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PubMed2005

Fine particulate air pollution and cardiorespiratory effects in the elderly.

BACKGROUND: Past studies of air pollution effects among sensitive subgroups have produced inconsistent results. Our objective was to determine relationships between various measures of air pollution and cardiorespiratory effects in older subjects. METHODS: We conducted a study that included repeated measurements of pulmonary function (arterial oxygen saturation) and cardiac function (heart rate and blood pressure) in a panel of 88 subjects (>57 years of age) in Seattle during the years 1999 to 2001. Subjects were healthy or had lung or heart disease. Each subject participated in sessions of 10 consecutive days of exposure monitoring and collection of health outcomes for up to 2 sessions. Associations between health outcomes and indoor, outdoor, and personal measures of particulate matter </=2.5 micrometers (PM2.5) or particulate matter </=10 micrometers (PM10) were evaluated using generalized estimating equations with an exchangeable working correlation matrix and robust standard errors. The model included terms for the within-subject, within-session effect; the within- subject, between-session effect; and an interaction term for medication usage. The model controlled for temperature, relative humidity, body mass index, and age. RESULTS: Associations between air pollution and health measurements were found primarily in healthy subjects. Healthy subjects taking no medications had decreases in heart rate associated with indoor and outdoor PM2.5 and PM10. Healthy subjects on medication had small increases in systolic blood pressure associated with indoor PM2.5 and outdoor PM10. Heterogeneity analysis found differences among the health groups for associations with particulate air pollution in heart rate but not in blood pressure. CONCLUSION: Modest concentrations of air pollutants were associated with small changes in cardiac function.

Aged↗
PubMed2006

Long-term exposure to urban air pollution and myocardial infarction.

BACKGROUND: Cohort studies have reported increased risks of cardiopulmonary mortality from long-term air pollution exposure, but the evidence is limited and inconclusive. We studied the association between long-term exposure to source-specific air pollution and myocardial infarction (MI) in a case-control study of first-time MI cases and population controls age 45 to 70 years in Stockholm county in 1992 to 1994. METHODS: Home addresses during several decades were combined with historical emission databases and dispersion models to obtain annual mean levels of pollutants from traffic and heating during 30 years for 1397 cases and 1870 controls. Nitrogen dioxide (NO2), carbon monoxide (CO), and particulate matter with an aerodynamic diameter less than 10 microm (PM10) were used as indicators of traffic emissions and sulfur dioxide (SO2) as an indicator of emissions from residential heating. RESULTS: There was no association between long-term average air pollution exposure and overall MI, but an increased risk of fatal MI was suggested, especially for out-of-hospital death. After adjustment for cardiovascular risk factors, the odds ratio for fatal MI associated with a 5th to 95th percentile difference in 30-year average exposure was 1.51 (95% confidence interval = 0.96-2.16) for NO2, 1.22 (0.98-1.52) for CO, 1.39 (0.94-2.07) for PM10, and 1.24 (0.77-2.02) for SO2. For out-of-hospital death, the odds ratio related to NO2 exposure was 2.17 (1.05-4.51). CONCLUSIONS: This study provides some support for an association between long-term air pollution exposure and fatal cardiovascular disease.

Aged↗
PubMed2006

Urban air pollution increases plasma fibrinogen and plasminogen activator inhibitor-1 levels in susceptible patients.

BACKGROUND: The cardiovascular effects on fibrinolytic activity by urban air pollution are still unknown. METHODS: Paired fasting blood samples during high and low air pollution days in Taipei were taken from a panel of 49 patients with coronary heart disease or multiple risk factors to study their fibrinolytic and inflammatory response to urban air pollution. Paired t-tests and mixed-effects models were used to determine the air pollution effects. RESULTS: Patients' plasma plasminogen activator inhibitor-1 levels were significantly increased when hourly concentrations of particulate matter with diameters less than 10 microm (PM10) were greater than 100 microg/m during the period 0800 to 1800 h. CONCLUSION: Urban air pollution has an adverse effect on plasma fibrinolytic function in a susceptible population.

Adult↗
PubMed2005

Asthma, genes, and air pollution.

OBJECTIVE: The objective of this article is to evaluate genetic risks associated with the pulmonary response to air pollutants, including particulates and ozone. METHODS: A comprehensive review of articles related to the genetics of asthma with particular attention to air pollution was conducted through a search of the National Library of Medicine's PubMed database. RESULTS: Asthma, which affects over 15 million people in the United States, is characterized by inflammation leading to reversible airflow obstruction. Triggered by exposure to numerous occupational and environmental agents, asthma has long been considered to occur more frequently in families, with upwards of a 50% higher rate in the offspring of parents with asthma. Asthma genetic studies have used two major methods: mapping techniques that pinpoint gene loci and studies that identify genes and polymorphisms associated with various asthma mechanisms such as inflammatory mediators. The most consistently replicated chromosomal regions associated with asthma have been chromosomes 2q, 5q, 6p, 12 q, and 13q. Because the formation of reactive oxygen species is a major aspect of the inflammatory process of asthma, genetic aberrations associated with antioxidants such as glutathione S-transferase (GST) may shed light on reasons why some people with asthma seem more at risk of exacerbations as a result of air pollution. People with a polymorphism at the GSTP 1 locus, which codes for GST, one of a family of pulmonary antioxidants, have higher rates of asthma. Children in Mexico City with the GSTM1 null genotype demonstrated significant ozone-related decrements in lung function. Animal studies support the key role of antioxidants in reducing the inflammatory response associated with exposure to diesel exhaust particles. CONCLUSIONS: Oxidative stress is a key mechanism underlying the toxic effects of exposure to some types of air pollution. Asthmatics with the null genotype for the antioxidant, GST, seem more at risk of the pulmonary effects of air pollution.

Air Pollution↗
PubMed1986

The changing prevalence of respiratory symptoms in atopic children in response to air pollution.

Following the promotion of anti-air pollution measures in steam power stations using crude oil, atmospheric concentrations of sulphur dioxide, nitrogen dioxide and suspended particulates have declined. These changes in atmospheric concentrations were accompanied by a decline in the prevalence of respiratory symptoms among schoolchildren living near the power stations. In analysing the correlation between air pollutant concentrations and the prevalence of respiratory symptoms, those with positive skin reactions to house dust extract (the positive group) showed a more significant correlation coefficient compared to those who had never had a positive skin reaction (the negative group). In addition, schoolchildren more heavily exposed to air pollutants showed the higher prevalence of respiratory symptoms than the others. With regard to the kind of air pollutants, both sulphur dioxide and nitrogen dioxide were more closely associated with the prevalence of respiratory symptoms than suspended particulates. This study has therefore demonstrated that the positive group is a useful population for monitoring the health effects associated with low-degree air pollution of gaseous agents.

Adolescent↗
PubMed2006

Breast cancer, oestrogens and environmental pollutants: a re-evaluation from a mixture perspective.

The continuing rise in breast cancer incidence rates in almost all Western countries cannot be explained entirely in terms of known risk factors of the disease process. Additional determinants need to be examined, among them exposure to environmental pollutants. With the demonstration that elevated levels of endogenous sex hormones and the use of hormones for the relief of menopausal symptoms are associated with the disease, the oestrogen hypothesis of breast cancer has received further empirical support. This has led to heightened concerns about the possible involvement of oestrogen-like pollutants, such as p,p'-Dichlorodiphenyldichloroethane (DDE). Case-control studies assessing whether women with breast cancer have elevated burdens of p,p'-DDE have produced results not suggestive of a link with cancer risks. However, possible effects of p,p'-DDE and other pollutants cannot be seen in isolation from sex hormones also present in serum. In view of the low potency of p,p'-DDE, and its low levels in serum, it seems unlikely that the chemical on its own will add significantly to the action of sex hormones. However, chemical analyses show that numerous pollutants with oestrogen-like effect profiles can be found in human tissues. Thus, the oestrogen hypothesis of breast cancer should be extended to encompass the multitude of these agents. Viewed from such a perspective, a putative role of organochlorines and other agents in breast cancer should not be dismissed prematurely. Instead, breast cancer epidemiology should face the reality of combined exposures and should take account of recent evidence from in vitro models demonstrating that a large number of oestrogen-like pollutants, all present at low levels, can act together to add to the internal oestrogenic load.

Breast Neoplasms↗
PubMed1997

Epidemiology of pollution-induced airway disease in Japan.

Air pollution has been implicated as one of the factors responsible for the increased incidence of allergic diseases seen over recent years. Epidemiological studies in Japan demonstrate that atopic subjects living in urban areas are more likely to suffer from the effects of air pollution, with increased coughing, sputum production, wheezing and throat irritation. Furthermore, animal studies show that high concentrations of pollutant gases can promote airway sensitization. The incidence of allergic rhinitis and asthma have been shown to be greater in areas where there is heavy traffic and hence high levels of automobile exhaust emissions. Intranasal administration of diesel exhaust particles in mice produces a stimulatory effect on immunoglobulin E production, and a similar finding has also been shown with suspended particulate matter in air. Air pollutants, such as ozone and nitrogen dioxide (NO2), have been shown to stimulate the production of granulocyte-macrophage colony stimulating factor, which may play a vital role in airway hyperreactivity and asthma. In comparative studies of asthma in urban and rural areas, history of airway infection and a younger age of onset were found to be significantly greater in urban areas. When the asthmatic patients were divided into two groups according to environmental NO2 levels (group I: NO2 > 30 ppb; group II: NO2 < 30 ppb), no significant difference regarding the various parameters was noted between the two groups, except for a greater severity of asthma in adults in group I, and a greater severity in children in group II. These studies imply that air pollution may be one reason for the increase in allergic diseases in Japan, but a definitive conclusion cannot be drawn, and further investigation is warranted.

Air Pollutants↗
PubMed2006

Is outdoor air pollution associated with physician visits for allergic rhinitis among the elderly in Toronto, Canada?

BACKGROUND: While a number of studies suggest that air pollution is associated with allergic rhinitis in children, findings among adults have been equivocal. The aim of this study was to examine the relationship between outdoor air pollution and physician visits for allergic rhinitis among individuals>or=65 years of age in Toronto, Canada. METHODS: Physician visits were identified by using data from the Ontario provincial health insurance plan that is made available to all residents. Our analyses are based on 52,691 physician visits for allergic rhinitis among individuals>or=65 years of age in the Toronto metropolitan area between 1995 and 2000. Generalized linear models were used to regress daily counts of physician visits against daily measures of gaseous and particulate components of air pollution after controlling for seasonality, potential confounders (temperature, relative humidity, aeroallergens), overdispersion and serial correlation. RESULTS: A large number of comparisons were undertaken, with most showing no statistically significant associations between daily levels of air pollution and the number of physician visits for rhinitis. In contrast, an interquartile increase in the 10-day average of ragweed particles increased the mean number of daily rhinitis consultations by 6.4% (95% CI=0.7-12.4%). CONCLUSIONS: Our findings suggest that outdoor air pollution is a poor predictor of physician visits for allergic rhinitis among the elderly.

Aged↗
PubMed1995

Impact of pollution and place of residence on atopic diseases among schoolchildren in Telemark County, Norway.

For estimation of the prevalence, degree of severity, and association with outdoor pollution, a questionnaire on asthma and other atopic diseases was distributed to the parents of 4666 7-13-year-olds, comprising all the children in 36 schools in Telemark County, Norway, including 37% of the schoolchildren in the county. The response rate was 94%. In a validity study employing clinical evaluations, the questionnaire-based diagnosis of asthma was found to have a sensitivity of 0.96 and a specificity of 0.88. The lifetime prevalence of asthma in Telemark was 9% (boys 11.3%, girls 6.6%; p < 0.001). There was no significant difference in the lifetime prevalence of asthma by pollution zone; 8.3% in heavily, 9.3% in moderately, and 9.2% in minimally polluted zones. The asthma prevalence was significantly higher (14.2%; p < 0.05) among boys in the coastal area of the county than in the mountainous area (8.9%). Both of these areas were in the minimal pollution zone. Of asthma cases, 67% were categorized as mild, 29% as moderate, and 4% as severe. The lifetime prevalence was 17.8% (boys 21.3%, girls 14.2%; p < 0.001) for allergic rhinitis, 13.2% (boys 11.4%, girls 15.2%; p < 0.001) for atopic eczema, and 29.6% (boys 31.7%, girls 27.4%; p < 0.01) for overall atopic disease (asthma, allergic rhinitis, eczema). These findings are not compatible with the hypothesis that outdoor pollution is associated with the lifetime prevalence of asthma in school-age children. The results also show that less than 0.5% of schoolchildren suffer from severe asthma.

Adolescent↗
PubMed1993

Psychological testing on schoolchildren before and after pollution of drinking water in North Cornwall.

The tap water supply in Camelford, North Cornwall and environs was contaminated by aluminium and other metals in 1988. Richmond tests were routinely given before and after the pollution and here scores are compared between 39 children from schools in the contaminated area and 64 children from Cornish schools outside the polluted area. The study was retrospective and it was not possible to determine whether or how much polluted water individuals had consumed. No differences were found between groups either before or after the pollution accident nor was there any evidence for any sub-group of the polluted group which had been affected. The limits of conclusions which can be drawn from data available are discussed.

Alum Compounds↗
PubMed2005

Ambient air pollution and acute myocardial infarction.

This review summarizes the nature of ambient air pollutants, which are either gaseous or particulate of various sizes, the latter determining their penetration into the body, the smallest even translocating from the lung into the systemic circulation. It presents the epidemiological evidence linking air pollution to overall mortality, cardiovascular mortality and myocardial infarction, making the distinction between acute and chronic exposure to the pollutants. It reviews mechanistic investigations that have evaluated the links among exposure to pollutants, thrombosis, pulmonary inflammation, arterial vasoconstriction and heart rate variability. It concludes by attempting to integrate current epidemiological and mechanistic observations into a pathophysiological framework that links ambient air pollution to acute myocardial infarction and cardiovascular mortality.

Air Pollution↗
PubMed1996

Industry response to SARA Title III: pollution prevention, risk reduction, and risk communication.

This paper reports results from a survey designed to: (1) evaluate changes in industrial pollution prevention practices since the passage of the landmark environmental legislation, the Emergency Planning and Community Right-to-Know Act of 1986, also known as SARA Title III, and (2) identify those factors that may contribute to an industrial facility engaging in pollution prevention and risk communication activities. The survey was conducted under a Cooperative Agreement between the U.S. Environmental Protection Agency and the Columbia University Center for Risk Communication. Evidence from the survey indicates that a wide variety of waste and pollution reduction activities have been undertaken since passage of the Act. Virtually all facilities surveyed in the pulp and paper, chemical, and petroleum and refining industries reported that they had reduced pollutants or wastes on at least one of ten measures, including reducing toxic air emissions. Most facilities indicated paying more attention to pollution prevention activities as a result of SARA Title III and half reported that their communication activities have also increased.

Communication↗
PubMed1992

Immune responses to pollutant mixtures from indoor sources.

Indoor air pollution occurs as an undesirable consequence of urbanization, energy conservation, indoor bioaerosol contamination, and use of synthetic materials and new technologies, and has become a worldwide concern. It is important to comprehend not only the diversity of pollutant hazards but also to develop novel methods and approaches that establish dose-response relationships, cause-and-effect relationships, and clinical relevance. Coincident with heightened public concern over indoor air pollution and its health consequences, a revolution in immunology has occurred. The immune system is recognized as an essential defensive and homeostatic mechanism. Unfortunately, the immune apparatus is exquisitely sensitive to toxic damage. Equally important, among the disciplines available to assess the health impact of indoor air pollutants, immunology has the capability to provide sensitive and specific tools that may accurately measure relevant clinical effects at tissue, cellular, and molecular levels. Furthermore, exciting new insights into shared communications networks between the immune, endocrine, and central nervous systems may provide future explanations for the myriad human complaints associated with indoor air pollutants.

Air Pollution, Indoor↗
PubMed2002

The role of sea spray in cleansing air pollution over ocean via cloud processes.

Particulate air pollution has been shown to strongly suppress precipitation from convective clouds over land. New observations show that precipitation from similar polluted clouds over oceans is much less affected, because large sea salt nuclei override the precipitation suppression effect of the large number of small pollution nuclei. Raindrops initiated by the sea salt grow by collecting small cloud droplets that form on the pollution particles, thereby cleansing the air. Therefore, sea salt helps cleanse the atmosphere of the air pollution via cloud processes. This implies that over oceans, the climatic aerosol indirect effects are significantly smaller than current estimates.

Air Pollution↗
PubMed2006

Mixed pollutant degradation by Methylosinus trichosporium OB3b expressing either soluble or particulate methane monooxygenase: can the tortoise beat the hare?

Methanotrophs have been widely investigated for in situ bioremediation due to their ubiquity and their ability to degrade halogenated hydrocarbons through the activity of methane monooxygenase (MMO). It has been speculated that cells expressing the soluble form of MMO (sMMO) are more efficient in cleaning up sites polluted with halogenated hydrocarbons due to its broader substrate range and relatively fast degradation rates compared cells expressing the other form of MMO, the particulate MMO (pMMO). To examine this issue, the biodegradation of mixtures of chlorinated solvents, i.e., trichloroethylene (TCE), trans-dichloroethylene (t-DCE), and vinyl chloride (VC), by Methylosinus trichosporium OB3b in the presence of methane using either form of MMO was investigated over longer time frames than those commonly used, i.e., days instead of hours. Growth of M. trichosporium OB3b along with pollutant degradation were monitored and analyzed using a simple comparative model developed from the Omega model created for analysis of the competitive binding of oxygen and carbon dioxide by ribulose bisphosphate carboxylase. From these findings, it appears that at concentrations of VC, t-DCE, and TCE greater than 10 microM each, methanotrophs expressing pMMO have a competitive advantage over cells expressing sMMO due to higher growth rates. Despite such an apparent growth advantage, pMMO-expressing cells degraded less of these substrates at these concentrations than sMMO-expressing cells during active growth. If the concentrations were increased to 100 muM, however, not only did pMMO-expressing cells grow faster, they degraded more of these pollutants and did so in a shorter amount of time. These findings suggest that the relative rates of growth substrate and pollutant degradation are important factors in determining which form of MMO should be considered for pollutant degradation.

Biodegradation, Environmental↗
PubMed1982

Distribution of bacterial plasmids in clean and polluted sites in a South Wales river.

We isolated 400 aerobic heterotrophic bacteria from the sediment of unpolluted and polluted sites in a fast-flowing south Wales river. Isolates were subjected to taxonomic tests and screened for the presence of plasmid DNA by alkaline lysis and agarose gel techniques. There were no significant differences between sites in either the total percentage of isolates containing plasmids (unpolluted site, 9.4%; polluted site, 15%) or in the percentage of non-Pseudomonas-like isolates containing plasmids (unpolluted site, 15%; polluted site, 10%). There were significantly more Pseudomonas-like isolates with plasmids at the polluted site than at the unpolluted site (unpolluted site, 7%; polluted site, 18%). This presumably reflected a response of the nutritionally versatile Pseudomonas-like isolates to conditions at that site. The majority (86%) of the plasmids detected had molecular masses between 35 and 312 megadaltons. These plasmids were large enough to carry genes for conjugal transfer, suggesting the possibility of such transfer in this environment.

Bacteria↗
PubMed2004

A previously unexposed forest soil microbial community degrades high levels of the pollutant 2,4,6-trichlorophenol.

2,4,6-trichlorophenol (2,4,6-TCP) is a hazardous pollutant that is efficiently degraded by some aerobic soil bacterial isolates under laboratory conditions. The degradation of this pollutant in soils and its effect on the soil microbial community are poorly understood. We report here the ability of a previously unexposed forest soil microbiota to degrade high levels of 2,4,6-TCP and describe the changes in the soil microbial community found by terminal restriction fragment length polymorphism (T-RFLP) analysis. After 30 days of incubation, about 50% degradation of this pollutant was observed in soils amended with 50 to 5,000 ppm of 2,4,6-TCP. The T-RFLP analysis showed that the soil bacterial community was essentially unchanged after exposure to up to 500 ppm of 2,4,6-TCP. However, a significant decrease in richness was found with 2,000 and 5,000 ppm of 2,4,6-TCP, even though the removal of this pollutant remained high. The introduction of Ralstonia eutropha JMP134 or R. eutropha MS1, two efficient 2,4,6-TCP degraders, to this soil did not improve degradation of this pollutant, supporting the significant bioremediation potential of this previously unexposed, endogenous forest soil microbial community.

Bacteria↗
PubMed2006

Air pollution and cardiovascular admissions association in Spain: results within the EMECAS project.

OBJECTIVE: To evaluate the short term effect of air pollution on cardiovascular admissions in 14 Spanish cities METHODS: The period under study was from 1995 to 1999. Daily emergency admissions for all cardiovascular diseases (CVD) and heart diseases (HD) were obtained from hospital records, and the corresponding daily levels of particulates, SO2, NO2, CO, and ozone were recorded. The magnitude of association was estimated using Poisson generalised additive models controlling for confounding and overdispersion. For each cause, lagged effects, up to three days, of each pollutant were examined and combined estimates were obtained. For ozone the analyses were restricted to the warm period. One and two pollutant models were performed. RESULTS: Associations were more consistent in lag 0 (concurrent day) and 1 (lag 0-1), except in the case of ozone where there was a more delayed relation (lag 2-3). For combined estimates an increase of 10 microg/m3 in the PM10 levels in lag 0-1 was associated with an increase of 0.9% (95% CI: 0.4 to 1.5%) in the number of hospital admissions for CVD, and 1.6% (0.8 to 2.3%) for HD. For ozone the corresponding estimates for lag 2-3 were 0.7% (0.3 to 1.0) for CVD, and 0.7% (0.1 to 1.2) for HD. An increase of 1 mg/m3 in CO levels was associated with an increase of 2.1% (0.7 to 3.5%) in CVD admissions, and 4.2% (1.3 to 7.1%) in HD admissions. SO2 and NO2 estimates were more sensitive in two pollutant models CONCLUSIONS: A short term association between increases in daily levels of air pollutants and the number of daily admissions for cardiovascular diseases, with specificity for heart diseases, has been described in Spanish cities.

Aged↗