The opium poppy was cultivated in lower Mesopotamia as long ago as 3400 BC. The chemical analysis of opium in the 19th century revealed that most of its activity could be ascribed to two ingredients, codeine and morphine.
Heroin was first synthesized in 1874 by C.R. Alder Wright, an English chemist working at St. Mary's Hospital Medical School in London, England. He had been experimenting with combining morphine with various acids. He boiled anhydrous morphine alkaloid with acetic anhydride over a stove for several hours and produced a more potent, acetylated form of morphine, now called diacetylmorphine. The compound was sent to F.M. Pierce of Owens College in Manchester for analysis, who reported the following to Wright:
Doses ... were subcutaneously injected into young dogs and rabbits ... with the following general results ... great prostration, fear, and sleepiness speedily following the administration, the eyes being sensitive, and pupils constrict, considerable salivation being produced in dogs, and slight tendency to vomiting in some cases, but no actual emesis. Respiration was at first quickened, but subsequently reduced, and the heart's action was diminished, and rendered irregular. Marked want of coordinating power over the muscular movements, and loss of power in the pelvis and hind limbs, together with a diminution of temperature in the rectum of about 4° (rectal failure).
Wright's invention, however, did not lead to any further developments, and heroin only became popular after it was independently re-synthesized 23 years later by another chemist, Felix Hoffmann. Hoffmann, working at the Bayer pharmaceutical company in Elberfeld, Germany, was instructed by his supervisor Heinrich Dreser to acetylate morphine with the objective of producing codeine, a natural derivative of the opium poppy, similar to morphine but less potent and less addictive. But instead of producing codeine, the experiment produced a substance that was actually three times more potent than morphine itself. Bayer would name the substance "heroin", probably from the word heroisch, German for heroic, because in field studies people using the medicine felt "heroic".
From 1898 through to 1910 heroin was marketed as a non-addictive morphine substitute and cough medicine for children. Bayer marketed heroin as a cure for morphine addiction before it was discovered that heroin is converted to morphine when metabolized in the liver. The company was somewhat embarrassed by this new finding and it became a historical blunder for Bayer.
As with aspirin, Bayer lost some of its trademark rights to heroin following the German defeat in World War I.
In the United States the Harrison Narcotics Tax Act was passed in 1914 to control the sale and distribution of heroin. The law did allow heroin to be prescribed and sold for medical purposes. In particular, recreational users could often still be legally supplied with heroin. In 1924, the United States Congress passed additional legislation banning the sale, importation or manufacture of heroin in the United States. It is now a Schedule I substance, and is thus illegal there.

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Heroin is produced for the black market through processes of opium refinement. While the production of drugs like LSD requires considerable expertise in chemistry and access to constituents which are now tightly controlled, the refinement of the first three grades of heroin from opium is a relatively simple process requiring only moderate technical expertise and common chemicals. The final grade of heroin favoured in the West is more difficult to produce and involves a potentially dangerous chemical procedure.
First, morphine is isolated from crude opium by being dissolved in water, reacted with lime fertilizer such that the morphine precipitates out, and then reacted again with ammonia. What remains is then mechanically filtered to yield a final product of morphine weighing about 90% less than the original quantity of opium. The morphine is reacted with acetic anhydride — a chemical also used in the production of aspirin — in a five-step process used by most refineries in the Golden Triangle. The first step is to cook the morphine at 85 °C (185 °F) for six hours with an equivalent weight of acetic anhydride. In the second, a treatment of water and hydrochloric acid then purifies the product moderately. When the chemists add sodium carbonate, the particulates settle. Step four involves heating the heroin in a mixture of alcohol and activated charcoal until the alcohol evaporates. The fifth step is optional, as it only changes the heroin into a finer white powder, more easily injectable; this so-called "no. 4 heroin" is principally exported to the Western markets. In this last, most dangerous step, the heroin (after being dissolved in alcohol), precipitates out in tiny white flakes when a mixture of ether and hydrochloric acid is injected; this step is dangerous because the ether may explode, leveling or severely damaging the refinery (as has happened to a number of such facilities).
The purity of the extracted morphine determines in large part the quality of the resulting heroin.
Heroin is also rarely made from codeine by first demethylating with pyridine followed by acetylation with acetic anhydride. The resulting product is an impure mixture of heroin and monoacetylmorphine known as Home Bake.

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For intravenous users of heroin (and any other substance), the use of non-sterile needles and syringes and other related equipment leads to the risk of contracting blood-borne pathogens such as HIV and hepatitis, as well as the risk of contracting bacterial or fungal endocarditis and possibly venous sclerosis.
Poisoning from contaminants added to "cut" or dilute heroin
Chronic constipation
Heroin-induced toxic leukoencephalopathy (very rare, smokers only, the causal reason is currently unknown)
Addiction and constantly growing tolerance. Like all opiates and opioids, long term use can lead to physical addiction.
Decreased kidney function. (although it is not currently known if this is due to adulterants used in the cut)
Many countries and local governments have begun funding programs that supply sterile needles to people who inject illegal drugs in an attempt to reduce these contingent risks and especially the contraction and spread of blood-borne diseases. The Drug Policy Alliance reports that up to 75% of new AIDS cases among women and children are directly or indirectly a consequence of drug use by injection. But despite the immediate public health benefit of needle exchanges, some see such programs as tacit acceptance of illicit drug use. The United States federal government does not operate needle exchanges, although some state and local governments do support needle exchange programs. Needle exchanges have been instrumental in arresting the spread of HIV/AIDS in many communities with a significant heroin using population,[citation needed] Australia being a leader due to its early inception of needle exchanges. Needle exchange programs have also been attributed to saving the public significant amounts of tax money by preventing medical costs which would have been required otherwise for the treatment of diseases spread through the practice of sharing and reusing needles.
A heroin overdose is usually treated with an opioid antagonist, such as naloxone (Narcan), which has a high affinity for opioid receptors but does not activate them. This blocks heroin and other opioid antagonists and causes an immediate return of consciousness and the beginning of withdrawal symptoms when administered intravenously. The half-life of this antagonist is usually much shorter than that of the opiate drugs it is used to block, so the antagonist usually has to be re-administered multiple times until the opiate has been metabolized by the body.
Depending on drug interactions and numerous other factors, death from overdose can take anywhere from several minutes to several hours due to anoxia because the breathing reflex is suppressed by µ-opioids. An overdose is immediately reversible with an opioid antagonist injection. Heroin overdoses can occur due to an unexpected increase in the dose or purity or due to diminished opiate tolerance. However, most fatalities reported as overdoses are probably caused by interactions with other depressant drugs like alcohol or benzodiazepines.
The LD50 for a physically addicted person is prohibitively high,[citation needed] to the point that there is no general medical consensus on where to place it. Several studies done in the 1920s gave users doses of 1,600–1,800 mg of heroin in one sitting, and no adverse effects were reported. This is approximately 16–18 times a normal recreational dose.[citation needed] Even for a non-user, the LD50 can be placed above 350 mg[citation needed] though some sources give a figure of between 75 and 375 mg for a 75 kg person.
Street heroin is of widely varying and unpredictable purity. This means that the user may prepare what they consider to be a moderate dose while actually taking far more than intended. Also, those who use the drug after a period of abstinence have tolerances below what they were during active addiction. If a dose comparable to their previous use is taken, an effect greater to what the user intended is caused, in extreme cases an overdose could result.
It has been speculated that an unknown portion of heroin related deaths are the result of an overdose or allergic reaction to quinine, which may sometimes be used as a cutting agent.
A final source of overdose in users comes from place conditioning. Heroin use, like other drug using behaviors, is highly ritualized. While the mechanism has yet to be clearly elucidated, it has been shown that longtime heroin users, immediately before injecting in a common area for heroin use, show an acute increase in metabolism and a surge in the concentration of opiate-metabolizing enzymes. This acute increase, a reaction to a location where the user has repeatedly injected heroin, imbues him or her with a strong (but temporary) tolerance to the toxic effects of the drug. When the user injects in a different location, this place-conditioned tolerance does not occur, giving the user a much lower-than-expected ability to metabolize the drug. The user's typical dose of the drug, in the face of decreased tolerance, becomes far too high and can be toxic, leading to overdose.
A small percentage of heroin smokers may develop symptoms of toxic leukoencephalopathy. This is believed to be caused by an uncommon adulterant that is only active when heated. Symptoms include slurred speech and difficulty walking.

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