Exposure to air pollution is associated with adverse cardiopulmonary health effects in international travellers.

BACKGROUND: With the number of annual global travellers reaching 1.2 billion, many individuals encounter greater levels of air pollution when they travel abroad to megacities around the world. This study's objective was to determine if visits to cities abroad with greater levels of air pollution adversely impact cardiopulmonary health. METHODS: A total of 34 non-smoking healthy adult participants who travelled abroad to selected cities from the New York City (NYC) metropolitan area were pre-trained to measure lung function, blood pressure and heart rate (HR)/HR variability (HRV) and record symptoms before, during and after travelling abroad. Outdoor particulate matter (PM)2.5 concentrations were obtained from central monitors in each city. Associations between PM exposure concentrations and cardiopulmonary health endpoints were analysed using a mixed effects statistical design. RESULTS: East and South Asian cities had significantly higher PM2.5 concentrations compared with pre-travel NYC PM2.5 levels, with maximum concentrations reaching 503 µg/m3. PM exposure-related associations for lung function were statistically significant and strongest between evening Forced Expiratory Volume in the first second (FEV1) and same-day morning PM2.5 concentrations; a 10-µg/m3 increase in outdoor PM2.5 was associated with a mean decrease of 7 mL. Travel to a highly polluted city (PM2.5 > 100 µg/m3) was associated with a 209-ml reduction in evening FEV1 compared with a low polluted city (PM2.5 < 35 µg/m3). In general, participants who travelled to East and South Asian cities experienced increased respiratory symptoms/scores and changes in HR and HRV. CONCLUSIONS: Exposure to increased levels of PM2.5 in cities abroad caused small but statistically significant acute changes in cardiopulmonary function and respiratory symptoms in healthy young adults. These data suggest that travel-related exposure to increased PM2.5 adversely impacts cardiopulmonary health, which may be particularly important for travellers with pre-existing respiratory or cardiac disease.

Malignant human cell transformation of Marcellus Shale gas drilling flow back water.

The rapid development of high-volume horizontal hydraulic fracturing for mining natural gas from shale has posed potential impacts on human health and biodiversity. The produced flow back waters after hydraulic stimulation are known to carry high levels of saline and total dissolved solids. To understand the toxicity and potential carcinogenic effects of these wastewaters, flow back waters from five Marcellus hydraulic fracturing oil and gas wells were analyzed. The physicochemical nature of these samples was analyzed by inductively coupled plasma mass spectrometry and scanning electron microscopy/energy dispersive X-ray spectroscopy. A cytotoxicity study using colony formation as the endpoint was carried out to define the LC50 values of test samples using human bronchial epithelial cells (BEAS-2B). The BEAS-2B cell transformation assay was employed to assess the carcinogenic potential of the samples. Barium and strontium were among the most abundant metals in these samples and the same metals were found to be elevated in BEAS-2B cells after long-term treatment. BEAS-2B cells treated for 6weeks with flow back waters produced colony formation in soft agar that was concentration dependent. In addition, flow back water-transformed BEAS-2B cells show better migration capability when compared to control cells. This study provides information needed to assess the potential health impact of post-hydraulic fracturing flow back waters from Marcellus Shale natural gas mining.

Air quality in New York City hookah bars.

BACKGROUND: Hookahs are increasingly being used in the USA 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. This study investigated levels of multiple indices of indoor air pollution in hookah bars in NYC. METHODS: Air samples were collected in 8 hookah bars in NYC. Along with venue characteristics, real-time measurements of fine particulate matter (PM2.5), black carbon (BC), and carbon monoxide (CO), and 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/m(3), whereas the filter-based total PM mean was 691.3 (592.6) µg/m(3). The mean real time BC level was 4.1 (2.3) µg/m(3), OC was 237.9 (112.3) µg/m(3), and CO was 32 (16) ppm. Airborne nicotine was present in all studied hookah bars (4.2 (1.5) µg/m(3)). 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 that may present a 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.

Rapid doubling of Alzheimer's amyloid-ß40 and 42 levels in brains of mice exposed to a nickel nanoparticle model of air pollution.

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-ß peptides Aß40 and Aß42, as well as Aß42/40 (p <0.01). CONCLUSIONS: These effects on elevation of brain Aß 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.