EHPnet: Greener Education Materials for Chemists

Research The incidence of asthma has escalated over the past 20 years. Increasingly, initial asthma episodes are observed early in life (Holt 1998; Weiss 1998). In 2004, nearly 30% of the 30 million diagnosed asthmatics in the United States were < 18 years of age. The highest asthma prevalence rate (148/1,000) exists in 5-to 17-year-olds (American Lung Association 2006). Despite the often early onset of this disease, chronic adult asthmatics comprise the majority of asthma patients. Stresses in the fetal environment can promote early onset of chronic adult diseases. Initial epidemiologic studies related maternal nutritional deficits to low live birth weights and to premature cardiovascular disease in adult human offspring (reviewed by Barker 2002). In humans, neurologic response to fetal stress has been recently reviewed (Amiel-Tison et al. 2004). In experimental studies, fetal anemia in sheep (Davis et al. 2005) and hypoxia in pregnant rats (Li et al. 2004) have resulted in chronic disease in adult offspring. In pregnant mice, viral infection (Niklasson et al. 2006), pesticide treatment (Cory-Slechta et al. 2005), and environmental tobacco smoke (ETS) exposure (Yang et al. 2004) have also resulted in chronic adult disease in offspring. Exposure to ETS has been associated with exacerbated asthmatic responses in children (Gilliland et al. 2000; Lindfors et al 1999; Mannino et al. 2001). Altered lung function, increased risk of asthma, and persistent lung function deficits in children have been linked with in utero exposure to maternal smoking and/or postnatal exposure to ETS (Gilliland action of tobacco smoke exposure with sensi-tization to nontobacco allergens may increase the prevalence of allergy and asthma (Oryszczyn et al. 2000). Detailed experimental studies focused on proasthmatic responses resulting from in utero ETS exposure combined with postnatal exposure to nontobacco antigens have not been reported. In rodent models of allergic asthma, ovalbumin (OVA) is a commonly employed antigen for eliciting allergic responses. Sensitization by intraperitoneal (ip) injection , followed by inhalation challenge with OVA elicits expansion of the T helper-2 (Th2) lymphocyte population. Production of Th2 cytokines follows, leading to airway hyperresponsiveness (AHR) and inflammation characterized by eosinophilia and OVA-specific IgE (Zhang et al. 1997). This sensitization/challenge protocol fails to mimic the typical human experience of aerosol-only sensitization and challenge (Bice et al. 2000; Persson et al. 1997). However, aerosol-only OVA exposure of mice results in little or no OVA-specific serum IgE, and no eosinophilic inflammatory response. This has been attributed to the induction …