Athletic performance and urban air pollution.

Air pollution may affect athletic performance. In Los Angeles, contaminants include carbon monoxide, ozone, peroxyacetylnitrate (PAN) and nitrogen oxides, whereas in older European cities, such as Sarajevo, "reducing smog" of sulfur dioxide is the main hazard. The carbon monoxide and ozone levels expected in Los Angeles this summer could affect the athletes'' performance in endurance events at the Olympic Games. Carbon monoxide may also impair psychomotor abilities, and PAN causes visual disturbances. The only likely physiologic consequence from reducing smog is an increase in the workload of the respiratory system and thus a decrease in endurance performance. While carbon monoxide has been blamed for myocardial infarctions, nitrogen oxides for pulmonary edema and sulfur dioxide for deaths due to respiratory failure, the only illnesses that are likely to be more frequent than usual among young athletes exposed to high levels of these pollutants are upper respiratory tract infections. Therapeutic tactics include the avoidance of pollution, the administration of oxygen, vitamin C and vitamin E, and general reassurance.     

大气污染对城市植被的生态胁迫效应综述

快速的城市化进程使得城市大气污染日趋严重,造成了城市植被的退化及其生态服务功能的下降。大气中的O₃、紫外(UV-B)辐射、重金属、SO₂等污染物及其复合污染从分子、细胞、个体、种群、群落和生态系统各个水平上都对城市植被造成了胁迫效应。本文从微观实验法和宏观高光谱遥感法两方面对已有的研究方法进行了分析和总结后,提出了以下几个今后需要关注的研究领域:开展野外和长期胁迫实验、植物受胁迫机理及多种因子复合胁迫研究等;同时指出应重视建筑物在城市大气污染生态胁迫中的重要作用,并在今后加强城市行道树相关方面的研究。     

Temporal variation in the genotoxic potential of urban air particulate matter

The main aim of this study was to compare the genotoxic potential of organic extracts from urban air particles collected in three different sampling periods in the center of Prague (Czech Republic). For this purpose, we analyzed the DNA adduct forming activity of extractable organic matter (EOM) from urban air particles <10 microm (PM10) in the human hepatoma cell line HepG2. DNA adducts were analyzed by (32)P-postlabelling with nuclease P1 enrichment. PM10 concentrations were 36.9 microg/m(3), 62.6mug/m(3) and 39.0 microg/m(3), in summer 2000, winter 2001 and winter 2005, respectively. The corresponding EOM contents were 5.0 microg/m(3) (13.9% of PM10), 14.9 microg/m(3) (23.8%) and 6.7 microg/m(3) (17.2%). The total DNA adduct levels induced by 10 microg EOM/ml were 4.7, 19.5 and 37.2 adducts/10(8) nucleotides in summer 2000, winter 2001 and winter 2005, respectively. However, when the EOM quantities per cubic meter of air were taken into consideration, the summer sample exhibited a 10-fold lower genotoxicity than did those of winter, while the difference between the winter samples was not significant: 23.4 in summer 2000, 291 in winter 2001 and 249 in winter 2005 (in relative units). Although the PM10 concentration in air and the EOM content in particles in winter 2005 were significantly lower than in winter 2001, the genotoxic potential of the ambient air in these samples was almost equal. There were significant positive correlations between the B[a]P and c-PAH content in EOM from various sampling periods and the total DNA adduct levels detected in the EOM-treated samples. These findings support the hypothesis that the B[a]P and c-PAH content in EOM is the most important factor that determines its genotoxic potential. Thus, estimating the genotoxic potential of the ambient air and predicting health risk should be based mainly on the c-PAH concentration and the biological activity of the extracts, while the mass of particles and the EOM content do not seem to be crucial determinants of ambient air genotoxicity.     

Molecular genetic approaches to the study of cellular senescence.

Normal cells in culture exhibit limited division potential, which is used as a model for cellular aging. In contrast, tumor-derived, carcinogen- or virus-transformed cells are capable of dividing indefinitely (immortal). Fusion of normal with immortal human cells yielded hybrids having limited life span, indicating that cellular senescence is a dominant phenotype and that immortality is recessive. Fusions of various immortal human cell lines with each other led to the identification of four complementation groups for indefinite division. In order to identify the chromosomes and genes involved in growth regulation, that had been modified in immortal cells, we used the technique of microcell fusion to introduce either a normal human chromosome 11 or 4 into cell lines representative of the different complementation groups. Chromosome 11 had no effect on the in vitro life span of the different immortal human tumor lines. However, when a normal human chromosome 4 was introduced into cell lines assigned to complementation group B, the cells lost the immortal phenotype. No effect on the proliferation potential of cell lines representative of the other complementation groups was observed. These results suggest that a gene(s) on human chromosome 4 has been modified in immortal cell lines assigned to complementation group B, to allow escape from senescence. They also provide evidence for a genetic basis for cellular aging.     

Molecular approaches to the study of myiasis-causing larvae

Among arthropod diseases affecting animals, larval infections - myiases - of domestic and wild animals have been considered important since ancient times. Besides the significant economic losses to livestock worldwide, myiasis-causing larvae have attracted the attention of scientists because some parasitise humans and are of interest in forensic entomology. In the past two decades, the biology, epidemiology, immunology, immunodiagnosis and control methods of myiasis-causing larvae have been focused on and more recently the number of molecular studies have also begun to increase. The 'new technologies' (i.e. molecular biology) are being used to study taxonomy, phylogenesis, molecular identification, diagnosis (recombinant antigens) and vaccination strategies. In particular, more in depth molecular studies have now been performed on Sarcophagidae, Calliphoridae and flies of the Oestridae sister group. This review discusses the most topical issues and recent studies on myiasis-causing larvae using molecular approaches. In the first part, PCR-based techniques and the genes that have already been analysed, or are potentially useful for the molecular phylogenesis and identification of myiasis-causing larvae, are described. The second section deals with the more recent advances concerning taxonomy, phylogenetics, population studies, molecular identification, diagnosis and vaccination.     

Epidemiological studies regarding the effects of air pollution

Studies on large samples of the population are an indispensable prerequisite for investigations into the validity and reliability of threshold levels stipulated for atmospheric pollutants purity under real conditions. Children represent suitable groups for such studies, also in the context of meaningful and effective prophylaxis. Epidemiological studies conducted over several years show that there are differences between the anthropometric, hematological and immunological parameters of subjects living in regions with major pollution loads and in so-called "clean air" regions. Conclusions are drawn regarding the work performed by national hygiene authorities, and a method is proposed for the continuation of epidemiological studies in qualitatively and quantitatively differently loaded regions as a contribution to establishing a uniform register of effects.     

Particulate urban air pollution affects the functional morphology of mouse placenta

In humans, adverse pregnancy outcomes (low birth weight, prematurity, and intrauterine growth retardation) are associated with exposure to urban air pollution. Experimental data have also shown that such exposure elicits adverse reproductive outcomes. We hypothesized that the effects of urban air pollution on pregnancy outcomes could be related to changes in functional morphology of the placenta. To test this, future dams were exposed during pregestational and gestational periods to filtered or nonfiltered air in exposure chambers. Placentas were collected from near-term pregnancies and prepared for microscopical examination. Fields of view on vertical uniform random tissue slices were analyzed using stereological methods. Volumes of placental compartments were estimated, and the labyrinth was analyzed further in terms of its maternal vascular spaces, fetal capillaries, trophoblast, and exchange surface areas. From these primary data, secondary quantities were derived: vessel calibers (expressed as diameters), trophoblast thickness (arithmetic mean), and total and mass-specific morphometric diffusive conductances for oxygen of the intervascular barrier. Two-way analysis of variance showed that both periods of exposure led to significantly smaller fetal weights. Pregestational exposure to nonfiltered air led to significant increases in fetal capillary surface area and in total and mass-specific conductances. However, the calibers of maternal blood spaces were reduced. Gestational exposure to nonfiltered air was associated with reduced volumes, calibers, and surface areas of maternal blood spaces and with greater fetal capillary surfaces and diffusive conductances. The findings indicate that urban air pollution affects placental functional morphology. Fetal weights are compromised despite attempts to improve diffusive transport across the placenta.     

Sensitivity analysis of common statistical models used to study the short-term effects of air pollution on health

The relationship between photochemical air pollutants (nitrogen dioxide and ozone) and emergency room admissions for asthma in Madrid (Spain) for the period 1995-1998 was analysed using the statistical models commonly used to studying the short-term effects of air pollution on health: linear and Cochrane-Orcutt regression, standard Poisson and Poisson corrected by overdispersion, Poisson autoregressive models, and generalised additive models. Linear regression models presented residual autocorrelation, Poisson regression models also showed overdispersion, and generalised additive models did not show residual autocorrelation and overdispersion was substantially reduced. Linear models provided biased estimates because our health outcome is non-normally distributed. Estimates from Poisson regression allowing for overdispersion and autocorrelation did not differ substantially from those reported by generalised additive models, which present the best model fit in terms of the absence of autocorrelation and reduction of overdispersion.     

Molecular approaches to study control of glucose homeostasis

Type 2 diabetes is a polygenic disease that can lead to severe complications in multiple tissues. Rodent models have been used widely for investigating the pathophysiology underlying type 2 diabetes and for examining the potential link with obesity, largely due to the limitations of invasive testing and of studying detailed molecular mechanisms in human tissues. Among rodents, the mouse model is especially popular because mice are easy to manipulate genetically, have a short generation time, and are relatively inexpensive. The most commonly used inbred mouse strains are reviewed in addition to several genetically engineered mouse models that have been generated to study type 2 diabetes in the context of obesity, with a focus on insulin, leptin, and peroxisome proliferator-activated receptor (PPAR) signaling pathways.     

Molecular approaches to nerve regeneration.

Current research into regeneration of the nervous system has focused on defining the molecular events that occur during regeneration. One well-characterized system for studying nerve regeneration is the sciatic nerve of rat. Numerous studies have characterized the sequence of events that occur after a crush injury to the sciatic nerve (Cajal 1928; Hall 1989). These events include axon and myelin breakdown, changes in the permeability of the blood vessels, proliferation of Schwann cells, invasion of macrophages, and the phagocytosis of myelin fragments by Schwann cells and macrophages. The distal segment of the injured sciatic nerve provides a supportive environment for the regeneration of the nerve fibres (Cajal 1928; David & Aguayo 1981). Within a period of weeks, the injured sciatic nerve is able to regrow and successfully reinnervate the appropriate targets. Some of the molecules that provide trophic support for the regrowing nerve fibres have been identified, including nerve growth factor (NGF) (Heumann et al. 1987) and glial maturation factor beta (Bosch et al. 1989). Another class of molecules show changes in their rates of synthesis during regeneration, including both proteins (Skene & Shooter 1983; Muller et al. 1986) and mRNA species (Trapp et al. 1988; Meier et al. 1989). To better understand nerve regeneration, we have taken two, parallel molecular approaches to study the events associated with regeneration. The first of these is to study in detail the mechanism of action of a molecule that has been implicated in the regeneration process, nerve growth factor. The second approach is to identify novel gene sequences which are regulated during regeneration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Molecular approaches to the study of mesoderm formation in amphibians

The mesoderm is the region of the embryo that gives rise to muscle, blood and connective tissues; it becomes segregated from the ectoderm and endoderm at gastrulation. Embryological studies have revealed, however, that the potential for certain embryonic cells to become part of the mesoderm is established well before gastrulation, most likely through an extracellular signalling process termed ‘induction’. The recent characterization of mesoderm-specific mRNAs and proteins now permits an analysis of the very earliest events involved in the specification of the mesoderm at the molecular level. Such experiments should contribute to our understanding of the mechanisms involved in controlling cell differentiation.     

Acute effects of air pollution changes in schoolchildren: the Gardanne coal basin study

In the literature, studies devoted to shortterm effects of air pollution episodes in children have provided controversial results. To evaluate if acute air pollution changes in the Gardanne coal basin (France) could have deleterious effects on children's pulmonary function, we studied 160 children on two different days. Each in-school examination consisted of a short questionnaire and a spirometric assessment. The area included districts of high and low pollution levels. In the former, the two examinations took place at different air pollution levels whereas, in the latter, the air pollution levels were comparable. We obtained higher spirometric values during the second examination, regardless of air pollution changes and suggesting a learning effect, which vanished when we used FEV₁/FVC ratio. The difference in FEV₁/FVC between days of low and high pollution was significant but merely equal to 2%. There was no change of clinical symptom score.     

Dietary and pharmacological intervention to mitigate the cardiopulmonary effects of air pollution toxicity

BackgroundExposure to air pollution contributes importantly to excess morbidity and mortality. And while regulatory actions under the “Clean Air Act” have saved millions of lives by improving air quality, there are still millions of people in the U.S. who live in areas where particulate air pollution (PM) levels exceed the U.S. Environmental Protection Agency's National Ambient Air Quality Standards. Therefore, apart from such localities working to attain such standards the protection of the health of public and in particular those at high risk might benefit from interventional strategies that would ameliorate air pollution's adverse health effects. Because inflammation and oxidative stress appear to mediate the health effects of air pollution, one interventional approach to consider is the use of dietary supplementation or medication with anti-inflammatory or antioxidant properties to block the biological responses that initiate the pathophysiological process that culminates in adverse health effects.Scope of reviewThis article reviews the capability of dietary supplementation, such as antioxidant vitamins, polyunsaturated fatty acids, and medications as a strategy to mitigate air pollution-induced subclinical cardiopulmonary effects.Major conclusionsAntioxidant vitamins C and E protect the lungs against short-term ozone and PM exposure. Polyunsaturated fatty acids, such as fish oil and olive oil appear to offer protection against short-term air pollution-induced adverse cardiovascular responses.General significanceTaking dietary supplements or medications with antioxidant or anti-inflammatory properties has the potential to provide at least partial protection against air pollution-induced adverse health effects in those individuals who are known to be most susceptible, namely those with pre-existing respiratory and cardiovascular diseases. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.     

Attempt at quantitative estimation of genetic effects of chemical pollution of atmospheric air in urban populations]

Epidemiological investigation of spontaneous abortions and congenital anomalies in three towns of Ukraine has shown that mutation rate in Mariupol, the most contaminated town, as compared with relatively clean town is essentially higher. Genetical consequences due to environmental chemical pollution in Mariupol proved to be equivalent to the chronic influence of ionizing radiation for 30 years in the dose of 230 REM.     

大气污染规制对城市空气污染的防治成效——基于准实验分析

以2003年实施的大气污染防治重点城市政策为准自然实验,运用双重差分模型从区域层面分析了大气污染规制对城市空气污染治理的影响,研究发现：（1）大气污染规制在1%的显著性水平下降低了重点城市的工业二氧化硫排放强度,工业二氧化硫排放量以及城市PM2.5年均浓度值。（2）大气污染防治重点城市政策实施后的9年时间内有效减少了12215.8万t城市工业二氧化硫排放量,并且使得城市PM2.5年均浓度改善2.97μg/m3,下降比分别达到了36.2%和8.5%,平均每年减少了3.7%的城市工业二氧化硫排放量并降低0.944%的城市PM2.5浓度值。（3）大气污染防治重点城市政策对于城市空气污染治理主要是通过减少能源消耗量、增加城市污染治理力度、促进规制地区产业结构转型升级和提升生产技术水平等渠道予以实现。     

Molecular genetic approaches to understanding disease.

Molecular genetics has greatly increased the understanding of diseases in which there is a single gene defect such as cystic fibrosis. Discovering the gene responsible and its function not only helps determine the pathogenesis of the disease but also offers a possible treatment-gene therapy. Polygenic disorders such as diabetes may soon yield their secrets to the same approach. Animal models of genetic diseases are proving useful research tools, and transgenesis has made xenografting possible. Furthermore, antisense technology allows specific inhibition of undesirably overexpressed genes such as those driving unwanted vascular cell proliferation and restenosis after angioplasty. The completion of the human genome project should make the search for "disease" gene much quicker and will increase still further the importance of these gene based approaches toward diseases.