Ambient nitrogen dioxide is a widely available measure of traffic-related air pollution and is inconsistently associated with the prevalence of asthma symptoms in children. The use of this relationship to evaluate the health impact of policies affecting traffic management and traffic emissions is limited by the lack of a concentration-response function based on systematic review and meta-analysis of relevant studies. Using systematic methods, we identified papers containing quantitative estimates for nitrogen dioxide and the 12 month period prevalence of asthma symptoms in children in which the exposure contrast was within-community and dominated by traffic pollution. One estimate was selected from each study according to an a priori algorithm. Odds ratios were standardised to 10 μg/m3 and summary estimates were obtained using random- and fixed-effects estimates. Eighteen studies were identified. Concentrations of nitrogen dioxide were estimated for the home address (12) and/or school (8) using a range of methods; land use regression (6), study monitors (6), dispersion modelling (4) and interpolation (2). Fourteen studies showed positive associations but only two associations were statistically significant at the 5 % level. There was moderate heterogeneity (I2 = 32.8 %) and the random-effects estimate for the odds ratio was 1.06 (95 % CI 1.00 to 1.11). There was no evidence of small study bias. Individual studies tended to have only weak positive associations between nitrogen dioxide and asthma prevalence but the summary estimate bordered on statistical significance at the 5 % level. Although small, the potential impact on asthma prevalence could be considerable because of the high level of baseline prevalence in many cities. Whether the association is causal or indicates the effects of a correlated pollutant or other confounders, the estimate obtained by the meta-analysis would be appropriate for estimating impacts of traffic pollution on asthma prevalence.Electronic supplementary materialThe online version of this article (doi:10.1007/s11869-014-0265-8) contains supplementary material, which is available to authorized users.
Background
Post-traumatic stress disorder (PTSD) has been identified as a potential risk factor for developing dementia. There are currently, however, no meta-analyses quantifying this risk.
Aims
To systematically review and quantify the risk of future dementia associated with PTSD across populations. PROSPERO registration number CRD42019130392.
Method
We searched nine electronic databases up to 25 October 2019 for longitudinal studies assessing PTSD and risk of dementia. We used random- and fixed-effects meta-analyses to pool estimates across studies.
Results
PTSD was associated with a significant risk for all-cause dementia: pooled hazard ratio HR = 1.61 (95% CI 1.43–1.81, I2= 85.8%, P < 0.001; n = 1 693 678; 8 studies). Pooled HR was 1.61 (95% CI 1.46–1.78; I2= 80.9%, P < 0.001; n = 905 896; 5 studies) in veterans, and 2.11 (95% CI 1.03–4.33, I2= 91.2%, P < 0.001; n = 787 782; 3 studies) in the general population. The association between PTSD and dementia remained significant after excluding studies with high risk of bias (HR = 1.55, 95% CI 1.39–1.73, I2= 83.9%, P < 0.001; n = 1 684 928; 7 studies). Most studies included were retrospective and there was evidence of high heterogeneity.
Conclusions
This is the first meta-analysis quantifying the association of PTSD and risk of dementia showing that PTSD is a strong and potentially modifiable risk factor for all-cause dementia. Future studies investigating potential causal mechanisms, and the protective value of treating PTSD are needed.
Our data support a link between the initiation of RTV-boosted/lopinavir-based ART preconception and PTD in subsequent pregnancies, with implications for treatment guidelines. Continued monitoring of PTD risk is needed as increasing numbers of pregnancies are conceived on new drugs.
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