Abstract
BackgroundStrong relationships between exposure to childhood traumatic stressors and smoking behaviours inspire the question whether these adverse childhood experiences (ACEs) are associated with an increased risk of lung cancer during adulthood.MethodsBaseline survey data on health behaviours, health status and exposure to adverse childhood experiences (ACEs) were collected from 17,337 adults during 1995-1997. ACEs included abuse (emotional, physical, sexual), witnessing domestic violence, parental separation or divorce, or growing up in a household where members with mentally ill, substance abusers, or sent to prison. We used the ACE score (an integer count of the 8 categories of ACEs) as a measure of cumulative exposure to traumatic stress during childhood. Two methods of case ascertainment were used to identify incident lung cancer through 2005 follow-up: 1) hospital discharge records and 2) mortality records obtained from the National Death Index.ResultsThe ACE score showed a graded relationship to smoking behaviors. We identified 64 cases of lung cancer through hospital discharge records (age-standardized risk = 201 × 100,000-1 population) and 111 cases of lung cancer through mortality records (age-standardized mortality rate = 31.1 × 100,000-1 person-years). The ACE score also showed a graded relationship to the incidence of lung cancer for cases identified through hospital discharge (P = 0.0004), mortality (P = 0.025), and both methods combined (P = 0.001). Compared to persons without ACEs, the risk of lung cancer for those with ≥ 6 ACEs was increased approximately 3-fold (hospital records: RR = 3.18, 95%CI = 0.71-14.15; mortality records: RR = 3.55, 95%CI = 1.25-10.09; hospital or mortality records: RR = 2.70, 95%CI = 0.94-7.72). After a priori consideration of a causal pathway (i.e., ACEs → smoking → lung cancer), risk ratios were attenuated toward the null, although not completely. For lung cancer identified through hospital or mortality records, persons with ≥ 6 ACEs were roughly 13 years younger on average at presentation than those without ACEs.ConclusionsAdverse childhood experiences may be associated with an increased risk of lung cancer, particularly premature death from lung cancer. The increase in risk may only be partly explained by smoking suggesting other possible mechanisms by which ACEs may contribute to the occurrence of lung cancer.
Highlights
Strong relationships between exposure to childhood traumatic stressors and smoking behaviours inspire the question whether these adverse childhood experiences (ACEs) are associated with an increased risk of lung cancer during adulthood
An underlying thesis of the ACE Study is that stressful or traumatic childhood experiences have negative neurodevelopmental impacts that persist over the lifespan and that increase the risk of a variety of health and social problems [1]
Anda and colleagues [2] hypothesized that observed associations between adverse childhood experiences (ACEs) and early smoking initiation as well as other smoking behaviours in adulthood may be partly explained by the adoption of smoking as a means of self-medicating to deal with affective disorders through the psychoactive actions of nicotine
Summary
Strong relationships between exposure to childhood traumatic stressors and smoking behaviours inspire the question whether these adverse childhood experiences (ACEs) are associated with an increased risk of lung cancer during adulthood. An underlying thesis of the ACE Study is that stressful or traumatic childhood experiences have negative neurodevelopmental impacts that persist over the lifespan and that increase the risk of a variety of health and social problems [1]. The epidemiological findings parallel advances in the neurobiological understanding of tobacco dependence [4,5,6] as well as that for the consequences of exposure to childhood traumatic stressors [7], including cancer [8], providing biologic plausibility to observed associations between child maltreatment and adverse health outcomes later in life [9,10,11,12]. Disruptions in HPA signaling may sustain inflammatory processes (processes shown to have a role in the development of some cancers [14]) through altered release of glucocorticoid hormones and disturbances in the balance between pro- and anti-inflammatory mechanisms thereby affecting immune activation and inflammation [15,16,17]
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