Background: Particulate air pollution has been associated with increased cardiovascular deaths and hospital admissions. To help understand the mechanisms, the types of particles most involved, and the types of persons most susceptible, the association between exposure to summertime air pollution and heart rate variability (HRV) was examined in a panel study of 28 elderly subjects. Methods: Subjects were seen once a week for up to 12 weeks and HRV (SDNN, r-MSSD, PNN 50 , low frequency/high frequency ratio (LFHFR)) was measured for approximately 30 minutes at each session using a defined protocol. Temperature, day of the week, and hour of the day were controlled, and dummy variables for each subject were controlled for subject specific risk factors. Results: PM 2.5 was associated with r-MSSD (210.1% change for an interquartile range (IQR) increase in exposure (95% CI 22.8 to 216.9)) and PNN 50 , but stronger associations were seen with black carbon, an indicator of traffic particles, which was also associated with SDNN (24.6% per IQR (95% CI 22.0 to 27.2)) and LFHFR. Secondary particles were more weakly associated with r-MSSD, as was ozone. No associations were seen with SO 2 or NO 2 . CO had similar patterns of association to black carbon, which disappeared after controlling for black carbon. Black carbon had a substantially higher effect on SDNN in subjects who had had a previous myocardial infarction (212.7%, 95% CI 25.7 to 219.25). Conclusions: Particles, especially from traffic, are associated with disturbances of autonomic control of the heart.

Background: Animal models suggest that the cardiovascular effects of air pollution result in part from inflammation caused by proinflammatory mediators originating in the lung. In a human study of the cardiovascular effects of air pollution, we aimed to evaluate the potential association between air pollution levels and the fraction of exhaled nitric oxide (FE NO ), a non-invasive measure of airway inflammation. Methods: Breath samples were collected weekly between September and December 2000 in a community based group of elderly subjects (median age 70.7 years) in Steubenville, Ohio. The samples were analysed for NO. Air pollution levels were measured concurrently at a central site monitor. Results: An increase in the 24 hour average PM 2.5 concentration of 17.7 mg/m 3 was associated with an increase in FE NO of 1.45 ppb (95% CI 0.33 to 2.57) in models adjusted for subject, week of study, day of the week, hour of the day, ambient barometric pressure, temperature, and relative humidity. This represents a change of approximately 15% compared with the mean FE NO in the cohort (9.9 ppb). A significant association was also observed for a 24 hour moving average of ambient NO (0.83 ppb increase, 95% CI 0.26 to 1.40). In two-pollutant models, the magnitude and precision of the PM 2.5 effect was not reduced and the ambient NO effect was no longer significant. The associations between FE NO and PM 2.5 were significantly higher in subjects with a doctor's diagnosis of COPD (p value for interaction = 0.03). Conclusions: Ambient pollution may lead to airway inflammation as measured by FE NO . These subclinical inflammatory changes may be an important step in the pathogenesis of the cardiopulmonary effects induced by exposure to air pollution.

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Background Few studies have examined how developing obesity in early adulthood affects the course of asthma. Objective We analyzed lung function and asthma impairment and risk among non-obese children with asthma, comparing those who were obese in young adulthood to those who remained non-obese. Methods Post-hoc analysis of 771 subjects with mild-moderate asthma who were not obese (pediatric definition, body mass index (BMI) <95th percentile) when enrolled in the Childhood Asthma Management Program at ages 5–12 years. Subjects were then followed to age ≥ 20 years. For visits at ages ≥ 20 years, spirometry values as percent predicted and recent asthma symptom scores and prednisone exposure were compared between 579 subjects who were non-obese at all visits and 151 who obese (adult definition of BMI ≥ 30 kg/m2) on at least one visit (median number of visits when obese = 4, IQR 2–7). Results Compared to participants who were non-obese (BMI 23.4 ± 2.6 kg/m2), those who became obese (BMI 31.5 ± 3.8 kg/m2) had significant decreases in FEV1/FVC (p<0.0003) and FEV1 (p = 0.001), without differences in FVC (p=0.15) during visits at ages ≥ 20 years. For each unit increase of BMI, FEV1 percent predicted decreased by 0.29 (p=0.0009). The relationship between BMI and lung function was not confounded by sex or BMI at baseline. Asthma impairment (symptom scores) and risk (prednisone use) did not differ between the two groups. Conclusion Becoming obese in early adulthood was associated with increased airway obstruction, without impact on asthma impairment or risk.