Sarah Robertson

Exposures and health outcomes in relation to bioaerosol emissions from composting facilities: a systematic review of occupational and community studies.

The number of composting sites in Europe is rapidly increasing, due to efforts to reduce the fraction of waste destined for landfill, but evidence on possible health impacts is limited. This article systematically reviews studies related to bioaerosol exposures within and near composting facilities and associated health effects in both community and occupational health settings. Six electronic databases and bibliographies from January 1960 to July 2014 were searched for studies reporting on health outcomes and/or bioaerosol emissions related to composting sites. Risk of bias was assessed using a customized score. Five hundred and thirty-six papers were identified and reviewed, and 66 articles met the inclusion criteria (48 exposure studies, 9 health studies, 9 health and exposure studies). Exposure information was limited, with most measurements taken in occupational settings and for limited time periods. Bioaerosol concentrations were highest on-site during agitation activities (turning, shredding, and screening). Six studies detected concentrations of either Aspergillus fumigatus or total bacteria above the English Environment Agency’s recommended threshold levels beyond 250 m from the site. Occupational studies of compost workers suggested elevated risks of respiratory illnesses with higher bioaerosol exposures. Elevated airway irritation was reported in residents near composting sites, but this may have been affected by reporting bias. The evidence base on health effects of bioaerosol emissions from composting facilities is still limited, although there is sufficient evidence to support a precautionary approach for regulatory purposes. While data to date are suggestive of possible respiratory effects, further study is needed to confirm this and to explore other health outcomes.

CD36 Mediates Endothelial Dysfunction Downstream of Circulating Factors Induced by O3 Exposure

Inhaled pollutants induce the release of vasoactive factors into the systemic circulation, but little information is available regarding the nature of these factors or their receptors. The pattern recognition receptor CD36 interacts with many damage-related circulating molecules, leading to activation of endothelial cells and promoting vascular inflammation; therefore, we hypothesized that CD36 plays a pivotal role in mediating cross talk between inhaled ozone (O3)-induced circulating factors and systemic vascular dysfunction. O3 exposure (1 ppm × 4h) induced lung inflammation in wild-type (WT) mice, which was absent in the CD36 deficient (CD36(-/-)) mice. Acetylcholine (ACh)-evoked vasorelaxation was impaired in isolated aortas from O3-exposed WT mice but not in vessels from CD36(-/-) mice. To delineate whether vascular impairments were caused by lung inflammation or CD36-mediated generation of circulating factors, naïve aortas were treated with diluted serum from control or O3-exposed WT mice, which recapitulated the impairments of vasorelaxation observed after inhalation exposures. Aortas from CD36(-/-) mice were insensitive to the effects of O3-induced circulating factors, with robust vasorelaxation responses in the presence of serum from O3-exposed WT mice. Lung inflammation was not a requirement for production of circulating vasoactive factors, as serum from O3-exposed CD36(-/-) mice could inhibit vasorelaxation in naïve WT aortas. These results suggest that O3 inhalation induces the release of circulating bioactive factors capable of impairing vasorelaxation to ACh via a CD36-dependent signaling mechanism. Although lung inflammatory and systemic vascular effects were both dependent on CD36, the presence of circulating factors appears to be independent of CD36 and inflammatory responses.

Microglial priming through the lung–brain axis: the role of air pollution–induced circulating factors

Air pollution is implicated in neurodegenerative disease risk and progression and in microglial activation, but the mechanisms are unknown. In this study, microglia remained activated 24 h after ozone (O3) exposure in rats, suggesting a persistent signal from lung to brain. Ex vivo analysis of serum from O3‐treated rats revealed an augmented microglial proinflammatory response and β‐amyloid 42 (Aβ42) neurotoxicity independent of traditional circulating cytokines, where macrophage‐1 antigen‐mediated microglia proinflammatory priming. Aged mice exhibited reduced pulmonary immune profiles and the most pronounced neuroinflammation and microglial activation in response to mixed vehicle emissions. Consistent with this premise, cluster of differentiation 36 (CD36)–/– mice exhibited impaired pulmonary immune responses concurrent with augmented neuroinflammation and microglial activation in response to O3. Further, aging glia were more sensitive to the proinflammatory effects of O3 serum. Together, these findings outline the lung‐brain axis, where air pollutant exposures result in circulating, cytokine‐independent signals present in serum that elevate the brain proinflammatory milieu, which is linked to the pulmonary response and is further augmented with age.—Mumaw, C. L., Levesque, S., McGraw, C., Robertson, S., Lucas, S., Stafflinger, J. E., Campen, M. J., Hall, P., Norenberg, J. P., Anderson, T., Lund, A. K., McDonald, J. D., Ottens, A. K., Block, M. L. Microglial priming through the lung‐brain axis: the role of air pollution‐induced circulating factors. FASEB J. 30, 1880–1891 (2016). www.fasebj.org

OZONE INHALATION IMPAIRS CORONARY ARTERY DILATION VIA INTRACELLULAR OXIDATIVE STRESS: EVIDENCE FOR SERUM-BORNE FACTORS AS DRIVERS OF SYSTEMIC TOXICITY

Ambient ozone (O3) levels are associated with cardiovascular morbidity and mortality, but the underlying pathophysiological mechanisms driving extrapulmonary toxicity remain unclear. This study examined the coronary vascular bed of rats in terms of constrictive and dilatory responses to known agonists following a single O3 inhalation exposure. In addition, serum from exposed rats was used in ex vivo preparations to examine whether bioactivity and toxic effects of inhaled O3 could be conveyed to extrapulmonary systems via the circulation. We found that 24 h following inhalation of 1 ppm O3, isolated coronary vessels exhibited greater basal tone and constricted to a greater degree to serotonin stimulation. Vasodilation to acetylcholine (ACh) was markedly diminished in coronary arteries from O3-exposed rats, compared with filtered air-exposed controls. Dilation to ACh was restored by combined superoxide dismutase and catalase treatment, and also by NADPH oxidase inhibition. When dilute (10%) serum from exposed rats was perfused into the lumen of coronary arteries from unexposed, naïve rats, the O3-induced reduction in vasodilatory response to ACh was partially recapitulated. Furthermore, following O3 inhalation, serum exhibited a nitric oxide scavenging capacity, which may partially explain blunted ACh-mediated vasodilatory responses. Thus, bioactivity from inhalation exposures may be due to compositional changes of the circulation. These studies shed light on possible mechanisms of action that may explain O3-associated cardiac morbidity and mortality in humans.

Engine exhaust particulate and gas phase contributions to vascular toxicity

Abstract Cardiovascular health effects of near-roadway pollution appear more substantial than other sources of air pollution. The underlying cause of this phenomenon may simply be concentration-related, but the possibility remains that gases and particulate matter (PM) may physically interact and further enhance systemic vascular toxicity. To test this, we utilized a common hypercholesterolemic mouse model (Apolipoprotein E-null) exposed to mixed vehicle emission (MVE; combined gasoline and diesel exhausts) for 6 h/d × 50 d, with additional permutations of removing PM by filtration and also removing gaseous species from PM by denudation. Several vascular bioassays, including matrix metalloproteinase-9 protein, 3-nitrotyrosine and plasma-induced vasodilatory impairments, highlighted that the whole emissions, containing both particulate and gaseous components, was collectively more potent than MVE-derived PM or gas mixtures, alone. Thus, we conclude that inhalation of fresh whole emissions induce greater systemic vascular toxicity than either the particulate or gas phase alone. These findings lend credence to the hypothesis that the near-roadway environment may have a more focused public health impact due to gas–particle interactions.

Ambient air pollution and thrombosis

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.

A systematic review of the public health risks of bioaerosols from intensive farming

BACKGROUND Population growth, increasing food demands, and economic efficiency have been major driving forces behind farming intensification over recent decades. However, biological emissions (bioaerosols) from intensified livestock farming may have the potential to impact human health. Bioaerosols from intensive livestock farming have been reported to cause symptoms and/or illnesses in occupational-settings and there is concern about the potential health effects on people who live near the intensive farms. As well as adverse health effects, some potential beneficial effects have been attributed to farm exposures in early life. The aim of the study was to undertake a systematic review to evaluate potential for adverse health outcomes in populations living near intensive livestock farms. MATERIAL AND METHODS Two electronic databases (PubMed and Scopus) and bibliographies were searched for studies reporting associations between health outcomes and bioaerosol emissions related to intensive farming published between January 1960 and April 2017, including both occupational and community studies. Two authors independently assessed studies for inclusion and extracted data. Risk of bias was assessed using a customized score. RESULTS 38 health studies met the inclusion criteria (21 occupational and 1 community study measured bioaerosol concentrations, 16 community studies using a proxy measure for exposure). The majority of occupational studies found a negative impact on respiratory health outcomes and increases in inflammatory biomarkers among farm workers exposed to bioaerosols. Studies investigating the health of communities living near intensive farms had mixed findings. All four studies of asthma in children found increased reported asthma prevalence among children living or attending schools near an intensive farm. Papers principally investigated respiratory and immune system outcomes. CONCLUSIONS The review indicated a potential impact of intensive farming on childhood respiratory health, based on a small number of studies using self-reported outcomes, but supported by findings from occupational studies. Further research is needed to measure and monitor exposure in community settings and relate this to objectively measured health outcomes.