Researchers: Black Mold Toxins Could Affect Sense Of Smell

Certain toxins produced by black mold, that fungus found everywhere from damp basements to thousands of buildings in hurricane-ravaged New Orleans and the U.S. Gulf coast, are capable of killing nerve cells essential for the sense of smell, Michigan State University (MSU) researchers in the Center for Integrative Toxicology announced on March 1.

According to the MSU researchers, these toxins found in black mold, also known as Stachybotrys chartarum, specifically killed olfactory sensory neurons in the nasal airways of exposed mice. These nasal neuronal cells are known to detect odors and send electrical signals to the parts of the brain that are necessary for the sense of smell, or olfaction.

"Essentially, this toxin is killing off the cells needed for the sense of smell," said Jack Harkema, a university distinguished professor of pathobiology and diagnostic investigation and one of the MSU researchers. "This is the first animal study to really show that a toxin derived from the spores of black mold may cause significant damage in the nose and the frontal part of the brain involved in olfaction."

In addition, they found that the mice that inhaled these fungal toxins developed rhinitis, inflammation of the nasal passages. Mild inflammation also was detected in the animals' olfactory bulbs, the part of the brain directly connected to the olfactory nerves from the nose. Olfactory bulbs relay the smell signals from the nose to other parts of the brain that are involved in olfaction.

"The mice used in the study were allowed to sniff a single small dose of the toxin, which is known as satratoxin G," said James Pestka, a professor of food science and human nutrition. "The amount of toxin given to the mice would be close to estimated amounts that a person, without respiratory protection, may inhale when working in a room heavily contaminated with black mold."

"In every mouse that received the single dose of satratoxin G," said Zahidul Islam, a research assistant professor in Pestka's laboratory, "there was a large loss of olfactory sensory neurons through a process called programmed cell death or apoptosis, and all of these same mice also developed secondary inflammation in the nose and olfactory bulbs of the brain."

Harkema asked, "Are our noses more or less sensitive to this toxin, and other similar fungal toxins? This is really a crucial question yet to be answered. We also need to develop better ways of detecting these toxins in the contaminated air of water-damaged buildings, so that we can protect the public from toxic exposure."

Exposure to black mold has been linked to another dangerous respiratory disorder called pulmonary hemorrhage. A number of infants in the Cleveland area who lived in mold-contaminated homes were reported in the mid-1990s to have developed this lung disorder and some even died as a result of this condition. This bleeding disorder of the lungs appeared to be caused by something in the air of the infants' home environments, most likely toxins produced by Stachybotrys chartarum or similar fungi.

"Also, it has been reported that there are neurological conditions in people who have inhabited mold-contaminated buildings or homes," Harkema said. "They've claimed to suffer from memory loss or other neurological symptoms. As we all know, memory can be triggered by what we smell. Our studies in mice suggest that airborne toxins from mold may damage our ability to smell."

A recent Institute of Medicine report said "critical gaps" exist in the knowledge of the effects of black mold and its relationship to what is known as "damp building syndrome."

"What our laboratory research, and those of others, will do is allow us to better understand the cellular mechanisms underlying the toxin causing injury in the nose and brain," Pestka said. "It is crucial, however, that others also conduct well-designed human epidemiological studies so that we can better determine the overall human health impact of exposure to airborne toxins from black mold."

This article originally appeared in the 03/01/2006 issue of Environmental Protection.

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