Pulmonary phthalate exposure and asthma - is PPAR a plausible mechanistic link?

Due to their extensive use as plasticisers in numerous consumer products, phthalates have become ubiquitous environmental contaminants. An increasing number of epidemiological studies suggest that exposure to phthalates may be associated with worsening or development of airway diseases. Peroxisome Proliferation Activated Receptors (PPAR)s, identified as important targets for phthalates in early studies in rodent liver, have been suggested as a possible mechanistic link. In this review we discuss the likelihood of an involvement of PPARs in asthma development and exacerbation due to pulmonary phthalate exposure. First, we go through the literature on indoor air levels of phthalates and pulmonary phthalate kinetics. These data are then used to estimate the pulmonary phthalate levels due to inhalation exposure. Secondly, the literature on phthalate-induced activation or modulation of PPARs is summarized. Based on these data, we discuss whether pulmonary phthalate exposure is likely to cause PPAR activation, and if this is a plausible mechanism for adverse effects of phthalates in the lung. It is concluded that the pulmonary concentrations of some phthalates may be sufficient to cause a direct activation of PPARs. Since PPARs mainly mediate anti-inflammatory effects in the lungs, a direct activation is not a likely molecular mechanism for adverse effects of phthalates. However, possible modulatory effects of phthalates on PPARs deserve further investigation, including partial antagonist effects and/or cross talk with other signalling pathways. Moreover other mechanisms, including interactions between phthalates and other receptors, could also contribute to possible adverse pulmonary effects of phthalates

Emission factors from residential combustion appliances burning Portuguese biomass fuels

Smoke from residential wood burning has been identified as a major contributor to air pollution, motivating detailed emission measurements under controlled conditions. A series of experiments were performed to compare the emission levels from two types of wood-stoves to those of fireplaces. Eight types of biomass were burned in the laboratory: wood from seven species of trees grown in the Portuguese forest (Pinus pinaster, Eucalyptus globulus, Quercus suber, Acacia longifolia, Quercus faginea, Olea europaea and Quercus ilex rotundifolia) and briquettes produced from forest biomass waste. Average emission factors were in the ranges 27.5–99.2 g CO kg 1, 552–1660 g CO2 kg 1, 0.66– 1.34 g NO kg 1, and 0.82–4.94 g hydrocarbons kg 1 of biomass burned (dry basis). Average particle emission factors varied between 1.12 and 20.06 g kg 1 biomass burned (dry basis), with higher burn rates producing significantly less particle mass per kg wood burned than the low burn rates. Particle mass emission factors from wood-stoves were lower than those from the fireplace. The average emission factors for organic and elemental carbon were in the intervals 0.24–10.1 and 0.18–0.68 g kg 1 biomass burned (dry basis), respectively. The elemental carbon content of particles emitted from the energyefficient ‘‘chimney type’’ logwood stove was substantially higher than in the conventional cast iron stove and fireplace, whereas the opposite was observed for the organic carbon fraction. Pinus pinaster, the only softwood species among all, was the biofuel with the lowest emissions of particles, CO, NO and hydrocarbons

PAH emissions from an African cookstove

Combustion of wood and other biomass is a significant contributor to poor air quality in many developing countries. Emissions of particulates and Polycyclic Aromatic Hydrocarbons (PAH) are a major health hazard, particularly in Africa where the use of domestic cookstoves has increased alongside population expansion. Because of economic factors firewood is commonly used in place of the more expensive charcoal; particularly in rural areas. This work conducts a study of PAH emissions from an African cookstove comparing the combustion of both charcoal and firewood. It is demonstrated that PAH and particulate emissions are much higher from the firewood compared to the charcoal. The difference in levels can be interpreted due to the importance of the pyrolysis reactions of the volatile components of wood in PAH formation, whereas these volatiles emissions are much smaller from charcoal. Analysis of the combustion phases (flaming, smouldering) is undertaken and a computer model has been developed to link the composition of the fuels to the emissions of the PAH and particulates. The modelled PAH levels are shown to follow a similar trend to the experimental results

Bisphenol A Is More Potent than Phthalate Metabolites in Reducing Pancreatic β-Cell Function

Bisphenol A (BPA) and phthalates are common environmental contaminants that have been proposed to influence incidence and development of types 1 and 2 diabetes. Thus, effects of BPA and three phthalate metabolites (monoisobutyl phthalate (MiBP), mono-n-butyl phthalate (MnBP), and mono-(2-ethylhexyl) phthalate (MEHP)) were studied in the pancreatic β-cell line INS-1E, after 2–72 h of exposure to 5–500 μM. Three endpoints relevant to accelerated development of types 1 or 2 diabetes were investigated: β-cell viability, glucose-induced insulin secretion, and β-cell susceptibility to cytokine-induced cell death. BPA and the phthalate metabolites reduced cellular viability after 72 h of exposure, with BPA as the most potent chemical. Moreover, BPA, MEHP, and MnBP increased insulin secretion after 2 h of simultaneous exposure to chemicals and glucose, with potency BPA > MEHP > MnBP. Longer chemical exposures (24–72 h) showed no consistent effects on glucose-induced insulin secretion, and none of the environmental chemicals affected susceptibility to cytokine-induced cell death. Overall, BPA was more potent than the investigated phthalate metabolites in affecting insulin secretion and viability in the INS-1E pancreatic β-cells. In contrast to recent literature, concentrations with relevance to human exposures (1–500 nM) did not affect the investigated endpoints, suggesting that this experimental model displayed relatively low sensitivity to environmental chemical exposure

Enniatin B-induced cell death and inflammatory responses in RAW 267.4 murine macrophages.

International audienceThe mycotoxin enniatin B (EnnB) is predominantly produced by species of the Fusarium genera, and often found in grain. The cytotoxic effect of EnnB has been suggested to be related to its ability to form ionophores in cell membranes. The present study examines the effects of EnnB on cell death, differentiation, proliferation and pro-inflammatory responses in the murine monocyte-macrophage cell line RAW 264.7. Exposure to EnnB for 24 h caused an accumulation of cells in the G0/G1-phase with a corresponding decrease in cyclin D1. This cell cycle-arrest was possibly also linked to the reduced cellular ability to capture and internalize receptors as illustrated by the lipid marker ganglioside GM1. EnnB also increased the number of apoptotic, early apoptotic and necrotic cells, as well as cells with elongated spindle-like morphology. The Neutral Red assay indicated that EnnB induced lysosomal damage; supported by transmission electron microscopy (TEM) showing accumulation of lipids inside the lysosomes forming lamellar structures/myelin bodies. Enhanced levels of activated caspase-1 were observed after EnnB exposure and the caspase-1 specific inhibitor ZYVAD-FMK reduced EnnB-induced apoptosis. Moreover, EnnB increased the release of interleukin-1 beta (IL-1β) in cells primed with lipopolysaccharide (LPS), and this response was reduced by both ZYVAD-FMK and the cathepsin B inhibitor CA-074Me. In conclusion, EnnB was found to induce cell cycle arrest, cell death and inflammation. Caspase-1 appeared to be involved in the apoptosis and release of IL-1β and possibly activation of the inflammasome through lysosomal damage and leakage of cathepsin B

Overvåking av Indre Oslofjord i 2013 - Vedleggsrapport

Her rapporteres resultatene fra overvåkingen i Indre Oslofjord i 2013. En mindre omfattende beskrivelse av resultatene er gitt i NIVA rapport nr. 6697. Undersøkelsene omfatter fysiske, kjemiske og biologiske forhold. Overvåkingen ble gjennomført i samarbeid med Universitetet i Oslo. Vannutskiftningen i Indre Oslofjord var i 2013 god. Oksygenforholdene i Bunnefjorden viser en endring i positiv retning fra 2001, sammenfallende i tid med når dyputslippet fra det nye Bekkelaget renseanlegg ble satt i drift. Også i Vestfjorden antydes en forbedring i oksygensituasjonen. Den totale algebiomassen integrert over året var ca. 10 % lavere enn de to foregående årene, mens mengden klorofyll i 2013 var omtrent i samme nivå som gjennomsnittet for perioden 2002-2010. De lokale næringssalttilførslene til Indre Oslofjord har blitt betydelig redusert siden midten av 1970-tallet til 2003, men har siden økt frem til 2007, hvor etterverdiene har ligget omtrent på samme nivå. Kapasiteten på rensing av kommunalt avløpsvann er i ferd med å bli sprengt. Midlere siktedyp var i 2013 i samme nivå eller svakt høyere enn middelverdien for årene 2002-2010. I 2013 ble det observert mye reker (unntatt ved Vesthullet). Det var også uvanlig mange rekearter ved Hellvik i Bunnefjorden og i Lysakerfjorden. Forekomsten av tang viste en positiv utvikling i Vestfjorden og Bunnefjorden, og negativ utvikling i sørlige deler av Vestfjorden og Drøbak-området. Øyepål var den dominerende fiskearten på dypt vann. Både gapeflyndre, hvitting og sølvtorsk og til dels sypike var også blant de mer tallrike artene. Rekrutteringen av torsk i Oslofjorden har ligget under gjennomsnittet for Skagerrak. I 2013 var fangsten av ørret i Indre Oslofjord 3.5 ganger større enn langtidsgjennomsnittet for Skagerrak. Resultatene fra de siste ti årene har generelt vist tegn til gradvis mindre effekter av miljøgifter på torsken i Indre Oslofjord, men påvirkningen er likevel større enn i Ytre Oslofjord