Effects of Inhaled Hexachlorobenzene Aerosols on Rat Pulmonary Host Defenses

Sherwood, Robert; Thomas, Peter T.; O’Shea, William J.; Bradof, Jeannie N.; Ratajczak, Helen V.; Graham, Judith A.; Aranyi, Catherine

doi:10.1177/074823378900500306

“…Slight changes in humoral and pulmonary cellular defenses have been observed in a study that investigated the effect of single or multiple inhalation exposures to HCB (64) in male Sprague-Dawley rats. Recently it was shown that exposure of Wistar rats to (Table 3).…”

Section: Accidental Human Poisoning In Turkeymentioning

confidence: 99%

The role of the immune system in hexachlorobenzene-induced toxicity.

Michielsen

¹

,

Loveren

²

,

Vos

³

1999

Environ Health Perspect

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Hexachlorobenzene (HCB) is a persistent environmental pollutant. The toxicity of HCB has been extensively studied after an accidental human poisoning in Turkey and more recently it has been shown that HCB has immunotoxic properties in laboratory animals and probably also in man. Oral exposure of rats to HCB showed stimulatory effects on spleen and lymph node weights and histology, increased serum IgM levels, and an enhancement of several parameters of immune function. Moreover, more recent studies indicate that HCB-induced effects in the rat may be related to autoimmunity. In Wistar rats exposed to HCB, IgM antibodies against several autoantigens were elevated; in the Lewis rat, HCB differently modulated two experimental models of autoimmune disease. Oral exposure of rats to HCB induces skin and lung pathology in the rat. Recently several studies have been conducted to investigate whether these skin and lung lesions can be related to HCB-induced immunomodulation, and these studies will be discussed in this review. HCB-induced skin and lung lesions probably have a different etiology; pronounced strain differences and correlation of skin lesions with immune parameters suggest a specific involvement of the immune system in HCB-induced skin lesions. The induction of lung lesions by HCB was thymus independent. Thymus-dependent T cells were not likely to be required for the induction of skin lesions, although T cells enhanced the rate of induction and the progression of the skin lesions. No deposition of autoantibodies was observed in nonlesional or lesional skin of HCB-treated rats. Therefore, we concluded that it is unlikely that the mechanism by which most allergic or autoimmunogenic chemicals work, i.e., by binding to macromolecules of the body and subsequent T-and B-cell activation, is involved in the HCB-induced immunopathology in the rat. Such a thymus-independent immunopathology is remarkable, as HCB strongly modulates T-cell-mediated immune parameters. This points at a very complex mechanism and possible involvement of multiple factors in the immunopathology of HCB.

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“…Short-term exposure to 35 mg/m3 HCB aerosols for 1 or 4 days significantly reduced the capacity of alveolar macrophages to phagocytize radiolabeled red cells as well as viable Klebsiella pneumoniae bacteria, suggesting impaired pulmonary host defense (33). Lymphoproliferative responses to Tand B-cell mitogens in these studies in the lung-associated and mesenteric lymph nodes exhibited differential.…”

Section: Hexachiorobenzenementioning

confidence: 69%

Pesticide-induced immunotoxicity: are Great Lakes residents at risk?

Thomas

¹

1995

Environ Health Perspect

23

0

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Several organophosphate and organochlorine compounds, including pesticides commonly found in the Great Lakes basin, have the potential to induce immunotoxicity. Because of biomagnification and accumulation in the food chain, Great Lakes residents may inadvertently be exposed to these compounds and thus face increased risk of immune dysfunction. In spite of the laboratory animal data and evidence from occupational exposures that suggest immunotoxicity, there is no definitive evidence as yet that environmental exposure to these xenobiotics poses a significant threat to the human immune system that is sufficient to predispose residents of the Great Lakes basin to increased disease. However, uncertainties with regard to exposure levels, predictability of tests, suitability of the animal models, and immune reserve cannot be ruled out when making risk assessment decisions such as this.

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“…Barnett et al (30) reported that in the absence of changes in splenic B-and Tcell mitogenesis, antigen-specific delayedtype hypersensitivity and mixed lymphocyte culture responses were suppressed in mice exposed perinatally to up to 5 mg/kg HCB. On the other hand, combined prenatal and postnatal exposure of rats to as little as 4 mg/kg HCB significantly increased immunoglobulins M and G (IgM, IgG) antibody titers to tetanus toxoid as well as delayed hypersensitivity to ovalbumin in a dose-dependent manner relative to controls (31 (33). Lymphoproliferative responses to T-and B-cell mitogens in these studies in the lung-associated and mesenteric lymph nodes exhibited differential.…”

Section: Hexachiorobenzenementioning

confidence: 82%

Pesticide-Induced Immunotoxicity: Are Great Lakes Residents at Risk?

Thomas¹

1995

Environmental Health Perspectives

Self Cite

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Several organophosphate and organochlorine compounds, including pesticides commonly found in the Great Lakes basin, have the potential to induce immunotoxicity. Because of biomagnification and accumulation in the food chain, Great Lakes residents may inadvertently be exposed to these compounds and thus face increased risk of immune dysfunction. In spite of the laboratory animal data and evidence from occupational exposures that suggest immunotoxicity, there is no definitive evidence as yet that environmental exposure to these xenobiotics poses a significant threat to the human immune system that is sufficient to predispose residents of the Great Lakes basin to increased disease. However, uncertainties with regard to exposure levels, predictability of tests, suitability of the animal models, and immune reserve cannot be ruled out when making risk assessment decisions such as this. -Environ Health Perspect 1 03(Suppl 9): 55-61 (1995)

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Effects of Inhaled Hexachlorobenzene Aerosols on Rat Pulmonary Host Defenses

Cited by 7 publications

References 25 publications

The role of the immune system in hexachlorobenzene-induced toxicity.

The role of the immune system in hexachlorobenzene-induced toxicity.

Pesticide-induced immunotoxicity: are Great Lakes residents at risk?

Pesticide-Induced Immunotoxicity: Are Great Lakes Residents at Risk?

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