Victims of War must be loyal to deserve protection: International law and national legislation on enemy aliens 1907-1918

In international law the internment of civilians has only been regulated in writing in the context of the 4th Geneva Convention of 1949. Nevertheless this did not mean that civilians were not protected by at least some rules of customary international law before that date and especially in World War I. Furthermore specialists of international law expected states – at least those considered to be part of the community of civilized nations – to continue to treat all men equal before the law even in wartime. As research already conducted (Bird, Panayi, Fischer) has shown, this was not the case during World War I. Based on these findings the presentation proposed here wants to look into the development of international law and into some national preparations for treating so called “enemy aliens” in the period before 1914 (Austria-Hungary, Australia, United Kingdom), in order to see to what extent principles of international law protecting civilians from the consequences of war can be detected in the pre-war preparations. As far as can be judged so far the issue of loyalty was central in this context. Looking at the war itself, the presentation proposed here will try to look at how far the principles of international law alluded to above continued to influence the policies on “enemy aliens” in the countries mentioned and to see, how the International Committee of the Red Cross tried to use them to legitimize and expand its protective policies in regard to civilians interned in belligerent as well as neutral countries throughout the war.

Aircraft noise, air pollution, and mortality from myocardial infarction

Objective: Myocardial infarction has been associated with both transportation noise and air pollution. We examined residential exposure to aircraft noise and mortality from myocardial infarction, taking air pollution into account. Methods: We analyzed the Swiss National Cohort, which includes geocoded information on residence. Exposure to aircraft noise and air pollution was determined based on geospatial noise and air-pollution (PM10) models and distance to major roads. We used Cox proportional hazard models, with age as the timescale. We compared the risk of death across categories of A-weighted sound pressure levels (dB(A)) and by duration of living in exposed corridors, adjusting for PM10 levels, distance to major roads, sex, education, and socioeconomic position of the municipality. Results: We analyzed 4.6 million persons older than 30 years who were followed from near the end of 2000 through December 2005, including 15,532 deaths from myocardial infarction (ICD-10 codes I 21, I 22). Mortality increased with increasing level and duration of aircraft noise. The adjusted hazard ratio comparing ≥60 dB(A) with <45 dB(A) was 1.3 (95% confidence interval = 0.96-1.7) overall, and 1.5 (1.0-2.2) in persons who had lived at the same place for at least 15 years. None of the other endpoints (mortality from all causes, all circulatory disease, cerebrovascular disease, stroke, and lung cancer) was associated with aircraft noise. Conclusion: Aircraft noise was associated with mortality from myocardial infarction, with a dose-response relationship for level and duration of exposure. The association does not appear to be explained by exposure to particulate matter air pollution, education, or socioeconomic status of the municipality.

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

Background/Objectives Ambient air pollution can alter cytokine concentrations as shown in vitro and following short-term exposure to high air pollution levels in vivo. Exposure to pollution during late pregnancy has been shown to affect fetal lymphocytic immunophenotypes. However, effects of prenatal exposure to moderate levels of air pollutants on cytokine regulation in cord blood of healthy infants are unknown. Methods In a birth cohort of 265 healthy term-born neonates, we assessed maternal exposure to particles with an aerodynamic diameter of 10 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.

A prospective study of the impact of air pollution on respiratory symptoms and infections in infants

Rationale: There is increasing evidence that short-term exposure to air pollution has a detrimental effect on respiratory health, but data from healthy populations, particularly infants, are scarce. Objectives: To assess the association of air pollution with frequency and severity of respiratory symptoms and infections measured weekly in healthy infants. Methods: In a prospective birth cohort of 366 infants of unselected mothers, respiratory health was assessed weekly by telephone interviews during the first year of life (19,106 total observations). Daily mean levels of particulate matter (PM10), nitrogen dioxide (NO2), and ozone (O3) were obtained from local monitoring stations. We determined the association of the preceding week's pollutant levels with symptom scores and respiratory tract infections using a generalized additive mixed model with an autoregressive component. In addition, we assessed whether neonatal lung function influences this association and whether duration of infectious episodes differed between weeks with normal PM10 and weeks with elevated levels. Measurements and Main Results: We found a significant association between air pollution and respiratory symptoms, particularly in the week after respiratory tract infections (risk ratio, 1.13 [1.02-1.24] per 10 μg/m(3) PM10 levels) and in infants with premorbid lung function. During times of elevated PM10 (>33.3 μg/m(3)), duration of respiratory tract infections increased by 20% (95% confidence interval, 2-42%). Conclusions: Exposure to even moderate levels of air pollution was associated with increased respiratory symptoms in healthy infants. Particularly in infants with premorbid lung function and inflammation, air pollution contributed to longer duration of infectious episodes with a potentially large socioeconomic impact.

Air pollution during pregnancy and neonatal outcome: a review

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.

Air pollution during pregnancy and lung function in newborns: a birth cohort study

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.

[Air pollution and asthma in childhood].

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

Is there a common pattern of future gas-phase air pollution in Europe under diverse climate change scenarios?

Climate change alone influences future levels of tropospheric ozone and their precursors through modifications of gas-phase chemistry, transport, removal, and natural emissions. The goal of this study is to determine at what extent the modes of variability of gas-phase pollutants respond to different climate change scenarios over Europe. The methodology includes the use of the regional modeling system MM5 (regional climate model version)-CHIMERE for a target domain covering Europe. Two full-transient simulations covering from 1991–2050 under the SRES A2 and B2 scenarios driven by ECHO-G global circulation model have been compared. The results indicate that the spatial patterns of variability for tropospheric ozone are similar for both scenarios, but the magnitude of the change signal significantly differs for A2 and B2. The 1991–2050 simulations share common characteristics for their chemical behavior. As observed from the NO2 and α-pinene modes of variability, our simulations suggest that the enhanced ozone chemical activity is driven by a number of parameters, such as the warming-induced increase in biogenic emissions and, to a lesser extent, by the variation in nitrogen dioxide levels. For gas-phase pollutants, the general increasing trend for ozone found under A2 and B2 forcing is due to a multiplicity of climate factors, such as increased temperature, decreased wet removal associated with an overall decrease of precipitation in southern Europe, increased photolysis of primary and secondary pollutants as a consequence of lower cloudiness and increased biogenic emissions fueled by higher temperatures.