The environmental exposures that contribute to emergence of ALL is contentious and a subject of ongoing debate.

High levels of radiation exposure from nuclear fallout is a known risk factor for developing leukemia. Evidence whether less radiation, as from x-ray imaging during pregnancy, increases risk of disease remains inconclusive. Studies that have identified an association between x-ray imaging during pregnancy and ALL found only a slightly increased risk. Exposure to strong electromagnetic radiation from power lines has also been associated with a slightly increased risk of ALL. This result is questioned as no causal mechanism linking electromagnetic radiation with cancer is known.

High birth weight (greater than 4000g or 8.8lbs) is also associated with a small increased risk. The mechanism connecting high birth weight to ALL is also not known.

Evidence suggests that secondary leukemia can develop in individuals treated with certain types of chemotherapy, such as epipodophyllotoxins and cyclophosphamide.

Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women. How it is handled depends primarily on the type of leukemia. Nearly all leukemias appearing in pregnant women are acute leukemias. Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester. Chronic myelogenous leukemia can be treated with relative safety at any time during pregnancy with Interferon-alpha hormones. Treatment for chronic lymphocytic leukemias, which are rare in pregnant women, can often be postponed until after the end of the pregnancy.

High amounts of ionizing radiation exposure can increase the risk of AML. Survivors of the atomic bombings of Hiroshima and Nagasaki had an increased rate of AML, as did radiologists exposed to high levels of X-rays prior to the adoption of modern radiation safety practices. People treated with ionizing radiation after treatment for prostate cancer, non-Hodgkin lymphoma, lung cancer, and breast cancer have the highest chance of acquiring AML, but this increased risk returns to the background risk observed in the general population after 12 years.

Some people have a genetic predisposition towards developing leukemia. This predisposition is demonstrated by family histories and twin studies. The affected people may have a single gene or multiple genes in common. In some cases, families tend to develop the same kinds of leukemia as other members; in other families, affected people may develop different forms of leukemia or related blood cancers.

In addition to these genetic issues, people with chromosomal abnormalities or certain other genetic conditions have a greater risk of leukemia. For example, people with Down syndrome have a significantly increased risk of developing forms of acute leukemia (especially acute myeloid leukemia), and Fanconi anemia is a risk factor for developing acute myeloid leukemia. Mutation in SPRED1 gene has been associated with a predisposition to childhood leukemia.

Chronic myelogenous leukemia is associated with a genetic abnormality called the Philadelphia translocation; 95% of people with CML carry the Philadelphia mutation, although this is not exclusive to CML and can be observed in people with other types of leukemia.

Exposure to anticancer chemotherapy, in particular alkylating agents, can increase the risk of subsequently developing AML. The risk is highest about three to five years after chemotherapy. Other chemotherapy agents, specifically epipodophyllotoxins and anthracyclines, have also been associated with treatment-related leukemias, which are often associated with specific chromosomal abnormalities in the leukemic cells.

Occupational chemical exposure to benzene and other aromatic organic solvents is controversial as a cause of AML. Benzene and many of its derivatives are known to be carcinogenic "in vitro". While some studies have suggested a link between occupational exposure to benzene and increased risk of AML, others have suggested the attributable risk, if any, is slight.

Leukemia is rarely associated with pregnancy, affecting only about 1 in 10,000 pregnant women. The management of leukemia in a pregnant patient depends primarily on the type of leukemia. Acute leukemias normally require prompt, aggressive treatment, despite significant risks of pregnancy loss and birth defects, especially if chemotherapy is given during the developmentally sensitive first trimester.

Acute promyelocytic leukemia represents 10-12% of AML cases. The median age is approximately 30–40 years, which is considerably younger than the other subtypes of AML (70 years). Incidence is higher among individuals of Latin American or South European origin. It can also occur as a secondary malignancy in those that receive treatment with topoisomerase II inhibitors (such as the anthracyclines and etoposide) due to the carcinogenic effects of these agents, with patients with breast cancer representing the majority of such patients. Around 40% of patients with APL also have a chromosomal abnormality such as trisomy 8 or isochromosome 17 which do not appear to impact on long-term outcomes.

CLL is primarily a disease of older adults, with a median age of 70 years at the time of diagnosis. Though less common, CLL sometimes affects people between 30 and 39 years of age. The incidence of CLL increases very quickly with increasing age.

In the United States during 2014, about 15,720 new cases are expected to be diagnosed, and 4,600 patients are expected to die from CLL. Because of the prolonged survival, which was typically about 10 years in past decades, but which can extend to a normal life expectancy, the prevalence (number of people living with the disease) is much higher than the incidence (new diagnoses). CLL is the most common type of leukemia in the UK, accounting for 38% of all leukemia cases. Approximately 3,200 people were diagnosed with the disease in 2011.

In Western populations, subclinical "disease" can be identified in 3.5% of normal adults, and in up to 8% of individuals over the age of 70. That is, small clones of B cells with the characteristic CLL phenotype can be identified in many healthy elderly persons. The clinical significance of these cells is unknown.

In contrast, CLL is rare in Asian countries, such as Japan, China, and Korea, accounting for less than 10% of all leukemias in those regions. A low incidence is seen in Japanese immigrants to the US, and in African and Asian immigrants to Israel.

Of all cancers involving the same class of blood cell, 7% of cases are CLL/SLL.

Rates of CLL are somewhat elevated in people exposed to certain chemicals. Under U.S. Department of Veterans' Affairs regulations, Vietnam veterans who served in-country or in the inland waterways of Vietnam and who later develop CLL are presumed to have contracted it from exposure to Agent Orange and may be entitled to compensation.

MBL has been found in less than 1% of asymptomatic adults under age 40, and in around 5% of adults older than 60. Exact numbers depend on the population studied and the sensitivity of the diagnostic technique.

Like CLL, it appears to be more common in males.

It is also a common finding among older adults with unexplained lymphocytosis.

Recent studies suggest that CLL is very often preceded by MBL,

and that MBL progresses to CLL requiring treatment at a rate of around 1-2% per year. Advancing age and high initial B cell count predispose to progression from MBL to CLL; however, only a small fraction of people with MBL die because of CLL.

Thus, MBL could be regarded as a premalignant condition from which some cases progress to CLL (much similar to the progression of some cases of monoclonal gammopathy of undetermined significance to multiple myeloma).

No treatment is required, but follow-up might be able to detect new diagnoses of CLL. However, this might lead to increased costs, repeated investigations, unnecessary anxiety about cancer and health insurance concerns, while there is no means to prevent progression to CLL.

The exact cause of most cases of childhood leukemia is not known. Most children with leukemia do not have any known risk factors. The immune system plays an important role in protecting the body's immune system. An alteration or defect in the immune system may increase the risk for developing cancer. The immune system can be damaged by different factors, such as exposure to different viruses, environmental factors, chemical factors and other various infections.

There also appears to be some evidence linking childhood leukemia to x-ray exposure. In a 2010 study by the University of California, Berkeley’s School of Public Health, researchers found that children with acute lymphoid leukemia (ALL) had almost twice the chance of having been exposed to three or more X-rays compared with children who did not have leukemia.

T-PLL is an extremely rare aggressive disease, and patients are not expected to live normal lifespans. Before the recent introduction of better treatments, such as alemtuzumab, the median survival time was 7.5 months after diagnosis. More recently, some patients have survived five years and more, although the median survival is still low.

Leukemia is rarely associated with pregnancy, affecting only about one in 10,000 pregnant women. Treatment for chronic lymphocytic leukemias can often be postponed until after the end of the pregnancy. If treatment is necessary, then giving chemotherapy during the second or third trimesters is less likely to result in pregnancy loss or birth defects than treatment during the first trimester.

About four men are diagnosed with this disease for every three women. Despite its overall rarity, it is also the most common type of mature T cell leukemia.

Prognosis is generally good relative to other leukemias. Because of the acuteness of onset compared to other leukemias, early death is comparatively more common. The cause of early death is most commonly severe bleeding, often intracranial hemorrhage. Early death from hemorrhage occurs in 5-10% of patients in countries with adequate access to healthcare and 20-30% of patients in less developed countries. Risk factors for early death due to hemorrhage include delayed diagnosis, late treatment initiation, and high white blood cell count on admission. Despite advances in treatment, early death rates have remained relatively constant.

Relapse rates are extremely low. Most deaths following remission are from other causes, such as second malignancies, which in one study occurred in 8% of patients. In this study, second malignancies accounted for 41% of deaths, and heart disease, 29%. Survival rates were 88% at 6.3 years and 82% at 7.9 years.

In another study, 10-year survival rate was estimated to be approximately 77%.

Little is yet known about the causes of MBL, but as it is a "forme fruste" of CLL the etiologies of these two conditions would be closely related. Genetic changes that can be found in CLL have also been found in MBL, and relatives of people with CLL have a much higher chance of having MBL (13% of first-degree relatives in one study).

One concern about MBL is related to blood transfusions. MBL was found in 0.14% of blood donors in one study. It is unknown whether blood transfusion can transmit MBL.

In the United States, about 500 patients are diagnosed with Richter's transformation each year.

This disease is rare, with fewer than 1 in 10,000 people being diagnosed with HCL during their lives. Men are four to five times more likely to develop hairy cell leukemia than women. In the United States, the annual incidence is approximately 3 cases per 1,000,000 men each year, and 0.6 cases per 1,000,000 women each year.

Most patients are white males over the age of 50, although it has been diagnosed in at least one teenager. It is less common in people of African and Asian descent compared to people of European descent.

It does not appear to be hereditary, although occasional familial cases that suggest a predisposition have been reported, usually showing a common Human Leukocyte Antigen (HLA) type.

As with many cancers, the cause of hairy cell leukemia is unknown. Exposure to tobacco smoke, ionizing radiation, or industrial chemicals (with the possible exception of diesel) does not appear to increase the risk of developing HCL. Farming and gardening appear to increase the risk of HCL in some studies.

Recent studies have identified somatic BRAF V600E mutations in all patients with the classic form of hairy cell leukemia thus sequenced, but in no patients with the variant form.

The U.S. Institute of Medicine (IOM) announced "sufficient evidence" of an association between exposure to herbicides and later development of chronic B-cell leukemias and lymphomas in general. The IOM report emphasized that neither animal nor human studies indicate an association of herbicides with HCL specifically. However, the IOM extrapolated data from chronic lymphocytic leukemia and non-Hodgkin lymphoma to conclude that HCL and other rare B-cell neoplasms may share this risk factor. As a result of the IOM report, the U.S. Department of Veterans Affairs considers HCL an illness presumed to be a service-related disability (see Agent Orange).

Human T-lymphotropic virus 2 (HTLV-2) has been isolated in a small number of patients with the variant form of HCL. In the 1980s, HTLV-2 was identified in a patient with a T-cell lymphoproliferative disease; this patient later developed hairy cell leukemia (a B cell disease), but HTLV-2 was not found in the hairy cell clones. There is no evidence that HTLV-II causes any sort of hematological malignancy, including HCL.

The prognosis is generally poor. The "RS score" (Richter syndrome score), which is an estimate of the patient's prognosis, is based on the patient's performance status, LDH, platelet count, the size of the lymphoma tumors, and the number of prior therapies already received. Overall, the median survival is between five and eight months. Untreated, RS is invariably fatal.

The Hodgkin's lymphoma variant of Richter's carries a better prognosis than the predominant diffuse large B-cell lymphoma type, but a worse prognosis than a "de novo" case of Hodgkin's.

The 5 year survival has been noted as 89% in at least one study from France of 201 patients with T-LGL leukemia.

Chloromas may occur in patients with a diagnosis of myelodysplastic syndrome (MDS) or myeloproliferative syndromes (MPS) (e.g. chronic myelogenous leukemia (CML), polycythemia vera, essential thrombocytosis, or myelofibrosis). The detection of a chloroma is considered "de facto" evidence these premalignant conditions have transformed into an acute leukemia requiring appropriate treatment. For example, presence of a chloroma is sufficient to indicate chronic myelogenous leukemia has entered its 'blast crisis' phase.

Of all cancers involving the lymphocytes, 1% of cases are WM.

WM is a rare disorder, with fewer than 1,500 cases occurring in the United States annually. The median age of onset of WM is between 60 and 65 years, with some cases occurring in late teens.

Leukemia is usually described either as "acute", which grows quickly, or "chronic", which grows slowly. One main type of acute leukemia is acute lymphocytic leukemia (ALL), which accounts for about 3 out of 4 cases of leukemia in children. ALL is a form of leukemia that affects the lymphocytes, a type of white blood cells which fights infection. When a patient has ALL, the bone marrow makes too many immature white blood cells and they do not mature correctly. Therefore, the white blood cells over-produce, crowding the other blood cells. The white blood cells also do not work correctly to fight infection.

Another type of acute leukemia is acute myelogenous leukemia (AML). AML is cancer of the blood in which too many myeloblasts, immature white blood cells, are produced in the bone marrow. The marrow continues to produce abnormal cells that crowd the other blood cells and do not work properly to fight infection. Almost all childhood leukemia is acute.

Chronic leukemias are more common in adults than in children, and although they tend to grow more slowly than acute leukemias, they are harder to treat. These chronic leukemias are divided into two types: chronic myelogenous leukemia (CML) and chronic lymphocytic leukemia (CLL). CML is rare in children, but does occur and is treatable in children the same as in adults. CML patients have too many immature white blood cells being produced, and the cells crowd the other healthy blood cells.

A specific chromosome rearrangement is also found in patients with CML, among the 46 chromosomes in human cells. Part of chromosome nine breaks off and attaches itself to chromosome 22, meaning there is an exchange of genetic material between chromosomes 9 and 22. The rearrangement of the chromosomes changes the positions and functions of certain genes, which causes uncontrolled cell growth.

CLL is another form of chronic leukemia, but is extremely rare in children. Juvenile myelomonocytic leukemia (JMML) is a form of leukemia that is neither chronic nor acute and occurs most often in children under the age of four. JMML begins from myeloid cells, but is not as fast-growing as AML or as slow as CML.

Acute mast cell leukemia is extremely aggressive and has a grave prognosis. In most cases, multi-organ failure including bone marrow failure develops over weeks to months. Median survival after diagnosis is only about 6 months.

Taken together, haematological malignancies account for 9.5% of new cancer diagnoses in the United States and 30,000 patients in the UK are diagnosed each year. Within this category, lymphomas are more common than leukemias.