The results presented in this review suggest that the impact of nutrition on obstructive lung disease is most evident for antioxidant vitamins, particularly vitamin C and, to a lesser extent, vitamin E. By decreasing oxidant insults to the lung, antioxidants could modulate the development of chronic lung diseases and lung function decrement. Antioxidant vitamins could also play an important role in gene-environment interactions in complex lung diseases such as childhood asthma. Data also suggest that omega-3 fatty acids may have a potentially protective effect against airway hyperreactivity and lung function decrements; however, relevant data are still sparse. Although epidemiologic data suggest that consumption of fresh fruit may reduce risk of noncarcinogenic airway limitation, there are no clear data on which nutrients might be most relevant. While some studies evaluate daily intake of vitamin C, other studies use fruit consumption as a surrogate for antioxidant intake. Given the dietary intercorrelations among antioxidant vitamins, particularly vitamin C, beta-carotene, and flavonoids, as well as other micronutrients, it may be difficult to isolate a specific effect. Some population subgroups with higher levels of oxidative stress, such as cigarette smokers, may be more likely to benefit from dietary supplementation, since some studies have suggested that antioxidant intake may have a greater impact in this group. Studies of lung function decrement and COPD in adults suggest that daily intake of vitamin C at levels slightly exceeding the current Recommended Dietary Allowance (60 mg/day among nonsmokers and 100 mg/day among smokers) may have a protective effect (20). In the Schwartz and Weiss (85) and Britton et al. (87) studies, an increase of 40 mg/day in vitamin C intake led to an approximate 20-ml increase in FEV1. Daily mean vitamin C intakes in these studies were 66 mg and 99.2 mg, respectively, and the highest intake level (178 mg/day) was approximately three times the Recommended Dietary Allowance. Although the amplitude of the effect was modest, if these effects accumulate over 20-30 years, they could have a meaningful impact on the rate at which pulmonary function declines, particularly in symptomatic subjects (85). Longitudinal data support the hypothesis that fresh fruit consumption has a beneficial impact on the lung (95). Among children, consumption of fresh fruit, particularly fruit high in vitamin C, has been related to a lower prevalence of asthma symptoms and higher lung function (64). This effect was observed event at low levels of fruit consumption (one or two servings per week vs. less than one serving per week), which suggests that a small increase in dietary intake could have a beneficial effect. Consumption of fish has also been related to lower airway hyperreactivity among children (75) and higher lung function in adults (100); however, longitudinal data do not provide evidence that increased omega-3 fatty acid intake protects against lung disease (101). Experimental studies of persons...

Most particulate matter (PM) health effects studies use outdoor (ambient) PM as a surrogate for personal exposure. However, people spend most of their time indoors exposed to a combination of indoor-generated particles and ambient particles that have infiltrated. Thus, it is important to investigate the differential health effects of indoor- and ambient-generated particles. We combined our recently adapted recursive model and a predictive model for estimating infiltration efficiency to separate personal exposure (E) to PM2.5 (PM with aerodynamic diameter ≤2.5 μm) into its indoor-generated (Eig) and ambient-generated (Eag) components for 19 children with asthma. We then compared Eig and Eag to changes in exhaled nitric oxide (eNO), a marker of airway inflammation. Based on the recursive model with a sample size of eight children, Eag was marginally associated with increases in eNO [5.6 ppb per 10-μg/m3 increase in PM2.5; 95% confidence interval (CI), −0.6 to 11.9; p = 0.08]. Eig was not associated with eNO (−0.19 ppb change per 10μg/m3). Our predictive model allowed us to estimate Eag and Eig for all 19 children. For those combined estimates, only Eag was significantly associated with an increase in eNO (Eag: 5.0 ppb per 10-μg/m3 increase in PM2.5; 95% CI, 0.3 to 9.7; p = 0.04; Eig: 3.3 ppb per 10-μg/m3 increase in PM2.5; 95% CI, −1.1 to 7.7; p = 0.15). Effects were seen only in children who were not using corticosteroid therapy. We conclude that the ambient-generated component of PM2.5 exposure is consistently associated with increases in eNO and the indoor-generated component is less strongly associated with eNO.

BackgroundTraffic-related air pollution is consistently associated with cardiovascular morbidity and mortality. Recent human and animal studies suggest that exposure to air pollutants affects vascular function. Diesel exhaust (DE) is a major source of traffic-related air pollution.ObjectivesOur goal was to study the effects of short-term exposure to DE on vascular reactivity and on mediators of vascular tone.MethodsIn a double-blind, crossover, controlled exposure study, 27 adult volunteers (10 healthy and 17 with metabolic syndrome) were exposed in randomized order to filtered air (FA) and each of two levels of diluted DE (100 or 200 μg/m3 of fine particulate matter) in 2-hr sessions. Before and after each exposure, we assessed the brachial artery diameter (BAd) by B-mode ultrasound and collected blood samples for endothelin-1 (ET-1) and catecholamines. Postexposure we also assessed endothelium-dependent flow-mediated dilation (FMD).ResultsCompared with FA, DE at 200 μg/m3 elicited a decrease in BAd (0.11 mm; 95% confidence interval, 0.02–0.18), and the effect appeared linearly dose related with a smaller effect at 100 μg/m3. Plasma levels of ET-1 increased after 200 μg/m3 DE but not after FA (p = 0.01). There was no consistent impact of DE on plasma catecholamines or FMD.ConclusionsThese results demonstrate that short-term exposure to DE is associated with acute endothelial response and vasoconstriction of a conductance artery. Elucidation of the signaling pathways controlling vascular tone that underlie this observation requires further study.

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Epidemiologic studies report consistent adverse health effects of particulate matter (PM) air pollution in population studies (U.S. EPA 2001). However, describing the adverse health effects of fine PM exposure at the individual subject level remains a high priority. Studies designed to provide information concerning these adverse effects include panel studies with subjects followed for several days or longer, clinical exposure studies, and toxicologic studies, including controlled exposures of human subjects. Panel studies are usually designed to combine intensive personal, indoor and/or outdoor air monitoring in conjunction with measures of specific health outcomes. Recent panel studies have concentrated on subjects believed to be susceptible to air pollution, such as those with preexisting respiratory or cardiac disease. As a consequence, the health end points commonly measured are lung function, symptoms and medication use, arterial oxygen saturation, blood pressure, and heart rate variability. Recent results from panel studies indicate several adverse health effects associated with exposure to PM with aerodynamic diameters ≤ 2.5 µm (PM 2.5 ). In the United States, decreased heart rate variability was associated with indoor or outdoor PM 2.5 in 26 elderly subjects in Baltimore, Maryland (Liao et al. 1999), in healthy subjects in Boston, Massachusetts (Magari et al.