Search

Background: Exposure to heat and particulate matter is a cause of increased mortality. Climate change and increasing climate variability exacerbate these problems. Experts require assessments with which health risks and the success of preventative measures can be estimated. We implemented an ecological study approach to assess these risks at both small and large scales of reference levels (Federal Republic of Germany and territorial authority)., Methods: We utilised a case-crossover design to investigate the relationship between exposure and mortality. This study design uses a logistic regression model. Analogously to a matched case-control study, the odds ratio maps the effect strength. The study period included the years 2002-2006., Results: The analysis demonstrated health risks from exposure to heat for the German population (OR 1.1529, 95% CI 1.1517-1.1541; adjusted OR 1.0658). Significant evidence of a health risk was also documented for exposure to particulate matter (PM 10; OR 1.2987, 95% CI 1.2951-1.3024; adjusted OR 1.0128). The risk does not significantly differ for women versus men; the variable age was also not significant at the level of the country-wide analysis, but for a few subordinate units of space. This study approach can be adapted for assessments at varying levels of reference and periods of time as well as for different populations., Discussion: The methodological approach is useful for a reproducible study design. Nevertheless, other influencing factors such as ozone or PM 2.5 should be incorporated in subsequent analyses to clarify whether these factors skew the results. Further analysis would also be useful to investigate if and to what extent socio-structural and socio-economic factors affect the associated risk.

Airborne microorganisms occur ubiquitously in the ambient air. Besides allergic and irritative-toxic effects, they can cause infections after inhalation. Occupational studies have shown that an increased incidence of respiratory diseases is found in adequately exposed workers. In addition to respiratory diseases, severe systemic infections can also occur in particular cases, such as in the case of a hantavirus infection that is recognized as an occupational disease. In studies from environmental medicine, respiratory diseases have also been observed in residents living in the vicinity of livestock facilities and evaporative cooling towers. In the latter case, an infection risk may be caused by inhalation of legionella-contaminated aerosol from the exhaust air of such systems.Currently, there are no health-related exposure limits for airborne microorganisms released from such facilities. Environmental risk assessment can be carried out on the basis of the guideline VDI 4250 part 1, which relies on an excess of natural background concentration by facility-specific emissions. For the approval practice, the LAI-Leitfaden Bioaerosole is a uniform, standardized method for the determination and assessment of bioaerosol exposure.In indoor spaces, only a few mold types, such as Aspergillus fumigatus are able to trigger infections by local or systemic infection of the human organism. In particular, persons with an immune deficiency or allergies must be informed about the risks of mold exposure in indoor air. In general, mold growth in indoor spaces is a hygienic problem and must not be accepted as a matter of principle.

Background: It is not known/is disputed whether introduction of low emission zones (LEZs) leads to a reduction of fine dust pollutants., Methods: Data on PM10 concentrations obtained from measurement stations within and outside of LEZs from 19 German cities (Augsburg, Berlin, Dortmund, Duisburg, Düsseldorf, Essen, Frankfurt a. M., Hannover, Herrenberg, Ilsfeld, Karlsruhe, Köln, Ludwigsburg, Mannheim, München, Reutlingen, Stuttgart, Tübingen, Wuppertal) were analyzed in order to investigate the effect of banning vehicles ("tier 1") of the pollutant group 1 (without stickers) on the pollutant concentration, i.e, this study focused on LEZs that restricted cars of EURO 1 standard without appropriate retrofitting systems from entering these zones. For the period from about 2005 until the end of 2009, data from continuous half-hour measurements as well as gravimetrically determined daily measurements of PM10 were collected. The analysis consisted of four pairwise corresponding measurement values as matched quadruples of two index and two reference values (index stations are inside, and reference stations are outside the LEZs). One index value and the simultaneous reference value were measured during the active LEZ period, and the other pair of values was measured before the LEZ was introduced. The pairs of values had a difference in time of 364 days or a multiple of 364 days keeping the season, weekday and time of day constant within the quadruple. Differences in index values were regressed on differences in reference values while meteorological parameters (height of the inversion base, amount of precipitation, wind velocity), school holidays, period of environmental bonus paid, periods when trucks were banned as well as baseline data at index and reference stations were taken into account as covariates in so-called "fixed effects" regression analyses of the quadruples (difference score method in the two-period case). The statistical approach was successfully validated prior to this study in an analysis of simulated data from FU Berlin., Results: 2,110,803 quadruples of continuous PM10 and 15,735 gravimetric quadruples were identified leading to 61,169 quadruples based on daily PM10 averages. The analyses showed that best LEZ effect estimates for fine dust reduction were (at all index stations) ≤ 0.2 μg/m3, i. e., a relative PM10 reduction ≤ 1 %. Best estimates at all index stations near traffic (excluding urban background and industry index stations) were below 1 μg/m3 (less than 5 %, respectively)., Conclusions: Effects were smaller than predicted prior to the introduction of LEZs. This study is the first that investigated comprehensively the effectiveness of "tier 1" LEZs in Germany on PM10 reduction with a homogeneous approach in data collection and analysis and taking into account the most relevant confounding factors., (© Georg Thieme Verlag KG Stuttgart · New York.)

Evidence accumulated during the mid-1990 s that ambient particulate air pollution aerosol particles may not only exacerbate respiratory diseases but also be a risk factor for cardiovascular disease exacerbation. The aim of the studies described here was to assess the impact of the 1985 smog episode on the risk factor profile in the randomly selected population-based sample of the MONICA survey 1984/85 (S1). During a 13-day period in January 1985 sulphur dioxide concentrations increased four times and concentrations of total suspended atmospheric particles doubled. The impact of this time period on plasma viscosity, plasma C-reactive protein concentrations, heart rate and blood pressure was investigated. Regression models were used to assess these associations adjusting for individual risk factors such as gender, age, body mass index, serum total cholesterol and HDL-cholesterol, smoking, physical activity and medication for cardiovascular diseases and for weather conditions during the survey period. An increase in plasma viscosity, C-reactive protein and heart rate was estimated during the air pollution episode. There was also an increase in blood pressure, but this appeared to be attributable to the weather conditions during the air pollution episode. All the four outcomes were associated with the sulphur dioxide concentrations and the total suspended particle concentrations during the survey. These results indicate that ambient air pollution, particularly ambient particulate air pollution may induce systemic inflammation and modulate the autonomic function of the heart. These pathomechanisms may contribute to the observed associations between ambient air pollution concentrations and cardiovascular disease exacerbation such as hospitalisation and mortality due to cardiovascular diseases.

Recent studies in Germany after re-unification did not show any a link between air-pollution and the prevalence of asthma. The data indicate that there is a tendency for increasing rates of allergic rhinitis and asthma-related symptoms in the eastern part of Germany. It is not clear whether this is due to a true increase in morbidity or a higher sensitivity to environmental problems in the public and among the doctors. However, there are observations compatible with the hypothesis that viral respiratory RSV infections early in childhood somehow prevent the expression of allergic disease later in life. On the other hand the increasing rate of asthmatic disease is due to later childhood RV-infections in children displaying allergic rhinitis. These risks childhood asthma need more detailed attention interest in future studies.

Public health costs ascribable to air pollution are socialized in our society. To quantify the damage to public health, epidemiologic studies are needed. We present the methods and epidemiologic background data which form the basis for estimating the public health effect ascribable to air pollution. The figures are presented per 1 million "average" Swiss population and per 10 micrograms/m3 increase in long-term annual mean particulate pollution (PM10). Quantification was restricted to the health effects given below (due to lack of complete data for other effects or to avoid duplicating health effects which may be described by overlapping measurements). In parenthesis we present (1) the mean effect estimates (+/-1 SE) (% increase per 10 micrograms/m3 increment in PM10) derived from national and international epidemiologic studies, and (2) the expected absolute additional health effects (+/-1 SE) per 1 million Swiss population and per 10 micrograms/m3 increment in PM10, based on Swiss population statistics: total mortality (long-term estimates from the 2 US cohort studies) (+4.4% [+/-1.1]/349 [+/-91] premature deaths per year); prevalence of chronic bronchitis in adults (+25% [+8.4]/increase in long-term prevalence by 3,513 [+/-1.475]); bronchitis among children (35% [+/-13]/5,180 [+/-2,590] additional children sufferers in a year); repeated cough among children (+54% [+/-8.8]/23,490 [+/-5,873] additional children per year); cough/phlegm in adults (+12.8% [+/-7.8]/1.56 [+/-1.08] million person-days per year); hospital admissions for respiratory diseases (+1.47% [+/-0.5]/71 [+/-24] additional admissions or 1,104 (+/-390) hospital days); admissions for cardiovascular diseases (+0.9% [+/-0.25]/70 [+19] admissions; 970 (+/-270) hospital days); restricted activity days (+10.5% [+/-0.77]/0.42 [+/-0.03] million person-days); days with asthma attacks among the 6.7% asthmatics (Swiss prevalence) (+5.3% [+/-2.1]/ 240,000 [+/-102,000] additional person-days). Conservative assumptions were used throughout the study and thus the true effects are likely to be larger. Estimates of Swiss population exposure distribution would be needed to apply these results to the entire population. This step, and monetary quantification of these total effects, were the second and third elements (not shown in this report) of this Swiss government funded project. Although individual relative risks of air pollution are rather slight, the public health burden of even moderate pollution may be substantial.

The evidence for the adverse health effects of today's "normal" air pollution relies heavily on epidemiologic studies. Given the major impact of these effects on environmental, economic and social policy, the causality of epidemiologic findings becomes a central issue. The scientific process of establishing causality based on the air pollution epidemiology literature is reviewed. It consists of two steps: first, the quality and validity of each epidemiologic study must be rigorously assessed (design, selection, confounding); second, the overall evidence across all valid studies must be appraised. Of major importance are the consistency of results between replicate studies and the coherence of effects across a variety of different pathophysiologically or logically interrelated epidemiologic health outcomes, such as respiratory symptoms, exacerbations of respiratory diseases, use of health care, sick absenteeism, or, among the most sensitive subjects, mortality. Demonstration of a dose-response association is crucial and has been shown in many studies. Valid studies may use varied indicators of the air pollution mixtures, such as particulate matter, NO2, SO2, or others. However, epidemiology is incapable of investigating the biologic pathophysiologic mechanisms, which require experimental studies. Such studies may increase the biologic plausibility of epidemiologic findings. Given the common sources of many of the air pollution indicators used in epidemiology, a knowledge of pathophysiologic mechanisms is not a prerequisite for public health action aimed at improving air quality in cities.

The GDR is the country with the highest degree of air pollution in Europe. The oil crisis and the subsequent substitution of oil, coal and gas by lignite has led to an enormous increase of SO2-emissions. The highest air pollution concentrations are found in the industrial centres of Halle and Leipzig. The end of the socialist system in the GDR and the financial, economical and social union with the FRG is also the beginning of fundamental changes in the field of environmental protection, -regulations and -management. In June the Volkskammer passed a law for the assimilation of GDR environmental regulations to FRG-right presented by the common environmental commission. Subsequently, the old structure of the Hygiene Inspectorates has to be reorganised to ensure an efficient environmental control. The development of environmental epidemiology, the investigation of diseases caused by environmental pollutions should play an important role in environmental research.