Parental lung cancer as predictor of cancer risks in offspring: Clues about multiple routes of harmful influence?

Abstract

The carcinogenic effects of active smoking have been demonstrated for many sites, but the effects of passive smoking and exposures during pregnancy and breastfeeding are less well documented. We examined whether 0–70‐year‐old offspring of parents with lung cancer are at a risk of cancer that cannot be explained by their smoking or familial risk. It was assumed that known target sites for tobacco carcinogenesis would be affected, if any. The nationwide Swedish Family‐Cancer Database with cancers recorded from 1958 to 2002 was used to calculate age‐specific standardized incidence ratios (SIRs). Among offspring of affected mothers, increased risks were observed for upper aerodigestive (SIR 1.45), nasal (2.93), lung (1.71) and bladder (1.52) cancers and for kidney cancer (6.41) in one age group. The risk of bladder cancer was found in younger age groups than that of lung cancer. Cancers at many of these sites, but not the kidney or the bladder, were in excess in offspring of affected fathers. Nasal cancer was even increased when either parent was diagnosed with lung cancer; the highest risk was for nasal adenoid cystic carcinoma (7.73). The data suggest that passive smoking during childhood is associated with an increase risk of nasal cancer. For bladder and kidney cancers, a contribution by tobacco carcinogens is implicated through breastfeeding and in utero exposure. © 2005 Wiley‐Liss, Inc.

Risk of Bladder Cancer Associated with Family History of Cancer: Do Low-Penetrance Polymorphisms Account for the Increase in Risk?

“…The fact that both family history of tobacco-related cancer and personal history of smoking were associated with an increased risk for bladder cancer points to two potential explanations: first, that shared exposures within families such as in utero exposure to tobacco compounds, exposure to tobacco carcinogens through breast-feeding, and ETS during childhood, as well as the intensity of the smoking habit among relatives, may account for cancer clusters in relatives (34); second, that a susceptibility polymorphism, or a combination of them, is segregated within families predisposing relatives to cancer in the presence of tobacco exposure. We explored the hypothesis that ETS might contribute to the familial clustering of bladder cancer among the nonsmoker subjects by adjusting the logistic regression models for childhood ETS.…”

Environment‐induced epigenetic reprogramming in genomic regulatory elements in smoking mothers and their children

“…One of the most common hazardous prenatal exposures is maternal smoking. Prenatal exposure to tobacco smoke was described as a risk factor for a multitude of different diseases in the child, including lung diseases, obesity, and cancer (Hemminki & Chen, 2006;Oken et al, 2008;Neuman et al, 2012). Several studies have focused on DNA methylation in cord blood to elucidate the influence of smoking and other prenatal exposures on the newborn's epigenome by analyzing global DNA methylation changes (i.e., in repetitive elements) or methylation of a limited number of preselected CpG probes (i.e., 27k methylation or 450k arrays) (Breton et al, 2009;Joubert et al, 2012;Murphy et al, 2012;Markunas et al, 2014;Kupers et al, 2015;Richmond et al, 2015).…”

Adverse health effects related to tobacco smoke exposure in a cohort of three‐year olds

“…Foetal tobacco smoke exposure increases the risk for sudden infant death syndrome, low birthweight, preterm birth, behavioural problems, cognitive developmental delay and reading and writing disability (3). Others show long‐term effects like cardiovascular disease (5), cancer (6) and asthma in adulthood (7). Development of allergy is controversial, because both negative and positive associations have been shown in different studies (3).…”