Wind turbine syndrome or wind farm syndrome is a psychosomatic disorder primarily caused by anxiety generated by heightened awareness of turbines – the "nocebo effect" – prompted by proponents of the idea that wind turbines have adverse health effects. While proponents claim that a number of effects including death, cancer and congenital abnormality have been caused by wind farms, the distribution of recorded events correlates with media coverage of wind farm syndrome itself, and not with the presence or absence of wind farms. It is not recognised by any international disease classification system and does not appear in any title or abstract in the United States National Library of Medicine's PubMed database. The Center for Media and Democracy's "SourceWatch" website has identified at least one Australian fossil fuel industry funded astroturfing group as involved in promoting the idea of wind turbine syndrome. An investigation led to the foundation being stripped of its status as a health promotion charity.

A 2011 literature review stated that wind turbines can be associated with some health effects, such as sleep disturbance, and argued that the health effects reported by those living near wind turbines were probably caused not by the turbines themselves but rather by "physical manifestation from an annoyed state."

Eighteen research reviews about wind turbines and health, published since 2003, all concluded that there was very little evidence that wind turbines were harmful in any direct way.

A meta study published in 2014 concluded:

- Infrasound is emitted by wind turbines. The levels of infrasound at customary distances to homes are typically well below audibility thresholds.

- Components of wind turbine sound, including infrasound and low-frequency sound, have not been shown to present unique health risks to people living near wind turbines.

- Among the cross-sectional studies of better quality, no clear or consistent association is seen between wind turbine noise and any reported disease or other indicator of harm to human health.

- Annoyance associated with living near wind turbines is a complex phenomenon related to personal factors. Noise from turbines plays a minor role in comparison with other factors in leading people to report annoyance in the context of wind turbines

In Ontario, Canada, the Ministry of the Environment created noise guidelines to limit wind turbine noise levels 30 metres away from a dwelling or campsite to 40 dB(A). These regulations also set a minimum distance of for a group of up to five relatively quiet [102 dB(A)] turbines within a radius, rising to for a group of 11 to 25 noisier (106-107 dB(A)) turbines. Larger facilities and noisier turbines would require a noise study.

Modern wind turbines produce significantly less noise than older designs. Turbine designers work to minimise noise, as noise reflects lost energy and output. Noise levels at nearby residences may be managed through the siting of turbines, the approvals process for wind farms, and operational management of the wind farm.

Bronchiolitis obliterans has many possible causes, including collagen vascular disease, transplant rejection in organ transplant patients, viral infection (respiratory syncytial virus, adenovirus, HIV, cytomegalovirus), Stevens-Johnson syndrome, Pneumocystis pneumonia, drug reaction, aspiration and complications of prematurity (bronchopulmonary dysplasia), and exposure to toxic fumes, including diacetyl, sulfur dioxide, nitrogen dioxide, ammonia, chlorine, thionyl chloride, methyl isocyanate, hydrogen fluoride, hydrogen bromide, hydrogen chloride, hydrogen sulfide, phosgene, polyamide-amine dyes, mustard gas and ozone. It can also be present in patients with rheumatoid arthritis. Certain orally administrated emergency medications, such as activated charcoal, have been known to cause it when aspirated. The ingestion of large doses of papaverine in the vegetable Sauropus androgynus has caused it. Additionally, the disorder may be idiopathic (without known cause).

There are many industrial inhalants that are known to cause various types of bronchiolitis, including bronchiolitis obliterans.

Industrial workers who have presented with bronchiolitis:

- nylon-flock workers

- workers who spray prints onto textiles with polyamide-amine dyes

- battery workers who are exposed to thionyl chloride fumes

- workers at plants that use or manufacture flavorings, e.g. diacetyl butter-like flavoring

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease found in people who have had multiple head injuries. Symptoms may include behavioral problems, mood problems, and problems with thinking. This typically does not begin until years after the injuries. It often gets worse over time and can result in dementia. It is unclear if the risk of suicide is altered.

Most documented cases have occurred in athletes involved in contact sports such as football, wrestling, ice hockey, and soccer. Other risk factors include being in the military, prior domestic violence, and repeated banging of the head. The exact amount of trauma required for the condition to occur is unknown. Definitive diagnosis can only occur at autopsy. It is a form of tauopathy.

As of 2017 there is no specific treatment. Rates of disease have been found to be about 30% among those with a history of multiple head injuries. Population rates, however, are unclear. Research into brain damage as a result of repeated head injuries began in the 1920s, at which time the condition was known as "punch drunk". Changing the rules in some sports has been discussed as a means of prevention.

Symptoms of CTE, which occur in four stages, generally appear 8 to 10 years after an athlete experiences repetitive mild traumatic brain injury.

First-stage symptoms include attention deficit hyperactivity disorder as well as confusion, disorientation, dizziness, and headaches. Second-stage symptoms include memory loss, social instability, impulsive behavior, and poor judgment. Third and fourth stages include progressive dementia, movement disorders, hypomimia, speech impediments, sensory processing disorder, tremors, vertigo, deafness, depression and suicidality.

Additional symptoms include dysarthria, dysphagia, cognitive disorder such as amnesia, and ocular abnormalities, such as ptosis.

The condition manifests as dementia, or declining mental ability, problems with memory, dizzy spells or lack of balance to the point of not being able to walk under one's own power for a short time and/or Parkinsonism, or tremors and lack of coordination. It can also cause speech problems and an unsteady gait. Patients with DP may be prone to inappropriate or explosive behavior and may display pathological jealousy or paranoia.

Severe disease is more common in babies and young children, and in contrast to many other infections, it is more common in children who are relatively well nourished. Other risk factors for severe disease include female sex, high body mass index, and viral load. While each serotype can cause the full spectrum of disease, virus strain is a risk factor. Infection with one serotype is thought to produce lifelong immunity to that type, but only short-term protection against the other three. The risk of severe disease from secondary infection increases if someone previously exposed to serotype DENV-1 contracts serotype DENV-2 or DENV-3, or if someone previously exposed to DENV-3 acquires DENV-2. Dengue can be life-threatening in people with chronic diseases such as diabetes and asthma.

Polymorphisms (normal variations) in particular genes have been linked with an increased risk of severe dengue complications. Examples include the genes coding for the proteins known as TNFα, mannan-binding lectin, CTLA4, TGFβ, DC-SIGN, PLCE1, and particular forms of human leukocyte antigen from gene variations of HLA-B. A common genetic abnormality, especially in Africans, known as glucose-6-phosphate dehydrogenase deficiency, appears to increase the risk. Polymorphisms in the genes for the vitamin D receptor and FcγR seem to offer protection against severe disease in secondary dengue infection.

The mortality rate of chikungunya is slightly less than 1 in 1000. Those over the age of 65, neonates, and those with underlying chronic medical problems are most likely to have severe complications. Neonates are vulnerable as it is possible to vertically transmit chikungunya from mother to infant during delivery, which results in high rates of morbidity, as infants lack fully developed immune systems. The likelihood of prolonged symptoms or chronic joint pain is increased with increased age and prior rheumatological disease.

Most people with dengue recover without any ongoing problems. The fatality rate is 1–5%, and less than 1% with adequate treatment; however those who develop significantly low blood pressure may have a fatality rate of up to 26%. Dengue is common in more than 110 countries. In 2013 it causes about 60 million symptomatic infections worldwide, with 18% admitted to hospital and about 13,600 deaths. The worldwide cost of dengue case is estimated US$9 billion. For the decade of the 2000s, 12 countries in Southeast Asia were estimated to have about 3 million infections and 6,000 deaths annually. It is reported in at least 22 countries in Africa; but is likely present in all of them with 20% of the population at risk. This makes it one of the most common vector-borne diseases worldwide.

Infections are most commonly acquired in the urban environment. In recent decades, the expansion of villages, towns and cities in the areas in which it is common, and the increased mobility of people has increased the number of epidemics and circulating viruses. Dengue fever, which was once confined to Southeast Asia, has now spread to Southern China, countries in the Pacific Ocean and America, and might pose a threat to Europe.

Rates of dengue increased 30 fold between 1960 and 2010. This increase is believed to be due to a combination of urbanization, population growth, increased international travel, and global warming. The geographical distribution is around the equator. Of the 2.5 billion people living in areas where it is common 70% are from Asia and the Pacific. An infection with dengue is second only to malaria as a diagnosed cause of fever among travelers returning from the developing world. It is the most common viral disease transmitted by arthropods, and has a disease burden estimated at 1,600 disability-adjusted life years per million population. The World Health Organization counts dengue as one of seventeen neglected tropical diseases.

Like most arboviruses, dengue virus is maintained in nature in cycles that involve preferred blood-sucking vectors and vertebrate hosts. The viruses are maintained in the forests of Southeast Asia and Africa by transmission from female "Aedes" mosquitoes—of species other than "A. aegypti"—to their offspring and to lower primates. In towns and cities, the virus is primarily transmitted by the highly domesticated "A. aegypti". In rural settings the virus is transmitted to humans by "A. aegypti" and other species of "Aedes" such as "A. albopictus". Both these species had expanding ranges in the second half of the 20th century. In all settings the infected lower primates or humans greatly increase the number of circulating dengue viruses, in a process called amplification.

Observations during recent epidemics have suggested chikungunya may cause long-term symptoms following acute infection. This condition has been termed chronic chikungunya virus-induced arthralgia. Long-term symptoms are not an entirely new observation; long-term arthritis was observed following an outbreak in 1979. Common predictors of prolonged symptoms are advanced age and prior rheumatological disease.

During the La Reunion outbreak in 2006, more than 50% of subjects over the age of 45 reported long-term musculoskeletal pain with up to 60% of people reporting prolonged painful joints three years following initial infection. A study of imported cases in France reported that 59% of people still suffered from arthralgia two years after acute infection. Following a local epidemic of chikungunya in Italy, 66% of people reported muscle pains, joint pains, or asthenia at one year after acute infection.

Currently, the cause of these chronic symptoms is not fully known. Markers of autoimmune or rheumatoid disease have not been found in people reporting chronic symptoms. However, some evidence from humans and animal models suggests chikungunya may be able to establish chronic infections within the host. Viral antigen was detected in a muscle biopsy of a person suffering a recurrent episode of disease three months after initial onset. Additionally, viral antigen and viral RNA were found in macrophages in the synovial joint of a person experiencing a relapse of musculoskeletal disease 18 months after initial infection. Several animal models have also suggested chikungunya virus may establish persistent infections. In a mouse model, viral RNA was detected specifically in joint-associated tissue for at least 16 weeks after inoculation, and was associated with chronic synovitis. Similarly, another study reported detection of a viral reporter gene in joint tissue of mice for weeks after inoculation. In a nonhuman primate model, chikungunya virus was found to persist in the spleen for at least six weeks.

A robovirus is a zoonotic virus that is transmitted by a rodent vector (i.e., "ro"dent "bo"rne).

Roboviruses mainly belong to the Arenaviridae and Hantaviridae family of viruses. Like arbovirus ("ar"thropod "bo"rne) and tibovirus ("ti"ck "bo"rne) the name refers to its method of transmission, known as its vector. This is distinguished from a clade, which groups around a common ancestor. Some scientists now refer to arbovirus and robovirus together with the term ArboRobo-virus.

Rodent borne disease can be transmitted through different forms of contact such as rodent bites, scratches, urine, saliva, etc. Potential sites of contact with rodents include habitats such as barns, outbuildings, sheds, and dense urban areas. Transmission of disease through rodents can be spread to humans through direct handling and contact, or indirectly through rodents carrying the disease spread to ticks, mites, fleas (arboborne.