The following environmental factors have been shown to increase the risk of DCS:

- the magnitude of the pressure reduction ratio – a large pressure reduction ratio is more likely to cause DCS than a small one.

- repetitive exposures – repetitive dives within a short period of time (a few hours) increase the risk of developing DCS. Repetitive ascents to altitudes above within similar short periods increase the risk of developing altitude DCS.

- the rate of ascent – the faster the ascent the greater the risk of developing DCS. The US Navy Dive Manual indicates that ascent rates greater than about when diving increase the chance of DCS, while recreational dive tables such as the Bühlmann tables require an ascent rate of with the last taking at least one minute. An individual exposed to a rapid decompression (high rate of ascent) above has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.

- the duration of exposure – the longer the duration of the dive, the greater is the risk of DCS. Longer flights, especially to altitudes of and above, carry a greater risk of altitude DCS.

- underwater diving before flying – divers who ascend to altitude soon after a dive increase their risk of developing DCS even if the dive itself was within the dive table safe limits. Dive tables make provisions for post-dive time at surface level before flying to allow any residual excess nitrogen to outgas. However, the pressure maintained inside even a pressurized aircraft may be as low as the pressure equivalent to an altitude of above sea level. Therefore, the assumption that the dive table surface interval occurs at normal atmospheric pressure is invalidated by flying during that surface interval, and an otherwise-safe dive may then exceed the dive table limits.

- diving before travelling to altitude – DCS can occur without flying if the person moves to a high-altitude location on land immediately after diving, for example, scuba divers in Eritrea who drive from the coast to the Asmara plateau at increase their risk of DCS.

- diving at altitude – diving in water whose surface altitude is above — for example, Lake Titicaca is at — without using versions of decompression tables or dive computers that are modified for high-altitude.

Although the occurrence of DCS is not easily predictable, many predisposing factors are known. They may be considered as either environmental or individual.

Decompression sickness and arterial gas embolism in recreational diving are associated with certain demographic, environmental, and dive style factors. A statistical study published in 2005 tested potential risk factors: age, gender, body mass index, smoking, asthma, diabetes, cardiovascular disease, previous decompression illness, years since certification, dives in the last year, number of diving days, number of dives in a repetitive series, last dive depth, nitrox use, and drysuit use. No significant associations with risk of decompression sickness or arterial gas embolism were found for asthma, diabetes, cardiovascular disease, smoking, or body mass index. Increased depth, previous DCI, larger number of consecutive days diving, and being male were associated with higher risk for decompression sickness and arterial gas embolism. Nitrox and drysuit use, greater frequency of diving in the past year, increasing age, and years since certification were associated with lower risk, possibly as indicators of more extensive training and experience.

The cause is the most mysterious aspect of the disease. Commentators then and now put much blame on the generally poor sanitation, sewage and contaminated water supplies of the time, which might have harboured the source of infection. The first outbreak at the end of the Wars of the Roses means that it may have been brought over from France by the French mercenaries whom Henry VII used to gain the English throne. However, the "Croyland Chronicle" mentions that Thomas Stanley, 1st Earl of Derby used the "sweating sickness" as an excuse not to join with Richard III's army prior to the Battle of Bosworth.

Relapsing fever has been proposed as a possible cause. This disease, which is spread by ticks and lice, occurs most often during the summer months, as did the original sweating sickness. However, relapsing fever is marked by a prominent black scab at the site of the tick bite and a subsequent skin rash.

Noting symptom overlap with hantavirus pulmonary syndrome, several scientists proposed an unknown hantavirus as the cause. A critique of this hypothesis included the argument that, whereas sweating sickness was thought to be transmitted from human to human, hantaviruses are rarely spread in this way. However, infection via human-to-human contact has been proven in hantavirus outbreaks in Argentina.

The following factors increase some people's susceptibility to airsickness:

- Fatigue, stress, and anxiety, are some factors that can increase susceptibility to motion sickness of any type.

- The use of alcohol, drugs, and medications may also contribute to airsickness.

- Additionally, airsickness is more common in women (especially during menstruation or pregnancy), young children, and individuals prone to other types of motion sickness.

- Although airsickness is uncommon among experienced pilots, it does occur with some frequency in student pilots.

Ascending slowly is the best way to avoid altitude sickness. Avoiding strenuous activity such as skiing, hiking, etc. in the first 24 hours at high altitude reduces the symptoms of AMS. Alcohol and sleeping pills are respiratory depressants, and thus slow down the acclimatization process and should be avoided. Alcohol also tends to cause dehydration and exacerbates AMS. Thus, avoiding alcohol consumption in the first 24–48 hours at a higher altitude is optimal.

This disease is spread by insect vectors. The biological vector of the virus is the "Culicoides" (midges) species. However, this disease can also be transmitted by species of mosquitoes including "Culex", "Anopheles", and "Aedes", and species of ticks such as "Hyalomma" and "Rhipicephalus".

As of 2010 it caused around 9,000 deaths, down from 34,000 in 1990. As of 2000, the disability-adjusted life-years (9 to 10 years) lost due to sleeping sickness are 2.0 million. From 2010-2014, there was an estimated 55 million people at risk for "gambiense" African Trypanosomiasis and over 6 million people at risk for "rhodesiense" African Trypanosomiasis. In 2014, the World Health Organization reported 3,797 cases of Human African Trypanosomiasis when the predicted number of cases were to be 5,000. The number of total reported cases in 2014 is an 86% reduction to the total number of cases reported in 2000.

The disease has been recorded as occurring in 37 countries, all in sub-Saharan Africa. It occurs regularly in southeast Uganda and western Kenya, and killed more than 48,000 Africans in 2008. The Democratic Republic of the Congo is the most affected country in the world, accounting for 75% of the "Trypanosoma brucei gambiense" cases. The population at risk being about 69 million with one third of this number being at a 'very high' to 'moderate' risk and the remaining two thirds at a 'low' to 'very low' risk. The number of people being affected by the disease has declined. At this rate, sleeping sickness elimination is a possibility. The World Health Organization plans to eradicate sleeping sickness by the year 2020.

There is currently no treatment for AHS.

Control of an outbreak in an endemic region involves quarantine, vector control and vaccination. To prevent this disease, the affected horses are usually slaughtered, and the uninfected horses are vaccinated against the virus. Three vaccines currently exist, which include a polyvalent vaccine, a monovalent vaccine, and a monovalent inactivated vaccine. This disease can also be prevented by destroying the insect vector habitats using insecticides.

Pre-acclimatization is when the body develops tolerance to low oxygen concentrations before ascending to an altitude. It significantly reduces risk because less time has to be spent at altitude to acclimatize in the traditional way. Additionally, because less time has to be spent on the mountain, less food and supplies have to be taken up. Several commercial systems exist that use altitude tents, so called because they mimic altitude by reducing the percentage of oxygen in the air while keeping air pressure constant to the surroundings.

Travelers who are susceptible to motion sickness can minimize symptoms by:

- Choosing a window seat with a view of the ground or of lower clouds, such that motion can be detected. This will not work if the plane is flown in the clouds for a long duration.

- Choosing seats with the smoothest ride in regards to pitch (the seats over the wings in an airplane). (This may not be sufficient for sensitive individuals who need to see ground movement)

- Sitting facing forward while focusing on distant objects rather than trying to read or look at something inside the airplane.

- Eating dry crackers, olives or suck on a lemon, to dry out the mouth, lessening nausea.

- Drinking a carbonated beverage.

The symptoms and signs, as described by physician John Caius and others, were as follows: the disease began very suddenly with a sense of apprehension, followed by cold shivers (sometimes very violent), giddiness, headache, and severe pains in the neck, shoulders and limbs, with great exhaustion. After the cold stage, which might last from half an hour to three hours, the hot and sweating stage followed. The characteristic sweat broke out suddenly without any obvious cause. Accompanying the sweat, or after, was a sense of heat, headache, delirium, rapid pulse, and intense thirst. Palpitation and pain in the heart were frequent symptoms. No skin eruptions were noted by observers including Caius. In the final stages, there was either general exhaustion and collapse, or an irresistible urge to sleep, which Caius thought to be fatal if the patient was permitted to give way to it. One attack did not offer immunity, and some people suffered several bouts before dying. The disease tended to occur in summer and early autumn.

Currently there are few medically related prevention options for African Trypanosomiasis (i.e. no vaccine exists for immunity). Although the risk of infection from a tsetse fly bite is minor (estimated at less than 0.1%), the use of insect repellants, wearing long-sleeved clothing, avoiding tsetse-dense areas, implementing bush clearance methods and wild game culling are the best options to avoid infection available for local residents of affected areas.

At the 25th ISCTRC (International Scientific Council for Trypanosomiasis Research and Control) in Mombasa, Kenya, in October 1999, the idea of an African-wide initiative to control tsetse and trypanosomiasis populations was discussed. During the 36th summit of the Organization for African Unity in Lome, Togo, in July 2000, a resolution was passed to form the Pan African Tsetse and Trypanosomiasis Eradication Campaign (PATTEC). The campaign works to eradicate the tsetse vector population levels and subsequently the protozoan disease, by use of insecticide-impregnated targets, fly traps, insecticide-treated cattle, ultra-low dose aerial/ground spraying (SAT) of tsetse resting sites and the sterile insect technique (SIT). The use of SIT in Zanzibar proved effective in eliminating the entire population of tsetse flies but was expensive and is relatively impractical to use in many of the endemic countries afflicted with African trypanosomiasis.

Regular active surveillance, involving detection and prompt treatment of new infections, and tsetse fly control is the backbone of the strategy used to control sleeping sickness. Systematic screening of at-risk communities is the best approach, because case-by-case screening is not practical in endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to areas of high infection rates. Such screening efforts are important because early symptoms are not evident or serious enough to warrant patients with gambiense disease to seek medical attention, particularly in very remote areas. Also, diagnosis of the disease is difficult and health workers may not associate such general symptoms with trypanosomiasis. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir. A single case of sexual transmission of West African sleeping sickness has been reported.

Human milk sickness is uncommon today in the United States. Current practices of animal husbandry generally control the pastures and feed of cattle, and the pooling of milk from many producers lowers the risk of tremetol present in dangerous amounts. The poison tremetol is not inactivated by pasteurization. Although extremely rare, milk sickness can occur if a person drinks contaminated milk or eats dairy products gathered from a single cow or from a smaller herd that has fed on the white snakeroot plant. There is no cure, but treatment is available.

The vast majority of victims fully recover without significant lasting problems (sequelae). Death from latrodectism is reported as high as 5% to as low as 0.2%. In the United States, where antivenom is rarely used, there have been no deaths reported for decades.

Despite frequent reference to youth and old age being a predisposing factor it has been demonstrated that young children appear to be at lowest risk for a serious bite, perhaps owing to the rapid use of antivenom. Bite victims who are very young, old, hypotensive, pregnant or who have existing heart problems are reported to be the most likely to suffer complications. However, due to the low incidence of complications these generalizations simply refer to special complications (see Special circumstances).

The most common hypothesis for the cause of motion sickness is that it functions as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in a ship with no windows), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the discordance, the brain will come to the conclusion that the individual is hallucinating and further conclude that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.

An alternative theory, also known as the Nystagmus Hypothesis, has been proposed based on stimulation of the vagus nerves resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eye's six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherrington's Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherrington's Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, 10th nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.

Motion sickness is a condition in which a disagreement exists between visually perceived movement and the vestibular system's sense of movement. Depending on the cause, it can also be referred to as seasickness, car sickness, simulation sickness or airsickness.

Dizziness, fatigue and nausea are the most common symptoms of motion sickness. Sopite syndrome, in which a person feels fatigue or tiredness, is also associated with motion sickness. "Nausea" in Greek means seasickness ("naus" means ship). If the motion causing nausea is not resolved, the sufferer will usually vomit. Vomiting often will not relieve the feeling of weakness and nausea, which means the person might continue to vomit until the cause of the nausea is treated.

The term Winterbottom's sign derives from descriptions of the posterior cervical lymphadenopathy associated with African trypanosomiasis made by a slave trader using the sign to weed out the ill.

Morning sickness may be an evolved trait that protects the baby against toxins ingested by the mother. Evidence in support of this theory includes:

- Morning sickness is very common among pregnant women, which argues in favor of its being a functional adaptation and against the idea that it is a pathology.

- Fetal vulnerability to toxins peaks at around 3 months, which is also the time of peak susceptibility to morning sickness.

- There is a good correlation between toxin concentrations in foods, and the tastes and odors that cause revulsion.

Women who have "no" morning sickness are more likely to miscarry. This may be because such women are more likely to ingest substances that are harmful to the fetus.

In addition to protecting the fetus, morning sickness may also protect the mother. A pregnant woman's immune system is suppressed during pregnancy, presumably to reduce the chances of rejecting tissues of her own offspring. Because of this, animal products containing parasites and harmful bacteria can be especially dangerous to pregnant women. There is evidence that morning sickness is often triggered by animal products including meat and fish.

If morning sickness is a defense mechanism against the ingestion of toxins, the prescribing of anti-nausea medication to pregnant women may have the undesired side effect of causing birth defects or miscarriages by encouraging harmful dietary choices.

The cause of morning sickness is unknown. While some have claimed it to be due to psychological reasons, this is not supported by evidence.

Nausea and vomiting may also occur with molar pregnancy.

Bites from "Latrodectus" occur usually because of accidental contact with the spiders. The species are not aggressive to humans naturally, but may bite when trapped. As such, bite incidents may be described as accidents. Reports of epidemics were associated with agricultural areas in Europe in the last two centuries. However the European spider is associated with fields and humans come in contact only during harvest. For example, in the 1950s researchers believed that three bites happened each year and with an epidemic up to 180 each year.

Conversely, redback and North American black widows live in proximity with people and several thousand black widow bites are reported to Poison Control in the United States each year. About 800 are reported by medical personnel. Amongst those 800 bites only a dozen had major complications and none were fatal.

In Perth, Australia, for example there were 156 bites in children from redback spiders over 20 years. Twice as many boys were bitten as girls, mostly toddlers. A third of the children developed latrodectism and there were no deaths.

Winterbottom's sign is seen in the early phase of African trypanosomiasis, a disease caused by the parasites "Trypanosoma brucei rhodesiense" and "Trypanosoma brucei gambiense" which is more commonly known as African sleeping sickness. Dr. Anthony Martinelli describes Winterbottom's sign as the swelling of lymph nodes (lymphadenopathy) along the back of the neck, in the posterior cervical chain of lymph nodes, as trypanosomes travel in the lymphatic fluid and cause inflammation.

It may be suggestive of cerebral infection.

Some of the drugs associated with serum sickness are:

- allopurinol

- barbiturates

- captopril

- cephalosporins

- griseofulvin

- penicillins

- phenytoin

- procainamide

- quinidine

- streptokinase

- sulfonamides

- rituximab

- ibuprofen

- infliximab

Allergenic extracts, hormones and vaccines can also cause serum sickness.

Sweating sickness is "an acute, febrile, tickborne toxicosis characterized mainly by a profuse, moist eczema and hyperemia of the skin and visible mucous membranes." It affects cattle, mainly calves, mostly in southern and eastern Africa. It is caused by toxins that develop in some ticks of the "Hyalomma truncatum" species.

Milk sickness, also known as tremetol vomiting or, in animals, as trembles, is a kind of poisoning, characterized by trembling, vomiting, and severe intestinal pain, that affects individuals who ingest milk, other dairy products, or meat from a cow that has fed on white snakeroot plant, which contains the poison tremetol.

Although very rare today, milk sickness claimed thousands of lives among migrants to the Midwest in the early 19th century in the United States, especially in frontier areas along the Ohio River Valley and its tributaries where white snakeroot was prevalent. New settlers were unfamiliar with the plant and its properties. A notable victim was Nancy Hanks Lincoln, the mother of Abraham Lincoln, who died in 1818. Nursing calves and lambs may have died from their mothers' milk contaminated with snakeroot, although the adult cows and sheep showed no signs of poisoning. Cattle, horses, and sheep are the animals most often poisoned.

Anna Pierce Hobbs Bixby, called Dr. Anna on the frontier, is credited today by the American medical community with having identified white snakeroot as the cause of the illness. Told about the plant's properties by an elderly Shawnee woman she befriended, Bixby did testing to observe and document evidence. She wrote up her findings to share the discovery in the medical world. The Shawnee woman's name has been lost to history.