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.

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.

While radon presents the aforementioned risks in adults, exposure in children leads to a unique set of health hazards that are still being researched. The physical composition of children leads to faster rates of exposure through inhalation given that their respiratory rate is higher than that of adults, resulting in more gas exchange and more potential opportunities for radon to be inhaled. In addition to this potentially higher dose of radon inhalation, children have smaller lungs, which can become damaged much more quickly than adults’ lungs. For example, children who are exposed to radon and who live in a household where they are exposed to tobacco smoke have a 20 times greater risk of developing lung cancer.

The resulting health effects in children are similar to those of adults, predominantly including lung cancer and respiratory illnesses such as asthma, bronchitis, and pneumonia. While there have been numerous studies assessing the link between radon exposure and childhood leukemia, the results are largely varied. Many ecological studies show a positive association between radon exposure and childhood leukemia; however, most case control studies have produced a weak correlation. Genotoxicity has been noted in children exposed to high levels of radon, specifically a significant increase of frequency of aberrant cells was noted, as well as an “increase in the frequencies of single and double fragments, chromosome interchanges, [and] number of aberrations chromatid and chromosome type”.

UNSCEAR recommends a reference value of 9 nSv (Bq·h/m).

For example, a person living (7000 h/year) in a concentration of 40 Bq/m receives an effective dose of 1 mSv/year.

Studies of miners exposed to radon and its decay products provide a direct basis for assessing their lung cancer risk. The BEIR VI report, entitled "Health Effects of Exposure to Radon", reported an excess relative risk from exposure to radon that was equivalent to 1.8% per megabecquerel hours per cubic meter (MBq·h/m) (95% confidence interval: 0.3, 35) for miners with cumulative exposures below 30 MBq·h/m. Estimates of risk per unit exposure are 5.38×10 per WLM; 9.68×10/WLM for ever smokers; and 1.67×10 per WLM for never smokers.

According to the UNSCEAR modeling, based on these miner's studies, the excess relative risk from long-term residential exposure to radon at 100 Bq/m is considered to be about 0.16 (after correction for uncertainties in exposure assessment), with about a threefold factor of uncertainty higher or lower than that value.

In other words, the absence of ill effects (or even positive hormesis effects) at 100 Bq/m are compatible with the known data.

The ICPR 65 model follows the same approach, and estimates the relative lifelong risk probability of radon-induced cancer death to 1.23 × 10 per Bq/(m·year). This relative risk is a global indicator; the risk estimation is independent of sex, age, or smoking habit. Thus, if a smoker's chances of dying of lung cancer are 10 times that of a nonsmoker's, the relative risks for a given radon exposure will be the same according to that model, meaning that the absolute risk of a radon-generated cancer for a smoker is (implicitly) tenfold that of a nonsmoker.

The risk estimates correspond to a unit risk of approximately 3–6 × 10 per Bq/m, assuming a lifetime risk of lung cancer of 3%. This means that a person living in an average European dwelling with 50 Bq/m has a lifetime excess lung cancer risk of 1.5–3 × 10. Similarly, a person living in a dwelling with a high radon concentration of 1000 Bq/m has a lifetime excess lung cancer risk of 3–6%, implying a doubling of background lung cancer risk.

The BEIR VI model proposed by the National Academy of Sciences of the USA is more complex. It is a multiplicative model that estimates an excess risk per exposure unit. It takes into account age, elapsed time since exposure, and duration and length of exposure, and its parameters allow for taking smoking habits into account.

In the absence of other causes of death, the absolute risks of lung cancer by age 75 at usual radon concentrations of 0, 100, and 400 Bq/m would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong nonsmokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers.

There is great uncertainty in applying risk estimates derived from studies in miners to the effects of residential radon, and direct estimates of the risks of residential radon are needed.

As with the miner data, the same confounding factor of other carcinogens such as dust applies. Radon concentration is high in poorly ventilated homes and buildings and such buildings tend to have poor air quality, larger concentrations of dust etc. BEIR VI did not consider that other carcinogens such as dust might be the cause of some or all of the lung cancers, thus omitting a possible spurious relationship.

Approximately 21% of the adults affected by asthma report an aggravation of their symptoms while at work and an improvement when away, which implies that they may be suffering from occupational asthma. In the United States, occupational asthma is the most common occupational lung disease. Today, asthma affects as much as 15% of the Canadian population, a statistic reflective of other developed countries, and has increased fourfold in the last 20 years. Various reasons can be identified for this increase, including increase environmental pollution, better diagnostic ability, and greater awareness.

Smoking has a supra-additive effect in increasing the risk of lung cancer in those exposed to asbestos. Studies have shown an increased risk of lung cancer among smokers who are exposed to asbestos compared to nonsmokers.

At present, over 400 workplace substances have been identified as having asthmagenic or allergenic properties. Their existence and magnitude vary by region and industry and can include diisocyanates, acid anhydrides, plicatic acid, and platinum salts (all low molecular weight agents), and animal protein, enzymes, wheat, and latex (high-molecular weight agents). For example, in France the industries most affected are bakeries and cake-shops, automobile industry and hairdressers, whereas in Canada the principal cause is wood dust, followed by isocyanates. Furthermore, the most common cause of occupational asthma in the workplace are isocyanates. Isocyanates are used in the production of motor vehicles and in the application of orthopaedic polyurethane and fibreglass casts.

The occupations most at risk are: adhesive handlers (e.g. acrylate), animal handlers and veterinarians (animal proteins), bakers and millers (cereal grains), carpet makers (gums), electronics workers (soldering resin), forest workers, carpenters and cabinetmakers (wood dust), hairdressers (e.g. persulfate), health care workers (latex and chemicals such as glutaraldehyde), janitors and cleaning staff (e.g. chloramine-T), pharmaceutical workers (drugs, enzymes), seafood processors, shellac handlers (e.g. amines), solderers and refiners (metals), spray painters, insulation installers, plastics and foam industry workers (e.g. diisocyanates), textile workers (dyes) and users of plastics and epoxy resins (e.g. anhydrides)

The following tables show occupations that are known to be at risk for occupational asthma, the main reference for these is the Canadian Centre for Occupational Health and Safety.

Morbidity and mortality range from both extremes as the significance correlate with the underlying systemic disease.

Diseases commonly associated with asbestos include:

- Asbestosis: Progressive fibrosis of the lungs of varying severity, progressing to bilateral fibrosis, honeycombing of the lungs on radiological view with symptoms including rales and wheezing. Individuals who have been exposed to asbestos via home, environment, work should notify their doctors about exposure history.

- Asbestos warts: caused when the sharp fibers lodge in the skin and are overgrown causing benign callus-like growths.

- Pleural plaques: discrete fibrous or partially calcified thickened area which can be seen on X-rays of individuals exposed to asbestos. Although pleural plaques are themselves asymptomatic, in some patients this develops into pleural thickening.

- Diffuse pleural thickening: similar to above and can sometimes be associated with asbestosis. Usually no symptoms shown but if exposure is extensive, it can cause lung impairment.

- Pneumothorax: Some reports have also linked the condition of pneumothorax to asbestos related diseases.

It is important to consult a doctor, particularly if the following symptoms develop: shortness of breath, wheezing or hoarseness, persistent cough that worsens over time, blood in fluid coughed up, pain or tightening in chest, difficulty swallowing, swelling of neck or face, decreased appetite, weight loss, fatigue or anemia.

Prevention is through use of Stock coryza-free birds. In other areas culling of the whole flock is a good means of the disease control. Bacterin also is used at a dose of two to reduce brutality of the disease. Precise exposure has also has been used but it should be done with care. Vaccination of the chicks is done in areas with high disease occurrence. Treatment is done by using antibiotics such as erythromycin, Dihydrostreptomycin, Streptomycin sulphonamides, tylosin and Flouroquinolones .

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

There seems to be beneficial responses to clindamycin therapy as the lesions regress. This leads to the hypothesis that microorganisms may be playing a role in the initial stages of Kyrle disease.

A family with Kyrle disease were examined which their skin lesions were benign. However, when three of the young adult members were closely examined, they had posterior subcapsular cataracts and two of those three developed multiple tiny yellow-brown anterior stromal corneal opacities. In order to determine if there is any correlation between Kyrle disease and the ocular observations, more cases of Kyrle disease are to be analyzed.

All in all, since Kyrle disease is relatively rare, more cases need to be studied and analyzed in order to understand the underlying pathogenesis and to improve the management of the disease.

The reservoirs of the disease are carrier chickens which could be health but harboring the disease or chronically sick chickens. The disease affects all ages of chickens. The disease can persist in the flock for 2-3 weeks and signs of the disease are seen between 1–3 days post infection. Transmission of the disease is through direct interaction, airborne droplets and drinking contaminated water. Chicken having infection and those carriers contribute highly to the disease transmission

Early reports indicated that the disorder was affected by climate and growing conditions. Dry weather before harvest seemed to increase the condition. Light crops, heavy use of fertilizers, large fruit and early harvesting increased the condition. Fruit that were free of bitter pit at harvest were often severely affected after a short period of storage. Bitter pit has been widely reviewed over many decades.

The disorder became a major problem for exports from the Southern Hemisphere to Europe. The breakthrough in control came with the discovery in North America that the mineral calcium was low in affected fruit. This was confirmed elsewhere.

Sealpox is a cutaneous (skin) condition caused by parapoxvirus, usually affecting seal handlers who have been bitten by infected harbor or grey seals. First identified in 1969, it wasn't unequivocally proven to be transmissible to humans until 2005, though such transmission had been reported at least as early as 1987. It causes lesions that closely resemble those caused by orf. As many as 2% of seals in marine mammal rehabilitation facilities in North America may have it.

Urbach–Wiethe disease is very rare; there are fewer than 300 reported cases in medical literature. Although Urbach–Wiethe disease can be found worldwide, almost a quarter of reported diagnoses are in South Africa. Many of these are in patients of Dutch, German, and Khoisan ancestry. This high frequency is thought to be due to the founder effect. Due to its recessive genetic cause and the ability to be a carrier of the disease without symptoms, Urbach–Wiethe disease often runs in families. In some regions of South Africa, up to one in 12 individuals may be carriers of the disease. Most of the case studies involving Urbach–Wiethe disease patients involve only one to three cases and these cases are often in the same family. Due to its low incidence, it is difficult to find a large enough number of cases to adequately study the disease.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Currently, antibiotic drugs such as penicillin or tetracycline are the only effective methods for disease treatment. Within wild populations, disease control consists of reducing the amount of bacterial spores present in the environment. This can be done by removing contaminated carcasses and scat.

The affected fruit have dark spots, about ½ cm diameter, which occur on the skin and/or in the flesh The cells in the spots are dead (necrotic), and turn brown-black.

Thousand cankers disease can be spread by moving infected black walnut wood. Trees intended for shipment should be inspected for dieback and cankers and galleries after harvest. G. morbidia or the walnut twig beetle ("Pityophthorus juglandis") are not currently known to be moved with walnut seed . There is currently no chemical therapy or prevention available for the disease making it difficult to control the spread of the disease from the west to the eastern united states. Wood from infected trees can still be used for commercial value, but safety measures such as removing the bark, phloem, and cambium to reduce the risk of spreading the disease with shipment. Quarantines have been put in place in some states to reduce the potential movement of fungus or beetle from that region. On May 17th, 2010, the Director of the Michigan Department of Agriculture issued a quarantine from affected states to protect Michigan’s black walnut ecology and production. Contacting the appropriate entities about possible infections is important to stopping or slowing the spread of thousand cankers disease.

Cardiovascular disease affects low- and middle-income countries even more than high-income countries. There is relatively little information regarding social patterns of cardiovascular disease within low- and middle-income countries, but within high-income countries low income and low educational status are consistently associated with greater risk of cardiovascular disease. Policies that have resulted in increased socio-economic inequalities have been associated with greater subsequent socio-economic differences in cardiovascular disease implying a cause and effect relationship. Psychosocial factors, environmental exposures, health behaviours, and health-care access and quality contribute to socio-economic differentials in cardiovascular disease.

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease. Currently, PM is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m of PM long-term exposure, there was an estimated 8–18% CVD mortality risk. Women had a higher relative risk (RR) (1.42) for PM induced coronary artery disease than men (0.90) did. Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m of PM resulted in a 48% increase of CVD mortality risk. In addition, after only 5 days of exposure, a rise in systolic (2.8 mmHg) and diastolic (2.7 mmHg) blood pressure occurred for every 10.5 μg/m of PM. Other research has implicated PM in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. PM is also linked to carotid artery thickening and increased risk of acute myocardial infarction.

Urbach–Wiethe disease is typically not a life-threatening condition. The life expectancy of these patients is normal as long as the potential side effects of thickening mucosa, such as respiratory obstruction, are properly addressed. Although this may require a tracheostomy or carbon dioxide laser surgery, such steps can help ensure that individuals with Urbach–Wiethe disease are able to live a full life. Oral dimethyl sulfoxide (DMSO) has been shown to reduce skin lesions, helping to minimize discomfort for these individuals.

Thousand cankers disease is a recently recognized disease of certain walnuts ("Juglans" spp.). The disease results from the combined activity of the walnut twig beetle ("Pityophthorus juglandis") and a canker producing fungus, "Geosmithia morbida". Until July 2010 the disease was only known to the western United States where over the past decade it has been involved in several large scale die-offs of walnut, particularly black walnut, "Juglans nigra". However, in late July 2010 a well-established outbreak of the disease was found in the Knoxville, Tennessee area. This new finding is the first locating it within the native range of its susceptible host, black walnut.