| 1. |
- Landrigan, Philip, et al.
(author)
-
Reducing disease and death from Artisanal and Small-Scale Mining (ASM) - the urgent need for responsible mining in the context of growing global demand for minerals and metals for climate change mitigation
- 2022
-
In: Environmental Health. - : BioMed Central (BMC). - 1476-069X. ; 21:1
-
Journal article (peer-reviewed)abstract
- Artisanal and small-scale mining (ASM) takes place under extreme conditions with a lack of occupational health and safety. As the demand for metals is increasing due in part to their extensive use in 'green technologies' for climate change mitigation, the negative environmental and occupational consequences of mining practices are disproportionately felt in low- and middle-income countries. The Collegium Ramazzini statement on ASM presents updated information on its neglected health hazards that include multiple toxic hazards, most notably mercury, lead, cyanide, arsenic, cadmium, and cobalt, as well as physical hazards, most notably airborne dust and noise, and the high risk of infectious diseases. These hazards affect both miners and mining communities as working and living spaces are rarely separated. The impact on children and women is often severe, including hazardous exposures during the child-bearing age and pregnancies, and the risk of child labor. We suggest strategies for the mitigation of these hazards and classify those according to primordial, primary, secondary, and tertiary prevention. Further, we identify knowledge gaps and issue recommendations for international, national, and local governments, metal purchasers, and employers are given. With this statement, the Collegium Ramazzini calls for the extension of efforts to minimize all hazards that confront ASM miners and their families.
|
|
| 2. |
- Lundbäck, Magnus, 1976-
(author)
-
Cardiovascular effects of diesel exhaust : mechanistic and interventional studies
- 2009
-
Doctoral thesis (other academic/artistic)abstract
- Background: Air pollution is associated with negative health effects. Exposure to combustion-derived particulate matter (PM) air pollution has been related to increased incidence of cardiovascular and respiratory morbidity and mortality, specifically in susceptible populations. Ambient particles, with a diameter of less than 2.5 mm, have been suggested to be the strongest contributor to these health effects. Diesel exhaust (DE) is a major source of small combustion-derived PM air pollution world wide. In healthy volunteers, exposure to DE, has been associated with airway inflammation and impaired vasomotor function and endogenous fibrinolysis. The aims of this thesis were to further elucidate the underlying mechanisms to the reported cardiovascular effects following exposure to DE, with specific focus on endothelin-1 (ET-1). Additionally, the vascular effects of the major gaseous component of DE, nitrogen dioxide (NO2), were assessed together with the impact of an exhaust particle trap to reduce the observed negative vascular effects after DE exposure. Methods: In all studies healthy, non-smoking male volunteers were included and exposed for one hour during intermittent exercise in a randomised double-blind crossover fashion. In studies I-III, subjects were exposed to DE at a particulate matter concentration of approximately 300 μg/m3 and filtered air, on two different occasions. In study V an additional exposure was employed, during which DE was filtered through an exhaust particle trap. In study IV subjects were exposed to nitrogen dioxide (NO2) at 4 ppm or filtered air. In study I, thrombus formation and platelet activation were assessed using the Badimon ex vivo perfusion chamber and flow cytometry. Study II comprised the determination of arterial stiffness including pulse wave analysis and velocity. In studies III-V, vascular assessment was performed using venous occlusion plethysmography. In studies IV and V, the vascular responses to intra-arterially infused endothelial-dependent and endothelial-independent vasodilatators were registered. In study III, vascular responses to intra-arterial infusion of Endothelin-1 (ET-1) and ET-1-receptor antagonists were assessed. Venous occlusion phlethysmography was in all cases performed 4-6 hours following exposures. Blood samples for markers of inflammation, coagulation and platelet activation were collected before and throughout the study periods in studies III and V. Results: Exposure to DE increased ex vivo thrombus formation and arterial stiffness, in terms of augmentation index. DE inhalation impaired vasomotor function and endogenous fibrinolysis. The exhaust particle trap reduced the particle concentration by 98% and abolished the effects on vasomotor function, endogenous fibrinolysis and ex vivo thrombus formation. Plasma concentrations of ET-1 and its precursor big-ET-1 were unchanged following exposure. Dual endothelial receptor antagonism caused similar vasodilatation after both exposures, although vasodilatation to the endothelin-A receptor alone was blunted after DE exposure. ET-1 infusion induced vasoconstriction only following DE exposure. Exposure to nitrogen dioxide did not affect vascular function. Conclusion: Inhalation of diesel exhaust in young healthy men impaired important and complementary aspects of vascular function in humans; regulation of vascular tone and endogenous fibrinolysis as well as increased ex vivo thrombus formation. The use of an exhaust particle trap significantly reduced particle emissions and abolished the DE-induced vascular and prothrombotic effects. The adverse vascular effects following DE exposure do not appear to be directly mediated through the endothelin system. Neither is NO2 suggested to be a major arbiter of the DE-induced cardiovascular responses. Arterial stiffness is a non-invasive and easily accessible method and could thus be employed to address vascular function in larger field studies. Taken together, this thesis has given further knowledge about the mechanisms underlying the DE-induced vascular effects.
|
|
| 3. |
- Nawrot, Tim S, et al.
(author)
-
Oxidative properties of ambient PM2.5 and elemental composition : heterogeneous associations in 19 European cities
- 2009
-
In: Atmospheric Environment. - : Elsevier BV. - 1352-2310 .- 1873-2844. ; 43:30, s. 4595-4602
-
Journal article (peer-reviewed)abstract
- We assessed the extent to which constituents of PM2.5 (transition metals, sodium, chloride) contribute to the ability to generate hydroxyl radicals (OH) in vitro in PM2.5 sampled at 20 locations in 19 European centres participating in the European Community Respiratory Health Survey. PM2.5 samples (n = 716) were collected on filters over one year and the oxidative activity of particle suspensions obtained from these filters was then assessed by measuring their ability to generate OH in the presence of hydrogen peroxide. Associations between OH formation and the studied PM constituents were heterogeneous. The total explained variance ranged from 85% in Norwich to only 6% in Albacete. Among the 20 centres, 15 showed positive correlations between one or more of the measured transition metals (copper, iron, manganese, lead, vanadium and titanium) and OH formation. In 9 of 20 centres OH formation was negatively associated with chloride, and in 3 centres with sodium. Across 19 European cities, elements which explained the largest variations in OH formation were chloride, iron and sodium.
|
|
