Real-time air concentrations and turbulent fluxes of volatile organic compounds (VOCs) over historic closed landfills to assess their potential environmental impact.

For the first time, emission/deposition fluxes of volatile organic compounds (VOCs) and H2S from a historic closed landfill site in Southern Italy were determined by Eddy Covariance (EC) using Proton Transfer Reaction Time-of-Flight Mass Spectrometry (PTR-TOF-MS). This was done in two field campaigns of one week performed in July and October 2016, where fluxes of CO2 and CH4 were also measured. Many compounds not previously identified in the biogas were detected by PTR-TOF-MS, but only in July some of them produced positive fluxes exceeding the flux limit of detection. Methanol was the most emitted compound with an average flux of 44.20 ± 4.28 µg m-2 h-1, followed by toluene with a mean flux of 18.97 ± 2.47 µg m-2 h-1. Toluene fluxes were 10 times higher than those of benzene, fitting rather well with values previously measured in the biogas. VOCs emission fluxes of monoterpenes and highly reactive arenes did not reflect, however, the biogas composition. This, combined with tiny emissions of VOC oxidation products, suggests that landfill emissions underwent some photochemical degradation before being dispersed in the atmospheric boundary layer (ABL). Deposition fluxes of some VOCs emitted from the sea was also observed in July. No relevant VOC fluxes were instead measured in October, suggesting that temperature was the variable controlling most landfill emission. Albeit small, summer landfill emissions from the investigated site can have an impact on the population living nearby, because they contain or still generate compounds that causing nuisance.

Evidence that hereditary pancreatitis is genetically heterogeneous disorder.

Hereditary pancreatitis (HP) is an autosomal dominant disorder characterized by recurrent acute attacks of severe abdominal pain with an onset in early childhood. Many HP patients progress to complicated chronic pancreatitis and/or pancreatic cancer. Initially, a single mutation R117H in the cationic trypsinogen gene was detected in all affected members of five unrelated HP families. Further studies identified a second mutation (N21L) in two HP families without the R117H mutation. Before the association between cationic trypsinogen and HP was found, we detected a cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation (L327R) in all affected individuals of a family with HP. We therefore performed a mutational analysis for R117H and N21L in cationic trypsinogen in this and three additional unrelated families with HP. The R117H mutation was detected in all 9 affected members of three HP families and in 3 asymptomatic but at-risk relatives. However, neither the R117H nor the N21L mutation in the cationic trypsinogen were found in the HP family with the L327R alteration in CFTR. The L327R allele segregates with the disease within this HP family and was not detected on 360 unrelated Caucasian non-CF chromosomes. Although close to 800 different mutations have been detected in the CF gene of cystic fibrosis patients, L327R is a new alteration, not yet reported in connection with CF. The results of this study indicate that the CFTR gene may play a role in the etiology of minority of cases with HP and suggest that hereditary pancreatitis is genetically heterogeneous disease.