Atmospheric pollutants in S��o Paulo state, Brazil and effects on human health ��� a review

Funda����o de Amparo �� Pesquisa do Estado de S��o Paulo (FAPESP)

The impact of atmospheric particulate matter on cancer incidence and mortality in the city of Sao Paulo, Brazil

This study aimed to verify the impact of inhalable particulate matter (PM10) on cancer incidence and mortality in the city of Sao Paulo, Brazil. Statistical techniques were used to investigate the relationship between PM10 on cancer incidence and mortality in selected districts. For some types of cancer (skin, lung, thyroid, larynx, and bladder) and some periods, the correlation coefficients ranged from 0.60 to 0.80 for incidence. Lung cancer mortality showed more correlations during the overall period. Spatial analysis showed that districts distant from the city center showed higher than expected relative risk, depending on the type of cancer According to the study, urban PM10 can contribute to increased incidence of some cancers and may also contribute to increased cancer mortality. The results highlight the need to adopt measures to reduce atmospheric PM10 levels and the importance of their continuous monitoring.

Tr��fego veicular e mortalidade por doen��as do aparelho circulat��rio em homens adultos

OBJETIVO: Analisar a associa����o entre indicadores de exposi����o �� polui����o por tr��fego veicular e mortalidade por doen��as do aparelho circulat��rio em homens adultos. M��TODOS: Foram analisadas informa����es sobre vias e volume de tr��fego no ano de 2007 fornecidas pela companhia de engenharia de tr��fego local. Mortalidade por doen��as do aparelho circulat��rio no ano de 2005 entre homens ��� 40 anos foram obtidas do registro de mortalidade do Programa de Aprimoramento de Informa����es de Mortalidade do Munic��pio de S��o Paulo, SP. Dados socioecon��micos do Censo 2000 e informa����es sobre a localiza����o dos servi��os de sa��de tamb��m foram coletados. A exposi����o foi avaliada pela densidade de vias e volume de tr��fego para cada distrito administrativo. Foi calculada regress��o (�� = 5%) entre esses indicadores de exposi����o e as taxas de mortalidade padronizadas, ajustando os modelos para vari��veis socioecon��micas, n��mero de servi��os de sa��de nos distritos e autocorrela����o espacial. RESULTADOS: A correla����o entre densidade de vias e volume de tr��fego foi modesta (r�� = 0,28). Os distritos do centro apresentaram os maiores valores de densidade de vias. O modelo de regress��o espacial de densidade de vias indicou associa����o com mortalidade por doen��as do aparelho circulat��rio (p = 0,017). N��o se observou associa����o no modelo de volume de tr��fego. Em ambos os modelos ��� vias e volume de tr��fego (ve��culos leves/pesados) ��� a vari��vel socioecon��mica foi estatisticamente signi��� cante. CONCLUS��ES: A associa����o entre mortalidade por doen��as do aparelho circulat��rio e densidade de vias converge com a literatura e encoraja a realiza����o de mais estudos epidemiol��gicos em n��vel individual e com m��todos mais acurados de avalia����o da exposi����o.

Air pollution and health: bridging the gap from sources to health outcomes: conference summary

Air Pollution and Health: Bridging the Gap from Sources to Health Outcomes, an international specialty conference sponsored by the American Association for Aerosol Research, was held to address key uncertainties in our understanding of adverse health effects related to air pollution and to integrate and disseminate results from recent scientific studies that cut across a range of air pollution-related disciplines. The Conference addressed the science of air pollution and health within a multipollutant framework (herein "multipollutant" refers to gases and particulate matter mass, components, and physical properties), focusing on five key science areas: sources, atmospheric sciences, exposure, dose, and health effects. Eight key policy-relevant science questions integrated across various parts of the five science areas and a ninth question regarding findings that provide policy-relevant insights served as the framework for the meeting. Results synthesized from this Conference provide new evidence, reaffirm past findings, and offer guidance for future research efforts that will continue to incrementally advance the science required for reducing uncertainties in linking sources, air pollutants, human exposure, and health effects. This paper summarizes the Conference findings organized around the science questions. A number of key points emerged from the Conference findings. First, there is a need for greater focus on multipollutant science and management approaches that include more direct studies of the mixture of pollutants from sources with an emphasis on health studies at ambient concentrations. Further, a number of research groups reaffirmed a need for better understanding of biological mechanisms and apparent associations of various health effects with components of particulate matter (PM), such as elemental carbon, certain organic species, ultrafine particles, and certain trace elements such as Ni, V, and Fe(II), as well as some gaseous pollutants. Although much debate continues in this area, generation of reactive oxygen species induced by these and other species present in air pollution and the resulting oxidative stress and inflammation were reiterated as key pathways leading to respiratory and cardiovascular outcomes. The Conference also underscored significant advances in understanding the susceptibility of populations, including the role of genetics and epigenetics and the influence of socioeconomic and other confounding factors and their synergistic interactions with air pollutants. Participants also pointed out that short-and long-term intervention episodes that reduce pollution from sources and improve air quality continue to indicate that when pollution decreases so do reported adverse health effects. In the limited number of cases where specific sources or PM2.5 species were included in investigations, specific species are often associated with the decrease in effects. Other recent advances for improved exposure estimates for epidemiological studies included using new technologies such as microsensors combined with cell phone and integrated into real-time communications, hybrid air quality modeling such as combined receptor-and emission-based models, and surface observations used with remote sensing such as satellite data.

Water-soluble organic compounds in air particulate matter analyzed by HPLC-DAD-MS and HPLC-MS/MS: abundance, sources and transformation of carboxylic acids, nitrophenols and nitrated proteins

Wasserl��sliche organische Verbindungen (WSOCs) sind Hauptbestandteile atmosph��rischer Aerosole, die bis zu ~ 50% und mehr der organischen Aerosolfraktion ausmachen. Sie k��nnen die optischen Eigenschaften sowie die Hygroskopizit��t von Aerosolpartikeln und damit deren Auswirkungen auf das Klima beeinflussen. Dar��ber hinaus k��nnen sie zur Toxizit��t und Allergenit��t atmosph��rischer Aerosole beitragen.In dieser Studie wurde Hochleistungsfl��ssigchromatographie gekoppelt mit optischen Diodenarraydetektion und Massenspektrometrie (HPLC-DAD-MS und HPLC-MS/MS) angewandt, um WSOCs zu analysieren, die f��r verschiedene Aerosolquellen und -prozesse charakteristisch sind. Niedermolekulare Carbons��uren und Nitrophenole wurden als Indikatoren f��r die Verbrennung fossiler Brennstoffe und die Entstehung sowie Alterung sekund��rer organischer Aerosole (SOA) aus biogenen Vorl��ufern untersucht. Protein-Makromolek��le wurden mit Blick auf den Einfluss von Luftverschmutzung und Nitrierungsreaktionen auf die Allergenit��t prim��rer biologischer Aerosolpartikel ��� wie Pollen und Pilzsporen ��� untersucht.rnFilterproben von Grob- und Feinstaubwurden ��ber ein Jahr hinweg gesammelt und auf folgende WSOCs untersucht: die Pinen-Oxidationsprodukte Pins��ure, Pinons��ure und 3-Methyl-1,2,3-Butantricarbons��ure (3-MBTCA) sowie eine Vielzahl anderer Dicarbons��uren und Nitrophenole. Saisonale Schwankungen und andere charakteristische Merkmale werden mit Blick auf Aerosolquellen und -senken im Vergleich zu Daten anderen Studien und Regionen diskutiert. Die Verh��tlnisse von Adipins��ure und Phthals��ure zu Azelains��ure deuten darauf hin, dass die untersuchten Aerosolproben haupts��chlich durch biogene Quellen beeinflusst werden. Eine ausgepr��gte Arrhenius-artige Korrelation wurde zwischen der 3-MBTCA-��Konzentration und der inversen Temperatur beobachtet (R2 = 0.79, Ea = 126��10 kJ mol-1, Temperaturbereich 275���300 K). Modellrechnungen zeigen, dass die Temperaturabh��ngigkeit auf eine Steigerung der photochemischen Produktionsraten von 3-MBTCA durch erh��hte OH-Radikal-Konzentrationen bei erh��hten Temperaturen zur��ckgef��hrt werden kann. Im Vergleich zur chemischen Reaktionskinetik scheint der Einfluss von Gas-Partikel-Partitionierungseffekten nur eine untergeordnete Rolle zu spielen. Die Ergebnisse zeigen, dass die OH-initiierte Oxidation von Pinos��ure der geschwindigkeitsbestimmende Schritt der Bildung von 3-MBTCA ist. 3-MBTCA erscheint somit als Indikator f��r die chemische Alterung von biogener sekund��rer organischer Aerosole (SOA) durch OH-Radikale geeignet. Eine Arrhenius-artige Temperaturabh��ngigkeit wurde auch f��r Pin��ure beobachtet und kann durch die Temperaturabh��ngigkeit der biogenen Pinen-Emissionen als geschwindigkeitsbestimmender Schritt der Pins��ure-Bildung erkl��rt werden (R2 = 0.60, Ea = 84��9 kJ mol-1).rn rnF��r die Untersuchung von Proteinnitrierungreaktionen wurde nitrierte Protein��standards durch Fl��ssigphasenreaktion von Rinderserumalbumin (BSA) und Ovalbumin (OVA) mit Tetranitromethan (TNM) synthetisiert.Proteinnitrierung erfolgt vorrangig an den Resten der aromatischen Aminos��ure Tyrosin auf, und mittels UV-Vis-Photometrie wurde der Proteinnnitrierungsgrad (ND) bestimmt. Dieser ist definiert als Verh��ltnis der mittleren Anzahl von Nitrotyrosinresten zur Tyrosinrest-Gesamtzahl in den Proteinmolek��len. BSA und OVA zeigten verschiedene Relationen zwischen ND und TNM/Tyrosin-Verh��ltnis im Reaktionsgemisch, was vermutlich auf Unterschiede in den L��slichkeiten und den molekularen Strukturen der beiden Proteine zur��ck zu f��hren ist.rnDie Nitrierung von BSA und OVA durch Exposition mit einem Gasgemisch aus Stickstoffdioxid (NO2) und Ozon (O3) wurde mit einer neu entwickelten HPLC-DAD-��Analysemethode untersucht. Diese einfache und robuste Methode erlaubt die Bestimmung des ND ohne Hydrolyse oder Verdau der untersuchten Proteine und ern��glicht somit eine effiziente Untersuchung der Kinetik von Protein��nitrierungs-Reaktionen. F��r eine detaillierte Produktstudien wurden die nitrierten Proteine enzymatisch verdaut, und die erhaltenen Oligopeptide wurden mittels HPLC-MS/MS und Datenbankabgleich mit hoher Sequenz��bereinstimmung analysiert. Die Nitrierungsgrade individueller Nitrotyrosin-Reste (NDY) korrelierten gut mit dem Gesamt-Proteinnitrierungsgrad (ND), und unterschiedliche Verh��ltnisse von NDY zu ND geben Aufschluss ��ber die Regioselektivit��t der Reaktion. Die Nitrierungmuster von BSA und OVA nach Beahndlung mit TNM deuten darauf hin, dass die Nachbarschaft eines negativ geladenen Aminos��urerestes die Tyrosinnitrierung f��rdert. Die Behandlung von BSA durch NO2 und O3 f��hrte zu anderend Nitrierungemustern als die Behandlung mit TNM, was darauf hindeutet, dass die Regioselektivit��t der Nitrierung vom Nitrierungsmittel abh��ngt. Es zeigt sich jedoch, dass Tyrosinreste in Loop-Strukturen bevorzugt und unabh��ngig vom Reagens nitriert werden.Die Methoden und Ergebnisse dieser Studie bilden eine Grundlage f��r weitere, detaillierte Untersuchungen der Reaktionskinetik sowie der Produkte und Mechanismen von Proteinnitrierungreaktionen. Sie sollen helfen, die Zusammenh��nge zwischen verkehrsbedingten Luftschadstoffen wie Stickoxiden und Ozon und der Allergenit��t von Luftstaub aufzukl��ren.rn

Exposure to moderate air pollution during late pregnancy and cord blood cytokine secretion in healthy neonates

Background/Objectives Ambient air pollution can alter cytokine concentrations as shown in vitro and following short-term exposure to high air pollution levels in vivo. Exposure to pollution during late pregnancy has been shown to affect fetal lymphocytic immunophenotypes. However, effects of prenatal exposure to moderate levels of air pollutants on cytokine regulation in cord blood of healthy infants are unknown. Methods In a birth cohort of 265 healthy term-born neonates, we assessed maternal exposure to particles with an aerodynamic diameter of 10 ��m or less (PM10), as well as to indoor air pollution during the last trimester, specifically the last 21, 14, 7, 3 and 1 days of pregnancy. As a proxy for traffic-related air pollution, we determined the distance of mothers' homes to major roads. We measured cytokine and chemokine levels (MCP-1, IL-6, IL-10, IL-1��, TNF-�� and GM-CSF) in cord blood serum using LUMINEX technology. Their association with pollution levels was assessed using regression analysis, adjusted for possible confounders. Results Mean (95%-CI) PM10 exposure for the last 7 days of pregnancy was 18.3 (10.3���38.4 ��g/m3). PM10 exposure during the last 3 days of pregnancy was significantly associated with reduced IL-10 and during the last 3 months of pregnancy with increased IL-1�� levels in cord blood after adjustment for relevant confounders. Maternal smoking was associated with reduced IL-6 levels. For the other cytokines no association was found. Conclusions Our results suggest that even naturally occurring prenatal exposure to moderate amounts of indoor and outdoor air pollution may lead to changes in cord blood cytokine levels in a population based cohort.

Reduced Bayesian Hierarchical Models: Estimating Health Effects of Simultaneous Exposure to Multiple Pollutants

Quantifying the health effects associated with simultaneous exposure to many air pollutants is now a research priority of the US EPA. Bayesian hierarchical models (BHM) have been extensively used in multisite time series studies of air pollution and health to estimate health effects of a single pollutant adjusted for potential confounding of other pollutants and other time-varying factors. However, when the scientific goal is to estimate the impacts of many pollutants jointly, a straightforward application of BHM is challenged by the need to specify a random-effect distribution on a high-dimensional vector of nuisance parameters, which often do not have an easy interpretation. In this paper we introduce a new BHM formulation, which we call "reduced BHM", aimed at analyzing clustered data sets in the presence of a large number of random effects that are not of primary scientific interest. At the first stage of the reduced BHM, we calculate the integrated likelihood of the parameter of interest (e.g. excess number of deaths attributed to simultaneous exposure to high levels of many pollutants). At the second stage, we specify a flexible random-effect distribution directly on the parameter of interest. The reduced BHM overcomes many of the challenges in the specification and implementation of full BHM in the context of a large number of nuisance parameters. In simulation studies we show that the reduced BHM performs comparably to the full BHM in many scenarios, and even performs better in some cases. Methods are applied to estimate location-specific and overall relative risks of cardiovascular hospital admissions associated with simultaneous exposure to elevated levels of particulate matter and ozone in 51 US counties during the period 1999-2005.

[Air pollution and asthma in childhood].

Exposure to outdoor air pollutants and passive tobacco smoke are common but avoidable worldwide risk factors for morbidity and mortality of individuals. In addition to well-known effects of pollutants on the cardiovascular system and the development of cancer, in recent years the association between air pollution and respiratory morbidity has become increasingly apparent. Not only in adults, but also in children with asthma and in healthy children a clear harmful effect of exposure towards air pollutants has been demonstrated in many studies. Among others increased pollution has been shown to result in more frequent and more severe respiratory symptoms, more frequent exacerbations, higher need for asthma medication, poorer lung function and increased visits to the emergency department and more frequent hospitalisations. While these associations are well established, the available data on the role of air pollution in the development of asthma seems less clear. Some studies have shown that increased exposure towards tobacco smoke and air pollution leads to an increase in asthma incidence and prevalence; others were not able to confirm those findings. Possible reasons for this discrepancy are different definitions of the outcome asthma, different methods for exposure estimation and differences in the populations studied with differing underlying genetic backgrounds. Regardless of this inconsistency, several mechanisms have already been identified linking air pollution with asthma development. Among these are impaired lung growth and development, immunological changes, genetic or epigenetic effects or increased predisposition for allergic sensitisation. What the exact interactions are and which asthmatic phenotypes will be influenced most by pollutants will be shown by future studies. This knowledge will then be helpful in exploring possible preventive measures for the individual and to help policy makers in deciding upon most appropriate regulations on a population level.

Effects of air pollution on asthma hospitalization rates in different age groups in metropolitan cities of Korea

Many studies have shown relationships between air pollution and the rate of hospital admissions for asthma. A few studies have controlled for age-specific effects by adding separate smoothing functions for each age group. However, it has not yet been reported whether air pollution effects are significantly different for different age groups. This lack of information is the motivation for this study, which tests the hypothesis that air pollution effects on asthmatic hospital admissions are significantly different by age groups. Each air pollutant's effect on asthmatic hospital admissions by age groups was estimated separately. In this study, daily time-series data for hospital admission rates from seven cities in Korea from June 1999 through 2003 were analyzed. The outcome variable, daily hospital admission rates for asthma, was related to five air pollutants which were used as the independent variables, namely particulate matter <10 micrometers (��m) in aerodynamic diameter (PM10), carbon monoxide (CO), ozone (O3), nitrogen dioxide (NO2), and sulfur dioxide (SO2). Meteorological variables were considered as confounders. Admission data were divided into three age groups: children (<15 years of age), adults (ages 15-64), and elderly (��� 65 years of age). The adult age group was considered to be the reference group for each city. In order to estimate age-specific air pollution effects, the analysis was separated into two stages. In the first stage, Generalized Additive Models (GAMs) with cubic spline for smoothing were applied to estimate the age-city-specific air pollution effects on asthmatic hospital admission rates by city and age group. In the second stage, the Bayesian Hierarchical Model with non-informative prior which has large variance was used to combine city-specific effects by age groups. The hypothesis test showed that the effects of PM10, CO and NO2 were significantly different by age groups. Assuming that the air pollution effect for adults is zero as a reference, age-specific air pollution effects were: -0.00154 (95% confidence interval(CI)= (-0.0030,-0.0001)) for children and 0.00126 (95% CI = (0.0006, 0.0019)) for the elderly for PM 10; -0.0195 (95% CI = (-0.0386,-0.0004)) for children for CO; and 0.00494 (95% CI = (0.0028, 0.0071)) for the elderly for NO2. Relative rates (RRs) were 1.008 (95% CI = (1.000-1.017)) in adults and 1.021 (95% CI = (1.012-1.030)) in the elderly for every 10 ��g/m3 increase of PM10 , 1.019 (95% CI = (1.005-1.033)) in adults and 1.022 (95% CI = (1.012-1.033)) in the elderly for every 0.1 part per million (ppm) increase of CO; 1.006 (95%CI = (1.002-1.009)) and 1.019 (95%CI = (1.007-1.032)) in the elderly for every 1 part per billion (ppb) increase of NO2 and SO2, respectively. Asthma hospital admissions were significantly increased for PM10 and CO in adults, and for PM10, CO, NO2 and SO2 in the elderly.^

Associations between ambient levels of combustion pollutants and small for gestational age infants in Texas

There is scant evidence regarding the associations between ambient levels of combustion pollutants and small for gestational age (SGA) infants. No studies of this type have been completed in the Southern United States. The main objective of the project presented was to determine associations between combustion pollutants and SGA infants in Texas using three different exposure assessments. ^ Birth certificate data that contained information on maternal and infant characteristics were obtained from the Texas Department of State Health Services (TX DSHS). Exposure assessment data for the three aims came from: (1) U.S. Environmental Protection Agency (EPA) National Air Toxics Assessment (NATA), (2) U.S. EPA Air Quality System (AQS), and (3) TX Department of Transportation (DOT), respectively. Multiple logistic regression models were used to determine the associations between combustion pollutants and SGA. ^ For the first study looked at annual estimates of four air toxics at the census tract level in the Greater Houston Area. After controlling for maternal race, maternal education, tobacco use, maternal age, number of prenatal visits, marital status, maternal weight gain, and median census tract income level, adjusted ORs and 95% confidence intervals (CI) for exposure to PAHs (per 10 ng/m3), naphthalene (per 10 ng/m3), benzene (per 1 ��g/m3), and diesel engine emissions (per 10 ��g/m3) were 1.01 (0.97���1.05), 1.00 (0.99���1.01), 1.01 (0.97���1.05), and 1.08 (0.95���1.23) respectively. For the second study looking at Hispanics in El Paso County, AORs and 95% confidence intervals (CI) for increases of 5 ng/m3 for the sum of carcinogenic PAHs (�� c-PAHs), 1 ng/m3 of benzo[a]pyrene, and 100 ng/m3 in naphthalene during the third trimester of pregnancy were 1.02 (0.97���1.07), 1.03 (0.96���1.11), and 1.01 (0.97���1.06), respectively. For the third study using maternal proximity to major roadways as the exposure metric, there was a negative association with increasing distance from a maternal residence to the nearest major roadway (Odds Ratio (OR) = 0.96; 95% CI = 0.94���0.97) per 1000 m); however, once adjusted for covariates this effect was no longer significant (AOR = 0.98; 95% CI = 0.96���1.00). There was no association with distance weighted traffic density (DWTD). ^ This project is the first to look at SGA and combustion pollutants in the Southern United States with three different exposure metrics. Although there was no evidence of associations found between SGA and the air pollutants mentioned in these studies, the results contribute to the body of literature assessing maternal exposure to ambient air pollution and adverse birth outcomes. ^

Prevalence and risk factors of asthma and work -related asthma among U.S. adults: Data from the Third National Health and Nutrition Examination Survey, 1988--1994

This cross-sectional analysis of the data from the Third National Health and Nutrition Examination Survey was conducted to determine the prevalence and determinants of asthma and wheezing among US adults, and to identify the occupations and industries at high risk of developing work-related asthma and work-related wheezing. Separate logistic models were developed for physician-diagnosed asthma (MD asthma), wheezing in the previous 12 months (wheezing), work-related asthma and work-related wheezing. Major risk factors including demographic, socioeconomic, indoor air quality, allergy, and other characteristics were analyzed. The prevalence of lifetime MD asthma was 7.7% and the prevalence of wheezing was 17.2%. Mexican-Americans exhibited the lowest prevalence of MD asthma (4.8%; 95% confidence interval (CI): 4.2, 5.4) when compared to other race-ethnic groups. The prevalence of MD asthma or wheezing did not vary by gender. Multiple logistic regression analysis showed that Mexican-Americans were less likely to develop MD asthma (adjusted odds ratio (ORa) = 0.64, 95%CI: 0.45, 0.90) and wheezing (ORa = 0.55, 95%CI: 0.44, 0.69) when compared to non-Hispanic whites. Low education level, current and past smoking status, pet ownership, lifetime diagnosis of physician-diagnosed hay fever and obesity were all significantly associated with MD asthma and wheezing. No significant effect of indoor air pollutants on asthma and wheezing was observed in this study. The prevalence of work-related asthma was 3.70% (95%CI: 2.88, 4.52) and the prevalence of work-related wheezing was 11.46% (95%CI: 9.87, 13.05). The major occupations identified at risk of developing work-related asthma and wheezing were cleaners; farm and agriculture related occupations; entertainment related occupations; protective service occupations; construction; mechanics and repairers; textile; fabricators and assemblers; other transportation and material moving occupations; freight, stock and material movers; motor vehicle operators; and equipment cleaners. The population attributable risk for work-related asthma and wheeze were 26% and 27% respectively. The major industries identified at risk of work-related asthma and wheeze include entertainment related industry; agriculture, forestry and fishing; construction; electrical machinery; repair services; and lodging places. The population attributable risk for work-related asthma was 36.5% and work-related wheezing was 28.5% for industries. Asthma remains an important public health issue in the US and in the other regions of the world. ^

Ambient Air Pollution and Lung Cancer Risk in the Women's Health Initiative Observational Study

Thesis (Master's)--University of Washington, 2016-06

Monte Carlo Study of Particle Transport Problem in Air Pollution

2002 Mathematics Subject Classification: 65C05.

Air Pollution and High Density Lipoprotein Structure and Function

Thesis (Ph.D.)--University of Washington, 2016-06