Sodium chloride is believed to mitigate the reproduction of Velvet, however this treatment is not itself sufficient for the complete eradication of an outbreak. Additional, common medications added directly to the fish's environment include copper sulfate, methylene blue, formalin, malachite green and acriflavin, all of which can be found in common fish medications designed specifically to combat this disease. Additionally, because Velvet parasites derive a portion of their energy from photosynthesis, leaving a tank in total darkness for seven days provides a helpful supplement to chemical curatives. Finally, some enthusiasts recommend raising the water temperature of an infected fish's environment, in order to quicken the life cycle (and subsequent death) of Velvet parasites; however this tactic is not practical for all fish, and may induce immunocompromising stress.

Velvet (in an aquarium environment) is usually spread by contaminated tanks, fish, and tools (such as nets or testing supplies). There are also rare reports of frozen live foods (such as bloodworms) containing dormant forms of the species. Frequently, however, the parasite is endemic to a fish, and only causes a noticeable "outbreak" after the fish's immune system is compromised for some other reason. The disease is highly contagious and can prove fatal to fish.

Fungicidal agents such as azadirachtin and phytoallexin have been used against some muscardine pathogens. Silkworm breeders dust their cages with slaked lime to discourage fungal growth. In India a dust of chaff soaked in formalin is applied to the larvae.

Muscardine is a disease of insects. It is caused by many species of entomopathogenic fungus. Many muscardines are known for affecting silkworms. Muscardine may also be called calcino.

While studying muscardine in silkworms in the 19th century, Agostino Bassi found that the causal agent was a fungus. This was the first demonstration of the germ theory of disease, the first time a microorganism was recognized as an animal pathogen.

There are many types of muscardine. They are often named for the color of the conidial layer each fungus leaves on its host.

Molds are ubiquitous, and mold spores are a common component of household and workplace dust. In large amounts they can be a health hazard to humans, potentially causing allergic reactions and respiratory problems.

Some molds produce mycotoxins that can pose serious health risks to humans and animals. "Toxic mold" refers to molds which produce mycotoxins, such as "Stachybotrys chartarum". Exposure to high levels of mycotoxins can lead to neurological problems and death. Prolonged exposure (for example, daily exposure) can be particularly harmful.

The smuts are multicellular fungi characterized by their large numbers of teliospores. The smuts get their name from a Germanic word for dirt because of their dark, thick-walled, and dust-like teliospores. They are mostly Ustilaginomycetes (of the class Teliomycetae, subphylum Basidiomycota) and can cause plant disease. The smuts are grouped with the other basidiomycetes because of their commonalities concerning sexual reproduction.

Smuts are cereal and crop pathogens that most notably affect members of the grass family ("Poaceae"). Economically important hosts include maize, barley, wheat, oats, sugarcane, and forage grasses. They eventually hijack the plants' reproductive systems, forming galls which darken and burst, releasing fungal teliospores which infect other plants nearby. Before infection can occur, the smuts need to undergo a successful mating to form dikaryotic hyphae (two haploid cells fuse to form a dikaryon).

Infants may develop respiratory symptoms as a result of exposure to "Penicillium", a fungal genus. Signs of mold-related respiratory problems in an infant include a persistent cough or wheeze. Increased exposure increases the probability of developing respiratory symptoms during the first year of life. Studies have indicated a correlation between the probability of developing asthma and exposure to "Penicillium".

Mold exposure has a variety of health effects, and sensitivity to mold varies. Exposure to mold may cause throat irritation, nasal stuffiness, eye irritation, cough and wheezing and skin irritation in some cases. Exposure to mold may heighten sensitivity, depending on the time and nature of exposure. People with chronic lung diseases are at higher risk for mold allergies, and will experience more severe reactions when exposed to mold. Damp indoor environments correlate with upper-respiratory-tract symptoms, such as coughing and wheezing in people with asthma.

Sugarcane smut or "Ustilago scitaminea Sydow" is caused by the fungus "Sporisorium scitamineum"; smut was previously known as "Ustilago scitaminea". The smut 'whip' is a curved black structure which emerges from the leaf whorl, and which aids in the spreading of the disease. Sugarcane smut causes significant losses to the economic value of a sugarcane crop. Sugarcane smut has recently been found in the eastern seaboard areas of Australia, one of the world's highest-yielding sugar areas.

For the sugarcane crop to be infected by the disease, large spore concentrations are needed. The fungi uses its "smut-whip" to ensure that the disease is spread to other plants, which usually occurs over a time period of three months. As the inoculum is spread, the younger sugarcane buds just coming out of the soil will be the most susceptible. Because water is necessary for spore germination, irrigation has been shown to be a factor in spreading the disease. Therefore, special precautions need to be taken during irrigation to prevent spreading of the smut.

Another way to prevent the disease from occurring in the sugarcane is to use fungicide. This can be done by either pre-plant soaking or post-plant spraying with the specific fungicide. Pre-plant soaking has been proven to give the best results in preventing the disease, but post-plant spraying is a practical option for large sugarcane cultivations.

There are a very small number of cases of human-to-human transmission of "B. dermatitidis" related to dermal contact or sexual transmission of disseminated blastomycosis of the genital tract among spouses.

Sex is another factor inconstantly linked to contraction of blastomycosis: though many studies show more men than women affected, some show no sex-related bias. As mentioned above, most cases are in middle aged adults, but all age groups are affected, and cases in children are not uncommon.

Exposure to cobalt metal dust is most common in the fabrication of tungsten carbide. Another potential source is wear and tear of metal-on-metal hip prostheses; however, this is a relatively uncommon phenomenon with 18 reported cases being documented in the medical literature.

Since lead has been used widely for centuries, the effects of exposure are worldwide. Environmental lead is ubiquitous, and everyone has some measurable blood lead level. Atmospheric lead pollution increased dramatically beginning in the 1950s as a result of the widespread use of leaded gasoline. Lead is one of the largest environmental medicine problems in terms of numbers of people exposed and the public health toll it takes. Lead exposure accounts for about 0.2% of all deaths and 0.6% of disability adjusted life years globally.

Although regulation reducing lead in products has greatly reduced exposure in the developed world since the 1970s, lead is still allowed in products in many developing countries. In all countries that have banned leaded gasoline, average blood lead levels have fallen sharply. However, some developing countries still allow leaded gasoline, which is the primary source of lead exposure in most developing countries. Beyond exposure from gasoline, the frequent use of pesticides in developing countries adds a risk of lead exposure and subsequent poisoning. Poor children in developing countries are at especially high risk for lead poisoning. Of North American children, 7% have blood lead levels above 10 μg/dL, whereas among Central and South American children, the percentage is 33 to 34%. About one fifth of the world's disease burden from lead poisoning occurs in the Western Pacific, and another fifth is in Southeast Asia.

In developed countries, people with low levels of education living in poorer areas are most at risk for elevated lead. In the US, the groups most at risk for lead exposure are the impoverished, city-dwellers, and immigrants. African-American children and those living in old housing have also been found to be at elevated risk for high blood lead levels in the US. Low-income people often live in old housing with lead paint, which may begin to peel, exposing residents to high levels of lead-containing dust.

Risk factors for elevated lead exposure include alcohol consumption and smoking (possibly because of contamination of tobacco leaves with lead-containing pesticides). Adults with certain risk factors might be more susceptible to toxicity; these include calcium and iron deficiencies, old age, disease of organs targeted by lead (e.g. the brain, the kidneys), and possibly genetic susceptibility.

Differences in vulnerability to lead-induced neurological damage between males and females have also been found, but some studies have found males to be at greater risk, while others have found females to be.

In adults, blood lead levels steadily increase with increasing age. In adults of all ages, men have higher blood lead levels than women do. Children are more sensitive to elevated blood lead levels than adults are. Children may also have a higher intake of lead than adults; they breathe faster and may be more likely to have contact with and ingest soil. Children of ages one to three tend to have the highest blood lead levels, possibly because at that age they begin to walk and explore their environment, and they use their mouths in their exploration. Blood levels usually peak at about 18–24 months old. In many countries including the US, household paint and dust are the major route of exposure in children.

Evidence suggests lead exposure is associated with high blood pressure, and studies have also found connections between lead exposure and coronary heart disease, heart rate variability, and death from stroke, but this evidence is more limited. People who have been exposed to higher concentrations of lead may be at a higher risk for cardiac autonomic dysfunction on days when ozone and fine particles are higher.

Disease states associated with carotenoderma include hypothyroidism, diabetes mellitus, anorexia nervosa, nephrotic syndrome, and liver disease. In hypothyroidism and diabetes mellitus, the underlying mechanism of hypercarotenemia is thought to be both impaired conversion of beta-carotene into retinol and the associated increased serum lipids. Diabetes mellitus has also been associated with carotenoderma through disease-specific diets that are rich in vegetables. In the nephrotic syndrome, the hypercarotenemia is related to the associated increased serum lipids, similar to the above entities.

It is of note that kidney dysfunction in general is associated with hypercarotenemia as a result of decreased excretion of carotenoids. Liver dysfunction, regardless of origin, causes hypercarotenemia as a result of the impaired conversion of carotenoids to retinol. This is of particular interest because jaundice and carotenoderma can coexist in the same patient. Anorexia nervosa causes carotenoderma mainly through diets that are rich in carotenoids and the associated hypothyroidism. It tends to be more common in the restricting subtype of this disease, and is associated with numerous other dermatologic manifestations, such as brittle hair and nails, lanugo-like body hair, and xerosis. Although Alzheimer's disease has been associated with carotenoderma in some reports, most studies on serum carotenoids in these patients show that their levels of carotenoids and retinol are depressed, and may be associated with the development of dementia. A true association between Alzheimer's disease and carotenoderma is unclear at this time. There have been case reports in the literature of increased serum carotenoids and carotenoderma that is unresponsive to dietary measures, with a genetic defect in carotenoid metabolic enzymes proposed. Canthaxanthin and astaxanthin are naturally occurring carotenoids that are used in the British and US food industry to add color to foods such as sausage and fish. Canthaxanthin has been used in over-the-counter “tanning pills” in the United States and Europe, but is not currently Food and Drug Administration (FDA)-approved for this purpose in the United States because of its adverse effects. These include hepatitis, urticaria, aplastic anemia, and a retinopathy characterized by yellow deposits and subsequent visual field defects.

Infants and small children are especially prone to carotenoderma because of the cooked, mashed, and pureed vegetables that they eat. Processing and homogenizing causes carotene to become more available for absorption. A small 2.5 ounce jar of baby food sweet potatoes or carrots contains about 400-500% of an infant's recommended daily value of carotene. In addition to that source of carotene, infants are usually prescribed a liquid vitamin supplement, such as Tri-Vi-Sol, which contains vitamin A.

The values of soluble cobalt salts has been estimated to be between 150 and 500 mg/kg. Thus, for a 100 kg person the LD would be about 20 grams.

There are three main mechanisms involved in hypercarotenemia: excessive dietary intake of carotenoids, increased serum lipids, and decreased metabolism of carotenoids. The most common reported cause of hypercarotenemia (and thus carotenoderma) is increased intake, either through increased dietary foods or nutritional supplements. This change takes approximately 4 to 7 weeks to be recognized clinically. Numerous ingested substances are rich in carotenoids. Increased serum lipids also cause hypercarotenemia because there are increased circulating lipoproteins that contain bound carotenoids. Finally, in certain disease states, the metabolism and conversion of carotenoids to retinol is slowed, which can lead to decreased clearance and increased plasma levels. Elevated serum beta-carotene does not necessarily result in carotenosis, but the latter is likely to show up when intake is more than 20 mg/day. Average adult intake in the U.S. around 2.3 mg/day. One medium-sized carrot has about 4.0 mg.

Carotenoderma can be divided into two major types, primary and secondary. Primary carotenoderma is that developing from increased oral ingestion of carotenoids, whereas secondary carotenoderma is caused from underlying disease states that increase serum carotenoids with normal oral intake of these compounds. Primary and secondary carotenoderma can coexist in the same patient.

Foods associated with high levels of carotenoids include:

Cork is often harvested from the cork oak ("Quercus suber") and stored in slabs in a hot and humid environment until covered in mold. Cork workers may be exposed to organic dusts in this process, leading to this disease.

Radon () is a radioactive, colorless, odorless, tasteless noble gas, occurring naturally as the decay product of radium. It is one of the densest substances that remains a gas under normal conditions, and is considered to be a health hazard due to its radioactivity. Its most stable isotope, Rn, has a half-life of 3.8 days. Due to its high radioactivity, it has been less well-studied by chemists, but a few compounds are known.

Radon is formed as part of the normal radioactive decay chain of uranium into Pb. Uranium has been present since the earth was formed and its most common isotope has a very long half-life (4.5 billion years), which is the time required for one-half of uranium to break down. Thus, uranium and radon, will continue to occur for millions of years at about the same concentrations as they do now.

Radon is responsible for the majority of the mean public exposure to ionizing radiation. It is often the single largest contributor to an individual's background radiation dose, and is the most variable from location to location. Radon gas from natural sources can accumulate in buildings, especially in confined areas such as attics, and basements. It can also be found in some spring waters and hot springs.

According to a 2003 report "EPA's Assessment of Risks from Radon in Homes" from the United States Environmental Protection Agency, epidemiological evidence shows a clear link between lung cancer and high concentrations of radon, with 21,000 radon-induced U.S. lung cancer deaths per year—second only to cigarette smoking. Thus in geographic areas where radon is present in heightened concentrations, radon is considered a significant indoor air contaminant.

Some systemic diseases can become symptomatic as a skin disorder. These include many endocrine (hormonal) abnormalities, such as hypothyroidism, Cushing's Syndrome (hyperadrenalcorticism), and tumors of the ovaries or testicles.

Atopy is a hereditary and chronic (lifelong) allergic skin disease. Signs usually begin between 6 months and 3 years of age, with some breeds of dog, such as the Golden Retriever showing signs at an earlier age. Dogs with atopic dermatitis are itchy, especially around the eyes, muzzle, ears and feet. In severe cases the irritation is generalised. If the allergens are seasonal, the signs of irritation are similarly seasonal. Many dogs with house dust mite allergy have perennial disease. Some of the allergens associated with atopy in dogs include pollens of trees, grasses and weeds, as well as molds and House dust mite. Ear and skin infections with the bacteria "Staphylococcus pseudintermedius" and the yeast "Malassezia pachydermatis" are common secondary to atopic dermatitis.

Food allergy can be associated with identical signs and some authorities consider food allergy to be a type of atopic dermatitis.

Diagnosis of atopic dermatitis is by elimination of other causes of irritation including fleas, scabies and other parasites such as Cheyletiella and lice. Food allergy can be identified through the use of elimination diet trials in which a novel or hydrolysed protein diet is used for a minimum of 6 weeks and allergies to aeroallergens can be identified using intradermal allergy testing and/or blood testing (allergen-specific IgE ELISA).

Treatment includes avoidance of the offending allergens if possible, but for most dogs this is not practical or effective. Other treatments modulate the adverse immune response to allergens and include antihistamines, steroids, ciclosporin and immunotherapy (a process in which allergens are injected to try to induce tolerance). In many cases shampoos, medicated wipes and ear cleaners are needed to try to prevent the return of infections.

New research into T-cell receptor peptides and their effects on dogs with severe, advanced atopic dermatitis are being investigated.

Radon concentration is usually measured in the atmosphere in becquerels per cubic meter (Bq/m), which is an SI derived unit. As a frame of reference, typical domestic exposures are about 100 Bq/m indoors and 10-20 Bq/m outdoors. In the US, radon concentrations are often measured in picocuries per liter (pCi/l), with 1 pCi/l = 37 Bq/m.

The mining industry traditionally measures exposure using the "working level" (WL) index, and the cumulative exposure in "working level months" (WLM): 1 WL equals any combination of short-lived Rn progeny (Po, Pb, Bi, and Po) in 1 liter of air that releases 1.3 × 10 MeV of potential alpha energy; one WL is equivalent to 2.08 × 10 joules per cubic meter of air (J/m). The SI unit of cumulative exposure is expressed in joule-hours per cubic meter (J·h/m). One WLM is equivalent to 3.6 × 10 J·h/m. An exposure to 1 WL for 1 working month (170 hours) equals 1 WLM cumulative exposure.

A cumulative exposure of 1 WLM is roughly equivalent to living one year in an atmosphere with a radon concentration of 230 Bq/m.

The radon (Rn) released into the air decays to Pb and other radioisotopes. The levels of Pb can be measured. The rate of deposition of this radioisotope is dependent on the weather.

Suberosis, also known as corkhandler's disease or corkworker's lung, is a type of hypersensitivity pneumonitis usually caused by the fungus "Penicillium glabrum" (formerly called "Penicillum frequentans") from exposure to moldy cork dust. "Chrysonilia sitophilia", "Aspergillus fumigatus", uncontaminated cork dust, and "Mucor macedo" may also have significant roles in the pathogenesis of the disease.

Some ways to prevent airborne diseases include washing hands, using appropriate hand disinfection, getting regular immunizations against diseases believed to be locally present, wearing a respirator and limiting time spent in the presence of any patient likely to be a source of infection.

Exposure to a patient or animal with an airborne disease does not guarantee receiving the disease. Because of the changes in host immunity and how much the host was exposed to the particles in the air makes a difference to how the disease affects the body.

Antibiotics are not prescribed for patients to control viral infections. They may however be prescribed to a flu patient for instance, to control or prevent bacterial secondary infections. They also may be used in dealing with air-borne bacterial primary infections, such as pneumonic plague.

Additionally the Centers for Disease Control and Prevention (CDC) has told consumers about vaccination and following careful hygiene and sanitation protocols for airborne disease prevention. Consumers also have access to preventive measures like UV Air purification devices that FDA and EPA-certified laboratory test data has verified as effective in inactivating a broad array of airborne infectious diseases. Many public health specialists recommend social distancing to reduce the transmission of airborne infections.

Ultraviolet (UV) radiation is implicated in cattle with no pigmentation around the eyelids and cattle with prominently placed eyes. Exudate from the sun-burnt skin around the eyes can contain bacteria and attracts flies. UV light also directly damages the corneal epithelium, leading to a breakdown in host innate immunity.

Dust, dried-up plants, tall vegetation, and oversized or incorrectly placed ear tags may cause mechanical damage to the eye and facilitate bacterial colonization.

The disease may be complicated by concurrent infection with viruses such as infectious bovine rhinotracheitis virus (bovine herpesvirus 1) or adenovirus, bacteria such as "Mycoplasma boviculi" or "Listeria monocytogenes", or infestation by "Thelazia", a nematode.

Vitamin A deficiency is also implicated.

IBK is most prevalent in summer and early autumn.

A recent Meat and Livestock Australia report "estimates that the disease costs Australian beef producers AU$23.5 million annually in lost production and treatment costs".

Fungi are ubiquitous organisms that play a vital role in decomposing organic matter. Many species of fungi live on the human body and some will infect nails causing a condition called onychomycosis. There are oral and topical antifungal therapies for this condition, however, in some instances cutting, filing, or abrading the nail may be necessary to improve cure rates. Thickened nails caused by injury, infection, diabetes, psoriasis, or vascular disease may require the use of a mechanical therapy, which can expose the healthcare worker to microbial dust.

Exposure to nail dust was first discussed and described in the literature as an occupational hazard in the early 70’s. In 1975, two female chiropodists were diagnosed with allergic hypersensitivity to nail dust Since that time, there have been a number of occupational-related complaints pertaining to airborne nail dust exposure and efforts have been made to study the podiatric professionals to determine related symptoms. Biological dust from the hand and foot care procedures may deposit in the conjunctiva, nose, and throughout the respiratory tract. The local irritation of these areas can lead to conjunctivitis, itching, tearing, rhinitis, sneezing, asthmatic attacks, bronchitis, and coughing.

The literature suggests that nail dust can be a respiratory sensitizer, which is defined as a substance that when breathed in can trigger an irreversible allergic reaction in the respiratory system. Sensitization does not usually take place immediately, but rather after months or years of exposure to the agent. Once sensitized, even the smallest amount of the substance can trigger asthma, rhinitis, or conjunctivitis that may exhibit the following symptoms: coughing, wheezing, chest tightness, runny or stuffy nose, and watery or prickly eyes. Millar found that within the podiatry profession there is four times the national prevalence of asthma. Hypersensitivity reactions are the most probable disposition for healthcare workers inhaling nail dust, although more serious lung pathology can not be ruled out

It is widely known and accepted that fungi will induce asthma, but it is estimated that only 10% of the population has allergic antibodies to fungal antigens, and half of them, that is 5% of the population, would be asymptomatic, further complicating the link between the fungal dust and troubling symptoms. "Trichophyton rubrum" is the most common fungal cause of nail dystrophy. Studies conducted in England found that the prevalence of "trichophyton rubrum" antibodies in podiatrists ranged from 14%-31%. This is evidence that the podiatrist is heavily exposed to "trichophyton rubrum" as observed in increased precipitating antibodies compared to the general population. It has been suggested that absorption of "trichophyton" fungal antigens can give rise to immunoglobulin E (IgE) antibody production, sensitization of the airways, and symptomatic asthma and rhinitis.

Nail work requiring clipping and drilling is also a potential cause for ocular injury and infection to the podiatrists, podiatric staff, and patients that are exposed to nail fragments and high-speed drills used for grinding. Possible ocular hazards result from exposure to foreign bodies, allergens, bacteria, viruses, fungi and protozoa that can be introduced at the time of eye trauma, or enter as a consequence of damage to the ocular structures; permitting the entry of opportunistic infection. The high-speed rotation of podiatry drill burrs potentially expose the healthcare worker to aerosols containing bloodborne pathogens such as Hepatitis B, Hepatitis C, or HIV. Davies et al. surveyed podiatrists and found that 41% of them complained of eye problems, particularly soreness, burning, itching and excess lacrimation.

A 1990 case illustrates the potential for ocular trauma to the healthcare provider: A podiatrist suffered a lacerated cornea when hit by a metallic shard from the grinding bit or by a fragment from the patient’s toenail. The podiatrist reported fleeting periods of blurriness for several months following the incident. The healthcare worker’s exposure to foreign bodies is not well documented in the literature like they are with dental staff using similar equipment; however, many of these incidents are certain to go unreported. The healthcare provider’s risk of injury during nail care, however slight, warrants the use of simple and inexpensive preventative measures.