Immunotoxicology of Inhaled Compounds—Assessing Risks of Local Immune Suppression and Hypersensitivity

Selgrade, MaryJane K.; Gilmour, M. Ian

doi:10.1080/15287390600591579

Cited by 4 publications

(5 citation statements)

References 88 publications

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“…Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform antiphagocytic capsule with a subsequent increased rate and severity of respiratory infection (Selgrade and Gilmour, 2006). We further reported quantitative relationships between ozone suppression of AM function in humans and mice, following both in vivo and in vitro exposures, suggesting that these effects may enhance susceptibility to infection in humans (Selgrade, 1999).…”

Section: R E S E a R C H A R T I C L Ementioning

confidence: 77%

“…The S. zooepidemicus infectivity model was used extensively from the late 1970s through the early 1990s to assess the potential for a variety of air pollutants to reduce resistance to bacterial infection in the lung (Selgrade and Gilmour, 2006). The mechanism underlying increased susceptibility to infection featured dose-dependent reductions in AM function, which allowed the bacteria to adapt by developing an antiphagocytic capsule .…”

Section: Discussionmentioning

confidence: 99%

“…One of the most sensitive indicators of air pollutant toxicity is the Streptococcus zooepidemicus infectivity model. Increased mortality has been demonstrated in mice exposed by inhalation to numerous air pollutants including ozone, NO 2 , and SO 2 (Selgrade and Gilmour, 2006), prior to being infected by aerosolized S. zooepidemicus (a relatively avirulent, group C Streptococcus). The effects have commonly been associated with decrements in alveolar macrophage (AM) function as well as reduced bactericidal activity of the lung lining fluid (Hurst et al, 1970;Gardner et al, 1971;Goldstein et al, 1978).…”

Section: Introductionmentioning

confidence: 99%

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Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform

Selgrade

Gilmour

2010

Journal of Immunotoxicology

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Section: R E S E a R C H A R T I C L Ementioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform

Selgrade

Gilmour

2010

Journal of Immunotoxicology

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“…Therefore, route of exposure is potentially more important for immunotoxicity endpoints, and since local immunotoxicological effects may occur independent of systemic immunity, a separate evaluation of local immune responses may be appropriate. For example, chemical immunotoxicity may suppress immune function at the site of exposure, such as inhalation-dependent suppression of the resident macrophage populations of the lung, without affecting immune function of macrophages elsewhere in the body [149].…”

Section: Exposure Assessmentmentioning

confidence: 99%

Immunotoxicology and Its Application in Risk Assessment

Rooney

Luebke

Selgrade

et al. 2012

Experientia Supplementum

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Immunotoxicology is the study of undesired modulation of the immune system by extrinsic factors. Toxicological assessments have demonstrated that the immune system is a target following exposure to a diverse group of xenobiotics including ultraviolet radiation, chemical pollutants, therapeutics, and recreational drugs. There is a well-established cause and effect relationship between suppression of the immune response and reduced resistance to infections and certain types of neoplasia. In humans, mild-to-moderate suppression of the immune response is linked to reduced resistance to common community-acquired infections, whereas opportunistic infections, which are very rare in the general population, are common in individuals with severe suppression. Xenobiotic exposure may also result in unintended stimulation of immune function. Although a cause and effect relationship between unintended stimulation of the immune response and adverse consequences has yet to be established, evidence does suggest that hypersensitivity, autoimmunity, and pathological inflammation may be exacerbated in susceptible populations exposed to certain xenobiotics. Xenobiotics can act as allergens and elicit hypersensitivity responses, or they can modulate hypersensitivity responses to other allergens such as pollen or dust mite by acting as adjuvants, enhancing the development or expression of hypersensitivity. Allergic contact dermatitis, allergic rhinitis, and asthma are the most commonly encountered types of hypersensitivity reactions resulting from chemical exposure. The immunologic effectors and mechanisms involved in autoimmune reactions are the same as those associated with responses to foreign antigens; however, the reactions are directed against the host's own cells. Thus, chemicals that induce immune suppression, nonspecific immunostimulation, or hypersensitivity may also impact autoimmunity. Risk assessment for immunotoxicity should be performed using the same approaches and principles for other noncancer effects. However, since xenobiotics may have effects on more than one aspect of immune function, immunotoxicity data should be evaluated separately for evidence of suppression, stimulation, hypersensitivity, and autoimmunity.

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“…A number of chemicals suppress a variety of immune responses in laboratory rodents, and there is some indication that many chemicals affect immune functions in humans (Selgrade, 2010). One well-documented example is decreased alveolar macrophage function following exposure to several air pollutants accompanied by enhanced risk of certain bacterial infections (Selgrade and Gilmour, 2006). Data on ozone indicate that cells from both species respond almost identically as measured by macrophage phagocytic capability.…”

Section: Exposure To Toxicants Increases Susceptibility To Microbial mentioning

confidence: 99%

Cumulative Risk: Toxicity and Interactions of Physical and Chemical Stressors

Rider

Boekelheide

Catlin

et al. 2013

Toxicological Sciences

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Recent efforts to update cumulative risk assessment procedures to incorporate nonchemical stressors ranging from physical to psychosocial reflect increased interest in consideration of the totality of variables affecting human health and the growing desire to develop community-based risk assessment methods. A key roadblock is the uncertainty as to how nonchemical stressors behave in relationship to chemical stressors. Physical stressors offer a reasonable starting place for measuring the effects of nonchemical stressors and their modulation of chemical effects (and vice versa), as they clearly differ from chemical stressors; and "doses" of many physical stressors are more easily quantifiable than those of psychosocial stressors. There is a commonly held belief that virtually nothing is known about the impact of nonchemical stressors on chemically mediated toxicity or the joint impact of coexposure to chemical and nonchemical stressors. Although this is generally true, there are several instances where a substantial body of evidence exists. A workshop titled "Cumulative Risk: Toxicity and Interactions of Physical and Chemical Stressors" held at the 2013 Society of Toxicology Annual Meeting provided a forum for discussion of research addressing the toxicity of physical stressors and what is known about their interactions with chemical stressors, both in terms of exposure and effects. Physical stressors including sunlight, heat, radiation, infectious disease, and noise were discussed in reference to identifying pathways of interaction with chemical stressors, data gaps, and suggestions for future incorporation into cumulative risk assessments.

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Immunotoxicology of Inhaled Compounds—Assessing Risks of Local Immune Suppression and Hypersensitivity

Cited by 4 publications

References 88 publications

Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform

Suppression of pulmonary host defenses and enhanced susceptibility to respiratory bacterial infection in mice following inhalation exposure to trichloroethylene and chloroform

Immunotoxicology and Its Application in Risk Assessment

Cumulative Risk: Toxicity and Interactions of Physical and Chemical Stressors

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