These preliminary results suggest, for the first time, an association between MBL level and respiratory tract infections in young men and a possible association between infections and MBL2 polymorphisms.

BackgroundFamily history of asthma and other allergic diseases have been linked to the risk of childhood asthma previously, but little is known about their effect on the age-of-onset and persistency of asthma until young adulthood.MethodsWe assessed the effect of the family history of asthma and allergic diseases on persistent vs. transient, and early- vs. late-onset persistent asthma in The Espoo Cohort Study 1991–2011, a population-based cohort study of 1623 subjects (follow-up rate 63.2%). The determinants were any family history (any parent or sibling); maternal; paternal; siblings only; parents only; and both siblings and parents. Analyses were conducted separately for asthma and allergic diseases while taking the other disease into account as a confounding factor. The outcomes were persistent, transient, early-onset persistent (<13 years) and late-onset persistent asthma. Adjusted risk ratios (RR) were calculated applying Poisson regression. Q-statistics were used to assess heterogeneity between RRs.ResultsFamily history was associated with the different subtypes but the magnitude of effect varied quantitatively. Any family history of asthma was a stronger determinant of persistent (adjusted RR = 2.82, 95% CI 1.99-4.00) than transient asthma (1.65, 1.03-2.65) (heterogeneity: P = 0.07) and on early-onset than late-onset persistent asthma. Also any family history of allergic diseases was a stronger determinant of persistent and early-onset asthma. The impact of paternal asthma continued to young adulthood (early-onset: 3.33, 1.57-7.06 vs. late-onset 2.04, 0.75-5.52) while the influence of maternal asthma decreased with age (Early-onset 3.94, 2.11-7.36 vs. Late-onset 0.88, 0.28-2.81). Paternal allergic diseases did not follow the pattern of paternal asthma, since they showed no association with late-onset asthma. Also the effect estimates for other subtypes were lower than in other hereditary groups (persistent 1.29, 0.75-2.22 vs. transient 1.20, 0.67-2.15 and early-onset 1.86, 0.95-3.64 vs. late-onset 0.64, 0.22-1.80).ConclusionsFamily history of asthma and allergic diseases are strong determinants of asthma, but the magnitude of effect varies according to the hereditary group so that some subtypes have a stronger hereditary component, and others may be more strongly related to environmental exposures. Our results provide useful information for assessing the prognosis of asthma based on a thorough family history.

Short-term cold exposure increases central aortic blood pressure and cardiac workload, and myocardial oxygen demand slightly increases in relation to blood supply in untreated hypertensive middle-aged men. Because of the higher baseline blood pressure among hypertensive subjects, the cold-induced rise in central aortic blood pressure may increase the risk of adverse cardiovascular health effects.

BACKGROUND:There is some evidence that prenatal exposure to low-level air pollution increases the risk of preterm birth (PTB), but little is known about synergistic effects of different pollutants. OBJECTIVES:We assessed the independent and joint effects of prenatal exposure to air pollution during the entire duration of pregnancy. METHODS:The study population consisted of the 2,568 members of the Espoo Cohort Study, born between 1984 and 1990, and living in the City of Espoo, Finland. We assessed individual-level prenatal exposure to ambient air pollutants of interest at all the residential addresses from conception to birth. The pollutant concentrations were estimated both by using regional-to-city-scale dispersion modelling and land-use regression-based method. We applied Poisson regression analysis to estimate the adjusted risk ratios (RRs) with their 95% confidence intervals (CI) by comparing the risk of PTB among babies with the highest quartile (Q4) of exposure during the entire duration of pregnancy with those with the lower exposure quartiles (Q1-Q3). We adjusted for season of birth, maternal age, sex of the baby, family's socioeconomic status, maternal smoking during pregnancy, maternal exposure to environmental tobacco smoke during pregnancy, single parenthood, and exposure to other air pollutants (only in multi-pollutant models) in the analysis. RESULTS:In a multi-pollutant model estimating the effects of exposure during entire pregnancy, the adjusted RR was 1.37 (95% CI: 0.85, 2.23) for PM2.5 and 1.64 (95% CI: 1.15, 2.35) for O3. The joint effect of PM2.5 and O3 was substantially higher, an adjusted RR of 3.63 (95% CI: 2.16, 6.10), than what would have been expected from their independent effects (0.99 for PM2.5 and 1.34 for O3). The relative risk due to interaction (RERI) was 2.30 (95% CI: 0.95, 4.57). DISCUSSION:Our results strengthen the evidence that exposure to fairly low-level air pollution during pregnancy increases the risk of PTB. We provide novel observations indicating that individual air pollutants such as PM2.5 and O3 may act synergistically potentiating each other's adverse effects.