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.

According to the linear no-threshold model, any exposure to ionizing radiation, even at doses too low to produce any symptoms of radiation sickness, can induce cancer due to cellular and genetic damage. Under the assumption, survivors of acute radiation syndrome face an increased risk of developing cancer later in life. The probability of developing cancer is a linear function with respect to the effective radiation dose. In radiation-induced cancer, the speed at which the condition advances, the prognosis, the degree of pain, and every other feature of the disease are not believed to be functions of the radiation dosage.

However, some studies contradict the linear no-threshold model. These studies indicate that some low levels of radiation do not increase cancer risk at all, and that there may exist a threshold dosage of ionizing radiation below which exposure should be considered safe. Nonetheless the 'no safe amount' assumption is the basis of US and most national regulatory policies regarding "man-made" sources of radiation.

During spaceflight, particularly flights beyond low Earth orbit, astronauts are exposed to both galactic cosmic radiation (GCR) and solar particle event (SPE) radiation. Evidence indicates past SPE radiation levels which would have been lethal for unprotected astronauts. GCR levels which might lead to acute radiation poisoning are less well understood.

Radiation burns are caused by exposure to high levels of radiation. Levels high enough to cause burn are generally lethal if received as a whole-body dose, whereas they may be treatable if received as a shallow or local dose.

Chronic radiation syndrome is a constellation of health effects that occur after months or years of chronic exposure to high amounts of ionizing radiation. Chronic radiation syndrome develops with a speed and severity proportional to the radiation dose received, i.e., it is a deterministic effect of radiation exposure, unlike radiation-induced cancer. It is distinct from acute radiation syndrome in that it occurs at dose rates low enough to permit natural repair mechanisms to compete with the radiation damage during the exposure period. Dose rates high enough to cause the acute form (> ~0.1 Gy/h) are fatal long before onset of the chronic form. The lower threshold for chronic radiation syndrome is between 0.7 and 1.5 Gy, at dose rates above 0.1 Gy/yr. This condition is primarily known from the Kyshtym disaster, where 66 cases were diagnosed, and has received little mention in Western literature. A future ICRP publication, currently in draft, may recognize the condition but with higher thresholds.

In 2013, Alexander V. Akleyev described the chronology of the clinical course or CRS while presenting at ConRad in Munich, Germany. In his presentation, he defined the latent period as being 1-5 years, and the formation coinciding with the period of maximum radiation dose. The recovery period was described as being 3-12 months after exposure ceased. He concluded that "CRS represents a systemic response of the body as a whole to the chronic total body exposure in man." In 2014, Akleyev's book "Comprehensive analysis of chronic radiation syndrome, covering epidemiology, pathogenesis, pathoanatomy, diagnosis and treatment" was published by Springer.

The ultraviolet radiation from tanning beds increases the risk of melanoma. The International Agency for Research on Cancer finds that tanning beds are "carcinogenic to humans" and that people who begin using tanning devices before the age of thirty years are 75% more likely to develop melanoma.

Those who work in airplanes also appear to have an increased risk, believed to be due to greater exposure to UV.

Ultraviolet UVB light (wavelengths between 315 – 280 nm) from the sun is absorbed by skin cell DNA and results in a type of direct DNA damage called cyclobutane pyrimidine dimers (CPDs). Thymine-thymine, cytosine-cytosine or cytosine-thymine dimers are formed by the joining of two adjacent pyrimidine bases within a DNA strand. Somewhat similarly to UVB, UVA light (longer wavelengths between 400 – 315 nm) from the sun or from tanning beds can also be directly absorbed by skin DNA (at about 100 to 1000 fold lower efficiency than UVB is absorbed).

Studies suggest that exposure to ultraviolet radiation (UVA and UVB) is one of the major contributors to the development of melanoma. Occasional extreme sun exposure (resulting in "sunburn") is causally related to melanoma. Melanoma is most common on the back in men and on legs in women (areas of intermittent sun exposure). The risk appears to be strongly influenced by socio-economic conditions rather than indoor versus outdoor occupations; it is more common in professional and administrative workers than unskilled workers. Other factors are mutations in or total loss of tumor suppressor genes. Use of sunbeds (with deeply penetrating UVA rays) has been linked to the development of skin cancers, including melanoma.

Possible significant elements in determining risk include the intensity and duration of sun exposure, the age at which sun exposure occurs, and the degree of skin pigmentation. Melanoma rates tend to be highest in countries settled by migrants from northern Europe that have a large amount of direct, intense sunlight that the skin of the settlers is not adapted to, most notably Australia. Exposure during childhood is a more important risk factor than exposure in adulthood. This is seen in migration studies in Australia.

Having multiple severe sunburns increases the likelihood that future sunburns develop into melanoma due to cumulative damage. The sun and tanning beds are the main sources of UV radiation that increase the risk for melanoma and living close to the equator increases exposure to UV radiation.

Fluoroscopy may cause burns if performed repeatedly or for too long.

Similarly, Computed Tomography and traditional Projectional Radiography have the potential to cause radiation burns if the exposure factors and exposure time are not appropriately controlled by the operator.

A study of radiation induced skin injuries has been performed by the Food and Drug Administration (FDA) based on results from 1994, followed by an advisory to minimize further fluoroscopy-induced injuries. The problem of radiation injuries due to fluoroscopy has been further investigated in review articles in 2000, 2001, 2009 and 2010.

As many as 50–70% of people who survive traffic accidents have facial trauma. In most developed countries, violence from other people has replaced vehicle collisions as the main cause of maxillofacial trauma; however in many developing countries traffic accidents remain the major cause. Increased use of seat belts and airbags has been credited with a reduction in the incidence of maxillofacial trauma, but fractures of the mandible (the jawbone) are not decreased by these protective measures. The risk of maxillofacial trauma is decreased by a factor of two with use of motorcycle helmets. A decline in facial bone fractures due to vehicle accidents is thought to be due to seat belt and drunk driving laws, strictly enforced speed limits and use of airbags. In vehicle accidents, drivers and front seat passengers are at highest risk for facial trauma.

Facial fractures are distributed in a fairly normal curve by age, with a peak incidence occurring between ages 20 and 40, and children under 12 suffering only 5–10% of all facial fractures. Most facial trauma in children involves lacerations and soft tissue injuries. There are several reasons for the lower incidence of facial fractures in children: the face is smaller in relation to the rest of the head, children are less often in some situations associated with facial fractures such as occupational and motor vehicle hazards, there is a lower proportion of cortical bone to cancellous bone in children's faces, poorly developed sinuses make the bones stronger, and fat pads provide protection for the facial bones.

Head and brain injuries are commonly associated with facial trauma, particularly that of the upper face; brain injury occurs in 15–48% of people with maxillofacial trauma. Coexisting injuries can affect treatment of facial trauma; for example they may be emergent and need to be treated before facial injuries. People with trauma above the level of the collar bones are considered to be at high risk for cervical spine injuries (spinal injuries in the neck) and special precautions must be taken to avoid movement of the spine, which could worsen a spinal injury.

While needlestick injuries have the potential to transmit bacteria, protozoa, viruses and prions, the risk of contracting hepatitis B, hepatitis C, and HIV is the highest. The World Health Organization estimated that in 2000, 66,000 hepatitis B, 16,000 hepatitis C, and 1,000 HIV infections were caused by needlestick injuries. In places with higher rates of blood-borne diseases in the general population, healthcare workers are more susceptible to contracting these diseases from a needlestick injury.

Hepatitis B carries the greatest risk of transmission, with 10% of exposed workers eventually showing seroconversion and 10% having symptoms. Higher rates of hepatitis B vaccination among the general public and healthcare workers have reduced the risk of transmission; non-healthcare workers still have a lower HBV vaccine rate and therefore a higher risk. The hepatitis C transmission rate has been reported at 1.8%, but newer, larger surveys have shown only a 0.5% transmission rate. The overall risk of HIV infection after percutaneous exposure to HIV-infected material in the health care setting is 0.3%. Individualized risk of blood-borne infection from a used biomedical sharp is further dependent upon additional factors. Injuries with a hollow-bore needle, deep penetration, visible blood on the needle, a needle located in a deep artery or vein, or a biomedical device contaminated with blood from a terminally ill patient increase the risk for contracting a blood-borne infection.

After a needlestick injury, certain procedures must be followed to minimize the risk of infection. Lab tests of the recipient should be obtained for baseline studies, including HIV, acute hepatitis panel (HAV IgM, HBsAg, HB core IgM, HCV) and for immunized individuals, HB surface antibody. Unless already known, the infectious status of the source needs to be determined. Unless the source is known to be negative for HBV, HCV, and HIV, post-exposure prophylaxis (PEP) should be initiated, ideally within one hour of the injury.

In 2007, the World Health Organization estimated annual global needlestick injuries at 2 million per year, and another investigation estimated 3.5 million injuries yearly. The European Biosafety Network estimated 1 million needlestick injuries annually in Europe. The US Occupational Safety and Health Administration (OSHA) estimates 5.6 million workers in the healthcare industry are at risk of occupational exposure to blood-borne diseases via percutaneous injury. The US Centers for Disease Control and Prevention (CDC) estimates more than 600,000 needlestick injuries occur among healthcare workers in the US annually.

Among healthcare workers, nurses and physicians appear especially at risk; those who work in an operating room environment are at the highest risk. An investigation among American surgeons indicates that almost every surgeon experienced at least one such injury during their training. More than half of needlestick injuries that occur during surgery happen while surgeons are sewing the muscle or fascia. Within the medical field, specialties differ in regard to the risk of needlestick injury: surgery, anesthesia, otorhinolaryngology (ENT), internal medicine, and dermatology have high risk, whereas radiology and pediatrics have relatively low rates of injury.

In the United States, approximately half of all needlestick injuries affecting health care workers are not reported, citing the long reporting process and its interference with work as their reason for not reporting an incident. The availability of hotlines, witnesses, and response teams can increase the percentage of reports. Physicians are particularly likely to leave a needlestick unreported, citing worries about loss of respect or a low risk perception. Low risk perception can be caused by poor knowledge about risk, or an incorrect estimate of a particular patient's risk. Surveillance systems to track needlestick injuries include the National Surveillance System for Healthcare Workers (NaSH), a voluntary system in the northeastern United States, and the Exposure Prevention Information Network (EPINet), a recording and tracking system that also gathers data.

Common causes of head injury are motor vehicle traffic collisions, home and occupational accidents, falls, and assaults. Wilson's disease has also been indicative of head injury. According to the United States CDC, 32% of traumatic brain injuries (another, more specific, term for head injuries) are caused by falls, 10% by assaults, 16.5% by being struck or against something, 17% by motor vehicle accidents, 21% by other/unknown ways. In addition, the highest rate of injury is among children ages 0–14 and adults age 65 and older.

Melanomas are usually caused by DNA damage resulting from exposure to ultraviolet light from the sun. Genetics also plays a role.

Having more than fifty moles indicates an increased risk melanoma might arise. A weakened immune system makes it easier for cancer to arise due to the body’s weakened ability to fight cancer cells.

Injury is damage to the body caused by external force. This may be caused by accidents, falls, hits, weapons, and other causes. Major trauma is injury that has the potential to cause prolonged disability or death.

In 2013, 4.8 million people died from injuries, up from 4.3 million in 1990. More than 30% of these deaths were transport-related injuries. In 2013, 367,000 children under the age of five died from injuries, down from 766,000 in 1990. Injuries are the cause of 9% of all deaths, and are the sixth-leading cause of death in the world.

In children with uncomplicated minor head injuries the risk of intra cranial bleeding over the next year is rare at 2 cases per 1 million. In some cases transient neurological disturbances may occur, lasting minutes to hours. Malignant post traumatic cerebral swelling can develop unexpectedly in stable patients after an injury, as can post traumatic seizures. Recovery in children with neurologic deficits will vary. Children with neurologic deficits who improve daily are more likely to recover, while those who are vegetative for months are less likely to improve. Most patients without deficits have full recovery. However, persons who sustain head trauma resulting in unconsciousness for an hour or more have twice the risk of developing Alzheimer's disease later in life.

Head injury may be associated with a neck injury. Bruises on the back or neck, neck pain, or pain radiating to the arms are signs of cervical spine injury and merit spinal immobilization via application of a cervical collar and possibly a long board.If the neurological exam is normal this is reassuring. Reassessment is needed if there is a worsening headache, seizure, one sided weakness, or has persistent vomiting.

To combat overuse of Head CT Scans yielding negative intracranial hemorrhage, which unnecessarily expose patients to radiation and increase time in the hospital and cost of the visit, multiple clinical decision support rules have been developed to help clinicians weigh the option to scan a patient with a head injury. Among these are the Canadian Head CT rule, the PECARN Head Injury/Trauma Algorithm, and the New Orleans/Charity Head Injury/Trauma Rule all help clinicians make these decisions using easily obtained information and noninvasive practices.

Ionizing radiation is classified as a neurotoxicant. A 2004 cohort study concluded that irradiation of the brain with dose levels overlapping those imparted by computed tomography can, in at least some instances, adversely affect intellectual development. Prenatal exposure to ionizing radiation at the 8-15 and 16–25 weeks after ovulation was found to induce severe mental retardation as well as variation in intelligence quotient (IQ) and school performance. It is uncertain, if there exist a threshold, under which one or more of these effects, of prenatal exposure to ionizing radiation, do not exist. Cumulative equivalent doses above 500 mSv of ionizing radiation to the head were proven with epidemiological evidences to cause cerebro-vascular atherosclerotic damage. The equivalent dose of 500 mGy x-rays is 500 mSv.

Radiation therapy was found to cause cognitive decline. Cognitive decline was especially apparent in young children, between the ages of 5 to 11. Studies found, for example, that the IQ of 5-year-old children declined each year after treatment by additional several IQ points, thereby the child's IQ decreased and decreased while growing older.

Injury mechanisms such as falls, assaults, sports injuries, and vehicle crashes are common causes of facial trauma in children as well as adults. Blunt assaults, blows from fists or objects, are a common cause of facial injury. Facial trauma can also result from wartime injuries such as gunshots and blasts.

Animal attacks and work-related injuries such as industrial accidents are other causes. Vehicular trauma is one of the leading causes of facial injuries. Trauma commonly occurs when the face strikes a part of the vehicle's interior, such as the steering wheel. In addition, airbags can cause corneal abrasions and lacerations (cuts) to the face when they deploy.

The consequences of whiplash range from mild pain for a few days (which is the case for most people), to severe disability. It seems that around 50% will have some remaining symptoms.

Alterations in resting state cerebral blood flow have been demonstrated in patients with chronic pain after whiplash injury. There is evidence for persistent inflammation in the neck in patients with chronic pain after whiplash injury.

There has long been a proposed link between whiplash injuries and the development of temporomandibular joint dysfunction (TMD). A recent review concluded that although there are contradictions in the literature, overall there is moderate evidence that TMD can occasionally follow whiplash injury, and that the incidence of this occurrence is low to moderate.

The presence of HPV within the tumour has been realised to be an important factor for predicting survival since the 1990s. Tumor HPV status is strongly associated with positive therapeutic response and survival compared with HPV-negative cancer, independent of the treatment modality chosen and even after adjustment for stage. While HPV+OPC patients have a number of favourable demographic features compared to HPV-OPC patients, such differences account for only about ten per cent of the survival difference seen between the two groups. Response rates of over 80% are reported in HPV+ cancer and three-year progression free survival has been reported as 75–82% and 45–57%, respectively, for HPV+ and HPV- cancer, and improving over increasing time. It is likely that HPV+OPC is inherently less maligant than HPV-OPC, since patients treated by surgery alone have a better survival after adjustment for stage. In one study, less than 50% of patients with HPV-OPC were still alive after five years, compared to more than 70% with HPV+OPC and an equivalent stage and disease burden.

In RTOG clinical trial 0129, in which all patients with advanced disease received radiation and chemotherapy, a retrospective analysis (recursive-partitioning analysis, or RPA) at three years identified three risk groups for survival (low, intermediate, and high) based on HPV status, smoking, T stage and N stage ("see" Ang et al., Fig. 2). HPV status was the major determinant of survival, followed by smoking history and stage. 64% were HPV+ and all were in the low and intermediate risk group, with all non-smoking HPV+ patients in the low risk group. 82% of the HPV+ patients were alive at three years compared to 57% of the HPV- patients, a 58% reduction in the risk of death. Locoregional failure is also lower in HPV+, being 14% compared to 35% for HPV-. HPV positivity confers a 50–60% lower risk of disease progression and death, but the use of tobacco is an independently negative prognostic factor. A pooled analysis of HPV+OPC and HPV-OPC patients with disease progression in RTOG trials 0129 and 0522 showed that although less HPV+OPC experienced disease progression (23 v. 40%), the median time to disease progression following treatment was similar (8 months). The majority (65%) of recurrences in both groups occurred within the first year after treatment and were locoregional. HPV+ did not reduce the rate of metastases (about 45% of patients experiencing progression), which are predominantly to the lungs (70%), although some studies have reported a lower rate. with 3-year distant recurrence rates of about 10% for patients treated with primary radiation or chemoradiation. Even if recurrence or metastases occur, HPV positivity still confers an advantage.

By contrast tobacco usage is an independently negative prognostic factor, with decreased response to therapy, increased disease recurrence rates and decreased survival. The negative effects of smoking, increases with amount smoked, particularly

if greater than 10 pack-years. For patients such as those treated on RTOG 0129 with primary chemoradiation, detailed nomograms have been derived from that dataset combined with RTOG 0522, enabling prediction of outcome based on a large number of variables. For instance, a 71 year old married non-smoking high school graduate with a performance status (PS) of 0, and no weight loss or anaemia and a T3N1 HPV+OPC would expect to have a progression-free survival of 92% at 2 years and 88% at 5 years. A 60 year old unmarried nonsmoking high school graduate with a PS of 1, weight loss and anaemia and a T4N2 HPV+OPC would expect to have a survival of 70% at two years and 48% at five years. Less detailed information is available for those treated primarily with surgery, for whom less patients are available, as well as low rates of recurrence (7–10%), but features that have traditionally been useful in predicting prognosis in other head and neck cancers, appear to be less useful in HPV+OPC. These patients are frequently stratified into three risk groups:

- Low risk: No adverse pathological features

- Intermediate risk: T3–T4 primary, perineural or lymphovascular invasion, N2 (AJCC 7)

- High risk: Positive margins, ECE

HPV+OPC patients are less likely to develop other cancers, compared to other head and neck cancer patients. A possible explanation for the favourable impact of HPV+ is "the lower probability of occurrence of 11q13 gene amplification, which is considered to be a factor underlying faster and more frequent recurrence of the disease" Presence of TP53 mutations, a marker for HPV- OPC, is associated with worse prognosis. High grade of p16 staining is thought to be better than HPV PCR analysis in predicting radiotherapy response.

The World Health Organization (WHO) developed the International Classification of External Causes of Injury (ICECI). Under this system, injuries are classified by

- mechanism of injury;

- objects/substances producing injury;

- place of occurrence;

- activity when injured;

- the role of human intent;

and additional modules. These codes allow the identification of distributions of injuries in specific populations and case identification for more detailed research on causes and preventive efforts.

The United States Bureau of Labor Statistics developed the Occupational Injury and Illness Classification System (OIICS). Under this system injuries are classified by

- nature,

- part of body affected,

- source and secondary source, and

- event or exposure.

The OIICS was first published in 1992 and has been updated several times since.

The Orchard Sports Injury Classification System (OSICS) is used to classify injuries to enable research into specific sports injuries.

An occupational injury is bodily damage resulting from working. The most common organs involved are the spine, hands, the head, lungs, eyes, skeleton, and skin. Occupational injuries can result from exposure to occupational hazards (physical, chemical, biological, or psychosocial), such as temperature, noise, insect or animal bites, blood-borne pathogens, aerosols, hazardous chemicals, radiation, and occupational burnout.

While many prevention methods are set in place, injuries may still occur due to poor ergonomics, manual handling of heavy loads, misuse or failure of equipment, exposure to general hazards, and inadequate safety training.

Up to 10% of invasive cancers are related to radiation exposure, including both ionizing radiation and non-ionizing ultraviolet radiation. Additionally, the majority of non-invasive cancers are non-melanoma skin cancers caused by non-ionizing ultraviolet radiation, mostly from sunlight. Sources of ionizing radiation include medical imaging and radon gas.

Ionizing radiation is not a particularly strong mutagen. Residential exposure to radon gas, for example, has similar cancer risks as passive smoking. Radiation is a more potent source of cancer when combined with other cancer-causing agents, such as radon plus tobacco smoke. Radiation can cause cancer in most parts of the body, in all animals and at any age. Children and adolescents are twice as likely to develop radiation-induced leukemia as adults; radiation exposure before birth has ten times the effect.

Medical use of ionizing radiation is a small but growing source of radiation-induced cancers. Ionizing radiation may be used to treat other cancers, but this may, in some cases, induce a second form of cancer. It is also used in some kinds of medical imaging.

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.

Non-ionizing radio frequency radiation from mobile phones, electric power transmission and other similar sources have been described as a possible carcinogen by the World Health Organization's International Agency for Research on Cancer. However, studies have not found a consistent link between mobile phone radiation and cancer risk.

Whiplash is the term commonly used to describe hyperflexion and hyperextension, and is one of the most common nonfatal car crash injuries. More than one million whiplash injuries occur each year due to car crashes. This is an estimate because not all cases of whiplash are reported. In a given year, an estimated 3.8 people per 1000 experience whiplash symptoms. "Freeman and co-investigators estimated that 6.2% of the US population have late whiplash syndrome". The majority of cases occur in patients in their late fourth decade. Unless a cervical strain has occurred with additional brain or spinal cord trauma mortality is rare.

Whiplash can occur at speeds of fifteen miles per hour or less; it is the sudden jolt, as one car hits another, that causes ones head to be abruptly thrown back and sideways. The more sudden the motion, the more bones, discs, muscles and tendons in ones neck and upper back will be damaged. Spinal cord injuries are responsible for about 6,000 deaths in the US each year and 5,000 whiplash injuries per year result in quadriplegia.

After 12 months, only 1 in 5 patients remain symptomatic, only 11.5% of individuals were able to return to work a year after the injury, and only 35.4% were able to get back to work at a similar level of performance after 20 years. Estimated indirect costs to industry are $66,626 per year, depending on the level and severity. Lastly, the total cost per year was $40.5 billion in 2008, a 317% increase over 1998.

In the United States, fire and hot liquids are the most common causes of burns. Of house fires that result in death, smoking causes 25% and heating devices cause 22%. Almost half of injuries are due to efforts to fight a fire. Scalding is caused by hot liquids or gases and most commonly occurs from exposure to hot drinks, high temperature tap water in baths or showers, hot cooking oil, or steam. Scald injuries are most common in children under the age of five and, in the United States and Australia, this population makes up about two-thirds of all burns. Contact with hot objects is the cause of about 20–30% of burns in children. Generally, scalds are first- or second-degree burns, but third-degree burns may also result, especially with prolonged contact. Fireworks are a common cause of burns during holiday seasons in many countries. This is a particular risk for adolescent males.

Exposure to particular substances have been linked to specific types of cancer. These substances are called "carcinogens".

Tobacco smoke, for example, causes 90% of lung cancer. It also causes cancer in the larynx, head, neck, stomach, bladder, kidney, esophagus and pancreas. Tobacco smoke contains over fifty known carcinogens, including nitrosamines and polycyclic aromatic hydrocarbons.

Tobacco is responsible for about one in five cancer deaths worldwide and about one in three in the developed world. Lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking rates since the 1950s followed by decreases in lung cancer death rates in men since 1990.

In Western Europe, 10% of cancers in males and 3% of cancers in females are attributed to alcohol exposure, especially liver and digestive tract cancers. Cancer from work-related substance exposures may cause between 2 and 20% of cases, causing at least 200,000 deaths. Cancers such as lung cancer and mesothelioma can come from inhaling tobacco smoke or asbestos fibers, or leukemia from exposure to benzene.