Exposure and harm to combustion-derived wood particles

The human respiratory system is the gateway of entry for inhaled detritus from anthropogenic (e.g. combustion-derived (CD) particulate matter (PM; e.g. diesel exhaust and wood-burning PM). Adult humans inhale 20m3 of air and suspended debris (gases and particles) into the airways daily. Inhalation exposure to CDPM (Figure 1) is known to increase the risk of morbidity and mortality of lung and heart diseases in all exposed individuals. The physicochemical properties of size, surface area and presence of transition metals have been implicated as drivers of the oxidative capacity of CDPM. However, the precise role of reactive organic compounds (ROC) in ambient aerosols, present either in the gas or particle phase has not been fully-investigated for their relevance in the induction of the observed adverse health effects. When addressing the toxicity of inhalation hazards such as wood smoke CDPM, a model that resembles the human lung responding to toxic challenges is required. In our in vitro exposure studies, we utilised normal human bronchial epithelial (NHBE) cells grown at the air-liquid interface (ALI) using filter-well technology (Prytherch et al 2011), to create an in vivo-like 3-dimensional lung model. This model is a fully-differentiated, pseudo-stratified, muco-ciliary epithelium containing basal, serous, Clara, goblet and ciliated cells. NHBE cells were exposed to wood smoke derived from Spruce, Beech and Birch at a dose of 152µg/cm2: carbon black (CB; negative control; Monarch 120, Cabot UK; DQ12 quartz (positive control). Following exposure (24 hours), tissue integrity (i.e. transepithelial electrical resistance (TEER) was measured to reveal minor disruption to bronchial tissue integrity (Figure 2). However, changes in cellular energy levels (i.e. ATP) between the types of wood smokes (Figure 3), could infer the smoke acted as an irritant to the lung environment. Wood smoke exposure can depress the immune system and damage the layer of cells in the lungs that protect and cleanse the airways. Further work on the biological and histological impacts of wood smoke will allow us to reveal mechanisms behind the changes observed, as well identifying biomarkers of cell damage by specific CDPM ROCs. For vulnerable populations, such as people with asthma, chronic respiratory disease and those with cardiovascular disease, wood smoke is particularly harmful, even at short exposures it can prove dangerous. Wood smoke interferes with normal lung development in infants and children. It also increases children’s risk of lower respiratory infections such as bronchitis and pneumonia. Prytherch, Z., Job, C., Marshall, H., Oreffo, V., Foster, M. and BéruBé, K.A. (2011) Macro. Bios. 11, 1467–77. This work was supported by HICE (www.hice-vi.eu)

Maternal smoking during pregnancy and child emotional problems: The relevance of maternal and child 5-HTTLPR genotype

Serotonin is involved in the development of neural circuits modulating emotional behavior. The short allele (s) of a polymorphism (5-HTTLPR) of the serotonin transporter gene is a risk factor for psychopathology in the presence of environmental stressors. Maternal smoking is associated with growth restriction of the human fetal brain and adverse effects of nicotine on the developing serotonin system have been documented. We hypothesized that maternal smoking interacts with both child and mother 5-HTTLPR genotype as a risk factor for later child emotional problems. In a sample of n=1,529 mother-child dyads, smoking habits were assessed by questionnaires during pregnancy. Child emotional problems were measured by the Child Behavior Checklist at the child's age of 3 years. Maternal smoking during pregnancy significantly increased the risk for emotional problems in children carrying the s-allele; beta=0.24, P=0.03 (mother-report), and beta=0.46, P=0.001 (father-report). In children heterozygous at 5-HTTLPR and exposed to maternal prenatal smoking (n=79) risk of emotional problems increased with each additional s-allele the mother carried. The associations between 5-HTTLPR and child emotional problems were not moderated by paternal prenatal smoking. These findings imply that the vulnerability for emotional problems in s-allele carriers may already originate in fetal life. (c) 2012 Wiley Periodicals, Inc

Developmental Risk I: Depression and the Developing Brain

This article discusses recent findings on the neurobiology of pediatric depression as well as the interplay between genetic and environmental factors in determining the risk for the disorder. Utilizing data from both animal and human studies, the authors focus on the evolving understanding of the developmental neurobiology of emotional regulation, cognitive function and social behavior as it applies to the risk and clinical course of depression. Treatment implications and directions for future research are also discussed