Organ system studies immunologic

NO has complex roles in immunological host responses against viruses, and especially against HIV-1 infection. In HIV-1 infection, NO cannot be rigidly classified as an anti-inflammatory or proinflammatory molecule, but it can be deemed a true inflammatory mediator. Many studies support a proviral effect of NO in HIV-1 infection, mainly based on stimulation of viral replication, and on toxic effects on various cells, including central nervous system cells, via oxidative injury that may cause cellular and organ dysfunction, and immunosuppression and immunopathology, especially in the central nervous system. 

Immunotoxicity. There are currently no data on the effects of 2-hexanone on the human immune system via any route of exposure. Animal data included an inhalation study in which there was a 40% decrease in peripheral white blood cells in rats exposed to 2-hexanone (Katz et al. 1980). In addition, 2,5-hexanedione, a metabolite of 2-hexanone, was shown to adversely affect lymphoid organs of the immune system in rats and to cause impairment of immunity in mice (Upreti and Shanker 1987). Immunological assessments, including analysis of peripheral blood components and effects on lymphoid tissue, conducted as part of intermediate-or chronic-duration studies and skin sensitization tests would be useful in developing a dose-response relationship and assessing the potential risk to chronically exposed persons in the vicinity of hazardous waste sites or to exposed workers. 

Knowing some potential target organs and systems affected by various tin compounds, it may be possible to develop biomarkers specific to effects. Examples include immunological and neurobehavioral tests as compound-specific pulmonary, liver, and kidney function studies. The primary objective of such biomarkers would be to predict adverse health effects in exposed individuals and populations. 

This section presents information on human health effects, including those known to be associated and those possibly associated with exposure to CDDs (primarily 2,3,7,8-TCDD). Since limited data exist to assign a specific route of exposure (inhalation, oral, dermal) to human studies, the information in this section is organized by health effects—death, systemic, immunological, neurological, developmental, reproductive, genotoxic, and carcinogenic effects. These data are discussed in terms of three exposure periods—acute (14 days or less), intermediate (15-364 days), and chronic (365 days or more). 

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