Over the past three or four decades, there have been important advances in the understanding of the actions, exposure-response characteristics, and mechanisms of action of many common air pollutant

https://www.jstor.org/stable/pdfplus/3431520.pdf

Human Health Effects of Air Pollution

The general public, especially patients with upper or lower respiratory symptoms, is aware from media reports that adverse respiratory effects can occur from air pollution. It is important for the allergist to have a current knowledge of the potential health effects of air pollution and how they might affect their patients to advise them accordingly. Specifically, the allergist–clinical immunologist should be keenly aware that both gaseous and particulate outdoor pollutants might aggravate or enhance the underlying pathophysiology of both the upper and lower airways. Epidemiologic and laboratory exposure research studies investigating the health effects of outdoor air pollution each have advantages and disadvantages. Epidemiologic studies can show statistical associations between levels of individual or combined air pollutants and outcomes, such as rates of asthma, emergency visits for asthma, or hospital admissions, but cannot prove a causative role. Human exposure studies, animal models, and tissue or cellular studies provide further information on mechanisms of response but also have inherent limitations. The aim of this rostrum is to review the relevant publications that provide the appropriate context for assessing the risks of air pollution relative to other more modifiable environmental factors in patients with allergic airways disease.

Health effects of air pollution

Children's exposure to air pollution is a special concern because their immune system and lungs are not fully developed when exposure begins, raising the possibility of different responses than seen in adults. In addition, children spend more time outside, where the concentrations of pollution from traffic, powerplants, and other combustion sources are generally higher. Although air pollution has long been thought to exacerbate minor acute illnesses, recent studies have suggested that air pollution, particularly traffic-related pollution, is associated with infant mortality and the development of asthma and atopy. Other studies have associated particulate air pollution with acute bronchitis in children and demonstrated that rates of bronchitis and chronic cough declined in areas where particle concentrations have fallen. More mixed results have been reported for lung function. Overall, evidence for effects of air pollution on children have been growing, and effects are seen at concentrations that are common today. Although many of these associations seem likely to be causal, others require and warrant additional investigation.

http://coep.pharmacy.arizona.edu/HOPE/andrea/Air%20pollution%20and%20children%27s%20health.pdf

Air Pollution and Children's Health

An acute (2 h) exposure of humans to 0.4 ppm ozone initiates biochemical changes in the lung that result in the production of components mediating inflammation and acute lung damage as well as components having the potential to lead to long-term effects such as fibrosis. However, many people are exposed to lower levels of ozone than this, but for periods of several hours. Therefore, it is important to determine if a prolonged exposure to low levels of ozone is also capable of causing cellular and biochemical changes in the lung. Nonsmoking males were randomly exposed to filtered air and either 0.10 ppm ozone or 0.08 ppm ozone for 6.6 h with moderate exercise (40 liters/min). Bronchoalveolar lavage (BAL) was performed 18 h after each exposure, and cells and fluid were analyzed. The BAL fluid of volunteers exposed to 0.10 ppm ozone had significant increases in neutrophils (PMNs), protein, prostaglandin E2 (PGE2), fibronectin, interleukin-6 (IL-6), and lactate dehydrogenase (LDH) compared with BAL fluid from the same volunteers exposed to filtered air. In addition, there was a decrease in the ability of alveolar macrophages to phagocytize yeast via the complement receptor. Exposure to 0.08 ppm ozone resulted in significant increases in PMNs, PGE2, LDH, IL-6, alpha 1-antitrypsin, and decreased phagocytosis via the complement receptor. However, BAL fluid protein and fibronectin were no longer significantly elevated. We conclude that exposure of humans to as low a level as 0.08 ppm for 6.6 h is sufficient to initiate an inflammatory reaction in the lung.

Exposure of humans to ambient levels of ozone for 6.6 hours causes cellular and biochemical changes in the lung.

Epidemiologic investigation has established an association between exposure to particulate matter (PM) and human health in the Utah Valley. Reduction of particle mass during the temporary closure of a local steel mill was associated with diminished morbidity and mortality. We tested the hypothesis that the biologic effect of PM would reflect findings of epidemiology with a greater injury after exposure to an equal mass of particles from those years in which the mill was in operation. Filters containing PM were collected prior to closure of the steel mill, during the closure, and after its reopening. Aqueous extracts of the filters were prepared. One of three extracts (500 microg) was instilled through the bronchoscope into the lungs of nonsmoking volunteers. Twenty-four hours later, the same subsegment was lavaged. Exposure to aqueous extracts of PM collected before closure and after reopening of the steel mill provoked a greater inflammatory response relative to PM extract acquired during the plant shutdown. This is the first demonstration that pulmonary effects after experimental exposure of humans to PM can correlate with health outcomes observed in epidemiologic studies of the same material under normal exposure conditions. Findings suggest that mass may not be the most appropriate metric to use in assessing health effects after PM exposure but rather specific components must be identified and assessed.

Inflammatory lung injury after bronchial instillation of air pollution particles.

Although ozone (O3) has been shown to induce inflammation in the lungs of animals, very little is known about its inflammatory effects on humans In this study, 11 healthy nonsmoking men, 18 to 35 yr of age (mean, 254 +/- 35), were exposed once to 04 ppm O3 and once to filtered air for 2 h with intermittent exercise Eighteen hours later, bronchoalveolar lavage (BAL) was performed and the cells and fluid were analyzed for various indicators of inflammation There was an 82-fold increase in the percentage of polymorphonuclear leukocytes (PMN) in the total cell population, and a small but significant decrease in the percentage of macrophages after exposure to O3 Immunoreactive neutrophil elastase often associated with inflammation and lung damage increased by 38-fold in the fluid while its activity increased 206-fold in the lavaged cells A 2-fold increase in the levels of protein, albumin, and IgG suggested increased vascular permeability of the lung Several biochemical markers that could act as chemotactic or regulatory factors in an inflammatory response were examined in the BAL fluid (BALF) The level of complement fragment C3 alpha was increased by 17-fold The chemotactic leukotriene B4 was unchanged while prostaglandin E2 increased 2-fold In contrast, three enzyme systems of phagocytes with potentially damaging effects on tissues and microbes, namely, NADPH-oxidase and the lysosomal enzymes acid phosphatase and beta-glucuronidase, were increased neither in the lavaged fluid nor cells In addition, the amounts of fibrogenic-related molecules were assessed in BALF(ABSTRACT TRUNCATED AT 250 WORDS)

Walter J. Kozumbo

Papers

Ozone-induced inflammation in the lower airways of human subjects.