Exposure to ambient air pollutants and short-term risk for exacerbations of allergic rhinitis: A time-stratified, case-crossover study in the three largest urban agglomerations in Poland.

Allergic rhinitis (AR) affects 10 % of the world population, with an increased prevalence in regions with substantial air pollution, but the association between exposure to air pollutants and the short-term risk of AR exacerbations is unclear. We used a time-series approach to analyze the risk of hospital admissions due to AR over 8 days from exposure to various air pollutants. Distributed lag nonlinear models were used to analyze data gathered between 2012 and 2018 in the three largest urban agglomerations in Poland. The analyses were carried out separately for the warm (April - September) and cold seasons (October - March). Overall, there were 1407 admissions due to AR. In the warm season, the rate ratio (95 % confidence interval) for admission per 10 µg/m3 was 1.202 (1.044, 1.384) for particulate matter less than 10 µm (PM10); 1.094 (0.896, 1.335) for particulate matter less than 2.5 µm (PM2.5); 0.946 (0.826, 1.085) for nitrogen dioxide (NO2); 0.837 (0.418, 1.677) for sulfur dioxide (SO2); and 1.112 (1.011, 1.224) for ozone (O3). In the cold season, the rate ratio for admission per 10 µg/m3 was 1.035 (0.985, 1.088) for PM10; 1.041 (0.977, 1.108) for PM2.5; 1.252 (1.122, 1.398) for NO2; 0.921 (0.717, 1.181) for SO2; and 1.030 (1.011, 1.050) for O3. In conclusion, the risk of admission due to AR increased significantly after exposure to O3 in the warm and cold seasons. Exposure to PM10 was associated with a significantly increased risk of AR hospitalizations in the warm season only, whereas exposure to NO2 was associated with a significantly increased risk of AR admission in the cold season.

Air pollution and long-term risk of hospital admission due to chronic obstructive pulmonary disease exacerbations in Poland: a time-stratified, case-crossover study.

INTRODUCTION: Airborne pollutants may worsen the course of chronic obstructive pulmonary disease (COPD). Previous studies have shown that both particulate and gaseous pollutants increase airway inflammation, which may lead to an exacerbation of COPD. OBJECTIVES: The aim of the study was to investigate the association between exposure to airborne pollutants and the risk of COPD exacerbations in 3 the largest urban agglomerations in Poland: Warsaw, Kraków, and Tricity. PATIENTS AND METHODS: We used a case­crossover approach to analyze data from the years 2011-2018. This time­series study used distributed lag linear-nonlinear models to analyze the risk of hospital admission due to COPD exacerbations during 21 days following the exposure to particulate matter (PM), NO2, and SO2. RESULTS: Overall, there were 26 948 admissions due to COPD exacerbations. During 21 days after exposure, the rate ratio (95% CI) for admissions per 10 µg/m3 was 1.028 (1.008-1.049) for PM10, 1.030 (1.006-1.055) for PM2.5, 1.032 (0.988-1.078) for NO2, and 1.145 (1.038-1.262) for SO2. The risk for admission peaked at 10 days after the exposure to PM10 and PM2.5, whereas for NO2 and SO2 the risk was the greatest on the day of exposure. The proportion (95% CI) of hospitalizations attributable to air pollution was 9.08% (3.10%-15.08%) for PM10, 7.61% (1.27%-13.49%) for PM2.5, 9.77% (-3.63% to 21.48%) for NO2, and 7.70% (2.30%-12.84%) for SO2. CONCLUSIONS: PM2.5, PM10, NO2, and SO2 pollution was associated with an increased risk of COPD exacerbations that needed hospitalization. There were different risk patterns for particulate and gaseous pollutants. Improving air quality in Polish cities could reduce the burden of COPD.

Inflammation Related to Obesity in the Etiopathogenesis of Gastroenteropancreatic Neuroendocrine Neoplasms.

Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are rare neoplasms, which, due to their heterogeneous nature, non-specific symptoms, and lack of specific tumor markers pose many diagnostic and clinical challenges. In recent years, the effectiveness of GEP-NEN diagnosis has increased, which is probably associated with the greater availability of diagnostic tests and the cooperation of many experienced specialists in various scientific disciplines. In addition to the possible genetic etiology, the cause of GEP-NET development is not fully understood. Inflammation and obesity are known risks that contribute to the development of many diseases. Chronic inflammation accompanying obesity affects the hormonal balance and cell proliferation and causes the impairment of the immune system function, leading to neoplastic transformation. This review explores the role of inflammation and obesity in GEP-NETs. The exact mechanisms inducing tumor growth are unknown; however, the profile of inflammatory factors released in the GEP-NET tumor microenvironment is responsible for the progression or inhibition of tumor growth. Both the excess of adipose tissue and the impaired function of the immune system affect not only the initiation of cancer but also reduce the comfort and lifetime of patients.

Differences in carotid artery atherosclerosis between men and women in the early phase after ischemic event.

OBJECTIVES: There is little data about sex differences in carotid atherosclerosis in the early phase after an ischemic event. The aim of this study was to examine the carotid artery atherosclerosis differences between men and women in early phase after TIA or stroke. METHODS: Consecutive patients with recent ischemic event, admitted during the first week after symptom onset were examined with ultrasound. Sex differences in degree of stenosis, number of plaques and plaque morphology were compared. Plaque morphology was assessed by gray-scale median (GSM), according to which lower values were associated with hemorrhagic/necrotic core indicating plaque instability. RESULTS: Of the 316 patients with ischemic events, 196 (50.5% male) entered the study. Men had more often moderate as well as severe ipsilateral carotid stenosis (12.1% vs 7.2% for moderate and 12.1% vs 2.1% for severe; p=0.024). Men had more often the largest plaque hypoechogenic contralateral (62.6% vs 37.1%, p=0.0008), but not ipsilateral. Men had 3 or more hypoechogenic plaques (24.2% vs 4.1%, p=0.0001; 17.2% vs 4.1%, p<0.0001) both ipsi and contralateral respectively. Male sex was a risk factor for having 3 or more ipsilateral hypoechogenic plaques (p=0.002, OR=20 CI 95% [5.5-75]. CONCLUSIONS: Men had more often carotid stenosis and higher number of hypoechogenic plaques.

Clonal distribution of bone sialoprotein-binding protein gene among Staphylococcus aureus isolates associated with bloodstream infections.

Staphylococcus aureus is a leading cause of bloodstream infections (BSI) and diseases that may be caused by hematogenous spread. The staphylococcal adhesin, for which the association with the infections emerging as a complication of septicemia has been well documented, is a bone sialoprotein-binding protein (Bbp). The aim of the study was to assess the prevalence of a bbp gene in S. aureus bloodstream isolates associated with BSI and to investigate to what degree the distribution of this gene is linked to the clonality of the population. Spa typing, used in order to explore the genetic population structure of the isolates, yielded 29 types. Six spa clusters and seven singletons were identified. The most frequent was spa clonal complex CC021 associated with MLST CC30 (38%). The bbp gene was found in 47% of isolates. Almost all isolates (95%) clustered in spa clonal complex CC021 were positive for this gene. All isolates carrying the bbp gene were sensitive to methicillin, and if clustered in the spa CC021, belonged to agr group III. Our study shows that Bbp is not strictly associated with BSI. However, one may conclude that for clonally related S. aureus strains most commonly causing BSI, the risk of Bbp-mediated complications of septicemia is expected to be higher than for other strains.