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PubMed2001

Assessment of deaths attributable to air pollution: should we use risk estimates based on time series or on cohort studies?

Epidemiologic studies are crucial to the estimation of numbers of deaths attributable to air pollution. In this paper, the authors present a framework for distinguishing estimates of attributable cases based on time-series studies from those based on cohort studies, the latter being 5-10 times larger. The authors distinguish four categories of death associated with air pollution: A) air pollution increases both the risk of underlying diseases leading to frailty and the short term risk of death among the frail; B) air pollution increases the risk of chronic diseases leading to frailty but is unrelated to timing of death; C) air pollution is unrelated to risk of chronic diseases but short term exposure increases mortality among persons who are frail; and D) neither underlying chronic disease nor the event of death is related to air pollution exposure. Time-series approaches capture deaths from categories A and C, whereas cohort studies assess cases from categories A, B, and C. In addition, years of life lost can only be derived from cohort studies, where time to death is the outcome, while in time-series studies, death is a once-only event (no dimension in time). The authors conclude that time-series analyses underestimate cases of death attributable to air pollution and that assessment of the impact of air pollution on mortality should be based on cohort studies.

Air Pollutants↗
PubMed2005

Years of life lost attributable to air pollution in Switzerland: dynamic exposure-response model.

BACKGROUND: There is debate on how the effect of air pollution should be assessed. We propose an approach to estimate its impact on adult and infant mortality that integrates data from long-term epidemiological studies and studies of interventions to reduce pollution. We use the method to estimate the number of years of life lost (YLLs) attributable to air pollution during 1 year in Switzerland. METHODS: A dynamic exposure-response model was implemented, which uses an exponential function (exp(-kt)) to model the change in mortality after cessation of air pollution. The model was populated with relative risk estimates and estimates of time constant k from the literature. Air pollution exposure in Switzerland was modelled using data from emission inventories. YLLs attributable to air pollution were calculated by taking the difference between observed survival probabilities in Switzerland in 2000 and modified survival probabilities, assuming no air pollution during the year 2000. RESULTS: Meta-analyses of three studies of adult mortality and five studies of infant mortality gave relative risks of 1.059 (95% confidence interval (CI) 1.031-1.088) and 1.056 (95% CI 1.026-1.088) per 10 mug/m(3) increase in PM10 concentration. Time constants k derived from two studies of the effects of the closing down of a steel mill in the Utah Valley and of the coal ban in Dublin were 0.88 and 0.11. Assuming a time constant k of 0.5 resulted in 42 400 (95% CI 22 600-63 600) YLLs, with 4.0% being ascribed to infant deaths. A total of 39% of the effect occurred in the same year and 80% within 5 years. The estimated number of YLLs was little affected by the choice of the time constant. CONCLUSIONS: In contrast to traditional steady-state models the dynamic model allows changes in mortality following short-term increases or decreases in air pollution levels to be quantified. This type of information is of obvious interest to policy makers.

Adult↗
PubMed2005

Air pollution and the heart.

Despite legislation, leading to dramatic decreases in levels of air pollution since the time of the great smogs, a large body of epidemiological evidence has demonstrated that pollution continues to have adverse effects on human health. One striking finding from the epidemiological data is that patients with cardiovascular disease are susceptible to acute rises in ambient pollutants. Mortality and hospital admissions for myocardial infarction, congestive cardiac failure and cardiac arrhythmia all increase with a rise in the concentration of both particulate and gaseous pollutants. Before concluding that this association is a causal one, plausible pathophysiological mechanisms are required. Evidence is accumulating in support of two mechanistic hypotheses: inhalation of pollutants might provoke a local inflammatory response with the consequent release into the circulation of pro-thrombotic and inflammatory cytokines. A systemic response of this nature would put individuals with coronary atheroma at increased risk of cardiac events; exposure to pollutants may have an adverse effect on cardiac autonomic control, leading to an increased risk of arrhythmia in susceptible patients. Clarification of the pollutants involved and the precise mechanisms of action is essential in designing measures by which susceptible individuals might be protected from the adverse cardiovascular effects of air pollution.

Air Pollution↗
PubMed1981

Seasonal relationship of sudden infant death syndrome and environmental pollutants.

Evidence that chronic hypoxia precedes death from sudden infant death syndrome (SIDS) is mounting. Prolonged exposure to moderate levels of pollutants could be a contributing factor to hypoxia. Levels of carbon monoxide (CO), sulphur dioxide (SO2), nitrogen dioxide (NO2) and hydrocarbons (HC) are highest in the winter when incidence of SIDS is increased. SIDS cases in Los Angeles County were correlated with daily mean levels of these pollutants, temperature, barometric pressure and monthly lead levels with the aid of time series analyses. Peaks in CO, SO2, NO2, HC and lead preceded the seasonal increase in SIDS by seven weeks. Theoretical considerations, such as the hypoxia-inducing effects of CO, support the hypothesis that this temporal relation has functional significance. Three additional findings provided evidence for this hypothesis: 1) SIDS infants born during months of low pollution lived longer than those born during months of high pollution. 2) SIDS infants born in a district with low pollution lived longer than those born in a district with high pollution. 3) The bimonthly rate of SIDS was directly proportional to the level of CO pollution to which the infants had been exposed between conception and two months of age. The role of pollution levels as a predisposing factor in risk for SIDS cannot be summarily dismissed.

Air Pollutants↗
PubMed2006

Effects of exposure to air pollution on blood coagulation.

BACKGROUND: Consistent evidence has indicated that air pollution increases the risk of cardiovascular diseases. The underlying mechanisms linking air pollutants to increased cardiovascular risk are unclear. OBJECTIVES: We investigated the association between the pollution levels and changes in such global coagulation tests as the prothrombin time (PT) and the activated partial thromboplastin time (APTT) in 1218 normal subjects from the Lombardia Region, Italy. Plasma fibrinogen and naturally occurring anticoagulant proteins were also evaluated. METHODS: Hourly concentrations of particulate (PM10) and gaseous pollutants (CO, NO2, SO2, and O3) were obtained from 53 monitoring sites covering the study area. Generalized additive models were applied to compute standardized regression coefficients controlled for age, gender, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends. RESULTS: The PT became shorter with higher ambient air concentrations at the time of the study of PM10 (coefficient = -0.06; P < 0.05), CO (coefficient = -0.11; P < 0.001) and NO2 (coefficient =-0.06; P < 0.05). In the 30 days before blood sampling, the PT was also negatively associated with the average PM(10) (coefficient = -0.08; P < 0.05) and NO2 (coefficient = -0.08; P < 0.05). No association was found between the APTT and air pollutant levels. In addition, no consistent relations with air pollution were found for fibrinogen, antithrombin, protein C and protein S. CONCLUSIONS: This investigation shows that air pollution is associated with changes in the global coagulation function, suggesting a tendency towards hypercoagulability after short-term exposure to air pollution. Whether these changes contribute to trigger cardiovascular events remains to be established.

Adolescent↗
PubMed1994

Air pollution and asthma.

The role of air pollution in the increased prevalence and morbidity of asthma has been widely debated, but results to date indicate that the normally encountered levels of air pollution are unlikely to contribute to a worsening of asthma. When the levels of sulphur dioxide (SO2) are exceptionally high it is possible that asthmatic patients may have increased symptoms after exertion, since this irritant gas acts as a trigger to bronchoconstriction. There is also evidence that suspended particles may also act as an inciter of asthma symptoms when concentrations are high. Experimentally, ozone in high concentrations may increase airway responsiveness in both normal and asthmatic subjects by inducing airway inflammation, but asthmatic individuals show the same responses as normal subjects and there is little or no evidence to link increases in ambient ozone with an increase in asthma. There is little evidence that nitrogen dioxide (NO2), even at the peak levels recorded, has any significant effect on airway function in normal or asthmatic individuals. Other air pollutants which are present in lower concentrations have not been studied as extensively, but there is no convincing evidence that they cause significant respiratory symptoms in asthmatic patients. It is still possible that combinations of air pollutants may have greater effects on airway function than exposure to a single pollutant, although there is little evidence to support this. Epidemiological evidence provides little support for the idea that atmospheric pollution levels are related to the frequency of asthma symptoms or the frequency of attacks. More importantly, there is no evidence that asthma prevalence or aetiology is related to the level of air pollution. A review of currently available information therefore provides little evidence for the widely expressed view that atmospheric pollution is related to increased prevalence or morbidity of asthma or is related to the causation of asthma.

Adult↗
PubMed1995

Effects of air pollution on symptoms and peak expiratory flow measurements in subjects with obstructive airways disease.

BACKGROUND: Evidence from laboratory studies suggests that air pollution can produce bronchoconstriction and respiratory symptoms in selected subjects, but the relevance of these findings to exposure to natural pollution is unclear. This study was performed to determine whether air pollution at typical levels found in the UK has demonstrable effects on respiratory function and symptoms in subjects with airways disease. METHODS: Seventy five adult patients with diagnoses of asthma or chronic obstructive pulmonary disease (COPD) were studied for a period of four weeks during which they kept records of their peak expiratory flow (PEF) rates, symptoms (wheeze, dyspnoea, cough, throat and eye irritation), and bronchodilator use. Thirty six patients in whom the provocative dose of methacholine causing a 20% fall in FEV1 was below 12.25 mumol were classified as reactors. Ambient air pollution was measured with absorption spectroscopy. RESULTS: There were modest but significant increases in PEF variability, bronchodilator use, and wheeze with increasing sulphur dioxide levels; bronchodilator use, dyspnoea, eye irritation, and minimum PEF readings were related to ozone levels. In the subgroup of reactors falls in mean and minimum peak flow and increases in wheeze, dyspnoea, and bronchodilator use were associated with increases in levels of both sulphur dioxide and ozone. Some associations were seen with pollution levels on the same day, but for others the pollution effects appeared to be delayed by 24 or 48 hours. Pollution levels did not breach the WHO guide levels during the course of the study. CONCLUSIONS: Increases in environmental levels of ozone and sulphur dioxide are associated with adverse changes in peak flow measurements and both ocular and respiratory symptoms in subjects with obstructive airways disease. Although the peak flow and symptom changes were modest, they occurred at pollution levels below current WHO guide levels.

Adult↗
PubMed1998

Air pollution, pollens, and daily admissions for asthma in London 1987-92.

BACKGROUND: A study was undertaken to investigate the relationship between daily hospital admissions for asthma and air pollution in London in 1987-92 and the possible confounding and modifying effects of airborne pollen. METHODS: For all ages together and the age groups 0-14, 15-64 and 65+ years, Poisson regression was used to estimate the relative risk of daily asthma admissions associated with changes in ozone, sulphur dioxide, nitrogen dioxide and particles (black smoke), controlling for time trends, seasonal factors, calendar effects, influenza epidemics, temperature, humidity, and autocorrelation. Independent effects of individual pollutants and interactions with aeroallergens were explored using two pollutant models and models including pollen counts (grass, oak and birch). RESULTS: In all-year analyses ozone was significantly associated with admissions in the 15-64 age group (10 ppb eight hour ozone, 3.93% increase), nitrogen dioxide in the 0-14 and 65+ age groups (10 ppb 24 hour nitrogen dioxide, 1.25% and 2.96%, respectively), sulphur dioxide in the 0-14 age group (10 micrograms/m3 24 hour sulphur dioxide, 1.64%), and black smoke in the 65% age group (10 micrograms/m3 black smoke, 5.60%). Significant seasonal differences were observed for ozone in the 0-14 and 15-64 age groups, and in the 0-14 age group there were negative associations with ozone in the cool season. In general, cumulative lags of up to three days tended to show stronger and more significant effects than single day lags. In two-pollutant models these associations were most robust for ozone and least for nitrogen dioxide. There was no evidence that the associations with air pollutants were due to confounding by any of the pollens, and little evidence of an interaction between pollens and pollution except for synergism of sulphur dioxide and grass pollen in children (p < 0.01). CONCLUSIONS: Ozone, sulphur dioxide, nitrogen dioxide, and particles were all found to have significant associations with daily hospital admissions for asthma, but there was a lack of consistency across the age groups in the specific pollutant. These associations were not explained by confounding by airborne pollens nor was there convincing evidence that the effects of air pollutants and airborne pollens interact in causing hospital admissions for asthma.

Adolescent↗
PubMedDate not supplied

Lung function and methacholine responsiveness among adolescents in an air-polluted area.

BACKGROUND: Outdoor air pollution is hazardous to human pulmonary health. Airway inflammation is an important cause of bronchial hyperresponsiveness. Information is not univocal about the potential effects of prolonged exposure to environmental air pollutants on lung function. OBJECTIVES: A cross-sectional study was performed to assess bronchial responsiveness to methacholine in children living in an air-polluted area. Afterwards, the same study protocol was repeated in children of similar age living in mountain valleys with virtually no air pollution. METHODS: Every child underwent a lung function test, skin tests to common allergens, total serum levels of IgE, and a challenge to methacholine at increasing doses (PD20 FEV1). Subjects were 246 children 11-12 years old living in an air-polluted area, and 285 children 11-13 years old living in mountain valleys. Respectively, 156 and 161 were negative to skin tests and had serum total IgE<100 IU/ml, and had no asthma or other recurrent or ongoing respiratory symptoms. RESULTS: Lung function data, adjusted for the effect of potential confounders showed significantly lower FVC, and even more so FEV1, in the children from the polluted area. After the exclusion of subjects with positive skin tests and serum total IgE>100 IU/ml and those with history of asthma or respiratory disorders, there were higher percentages of positive responses in the challenge to methacholine in children from the polluted area (28.9 vs. 15.5%, p<0.001). CONCLUSIONS: These data may corroborate the possible importance of long exposure to air pollutants on the prevalence of bronchial aspecific hyperresponsiveness in otherwise normal children.

Adolescent↗
PubMed2002

The public health relevance of air pollution abatement.

Assuming a causal relationship between current levels of air pollution and morbidity/mortality, it is crucial to estimate the public health relevance of the problem. The derivation of air pollution attributable cases faces inherent uncertainties and requires influential assumptions. Based on the results of the trinational impact assessment study of Austria, France, and Switzerland, where prudent estimates of the air pollution attributable cases (mortality, chronic bronchitis incidence, hospital admissions, acute bronchitis among children, restricted activity days, asthma attacks) have been made, influential uncertainties are quantified in this review. The public health impact of smoking, environmental tobacco smoke, and air pollution on the prevalence of chronic cough/phlegm are outlined. Despite all methodological caveats, impact assessment studies clearly suggest that public health largely benefits from better air quality. The studies are selective underestimates as they are strongly driven by mortality, but do not include full quantification of the impact on morbidity and their consequences on quality of life among the diseased and the caregivers. Air pollution abatement strategies are usually political in nature, targeting at polities, regulation and technology in mobile or stationary sources rather than at individuals. It is of note that key clean air strategies converge into abatement of climate change. In general, energy consumption is very closely related to both air pollution and greenhouse gases. The dominant causes of both problems are the excessive and inefficient combustion of fossil fuel. Thus, for many policy options, the benefit of air pollution abatement will go far beyond what prudent health-impact assessments may derive. From a climate change and air pollution perspective, improved energy efficiency and a strong and decisive departure from the "fossil fuel" combustion society is a science-based must. Health professionals must raise their voices in the political decision process to give strong support for clean air policies, both on a national and international level.

Air Pollution↗
PubMed2003

Air pollution and case fatality of SARS in the People's Republic of China: an ecologic study.

BACKGROUND: Severe acute respiratory syndrome (SARS) has claimed 349 lives with 5,327 probable cases reported in mainland China since November 2002. SARS case fatality has varied across geographical areas, which might be partially explained by air pollution level. METHODS: Publicly accessible data on SARS morbidity and mortality were utilized in the data analysis. Air pollution was evaluated by air pollution index (API) derived from the concentrations of particulate matter, sulfur dioxide, nitrogen dioxide, carbon monoxide and ground-level ozone. Ecologic analysis was conducted to explore the association and correlation between air pollution and SARS case fatality via model fitting. Partially ecologic studies were performed to assess the effects of long-term and short-term exposures on the risk of dying from SARS. RESULTS: Ecologic analysis conducted among 5 regions with 100 or more SARS cases showed that case fatality rate increased with the increment of API (case fatality = - 0.063 + 0.001 * API). Partially ecologic study based on short-term exposure demonstrated that SARS patients from regions with moderate APIs had an 84% increased risk of dying from SARS compared to those from regions with low APIs (RR = 1.84, 95% CI: 1.41-2.40). Similarly, SARS patients from regions with high APIs were twice as likely to die from SARS compared to those from regions with low APIs. (RR = 2.18, 95% CI: 1.31-3.65). Partially ecologic analysis based on long-term exposure to ambient air pollution showed the similar association. CONCLUSION: Our studies demonstrated a positive association between air pollution and SARS case fatality in Chinese population by utilizing publicly accessible data on SARS statistics and air pollution indices. Although ecologic fallacy and uncontrolled confounding effect might have biased the results, the possibility of a detrimental effect of air pollution on the prognosis of SARS patients deserves further investigation.

Air Pollutants↗
PubMed2002

Effects of air pollutants on acute stroke mortality.

The relationship between stroke and air pollution has not been adequately studied. We conducted a time-series study to examine the evidence of an association between air pollutants and stroke over 4 years (January 1995-December 1998) in Seoul, Korea. We used a generalized additive model to regress daily stroke death counts for each pollutant, controlling for seasonal and long-term trends and meteorologic influences, such as temperature, relative humidity, and barometric pressure. We observed an estimated increase of 1.5% [95% confidence interval (CI), 1.3-1.8%] and 2.9% (95% CI, 0.3-5.5%) in stroke mortality for each interquartile range increase in particulate matter < 10 microm aerodynamic diameter (PM(10)) and ozone concentrations in the same day. Stroke mortality also increased 3.1% (95% CI, 1.1-5.1%) for nitrogen dioxide, 2.9% (95% CI, 0.8-5.0%) for sulfur dioxide, and 4.1% (95% CI, 1.1-7.2%) for carbon monoxide in a 2-day lag for each interquartile range increase in single-pollutant models. When we examined the associations among PM(10) levels stratified by the level of gaseous pollutants and vice versa, we found that these pollutants are interactive with respect to their effects on the risk of stroke mortality. We also observed that the effects of PM(10) on stroke mortality differ significantly in subgroups by age and sex. We conclude that PM(10) and gaseous pollutants are significant risk factors for acute stroke death and that the elderly and women are more susceptible to the effect of particulate pollutants.

Adolescent↗
PubMed2000

Long-term health effects of particulate and other ambient air pollution: research can progress faster if we want it to.

There is need for the assessment of long-term effects of outdoor air pollution. In fact, a considerable part of the large amount of U.S. research money that has been dedicated to investigate effects of ambient particulate pollution should be invested to address long-term effects. Studies that follow the health status of large numbers of subjects across long periods of time (i.e., cohort studies) should be considered the key research approach to address these questions. However, these studies are time consuming and expensive. We propose efficient strategies to address these questions in less time. Apart from long-term continuation of the few ongoing air pollution cohort studies in the United States, data from large cohorts that were established decades ago may be efficiently used to assess cardiorespiratory effects and to target research on detection of the most susceptible subgroups in the population, which may be related to genetic, molecular, behavioral, societal, and/or environmental factors. This approach will be efficient only if the available air pollution monitoring data will be used to spatially model long-term outdoor pollution concentrations across a given country for each year with available pollution data. Such concentration maps will allow researchers to impute outdoor air pollution levels at any residential location, independent of the location of monitors. Exposure imputation may be based on residential location(s) of participants in long-standing cardiorespiratory cohort studies, which can be matched to pollutant levels using geographic information systems. As shown in European impact assessment studies, such maps may be derived relatively quickly.

Air Pollutants↗
PubMed2003

Asthma symptoms in Hispanic children and daily ambient exposures to toxic and criteria air pollutants.

Although acute adverse effects on asthma have been frequently found for the U.S. Environmental Protection Agency's principal criteria air pollutants, there is little epidemiologic information on specific hydrocarbons from toxic emission sources. We conducted a panel study of 22 Hispanic children with asthma who were 10-16 years old and living in a Los Angeles community with high traffic density. Subjects filled out symptom diaries daily for up to 3 months (November 1999 through January 2000). Pollutants included ambient hourly values of ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide and 24-hr values of volatile organic compounds (VOCs), particulate matter with aerodynamic diameter < 10 microm (PM10, and elemental carbon (EC) and organic carbon (OC) PM10 fractions. Asthma symptom severity was regressed on pollutants using generalized estimating equations, and peak expiratory flow (PEF) was regressed on pollutants using mixed models. We found positive associations of symptoms with criteria air pollutants (O3, NO2, SO2, PM10), EC-OC, and VOCs (benzene, ethylbenzene, formaldehyde, acetaldehyde, acetone, 1,3-butadiene, tetrachloroethylene, toluene, m,p-xylene, and o-xylene). Selected adjusted odds ratios for bothersome or more severe asthma symptoms from interquartile range increases in pollutants were, for 1.4 ppb 8-hr NO2, 1.27 [95% confidence interval (CI), 1.05-1.54]; 1.00 ppb benzene, 1.23 (95% CI, 1.02-1.48); 3.16 ppb formaldehyde, 1.37 (95% CI, 1.04-1.80); 37 microg/m3 PM10, 1.45 (95% CI, 1.11-1.90); 2.91 microg/m3 EC, 1.85 (95% CI, 1.11-3.08); and 4.64 microg/m3 OC, 1.88 (95% CI, 1.12-3.17). Two-pollutant models of EC or OC with PM10 showed little change in odds ratios for EC (to 1.83) or OC (to 1.89), but PM10 decreased from 1.45 to 1.0. There were no significant associations with PEF. Findings support the view that air toxins in the pollutant mix from traffic and industrial sources may have adverse effects on asthma in children.

Adolescent↗
PubMed1978

Plants as bioassay systems for monitoring atmospheric pollutants.

Plant species act as natural bioindicators of atmospheric pollutants. Plants can be used as bioassay systems for monitoring atmospheric pollutants. Plant injury symptoms, altered growth and reproductive pattern, changes in yield and/or productivity, and changes in species distribution can be used singly or in combination as monitoring devices. The results must be accepted as semiquantitative, but within that constraint, air quality can be sufficiently well defined to enable the setting of air quality standards. Genetic variability of higher plant species has yielded cultivars which display a range of tolerance to gaseous and particulate atmospheric pollutants. Asexual propagation of these cultivars provides pollutant-sensitive and pollutant-tolerant plant material which can be grown on selected sites for observation. Gymnosperm and Angiosperm species as well as species of lichens and mosses have been used to establish field monitoring networks in Europe, Canada, and the United States. White pine, shade tobacco, mosses, and lichens have proven particularly useful as bioassay tools. Pollen from pollutant-sensitive and pollutant-tolerant plant cultivars has also been used as a sensitive laboratory bioassay tool for studying air quality. Epiphytic mosses are particularly efficient as monitors of particulate pollutants, especially heavy metals, some of which may act as chemical mutagens. The cost, complexity, and lack of reliability of instrumented systems for air quality monitoring make imperative the need to develop successful plant bioassay systems for monitoring air quality.

Air Pollutants↗
PubMed2006

[Effects of air pollution on children's health in a city in Southeastern Brazil].

OBJECTIVE: Of the effects of air pollution on children's health, increased pneumonia admission rate is one of the most important. The study aimed at estimating the association between pneumonia admissions and increased air pollutants. METHODS: An ecological time-series study was carried out in the municipality of São José dos Campos, Southeastern Brazil, in the years 2000 and 2001. Daily records of pneumonia admissions, air pollutants (SO2, O3, and PM10) and weather conditions (temperature and humidity) were analyzed. The correlations between the study variables were estimated using Pearson's correlation. The associations between pneumonia and air pollutants were estimated using generalized additive Poisson regression models. The percentage increase (and their respective 95% CI) in pneumonia admission rate was estimated for the interquartile range of each air pollutant studied. RESULTS: The three pollutants analyzed presented lagged effects on pneumonia admission rate, beginning at lag 3 or 4 and lasting for no more than two days. The 8-day cumulative effect estimate showed that an increase of 24.7 mg/m3 in PM10 concentration increased pneumonia admission rate in 9.8%. CONCLUSIONS: The study corroborates that adverse health effects of air pollutants can be observed even in medium-sized cities. The magnitude of the effect was similar to that found in the city of São Paulo. Moreover, children are highly susceptible to air pollution exposure.

Air Pollution↗
PubMed2004

Air pollution and neonatal deaths in São Paulo, Brazil.

Air pollution has been associated with health effects on different age groups. The present study was designed to assess the impact of daily changes in air pollutants (NO2, SO2, CO, O3, and particle matter (PM10)) on total number of daily neonatal deaths (those that occur between the first and the 28th days of life) in São Paulo, from January 1998 to December 2000, since adverse outcomes such as neonatal deaths associated with air pollution in Brazil have not been evaluated before. Generalized additive Poisson regression models were used and nonparametric smooth functions (loess) were adopted to control long-term trend, temperature, humidity, and short-term trends. A linear term was used for holidays. The association between air pollutants and neonatal deaths showed a short time lag. Interquartile range increases in PM10 (23.3 microg/m(3)) and SO2 (9.2 microg/m(3)) were associated with increases of 4% (95% CI, 2-6) and 6% (95% CI, 4-8), respectively. Instead of adopting a two-pollutant model we created an index to represent PM10 and SO2 effects. For an interquartile range increase in the index an increase of 6.3% (95% CI, 6.1-6.5) in neonatal deaths was observed. These results agree with previous studies performed by our group showing the deleterious effects of air pollutants during the perinatal period. The method reported here represents an alternative approach to analyze the relationship between highly correlated pollutants and public health problems, reinforcing the idea of the synergic effects of air pollutants in public health.

Air Pollutants↗
PubMed2005

Effects of environmental pollution on microsatellite DNA diversity in wood mouse (Apodemus sylvaticus) populations.

Ten microsatellite DNA loci were surveyed to investigate the effects of heavy metal pollution on the genetic diversity and population genetic structure of seven wood mouse (Apodemus sylvaticus) populations along a heavy metal pollution gradient away from a nonferrous smelter in the south of Antwerp (Flanders, Belgium). Analysis of soil heavy metal concentrations showed that soil Ag, As, Cd, Cu, and Pb decreased with increasing distance from the smelter. Genetic analyses revealed high levels of genetic variation in all populations, but populations from the most polluted sites in the gradient did not differ from those of less-polluted sites in terms of mean observed and expected heterozygosity level and mean allelic richness. No correlation was found between measures of genetic diversity and the degree of heavy metal pollution. However, an analysis of molecular variance and a neighbor-joining tree suggested a contamination-related pattern of genetic structuring between the most polluted and less polluted sites. Pairwise F(ST) values indicated that populations were significantly genetically differentiated, and assignment tests and direct estimates of recent migration rates suggested restricted gene flow among populations. Additionally, genetic differentiation increased significantly with geographical distance, which is consistent with an isolation-by-distance model. We conclude that, at least for our microsatellite DNA markers, genetic diversity in the studied wood mouse populations is not affected greatly by the heavy metal pollution.

Alleles↗