Associations between ambient temperature and enteric infections by pathogen: a systematic review and meta-analysis

Background: Numerous studies have quantified the associations between ambient temperature and enteric infections, particularly all-cause enteric infections. However, the temperature sensitivity of enteric infections might be pathogen dependent. Here, we sought to identify pathogen-specific associations between ambient temperature and enteric infections.Methods: We did a systematic review and meta-analysis by searching PubMed, Web of Science, and Scopus for peerreviewed research articles published from Jan 1, 2000, to Dec 31, 2019, and also hand searched reference lists of included articles and excluded reviews. We included studies that quantified the effects of ambient temperature increases on common pathogen-specific enteric infections in humans. We excluded studies that expressed ambient temperature as a categorical or diurnal range, or in a standardised format. Two authors screened the search results, one author extracted data from eligible studies, and four authors verified the data. We obtained the overall risks by pooling the relative risks of enteric infection by pathogen for each 1°C temperature rise using random-effects modelling and robust variance estimation for the correlated effect estimates. Between-study heterogeneity was measured using I², τ², and Q-statistic. Publication bias was determined using funnel plot asymmetry and the trimand-fill method. Differences among pathogen-specific pooled estimates were determined using subgroup analysis of taxa-specific meta-analysis. The study protocol was not registered but followed the PRISMA guidelines.Findings: We identified 2981 articles via database searches and 57 articles from scanning reference lists of excluded reviews and included articles, of which 40 were eligible for pathogen-specific meta-analyses. The overall increased risks of incidence per 1°C temperature rise, expressed as relative risks, were 1·05 (95% CI 1·04–1·07; I² 97%) for salmonellosis, 1·07 (1·04–1·10; I² 99%) for shigellosis, 1·02 (1·01–1·04; I² 98%) for campylobacteriosis, 1·05 (1·04–1·07; I² 36%) for cholera, 1·04 (1·01–1·07; I² 98%) for Escherichia coli enteritis, and 1·15 (1·07–1·24; I² 0%) for typhoid. Reduced risks per 1°C temperature increase were 0·96 (95% CI 0·90–1·02; I² 97%) for rotaviral enteritis and 0·89 (0·81–0·99; I² 96%) for noroviral enteritis. There was evidence of between-pathogen differences in risk for bacterial infections but not for viral infections.Interpretation: Temperature sensitivity of enteric infections can vary according to the enteropathogen causing the infection, particularly for bacteria. Thus, we encourage a pathogen-specific health adaptation approach, such as vaccination, given the possibility of increasingly warm temperatures in the future

Association between Ambient Temperature and Severe Diarrhoea in the National Capital Region, Philippines

Epidemiological studies have quantified the association between ambient temperature and diarrhoea. However, to our knowledge, no study has quantified the temperature association for severe diarrhoea cases. In this study, we quantified the association between mean temperature and two severe diarrhoea outcomes, which were mortality and hospital admissions accompanied with dehydration and/or co-morbidities. Using a 12-year dataset of three urban districts of the National Capital Region, Philippines, we modelled the non-linear association between weekly temperatures and weekly severe diarrhoea cases using a two-stage time series analysis. We computed the relative risks at the 95th (30.4 °C) and 5th percentiles (25.8 °C) of temperatures using minimum risk temperatures (MRTs) as the reference to quantify the association with high- and low-temperatures, respectively. The shapes of the cumulative associations were generally J-shaped with greater associations towards high temperatures. Mortality risks were found to increase by 53.3% [95% confidence interval (CI): 29.4%; 81.7%)] at 95th percentile of weekly mean temperatures compared with the MRT (28.2 °C). Similarly, the risk of hospitalised severe diarrhoea increased by 27.1% (95% CI: 0.7%; 60.4%) at 95th percentile in mean weekly temperatures compared with the MRT (28.6 °C). With the increased risk of severe diarrhoea cases under high ambient temperature, there may be a need to strengthen primary healthcare services and sustain the improvements made in water, sanitation, and hygiene, particularly in poor communities

Global projections of temperature-attributable mortality due to enteric infections: a modelling study

Background: Mortality due to enteric infections is projected to increase because of global warming; however, the different temperature sensitivities of major enteric pathogens have not yet been considered in projections on a global scale. We aimed to project global temperature-attributable enteric infection mortality under various future scenarios of sociodemographic development and climate change.Methods: In this modelling study, we generated global projections in two stages. First, we forecasted baseline mortality from ten enteropathogens (non-typhoidal salmonella, Shigella, Campylobacter, cholera, enteropathogenic Escherichia coli, enterotoxigenic E coli, typhoid, rotavirus, norovirus, and Cryptosporidium) under several future sociodemographic development and health investment scenarios (ie, pessimistic, intermediate, and optimistic). We then estimated the mortality change from baseline attributable to global warming using the product of projected annual temperature anomalies and pathogen-specific temperature sensitivities.Findings: We estimated that in the period 2080–95, the global mean number of temperature-attributable deaths due to enteric infections could be as low as 6599 (95% empirical CI 5441–7757) under the optimistic sociodemographic development and climate change scenario, or as high as 83 888 (67 760–100 015) under the pessimistic scenario. Most of the projected temperature-attributable deaths were from shigellosis, cryptosporidiosis, and typhoid fever in sub-Saharan Africa and South Asia. Considerable reductions in the number of attributable deaths were from viral infections, such as rotaviral and noroviral enteritis, which resulted in net reductions in attributable enteric infection mortality under optimistic scenarios for Latin America and the Caribbean and East Asia and the Pacific.Interpretation: Temperature-attributable mortality could increase under warmer climate and unfavourable sociodemographic conditions. Mitigation policies for limiting global warming and sociodemographic development policies for low-income and middle-income countries might help reduce mortality from enteric infections in the future.Funding: Japan Society for the Promotion of Science, Japan Science and Technology Agency, and Spanish Ministry of Economy, Industry, and Competitiveness

Heat-related cardiorespiratory mortality: effect modification by air pollution across 482 cities from 24 countries

Background Evidence on the potential interactive effects of heat and ambient air pollution on cause-specific mortality is inconclusive and limited to selected locations. Objectives We investigated the effects of heat on cardiovascular and respiratory mortality and its modification by air pollution during summer months (six consecutive hottest months) in 482 locations across 24 countries. Methods Location-specific daily death counts and exposure data (e.g., particulate matter with diameters ≤ 2.5 µm [PM2.5]) were obtained from 2000 to 2018. We used location-specific confounder-adjusted Quasi-Poisson regression with a tensor product between air temperature and the air pollutant. We extracted heat effects at low, medium, and high levels of pollutants, defined as the 5th, 50th, and 95th percentile of the location-specific pollutant concentrations. Country-specific and overall estimates were derived using a random-effects multilevel meta-analytical model. Results Heat was associated with increased cardiorespiratory mortality. Moreover, the heat effects were modified by elevated levels of all air pollutants in most locations, with stronger effects for respiratory than cardiovascular mortality. For example, the percent increase in respiratory mortality per increase in the 2-day average summer temperature from the 75th to the 99th percentile was 7.7% (95% Confidence Interval [CI] 7.6-7.7), 11.3% (95%CI 11.2-11.3), and 14.3% (95% CI 14.1-14.5) at low, medium, and high levels of PM2.5, respectively. Similarly, cardiovascular mortality increased by 1.6 (95%CI 1.5-1.6), 5.1 (95%CI 5.1-5.2), and 8.7 (95%CI 8.7-8.8) at low, medium, and high levels of O3, respectively. Discussion We observed considerable modification of the heat effects on cardiovascular and respiratory mortality by elevated levels of air pollutants. Therefore, mitigation measures following the new WHO Air Quality Guidelines are crucial to enhance better health and promote sustainable development

Temporal variations in the short-term effects of ambient air pollution on cardiovascular and respiratory mortality: a pooled analysis of 380 urban areas over a 22-year period

Background: Ambient air pollution, including particulate matter (such as PM10 and PM2·5) and nitrogen dioxide (NO2), has been linked to increases in mortality. Whether populations’ vulnerability to these pollutants has changed over time is unclear, and studies on this topic do not include multicountry analysis. We evaluated whether changes in exposure to air pollutants were associated with changes in mortality effect estimates over time. Methods: We extracted cause-specific mortality and air pollution data collected between 1995 and 2016 from the Multi-Country Multi-City (MCC) Collaborative Research Network database. We applied a two-stage approach to analyse the short-term effects of NO2, PM10, and PM2·5 on cause-specific mortality using city-specific time series regression analyses and multilevel random-effects meta-analysis. We assessed changes over time using a longitudinal meta-regression with time as a linear fixed term and explored potential sources of heterogeneity and two-pollutant models. Findings: Over 21·6 million cardiovascular and 7·7 million respiratory deaths in 380 cities across 24 countries over the study period were included in the analysis. All three air pollutants showed decreasing concentrations over time. The pooled results suggested no significant temporal change in the effect estimates per unit exposure of PM10, PM2·5, or NO2 and mortality. However, the risk of cardiovascular mortality increased from 0·37% (95% CI –0·05 to 0·80) in 1998 to 0·85% (0·55 to 1·16) in 2012 with a 10 μg/m3 increase in PM2·5. Two-pollutant models generally showed similar results to single-pollutant models for PM fractions and indicated temporal differences for NO2. Interpretation: Although air pollution levels decreased during the study period, the effect sizes per unit increase in air pollution concentration have not changed. This observation might be due to the composition, toxicity, and sources of air pollution, as well as other factors, such as socioeconomic determinants or changes in population distribution and susceptibility. Funding: None. © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 licenseAG was supported by the European Union's Horizon 2020 Project Exhaustion (grant number 820655). FS was supported by the Italian Ministry of University and Research, Department of Excellence project 2023–2027 ReDS “Rethinking Data Science”—Department of Statistics, Computer Science and Applications, University of Florence. AMV-C acknowledges funding from the Swiss National Science Foundation (grant number TMSGI3_211626). JJKJ was supported by the Academy of Finland (grant number 310372; Global Health Risks Related to Atmospheric Composition and Weather Consortium)

Variation in Uteroglobin-Related Protein 1 (UGRP1) gene is associated with Allergic Rhinitis in Singapore Chinese

<p>Abstract</p> <p>Background</p> <p>Uteroglobin-Related Protein 1 (<it>UGRP1</it>) is a secretoglobulin protein which has been suggested to play a role in lung inflammation and allergic diseases. UGRP1 has also been shown to be an important pneumoprotein, with diagnostic potential as a biomarker of lung damage. Previous genetic studies evaluating the association between variations on <it>UGRP1 </it>and allergic phenotypes have yielded mixed results. The aim of this present study was to identify genetic polymorphisms in <it>UGRP1 </it>and investigate if they were associated with asthma and allergic rhinitis in the Singapore Chinese population.</p> <p>Methods</p> <p>Resequencing of the <it>UGRP1 </it>gene was conducted on 40 randomly selected individuals from Singapore of ethnic Chinese origin. The polymorphisms identified were then tagged and genotyped in a population of 1893 Singapore Chinese individuals. Genetic associations were evaluated in this population comparing 795 individuals with allergic rhinitis, 718 with asthma (of which 337 had both asthma and allergic rhinitis) and 717 healthy controls with no history of allergy or allergic diseases.</p> <p>Results</p> <p>By resequencing the <it>UGRP1 </it>gene within our population, we identified 11 novel and 16 known single nucleotide polymorphisms (SNPs). TagSNPs were then genotyped, revealing a significant association between rs7726552 and allergic rhinitis (Odds Ratio: 0.81, 95% Confidence Interval: 0.66-0.98, P = 0.039). This association remained statistically significant when it was analyzed genotypically or when stratified according to haplotypes. When variations on <it>UGRP1 </it>were evaluated against asthma, no association was observed.</p> <p>Conclusion</p> <p>This study documents the association between polymorphisms in <it>UGRP1 </it>and allergic rhinitis, suggesting a potential role in its pathogenesis.</p

Joint effect of heat and air pollution on mortality in 620 cities of 36 countries

Background The epidemiological evidence on the interaction between heat and ambient air pollution on mortality is still inconsistent. Objectives To investigate the interaction between heat and ambient air pollution on daily mortality in a large dataset of 620 cities from 36 countries. Methods We used daily data on all-cause mortality, air temperature, particulate matter ≤ 10 μm (PM10), PM ≤ 2.5 μm (PM2.5), nitrogen dioxide (NO2), and ozone (O3) from 620 cities in 36 countries in the period 1995–2020. We restricted the analysis to the six consecutive warmest months in each city. City-specific data were analysed with over-dispersed Poisson regression models, followed by a multilevel random-effects meta-analysis. The joint association between air temperature and air pollutants was modelled with product terms between non-linear functions for air temperature and linear functions for air pollutants. Results We analyzed 22,630,598 deaths. An increase in mean temperature from the 75th to the 99th percentile of city-specific distributions was associated with an average 8.9 % (95 % confidence interval: 7.1 %, 10.7 %) mortality increment, ranging between 5.3 % (3.8 %, 6.9 %) and 12.8 % (8.7 %, 17.0 %), when daily PM10 was equal to 10 or 90 μg/m3, respectively. Corresponding estimates when daily O3 concentrations were 40 or 160 μg/m3 were 2.9 % (1.1 %, 4.7 %) and 12.5 % (6.9 %, 18.5 %), respectively. Similarly, a 10 μg/m3 increment in PM10 was associated with a 0.54 % (0.10 %, 0.98 %) and 1.21 % (0.69 %, 1.72 %) increase in mortality when daily air temperature was set to the 1st and 99th city-specific percentiles, respectively. Corresponding mortality estimate for O3 across these temperature percentiles were 0.00 % (-0.44 %, 0.44 %) and 0.53 % (0.38 %, 0.68 %). Similar effect modification results, although slightly weaker, were found for PM2.5 and NO2. Conclusions Suggestive evidence of effect modification between air temperature and air pollutants on mortality during the warm period was found in a global dataset of 620 cities.Massimo Stafoggia, Francesca K. de’ Donato, Masna Rai and Alexandra Schneider were partially supported by the European Union’s Horizon 2020 Project Exhaustion (Grant ID: 820655). Jan Kyselý and Aleš Urban were supported by the Czech Science Foundation project (22-24920S). Joana Madureira was supported by the Fundação para a Ciência e a Tecnologia (FCT) (grant SFRH/BPD/115112/2016). Masahiro Hashizume was supported by the Japan Science and Technology Agency (JST) as part of SICORP, Grant Number JPMJSC20E4. Noah Scovronick was supported by the NIEHS-funded HERCULES Center (P30ES019776). South African Data were provided by Statistics South Africa, which did not have any role in conducting the study. Antonio Gasparrini was supported by the Medical Research Council-UK (Grants ID: MR/V034162/1 and MR/R013349/1), the Natural Environment Research Council UK (Grant ID: NE/R009384/1), and the European Union’s Horizon 2020 Project Exhaustion (Grant ID: 820655)

Effects of Desert Dust and Sandstorms on Human Health: A Scoping Review

Abstract Desert dust and sandstorms are recurring environmental phenomena that are reported to produce serious health risks worldwide. This scoping review was conducted to identify the most likely health effects of desert dust and sandstorms and the methods used to characterize desert dust exposure from the existing epidemiological literature. We systematically searched PubMed/MEDLINE, Web of Science, and Scopus to identify studies that reported the effects of desert dust and sandstorms on human health. Search terms referred to desert dust or sandstorm exposure, names of major deserts, and health outcomes. Health effects were cross‐tabulated with study design variables (e.g., epidemiological design and methods to quantify dust exposure), desert dust source, health outcomes and conditions. We identified 204 studies that met the inclusion criteria for the scoping review. More than half of the studies (52.9%) used a time‐series study design. However, we found a substantial variation in the methods used to identify and quantify desert dust exposure. The binary metric of dust exposure was more frequently used than the continuous metric for all desert dust source locations. Most studies (84.8%) reported significant associations between desert dust and adverse health effects, mainly for respiratory and cardiovascular mortality and morbidity causes. Although there is a large body of evidence on the health effects of desert dust and sandstorms, the existing epidemiological studies have significant limitations related to exposure measurement and statistical analysis that potentially contribute to inconsistencies in determining the effect of desert dust on human health

The non-linear and lagged short-term relationship between rainfall and leptospirosis and the intermediate role of floods in the Philippines

Background: Leptospirosis is a worldwide bacterial zoonosis. Outbreaks of leptospirosis after heavy rainfall and flooding have been reported. However, few studies have formally quantified the effect of weather factors on leptospirosis incidence. We estimated the association between rainfall and leptospirosis cases in an urban setting in Manila, the Philippines, and examined the potential intermediate role of floods in this association. Methods/Principal findings: Relationships between rainfall and the weekly number of hospital admissions due to leptospirosis from 2001 to 2012 were analyzed using a distributed lag non-linear model in a quasi-Poisson regression framework, controlling for seasonally varying factors other than rainfall. The role of floods on the rainfall?leptospirosis relationship was examined using an indicator. We reported relative risks (RRs) by rainfall category based on the flood warning system in the country. The risk of post-rainfall leptospirosis peaked at a lag of 2 weeks (using 0 cm/week rainfall as the reference) with RRs of 1.30 (95% confidence interval: 0.99?1.70), 1.53 (1.12?2.09), 2.45 (1.80?3.33), 4.61 (3.30?6.43), and 13.77 (9.10?20.82) for light, moderate, heavy, intense and torrential rainfall (at 2, 5, 16, 32 and 63 cm/week), respectively. After adjusting for floods, RRs (at a lag of 2 weeks) decreased at higher rainfall levels suggesting that flood is on the causal pathway between rainfall and leptospirosis. Conclusions: Rainfall was strongly associated with increased hospital admission for leptospirosis at a lag of 2 weeks, and this association was explained in part by floods