title: Influenza virus infection in mice after exposure to coal dust and diesel engine emissions.
abstract: Influenza virus infection initiated after aerosol exposure of CD-1, white Swiss mice for durations of 1, 3, and 6 months to respirable particulates maintained at 2 mg/m3 of either coal dust (CD), diesel engine emissions (DEE), a combination of both (CD/DEE), or to filtered air (control) was studied. The course of infection in mice previously exposed for 1 month to various particulates did not differ appreciably among the four animal groups with respect to mortality, virus growth in lungs, interferon levels, or hemagglutinin antibody response. In mice exposed for 3 and 6 months to different particulates, the mortality response was similar among all animal groups. However, the percentage of animals showing lung consolidation was significantly higher in the 3-month groups exposed to DEE (96.5%) and CD/DEE (97%) than in the control (61.2%); in the 6-month groups, the percentages were twice that of the control for both DEE- and CD/DEE-exposed animals. Complementing these observations of both 3- and 6-month-exposed animals was the higher virus growth levels attained in the DEE and CD/DEE animals with concomitant depressed interferon levels which were the inverse of findings noted in the control group. Hemagglutinin-antibody levels in particulate-exposed animals, especially at the 6-month interval, were fourfold less than the control. Histopathologic examination of lungs revealed no qualitative differences in the inflammatory response at any one specified time interval of exposure to influenza virus among the control and particulate-exposed animal groups. However, there were differences in severity of reaction in relation to the particulate component of the exposures. Focal macular collections of pigment-laden macrophages were seen only in DEE and CD/DEE but not in CD animals after 3- and 6-month exposures. The findings of this study indicated that the severity of influenza virus infection is more pronounced in mice exposed to diesel engine emissions than in control animals and it is not appreciably accentuated by coal dust.
authors.forename: N
authors.initials: N
authors.lastname: Hahon
authors.forename: J A
authors.initials: JA
authors.lastname: Booth
authors.forename: F
authors.initials: F
authors.lastname: Green
authors.forename: T R
authors.initials: TR
authors.lastname: Lewis
mesh_terms: D000818:Animals; D000914:Antibodies, Viral / Q000032:analysis; D003031:Coal / Q000009:adverse effects*; D004391:Dust / Q000009:adverse effects*; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D007372:Interferons / Q000032:analysis; D008168:Lung / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D009976:Orthomyxoviridae Infections / Q000276:immunology* / Q000473:pathology; D013997:Time Factors; D001335:Vehicle Emissions / Q000633:toxicity*; D014779:Virus Replication
chemical_list: D000914:Antibodies, Viral; D003031:Coal; D004391:Dust; D001335:Vehicle Emissions; D007372:Interferons