American Thoracic Society Journal News Tips for September

September 19, 2001

Antioxidant supplements reduce the effects of ozone gas

Antioxidant supplements given to vitamin C-depleted subjects reduced the effects of ozone gas. Ozone, which affects millions of Americans on a regular basis, is a highly reactive gas that is the major constituent of photochemical smog. Published studies reveal that ozone induces transient functional and inflammatory changes in the lung, as well as causes decreased lung function test results. The effects of ozone are believed to come from oxidant damage to cell structures. In this research, investigators studied 32 healthy, nonsmoking males and females, 18 to 35 years of age, who were on an antioxidant-restricted diet for a 3-week period. After one week, following exposure to filtered air and several tests, they were divided into two groups: one received a placebo while the other took antioxidant supplements, which each group respectively consumed in addition to their vitamin C-restricted diet. Next, the two groups were exposed to 0.4 parts per million (ppm) of ozone gas for 2 hours, while they performed moderate exercise intermittently. Then they underwent a lung air passage "wash out," or bronchoalveolar lavage. Those who had received supplements had 85 percent greater levels of vitamin C, 28 percent higher levels of vitamin E, and levels of an antioxidant precursor of vitamin A higher by 27 percent. Compared with those taking the placebo, the supplemented group showed a 24 percent improvement in one basic lung test and a 30 percent increase in the other. However, the tests for inflammatory response in the lungs showed no differences between the two groups. The investigators believe that antioxidant supplementation could represent a safe and effective way to improve pulmonary function response to ozone, even though study results demonstrated no effect on inflammatory response in the lungs provoked by this common air pollutant. The article appears in the first of two September issues of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.

Proinflammatory cell messengers caused by atmospheric pollutants could play important role on cardiopulmonary disease

Canadian scientists reported that tiny atmospheric particles and other forms of acute atmospheric pollution stimulate large scavenger cells in the tiny air sacs of the lung (alveolar macophages) to produce proinflammatory intercellular messengers called cytokines which they believe play an important role in cardiopulmonary illness and mortality. The researchers cite alveolar macrophages as the most likely link between the lung inflammation process and the human systemic response to pollutants because these cells are responsible for ingesting and clearing inhaled particles. Epidemiological studies have shown a significant association between exposure to tiny ambient air particles and greater illness and death from cardiopulmonary disease. The investigators studied serum samples from 30 healthy males, 19 to 24 years of age, taken at the time they fought serious fires in Southeast Asia in 1997. They also incubated other human alveolar macrophages with particle suspensions of residual fly ash, ambient urban particles from a large Canadian city, inert carbon particles, and latex particles of various sizes. The investigators found that the same cytokines, which elicited a proinflammatory response when alveolar macrophages were exposed to urban particles, were present in the serum samples collected from the young adult males during the hazy smoke period of the Southeast Asia fires. They postulate that these cytokines contributed to the systemic response caused by air pollution, and believe further studies are needed to establish a clear link between the circulating cytokines and the adverse cardiopulmonary effects seen in susceptible individuals exposed to air pollution. The research is published in the first of two September issues of the American Thoracic Society peer-reviewed American Journal of Respiratory and Critical Care Medicine.

Diabetics have twice the risk for hospital admissions from heart disease associated with tine airborne particles

Diabetics have twice the risk for hospital admissions for heart disease associated with higher concentrations of tiny airborne particles (PM10) than nondiabetics. Researchers examined Medicare data for Cook County, Illinois, for the period from 1988 to 1994. They found twice the PM10-associated risk for heart disease in diabetics than in nondiabetics in Medicare recipients both over and under age 75. Diabetes is a highly prevalent illness in the United States. Data from the Third National Health and Nutrition Survey showed that 5.1 percent of the U.S. population over age 20 had diagnosed diabetes, with an estimated 2.7 percent more persons believed to be undiagnosed. The researchers found a significant interaction for hospital admissions for heart disease in their PM10 data, with more than twice the risk in persons with diabetes. Both diabetes and airborne particles have been associated with increased heart rate variability, more risk factors for thrombosis, and additional systemic markers for inflammation. According to the authors, these similarities indicate that airborne particles and diabetes affect some of the same pathways, and raise the possibility of a synergistic effect. In contrast to heart disease admissions, they found only weak evidence that diabetes modified the risk of PM10-induced respiratory symptoms. The study appears in the first of two issues for September of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine.
For the complete text of articles, please see the ATS Journal Online Website at For the contact information on a specific investigator, to request a complimentary journalist subscription to ATS journals online, or if you would like additional details from the monthly postal or e-mail news releases provided only to journalists, contact Cathy Carlomagno at 212-315-6442, by fax at 212-315-6456, or by e-mail at 

American Thoracic Society

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