Urban air pollution and chronic obstructive pulmonary disease-related emergency department visits.

BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) can have recurrent disease exacerbations triggered by several factors, including air pollution. Visits to the emergency respiratory department can be a direct result of short-term exposure to air pollution. The aim of this study was to investigate the relationship between the daily number of COPD emergency department visits and the daily environmental air concentrations of PM(10), SO(2), NO(2), CO and O(3) in the City of São Paulo, Brazil. METHODS: The sample data were collected between 2001 and 2003 and are categorised by gender and age. Generalised linear Poisson regression models were adopted to control for both short- and long-term seasonal changes as well as for temperature and relative humidity. The non-linear dependencies were controlled using a natural cubic spline function. Third-degree polynomial distributed lag models were adopted to estimate both lag structures and the cumulative effects of air pollutants. RESULTS: PM(10) and SO(2) readings showed both acute and lagged effects on COPD emergency department visits. Interquartile range increases in their concentration (28.3 microg/m(3) and 7.8 microg/m(3), respectively) were associated with a cumulative 6-day increase of 19% and 16% in COPD admissions, respectively. An effect on women was observed at lag 0, and among the elderly the lag period was noted to be longer. Increases in CO concentration showed impacts in the female and elderly groups. NO(2) and O(3) presented mild effects on the elderly and in women, respectively. CONCLUSION: These results indicate that air pollution affects health in a gender- and age-specific manner and should be considered a relevant risk factor that exacerbates COPD in urban environments.

Effect of air pollution on diabetes and cardiovascular diseases in São Paulo, Brazil.

Type 2 diabetes increases the risk of cardiovascular mortality and these patients, even without previous myocardial infarction, run the risk of fatal coronary heart disease similar to non-diabetic patients surviving myocardial infarction. There is evidence showing that particulate matter air pollution is associated with increases in cardiopulmonary morbidity and mortality. The present study was carried out to evaluate the effect of diabetes mellitus on the association of air pollution with cardiovascular emergency room visits in a tertiary referral hospital in the city of São Paulo. Using a time-series approach, and adopting generalized linear Poisson regression models, we assessed the effect of daily variations in PM10, CO, NO2, SO2, and O3 on the daily number of emergency room visits for cardiovascular diseases in diabetic and non-diabetic patients from 2001 to 2003. A semi-parametric smoother (natural spline) was adopted to control long-term trends, linear term seasonal usage and weather variables. In this period, 45,000 cardiovascular emergency room visits were registered. The observed increase in interquartile range within the 2-day moving average of 8.0 microg/m(3) SO2 was associated with 7.0% (95%CI: 4.0-11.0) and 20.0% (95%CI: 5.0-44.0) increases in cardiovascular disease emergency room visits by non-diabetic and diabetic groups, respectively. These data indicate that air pollution causes an increase of cardiovascular emergency room visits, and that diabetic patients are extremely susceptible to the adverse effects of air pollution on their health conditions.

Effect of air pollution on diabetes and cardiovascular diseases in São Paulo, Brazil

Type 2 diabetes increases the risk of cardiovascular mortality and these patients, even without previous myocardial infarction, run the risk of fatal coronary heart disease similar to non-diabetic patients surviving myocardial infarction. There is evidence showing that particulate matter air pollution is associated with increases in cardiopulmonary morbidity and mortality. The present study was carried out to evaluate the effect of diabetes mellitus on the association of air pollution with cardiovascular emergency room visits in a tertiary referral hospital in the city of São Paulo. Using a time-series approach, and adopting generalized linear Poisson regression models, we assessed the effect of daily variations in PM10, CO, NO2, SO2, and O3 on the daily number of emergency room visits for cardiovascular diseases in diabetic and non-diabetic patients from 2001 to 2003. A semi-parametric smoother (natural spline) was adopted to control long-term trends, linear term seasonal usage and weather variables. In this period, 45,000 cardiovascular emergency room visits were registered. The observed increase in interquartile range within the 2-day moving average of 8.0 µg/m³ SO2 was associated with 7.0 percent (95 percentCI: 4.0-11.0) and 20.0 percent (95 percentCI: 5.0-44.0) increases in cardiovascular disease emergency room visits by non-diabetic and diabetic groups, respectively. These data indicate that air pollution causes an increase of cardiovascular emergency room visits, and that diabetic patients are extremely susceptible to the adverse effects of air pollution on their health conditions.

Efficacy of theophylline in people with stable chronic obstructive pulmonary disease: a systematic review and meta-analysis.

OBJECTIVES: To determine the efficacy of oral theophylline compared with placebo in people with stable chronic obstructive pulmonary disease (COPD). METHODS: Systematic review of randomized-controlled trials comparing oral theophylline with placebo for a minimum of 7 days in people with stable COPD. RESULTS: Twenty randomized-controlled trials were included in this review. The following outcomes showed significant improvement with theophylline compared with placebo: FEV1 and FVC both improved with theophylline (weighted mean difference [WMD] 0.10 L; 95% confidence interval [95% CI] 0.04-0.16 and WMD 0.21 L; 95% CI 0.10-0.32, respectively). VO2 max also improved with theophylline (WMD 195.27mL/ min; 95% CI 112.71-277.83), as did PaO2 and PaCO2 (WMD 3.18 mmHg; 95% CI 1.23-5.13 and WMD -2.36mmHg; 95% CI -3.52 to -1.21, respectively). Patients preferred theophylline over placebo (relative risk 2.27; 95% CI 1.26-4.11). Theophylline increased the risk of nausea compared with placebo (RR 7.67; 95% CI 1.47-39.94). CONCLUSION: This review has shown that theophylline still has a role in the management of stable COPD, and is preferred by patients over placebo. However, the benefits of theophylline in stable COPD have to be weighed against the risk of adverse effects.

Oral theophylline for chronic obstructive pulmonary disease.

BACKGROUND: Oral theophylline has, for many years, been used as a bronchodilator in patients with COPD. Despite the introduction of new drugs, and its narrow therapeutic index, theophylline is still recommended for COPD treatment. OBJECTIVES: To determine the effectiveness of oral theophylline when compared to placebo in patients with stable COPD. SEARCH STRATEGY: The Cochrane Airways Review Group and Cochrane Controlled Clinical Registers were searched. SELECTION CRITERIA: All studies were randomised controlled trials (RCTs). DATA COLLECTION AND ANALYSIS: Data were independently abstracted and the methodological quality assessed by two reviewers. MAIN RESULTS: Twenty RCTs met the inclusion criteria. Concomitant therapy varied from none to any other bronchodilator plus corticosteroid (oral and inhaled). The following outcomes were significantly different when compared to placebo. FEV1 improved with treatment: Weighted Mean Difference (WMD) 100 ml; 95% Confidence Interval (95%CI) 40, 160 ml. Similarly for FVC: WMD 210 ml 95%CI 100, 320. Two studies reported an improvement in VO2max; WMD 195 ml/min, 95%CI 113,27). At rest, PaO2 and PaCO2 both improved with treatment (WMD 3.2 mmHg; 95%CI = 1.2, 5., and WMD -2.4 mmHg; 95%CI = -3.5, -1.2, respectively). Walking distance tests did not improve (4 studies, Standardised Mean Difference 0.30, 95%CI -0.01, 0.62), neither did Visual Analogue Score for breathlessness isn two small studies (WMD 3.6, 95%CI -4.6, 11.8). The Relative Risk (RR) of nausea was greater with theophylline (RR 7.7; 95%CI 1.5, 39.9). However, patients' preference for theophylline was greater than that for placebo (RR 2.27; 95%CI = 1.26, 4.11). Very few patient withdrew from these studies for any reason. REVIEWER'S CONCLUSIONS: Theophylline has a modest effect on FEV1 and FVC and slightly improves arterial blood gas tensions in moderate to severe COPD. These benefits were seen in patients receiving a variety of different concomitant therapies. Improvement in exercise performance depended on the method of testing. There was a very low dropout rate in the studies that could be included in this review, which suggests that recruited patients may have been known by the investigators to be theophylline tolerant. This may limit the generalisability of these studies.

Pulmonary emphysema induced by passive smoking: an experimental study in rats

We describe a short time model for inducing experimental emphysema in rats chronic tobacco smoke inhalation. Three groups of male Wistar rats (6 months old) were studied: controls (N = 8), rats intoxicated for 45 days (s-45, N = 7) or for 90 days (s-90, N = 8). The exposed animals were intoxicated 3 times a day (10 cigarettes per exposure period), 5 days a week. Pulmonary damage was assessed by means of functional tests and quantitative pathological examination of the airways and lung parenchyma. The s-45 and s-90 animals were similar in terms of functional residual capacity (FRC) corrected for body weight (FRC/kg) but both groups of smoking rats exhibited significantly higher FRC/kg values than the controls (s-45=6.33; s-90=6.46; controls=3.78;P<0.05). When the two groups of smoking rats were pooled together and compared to controls, they showed decreased lung elastance (1.6 vs 2.19; P = 0.046) and increased mean linear intercept (Lm) (85.14 vs 66.44; P = 0.025). The s-90 animals presented higher inflammation and muscular hypertrophy at the level of the axial bronchus than the controls (P<0.05). When smoking groups were pooled and compared to controls, they presented significantly higher inflammation at the lateral level (P = 0.028), as well as airway secretory hyperplasia (P = 0.024) and smooth muscle hypertrophy ( P = 0.005) at the axial level. Due to its simplicity, low cost and short duration, this technique may be a useful model to obtain new information about airspace remodeling due to chronic tobacco consumption.

Pulmonary emphysema induced by passive smoking: an experimental study in rats.

We describe a short time model for inducing experimental emphysema in rats by chronic tobacco smoke inhalation. Three groups of male Wistar rats (6 months old) were studied: controls (N = 8), rats intoxicated for 45 days (s-45, N = 7) or for 90 days (s-90, N = 8). The exposed animals were intoxicated 3 times a day (10 cigarettes per exposure period), 5 days a week. Pulmonary damage was assessed by means of functional tests and quantitative pathological examination of the airways and lung parenchyma. The s-45 and s-90 animals were similar in terms of functional residual capacity (FRC) corrected for body weight (FRC/kg) but both groups of smoking rats exhibited significantly higher FRC/kg values than the controls (s-45 = 6.33; s-90 = 6.46; controls = 3.78; P < 0.05). When the two groups of smoking rats were pooled together and compared to controls, they showed decreased lung elastance (1.6 vs 2.19; P = 0.046) and increased mean linear intercept (Lm) (85.14 vs 66.44; P = 0.025). The s-90 animals presented higher inflammation and muscular hypertrophy at the level of the axial bronchus than the controls (P < 0.05). When smoking groups were pooled and compared to controls, they presented significantly higher inflammation at the lateral level (P = 0.028), as well as airway secretory hyperplasia (P = 0.024) and smooth muscle hypertrophy (P = 0.005) at the axial level. Due to its simplicity, low cost and short duration, this technique may be a useful model to obtain new information about airspace remodeling due to chronic tobacco consumption.