An estimated 48,000 cancers are diagnosed yearly in the US that come from occupational causes; this represents approximately 4-10% of total cancer in the United States. It is estimated that 19% of cancers globally are attributed to environmental exposures (including work-related exposures).

Occupational exposure to chemicals, dusts, radiation, and certain industrial processes have been tied to occupational cancer. Exposure to cancer-causing chemicals, also called Carcinogens, may cause mutations that allow cells to grow out of control, causing cancer. Carcinogens in the workplace may include chemicals like anilines, chromates, dinitrotoluenes, arsenic and inorganic arsenic compounds, beryllium and beryllium compounds, cadmium compounds, and nickel compounds. Dusts that can cause cancer leather or wood dusts, asbestos, crystalline forms of silica, coal tar pitch volatiles, coke oven emissions, diesel exhaust and environmental tobacco smoke. sunlight; radon gas; and industrial, medical, or other exposure to ionizing radiation can all cause cancer in the workplace. Industrial processes associated with cancer include aluminum production; iron and steel founding; and underground mining with exposure to uranium or radon.

Other factors that play a role in cancer include:

- Personal characteristics such as age, sex, and race

- Family history of cancer

- Diet and personal habits such as cigarette smoking and alcohol consumption

- The presence of certain medical conditions or past medical treatments, including chemotherapy, radiation treatment, or some immune-system suppressing drugs.

- Exposure to cancer-causing agents in the environment (for example, sunlight, radon gas, air pollution, and infectious agents)

Cancer is a stochastic effect of radiation, meaning that it only has a probability of occurrence, as opposed to deterministic effects which always happen over a certain dose threshold. The consensus of the nuclear industry, nuclear regulators, and governments, is that the incidence of cancers due to ionizing radiation can be modeled as increasing linearly with effective radiation dose at a rate of 5.5% per sievert. Individual studies, alternate models, and earlier versions of the industry consensus have produced other risk estimates scattered around this consensus model. There is general agreement that the risk is much higher for infants and fetuses than adults, higher for the middle-aged than for seniors, and higher for women than for men, though there is no quantitative consensus about this. This model is widely accepted for external radiation, but its application to internal contamination is disputed. For example, the model fails to account for the low rates of cancer in early workers at Los Alamos National Laboratory who were exposed to plutonium dust, and the high rates of thyroid cancer in children following the Chernobyl accident, both of which were internal exposure events. The European Committee on Radiation Risk calls the ICRP model "fatally flawed" when it comes to internal exposure.

Radiation can cause cancer in most parts of the body, in all animals, and at any age, although radiation-induced solid tumors usually take 10–15 years, and can take up to 40 years, to become clinically manifest, and radiation-induced leukemias typically require 2–10 years to appear. Some people, such as those with nevoid basal cell carcinoma syndrome or retinoblastoma, are more susceptible than average to developing cancer from radiation exposure. Children and adolescents are twice as likely to develop radiation-induced leukemia as adults; radiation exposure before birth has ten times the effect.

Radiation exposure can cause cancer in any living tissue, but high-dose whole-body external exposure is most closely associated with leukemia, reflecting the high radiosensitivity of bone marrow. Internal exposures tend to cause cancer in the organs where the radioactive material concentrates, so that radon predominantly causes lung cancer, iodine-131 is most likely to cause thyroid cancer, etc.

Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies. Clear evidence establishes ultraviolet radiation, especially the non-ionizing medium wave UVB, as the cause of most non-melanoma skin cancers, which are the most common forms of cancer in the world.

Skin cancer may occur following ionizing radiation exposure following a latent period averaging 20 to 40 years. A Chronic radiation keratosis is a precancerous keratotic skin lesion that may arise on the skin many years after exposure to ionizing radiation. Various malignancies may develop, most frequency basal-cell carcinoma followed by squamous-cell carcinoma. Elevated risk is confined to the site of radiation exposure. Several studies have also suggested the possibility of a causal relationship between melanoma and ionizing radiation exposure. The degree of carcinogenic risk arising from low levels of exposure is more contentious, but the available evidence points to an increased risk that is approximately proportional to the dose received. Radiologists and radiographers are among the earliest occupational groups exposed to radiation. It was the observation of the earliest radiologists that led to the recognition of radiation-induced skin cancer—the first solid cancer linked to radiation—in 1902. While the incidence of skin cancer secondary to medical ionizing radiation was higher in the past, there is also some evidence that risks of certain cancers, notably skin cancer, may be increased among more recent medical radiation workers, and this may be related to specific or changing radiologic practices. Available evidence indicates that the excess risk of skin cancer lasts for 45 years or more following irradiation.

Around 75% of cases are caused by alcohol and tobacco use.

Tobacco smoke is one of the main risk factors for head and neck cancer and one of the most carcinogenic compounds in tobacco smoke is acrylonitrile. (See Tobacco smoking). Acrylonitrile appears to indirectly cause DNA damage by increasing oxidative stress, leading to increased levels of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and formamidopyrimidine in DNA (see image). Both 8-oxo-dG and formamidopyrimidine are mutagenic. DNA glycosylase NEIL1 prevents mutagenesis by 8-oxo-dG and removes formamidopyrimidines from DNA.

However, cigarette smokers have a lifetime increased risk for head and neck cancers that is 5- to 25-fold increased over the general population.

The ex-smoker's risk for squamous cell cancer of the head and neck begins to approach the risk in the general population twenty years after smoking cessation. The high prevalence of tobacco and alcohol use worldwide and the high association of these cancers with these substances makes them ideal targets for enhanced cancer prevention.

Smokeless tobacco is cause of oral and pharyngeal cancers (oropharyngeal cancer). Cigar smoking is an important risk factor for oral cancers as well.

Other environmental carcinogens suspected of being potential causes of head and neck cancer include occupational exposures such as nickel refining, exposure to textile fibers, and woodworking. Use of marijuana, especially while younger, is linked to an increase in squamous-cell carcinoma cases while other studies suggest use is not shown to be associated with oral squamous cell carcinoma, or associated with decreased squamous cell carcinoma.

Excessive consumption of processed meats and red meat were associated with increased rates of cancer of the head and neck in one study, while consumption of raw and cooked vegetables seemed to be protective.

Vitamin E was not found to prevent the development of leukoplakia, the white plaques that are the precursor for carcinomas of the mucosal surfaces, in adult smokers.

Another study examined a combination of Vitamin E and beta carotene in smokers with early-stage cancer of the oropharynx, and found a worse prognosis in the vitamin users.

In a recent research carried on white American population in 2012, it was found that people with a germline mutation in their BAP1 gene are at higher risk of developing mesothelioma and uveal melanoma.

Working with asbestos is the most common risk factor for mesothelioma. However, mesothelioma has been reported in some individuals without any known exposure to asbestos.

Asbestos can cause lung cancer that is identical to lung cancer from other causes. Exposure to asbestos is associated with all major histological types of lung carcinoma (adenocarcinoma, squamous cell carcinoma, large-cell carcinoma and small-cell carcinoma). The latency period between exposure and development of lung cancer is 20 to 30 years. It is estimated that 3%-8% of all lung cancers are related to asbestos. The risk of developing lung cancer depends on the level, duration, and frequency of asbestos exposure (cumulative exposure). Smoking and individual susceptibility are other contributing factors towards lung cancer. Smokers who have been exposed to asbestos are at far greater risk of lung cancer. Smoking and asbestos exposure have a multiplicative (synergistic) effect on the risk of lung cancer. Symptoms include chronic cough, chest pain, breathlessness, haemoptysis (coughing up blood), wheezing or hoarseness of the voice, weight loss and fatigue. Treatment involves surgical removal of the cancer, chemotherapy, radiotherapy, or a combination of these (multimodality treatment). Prognosis is generally poor unless the cancer is detected in its early stages. Out of all patients diagnosed with lung cancer, only 15% survive for five years after diagnosis.

Tobacco smoking is the main known contributor to urinary bladder cancer; in most populations, smoking is associated with over half of bladder cancer cases in men and one-third of cases among women, however these proportions have reduced over recent years since there are fewer smokers in Europe and North America. There is an almost linear relationship between smoking duration (in years), pack years and bladder cancer risk. A risk plateau at smoking about 15 cigarettes a day can be observed (meaning that those who smoke 15 cigarettes a day are approximately at the same risk as those smoking 30 cigarettes a day). Quitting smoking reduces the risk, however former smokers will most likely always be at a higher risk of bladder cancer compared to never smokers. Passive smoking has not been proven to be involved.

Thirty percent of bladder tumors probably result from occupational exposure in the workplace to carcinogens such as benzidine. 2-Naphthylamine, which is found in cigarette smoke, has also been shown to increase bladder cancer risk. Occupations at risk are bus drivers, rubber workers, motor mechanics, leather (including shoe) workers, blacksmiths, machine setters, and mechanics. Hairdressers are thought to be at risk as well because of their frequent exposure to permanent hair dyes.

In addition to these major risk factors there are also numerous other modifiable factors that are less strongly (i.e. 10–20% risk increase) associated with bladder cancer, for example, obesity. Although these could be considered as minor effects, risk reduction in the general population could still be achieved by reducing the prevalence of a number of smaller risk factor together.

It has been suggested that mutations at HRAS, KRAS2, RB1, and FGFR3 may be associated in some cases.

A 2008 study commissioned by the World Health Organisation concluded that "specific fruit and vegetables may act to reduce the risk of bladder cancer." Fruit and yellow-orange vegetables, particularly carrots and those containing selenium, are probably associated with a moderately reduced risk of bladder cancer. Citrus fruits and cruciferous vegetables were also identified as having a possibly protective effect. However an analysis of 47,909 men in the Health Professionals Follow-Up Study showed little correlation between cancer reduction and high consumption of fruits and vegetables overall, or yellow or green leafy vegetables specifically, compared to the statistically significant reduction among those men who consumed large amounts of cruciferous vegetables.

In a 10-year study involving almost 49,000 men, researchers found that men who drank at least 1,44 L of water (around 6 cups) per day had a significantly reduced incidence of bladder cancer when compared with men who drank less. It was also found that: "the risk of bladder cancer decreased by 7% for every 240 mL of fluid added". The authors proposed that bladder cancer might partly be caused by the bladder directly contacting carcinogens that are excreted in urine, although this has not yet been confirmed in other studies.

Many studies have examined the effects of pesticide exposure on the risk of cancer. Associations have been found with: leukemia, lymphoma, brain, kidney, breast, prostate, pancreas, liver, lung, and skin cancers. This increased risk occurs with both residential and occupational exposures. Increased rates of cancer have been found among farm workers who apply these chemicals. A mother's occupational exposure to pesticides during pregnancy is associated with an increases in her child's risk of leukemia, Wilms' tumor, and brain cancer. Exposure to insecticides within the home and herbicides outside is associated with blood cancers in children.

Malignant mesothelioma is an aggressive and incurable tumour caused by asbestos arising from mesothelial cells of the pleura, peritoneum (the lining of the abdominal cavity) and rarely elsewhere. Pleural mesothelioma is the most common type of mesothelioma, representing about 75 percent of cases. Peritoneal mesothelioma is the second most common type, consisting of about 10 to 20 percent of cases. Mesothelioma appears from 20 to 50 years after the initial exposure to asbestos. The symptoms include shortness of breath, chronic chest pain, cough, and weight loss. Diagnosing mesothelioma is often difficult and can include physical examination, chest X-ray and lung function tests, followed by CT scan and MRI. A biopsy is needed to confirm a diagnosis of malignant mesothelioma. Mesothelioma has a poor prognosis, with most patients dying within 1 year of diagnosis. The treatment strategies include surgery, radiotherapy, chemotherapy or multimodality treatment. Several tumour biomarkers (soluble mesothelin-related protein (SMRP), osteopontin and fibulin3) have been evaluated for diagnostic purposes to allow early detection of this disease. Novel biomarkers such as volatile organic compounds measured in exhaled breath are also promising.

Evidence links pesticide exposure to worsened neurological outcomes.

The United States Environmental Protection Agency finished a 10-year review of the organophosphate pesticides following the 1996 Food Quality Protection Act, but did little to account for developmental neurotoxic effects, drawing strong criticism from within the agency and from outside researchers. Comparable studies have not been done with newer pesticides that are replacing organophosphates.

Besides causing silicosis, inhalation of silica can cause or exacerbate COPD. It can also impair lung function in general and cause cancer by oxidation damage. It is classified as a "known human carcinogen" (Group 1 carcinogen) by the IARC. Exposure is common for people working in tunneling, quarrying, construction, sandblasting, roadway repair, mining, and foundry work.

Tobacco smoke is a known carcinogen. Workers in the hospitality industry may be exposed to tobacco smoke in the workplace, especially in environments like casinos and bars/restaurants.

Squamous cell carcinoma of eye tissues is one of the most frequent neoplasms of cattle.

A 2015 SBU-report including a systematic review of non-chemical riskfactors for occupation cardiovascular disease found an association between certain occupational risk factors and developing cardiovascular disease in those:

- With mentally stressfull work with a lack of control of their own working situation — with a effort-reward imbalance

- Who experience low social support at work; who experience injustice or experience insufficient opportunities for personal development; or those who experience job insecurity

- Those who work night schedules; or have long working weeks

- Those who are exposed to noise

Specifically the risk of stroke was also increased by:

- Exposure to ionizing radiation

Hypertension develops more often in those who experience job strain and who have shift-work. Differences between women and men in risk are small, however men risk suffering and dieing of heart attacks or stroke twice as often as women during working life.

Chimney sweeps' carcinoma is a squamous cell carcinoma of the skin of the scrotum. Warts caused by the irritation from soot particles, if not excised, developed into a scrotal cancer. This then invaded the dartos, enlarged the testicle, and proceeded up the spermatic cord into the abdomen where it proved fatal.

The age-standardized 5-year relative survival rate is 23.6%. Patients with this tumor are 46 times more likely to die than matched members of the general population. It is important to note that prognosis across age groups is different especially during the first three years post-diagnosis. When the elderly population is compared with young adults, the excess hazard ratio (a hazard ratio that is corrected for differences in mortality across age groups) decreases from 10.15 to 1.85 at 1 to 3 years, meaning that the elderly population are much more likely to die in the first year post-diagnosis when compared to young adults (aged 15 to 40), but after three years, this difference is reduced markedly.

Typical median survival for anaplastic astrocytoma is 2–3 years. Secondary progression to glioblastoma multiforme is common. Radiation, younger age, female sex, treatment after 2000, and surgery were associated with improved survival in AA patients.

Cancer can be considered a very large and exceptionally heterogeneous family of malignant diseases, with squamous cell carcinomas comprising one of the largest subsets.

People may be exposed to toxic chemicals or similar dangerous substances from pharmaceutical products, consumer products, the environment, or in the home or at work. Many toxic tort cases arise either from the use of medications, or through exposure at work.

Pharmaceutical injuries can occur when a person is injured by a dangerous, defective or contaminated medication. Many pharmaceutical toxic injury cases are mass tort cases, as most medications are consumed by thousands of people. The cases are often litigated against drug manufacturers and distributors, and potentially against prescribing physicians. When prosecuted against drug manufacturers and distributors, pharmaceutical toxic tort cases differ from medical malpractice suits in that pharmaceutical toxic tort cases are essentially product liability cases, the defective product being the drug.

A 2017 SBU report found evidence that workplace exposure to silica dust, engine exhaust or welding fumes is associated with heart disease. Associations also exist for exposure to arsenic, benzopyrenes, lead, dynamite, carbon disulphide, carbon monoxide, metalworking fluids and occupational exposure to tobacco smoke. Working with the electrolytic production of aluminium or the production of paper when the sulphate pulping process is used is associated with heart disease. An association was also found between heart disease and exposure to compounds which are no longer permitted in certain work environments, such as phenoxy acids containing TCDD(dioxin) or asbestos.

Workplace exposure to silica dust or asbestos is also associated with pulmonary heart disease. There is evidence that workplace exposure to lead, carbon disulphide, phenoxyacids containing TCDD, as well as working in an environment where aluminium is being electrolytically produced, is associated with stroke.

Occupational lung diseases include asbestosis among asbestos miners and those who work with friable asbestos insulation, as well as black lung (coalworker's pneumoconiosis) among coal miners, silicosis among miners and quarrying and tunnel operators and byssinosis among workers in parts of the cotton textile industry.

Occupational asthma has a vast number of occupations at risk.

Bad indoor air quality may predispose for diseases in the lungs as well as in other parts of the body.