title: Inhaled lead affects lung pathology and inflammation in sensitized and control guinea pigs.
abstract: The association between lead exposure and respiratory diseases including asthma is controversial. Some studies indicate that exposure to environmental lead pollution may cause asthma; however, there is not sufficient data in this regard. The effect of lead on lung pathological findings and serum inflammatory mediators in sensitized and non-sensitized guinea pigs exposed to inhaled lead was examined. Eleven animal groups including control, sensitized, three groups of non sensitized animals, three groups during sensitization, and three groups after sensitization exposed to aerosol of three lead concentrations (n = 6 for each group) were studied. Serum inflammatory mediators levels and lung pathological changes were evaluated. All pathological changes and serum ET-1, EPO, NO levels were significantly higher in the sensitized and non sensitized animals exposed to lead than control group (p < 0.05 to p < 0.001). There was no significant difference between non sensitized groups exposed to high lead concentration and sensitized group. Serum inflammatory mediators levels and pathological findings in sensitized groups exposed to lead both during and after sensitization were significantly higher than sensitized non exposed group (p < 0.05 to p < 0.001). The data of exposed animals to high lead concentration were significantly higher than those of medium and low concentrations; those of medium concentration were also higher than low concentration (p < 0.05 to p < 0.001). In summary, the present study indicates that exposure to inhaled lead is able to induce respiratory changes similar to asthma. In addition, the results indicated that exposure to environmental lead is able to aggravate asthma severity both during development of asthma or after its manifestation.
authors.affiliation: Neurogenic Inflammation Research Centre and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
authors.forename: Mohammad Hossein
authors.initials: MH
authors.lastname: Boskabady
authors.affiliation: Department of Pathology, Mashhad University of Medical Sciences, Mashhad, Iran.
authors.forename: Sayed Abas
authors.initials: SA
authors.lastname: Tabatabai
authors.affiliation: Neurogenic Inflammation Research Centre and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
authors.forename: Tahereh
authors.initials: T
authors.lastname: Farkhondeh
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D019332:Endothelin-1 / Q000097:blood; D047209:Eosinophil Peroxidase / Q000097:blood; D005260:Female; D006168:Guinea Pigs; D006967:Hypersensitivity / Q000097:blood / Q000473:pathology*; D007249:Inflammation / Q000097:blood / Q000139:chemically induced* / Q000473:pathology; D007854:Lead / Q000633:toxicity*; D008168:Lung / Q000187:drug effects* / Q000473:pathology; D008297:Male; D009569:Nitric Oxide / Q000097:blood; D010047:Ovalbumin
chemical_list: D019332:Endothelin-1; D007854:Lead; D009569:Nitric Oxide; D010047:Ovalbumin; D047209:Eosinophil Peroxidase
keywords: asthma; inflammatory mediator; lead acetate; lung pathological changes; sensitized animals