Suchergebnisse

The objective of this study was to link arsenic exposure and influenza A (H1N1) infection‐induced respiratory effects to assess the impact of arsenic‐contaminated drinking water on exacerbation risk of A (H1N1)‐associated lung function. The homogeneous Poisson process was used to approximate the related processes between arsenic exposure and influenza‐associated lung function exacerbation risk. We found that (i) estimated arsenic‐induced forced expiratory volume in 1 second (FEV1) reducing rates ranged from 0.116 to 0.179 mL/μg for age 15–85 years, (ii) estimated arsenic‐induced A (H1N1) viral load increasing rate was 0.5 mL/μg, (iii) estimated A (H1N1) virus‐induced FEV1 reducing rate was 0.10 mL/logTCID50, and (iv) the relationship between arsenic exposure and A (H1N1)‐associated respiratory symptoms scores (RSS) can be described by a Hill model. Here we showed that maximum RSS at day 2 postinfection for Taiwan, West Bengal (India), and the United States were estimated to be in the severe range of 0.83, 0.89, and 0.81, respectively, indicating that chronic arsenic exposure and A (H1N1) infection together are most likely to pose potential exacerbations risk of lung function, although a 50% probability of lung function exacerbations risk induced by arsenic and influenza infection was within the mild and moderate ranges of RSS at day 1 and 2 postinfection. We concluded that avoidance of drinking arsenic‐containing water could significantly reduce influenza respiratory illness and that need will become increasingly urgent as the novel H1N1 pandemic influenza virus infects people worldwide.

The purpose of this study was to examine tuberculosis (TB) population dynamics and to assess potential infection risk in Taiwan. A well‐established mathematical model of TB transmission built on previous models was adopted to study the potential impact of TB transmission. A probabilistic risk model was also developed to estimate site‐specific risks of developing disease soon after recent primary infection, exogenous reinfection, or through endogenous reactivation (latently infected TB) among Taiwan regions. Here, we showed that the proportion of endogenous reactivation (53–67%) was larger than that of exogenous reinfection (32–47%). Our simulations showed that as epidemic reaches a steady state, age distribution of cases would finally shift toward older age groups dominated by latently infected TB cases as a result of endogenous reactivation. A comparison of age‐weighted TB incidence data with our model simulation output with 95% credible intervals revealed that the predictions were in an apparent agreement with observed data. The median value of overall basic reproduction number (R0) in eastern Taiwan ranged from 1.65 to 1.72, whereas northern Taiwan had the lowest R0 estimate of 1.50. We found that total TB incidences in eastern Taiwan had 25–27% probabilities of total proportion of infected population exceeding 90%, whereas there were 36–66% probabilities having exceeded 20% of total proportion of infected population attributed to latently infected TB. We suggested that our Taiwan‐based analysis can be extended to the context of developing countries, where TB remains a substantial cause of elderly morbidity and mortality.