Childhood Social Environment and Hodgkin's Disease

Nancy Gutensohn, Philip Cole

New England Journal of Medicine · 1981 · 318 citations · 34 references

Concepts

TL;DR

The epidemiologic similarities between Hodgkin's disease in the young and paralytic poliomyelitis suggest that Hodgkin's disease may be a rare consequence of a common infection, with the probability of oncogenesis increasing with age at the time of infection. The study aimed to investigate the association of Hodgkin's disease with childhood factors that influence age of exposure to infectious agents. The authors examined 225 cases and 447 controls aged 15 to 39 years to assess these associations. Risk was markedly lower among individuals with five or more siblings, later birth order, or multiple-family homes, and cases had fewer playmates, better-educated mothers, and twice the rate of infectious mononucleosis, suggesting that delayed early infection exposure reduces Hodgkin's disease risk, consistent with a viral origin. Published in N Engl J Med 1981, 304:135–40.

Abstract

The epidemiologic similarities between Hodgkin's disease in the young and paralytic poliomyelitis suggest that Hodgkin's disease may be a rare consequence of a common infection, with the probability of oncogenesis increasing with age at the time of infection. In a study of 225 cases and 447 controls 15 to 39 years of age, we investigated the association of Hodgkin's disease with factors in childhood that influence age of exposure to infectious agents. Risk among persons with five or more siblings was nearly half that among those with one or none; risk was also reduced among persons of late birth order. Subjects who had lived in multiple-family homes had half the risk of those in single-family housing. Cases had fewer playmates and better-educated mothers than did controls, and cases had twice the rate of infectious mononucleosis. Risk is therefore associated with a set of factors that tend to decrease or delay early exposure to infections, and this association might be explained by a viral origin of the disease, with age at infection as a major modifier of risk. (N Engl J Med. 1981; 304:135–40.)

References

34