INDUCTION OF DEPRESSION BY EXPOSURE TO DAMP ...

A study assessed the level of neuronal damage in the hippocampus of adult male
rats caused by quinolinic acid, IL-1β, and TNF-α (Stone and Behan, 2007). The study
findings revealed that low doses of quinolinic acid, IL-1β or TNF-α did not induce
neuronal damage, but a combination of quinolinic acid and IL-1β resulted in significant
neuronal damage. Higher doses of these two compounds nearly decimated the pyramidal
cells.
Microglia activation results in the production of quinolinic acid from the breakdown
of tryptophan, which is also a precursor for serotonin. Wichers et al. completed an
elegant study that correlated tryptophan degradation, and thus the production of the
neurotoxic compounds, with increases in depressive symptoms during TNF-α treatment
in patients with chronic hepatitis C (Wichers et al., 2005). This study did not find a
correlation between tryptophan availability and depression, however. Being that
tryptophan is a precursor to serotonin, some studies have concluded that the decrease in
tryptophan availability affects serotonin levels, and thus depressive symptoms (Capuron
et al., 2002). However, studies that suggest a reduction of tryptophan as being causative
for depression must be sure to include measurements of the buildup of neurotoxic
compounds from tryptophan degradation (Bonaccorso et al., 2002).
Damp Buildings and Inflammation
A growing body of studies has assessed neurological symptoms in people exposed to
damp buildings. Most reported only on the presence of mold growth. However, the
findings of these studies cannot be narrowly viewed as evidence that mold was the only
or the most pertinent agent to induce such symptoms, as other agents are also present in
damp environments. The general assertion is that occupant health effects are primarily
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