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      Air pollution and its impacts on health in Vitoria, Espirito Santo, Brazil

      Revista de Saúde Pública
      Faculdade de Saúde Pública da Universidade de São Paulo
      Child, Adult, Air Pollution, adverse effects, Respiratory Tract Diseases, epidemiology, Cardiovascular Diseases, epidemiology, Time Series Studies, Criança, Adulto, Poluição do Ar, efeitos adversos, Doenças Respiratórias, epidemiologia, Doenças Cardiovasculares, epidemiologia, Estudos de Séries Temporais

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          Abstract

          ABSTRACT OBJECTIVE To analyze the impact of air pollution on respiratory and cardiovascular morbidity of children and adults in the city of Vitoria, state of Espirito Santo. METHODS A study was carried out using time-series models via Poisson regression from hospitalization and pollutant data in Vitoria, ES, Southeastern Brazil, from 2001 to 2006. Fine particulate matter (PM10), sulfur dioxide (SO2), and ozone (O3) were tested as independent variables in simple and cumulative lags of up to five days. Temperature, humidity and variables indicating weekdays and city holidays were added as control variables in the models. RESULTS For each increment of 10 µg/m3 of the pollutants PM10, SO2, and O3, the percentage of relative risk (%RR) for hospitalizations due to total respiratory diseases increased 9.67 (95%CI 11.84-7.54), 6.98 (95%CI 9.98-4.17) and 1.93 (95%CI 2.95-0.93), respectively. We found %RR = 6.60 (95%CI 9.53-3.75), %RR = 5.19 (95%CI 9.01-1.5), and %RR = 3.68 (95%CI 5.07-2.31) for respiratory diseases in children under the age of five years for PM10, SO2, and O3, respectively. Cardiovascular diseases showed a significant relationship with O3, with %RR = 2.11 (95%CI 3.18-1.06). CONCLUSIONS Respiratory diseases presented a stronger and more consistent relationship with the pollutants researched in Vitoria. A better dose-response relationship was observed when using cumulative lags in polynomial distributed lag models.

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          Clearing the air: a review of the effects of particulate matter air pollution on human health.

          The World Health Organization estimates that particulate matter (PM) air pollution contributes to approximately 800,000 premature deaths each year, ranking it the 13th leading cause of mortality worldwide. However, many studies show that the relationship is deeper and far more complicated than originally thought. PM is a portion of air pollution that is made up of extremely small particles and liquid droplets containing acids, organic chemicals, metals, and soil or dust particles. PM is categorized by size and continues to be the fraction of air pollution that is most reliably associated with human disease. PM is thought to contribute to cardiovascular and cerebrovascular disease by the mechanisms of systemic inflammation, direct and indirect coagulation activation, and direct translocation into systemic circulation. The data demonstrating PM's effect on the cardiovascular system are strong. Populations subjected to long-term exposure to PM have a significantly higher cardiovascular incident and mortality rate. Short-term acute exposures subtly increase the rate of cardiovascular events within days of a pollution spike. The data are not as strong for PM's effects on cerebrovascular disease, though some data and similar mechanisms suggest a lesser result with smaller amplitude. Respiratory diseases are also exacerbated by exposure to PM. PM causes respiratory morbidity and mortality by creating oxidative stress and inflammation that leads to pulmonary anatomic and physiologic remodeling. The literature shows PM causes worsening respiratory symptoms, more frequent medication use, decreased lung function, recurrent health care utilization, and increased mortality. PM exposure has been shown to have a small but significant adverse effect on cardiovascular, respiratory, and to a lesser extent, cerebrovascular disease. These consistent results are shown by multiple studies with varying populations, protocols, and regions. The data demonstrate a dose-dependent relationship between PM and human disease, and that removal from a PM-rich environment decreases the prevalence of these diseases. While further study is needed to elucidate the effects of composition, chemistry, and the PM effect on susceptible populations, the preponderance of data shows that PM exposure causes a small but significant increase in human morbidity and mortality. Most sources agree on certain "common sense" recommendations, although there are lonely limited data to support them. Indoor PM exposure can be reduced by the usage of air conditioning and particulate filters, decreasing indoor combustion for heating and cooking, and smoking cessation. Susceptible populations, such as the elderly or asthmatics, may benefit from limiting their outdoor activity during peak traffic periods or poor air quality days. These simple changes may benefit individual patients in both short-term symptomatic control and long-term cardiovascular and respiratory complications.
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            The distributed lag between air pollution and daily deaths.

            Many studies have reported associations between air pollution and daily deaths. Those studies have not consistently specified the lag between exposure and response, although most have found associations that persisted for more than 1 day. A systematic approach to specifying the lag association would allow better comparison across sites and give insight into the nature of the relation. To examine this question, I fit unconstrained and constrained distributed lag relations to the association between daily deaths of persons 65 years of age and older with PM10 in 10 U.S. cities (New Haven, Birmingham, Pittsburgh, Canton, Detroit, Chicago, Minneapolis, Colorado Springs, Spokane, and Seattle) that had daily monitoring for PM10. After control for temperature, humidity, barometric pressure, day of the week, and seasonal patterns, I found evidence in each city that the effect of a single day's exposure to PM10 was manifested across several days. Averaging over the 10 cities, the overall effect of an increase in exposure of 10 microg/m3 on a single day was a 1.4% increase in deaths (95% confidence intervals (CI) = 1.15-1.68) using a quadratic distributed lag model, and a 1.3% increase (95% CI = 1.04-1.56) using an unconstrained distributed lag model. In contrast, constraining the model to assume the effect all occurs in one day resulted in an estimate of only 0.65% (95% CI = 0.49-0.81), indicating that this constraint leads to a substantial underestimate of effect. Combining the estimated effect at each day's lag across the 10 cities showed that the effect was spread over several days and did not reach zero until 5 days after the exposure. Given the distribution of sensitivities likely in the general population, this result is biologically plausible. I also found a protective effect of barometric pressure in all 10 locations.
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              A meta-analysis of time-series studies of ozone and mortality with comparison to the national morbidity, mortality, and air pollution study.

              Although many time-series studies of ozone and mortality have identified positive associations, others have yielded null or inconclusive results, making the results of these studies difficult to interpret. We performed a meta-analysis of 144 effect estimates from 39 time-series studies, and estimated pooled effects by lags, age groups, cause-specific mortality, and concentration metrics. We compared results with pooled estimates from the National Morbidity, Mortality, and Air Pollution Study (NMMAPS), a time-series study of 95 large U.S. urban centers from 1987 to 2000. Both meta-analysis and NMMAPS results provided strong evidence of a short-term association between ozone and mortality, with larger effects for cardiovascular and respiratory mortality, the elderly, and current-day ozone exposure. In both analyses, results were insensitive to adjustment for particulate matter and model specifications. In the meta-analysis, a 10-ppb increase in daily ozone at single-day or 2-day average of lags 0, 1, or 2 days was associated with an 0.87% increase in total mortality (95% posterior interval = 0.55% to 1.18%), whereas the lag 0 NMMAPS estimate is 0.25% (0.12% to 0.39%). Several findings indicate possible publication bias: meta-analysis results were consistently larger than those from NMMAPS; meta-analysis pooled estimates at lags 0 or 1 were larger when only a single lag was reported than when estimates for multiple lags were reported; and heterogeneity of city-specific estimates in the meta-analysis were larger than with NMMAPS. This study provides evidence of short-term associations between ozone and mortality as well as evidence of publication bias.
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