Parental smoking and childhood leukemia.
Childhood leukemia is the most common cancer among children, representing 31% of all cancer cases occurring in children younger than the age of 15 years in the USA. There are only few known risk factors of childhood leukemia (sex, age, race, exposure to ionizing radiation, and certain congenital diseases, such as Down syndrome and neurofibromatosis), which account for only 10% of the childhood leukemia cases. Several lines of evidence suggest that childhood leukemia may be more due to environmental rather than genetic factors, although genes may play modifying roles. Human and animal studies showed that the development of childhood leukemia is a two-step process that requires a prenatal initiating event(s) plus a postnatal promoting event(s). Despite a substantial public health effort to reduce cigarette smoking, a large proportion of the US and world population still smoke. Tobacco smoke contains at least 60 known human or animal carcinogens, with the major chemical classes being volatile hydrocarbons, aldehydes, aromatic amines, polycyclic aromatic hydrocarbons, and nitrosamines; among these chemicals, only benzene is an established leukemogen, although other chemicals in the tobacco could interact with one another in a complex way to jointly attain a significant carcinogenic effect on the development of leukemia. Although tobacco smoke is an established risk factor for adult myeloid leukemia, the studies of association between parental smoking and childhood leukemia have produced inconsistent results. The majority of the studies on maternal smoking and childhood leukemia did not find a significant positive association and some even reported an inverse association. In contrast to studies of maternal smoking, studies of paternal smoking and childhood leukemia reported more positive associations but only by less than half of the studies. Future directions to be considered for improving the study of parental smoking and childhood leukemia are: 1) consider all sources of benzene exposure in addition to smoking, including occupational exposure and traffic exhausts; 2) childhood leukemia is a heterogeneous disease and epidemiologic studies of childhood leukemia can be greatly improved by grouping childhood leukemia into more homogeneous groups by molecular techniques (e.g., structural and numerical chromosomal changes); and 3) assess gene-environment interaction. It is hoped that through the continual effort, more will be uncovered regarding the causes of childhood leukemia. In the meantime, more effort should be spent on educating the parents to quit smoking, because parental smoking is known to affect many childhood diseases (e.g., asthma, respiratory tract infection, and otitis media) that are much more prevalent than childhood leukemia.
Chang
Jeffrey S
JS
Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, USA.
D000818:Animals; D002648:Child; D005333:Fetus / Q000187:drug effects; D006801:Humans; D007938:Leukemia / Q000209:etiology*; D009153:Mutagens / Q000633:toxicity; D010290:Parents; D012907:Smoking / Q000009:adverse effects*; D014028:Tobacco Smoke Pollution / Q000009:adverse effects
D009153:Mutagens; D014028:Tobacco Smoke Pollution