Comparing effects of inhaled particles across rodent test systems and between rodent test systems and humans is a key obstacle to the interpretation of common toxicological test systems for human risk assessment. These comparisons, correlation with effects and prediction of effects, are best conducted using measures of tissue dose in the respiratory tract. Differences in lung geometry, physiology and the characteristics of ventilation can give rise to differences in the regional deposition of particles in the lung in these species. Differences in regional lung tissue doses cannot currently be measured experimentally. Regional lung tissue dosimetry can however be predicted using models developed for rats, monkeys, and humans. A computational model of particle respiratory tract deposition and clearance was developed for BALB/c and B6C3F1 mice, creating a cross species suite of available models for particle dosimetry in the lung. Airflow and particle transport equations were solved throughout the respiratory tract of these mice strains to obtain temporal and spatial concentration of inhaled particles from which deposition fractions were determined. Particle inhalability (Inhalable fraction, IF) and upper respiratory tract (URT) deposition were directly related to particle diffusive and inertial properties. Measurements of the retained mass at several post-exposure times following exposure to iron oxide nanoparticles, micro and nanoscale C60 fullerene, and nanoscale silver particles were used to calibrate and verify model predictions of total lung dose. Interstrain (mice) and interspecies (mouse, rat, human) differences in particle inhalability, fractional deposition and tissue dosimetry are described for ultrafine, fine and coarse particles.

Background Hookahs (e.g., water pipes) are increasingly being used in the U.S. and elsewhere. Despite the popularity of hookah bars, there is a paucity of research assessing the health effects of hookah smoke, and although New York City (NYC) bans indoor tobacco smoking, hookah lounges claim that they only use herbal products without tobacco and are exempt. This study investigated levels of multiple indices of air pollution in the indoor air of hookah bars in NYC. Methods Air samples were collected in 8 hookah bars in NYC during the summer and fall of 2013. Along with venue characteristics, real-time measurements of fine particulate matter (PM2.5), black carbon (BC), and carbon monoxide (CO), and integrated samples of total gravimetric PM, elemental carbon (EC), organic carbon (OC), and nicotine were collected in 1–2 hour sessions. Results Overall, levels of indoor air pollution increased with increasing numbers of active hookahs smoked. The mean (SD) real time PM2.5 level was 1179.9 (939.4) µg/m3, whereas the filter-based total PM mean was 691.3 (592.6) µg/m3. The mean real time BC level was 4.1 (2.3) µg/m3, OC was 237.9 (112.3) µg/m3, and CO was 32 (16) ppm. Airborne nicotine was present in all studied hookah bars (4.2 (1.5) µg/m3). Conclusions These results demonstrate that despite the ban on smoking tobacco products, at the very least, some NYC hookah bars are serving tobacco-based hookahs, and have elevated concentrations of indoor air pollutants and toxicants that may present significant health threat to visitors and employees. Therefore, there is an urgent need for better air quality monitoring in such establishments and policies to combat this emerging public health threat.

Background: Over 20 genetic risk factors have been confirmed to associate with elevated risk for Alzheimer’s disease (AD), but the identification of environmental and/or acquired risk factors has been more elusive. At present, recognized acquired risks for AD include traumatic brain injury, hypercholesterolemia, obesity, hypertension, and type 2 diabetes. Methods: Based on reports associating various inhalants with AD pathology, we investigated the possibility that air pollution might contribute to AD risk by exposing wild-type mice to a standard air pollution modeling system employing nickel nanoparticle-enriched atmosphere for 3 hr. Results: Mice exposed to air pollution showed 72-129% increases in brain levels of both amyloid-β peptides Aβ40 and Aβ42, as well as Aβ42/40 (p <0.01). Conclusions: These effects on elevation of brain Aβ exceed those associated with trisomy 21, a known risk for early onset AD pathology, raising the possibility that clinical importance might be attached. Further work is required to establish the molecular and physiological basis for these phenomena. The rapid, dramatic effect, if verified, would suggest that inhalant exposures should be evaluated for their possible roles in contributing to the environmental risk for common forms of AD.

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The survival of cells in density-inhibited, confluent cultures maintained at 37 degrees C was examined following exposure to 137Cs gamma rays at low dose rates (0.023 or 0.153 Gy/h) or to 60Co gamma rays at a single high dose rate (0.70-0.75 Gy/min). Cells from an ataxia telangiectasia (AT) homozygote showed no dose-rate effect, whereas a three- to fivefold increase in D0 was observed for all other cell strains exposed at low dose rates. The magnitude of the dose-rate effect did not differ significantly among cells from persons with hereditary retinoblastoma, basal cell nevus syndrome, or AT-heterozygote compared with normal cell strains, and was not related to the size of the shoulder (extrapolation number) of the survival curve. Furthermore, no differences in the capacity for the repair of potentially lethal damage during confluent holding were observed among these latter cell strains.