939 resultados para air pollution, fetal growth, pregnancy, temperature, ultrasound


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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 µm 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-1ß, TNF-α 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 µg/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-1ß 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.

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There is increasing evidence of the adverse impact of prenatal exposure to air pollution. This is of particular interest, as exposure during pregnancy--a crucial time span of important biological development--may have long-term implications. The aims of this review are to show current epidemiological evidence of known effects of prenatal exposure to air pollution and present possible mechanisms behind this process. Harmful effects of exposure to air pollution during pregnancy have been shown for different birth outcomes: higher infant mortality, lower birth weight, impaired lung development, increased later respiratory morbidity, and early alterations in immune development. Although results on lower birth weight are somewhat controversial, evidence for higher infant mortality is consistent in studies published worldwide. Possible mechanisms include direct toxicity of particles due to particle translocation across tissue barriers or particle penetration across cellular membranes. The induction of specific processes or interaction with immune cells in either the pregnant mother or the fetus may be possible consequences. Indirect effects could be oxidative stress and inflammation with consequent hemodynamic alterations resulting in decreased placental blood flow and reduced transfer of nutrients to the fetus. The early developmental phase of pregnancy is thought to be very important in determining long-term growth and overall health. So-called "tracking" of somatic growth and lung function is believed to have a huge impact on long-term morbidity, especially from a public health perspective. This is particularly important in areas with high levels of outdoor pollution, where it is practically impossible for an individual to avoid exposure. Especially in these areas, good evidence for the association between prenatal exposure to air pollution and infant mortality exists, clearly indicating the need for more stringent measures to reduce exposure to air pollution.

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Post-natal exposure to air pollution is associated with diminished lung growth during school age. The current authors aimed to determine whether pre-natal exposure to air pollution is associated with lung function changes in the newborn. In a prospective birth cohort of 241 healthy term-born neonates, tidal breathing, lung volume, ventilation inhomogeneity and exhaled nitric oxide (eNO) were measured during unsedated sleep at age 5 weeks. Maternal exposure to particles with a 50% cut-off aerodynamic diameter of 10 microm (PM(10)), nitrogen dioxide (NO(2)) and ozone (O(3)), and distance to major roads were estimated during pregnancy. The association between these exposures and lung function was assessed using linear regression. Minute ventilation was higher in infants with higher pre-natal PM(10) exposure (24.9 mL x min(-1) per microg x m(-3) PM(10)). The eNO was increased in infants with higher pre-natal NO(2) exposure (0.98 ppb per microg x m(-3) NO(2)). Post-natal exposure to air pollution did not modify these findings. No association was found for pre-natal exposure to O(3) and lung function parameters. The present results suggest that pre-natal exposure to air pollution might be associated with higher respiratory need and airway inflammation in newborns. Such alterations during early lung development may be important regarding long-term respiratory morbidity.

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Exposure to air pollution during pregnancy is a potential cause of adverse birth outcomes such as preterm birth and stillbirth. The risk of exposure may be greater during vulnerable windows of the pregnancy which might only be weeks long. We demonstrate a method to find these windows based on smoothing the risk of weekly exposure using conditional autoregression. We use incidence density sampling to match cases with adverse birth outcomes to controls whose gestation lasted at least as long as the case. This matching means that cases and controls are have equal length exposure periods, rather than comparing, for example, cases with short gestations to controls with longer gestations. We demonstrate the ability of the method to find vulnerable windows using two simulation studies. We illustrate the method by examining the association between particulate matter air pollution and stillbirth in Brisbane, Australia.

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Previous studies have demonstrated the importance of weather variables in influencing the incidence of influenza. However, the role of air pollution is often ignored in identifying the environmental drivers of influenza. This research aims to examine the impacts of air pollutants and temperature on the incidence of pediatric influenza in Brisbane, Australia. Lab-confirmed daily data on influenza counts among children aged 0-14years in Brisbane from 2001 January 1st to 2008 December 31st were retrieved from Queensland Health. Daily data on maximum and minimum temperatures for the same period were supplied by the Australian Bureau of Meteorology. Winter was chosen as the main study season due to it having the highest pediatric influenza incidence. Four Poisson log-linear regression models, with daily pediatric seasonal influenza counts as the outcome, were used to examine the impacts of air pollutants (i.e., ozone (O3), particulate matter≤10μm (PM10) and nitrogen dioxide (NO2)) and temperature (using a moving average of ten days for these variables) on pediatric influenza. The results show that mean temperature (Relative risk (RR): 0.86; 95% Confidence Interval (CI): 0.82-0.89) was negatively associated with pediatric seasonal influenza in Brisbane, and high concentrations of O3 (RR: 1.28; 95% CI: 1.25-1.31) and PM10 (RR: 1.11; 95% CI: 1.10-1.13) were associated with more pediatric influenza cases. There was a significant interaction effect (RR: 0.94; 95% CI: 0.93-0.95) between PM10 and mean temperature on pediatric influenza. Adding the interaction term between mean temperature and PM10 substantially improved the model fit. This study provides evidence that PM10 needs to be taken into account when evaluating the temperature-influenza relationship. O3 was also an important predictor, independent of temperature.

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In order to determine the effect of maternal exercise on maternal nutritional status and fetal growth, young (Y = 45-50 days old) Wistar rats were divided into 4 groups of 5 to 8 animals: control pregnant (CP), control non-pregnant (CNP), exercise-trained (swimming 1 h/day, 5 days/week, for 19 days) pregnant (TP) and exercise-trained non-pregnant (TNP). Four equivalent groups of adult rats (A - 90-100 days old) were also formed. Serum glucose, total protein, albumin, hematocrit and liver glycogen were determined in female rats and pups. There were no statistical differences in serum glucose, total protein and albumin levels, litter size ot birth weight among exercise-trained animals, controls and their respective pups. Hematocrit was significantly lower in pups of exercise-trained young rats than in all other groups (YCP = 38.6 +/- 3.0; YTP = 32.6 +/- 2.1; ACP = 39.0 +/- 2.5; ATP = 39.2 +/- 2.9%). Liver glycogen levels were lower in pregnant than in non-pregnant rats but similar in exercise-trained and control rats of the same age and physiological status (YCNP = 4.1 +/- 0.2; YCP = 2.7 +/- 0.9; YTNP = 4.9 +/- 0.8; YTP = 2.7 +/-0.4; ACNP = 6.1 +/- 0.6; ACP = 3.1 +/- 0.8; ATNP = 6.6 +/- 0.8; ATP = 2.2 +/- 0.9 mg/100 mg). We conclude that pups of adult female rats are spared from the effects of this kind of exercise training during pregnancy. on the other hand, it appears that maternal adaptations to exercise training in young rats are able to preserve only some aspects of pup metabolism.

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Background In the last 20 years, there has been an increase in the incidence of allergic respiratory diseases worldwide and exposure to air pollution has been discussed as one of the factors associated with this increase. The objective of this study was to investigate the effects of air pollution on peak expiratory flow (PEF) and FEV1 in children with and without allergic sensitization. Methods Ninety-six children were followed from April to July, 2004 with spirometry measurements. They were tested for allergic sensitization (IgE, skin prick test, eosinophilia) and asked about allergic symptoms. Air pollution, temperature, and relative humidity data were available. Results Decrements in PEF were observed with previous 24-hr average exposure to air pollution, as well as with 310-day average exposure and were associated mainly with PM10, NO2, and O3 in all three categories of allergic sensitization. Even though allergic sensitized children tended to present larger decrements in the PEF measurements they were not statistically different from the non-allergic sensitized. Decrements in FEV1 were observed mainly with previous 24-hr average exposure and 3-day moving average. Conclusions Decrements in PEF associated with air pollution were observed in children independent from their allergic sensitization status. Their daily exposure to air pollution can be responsible for a chronic inflammatory process that might impair their lung growth and later their lung function in adulthood. Am. J. Ind. Med. 55:10871098, 2012. (c) 2012 Wiley Periodicals, Inc.

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BACKGROUND: A number of epidemiological studies have examined the adverse effect of air pollution on mortality and morbidity. Also, several studies have investigated the associations between air pollution and specific-cause diseases including arrhythmia, myocardial infarction, and heart failure. However, little is known about the relationship between air pollution and the onset of hypertension. OBJECTIVE: To explore the risk effect of particulate matter air pollution on the emergency hospital visits (EHVs) for hypertension in Beijing, China. METHODS: We gathered data on daily EHVs for hypertension, fine particulate matter less than 2.5 microm in aerodynamic diameter (PM(2.5)), particulate matter less than 10 microm in aerodynamic diameter (PM(10)), sulfur dioxide, and nitrogen dioxide in Beijing, China during 2007. A time-stratified case-crossover design with distributed lag model was used to evaluate associations between ambient air pollutants and hypertension. Daily mean temperature and relative humidity were controlled in all models. RESULTS: There were 1,491 EHVs for hypertension during the study period. In single pollutant models, an increase in 10 microg/m(3) in PM(2.5) and PM(10) was associated with EHVs for hypertension with odds ratios (overall effect of five days) of 1.084 (95% confidence interval (CI): 1.028, 1.139) and 1.060% (95% CI: 1.020, 1.101), respectively. CONCLUSION: Elevated levels of ambient particulate matters are associated with an increase in EHVs for hypertension in Beijing, China.

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Background: A number of epidemiological studies have been conducted to research the adverse effects of air pollution on mortality and morbidity. Hypertension is the most important risk factor for cardiovascular mortality. However, few previous studies have examined the relationship between gaseous air pollution and morbidity for hypertension. ---------- Methods: Daily data on emergency hospital visits (EHVs) for hypertension were collected from the Peking University Third Hospital. Daily data on gaseous air pollutants (sulfur dioxide (SO2) and nitrogen dioxide (NO2)) and particulate matter less than 10 μm in aerodynamic diameter (PM10) were collected from the Beijing Municipal Environmental Monitoring Center. A time-stratified case-crossover design was conducted to evaluate the relationship between urban gaseous air pollution and EHVs for hypertension. Temperature and relative humidity were controlled for. ---------- Results: In the single air pollutant models, a 10 μg/m3 increase in SO2 and NO2 were significantly associated with EHVs for hypertension. The odds ratios (ORs) were 1.037 (95% confidence interval (CI): 1.004-1.071) for SO2 at lag 0 day, and 1.101 (95% CI: 1.038-1.168) for NO2 at lag 3 day. After controlling for PM10, the ORs associated with SO2 and NO2 were 1.025 (95% CI: 0.987-1.065) and 1.114 (95% CI: 1.037-1.195), respectively.---------- Conclusion: Elevated urban gaseous air pollution was associated with increased EHVs for hypertension in Beijing, China.

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Although ambient air pollution exposure has been linked with poor health in many parts of the world, no previous study has investigated the effect on morbidity in the city of Adelaide, South Australia. To explore the association between particulate matter (PM) and hospitalisations, including respiratory and cardiovascular admissions in Adelaide, South Australia. Methods: For the study period September 2001 to October 2007, daily counts of all-cause, cardiovascular and respiratory hospital admissions were collected, as well as daily air quality data including concentrations of particulates, ozone and nitrogen dioxide. Visibility codes for presentweather conditions identified dayswhen airborne dust or smoke was observed. The associations between PM and hospitalisations were estimated using timestratified case-crossover analyses controlling for covariates including temperature, relative humidity, other pollutants, day of the week and public holidays. Mean PM10 concentrations were higher in the warm season, whereas PM2.5 concentrations were higher in the cool season. Hospital admissions were associated with PM10 in the cool season and with PM2.5 in both seasons. No significant effect of PM on all-age respiratory admissions was detected, however cardiovascular admissions were associated with both PM2.5 and PM10 in the cool season with the highest effects for PM2.5 (4.48%, 95% CI: 0.74%, 8.36% increase per 10 μg/m3 increase in PM2.5). These findings suggest that despite the city's relatively low levels of air pollution, PMconcentrations are associated with increases in morbidity in Adelaide. Further studies are needed to investigate the sources of PM which may be contributing to the higher cool season effects.

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This study examined the long-term trends in four air pollutants in Australia’s four largest cities between 1996 and 2011. There were long-term improvements in carbon monoxide and sulfur dioxide. Particulate matter levels (PM10) remained relatively constant. Ozone levels increased in all four cities when including the influence of temperature, and levels are predicted to increase further because of climate change.

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Though increased particulate air pollution has been consistently associated with elevated mortality, evidence regarding whether diminished particulate air pollution would lead to mortality reduction is limited. Citywide air pollution mitigation program during the 2010 Asian Games in Guangzhou, China, provided such an opportunity. Daily mortality from non-accidental, cardiovascular and respiratory diseases was compared for 51 intervention days (November 1–December 21) in 2010 with the same calendar date of baseline years (2006–2009 and 2011). Relative risk (RR) and 95% confidence interval (95% CI) were estimated using a time series Poisson model, adjusting for day of week, public holidays, daily mean temperature and relative humidity. Daily PM10 (particle with aerodynamic diameter less than 10 μm) decreased from 88.64 μg/m3 during the baseline period to 80.61 μg/m3 during the Asian Games period. Other measured air pollutants and weather variables did not differ substantially. Daily mortality from non-accidental, cardiovascular and respiratory diseases decreased from 32, 11 and 6 during the baseline period to 25, 8 and 5 during the Games period, the corresponding RR for the Games period compared with the baseline period was 0.79 (95% CI: 0.73–0.86), 0.77 (95% CI: 0.66–0.89) and 0.68 (95% CI: 0.57–0.80), respectively. No significant decreases were observed in other months of 2010 in Guangzhou and intervention period in two control cities. This finding supports the efforts to reduce air pollution and improve public health through transportation restriction and industrial emission control.