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EFFECTS OF FORMALDEHYDE AND PARTICLE-BOUND FORMALDEHYDE ON LUNG MACROPHAGE FUNCTIONS
Impact/Purpose:
Exposure to formaldehyde may occur at work, at home, and outdoors. Human studies, animal inhalation studies, and cell culture assays suggest that formaldehyde potentially can cause adverse effects on human health. Therefore, the Clean Air Act Amendments of 1990 defined formaldehyde as a toxic air pollutant subject to regulatory action. Emissions from motor vehicles using gasoline and diesel fuels contribute to the outdoor levels of formaldehyde. The projected use of methanol as an alternative fuel and in fuel blends may further increase outdoor formaldehyde levels because alcohol combustion yields more aldehydes than conventional fuel combustion.
In addition to gases, the combustion of fossil fuels produces respirable carbon-based particles that can deposit in the lower respiratory tract. Because gas molecules can bind to particle surfaces, these particles may serve as carriers and transport the bound gases deep into the lungs. Formaldehyde is a water-soluble gas that normally deposits in the upper respiratory tract. Adsorption of formaldehyde to particles could carry it deeper into the lungs and alter its toxic action.
Alveolar macrophages in the lower respiratory tract protect the lungs from inhaled microorganisms. Impairment of alveolar macrophage function could compromise a person's resistance to respiratory infection. The Health Effects Institute sponsored this study to examine the effects of inhaled formaldehyde, with and without carbon particles, on alveolar macrophages.
Description:
Dr. George Jakab and associates exposed mice to varying levels (ranging from 0.5 to 15 parts per million [ppm]) of formaldehyde alone or to formaldehyde (5 and 2.5 ppm) mixed with carbon black particles. Carbon black particles were chosen because of their similarity to combustion derived particles. Different alveolar macrophage functions were evaluated using two assays. First, the investigators measured the ability of alveolar macrophages to kill the bacteria staphylococcus aureus. Mice were exposed to pollutants either before, after, or at both times relative to inhaling the bacteria. The number of bacteria still alive in the lungs four hours after inhaling the bacteria was counted. Second, the investigators measured the ingesting, or phagocytic, capacity of the macrophages. Mice were exposed to the pollutants, and at intervals ranging from one to 60 days later, alveolar macrophages were washed out of the lungs and their phagocytic activity was measured. Chemical analyses of the interactions between formaldehyde and carbon black particles also were conducted to determine the amount of formaldehyde potentially available for interacting with lung cells.
An extremely high concentration (15 ppm) of formaldehyde, which is far higher than outdoor concentrations, was needed to impair the killing of S. Aureus when mice were exposed to formaldehyde after inhaling the bacteria. However, when mice were exposed to formaldehyde both before and after inhaling the bacteria, only 1 ppm of formaldehyde was needed to impair bacterial killing. Exposing mice to formaldehyde and carbon black particles had no effect on bacterial killing but did depress phagocytosis. This depression was not apparent until five days after exposure and was maximal 25 days after exposure. The chemical analyses revealed that only 1% of the formaldehyde was bound to the carbon black particles, which may account for the absence of an effect of the combined exposure on bacterial killing. It is not known why the combined exposure depressed alveolar macrophage phagocytosis or why this effect was delayed.
These experiments demonstrated that inhalation of formaldehyde can impair the capacity of mouse alveolar macrophages to kill certain bacteria ant that inhalation of formaldehyde mixed with carbon black particles can depress alveolar macrophage phagocytosis. However, the detection of these effects depended on exposure protocol and the time of assay after an exposure.