Genetic effects of bisulfite (sulfur dioxide)

Epidemiology studies associate increased pulmonary morbidity with episodes of high particulate air pollution (size range 0.1-10 microm diameter, PM10). Pneumonia, often viral in origin, is increased following episodes of high PM10 pollution. Therefore, this study was undertaken to investigate how PM10 alters airway inflammatory responses to respiratory syncytial virus (RSV), a frequent cause of viral pneumonia in infants and the elderly. Supernatants of unexposed and PM10-exposed alveolar macrophage (AM) cultured with uninfected or RSV-infected airway epithelial cells were assessed for a number of chemokines responsible for inflammatory responses in the lung. AM exposure to PM10 in the absence of infection resulted in a significant increase in interleukin (IL)-8 and macrophage inflammatory protein (MIP)-1alpha production but not in MIP-1beta or monocyte chemotactic protein (MCP)-1. AM responded to RSV infection by the production of IL-8, MIP-1alpha, MIP-1beta, and MCP-1, while RANTES was derived solely from the RSV-infected bronchial epithelial cell line BEAS-2B. In the presence of PM10, the AM response to RSV was blunted. RSV-induced MCP-1 was significantly decreased, and the levels of MIP-1 and IL-8 were lower than expected from a combined response to PM10 and RSV. Furthermore, AM analyzed for uptake of virus showed a 50% decrease in viral antigen when exposed to PM10 RSV-induced production of RANTES by epithelial cells was decreased in the presence of AM but not affected by PM10 exposure. Taken together, these results suggest that AM-regulated inflammatory responses to viral infection are altered by exposure to PM10 in a manner that may result in increased spread of infection and thus may increase viral pneumonia-related hospital admissions.

Exposure to urban air particulates alters the macrophage-mediated inflammatory response to respiratory viral infection

During a 5-d period that commenced on August 30, 1987, dry lightning strikes ignited more than 1,500 fires that destroyed in excess of 600,000 acres of California forests. To evaluate the public health impact of the smoke on the general population, all hospital emergency rooms located in the six counties most severely affected by smoke or fire were surveyed. Selected hospital information was abstracted for a 2 1/2-wk period during the fires and during two reference periods. During the period of major forest fire activity, visits of persons with asthma and chronic obstructive pulmonary disease increased in number (observed/expected ratios of 1.4 and 1.3, respectively), as did visits of persons with sinusitis, upper respiratory infections, and laryngitis. A few patients with acute respiratory or eye irritation also visited the emergency rooms. Even recognizing the limited sensitivity of emergency room surveys, the overall public health impact was relatively modest. The increased respiratory morbidity detected in this survey, however, supports the notion that persons with pre-existing respiratory disease represent a sensitive subpopulation, who should be targeted for purposes of public health intervention when exposure to forest fire smoke is likely.

The 1987 forest fire disaster in California: assessment of emergency room visits.

Macrophages The alveolar macrophage system has been extensively studied Alveolar macrophages are responsible for the physical removal of inhaled particles although the major clearance mechanism co

Lung defense mechanisms (second of two parts).

China has become the world's largest emitter of SO(2) since 2005, and aggressive deployment of flue gas desulfurization (FGD) at coal-fired power plants appeared in China when facing the formidable pressure of environment pollution. In this work, we estimate the annual emission from combustion sources at provincial levels in China from 1990 to 2007, with updated data investigations. We have implemented the method of transportation matrix to gain a better understanding of sulfur content of coal in consuming provinces, which in turn improved the inventory. The total emissions from combustion in 2007 were 28.3 Tg, half of which was contributed by coal-fired power plants. Meanwhile, the industrial boiler coal combustion and residential coal consumed in centralized heating were responsible for another 32% of the total emissions. From 1990 to 2007, annual SO(2) emission was fluctuated with two peaks (1996 and 2006), and total emission doubled from 15.4 Tg to 30.8 Tg, at an annual growth rate of 4.4% (6.3% since 2000). Due to the extensive application of FGD technology and the phase-out of small, high emitting units, the SO(2) emission began to decrease after 2006. Furthermore, the differences among estimates reported in literatures highlight a great need for further research to reduce the uncertainties with more detailed information on key sources and actual operation of devices.

Sulfur dioxide emissions from combustion in china: from 1990 to 2007.

Studies carried out in four distinct geographic areas of the United States involving 20,472 children and adults clearly linked excessive, acute respiratory disease with communities heavily polluted with sulfur dioxide and suspended sulfates. Pollution exposure of three years or longer was an important component in increased risk for acute respiratory disease. Laryngo- tracheobronchitis was the major condition productive of excess, acute, lower-respiratory disease in children in heavily polluted communities in the Salt Lake Basin and Rocky Mountain communities. The effect of pollution on excess, acute respiratory disease was found to be independent of socioeconomic status and cigarette smoking.

Marvin Hertz

Papers

The Effect of Sulfur Dioxide and Suspended Sulfates on Acute Respiratory Disease