It was further found that by combining both methods, i.e. 10 seconds with paper towels and 20 seconds with hot air, bacterial transfer by touching was reduced by 99%. This was demonstrated in one experiment where hands were touched against a chamois and the level of bacteria was 75,000. This dropped to 1,500 after the dual drying system was performed.
It was reported that on average individuals spent inadequate time in hand drying using public facilities--an average of six seconds with paper towels and 15 seconds with hot air. There is little reason to suggest that these times would be any different for workers in food facilities.
The research findings show that the hand drying practices of food handlers are a critical step in personal hygiene. This relates both to their own safety and that of the food they handle. With some microorganisms such as Escherichia coli O157 and Hepatitis A less than 100 units are required to be ingested to initiate an infection and therefore a review by food processing establishments is required of the procedures used and the equipment available for hand washing and drying.

Ciguatera
Each year in Australia a small, yet significant, number of people will develop an illness after eating certain species of tropical fish. This illness is known as ciguatera poisoning and in most victims there is an acute episode of illness lasting for a few weeks, while in some, chronic symptoms may persist for months or even years. Ciguatera poisoning is not confined to Australia but has been shown to have a circumtropical distribution, usually with a close association to coral reefs. It is caused by the ingestion of a powerful toxin, ciguatoxin (CTX), that occurs in the tissues of the offending fish and gives rise to considerable morbidity in that over 50,000 people may be affected each year.
Ciguatera poisoning has been reported to be the most frequent form of food-borne disease of a chemical nature in the USA with most cases emanating from Florida and Hawaii. Episodes of illness have been documented from the Caribbean and the Pacific regions. Cases also occur annually along the tropical coast of eastern Australia and major outbreaks have occurred in Sydney in the past 10 years. Cases of ciguatera poisoning have also occurred outside these regions where either tropical fish have been purchased or have been consumed in the tropics before returning to temperate regions.
The largest outbreak of ciguatera poisoning in Australia occurred in 1987 in the temperate city of Sydney. Sixty-three people were poisoned after eating Spanish mackerel marketed in Sydney but captured in a ciguatera endemic region of Harvey Bay in Queensland, just below the southern margin of the Great Barrier Reef some 1,300 km to the north of Sydney.  The most dramatic case of mass poisoning attributed to CTX and related compounds occurred in 1994 when 500 people in Madagascar were poisoned resulting in 98 deaths.
Originally it was believed that a single chemical entity, ciguatoxin (CTX) was responsible for the syndrome of human ciguatera intoxication, this may now need modification. Variants of the CTX molecule can occur in a number of species of tropical fish and the ratios of the different forms of CTX are also variable. It may be possible that the there are five toxins involved (CTX, maitotoxin, scaritoxin, okadaic scid and prorocentrolid) in the ciguatera syndrome. Other toxins including palytoxin and carchatoxins may contribute to the general ciguatera syndrome and may afford an explanation for the variability of symptoms reported in humans.
Over 100 species of fish have been listed worldwide as potential carriers of CTX. In Australia several species of primarily carnivorous fish including mackerel, barracuda and coral trout are responsible for human intoxication. Three species of fish, from reefs in the vicinity of Cairns, red bass, chinamen fish and paddletail have shown to have a high rate of toxicity of 4%, 7% and 18% respectively. It is believed that a dinoflagellate, Gambierdiscus harbours the toxin(s) and enters the fish tissues after being ingested.
CTX has profound effects upon the human nervous system. After ingestion of toxic fish, the course of the affliction often follows a reasonably predictable pattern. The initial symptoms are usually gastrointestinal and develop at an early stage some three to twelve hours (usually about six hours) after ingestion of toxic fish. These symptoms can include nausea, vomiting, diarrhoea and abdominal cramps. Some twelve to eighteen hours after consumption of the toxic fish, neurological symptoms usually begin to appear. These can include paraesthesia of the lips and extremities, arthralgia, myalgia, dental pain, convulsions, muscular paralysis, vertigo, severe headache, short-term memory loss, temperature perception reversals, diaphoresis and puritis. Some patients display psychological disturbances, manifested as anxiety and depression for months, and sometimes years after intoxication. Cardiovascular symptoms which include bradycardia, tachycardia, arrhythmia and hypotension are also evident in a number of victims. The variability of the duration and severity of dysfunction is a feature of the ciguatera syndrome. However, variations of the amount of toxin consumed and the physiological status of the victim may account for some of this difference in response.
There is no simple test developed, with a high sensitivity and specificity, for the detection of CTX in fish samples. Laboratory assessment is generally confined to injecting mice with an extract from the fish.
The treatment of ciguatera poisoning remains essentially symptomatic. The long-term symptoms of ciguatera poisoning  have been treated with variable success using a variety of agents including vitamin B₁₂, calcium gluconate, antihistamines and antidepressants.