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Title: Immunotoxicity of air pollutants

Abstract

The most common ubiquitous air pollutants, as well as some point source (e.g. metals) air pollutants, decrease the function of pulmonary host defense mechanisms against infection. Most of this knowledge is based on animal studies and involves cellular antibacterial defenses such as alveolar macrophages and mucociliary clearance. Information on viral infectivity is more sparse. Since there is no routine treatment for viral infections which have a relatively high rate of occurrence, this gap in knowledge is of concern. Given the major gaps in knowledge, resaonably accurate assessment of the immunotoxicity of air pollutants is not possible. When the limited data base is reviewed relative to ambient levels of the common pollutants, it appears that acute exposures to O3 and H2SO4 and chronic exposures to NO2 are the major exposures of concern for immunotoxic effects. It is critical to point out, however, that until information is available for chronic exposures to low levels of metals and for exposures to common organic vapors, the immunotoxicity of air pollutants cannot be assessed adequately.

Authors:
;
Publication Date:
Research Org.:
Health Effects Research Lab., Research Triangle Park, NC (USA)
OSTI Identifier:
6667159
Report Number(s):
PB-84-183649; EPA-600/D-84-096
Resource Type:
Technical Report
Resource Relation:
Other Information: Prepared in cooperation with Northrop Services, Inc., Research Triangle Park, NC
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; 54 ENVIRONMENTAL SCIENCES; AIR POLLUTION; TOXICITY; IMMUNOLOGY; RESPONSE MODIFYING FACTORS; BACTERIA; METALS; NITROGEN DIOXIDE; OZONE; PUBLIC HEALTH; SULFUR DIOXIDE; SULFURIC ACID; VIRAL DISEASES; VIRUSES; CHALCOGENIDES; DISEASES; ELEMENTS; HYDROGEN COMPOUNDS; INFECTIOUS DISEASES; INORGANIC ACIDS; MICROORGANISMS; NITROGEN COMPOUNDS; NITROGEN OXIDES; OXIDES; OXYGEN COMPOUNDS; PARASITES; POLLUTION; SULFUR COMPOUNDS; SULFUR OXIDES 560306* -- Chemicals Metabolism & Toxicology-- Man-- (-1987); 500200 -- Environment, Atmospheric-- Chemicals Monitoring & Transport-- (-1989)

Citation Formats

Graham, J.A., and Gardner, D.E. Immunotoxicity of air pollutants. United States: N. p., 1984. Web.
Graham, J.A., & Gardner, D.E. Immunotoxicity of air pollutants. United States.
Graham, J.A., and Gardner, D.E. 1984. "Immunotoxicity of air pollutants". United States. doi:.
@article{osti_6667159,
title = {Immunotoxicity of air pollutants},
author = {Graham, J.A. and Gardner, D.E.},
abstractNote = {The most common ubiquitous air pollutants, as well as some point source (e.g. metals) air pollutants, decrease the function of pulmonary host defense mechanisms against infection. Most of this knowledge is based on animal studies and involves cellular antibacterial defenses such as alveolar macrophages and mucociliary clearance. Information on viral infectivity is more sparse. Since there is no routine treatment for viral infections which have a relatively high rate of occurrence, this gap in knowledge is of concern. Given the major gaps in knowledge, resaonably accurate assessment of the immunotoxicity of air pollutants is not possible. When the limited data base is reviewed relative to ambient levels of the common pollutants, it appears that acute exposures to O3 and H2SO4 and chronic exposures to NO2 are the major exposures of concern for immunotoxic effects. It is critical to point out, however, that until information is available for chronic exposures to low levels of metals and for exposures to common organic vapors, the immunotoxicity of air pollutants cannot be assessed adequately.},
doi = {},
journal = {},
number = ,
volume = ,
place = {United States},
year = 1984,
month = 1
}

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  • Although a number of studies have demonstrated suppression of extrapulmonary immune responses following exposure to NO2, a ubiquitous ambient and indoor air pollutant, most of these studies have utilized extremely high concentrations of NO2 relative to the environment. The authors' intent was to assess effects of NO2 on extrapulmonary immune responses using an environmentally relevant exposure regimen. Rats were exposed for 1, 3, 13, 52, or 78 wk to air or a pattern of NO2 designed to mimic episodic pollution in urban areas at concentrations 2-5 times those commonly seen in such areas. Daily exposures consisted of 0.5 ppm formore » 16 h, a 6-h exposure spike during which the concentration rose to 1.5 ppm, remained there for 2 h, and then returned to 0.5 ppm, and a 2-h down time. There were no NO2-related changes in mitogen responses, although significant suppression of these responses in both air and NO2 groups was noted in spleen at 52 and 78 wk, and in PBL at 13, 52, and 78 wk, presumably due to aging. Suppression of NK-cell activity was noted after 3 wk of exposure but not after 1, 13, 52, or 78 wk of exposure. Age did not appear to affect NK-cell activity.« less
  • Weanling male Fischer 344 rats were exposed daily by gastric intubation for up to 15 weeks to the polychlorinated biphenyl (PCB) Aroclor 1254 at 0.1, 1, 10, or 25 mg/kg body weight. At 5, 10 and 15 weeks groups of rats were killed and immune functions were evaluated. The immune parameters examined included the following: body and lymphoid organ weights, mitogen stimulated lymphoproliferative (LP) responses, natural killer (NK) cell activity, mixed lymphocyte reaction (MLR), and cytotoxic T lymphocyte (CTL) response. After 10 and 15 weeks of dosing body weights were reduced in rats receiving 25 mg/kg PCB while thymus weightsmore » were decreased in rats receiving 10 and 25 mg/kg. NK cell activity was reduced in rats dosed for 15 weeks at 10 and 25 mg/kg. The LP response to phytohemagglutinin was enhanced in rats dosed for 15 weeks at 25 mg/kg PCB. Exposure of rats to PCB did not affect the MLR or CTL responses. Other groups of rats were exposed to cyclophosphamide (CY) and served as positive controls for the immune assays employed. CY induced alterations in all of the immune parameters measured, indicating that this is a sensitive battery of immune function tests which is capable of detecting immune alterations in the rat.« less
  • Benzene is widely used by chemical industries and exposure to benzene has been shown experimentally to be immunotoxic in adult animals. The present study addressed whether exposure of fetuses in utero to benzene compromises the development of fetal B lymphopoiesis and whether B-lymphocyte development recovers postnatally. Pregnant BALB/C dams were given intraperitoneal injections of benzene (100 mg/kg, twice daily) from day 12.5 of gestation through day 19.5 of gestation. Phenotypic analysis revealed that fetal liver cell suspensions from embryos exposed in utero contained fewer pre-B cells and B cells than corresponding controls. Fetal liver cell cultures established from these embryosmore » also produced fewer B cells. In contrast, pre-B cells were elevated in the livers of 8-day-old neonates that had been exposed to benzene in utero. Moreover, responsiveness to the B-cell mitogen, LPS, was significantly decreased in spleen cell cultures derived from these neonates. The results indicate that in utero exposure to high concentrations of benzene alters fetal B lymphopoiesis and may compromise immune responsiveness postnatally.« less
  • The immunotoxicity of 2,2`-dichlorodiethyl sulfide (sulfur mustard, SM),on humoral and cell-mediated immunity was compared with that of the nitrogen mustard 2-(bis(2-chloroethyl) amino)tetrahydro- 2H-1,3,2-oxazophosphorine 2-oxide (cyclophosphamide, CP). SM and CP had similar effects on thymic and splenic weights, spleen cell number, and the formation of antibody producing cells to sheep red blood cells (sRBC) when examined 5 days after exposure, but differed in their effects on body weights. Although there were no differences in the delayed hypersensitivity response to keyhole limpet hemocyanin, CP and SM had different effects in the L1210 tumor cell allograft rejection assay. CP, but not SM, decreasedmore » the 28 day survival rate of allogeneic mice exposed to a sublethal L1210 tumor challenge. The differing effects on survival to the L1210 tumor challenge could not be attributed to a direct cytotoxic effect of SM on the L1210 tumor cells as SM did not increase the survival rate or mediansurvival time of syngeneic mice exposed to a lethal L1210 tumor cell challenge. In summary, SM and CP had immunosuppressive effects in the humoral immune assay. Although neither compound suppressed the delayed hypersensitivity response, CP was found to suppress host resistance to L1210 tumor cells.« less
  • During our preliminary year of experimentation we have made an initial examination Off the immunotoxicological effects of JP-8 jet fuel exposure. Inbred C57BL6 mice were exposed to varying concentrations (either 500, 1000 or 2500 mg/m3) of aerosolized JP-8 jet fuel for a period of 7 days with an exposure period of 1 hour per day. Animal exposure was performed via nose-only presentation while the animals were held in individual subject loading tubes. The tubes were nose cone fitted to receiving adapters that originated from a common anodized aluminum exposure chamber. Nose only exposure was utilized to minimize ingestion of jetmore » fuel during self grooming. Animals were rotated on a daily basis through the 12 adapter positions on the exposure chamber. This rotation was done to minimize proximity to the jet fuel source as a variable in exposure concentration or composition. Exposure concentration was determined by a seven stage --cascade impactor, and were measured after each exposure (1,2). 24 hours after the last exposure the animals were sacrificed and examined for changes in immune system composition and function. The major immune system organ systems (i.e., spleen, thymus, lymph nodes, blood and bone marrow) were recovered and examined for changes in organ weight total cell numbers, immune cell components (by differential histochemical staining).« less