In Utero Exposure to Environmental Tobacco Smoke Potentiates Adult Responses to Allergen in BALB/c Mice

Abstract

BackgroundFetal stress has been linked to adult atherosclerosis, obesity, and diabetes. Epidemiology studies have associated fetal exposure to maternal smoking and postnatal exposure to environmental tobacco smoke (ETS) with increased asthma risk.ObjectiveWe tested the hypothesis, in a mouse model of asthma, that in utero ETS exposure alters airway function and respiratory immune responses in adults.MethodsPregnant Balb/c mice were exposed daily to ETS or HEPA-filtered air (AIR). Offspring inhaled aerosolized ovalbumin (OVA) or saline in weeks 7–8. Regardless of whether they inhaled OVA or saline, mice were sensitized by OVA injections in weeks 11 and 13 followed by OVA aerosol challenge in weeks 14–15. At three time points, we assessed OVA-specific serum immunoglobins, bronchoalveolar lavage cells and cytokines, lung and nasal histopathology, and airway hyperresponsiveness (AHR).ResultsAt 6 weeks, we found no significant differences between in utero ETS and AIR mice. At 10 weeks, following OVA aerosol, ETS mice displayed greater AHR than AIR mice (α = 0.05), unaccompanied by changes in histopathology, cytokine profile, or antibody levels. At 15 weeks, mice that had inhaled saline in weeks 7–8 developed airway inflammation: eosinophilia (α = 0.05), interleukin-5 (α = 0.05), and AHR (α = 0.05) were greater in ETS mice than in AIR mice. Mice that had inhaled OVA in weeks 7–8 demonstrated no airway inflammation after sensitization and challenge.ConclusionIn utero ETS exposure exacerbates subsequent adult responses to initial allergen exposure.

Exposure to psychosocial job strain during pregnancy and odds of asthma and atopic dermatitis among 7-year old children – a prospective cohort study

“…Several factors have been proposed to contribute to the increasing incidence of asthma and AD [eg, maternal smoking (9), alcohol consumption (10), eating habits (11,12), obesity (13), and work environment (14,15)]. Also maternal stress has been suggested to interfere with fetal immune development (16,17).…”

Effect of maternal exposure to ozone on reproductive outcome and immune, inflammatory, and allergic responses in the offspring

“…Both O 3 and diesel exposures increase prostaglandin E 2 (PGE 2 ) levels in the lung fluid of mice (Canning et al, 1991;Ahn et al, 2008), and blocking this activity with indomethacin in the case of O 3 has reversed health effects such as reduced phagocytosis (Canning et al, 1991) and increased susceptibility to infection (Gilmour et al, 1993). However, maternal exposure to cigarette smoke components by inhalation increases allergic sensitization in both experimental animals (Penn et al, 2007;Wu et al, 2009) and in humans (Strachan and Cook, 1998;Gilliland et al, 2006), and this may be due to a different profile of mediators produced in the lung. To better understand how these inhalation exposures to common air pollutants produce contrasting effects through maternal exposure, a comparative study is warranted using the efficient sensitization regimes to identify chemical components and biomarkers that differentially modulate fetal immune development.…”

“…Inhalation exposure to environmental or side stream tobacco smoke enhanced the offspring's immune responses to allergen (Penn et al, 2007) and increased lung resistance (Wu et al, 2009). Studies examining prenatal and neonatal inhalation exposures to DE in rats have also shown increases in allergen-specific IgE responses in adults (Watanabe and Ohsawa, 2002).…”

Air Pollution and Its Effects in the Respiratory System

“…Prenatal exposure to Environmental Tobacco Smoke (ETS) has been associated with an increased risk of asthma, and during the postnatal period, the exposure increases asthma exacerbations, as well as the risk for respiratory infections (Wang & Pinkerton, 2008). Studies in mice indicate that prenatal exposure to ETS increases allergic responses in postnatal period (Penn et al, 2007;Gern, 2010). The exposure to outdoor pollutants such as Particulate Matter (PM), carbon monoxide (CO), sulphur (SO 2 ), nitrogen (NOx), and ozone, decreases lung function during childhood www.intechopen.com (Mortimer et al, 2008).…”