The link between environmental agents and childhood cancer is not a new
concept. Environmental causes of childhood cancer have long been
suspected by many scientists but have been difficult to pin down, partly
because cancer in children is rare and because it is difficult to
identify past exposure levels in children, particularly during
potentially important periods such as pregnancy, in-utero, or
even prior to conception. Hence, many of the environmental agents
hypothesized for childhood leukemia remain speculative [1-3].
In this issue of Indian Pediatrics, Rau et
al. [4] investigated the presence of endosulfan in the bone marrow
of children with hematological malignancy residing in areas sprayed with
the pesticide (in South India). This is a case-control study in which
the authors report its presence in the bone marrow of 7/34 children
residing in these areas including 6 who had leukemia.
The authors themselves point out that this study does
not in any way prove that endosulfan is a cause of leukemia. As of date,
there are no available epidemiological studies linking endosulfan
exposure specifically to cancer in humans. It is important to understand
that an association between an exposure and cancer does not necessarily
mean that the exposure causes cancer. Most importantly, other possible
explanations of the observed association must be ruled out. The
consistency of an association is to be considered, and the association
must be temporally correct meaning that we must be sure that the
exposure actually preceded the development of the disease, which in this
case would include events taking place before birth, during conception,
embryogenesis and early postnatal life. Another important aspect in such
a study is the sample size and whether it is truly representative of the
population. As acknowledged by the authors, the small sample size, other
compounding factors like genetic susceptibility, exposure to other
carcinogens and their effects, are the limitations of this study.
Endosulfan, an off patent organochlorine insecticide
and acaricide was developed in the early 1950s and has been used
globally in agriculture to control insect pests. Although
industrialized nations have restricted or banned many organochlorine
pesticides, some of these chemicals (like endosulfans) are still used,
on the assumption that they pose little threat to the environment,
wildlife, or human health.
It has long been recognized that leukemia is a
heterogenous disease with a multifactorial and multistep pathogenesis
with a fetal origin being postulated by some [3,5]. Epidemiological
evidence suggests that ionizing radiation, certain chemicals (such as
benzene), viruses (human T-cell leukemia/lymphoma virus type I,
EpsteinBarr virus), and bacteria (Helicobacter pylori) may play
a part in the development of some subtypes of leukemia and lymphoma in
adults and children.
Finding causes of any disease is usually a long, slow
process. No one study is likely to prove that a particular exposure
definitely causes a particular cancer. However, each well designed and
well executed study with adequate sample size will bring us closer to
understanding the causes of these cancers within populations of
children.
1. Pearce MS, Hammal DM, Dorak MT, McNally RJ, Parker
L. Paternal occupational exposure to pesticides or herbicides as risk
factors for cancer in children and young adults: a case-control study
from the North of England. Arch Environ Occup Health. 2006;61:138-44.
2. UK Childhood Cancer Study Investigators. Childhood
cancer and residential proximity to power lines. Br J Cancer.
2000;83:1573-80.
3. Toren A, Rechavi G, Ramot B. Pediatric cancer:
Environmental and genetic aspects. Ped Hematol Oncol. 1996;13:319–31.
4. Rau A, Coutinho A, Avabratha KS, Rau AR, Warrier
RP. Pesticide (endosulfan) levels in the bone marrow of children with
hematological malignancies. Indian Pediatr. 2012;49:113-7.
5. Wiemels JL, Cazzaniga G, Daniotti M, Eden OB,
Addison GM, Masera G, et al. Prenatal origin of acute
lymphoblastic leukaemia in children. Lancet. 1999; 354:1499–1503.
6. Greaves M. Molecular genetics, natural history and the demise of
childhood leukaemia. Eur J Cancer. 1999; 35:173-85.