Ambient air pollution and thrombosis

Abstract Air pollution is a growing public health concern of global significance. Acute and chronic exposure is known to impair cardiovascular function, exacerbate disease and increase cardiovascular mortality. Several plausible biological mechanisms have been proposed for these associations, however, at present, the pathways are incomplete. A seminal review by the American Heart Association (2010) concluded that the thrombotic effects of particulate air pollution likely contributed to their effects on cardiovascular mortality and morbidity. The aim of the current review is to appraise the newly accumulated scientific evidence (2009–2016) on contribution of haemostasis and thrombosis towards cardiovascular disease induced by exposure to both particulate and gaseous pollutants. Seventy four publications were reviewed in-depth. The weight of evidence suggests that acute exposure to fine particulate matter (PM2.5) induces a shift in the haemostatic balance towards a pro-thrombotic/pro-coagulative state. Insufficient data was available to ascertain if a similar relationship exists for gaseous pollutants, and very few studies have addressed long-term exposure to ambient air pollution. Platelet activation, oxidative stress, interplay between interleukin-6 and tissue factor, all appear to be potentially important mechanisms in pollution-mediated thrombosis, together with an emerging role for circulating microvesicles and epigenetic changes. Overall, the recent literature supports, and arguably strengthens, the contention that air pollution contributes to cardiovascular morbidity by promoting haemostasis. The volume and diversity of the evidence highlights the complexity of the pathophysiologic mechanisms by which air pollution promotes thrombosis; multiple pathways are plausible and it is most likely they act in concert. Future research should address the role gaseous pollutants play in the cardiovascular effects of air pollution mixture and direct comparison of potentially susceptible groups to healthy individuals

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Not AvailableThe objective of the present investigation was to study the efficiency of an ISMav2 polymerase chain reaction (PCR) in detecting Mycobacterium avium subspecies paratuberculosis (MAP) DNA in archived alcohol-fixed sheep tissues and compare with Ziehl Neelesen (ZN) staining, bacterial culture on Herrold’s egg yolk medium and IS900 PCR on fresh tissues. Tissue samples preserved in 70% alcohol for 6–8 months from 23 naturally infected paratuberculosis sheep and 7 healthy sheep were used for DNA extraction. In PCR amplification targeting ISMav2 gene of MAP, 19 (82.6%) were found to be positive. Bacterial culture, ZN and fresh tissue IS900 PCR detected 65%, 100%, and 95% cases, respectively. It was concluded that alcohol could be an alternative fixative for transportation of tissues for molecular detection of MAP genome in tissues by ISMav2 PCR, which compared well with fresh tissue IS900 PCR for the diagnosis of paratuberculosis in sheep. This may be useful in tropical countries, where shipment of fresh tissues for molecular diagnosis may be expensive proposition and most of the times facilities for maintaining cold chain are not available.Not Availabl

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Heterogeneous ozone effects on the DNA methylome of bronchial cells observed in a crossover study.

We used a randomized crossover experiment to estimate the effects of ozone (vs. clean air) exposure on genome-wide DNA methylation of target bronchial epithelial cells, using 17 volunteers, each randomly exposed on two separated occasions to clean air or 0.3-ppm ozone for two hours. Twenty-four hours after exposure, participants underwent bronchoscopy to collect epithelial cells whose DNA methylation was measured using the Illumina 450 K platform. We performed global and regional tests examining the ozone versus clean air effect on the DNA methylome and calculated Fisher-exact p-values for a series of univariate tests. We found little evidence of an overall effect of ozone on the DNA methylome but some suggestive changes in PLSCR1, HCAR1, and LINC00336 DNA methylation after ozone exposure relative to clean air. We observed some participant-to-participant heterogeneity in ozone responses