Opioids affect the human body by binding to a group of related proteins conveniently known as opioid receptors. By connecting to these receptors in a certain manner, they convince receptor-bearing cells in the brain, spinal cord, and intestine to do useful things like reduce the sensation of pain (while making you feel warm and fuzzy), suppress coughing, and prevent an onslaught of diarrhea. In addition to opiates such as morphine and codeine, which are naturally produced by the opium poppy, we've figured out how to put together a whole slew of opioids using chemistry. This involves either modifying poppy-produced opiates, as is done to make heroin (from morphine) and oxycodone (from thebaine), or synthesizing entirely new drugs such as fentanyl from scratch.
Desmethylprodine, also known as 1-methyl-4-phenyl-4-propionoxypiperidine (MPPP), was invented by a pair of drug company scientists in 1947. Structurally, it's very similar to meperidine (pethidine, Demerol), another entirely synthetic opioid. Seeing as it wasn't any more effective than meperidine at killing pain, the drug company decided to nix its production. Nearly thirty years later, a chemistry grad student by the name of Barry Kidston read about MPPP and decided to try making some of it for personal use. While the first couple of batches yielded a successful means of getting high, the situation soon devolved into a plot fit for an imaginary TV show I'm calling Breaking Sad. Kidston got sloppy. He apparently started to rush through the chemical reactions used to make MPPP and then didn't purify the drug properly. As a result, an impurity called 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) ended up in the final product. If you put MPTP in your body, it's converted into a neurotoxic substance with a fine-tuned appetite for destruction. It specifically annihilates dopamine-releasing neurons in a part of the brain responsible for controlling muscle movements, resulting in permanent symptoms resembling those seen in people with Parkinson's disease (parkinsonism). Kidston ended up hospitalized with acute parkinsonism after unwittingly dosing himself with MPTP. Although doctors eventually figured out they could treat his condition with a L-DOPA, which boosts dopamine levels in the brain, Kidston shortly passed away after overdosing on cocaine and codeine. A couple of other folks also ended up in the hospital after using poorly made MPPP and having their brains partially wrecked by MPTP. In at least two cases, the drug was tested and found to consist mostly of MPTP with only trace amounts of MPPP!
|MPTP rains down destruction on neurons in the substantia nigra (Photo source)|
Heroin, a suped-up version of morphine, is sold on the street mixed with an assortment of materials intended to do some combination of (1) cheaply bulking up the drug so it can be sold for more money, (2) deceiving buyers into thinking the quality of the drug is better than it really is, so it can be sold for more money, (3) altering its effects in a desirable way, and (4) making it easier to use. Inexpensive materials used to dilute heroin include sugars, flour, and talc. Black tar heroin, a heroin-containing mixture named for its appearance and consistency, has been known to be bulked up by adding dirt or ground up paper previously soaked in black shoe polish. Yuck. Quinine, a plant-derived alkaloid used to treat malaria, is used to dilute heroin in part because it also has a bitter taste and apparently produces a sensation in the lungs resembling what you feel after injecting heroin. Another bitter heroin mimic is paracetamol (acetaminophen, Tylenol), which has the added bonuses of also being painkiller, albeit a way weaker one, and having a similar melting point. Fentanyl is an incredibly strong opioid sometimes added to crappy heroin to increase its potency. Then there's caffeine and procaine, which when mixed with heroin cause the opioid to vaporize at a lower temperature, making it easier to smoke. Additionally, procaine is a local anesthetic (a numbing agent) and so can reduce any pain caused by injecting the drug.
By far the nastiest accidental addition to heroin has to be people-eating bacteria such as Bacillus anthracis (causes anthrax) and Clostridium botulinum (causes botulism). They produce spores capable of surviving being heated up within a spoonful of heroin before it's injected into a vein or under the skin. In fact, the heat can cause the spores to germinate, priming them for action. Injection provides instant access to a human tissue buffet, and infections brought about in this manner are often horrendous (I highly recommend not doing an image search). Heroin can become contaminated with harmful bacteria during its production, shipment, sale, or use. Cases of anthrax in heroin users living in Western Europe have been explained as being the result of Bacillus anthracis spores getting into the drug as it's moved from Afghanistan via Turkey, possibly from the animal skins in which the drug is smuggled (livestock in the Middle East are occasionally killed by the bacterium) or because bone meal contaminated with spores is used to bulk up the drug prior to selling it. Spores of Clostridium botulinum, naturally found in soil, are thought to get into heroin via the materials added to bulk it up or from dirty tools used to administer the drug. Although C. botulinum requires an environment lacking in oxygen in order to flourish, and the tissues of the human body are typically well-supplied with oxygen via the blood flowing to and from them, a heroin user can inadvertently create oxygen-poor pockets within their body where the bacterium can grow and pump out toxins. Heroin doesn't dissolve well in water, so people looking to inject it into them typically use a solution of citric acid, heated gently, to facilitate dissolution. Repeatedly introducing an acid into the body results in tissue damage and scar formation, reducing blood flow and thus the local level of oxygen. And that's how you get infected with C. botulinum.
Brett MM, Hallas G, Mpamugo O. 2004. Wound botulism in the UK and Ireland. Journal of Medical Microbiology 53(Pt 6):555-561. [Full text]
Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96.
Fahn S, Sulzer D. 2004. Neurodegeneration and neuroprotection in Parkinson disease. NeuroRx 1(1):139-154. [Full text]
Price EP et al. 2012. Molecular epidemiologic investigation of an anthrax outbreak among heroin users, Europe. Emerging Infectious Diseases 18(8):1307-1313. [Full text]