Effect of inhaled industrial chemicals on systemic and local immune response

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

“…In contrast, systemic (hepatic) effects have been seen in mice exposed to chloroform at levels (NOEL 3 ppm) lower than the 100 ppm NOEL observed here. These effects on susceptibility to infection in the lung could not have been predicted based on earlier studies of effects on more traditional immunotoxicity endpoints assessed in the spleen following oral TCE exposure and in the spleen and lung-associated lymph node following inhalation chloroform exposure (Sanders et al, 1982;Ban et al, 2003;Peden-Adams et al, 2006). It is certainly reasonable to assume that immune cells at the portal of entry for both the chemical and the infectious agent could be the most vulnerable to the chemical and crucial in defending against infection.…”

“…Studies using traditional measures to assess systemic effects on the immune system (Luster et al, 1988) suggested that oral exposure to TCE suppresses immune responses in weanling mice (Sanders et al, 1982) and in offspring following gestational exposure (Peden-Adams et al, 2006). In an acute inhalation study of chloroform, exposures between 10 and 50 ppm caused minimal effects on the IgM response to sheep red blood cells in both the spleen and lung-associated lymph nodes as well as on interferon responses with a trend for these responses to be enhanced (Ban et al, 2003). Using endpoints similar to those used in our study, Aranyi and colleagues demonstrated enhanced mortality in mice exposed for 3 h/ day for 5 days to 10 ppm chloroform and then challenged with S. zooepidemicus (Aranyi et al, 1986).…”

Immunotoxicological profile of chloroform in female B6C3F1 mice when administered in drinking water

“…In addition, CHF administration for 14 or 90 days by gavage at doses of 50-250 mg/kg in CD-1 mice reduced the number of antibody-forming cells to the T-dependent antigen sheep erythrocytes up to 30%, demonstrating that CHF was immunotoxic when administered as a bolus dose (Munson et al, 1982). On the other hand, exposure to CHF by inhalation at 10-20 ppm produced an increase in local immune responses, including the production of antibody and interferon-gamma (IFN-) by lung-associated lymph nodes (Ban et al, 2003(Ban et al, , 2006.…”

Inhaled chemicals may enhance allergic airway inflammation in ovalbumin-sensitised mice

“…Different concentrations of the chemicals studied were tested with this OVA mouse model. The chemical concentrations tested with this OVA mouse model have already been used in a previous study on mice where they were found to cause an increase in the number of antibody-forming cells in lung-associated lymph nodes (Ban et al, 2003).…”

“…Little is known about the pathomechanism of the adjuvant effect of environmental chemicals. In a previous study, we showed that pulmonary exposure to certain chemicals, namely styrene, 1,1-dichloroethylene, chloroform and carbon tetrachloride, increased the IFN-␥ release in the lung-associated lymph nodes as well as the numbers of IgM producing B cells against sheep red blood cells (SRBCs) (Ban et al, 2003). These chemicals may therefore promote sensitisation through an adjuvant effect, i.e.…”