Childhood Cancers – An Excerpt – Chemical Carcinogenesis And Cancers by W.C. Hueper, M.D. (Chief Environment Cancer Section of National Cancer Institute) & W.D. Conway, PhD (Former Senior Chemist Environmental Cancer Section of National Cancer Institute) – 1964
d. Childhood Cancers
The observed rise in cancers during childhood may finally be cited as another illustration of the changing epidemiologic cancer panorama which may reflect the influence of the growing chemicalization of the human economy and its pollution with carcinogenic chemicals. Childhood cancers arising on an exogenous basis may have their origin from two sources. Carcinogens may be introduced into the fetal organism through a transplacental penetration of carcinogens with which the maternal organism came in contact before or during pregnancy (Hueper). Such exposures may result in the development of cancers as well as of “congenital” malformations in the offspring, according to observations made in experimental animals with various chemical carcinogens (ionizing radiation, thiouracil, methycholanthrene, urethane, selenium, 2-acetylaminfluorene, trypan blue) (Shay et al.; Nurnberger and Lipscomb; Porteous; Williams and Schrum; Dargeon; Saye, Watt, Foushee and Palmer; Wilson et al.; Wilson, Brent, and Jordon; Russell and Russell; Danforth; Schinz and Fritz-Niggli; Aaron et al.; Nishimura and Kiginuki; Gruenwald; Hisaoka; Ford, Paterson, and Treuting; Holmberg, Nelson and Wallgren; Manning and Carroll; Peller; Stewart, Webb, Giles and Hewitt; Wilson; Gillman et al.; Larsen). The co-existence of mongolism and leukemia increasingly reported in recent years may be one of the associations related to such transplacental action of carcinogens. (Ingalls; Steyn; O’Connor et al.; Fischler and Farchy; Schunk and Lehman).
Chemicals which modify the mitotic process should primarily be suspected as teratogenic and cancerigenic agents (Steyn; Lawrence and Donlan; Stewart and Barber; Tuchmann-Duplessis and Mercier-Parot).
The second route by which carcinogens are transferred from the mother to the child is through the milk. Many chemicals, including carcinogenic ones (arsenicals, goitrogenic chemicals, chloroform, methylcholanthrene, DDT isoniazid, sulfonamides, radioactive chemicals, mouse milk factor) are excreted with the milk (Clements; Briziarelli; Dao et al.; Sapeika; Shay et al.; Rieben and Druey). The production of cancers in the suckling offspring of mothers excreting such carcinogens with the milk has been reported. Conditions prevailing in modern postnatal life provide for infants an increasingly common contact with environmental and especially dietary, sanitary, and medicinal carcinogenic factors of various types (radioactive chemicals, waxes in milk, and mineral oil in vaccines, x-radiation, etc) sustained by the very young may be of especially serious significance as to the subsequent development of cancers in later life, because observations made recently on newborn animals have shown that such very young animals react with cancerous responses to much smaller doses of carcinogens than adult animals (Pietra et al.; Svec and Hlavayova; Roe et al.; Stich; Kelly and O’Gara; Fiore-Donati et al.; Smith and Rous; Poel and Kammer; Lijinsky; Boutwell and Bosch).
The recent increase in frequency of cancers in infants and children is strikingly illustrated by the fact that twenty years ago cancer was not listed among the ten most frequent causes of death in children, while it has become now the third most frequent cause among children one to four years of age (Ariel and Pack). During 1954 to 1956, the cancer death rate among white males rose from 9.2 per 100,000 population under age one, to 12.7 of the same number. Kiesewetter and Mason quoted statistical data of the U.S. Department of Health, Education, and Welfare as showing that in 1945 cancers accounted for 6.9 per cent of all deaths in children under fourteen years of age, while they formed 8.3 per cent of the causes of death among children in 1955. This percentage stood at 7.3 in 1948 (Andersen). Similar observations have been recorded in England (Campbell, Gaisford, Paterson and Steward; Brown and Doll). Apart from chemical factors, genetic influence as well as prenatal and postnatal exposures to ionizing radiation have been considered as possible causes of this development (Stewart and Barber). The importance of carcinogenic exposures sustained before puberty in the development of cancers later in life are indicated by the suggestion of Kennaway and Kennaway that cancers of the stomach are arising after the second twenty-five years of life may be predestined to occur by factors to which the body was exposed during the first twenty-five years. The existence of such time-relations between exposure to a carcinogen (smegma) during the first few years of life and the appearance of penile cancer in adult life is well established (Kennaway).
These observations and considerations supply a substantial scientific basis for the assumption that exposures of pregnant mothers and infants to environmental carcinogenic chemicals, including radioactive agents, sustained to an increasing degree during recent decades, are at least in part, responsible for the observed rise in cancers and especially leukemias, in childhood (Kiesewetter and Mason; Dargeon; Andersen; Ariel and Pack; Stewart and Barber; Burnett; Brown and Doll; Campbell, Gaisford, Paterson and Steward).
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