Marination increases the bioavailability of lead in game meat shot with lead ammunition.

As a consequence of the toxicological lead characteristics, a reduction of its exposure should consider all sources. Game meat might contain elevated levels of lead due to the use of lead ammunition. The aim of the present study was to investigate the effects of acidic marination on the bioavailability of ammunition-derived lead in game meat (Roe deer), using the growing pig as an animal model. Furthermore, the study should provide evidence that the large-area scattering of lead particles leads to noticeable differences in the individual lead intake per game meat portion. Pigs of group A (n 7) received lead-shot game meat, which was cooked in water. Pigs of group B (n 7) received lead-shot game meat, which was first marinated (wine and vinegar) and then cooked. The lead content of both game meat preparations was equal with 0⋅77-0⋅79 mg Pb/portion. Pigs of group C (n 4) received lead-free game meat, which was also marinated and cooked. Additionally, lead acetate was administered intravenously to group D pigs (n 4). Blood samples were taken on elevated time points before and after game meat intake/i.v.-application. The acidic marination increased the bioavailability of orally ingested lead, resulting in significantly higher blood lead concentrations. The bioavailability of lead was 2⋅7 % when game meat was just cooked and 15 % when the meat was marinated before. The considerable variation of the individual blood lead concentrations suggests that an inhomogeneous distribution of ammunition-derived lead particles (in terms of size and number) causes individually non-comparable lead intakes from the consumption of game meat.

Neutral polyfluorinated compounds in indoor air in Germany--the LUPE 4 study.

Perfluoroalkyl- and polyfluoroalkyl-substances (PFAS) have been detected in many types of environmental media and biota including humans. We determined volatile PFAS, including fluorotelomer alcohols (FTOHs), fluorotelomer acrylates (FTACs), perfluorooctane sulfonamides (FOSAs), and perfluorooctane sulfonamidoethanols (FOSEs), in indoor air of residences and schools in Germany. FTOHs, FTACs, FOSEs, and FOSAs were quantified with median levels in schools (in residences) of 11,783pg/m(3) (13,198pg/m(3)), 737pg/m(3) (450pg/m(3)), 130pg/m(3) (278pg/m(3)), and 243pg/m(3) (110pg/m(3)), respectively. Using our data and previously published results in a simplified model based on the medians and 95th percentiles, the "typical" and "high" daily non-dietary exposures were calculated to be 4.2ng/kg body weight (9.9ng/kgb.w.) for Σ-FTOHs and 0.1ng/kgb.w. (0.8ng/kgb.w.) for Σ-FOSEs/FOSAs in children. Inhalation was the dominant intake pathway for FTOHs; however, dust ingestion contributed significantly to the total intake of FOSEs/FOSAs. In organisms, 8:2 FTOH is degraded to perfluorooctanoate (PFOA). Assuming that 1% of 8:2 FTOH is converted to PFOA, 8:2 FTOH exposure in Germany has a negligible contribution to the total daily PFOA exposure, which is mainly driven by dietary intake.

Airborne allergens, endotoxins, and particulate matter in elementary schools, results from Germany (LUPE 2).

Allergic disorders are the most common childhood-related chronic diseases in developed countries. It is essential to assess the exposure, especially in schools, where children spend a large portion of their time. We aimed to investigate allergen and endotoxin levels in the air of schools and to observe seasonal variations of these factors. We evaluated airborne concentrations of house dust mites allergens (Der p 1, Der f 1), cat allergen (Fel d 1), and endotoxin in PM10 in 14 classrooms during the school days in the region of Munich, each over 20 consecutive days and in 1 classroom over the course of a year (at 83 days); we also tested outdoor air close to the schools. Endotoxin levels were quantified using two different analytical methods. In addition, indoor air climate parameters were measured. The median daily indoor CO2 and PM10 concentrations in the classrooms ranged from 423 to 3,135 ppm (median: 1,211 ppm) and 9 to 390 µg/m(3) (median: 127 µg/m(3)), respectively. Fel d 1 in the PM10 samples was the most frequently detected allergen, with levels from 0.02 to 1.15 ng/m(3) in a total of 301 samples (median: 0.19 ng/m(3), 95th percentile: 0.57 ng/m(3)). Der p 1 and Der f 1 were detected in only 51% and 19% of the samples, with 95th percentiles at 0.5 and 0.3 ng/m(3). Endotoxin levels in the PM10 and inhalable dust samples ranged from 0.5 to 84.1 EU/m(3) (median: 15.3 EU/m(3); 95th percentile: 58.2 EU/m(3)) and from 0.03 to 115 EU/m(3) (median: 8.4 EU/m(3); 95th percentile: 27.9 EU/m(3)). Fel d 1 and endotoxin were found in higher levels in the winter months. The results of the two different indoor sampling techniques for endotoxin were statistically significantly correlated. The results of airborne allergens indicate a generally low exposure level in classrooms. With regard to endotoxin, our study showed higher levels in schools compared with residences.

Airborne indoor particles from schools are more toxic than outdoor particles.

High concentrations of particulate matter (PM(10)) were measured in classrooms. This study addresses the hazard of indoor particles in comparison to the better-studied outdoor particles. Samples were taken from six schools during teaching hours. Genome-wide gene expression in human BEAS-2B lung epithelial cells was analyzed and verified by quantitative PCR. Polycyclic aromatic hydrocarbons, endotoxin, and cat allergen (Fel d 1) were analyzed by standard methods. Enhancement of allergic reactivity by PM(10) was confirmed in human primary basophils. Acceleration of human blood coagulation was determined with supernatants of PM(10)-exposed human peripheral blood monocytes. Indoor PM(10) induced serine protease inhibitor B2 (involved in blood coagulation) and inflammatory genes (such as CXCL6, CXCL1, IL6, IL8; all P < 0.001). Outdoor PM(10) induced xenobiotic metabolizing enzymes (cytochrome P450 [CYP] 1A1, CYP1B1, TIPARP; all P < 0.001). The induction of inflammatory genes by indoor PM(10) was explained by endotoxin (indoor 128.5 ± 42.2 EU/mg versus outdoor 13.4 ± 21.5 EU/mg; P < 0.001), the induction of CYP by outdoor polycyclic aromatic hydrocarbons (indoor 8.3 ± 4.9 ng/mg versus outdoor 16.7 ± 15.2 ng/mg; P < 0.01). The induction of serine protease inhibitor B2 was confirmed by a more rapid human blood coagulation (P < 0.05). Indoor PM(10) only affected allergic reactivity from human primary basophils from cat-allergic individuals. This was explained by varying Fel d 1 concentrations in indoor PM(10) (P < 0.001). Indoor PM(10), compared with outdoor PM(10), was six times higher and, on an equal weight basis, induced more inflammatory and allergenic reactions, and accelerated blood coagulation. Outdoor PM(10) had significantly lower effects, but induced detoxifying enzymes. Therefore, preliminary interventions for the reduction of classroom PM(10) seem reasonable, perhaps through intensified ventilation.

Comparability of portable nanoparticle exposure monitors.

Five different portable instrument types to monitor exposure to nanoparticles were subject to an intensive intercomparison measurement campaign. Four of them were based on electrical diffusion charging to determine the number concentration or lung deposited surface area (LDSA) concentration of airborne particles. Three out of these four also determined the mean particle size. The fifth instrument type was a handheld condensation particle counter (CPC). The instruments were challenged with three different log-normally distributed test aerosols with modal diameters between 30 and 180 nm, varying in particle concentration and morphology. The CPCs showed the highest comparability with deviations on the order of only ±5%, independent of the particle sizes, but with a strictly limited upper number concentration. The diffusion charger-based instruments showed comparability on the order of ±30% for number concentration, LDSA concentration, and mean particle size, when the specified particle size range of the instruments matched the size range of the aerosol particles, whereas significant deviations were found when a large amount of particles exceeded the upper or lower detection limit. In one case the reported number concentration was even increased by a factor of 6.9 when the modal diameter of the test aerosol exceeded the specified upper limit of the instrument. A general dependence of the measurement accuracy of all devices on particle morphology was not detected.

Indoor air contamination during a waterpipe (narghile) smoking session.

The smoke of waterpipe contains numerous substances of health concern, but people mistakenly believe that this smoking method is less harmful and addictive than cigarettes. An experiment was performed in a 57 m3 room on two dates with no smoking on the first date and waterpipe smoking for 4h on the second date. We measured volatile organic compounds (VOC), polycyclic aromatic hydrocarbons (PAH), metals, carbon monoxide (CO), nitrogen oxides (e.g. NO), as well as particle mass (PM), particle number concentration (PNC) and particle surface area in indoor air. High concentrations were observed for the target analytes during the 4-h smoking event. The median (90th percentile) values of PM(2.5), PNC, CO and NO were 393 (737 microg/m(3)), 289,000 (550,000 particles/cm(3)), 51 (65 ppm) and 0.11 (0.13 ppm), respectively. The particle size distribution has a maximum of particles relating to a diameter of 17 nm. The seven carcinogenic PAH were found to be a factor 2.6 higher during the smoking session compared to the control day. In conclusion, the observed indoor air contamination of different harmful substances during a WP session is high, and exposure may pose a health risk for smokers but in particular for non-smokers who are exposed to ETS.