Dr. Frederick Miller, an expert in inhalation dosimetry, from CIIT Centers for Health Research says somewhat smaller particles that can be breathed and lodge in the tracheobronchial area can cause more lasting irritation, even though they clear form the lungs in about 24 hours. Dr. Miller believes particles this size — some of which appear to be of an unusually high alkalinity (i.e. caustic) because of materials like gypsum board and concrete — may contribute to "fireman's cough" experienced by firemen and rescuers.
Dr. Miller says what was only a small component of the dust after the collapse of the towers were the far more dangerous fine particles that can lodge deep into the alveolar spaces of the lung. These particles can take months to clear, and thus have greater likelihood of causing problems. He says initially most of these fine particles were literally lifted out of the area by the gigantic dust plume visible in all the photographs and television images. It shot up for thousands of feet, initially transporting the smallest particles to the East River and out into the harbor. However, many of the earliest people on the scene, often working 12-hour shifts, didn't use respirators. Not only is it virtually impossible to know exactly the make up of the particles they breathed, they are the people who would have been exposed to any toxic vapors.
STUDIES OF AIRBORNE PARTICLES INDICATE ADVERSE HEALTH EFFECTS, ESPECIALLY FROM SMALLEST PARTICLES
— During the American Society of Investigative Pathology symposium on environmental toxicology, Dr. Jon Samet, Johns Hopkins University's Bloomberg School of Public Health, describes recent epidemiological studies that have prompted reassessment of Environmental Protection Agency standards for airborne particles in the United States, Canada, and Europe.
In the 1990s, new epidemiological studies found positive associations between levels and size of airborne particulate matter and the numbers of daily deaths, both from all causes and from cardiovascular and respiratory disease. The findings were replicated across a number of cities and regions. These results were unexpected, says Dr. Samet. As levels of particles -- the larger ones measured in earlier studies, not the smaller ones so much a part of modern consideration -- had been falling in American cities, many researchers had concluded that airborne particles no longer posed a threat to public health.
Not so, says Dr. Samet. Findings in contemporary community based studies continue to find worsening of the clinical status of people with chronic heart and lung disease, and increased risk for emergency and clinic visits, and hospitalizations, and even death. Based on epidemiological data, EPA standards set in 1997 set, for the first time, separate standards for small airborne particles.
ULTRAFINE PARTICLES BEHAVE DIFFERENTLY THAN FINE PARTICLES, SCIENTIST INVESTIGATES THEIR TOXIC POTENTIAL — Dr. Gunter Oberdorster, University of Rochester, recently discovered (1) that on a mass basis ultrafine particles have significantly greater power to cause inflammatory lung injury than larger-sized particles, and (2) inhaled ultrafine particles not only translocate within the respiratory and to the liver but also within hours after exposure appear in regions of the central nervous system, consistent with a mechanism of neuronal transport from the respiratory tract along sensory nerves.
This means that when we breathe in ultrafine particles, they can be taken up by the olfactory nerve endings in the nose and transported into the olfactory part of the brain and, perhaps, even to deeper brain regions. He describes how his laboratory found evidence for the movement of ultra-fine 30 nm carbon and metal particles from the respiratory tract into the brain. The original work was done using polytetrafluoroethylene fumes, a workplace aerosol consisting of ultra-fine 20 nm particles, but later studies looked at ultrafine carbon particles as surrogates for ambient particles like those generated by internal combustion engines.
BIOLOGICAL MECHANISM DISCOVERED THAT EXPLAINS WHY URBAN AIR POLLUTION CAUSES NEGATIVE HEALTH EVENTS
— Epidemiological evidence linking urban air pollution to increased heart attacks and other negative cardiovascular events is overwhelming. When particulate matter associated with pollution rises, so do cardiac and respiratory hospital admissions. The elderly and people with compromised cardiovascular and pulmonary systems are hardest hit, but people with diabetes or cancer are also more sensitive to air pollution. Other studies show that pregnant women exposed to high levels of air pollutants are more likely to have lower weight babies.
What's been missing, until now, is a convincing biological explanation of exactly how pollution causes these physical changes. Dr. Renaud Vincent, a scientist with Health Canada in Ottawa, provides an answer. Air pollution itself evokes vasoconstrictive peptides known to be involved in many of the diseases known to be more deadly when pollution levels are high.
ENVIRONMENTAL TOXICOLOGY SYMPOSIUM LOOKS AT HEALTH RISKS OF DIFFERING PARTICULATE MATTER AND ALZHEIMER'S DISEASE
— The adverse respiratory and cardiovascular health effects of air pollution are widely recognized. Now, a new study conducted in Mexico City suggests that exposure to a complex mixture of air pollutants, especially particulate matter, may play a crucial role in Alzheimer's disease and other neurodegenerative disorders. The research was done by Dr. Lilian Calderon-Garciduenas of the National Institute of Pediatrics in Mexico City and a postdoctoral student in the environmental pathology program at the University of North Carolina at Chapel Hill.
Dr. Calderon-Garciduenas described her research in urban air pollution and brain damage as part of an American Society of Investigative Pathology symposium on negative health effects of inhaled airborne particles. Although Dr. Calderon-Garciduenas also found evidence of pollution-related damage in brain cells in children as young as four in Mexico City, her studies of dogs most clearly suggest the cascade of events causing the neuropathology evident in the brains of these highly exposed canines and humans.
(American Society for Investigative Pathology)