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ToxSci Advance Access published online on October 5, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfj006
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received August 11, 2005
Accepted September 22, 2005

Immunotoxiocology

Effects of Prenatal Exposure to Cigarette Smoke on Offspring Tumor Susceptibility and Associated Immune Mechanisms

Sheung P. Ng 1, Allen E. Silverstone 2, Zhi-Wei Lai 2, and Judith T. Zelikoff 1*

1 New York University School of Medicine, Nelson Institute of Environmental Medicine, Tuxedo, New York 10987
2 SUNY Upstate Medical University, Department of Microbiology & Immunology, Syracuse, New York 13210

* To whom correspondence should be addressed.
Judith T. Zelikoff, E-mail: judyz{at}env.med.nyu.edu


  Abstract

Epidemiologic evidence suggests that prenatal exposure to intact (unfractionated) cigarette smoke (CS) increases the incidence of cancer in the offspring. A toxicologic study was carried out to examine the effects and underlying mechanisms of prenatal exposure to mainstream cigarette smoke (MCS) on offspring resistance to tumor challenge and surveillance mechanisms critical for the recognition and destruction of tumors. Pregnant B6C3F1 mice were exposed by inhalation to MCS for 5 d/wk (4 h/d from gestational day 4 to parturition) and smoke-induced effects on offspring host resistance to transplanted tumor cells, natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activity, cytokine levels, lymphoid organ immune cell subpopulations and histology were examined in 5-, 10- and 20-wk-old male and female offspring. At a concentration of smoke roughly equivalent to smoking <1 pack of cigarettes/d, prenatally-exposed male offspring challenged at 5 wk of age with EL4 lymphoma cells demonstrated a >2-fold increase in tumor incidence (relative to age-/gender-matched air-exposed offspring); tumors in prenatally smoke-exposed pups also grew significantly faster. CTL activity in the smoke-exposed 5- and 10-wk-old male pups was significantly less than that of the age-/gender-matched controls. No effects of prenatal CS exposure were observed on offspring NK activity, cytokine levels, lymphoid organ histology or immune cell subpopulations. Results demonstrated that exposure of pregnant mice to a relevant dose of MCS decreased offspring resistance against transplanted tumor cells and persistently reduced CTL activity in prenatally exposed pups. This study provides biological plausibility for the epidemiologic data indicating that children of mothers who smoke during pregnancy have a greater risk of developing cancer in later life.

Keywords: Cigarette smoke; developmental immunotoxicology; tumor surveillance mechanisms.
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