Exposure to Particulate Matter (PM) could function as an adjuvant depending on the city of origin in mice allergic asthma models. Therefore, our aim was to determine whether inhalation of fine particles (PM2.5) from Mexico City could act as an adjuvant inducing allergic sensitization and/or worsening the asthmatic response in guinea pig, as a suitable model of human asthma. Experimental groups were Non-Sensitized (NS group), sensitized with Ovalbumin (OVA) plus Aluminum hydroxide (Al(OH)3) as adjuvant (S + Adj group), and sensitized (OVA) without adjuvant (S group). All the animals were exposed to Filtered Air (FA) or concentrated PM2.5 (5 h/daily/3 days), employing an aerosol concentrator system, PM2.5 composition was characterized. Lung function was evaluated by barometric plethysmography (Penh index). Inflammatory cells present in bronchoalveolar lavage were counted as well as OVA-specific IgG1 and IgE were determined by ELISA assay. Our results showed in sensitized animals without Al(OH)3, that the PM2.5 exposure (609 ± 12.73 μg/m3) acted as an adjuvant, triggering OVA-specific IgG1 and IgE concentration. Penh index increased ∼9-fold after OVA challenge in adjuvant-sensitized animals as well as in S + PM2.5 group (∼6-fold), meanwhile NS + FA and S + FA lacked response. S + Adj + PM2.5 group showed an increase significantly of eosinophils and neutrophils in bronchoalveolar lavage. PM2.5 composition was made up of inorganic elements and Polycyclic Aromatic Hydrocarbons, as well as endotoxins and β-glucan, all these components could act as adjuvant. Our study demonstrated that acute inhalation of PM2.5 acted as an adjuvant, similar to the aluminum hydroxide effect, triggering allergic asthma in a guinea pig model. Furthermore, in sensitized animals with aluminum hydroxide an enhancing influence of PM2.5 exposure was observed as specific-hyperresponsiveness to OVA challenge (quickly response) and eosinophilic and neutrophilic airway inflammation. Fine particles from Mexico City is a complex mix, which play a significant role as adjuvant in allergic asthma.

Lead (Pb) is one of the most common environmental pollutants and causes adverse effects on human and animal health. This study aimed to evaluate the protective role of beta-glucan against hepatic and reproductive toxicity induced by lead acetate. A total of 28 Sprague Dawley male rats were distributed into four groups (n = 7). The control group was intraperitoneally injected saline (1 ml/kg b.w.) daily for 21 days, the Pb group was intraperitoneally injected lead acetate (15 mg/kg b.w.) daily for 21 days, the beta-glucan group was orally administrated beta-glucan (50 mg/kg b.w.) daily for 21 days, and the Pb + beta-glucan group was intraperitoneally injected lead acetate (15 mg/kg b.w.) daily following the oral administration of beta-glucan (50 mg/kg b.w.) daily for 21 days. Results showed that feed intake in the Pb + beta-glucan group was significantly increased in comparison with that of the Pb group (p < 0.001). We also found that liver malondialdehyde (MDA) level was increased significantly in the Pb group (p < 0.01), while glutathione (GSH) level (p < 0.05), glutathione peroxidase (GSH-Px) (p < 0.05), and catalase (CAT) (p < 0.01) activities were reduced when they were compared with control. Moreover, Pb administration increased expression of pro-apoptotic protein Bax, the ratio of Bax/Bcl-2, and decreased the expression of the antiapoptotic protein Bcl-2 (p < 0.01). Also, Pb was found to cause a significant decrease in sperm motility (p < 0.01) and sperm concentration (p < 0.05) but increase in sperm tails and total sperm anomalies (p < 0.05). These findings were partially preserved by the administration of beta-glucan. Taken together, these results indicated that beta-glucan has the potential to alleviate the Pb-induced toxicity.