Coal ash, also known as coal combustion residuals (CCRs), is the particulate residue that remains from burning coal. Depending on the chemical composition of the coal burned, this residue may contain toxic substances and pose a health risk to workers in coal-fired power plants.

Coal workers' pneumoconiosis (CWP), also known as black lung disease or black lung, is caused by long exposure to coal dust. It is common in coal miners and others who work with coal. It is similar to both silicosis from inhaling silica dust and to the long-term effects of tobacco smoking. Inhaled coal dust progressively builds up in the lungs and cannot be removed by the body; this leads to inflammation, fibrosis, and in worse cases, necrosis.

Coal workers' pneumoconiosis, severe state, develops after the initial, milder form of the disease known as anthracosis ("anthrac" — coal, carbon). This is often asymptomatic and is found to at least some extent in all urban dwellers due to air pollution. Prolonged exposure to large amounts of coal dust can result in more serious forms of the disease, "simple coal workers' pneumoconiosis" and "complicated coal workers' pneumoconiosis" (or progressive massive fibrosis, or PMF). More commonly, workers exposed to coal dust develop industrial bronchitis, clinically defined as chronic bronchitis (i.e. productive cough for 3 months per year for at least 2 years) associated with workplace dust exposure. The incidence of industrial bronchitis varies with age, job, exposure, and smoking. In nonsmokers (who are less prone to develop bronchitis than smokers), studies of coal miners have shown a 16% to 17% incidence of industrial bronchitis.

In 2013 CWP resulted in 25,000 deaths down from 29,000 deaths in 1990.

Occupational lung diseases are occupational diseases affecting the respiratory system, including occupational asthma, black lung disease (coalworker's pneumoconiosis), chronic obstructive pulmonary disease (COPD), mesothelioma, and silicosis. Infectious lung diseases can also be acquired in an occupational context. Exposure to substances like flock and silica can cause fibrosing lung disease, whereas exposure to carcinogens like asbestos and beryllium can cause lung cancer. Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.

Health effects of pesticides may be acute or delayed in those who are exposed. A 2007 systematic review found that "most studies on non-Hodgkin lymphoma and leukemia showed positive associations with pesticide exposure" and thus concluded that cosmetic use of pesticides should be decreased. Strong evidence also exists for other negative outcomes from pesticide exposure including neurological problems, birth defects, fetal death, and neurodevelopmental disorder.

According to The Stockholm Convention on Persistent Organic Pollutants, 9 of the 12 most dangerous and persistent chemicals are pesticides.

Pneumoconiosis is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust, often in mines and from agriculture.

In 2013, it resulted in 260,000 deaths, up from 251,000 deaths in 1990. Of these deaths, 46,000 were due to silicosis, 24,000 due to asbestosis and 25,000 due to coal workers pneumoconiosis.

Asbestosis is a fibrosing interstitial lung disease caused by exposure to forms of the mineral asbestos.

Positive indications on patient assessment:

- Shortness of breath

- Chest X-ray may show a characteristic patchy, subpleural, bibasilar interstitial infiltrates or small cystic radiolucencies called honeycombing.

Pneumoconiosis in combination with multiple pulmonary rheumatoid nodules in rheumatoid arthritis patients is known as Caplan's syndrome.

Simple CWP is marked by the presence of 1–2 mm nodular aggregations of anthracotic macrophages, supported by a fine collagen network, within the lungs. Those 1–2 mm in diameter are known as "coal macules", with larger aggregations known as "coal nodules". These structures occur most frequently around the initial site of coal dust accumulation — the upper regions of the lungs around respiratory bronchioles. The coal macule is the basic pathological feature of CWP and has a surrounding area of enlargement of the airspace, known as focal emphysema.

Continued exposure to coal dust following the development of simple CWP may progress to complicated CWP with progressive massive fibrosis (PMF), wherein large masses of dense fibrosis develop, usually in the upper lung zones, measuring greater than 1 cm in diameter, with accompanying decreased lung function. These cases generally require a number of years to develop. Grossly, the lung itself appears blackened. Pathologically, these consist of fibrosis with haphazardly-arranged collagen and many pigment-laden macrophages and abundant free pigment. Radiographically, CWP can appear strikingly similar to silicosis. In simple CWP, small rounded nodules (see ILO Classification) predominate, tending to first appear in the upper lung zones. The nodules may coalesce and form large opacities (>1 cm), characterizing complicated CWP, or PMF.

Mold health issues are potentially harmful effects of molds.

Molds (US usage; British English "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The United States Centers for Disease Control and Prevention reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination." When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins, or causing fungal infection (mycosis).

Lead: The exposure of lead in coal ash can cause major damage to the nervous system. Lead exposure can lead to kidney disease, hearing impairment, high blood pressure, delays in development, swelling of the brain, hemoglobin damage, and male reproductive problems. Both low levels and high levels of lead exposure can cause harm to the human body.

Cadmium: When coal ash dust is inhaled, high levels of cadmium is absorbed into the body. More specifically, the lungs directly absorb cadmium into the bloodstream. When humans are exposed to cadmium over a long period of time, kidney disease and lung disease can occur. In addition, cadmium exposure can be associated with hypertension. Lastly, chronic exposure of cadmium can cause bone weakness which increases the risk of bone fractures and osteoporosis.

Chromium: The exposure of chromium (IV) in coal ash can cause lung cancer and asthma when inhaled. When coal ash waste pollutes drinking water, chromium (IV) can cause ulcers in the small intestine and stomach when ingested. Lastly, skin ulcers can also occur when the exposure chromium (IV) in coal ash comes in contact with the skin.

Arsenic: When high amounts of arsenic is inhaled or ingested through coal ash waste, diseases such as bladder cancer, skin cancer, kidney cancer and lung cancer can develop. Ultimately, exposure of arsenic over a long period of time can cause mortality. Furthermore, low levels of arsenic exposure can cause irregular heartbeats, nausea, diarrhea, vomiting, peripheral neuropathy and vision impairment.

Mercury: Chronic exposure of mercury from coal ash can cause harm to the nervous system. When mercury is inhaled or ingested various health effects can occur such as vision impairment, seizures, numbness, memory loss and sleeplessness.

Boron: When coal ash dust is inhaled, the exposure of boron can cause discomfort in the throat, nose and eye. Moreover, when coal ash waste is ingested, boron exposure can be associated with kidney, liver, brain, and intestine impairment.

Molybdenum: When molybdenum is inhaled from coal ash dust, discomfort of the nose, throat, skin and eye can occur. As a result, short-term molybdenum exposure can cause an increase of wheezing and coughing. Furthermore, chronic exposure of molybdenum can cause loss of appetite, tiredness, headaches and muscle soreness.

Thallium: The exposure of thallium in coal ash dust can cause peripheral neuropathy when inhaled. Furthermore, when coal ash is ingested, thallium exposure can cause diarrhea and vomiting. In addition, thallium exposure is also associated with heart, liver, lung and kidney complications.

Silica: When silica is inhaled from coal ash dust, fetal lung disease or silicosis can develop. Furthermore, chronic exposure of silica can cause lung cancer. In addition, exposure to silica over a period of time can cause loss of appetite, poor oxygen circulation, breathing complications and fever.

Symptoms of mold exposure can include:

- Nasal and sinus congestion, runny nose

- Respiratory problems, such as wheezing and difficulty breathing, chest tightness

- Cough

- Throat irritation

- Sneezing / Sneezing fits

According to the International Labour Office (ILO), PMF requires the presence of large opacity exceeding 1 cm (by x-ray). By pathology standards, the lesion in histologic section must exceed 2 cm to meet the definition of PMF. In PMF, lesions most commonly occupy the upper lung zone, and are usually bilateral. The development of PMF is usually associated with a restrictive ventilatory defect on pulmonary function testing. PMF can be mistaken for bronchogenic carcinoma and vice versa. PMF lesions tend to grow very slowly, so any rapid changes in size, or development of cavitation, should prompt a search for either alternative cause or secondary disease.

Acute health problems may occur in workers that handle pesticides, such as abdominal pain, dizziness, headaches, nausea, vomiting, as well as skin and eye problems. In China, an estimated half million people are poisoned by pesticides each year, 500 of whom die. Pyrethrins, insecticides commonly used in common bug killers, can cause a potentially deadly condition if breathed in.

Occupational acne is caused by several different groups of industrial compounds, including coal tar derivatives, insoluble cutting oils, and chlorinated hydrocarbons (chlornaphthalenes, chlordiphenyls, and chlordiphenyloxides).

Common symptoms of mercury poisoning include peripheral neuropathy, presenting as paresthesia or itching, burning, pain, or even a sensation that resembles small insects crawling on or under the skin (formication); skin discoloration (pink cheeks, fingertips and toes); swelling; and desquamation (shedding or peeling of skin).

Mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate "S"-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-"O"-methyl transferase. Due to the body's inability to degrade catecholamines (e.g. epinephrine), a person suffering from mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure).

Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, or insomnia.

Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease. Desquamation (skin peeling) can occur with severe mercury poisoning acquired by handling elemental mercury.

Mercury poisoning is a type of metal poisoning due to mercury exposure. Symptoms depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. High level exposure to methylmercury is known as Minamata disease. Methylmercury exposure in children may result in acrodynia (pink's disease) in which the skin becomes pink and peels. Long-term complications may include kidney problems and decreased intelligence. The effects of long-term low-dose exposure to methylmercury is unclear.

Forms of mercury exposure include metal, vapor, salt, and organic compound. Most exposure is from eating fish, amalgam based dental fillings, or exposure at work. In fish, those higher up in the food chain generally have higher levels of mercury. Less commonly poisoning may occur as an attempt to end one's life. Human activities that release mercury into the environment include the burning of coal and mining of gold. Tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body.

Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury. In those with acute poisoning from inorganic mercury salts, chelation with either dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) appears to improve outcomes if given within a few hours of exposure. Chelation for those with long-term exposure is of unclear benefit. In certain communities that survive on fishing, rates of mercury poisoning among children have been as high as 1.7 per 100.

Progressive Massive Fibrosis (PMF), characterized by the development of large conglomerate masses of dense fibrosis (usually in the upper lung zones), can complicate silicosis and coal worker's pneumoconiosis. Conglomerate masses may also occur in other pneumoconioses, such as talcosis, berylliosis (CBD), kaolin pneumoconiosis, and pneumoconiosis from carbon compounds, such as carbon black, graphite, and oil shale. Conglomerate masses can also develop in sarcoidosis, but usually near the hilae and with surrounding paracitricial emphysema.

The disease arises firstly through the deposition of silica or coal dust (or other dust) within the lung, and then through the body's immunological reactions to the dust.

, one of the Four Big Pollution Diseases of Japan, occurred in the city of Yokkaichi in Mie Prefecture, Japan, between 1960 and 1972. The burning of petroleum and crude oil released large quantities of sulfur oxide that caused severe smog, resulting in severe cases of chronic obstructive pulmonary disease, chronic bronchitis, pulmonary emphysema, and bronchial asthma among the local inhabitants. The generally accepted sources of the sulfur oxide pollution were petrochemical processing facilities and refineries that were built in the area between 1957 and 1973.

Pulmonary Langerhans cell histiocytosis, silicosis, coal workers pneumoconiosis, carmustine related pulmonary fibrosis, respiratory broncholitis associated with interstitial lung disease.

- Lower lung predominance

Idiopathic pulmonary fibrosis, pulmonary fibrosis associated with connective tissue diseases, asbestosis, chronic aspiration

- Central predominance (perihilar)

Sarcoidosis, berylliosis

- Peripheral predominance

Idiopathic pulmonary fibrosis, chronic eosinophilic pneumonia, cryptogenic organizing pneumonia

Shortness of breath is often the symptom that most bothers people. It is commonly described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in". Different terms, however, may be used in different cultures. Typically the shortness of breath is worse on exertion of a prolonged duration and worsens over time. In the advanced stages, or end stage pulmonary disease it occurs during rest and may be always present. It is a source of both anxiety and a poor quality of life in those with COPD. Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.

In 1955, the Ministry of International Trade and Industry began its policy to transition Japan's primary fossil fuel source from coal to petroleum. To accomplish that goal, construction of the Daichi Petrochemical Complex was begun in 1956. The complex contained an oil refinery, a petrochemical plant, and a power station. This was the first petrochemical complex constructed in Japan.

In 1960, the government of Prime Minister Hayato Ikeda accelerated the growth of petrochemical production as part of its goal to double individual incomes of Japanese citizens over a 10-year period. Also in 1960, MITI announced that a second complex was to be constructed on reclaimed land in northern Yokkaichi. The second complex went online in 1963. As demand for ethylene and other petrochemicals rose, a third complex was constructed which began production in 1972. Yokkaichi transferred its energy production from coal to oil more quickly than the rest of the nation. The oil used in Yokkaichi was primarily imported from the Middle East, which contained 2% sulfur in sulfur containing compounds, resulting in a white-colored smog developing over the city.

A chronic cough is often the first symptom to develop. When it persists for more than three months each year for at least two years, in combination with sputum production and without another explanation, it is by definition chronic bronchitis. This condition can occur before COPD fully develops. The amount of sputum produced can change over hours to days. In some cases, the cough may not be present or may only occur occasionally and may not be productive. Some people with COPD attribute the symptoms to a "smoker's cough". Sputum may be swallowed or spat out, depending often on social and cultural factors. Vigorous coughing may lead to rib fractures or a brief loss of consciousness. Those with COPD often have a history of "common colds" that last a long time.

Pulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

- Lymphadenopathy

Sarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

An occupational disease is any chronic ailment that occurs as a result of work or occupational activity. It is an aspect of occupational safety and health. An occupational disease is typically identified when it is shown that it is more prevalent in a given body of workers than in the general population, or in other worker populations. The first such disease to be recognised, squamous-cell carcinoma of the scrotum, was identified in chimney sweep boys by Sir Percival Pott in 1775. Occupational hazards that are of a traumatic nature (such as falls by roofers) are not considered to be occupational diseases.

Under the law of workers' compensation in many jurisdictions, there is a presumption that specific disease are caused by the worker being in the work environment and the burden is on the employer or insurer to show that the disease came about from another cause. Diseases compensated by national workers compensation authorities are often termed occupational diseases. However, many countries do not offer compensations for certain diseases like musculoskeletal disorders caused by work (e.g. in Norway). Therefore, the term work-related diseases is utilized to describe diseases of occupational origin. This term however would then include both compensable and non-compensable diseases that have occupational origins.

Caplan's syndrome (or Caplan disease or Rheumatoid pneumoconiosis) is a combination of rheumatoid arthritis (RA) and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogenous and well-defined on chest X-ray.