese and Korean words for diabetes are based on the same ideographs (糖尿病) which mean "sugar urine disease".
In medieval Persia, Avicenna (980–1037) provided a detailed account on diabetes mellitus in The Canon of Medicine, "describing the abnormal appetite and the collapse of sexual functions," and he documented the sweet taste of diabetic urine. Like Aretaeus before him, Avicenna recognized a primary and secondary diabetes. He also described diabetic gangrene, and treated diabetes using a mixture of lupine,trigonella (fenugreek), and zedoary seed, which produces a considerable reduction in the excretion of sugar, a treatment which is still prescribed in modern times. Avicenna also "described diabetes insipidus very precisely for the first time", though it was later Johann Peter Frank (1745–1821) who first differentiated between diabetes mellitus and diabetes insipidus.
Although diabetes has been recognized since antiquity, and treatments of various efficacies have been known in various regions since themiddle Ages, and in legend for much longer, pathogenesis of diabetes has only been understood experimentally since about 1900. The discovery of a role for the pancreas in diabetes is generally ascribed to Joseph von Mering and Oskar Minkowski, who in 1889 found that dogs whose pancreas was removed developed all the signs and symptoms of diabetes and died shortly afterwards. In 1910, Sir Edward Albert Sharpey-Schafer suggested that people with diabetes were deficient in a single chemical that was normally produced by the pancreas—he proposed calling this substance insulin, from the Latin insula, meaning island, in reference to the insulin-producing islets of Langerhansin the pancreas.
The endocrine role of the pancreas in metabolism, and indeed the existence of insulin, was not further clarified until 1921, when Sir Frederick Grant Banting and Charles Herbert Best repeated the work of Von Mering and Minkowski, and went further to demonstrate they could reverse induced diabetes in dogs by giving them an extract from the pancreatic islets of Langerhans of healthy dogs. Banting, Best, and colleagues (especially the chemist Collip) went on to purify the hormone insulin from bovine pancreases at the University of Toronto. This led to the availability of an effective treatment—insulin injections—and the first patient was treated in 1922. For this, Banting and laboratory director MacLeod received the Nobel Prize in Physiology or Medicine in 1923; both shared their Prize money with others in the team who were not recognized, in particular best and Collip. Banting and Best made the patent available without charge and did not attempt to control commercial production. Insulin production and therapy rapidly spread around the world, largely as a result of this decision. Banting is honored by World Diabetes Day which is held on his birthday, November 14.
The distinction between what is now known as type 1 diabetes and type 2 diabetes was first clearly made by Sir Harold Percival (Harry) Himsworth, and published in January 1936.
Despite the availability of treatment, diabetes has remained a major cause of death. For instance, statistics reveal that the cause-specificmortality rate during 1927 amounted to about 47.7 per 100,000 population in Malta.
Other landmark discoveries include:
 Identification of the first of the sulfonylureas in 1942
 Reintroduction of the use of biguanides for Type 2 diabetes in the late 1950s. The initial phenformin was withdrawn worldwide (in the U.S. in 1977) due to its potential for sometimes fatal lactic acidosis and metformin was first marketed in France in 1979, but not until 1994 in the US.
 The determination of the amino acid sequence of insulin (by Sir Frederick Sanger, for which he received a Nobel Prize)
 The radioimmunoassay for insulin, as discovered by Rosalyn Yalow and Solomon Berson (gaining Yalow the 1977 Nobel Prize in Physiology or Medicine)
 The three-dimensional structure of insulin (PDB 2INS)
 Dr Gerald Reaven's identification of the constellation of symptoms now called metabolic syndrome in 1988
 Demonstration that intensive glycemic control in type 1 diabetes reduces chronic side effects more as glucose levels approach 'normal' in a large longitudinal study, and also in type 2 diabetics in other large studies
 Identification of the first thiazolidinedione as an effective insulin sensitizer during the 1990s
In 1980, U.S. biotech company Genentech developed human insulin. The insulin is isolated from genetically altered bacteria (the bacteria contain the human gene for synthesizing human insulin), which produce large quantities of insulin. The purified insulin is distributed to pharmacies for use by diabetes patients.
Society and culture
The 1990 "St. Vincent Declaration was the result of international efforts to improve the care accorded to those with diabetes. Doing so is important both in terms of quality of life and life expectancy but also economically—expenses due to diabetes have been shown to be a major drain on health-and productivity-related resources for healthcare systems and governments.
Several countries established more and less successful national diabetes programmes to improve treatment of the disease.
A study shows that diabetic patients with neuropathic symptoms such as numbness or tingling in feet or hands are twice as likely to beunemployed as those without the symptoms.

OZONE LAYER

Ozone layer

The ozone layer is a layer in Earth's atmosphere which contains relatively high concentrations of ozone (O₃). This layer absorbs 97–99% of the Sun's high frequency ultraviolet light, which is potentially damaging to life on Earth. It is mainly located in the lower portion of the stratosphere from approximately 13 km to 40 km above Earth, though the thickness varies seasonally and geographically. The ozone layer was discovered in 1913 by the French physicistsCharles Fabry and Henri Buisson. Its properties were explored in detail by the British meteorologist G. M. B. Dobson, who developed a simple spectrophotometer (the Dobsonmeter) that could be used to measure stratospheric ozone from the ground. Between 1928 and 1958 Dobson established a worldwide network of ozone monitoring stations which continues to operate today. The "Dobson unit", a convenient measure of the columnar density of ozone overhead, is named in his honor.

Origin of ozone

Ozone-oxygen cycle in the ozone layer.

The photochemical mechanisms that give rise to the ozone layer were discovered by the British physicist Sidney Chapman in 1930. Ozone in the Earth's stratosphere is created by ultraviolet light striking oxygen molecules containing two oxygen atoms (O₂), splitting them into individual oxygen atoms (atomic oxygen); the atomic oxygen then combines with unbroken O₂ to create ozone, O₃. The ozone molecule is also unstable (although, in the stratosphere, long-lived) and when ultraviolet light hits ozone it splits into a molecule of O₂ and an atom of atomic oxygen, a continuing process called the ozone-oxygen cycle, thus creating an ozone layer in the stratosphere, the region from about 10 to 50 km (32,000 to 164,000 feet) above Earth's surface. About 90% of the ozone in our atmosphere is contained in the stratosphere. Ozone concentrations are greatest between about 20 and 40 km, where they range from about 2 to 8 parts per million. If all of the ozone were compressed to the pressure of the air at sea level, it would be only a few millimeters thick

Ultraviolet light and ozone

Levels of ozone at various altitudes and blocking of ultraviolet radiation.

UV-B energy levels at several altitudes. Blue line shows DNA sensitivity. Red line shows surface energy level with 10% decrease in ozone

Although the concentration of the ozone in the ozone layer is very small, it is vitally important to life because it absorbs biologically harmful ultraviolet (UV) radiation coming from the Sun. UV radiation is divided into three categories, based on its wavelength; these are referred to as UV-A (400–315 nm), UV-B (315–280 nm), and UV-C (280–100 nm). UV-C, which would be very harmful to all living things, is entirely screened out by ozone at around 35 km altitude. UV-B radiation can be harmful to the skin and is the main cause of sunburn; excessive exposure can also cause genetic damage, resulting in problems such as skin cancer. The ozone layer is very effective at screening out UV-B; for radiation with a wavelength of 290 nm, the intensity at the top of the atmosphere is 350 million times stronger than at the Earth's surface. Nevertheless, some UV-B reaches the surface. Most UV-A reaches the surface; this radiation is significantly less harmful, although it can potentially cause genetic damage.

Distribution of ozone in the stratosphere

The thickness of the ozone layer—that is, the total amount of ozone in a column overhead—varies by a large factor worldwide, being in general smaller near the equator and larger towards the poles. It also varies with season, being in general thicker during the spring and thinner during the autumn in the northern hemisphere. The reasons for this latitude and seasonal dependence are complicated, involving atmospheric circulation patterns as well as solar intensity.

Since stratospheric ozone is produced by solar UV radiation, one might expect to find the highest ozone levels over the tropics and the lowest over Polar Regions. The same argument would lead one to expect the highest ozone levels in the summer and the lowest in the winter. The observed behavior is very different: most of the ozone is found in the mid-to-high latitudes of the northern and southern hemispheres, and the highest levels are found in the spring, not summer, and the lowest in the autumn, not winter in the northern hemisphere. During winter, the ozone layer actually increases in depth. This puzzle is explained by the prevailing stratospheric wind patterns, known as the Brewer-Dobson circulation. While most of the ozone is indeed created over the tropics, the stratospheric circulation then transports it pole ward and downward to the lower stratosphere of the high latitudes. However in the southern hemisphere, owing to the ozone hole phenomenon, the lowest amounts of column ozone found anywhere in the world are over the Antarctic in the southern spring period of September and October.

Brewer-Dobson circulation in the ozone layer.

The ozone layer is higher in altitude in the tropics, and lower in altitude in the extra tropics, especially in the Polar Regions. This altitude variation of ozone results from the slow circulation that lifts the ozone-poor air out of the troposphere into the stratosphere. As this air slowly rises in the tropics, ozone is produced by the overhead sun which photolyzes oxygen molecules. As this slow circulation bends towards the mid-latitudes, it carries the ozone-rich air from the tropical middle stratosphere to the mid-and-high latitudes lower stratosphere. The high ozone concentrations at high latitudes are due to the accumulation of ozone at lower altitudes.

The Brewer-Dobson circulation moves very slowly. The time needed to lift an air parcel from the tropical tropopause near 16 km (50,000 ft) to 20 km is about 4–5 months (about 30 feet (9.1 m) per day). Even though ozone in the lower tropical stratosphere is produced at a very slow rate, the lifting circulation is so slow that ozone can build up to relatively high levels by the time it reaches 26 km.

Ozone amounts over the continental United States (25°N to 49°N) are highest in the northern spring (April and May). These ozone amounts fall over the course of the summer to their lowest amounts in October, and then rise again over the course of the winter. Again, wind transport of ozone is principally responsible for the seasonal evolution of these higher latitude ozone patterns.

The total column amount of ozone generally increases as we move from the tropics to higher latitudes in both hemispheres. However, the overall column amounts are greater in the northern hemisphere high latitudes than in the southern hemisphere high latitudes. In addition, while the highest amounts of column ozone over the Arctic occur in the northern spring (March–April), the opposite is true over the Antarctic, where the lowest amounts of column ozone occur in the southern spring (September–October).

Ozone depletion

NASA projections of stratospheric ozone concentrations if chlorofluorocarbons had not been banned.

The ozone layer can be depleted by free radical catalysts, including nitric oxide (NO), nitrous oxide (N₂O), hydroxyl(OH), atomic chlorine (Cl), and atomic bromine (Br). While there are natural sources for all of these species, the concentrations of chlorine and bromine have increased markedly in recent years due to the release of large quantities of man-made organohalogen compounds, especially chlorofluorocarbons (CFCs) and bromofluorocarbons. These highly stable compounds are capable of surviving the rise to the stratosphere, where Cl and Br radicals are liberated by the action of ultraviolet light. Each radical is then free to initiate and catalyze a chain reaction capable of breaking down over 100,000 ozone molecules. The breakdown of ozone in the stratosphere results in the ozone molecules being unable to absorb ultraviolet radiation. Consequently, unabsorbed and dangerous ultraviolet-B radiation is able to reach the Earth’s surface. Ozone levels, over the northern hemisphere, have been dropping by 4% per decade. Over approximately 5% of the Earth's surface, around the north and south poles, much larger (but seasonal) declines have been seen; these are the ozone holes.

In 2009, nitrous oxide (N₂O) was the largest ozone-depleting substance emitted through human activities.

Regulation

In 1978, the United States, Canada and Norway enacted bans on CFC-containing aerosol sprays that are thought to damage the ozone layer. The European Community rejected an analogous proposal to do the same. In the U.S., chlorofluorocarbons continued to be used in other applications, such as refrigeration and industrial cleaning, until after the discovery of the Antarctic ozone hole in 1985. After negotiation of an international treaty (the Montreal Protocol), CFC production was sharply limited beginning in 1987 and phased out completely by 1996^.

On August 2, 2003, scientists announced that the depletion of the ozone layer may be slowing down due to the international ban on CFCs. Three satellites and three ground stations confirmed that the upper atmosphere ozone depletion rate has slowed down significantly during the past decade. The study was organized by the American Geophysical Union. Some breakdown can be expected to continue due to CFCs used by nations which have not banned them, and due to gases which are already in the stratosphere. CFCs have very long atmospheric lifetimes, ranging from 50 to over 100 years, so the final recovery of the ozone layer is expected to require several lifetimes.

Compounds containing C–H bonds have been designed to replace the function of CFC's (such as HCFC), since these compounds are more reactive and less likely to survive long enough in the atmosphere to reach the stratosphere where they could affect the ozone layer. While being less damaging than CFC's, HCFC's also have a significant negative impact on the ozone layer. HCFC's are also being phased out.