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.

Rapid population growth and urbanisation around the world has led to increasing waste generation rates. Composting of organic waste in large-scale facilities is part of a growing trend in the UK, and elsewhere, to better manage and re-use the organic waste. However, composting inevitably generates bioaerosols, which have been associated with human health effects. In 2015, we reported that there was some, albeit limited, qualitative evidence linking bioaerosol emissions from composting facilities to poor respiratory health in nearby residents. However, the limited evidence precluded any quantitative assessment. Since then, the number of operational industrial-scale composting facilities in England has increased by 9% - nearly twice the growth from 2012 to 2014. At the same time, rapid urbanisation has led to expansion of city borders with more people living near large composting facilities and exposed to bioaerosol pollution. It is essential that regulatory authorities have access to the most up to date and accurate information. In this update of a systematic review published in 2015, we review and summarise the evidence from more recent studies that have assessed bioaerosol exposures within and near composting facilities and their associated health effects in both community and occupational health settings. Specifically, we wanted to find out if new evidence has emerged since the previous review to strengthen and confirm its conclusions. Two electronic databases (Medline and Embase) and bibliographies were searched for studies reporting on health outcomes and/or exposure to bioaerosols from composting facilities published between 1 January 2014 and 15 June 2018. Identification of relevant articles and data extraction was undertaken and studies were assessed for risk of bias. 23 studies met the inclusion criteria (15 exposure studies, 4 health studies, 4 health and exposure studies (one of which used an exposure proxy)). The majority of studies were conducted in occupational settings, and over short time periods. Some progress has been made in the characterisation of bioaerosol emissions from these composting facilities, with the application of molecular-based methods. Whilst the latest health studies do not rely solely on subjective self-reported measures of health status but include more objective health measures, these studies were almost exclusively carried out in compost workers and were characterised by profound methodological limitations. Only one community health study was identified and used a proxy measure of bioaerosol exposure. Although this review identified an additional 23 studies since the earlier review, the conclusions remain largely unchanged. Given the absence of any consistent evidence on the toxicity of bioaerosols from composting facilities, there is insufficient evidence to provide a quantitative comment on the risk to nearby residents from exposure to compost bioaerosols. To improve risk assessment and to best advise on risk management, it is important to ensure that the research recommendations outlined in this review are addressed.

Nanomaterial inhalation represents a potential hazard for respiratory conditions such as asthma. Cerium dioxide nanoparticles (CeO2NPs) have the ability to modify disease outcome but have not been investigated for their effect on models of asthma and inflammatory lung disease. The aim of this study was to examine the impact of CeO2NPs in a house dust mite (HDM) induced murine model of asthma. Repeated intranasal instillation of CeO2NPs in the presence of HDM caused the induction of a type II inflammatory response, characterised by increased bronchoalveolar lavage eosinophils, mast cells, total plasma IgE and goblet cell metaplasia. This was accompanied by increases in IL-4, CCL11 and MCPT1 gene expression together with increases in the mucin and inflammatory regulators CLCA1 and SLC26A4. CLCA1 and SLC26A4 were also induced by CeO2NPs + HDM co-exposure in air liquid interface cultures of human primary bronchial epithelial cells. HDM induced airway hyperresponsiveness and airway remodelling in mice were not altered with CeO2NPs co-exposure. Repeated HMD instillations followed by a single exposure to CeO2NPs failed to produce changes in type II inflammatory endpoints but did result in alterations in the neutrophil marker CD177. Treatment of mice with CeO2NPs in the absence of HDM did not have any significant effects. RNA-SEQ was used to explore early effects 24 h after single treatment exposures. Changes in SAA3 expression paralleled increased neutrophil BAL levels, while no changes in eosinophil or lymphocyte levels were observed. HDM resulted in a strong induction of type I interferon and IRF3 dependent gene expression, which was inhibited with CeO2NPs co-exposure. Changes in the expression of genes including CCL20, CXCL10, NLRC5, IRF7 and CLEC10A suggest regulation of dendritic cells, macrophage functionality and IRF3 modulation as key early events in how CeO2NPs may guide pulmonary responses to HDM towards type II inflammation. CeO2NPs were observed to modulate the murine pulmonary response to house dust mite allergen exposure towards a type II inflammatory environment. As this type of response is present within asthmatic endotypes this finding may have implications for how occupational or incidental exposure to CeO2NPs should be considered for those susceptible to disease.

Purpose: To evaluate implantation potential of cleavage-stage embryos cultured in medium containing 2 ng/ml granulocyte–macrophage colony-stimulating factor (GM-CSF) versus control medium, according to embryo morphological quality and then transferred on day 3. Methods: Explorative secondary data analysis of a multicenter, randomized, placebo-controlled, double-blinded prospective study of 1149 couples with embryo transfer after IVF/ICSI. This analysis includes a subgroup of 422 subjects with either single-embryo transfer (SET, N = 286) or double-embryo transfer of two embryos with equivalent morphological quality (DET, N = 136). Implantation rate and live birth rate were assessed according to category of morphological embryo quality on day 3. Results: Culture with GM-CSF did not increase the implantation rate for embryos classified as poor quality. A trend towards greater benefit of GM-CSF on implantation and survival until live birth for top-quality embryos (TQEs) compared with poor-quality embryos was observed, although not statistically significant. For TQEs, the percentage of transferred embryos resulting in a live born baby was: 40.9 ± 5.3% (GM-CSF) versus 30.5 ± 4.6% (control) (P = 0.24; odds ratio [OR] 1.43, 95% confidence interval [CI] 0.79–2.59), and for embryos with less than 6 cells at day 3 this same rate was: 7.4 ± 3.3% (GM-CSF) versus 12.0 ± 4.0% (control) (P = 0.26; OR 0.53, 95% CI 0.17–1.61). Conclusion: This exploratory analysis is consistent with GM-CSF protecting morphologically normal embryos from culture-induced stress and does not support an effect of GM-CSF in rescuing poor-quality embryos. ClinicalTrials.gov identifier: NCT00565747.