Air Pollution - General

The American Thoracic Society   presents a document on lung diseases and the environment.

In a cohort of children with asthma from 12 Southern California communities, McConnell and coworkers   investigated the relationship between bronchitic symptoms and ambient particulate matter, particulate elemental and organic carbon, nitrogen dioxide, and other gaseous pollutants. Symptoms (assessed by questionnaire every year between 1996 and 1999) were associated with yearly variability of particulate matter with aerodynamic diameter less than 2.5 µm (odds ratio, 1.41), nitrogen dioxide (odds ratio, 1.07), organic carbon (odds ratio, 1.41), nitrogen dioxide (odds ratio, 1.07), and ozone (odds ratio, 1.06). The within-community associations were stronger in magnitude than the between-community associations. The effects of yearly variation of organic carbon and nitrogen dioxide were only modestly reduced after adjusting for other pollutants. The effects of all other pollutants were reduced after adjusting for organic carbon and nitrogen dioxide. The authors conclude that previous cross-sectional studies may have underestimated the effects of organic carbon and nitrogen dioxide on chronic bronchitic symptoms in children with asthma.

Nicotinamide adenine dinucleotide (phosphate) reduced:quinone oxidoreductase (NQO1) and glutathione S-transferase (GST) M1 are detoxifying enzymes induced in response to oxidative stress, as occurs during ozone exposure. To examine the relationship between significant polymorphisms in NQO1 and GSTM1 and risk of asthma, David and coworkers   studied 218 case-parent triads in children from Mexico City (which has the highest ozone levels in North America). The Pro187Ser polymorphism in NQO1 was not associated with risk of asthma. Among subjects with homozygous deletion of GSTM1, carriers of a serine allele were at reduced risk of asthma as compared with Pro/Pro homozygotes. The authors conclude that children who live in an area with high exposure to ozone and who carry at least one NQO1 Ser allele and are homozygous for the GSTM1 deletion are at a decreased risk of asthma.

To determine whether concentrated ambient air particles induce pulmonary inflammation in normal rats and in rats with chronic bronchitis, Saldiva and coworkers   exposed four groups of rats (some healthy and some with chronic bronchitis secondary to sulfur dioxide) to filtered air or to concentrated ambient air particles for five hours a day for three consecutive days. Concentrated ambient air particles caused an increase in neutrophils in the bronchoalveolar fluid of both the normal rats and the rats with chronic bronchitis. The particles caused an increase in the numerical density of neutrophils in the alveolar walls only in normal rats; the density was greater in the central regions than in the peripheral regions of the lung. A dose-dependent relationship was found between many components of concentrated ambient air particles (especially vanadium and bromine) and neutrophils and lymphocytes in bronchoalveolar fluid. The authors conclude that short-term exposure to concentrated ambient air particles induces a significant inflammatory reaction in the lungs of rats.

Particulate air pollution is associated with cardiovascular morbidity and mortality. To investigate this association, Nemmar and coworkers   studied the effect of intravenous and intratracheal administration of ultrafine (60 nm) polystyrene particles on thrombus formation in a hamster model. Intravenous administration of unmodified particles had no effect on thrombus formation. Intravenous administration of amine-polystyrene particles enhanced thrombosis at high but not at low concentrations. High concentrations of carboxylate-polystyrene particles inhibited thrombus formation. Intratracheal instillation of amino-polystyrene particles caused an increase in thrombus formation, whereas unmodified particles and carboxylate-polysterene particles had no effect. Unmodified particles did not alter the aggregation of platelets in human plasma induced by ADP, whereas carboxylate-polystyrene particles weakly enhanced platelet aggregation. Amine-polystyrene particles were sufficient to induce platelet aggregation on their own and strongly enhanced aggregation induced by ADP. The authors conclude that the presence of ultrafine particles in the circulation increases the tendency toward thrombosis, resulting in part from platelet activation and depending on the surface charge of the particles.

To determine whether antioxidant vitamins could modulate the adverse effect of air pollution on lung function in children, Romieu and coworkers   did a double-blind randomized study in 158 children with asthma who lived in Mexico City. During the 31-month study, the average maximum level of ozone was 102 ppb and the mean 24-hour average level of particulates with a mass median diameter of less than 10 µm (PM₁₀) was 57 µg per m³. Pulmonary function was measured twice weekly. In the placebo group, the children with moderate and severe asthma showed an inverse relationship between the level of ozone (on the day before spirometry) and peak expiratory flow (-15 ml per second per 10 ppb), forced expiratory flow (FEF_25–75, -13.3 ml per second per 10 ppb), and FEV₁ (-4.6 ml per 10 ppb). In children treated with vitamin E (50 mg daily) and vitamin C (250 mg daily), no association was seen between ozone and lung function. The authors conclude that antioxidant supplements might modulate the impact of exposure to ozone on the small airways of children with moderate to severe asthma.

To determine whether exposure to ambient air pollutants affects the growth of lung function in children, coworkers Gauderman and coworkers   studied 2,081 fourth-grade children (average age, 9.9 years). Exposure to acid vapor, nitrogen dioxide, particles with an aerodynamic diameter of less than 2.5 µm (PM_2.5), and elemental carbon were associated with significant deficits in the growth of lung function. Across the range of acid exposure, for example, the average annual growth rates of MMEF and FEV₁ were reduced by 11% and 5%, respectively. Exposure to acid vapor was associated with a decrease in the ratio of MMEF to FVC, whereas exposure to ozone was associated with a reduced rate of growth in PEF. Children spending more time outdoors experienced greater deficits in lung function. The authors conclude that exposure to ambient levels of air pollutants has a detrimental effect on growth of lung function in children.

To determine the relationship between exposure to air pollution related to traffic and the development of asthmatic symptoms, allergic diseases, and respiratory infections, Brauer and coworkers   studied a birth cohort of 4,146 children. Outdoor concentrations of traffic-related air pollutants were modeled for the home of each subject. Adjusted odds ratios for wheezing, physician-diagnosed asthma, infections of the ear, nose or throat, and serious colds at 2 years of age were associated with air pollutants; some of the associations reached borderline statistical significance. The authors conclude that traffic-related air pollution may be associated with the prevalence of respiratory illness at 2 years of age.

Citations 1-4 of 4 total displayed.

Nicotinamide Adenine Dinucleotide (Phosphate) Reduced:Quinone Oxidoreductase and Glutathione S-Transferase M1 Polymorphisms and Childhood Asthma

Gloria L. David, Isabelle Romieu, Juan Jose Sienra-Monge, William J. Collins, Matiana Ramirez-Aguilar, Blanca Estela del Rio-Navarro, Norma Isabel Reyes-Ruiz, Richard W. Morris, Jacqueline M. Marzec, and Stephanie J. London
Am. J. Respir. Crit. Care Med. 168: 1199 -1204. First published online as doi:10.1164/rccm.200305-684OC [Abstract] [Full text]  

Prospective Study of Air Pollution and Bronchitic Symptoms in Children with Asthma

Rob McConnell, Kiros Berhane, Frank Gilliland, Jassy Molitor, Duncan Thomas, Fred Lurmann, Edward Avol, W. James Gauderman, and John M. Peters
Am. J. Respir. Crit. Care Med. 168: 790 -797. First published online as doi:10.1164/rccm.200304-466OC [Abstract] [Full text]  

Contribution of Respiratory Disease to Nonrespiratory Mortality Associations with Air Pollution

Samantha F. De Leon, George D. Thurston, and Kazuhiko Ito
Am. J. Respir. Crit. Care Med. 167: 1117 -1123. First published online as doi:10.1164/rccm.200205-409OC [Abstract] [Full text]  

Proceedings of the First Jack Pepys Occupational Asthma Symposium

Am. J. Respir. Crit. Care Med. 167: 450-471. [Full text]