Critical Evaluation of Health Impacts from Urban Air Pollution (NO2 and PM): Abstract
There is no doubt that historical air pollution in terms of smokes, fumes, vapors, mist, and dust lead to severe health problems, excess morbidity and mortality. However, at present urban pollution levels of NO2 and PM10 are around two orders of magnitude lower. Nevertheless, several administrations state that such levels result into health effects and reduce the life expectancy. The “thousands additional annual deaths” due to air pollution are based on a few papers using wrong statistics, erroneous date and simple mathematical assumptions, not verified by true observations but wanted by governmental administrations (conflict between law and nature).
In most human clinical studies of healthy individuals, exposures to NO2 at concentrations less than 4 ppm do not cause symptoms or alter pulmonary function. In healthy individuals, exposures in the range of 1.5 to 2 ppm may increase airway responsiveness. From clinical studies it is seen that no effects result from NO2 concentrations less than 1 ppm (it is 10 times the 1-hour limit). Some (but some not) epidemiological studies show for sensitive persons irritations for less than 0.1 ppm NO2 but that is likely not because of NO2 but rather of the air pollution mixture. Traffic related concentrations between 0.02 and 0.04 ppm are thus out of any health relevance. Difference in findings from epidemiological studies has led to the conclusion that if an effect exists, it is subtle and difficult to distinguish from other environmental effects (EPA 1993). No data provide health’s effects at levels < 100 µg m–3. The current small (!) exceedance of the NO2 EU limit (40 μg m–3) results in political hysteria.
The results from Pope et al. (2002) concerns the mortality hazard have been used in a linear relationship to calculate the loss of life years (YPLL) due to PM2.5 to be 8.6 month in the EU and 10.2 month in Germany. UBA build on Wichman (2003) who used the papers by Pope et al. with additional wrong conclusions as discussed by Greim et al. (2003). Enstrom (2017 and citations therein) conclusive reanalyzed the data and found that there was no significant relationship between PM2.5 and death. The literature related to specific PM types (e.g. coal dust) also shows responses only at high concentrations (> 4 mg m–3). The studies show that effects would be expected with any inhaled particle (Wyzga and Rohr 2015 and citations therein). The question must be answered why ambient PM at levels more than hundred times smaller and changes of PM levels being < 1% of the above clinical limit should result in detectable health effects.
The claim that PM2.5 causes premature deaths is implausible because no etiologic mechanism has ever been established and because it involves the lifetime inhalation of only about 5 g of particles that are less than 2.5 µm in diameter (Enstrom 2017). The PM2.5 mortality relationship has been further challenged because the small increased risk could be due to well-known epidemiological biases, such as, the ecological fallacy, inaccurate exposure measurements, and confounding variables like co-pollutants.
Large discrepancies exist between workplace and ambient exposure limits. The permissible exposure limits (PEL) in the USA (OSHA) are (in mg m–3) 10 for respirable quartz, 2.4 for respirable fraction with less than 5% SiO2, 5 for total respirable fraction and 15 for total dust. In Germany, the limit (MAK) amounts 4 mg m–3 for the total respirable dust fraction and 1.5 mg m–3 for alveolar dust fraction. These values have been set up for 40 hours per week and 40 years working as maximum without expecting adverse health effects. It follows a long life maximally cumulative exposure of around 2500 g h m–3. For ambient PM (limit 40 µg m–3) it follows for 65 years life a maximally cumulative exposure of only 24 g h m–3. Urban dust will presently have a potential of about 3 μg m–3 soot. A person would be exposured over 65 years with 1.7 g h m–3 of this sooty PM.