Acute exposure to abuse‐like concentrations of toluene induces inflammation in mouse lungs and brain

Abstract

Toluene is an aromatic hydrocarbon commonly abused by young adolescents for its central nervous system depressant effects. Although toluene's pharmacological effects at high concentrations are relatively well-known, few studies have assessed toluene's effects on lung and brain tissues. The present study characterized the pathological effects of acute inhaled toluene exposure in the lungs and brains of male Swiss-Webster mice (N = 68). Using a static vapor exposure chamber, mice (PND 28) received a single 30-min toluene administration (0, 1000, 2000, or 4000 ppm). Lung and brain tissues were extracted 24-h post-exposure. Histology results revealed significant changes in the morphology of lung tissue (e.g., irregular cellular architecture) with the 2000-and 4000-ppm exposures expressing greater signs of pathology than control 0-ppm exposure. Markers of immune system activity (F4/80 and Ly-6G) and cellular proliferation (Ki-67) in the lung revealed no significant differences. Additionally, brain tissues were analyzed for changes of astrogliosis (glial fibrillary acidic protein [GFAP]) and oxidative stress (glutathione peroxidase [GPx]). GFAP showed increased astrogliosis in the striatum with 2000-ppm toluene showing significantly higher expression than control (p < 0.05) and a marginal effect in the hippocampus.No other markers showed significant changes. The increased signs of inflammation and cellular damage suggest that exposure to a single high concentration of toluene, typical of abuse, is capable of producing pathology in both lung and brain tissue.

Exposure to Crude Oil-Related Volatile Organic Compounds Associated with Lung Function Decline in a Longitudinal Panel of Children

“…The study, which showed not only the association between exposure to VOCs and increased systemic level of oxidative stress but also the association between markers of oxidative stress and parameters of lung function supports this hypothesis [ 14 ]. As VOCs are gaseous pollutants, their primary target tissue is the lung, and breathing elevated concentrations of VOCs could have direct toxic effects on cells through some possible mechanisms, such as inflammation and DNA repair pathways, in addition to oxidative stress [ 18 , 33 ]. In addition to genetic toxicity, epigenetic mechanisms appear to be involved.…”

“…To our knowledge, no health studies have looked into how long an accidental single exposure to large amounts of VOCs can affect lung function deterioration. Considering that even low levels of VOCs cause a loss of lung function in the general population [ 13 , 16 ], exposure to very high environmental concentrations of VOCs, albeit acutely, may have long-term adverse effects on lung function decline [ 18 ]. In addition, to the best of our knowledge, there are no children’s studies of a relationship between VOC exposure and lung function.…”