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High ambient temperature in pregnancy and risk of childhood acute lymphoblastic leukaemia: an observational study 孕期环境温度过高与儿童患急性淋巴细胞白血病的风险:一项观察性研究。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00121-9
Tormod Rogne PhD , Rong Wang PhD , Pin Wang PhD , Nicole C Deziel PhD , Prof Catherine Metayer PhD , Prof Joseph L Wiemels PhD , Kai Chen PhD , Joshua L Warren PhD , Prof Xiaomei Ma PhD

Background

High ambient temperature is increasingly common due to climate change and is associated with risk of adverse pregnancy outcomes. Acute lymphoblastic leukaemia is the most common malignancy in children, the incidence is increasing, and in the USA disproportionately affects Latino children. We aimed to investigate the potential association between high ambient temperature in pregnancy and risk of childhood acute lymphoblastic leukaemia.

Methods

We used data from California birth records (children born from Jan 1, 1982, to Dec 31, 2015) and California Cancer Registry (those diagnosed with childhood cancer in California from Jan 1, 1988, to Dec 31, 2015) to identify acute lymphoblastic leukaemia cases diagnosed in infants and children aged 14 years and younger and controls matched by sex, race, ethnicity, and date of last menstrual period. Ambient temperatures were estimated on a 1-km grid. The association between ambient temperature and acute lymphoblastic leukaemia was evaluated per gestational week, restricted to May–September, adjusting for confounders. Bayesian meta-regression was applied to identify critical exposure windows. For sensitivity analyses, we evaluated a 90-day pre-pregnancy period (assuming no direct effect before pregnancy), adjusted for relative humidity and particulate matter less than 2·5 microns in aerodynamic diameter, and constructed an alternatively matched dataset for exposure contrast by seasonality.

Findings

6849 cases of childhood acute lymphoblastic leukaemia were identified and, of these, 6258 had sufficient data for study inclusion. We also included 307 579 matched controls. Most of the study population were male (174 693 [55·7%] of the 313 837 included in the study) and of Latino ethnicity (174 906 [55·7%]). The peak association between ambient temperature and risk of acute lymphoblastic leukaemia was observed in gestational week 8, where a 5°C increase was associated with an odds ratio of 1·07 (95% CI 1·04–1·11). A slightly larger effect was seen among Latino children (OR 1·09 [95% CI 1·04–1·14]) than non-Latino White children (OR 1·05 [1·00–1·11]). The sensitivity analyses supported the results of the main analysis.

Interpretation

Our findings suggest an association between high ambient temperature in early pregnancy and risk of childhood acute lymphoblastic leukaemia. Further replication and investigation of mechanistic pathways might inform mitigation strategies.

Funding

Yale Center on Climate Change and Health, The National Center for Advancing Translational Science, National Institutes of Health.

背景:由于气候变化,环境温度过高的现象越来越普遍,这与不良妊娠结局的风险有关。急性淋巴细胞白血病是儿童最常见的恶性肿瘤,发病率正在上升,在美国,拉丁裔儿童的发病率更高。我们旨在研究孕期环境温度过高与儿童急性淋巴细胞白血病风险之间的潜在关联:我们利用加州出生记录(1982 年 1 月 1 日至 2015 年 12 月 31 日出生的儿童)和加州癌症登记(1988 年 1 月 1 日至 2015 年 12 月 31 日在加州确诊为儿童癌症的儿童)中的数据,确定了确诊为急性淋巴细胞白血病的 14 岁及以下婴幼儿病例,以及按性别、种族、民族和末次月经日期匹配的对照组。环境温度按 1 公里网格估算。环境温度与急性淋巴细胞白血病之间的关系按孕周进行评估,时间仅限于 5 月至 9 月,并对混杂因素进行了调整。采用贝叶斯元回归法确定关键暴露窗口。在敏感性分析中,我们评估了孕前 90 天(假设孕前无直接影响),调整了相对湿度和空气动力直径小于 2-5 微米的颗粒物,并构建了一个替代匹配数据集,用于按季节性进行暴露对比:我们发现了 6849 例儿童急性淋巴细胞白血病病例,其中 6258 例病例的数据足以纳入研究。我们还纳入了 307 579 例匹配对照。研究对象中大部分为男性(313 837 例研究对象中的 174 693 例[55-7%])和拉丁裔(174 906 例[55-7%])。环境温度与罹患急性淋巴细胞白血病风险之间的关系在孕 8 周达到顶峰,温度每升高 5°C,几率比为 1-07(95% CI 1-04-1-11)。拉丁裔儿童的影响(OR 1-09 [95% CI 1-04-1-14])略大于非拉丁裔白人儿童(OR 1-05 [1-00-1-11])。敏感性分析支持主要分析的结果:我们的研究结果表明,孕早期环境温度过高与儿童急性淋巴细胞白血病的发病风险有关。对机理途径的进一步复制和调查可能会为缓解策略提供依据:耶鲁大学气候变化与健康中心、国家促进转化科学中心、美国国立卫生研究院。
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引用次数: 0
All-cause, cardiovascular, and respiratory mortality and wildfire-related ozone: a multicountry two-stage time series analysis 全因、心血管和呼吸系统死亡率与野火相关臭氧:多国两阶段时间序列分析。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00117-7
Gongbo Chen PhD , Prof Yuming Guo PhD , Prof Xu Yue PhD , Rongbin Xu PhD , Wenhua Yu MPH , Tingting Ye MSc , Prof Shilu Tong PhD , Prof Antonio Gasparrini PhD , Prof Michelle L Bell PhD , Prof Ben Armstrong PhD , Prof Joel Schwartz PhD , Prof Jouni J K Jaakkola PhD , Eric Lavigne PhD , Prof Paulo Hilario Nascimento Saldiva PhD , Prof Haidong Kan PhD , Dominic Royé PhD , Aleš Urban PhD , Prof Ana Maria Vicedo-Cabrera PhD , Aurelio Tobias PhD , Prof Bertil Forsberg PhD , Ariana Zeka

Background

Wildfire activity is an important source of tropospheric ozone (O3) pollution. However, no study to date has systematically examined the associations of wildfire-related O3 exposure with mortality globally.

Methods

We did a multicountry two-stage time series analysis. From the Multi-City Multi-Country (MCC) Collaborative Research Network, data on daily all-cause, cardiovascular, and respiratory deaths were obtained from 749 locations in 43 countries or areas, representing overlapping periods from Jan 1, 2000, to Dec 31, 2016. We estimated the daily concentration of wildfire-related O3 in study locations using a chemical transport model, and then calibrated and downscaled O3 estimates to a resolution of 0·25° × 0·25° (approximately 28 km2 at the equator). Using a random-effects meta-analysis, we examined the associations of short-term wildfire-related O3 exposure (lag period of 0–2 days) with daily mortality, first at the location level and then pooled at the country, regional, and global levels. Annual excess mortality fraction in each location attributable to wildfire-related O3 was calculated with pooled effect estimates and used to obtain excess mortality fractions at country, regional, and global levels.

Findings

Between 2000 and 2016, the highest maximum daily wildfire-related O3 concentrations (≥30 μg/m3) were observed in locations in South America, central America, and southeastern Asia, and the country of South Africa. Across all locations, an increase of 1 μg/m3 in the mean daily concentration of wildfire-related O3 during lag 0–2 days was associated with increases of 0·55% (95% CI 0·29 to 0·80) in daily all-cause mortality, 0·44% (–0·10 to 0·99) in daily cardiovascular mortality, and 0·82% (0·18 to 1·47) in daily respiratory mortality. The associations of daily mortality rates with wildfire-related O3 exposure showed substantial geographical heterogeneity at the country and regional levels. Across all locations, estimated annual excess mortality fractions of 0·58% (95% CI 0·31 to 0·85; 31 606 deaths [95% CI 17 038 to 46 027]) for all-cause mortality, 0·41% (–0·10 to 0·91; 5249 [–1244 to 11 620]) for cardiovascular mortality, and 0·86% (0·18 to 1·51; 4657 [999 to 8206]) for respiratory mortality were attributable to short-term exposure to wildfire-related O3.

Interpretation

In this study, we observed an increase in all-cause and respiratory mortality associated with short-term wildfire-related O3 exposure. Effective risk and smoke management strategies should be implemented to protect the public from the impacts of wildfires.

Funding

Australian Research Council and the Australian National Health and Medical Research Council.

背景:野火活动是对流层臭氧(O3)污染的重要来源:野火活动是对流层臭氧(O3)污染的一个重要来源。然而,迄今为止还没有一项研究系统地考察了全球范围内野火相关的臭氧暴露与死亡率之间的关系:我们进行了多国两阶段时间序列分析。从多城市多国家(MCC)合作研究网络中,我们从 43 个国家或地区的 749 个地点获得了每日全因死亡、心血管死亡和呼吸系统死亡的数据,这些数据代表了 2000 年 1 月 1 日至 2016 年 12 月 31 日的重叠时期。我们使用化学传输模型估算了研究地点与野火相关的臭氧日浓度,然后将臭氧估算值校准并降级到 0-25° × 0-25° 的分辨率(赤道约 28 平方公里)。我们采用随机效应荟萃分析法,首先在地点层面,然后在国家、地区和全球层面进行汇总,研究了与野火相关的短期臭氧暴露(滞后期为 0-2 天)与日死亡率之间的关系。利用汇集效应估计值计算出每个地点与野火相关的臭氧导致的年超额死亡率,并利用该估计值得出国家、地区和全球层面的超额死亡率:2000年至2016年期间,在南美洲、中美洲、亚洲东南部和南非等地观测到了与野火相关的最高日臭氧浓度(≥30 μg/m3)。在所有地区,在滞后的 0-2 天内,与野火相关的臭氧日平均浓度每增加 1 μg/m3 就会导致每日全因死亡率增加 0-55%(95% CI 0-29 至 0-80),每日心血管死亡率增加 0-44%(-0-10 至 0-99),每日呼吸系统死亡率增加 0-82%(0-18 至 1-47)。在国家和地区层面上,每日死亡率与野火相关臭氧暴露的关联显示出很大的地域异质性。在所有地区,估计每年全因死亡率超额死亡率为 0-58%(95% CI 0-31 至 0-85;31 606 例死亡 [95% CI 17 038 至 46 027]),心血管死亡率为 0-41%(-0-10 至 0-91;5249 [-1244 至 11 620]),呼吸系统死亡率为 0-86%(0-18 至 1-51;4657 [999 至 8206]):在这项研究中,我们观察到短期暴露于与野火相关的 O3 会增加全因死亡率和呼吸系统死亡率。应实施有效的风险和烟雾管理策略,以保护公众免受野火的影响:澳大利亚研究委员会和澳大利亚国家健康与医学研究委员会。
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引用次数: 0
Urgent optimism for planetary health: lessons from the video game industry 对地球健康的迫切乐观:电子游戏产业的启示。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00110-4
Fatimah Ahamad , Jemilah Mahmood , Oliver Lacey-Hall , Menaka Ganeson , Hannah Zuhairah Ariff , Tai-Jie Lim
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引用次数: 0
Ambient air pollution and daily mortality in ten cities of India: a causal modelling study 印度十个城市的环境空气污染与日死亡率:因果模型研究。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00114-1
Jeroen de Bont PhD , Bhargav Krishna DrPH , Massimo Stafoggia PhD , Tirthankar Banerjee PhD , Hem Dholakia PhD , Amit Garg PhD , Vijendra Ingole PhD , Suganthi Jaganathan MPH , Prof Itai Kloog PhD , Kevin Lane PhD , Rajesh Kumar Mall PhD , Siddhartha Mandal PhD , Prof Amruta Nori-Sarma PhD , Prof Dorairaj Prabhakaran DM , Ajit Rajiva MESc , Abhiyant Suresh Tiwari MPH , Yaguang Wei PhD , Prof Gregory A Wellenius PhD , Prof Joel Schwartz PhD , Poornima Prabhakaran PhD , Petter Ljungman PhD

Background

The evidence for acute effects of air pollution on mortality in India is scarce, despite the extreme concentrations of air pollution observed. This is the first multi-city study in India that examines the association between short-term exposure to PM2·5 and daily mortality using causal methods that highlight the importance of locally generated air pollution.

Methods

We applied a time-series analysis to ten cities in India between 2008 and 2019. We assessed city-wide daily PM2·5 concentrations using a novel hybrid nationwide spatiotemporal model and estimated city-specific effects of PM2·5 using a generalised additive Poisson regression model. City-specific results were then meta-analysed. We applied an instrumental variable causal approach (including planetary boundary layer height, wind speed, and atmospheric pressure) to evaluate the causal effect of locally generated air pollution on mortality. We obtained an integrated exposure–response curve through a multivariate meta-regression of the city-specific exposure–response curve and calculated the fraction of deaths attributable to air pollution concentrations exceeding the current WHO 24 h ambient PM2·5 guideline of 15 μg/m3. To explore the shape of the exposure–response curve at lower exposures, we further limited the analyses to days with concentrations lower than the current Indian standard (60 μg/m3).

Findings

We observed that a 10 μg/m3 increase in 2-day moving average of PM2·5 was associated with 1·4% (95% CI 0·7–2·2) higher daily mortality. In our causal instrumental variable analyses representing the effect of locally generated air pollution, we observed a stronger association with daily mortality (3·6% [2·1–5·0]) than our overall estimate. Our integrated exposure–response curve suggested steeper slopes at lower levels of exposure and an attenuation of the slope at high exposure levels. We observed two times higher risk of death per 10 μg/m3 increase when restricting our analyses to observations below the Indian air quality standard (2·7% [1·7–3·6]). Using the integrated exposure–response curve, we observed that 7·2% (4·2%–10·1%) of all daily deaths were attributed to PM2·5 concentrations higher than the WHO guidelines.

Interpretation

Short-term PM2·5 exposure was associated with a high risk of death in India, even at concentrations well below the current Indian PM2·5 standard. These associations were stronger for locally generated air pollutants quantified through causal modelling methods than conventional time-series analysis, further supporting a plausible causal link.

Funding

Swedish Research Council for Sustainable Development.

背景:尽管印度的空气污染浓度极高,但有关空气污染对死亡率的急性影响的证据却很少。这是印度首次进行多城市研究,采用因果关系法研究 PM2-5 短期暴露与每日死亡率之间的关系,突出了当地产生的空气污染的重要性:我们在 2008 年至 2019 年期间对印度的十个城市进行了时间序列分析。我们使用一种新型混合全国时空模型评估了整个城市的 PM2-5 日浓度,并使用广义加性泊松回归模型估算了 PM2-5 对特定城市的影响。然后对特定城市的结果进行荟萃分析。我们采用了一种工具变量因果关系方法(包括行星边界层高度、风速和大气压力)来评估本地产生的空气污染对死亡率的因果效应。我们通过对特定城市的暴露-反应曲线进行多元元回归,得到了一条综合暴露-反应曲线,并计算了空气污染浓度超过世界卫生组织现行的 24 小时环境 PM2-5 指南(15 微克/立方米)所导致的死亡比例。为了探索较低暴露量下暴露-反应曲线的形状,我们进一步将分析限制在浓度低于印度现行标准(60 μg/m3)的日子:我们发现,PM2-5 的 2 天移动平均值每增加 10 微克/立方米,日死亡率就会增加 1-4%(95% CI 0-7-2-2)。在代表本地产生的空气污染影响的因果工具变量分析中,我们观察到与日死亡率的关联(3-6% [2-1-5-0])比我们的总体估计值更强。我们的综合暴露-反应曲线显示,暴露水平越低,斜率越陡,暴露水平越高,斜率越小。当我们将分析范围限制在低于印度空气质量标准的观测值时,我们发现每增加 10 μg/m3 的死亡风险要高出两倍(2-7% [1-7-3-6])。利用综合暴露-反应曲线,我们观察到,在所有每日死亡病例中,有7-2%(4-2%-10-1%)是由于PM2-5浓度高于世界卫生组织的指导标准:短期接触 PM2-5 与印度的高死亡风险有关,即使浓度远低于印度目前的 PM2-5 标准。与传统的时间序列分析相比,通过因果建模方法量化的当地产生的空气污染物的这些关联性更强,这进一步支持了可信的因果联系:瑞典可持续发展研究理事会。
{"title":"Ambient air pollution and daily mortality in ten cities of India: a causal modelling study","authors":"Jeroen de Bont PhD ,&nbsp;Bhargav Krishna DrPH ,&nbsp;Massimo Stafoggia PhD ,&nbsp;Tirthankar Banerjee PhD ,&nbsp;Hem Dholakia PhD ,&nbsp;Amit Garg PhD ,&nbsp;Vijendra Ingole PhD ,&nbsp;Suganthi Jaganathan MPH ,&nbsp;Prof Itai Kloog PhD ,&nbsp;Kevin Lane PhD ,&nbsp;Rajesh Kumar Mall PhD ,&nbsp;Siddhartha Mandal PhD ,&nbsp;Prof Amruta Nori-Sarma PhD ,&nbsp;Prof Dorairaj Prabhakaran DM ,&nbsp;Ajit Rajiva MESc ,&nbsp;Abhiyant Suresh Tiwari MPH ,&nbsp;Yaguang Wei PhD ,&nbsp;Prof Gregory A Wellenius PhD ,&nbsp;Prof Joel Schwartz PhD ,&nbsp;Poornima Prabhakaran PhD ,&nbsp;Petter Ljungman PhD","doi":"10.1016/S2542-5196(24)00114-1","DOIUrl":"10.1016/S2542-5196(24)00114-1","url":null,"abstract":"<div><h3>Background</h3><p>The evidence for acute effects of air pollution on mortality in India is scarce, despite the extreme concentrations of air pollution observed. This is the first multi-city study in India that examines the association between short-term exposure to PM<sub>2·5</sub> and daily mortality using causal methods that highlight the importance of locally generated air pollution.</p></div><div><h3>Methods</h3><p>We applied a time-series analysis to ten cities in India between 2008 and 2019. We assessed city-wide daily PM<sub>2·5</sub> concentrations using a novel hybrid nationwide spatiotemporal model and estimated city-specific effects of PM<sub>2·5</sub> using a generalised additive Poisson regression model. City-specific results were then meta-analysed. We applied an instrumental variable causal approach (including planetary boundary layer height, wind speed, and atmospheric pressure) to evaluate the causal effect of locally generated air pollution on mortality. We obtained an integrated exposure–response curve through a multivariate meta-regression of the city-specific exposure–response curve and calculated the fraction of deaths attributable to air pollution concentrations exceeding the current WHO 24 h ambient PM<sub>2·5</sub> guideline of 15 μg/m<sup>3</sup>. To explore the shape of the exposure–response curve at lower exposures, we further limited the analyses to days with concentrations lower than the current Indian standard (60 μg/m<sup>3</sup>).</p></div><div><h3>Findings</h3><p>We observed that a 10 μg/m<sup>3</sup> increase in 2-day moving average of PM<sub>2·5</sub> was associated with 1·4% (95% CI 0·7–2·2) higher daily mortality. In our causal instrumental variable analyses representing the effect of locally generated air pollution, we observed a stronger association with daily mortality (3·6% [2·1–5·0]) than our overall estimate. Our integrated exposure–response curve suggested steeper slopes at lower levels of exposure and an attenuation of the slope at high exposure levels. We observed two times higher risk of death per 10 μg/m<sup>3</sup> increase when restricting our analyses to observations below the Indian air quality standard (2·7% [1·7–3·6]). Using the integrated exposure–response curve, we observed that 7·2% (4·2%–10·1%) of all daily deaths were attributed to PM<sub>2·5</sub> concentrations higher than the WHO guidelines.</p></div><div><h3>Interpretation</h3><p>Short-term PM<sub>2·5</sub> exposure was associated with a high risk of death in India, even at concentrations well below the current Indian PM<sub>2·5</sub> standard. These associations were stronger for locally generated air pollutants quantified through causal modelling methods than conventional time-series analysis, further supporting a plausible causal link.</p></div><div><h3>Funding</h3><p>Swedish Research Council for Sustainable Development.</p></div>","PeriodicalId":48548,"journal":{"name":"Lancet Planetary Health","volume":"8 7","pages":"Pages e433-e440"},"PeriodicalIF":24.1,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2542519624001141/pdfft?md5=3a3f0a8cb2fb29dd6c3c9f7a1c4f0005&pid=1-s2.0-S2542519624001141-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141538776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Estimated effects of reductions in processed meat consumption and unprocessed red meat consumption on occurrences of type 2 diabetes, cardiovascular disease, colorectal cancer, and mortality in the USA: a microsimulation study 美国减少加工肉类消费和未加工红肉消费对 2 型糖尿病、心血管疾病、结直肠癌发病率和死亡率的影响估算:一项微观模拟研究。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00118-9
Joe Kennedy PhD , Peter Alexander PhD , Lindsey Smith Taillie PhD , Prof Lindsay M Jaacks PhD
<div><h3>Background</h3><p>High consumption of processed meat and unprocessed red meat is associated with increased risk of multiple chronic diseases, although there is substantial uncertainty regarding the relationship for unprocessed red meat. We developed a microsimulation model to estimate how reductions in processed meat and unprocessed red meat consumption could affect rates of type 2 diabetes, cardiovascular disease, colorectal cancer, and mortality in the US adult population.</p></div><div><h3>Methods</h3><p>We used data from two versions of the US National Health and Nutrition Examination Survey, one conducted during 2015–16 and one conducted during 2017–18, to create a simulated US population. The starting cohort was restricted to respondents aged 18 years or older who were not pregnant and had 2 days of dietary-recall data. First, we used previously developed risk models to estimate the baseline disease risk of an individual. For type 2 diabetes we used a logistic-regression model and for cardiovascular disease and colorectal cancer we used Cox proportional-hazard models. We then multiplied baseline risk by relative risk associated with individual processed meat and unprocessed red meat consumption. Prevented occurrences of type 2 diabetes, cardiovascular disease, colorectal cancer, and mortality were computed by taking the difference between the incidence in the baseline and intervention scenarios. All stages were repeated for ten iterations to correspond to a 10-year time span. Scenarios were reductions of 5%, 10%, 30%, 50%, 75%, and 100% in grams consumed of processed meat, unprocessed red meat, or both. Each scenario was repeated 50 times for uncertainty analysis.</p></div><div><h3>Findings</h3><p>The total number of individual respondents included in the simulated population was 8665, representing 242 021 876 US adults. 4493 (51·9%) of 8665 individuals were female and 4172 (48·1%) were male; mean age was 49·54 years (SD 18·38). At baseline, weighted mean daily consumption of processed meat was 29·1 g, with a 30% reduction being 8·7 g per day, and of unprocessed red meat was 46·7 g, with a 30% reduction being 14·0 g per day. We estimated that a 30% reduction in processed meat intake alone could lead to 352 900 (95% uncertainty interval 345 500–359 900) fewer occurrences of type 2 diabetes, 92 500 (85 600–99 900) fewer occurrences of cardiovascular disease, 53 300 (51 400–55 000) fewer occurrences of colorectal cancer, and 16 700 (15 300–17 700) fewer all-cause deaths during the 10-year period. A 30% reduction in unprocessed red meat intake alone could lead to 732 600 (725 700–740 400) fewer occurrences of type 2 diabetes, 291 500 (283 900–298 800) fewer occurrences of cardiovascular disease, 32 200 (31 500–32 700) fewer occurrences of colorectal cancer, and 46 100 (45 300–47 200) fewer all-cause deaths during the 10-year period. A 30% reduction in both processed meat and unprocessed red meat intake could lead to 1 073 400 (1 060 10
背景:加工肉类和未加工红肉的高消费量与多种慢性疾病风险的增加有关,但未加工红肉的关系还存在很大的不确定性。我们建立了一个微观模拟模型,以估计加工肉类和未加工红肉消费量的减少会如何影响美国成年人的 2 型糖尿病、心血管疾病、结肠直肠癌发病率和死亡率:我们使用两个版本的美国国家健康与营养调查数据(一个在 2015-16 年期间进行,另一个在 2017-18 年期间进行)创建了一个模拟美国人口。起始队列仅限于年龄在 18 岁或以上、未怀孕且有 2 天饮食回顾数据的受访者。首先,我们使用之前开发的风险模型来估算个人的基线疾病风险。对于 2 型糖尿病,我们使用了逻辑回归模型;对于心血管疾病和结直肠癌,我们使用了 Cox 比例危险模型。然后,我们将基线风险乘以与个人加工肉类和未加工红肉食用量相关的相对风险。2 型糖尿病、心血管疾病、结直肠癌和死亡率的预防发生率是通过计算基线方案和干预方案的发生率之差得出的。所有阶段重复进行十次迭代,时间跨度为 10 年。干预方案是将加工肉类、未加工红肉或两者的食用克数分别减少 5%、10%、30%、50%、75% 和 100%。每个方案重复 50 次,以进行不确定性分析:模拟人群中共有 8665 名受访者,代表了 242 021 876 名美国成年人。8665 人中有 4493 名女性(51-9%)和 4172 名男性(48-1%);平均年龄为 49-54 岁(SD 18-38)。基线时,加工肉类的加权平均日消费量为 29-1 克,减少 30% 则为每天 8-7 克;未加工红肉的加权平均日消费量为 46-7 克,减少 30% 则为每天 14-0 克。我们估计,仅将加工肉类的摄入量减少 30%,就可在 10 年内减少 352 900 例(95% 不确定区间为 345 500-359 900 例)2 型糖尿病,减少 92 500 例(85 600-99 900 例)心血管疾病,减少 53 300 例(51 400-55 000 例)结肠直肠癌,减少 16 700 例(15 300-17 700 例)全因死亡。如果仅将未加工红肉的摄入量减少 30%,则可在 10 年内减少 732 600 例(725 700-740 400 例)2 型糖尿病,减少 291 500 例(283 900-298 800 例)心血管疾病,减少 32 200 例(31 500-32 700 例)结肠直肠癌,减少 46 100 例(45 300-47 200 例)全因死亡。如果加工肉类和未加工红肉的摄入量均减少 30%,则可在 10 年内减少 1 073 400 例(1 060 100-1 084 700)2 型糖尿病,减少 382 400 例(372 100-391 000)心血管疾病,减少 84 400 例(82 100-86 200)结肠直肠癌,减少 62 200 例(60 600-64 400)全因死亡:解释:减少加工肉类的消费可以减轻美国一些慢性疾病的负担。然而,还需要进行更多的研究,以提高减少未加工红肉消费估计效果的确定性:资金来源:惠康信托基金会。
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引用次数: 0
Mobilising and evaluating existing heat adaptation measures to protect maternal and child health 动员和评估现有的热适应措施,以保护母婴健康。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00113-X
Dinesh Bhandari , Peng Bi , Jeffrey M Craig , Eddie Robinson , Wendy Pollock , Zerina Lokmic-Tomkins
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引用次数: 0
The emerging syndemic of climate change and non-communicable diseases 新出现的气候变化和非传染性疾病综合症。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00112-8
Ruth F Hunter , Leandro Garcia , Selina Dagless , Andy Haines , Tarra Penney , Chloe Clifford Astbury , Stephen Whiting , Kremlin Wickramasinghe , Francesca Racioppi , Gauden Galea , Hans Henri P Kluge
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引用次数: 0
Climate change adaptation for health: using case study systems-based approaches to formulating solutions and guiding policy 适应气候变化,促进健康:利用基于案例研究的系统方法制定解决方案和指导政策。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00111-6
Robin Fears , Montira Pongsiri , Peter F McGrath
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引用次数: 0
Mapping the distribution of Nipah virus infections: a geospatial modelling analysis 绘制尼帕病毒感染分布图:地理空间建模分析。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00119-0
Yan-Qun Sun MPH , Yuan-Yuan Zhang MSc , Mei-Chen Liu BSc , Jin-Jin Chen MSc , Ting-Ting Li BSc , Yan-Ning Liu BSc , Ling-Yu Zhang BSc , Tao Wang MPH , Lin-Jie Yu BSc , Tian-Le Che MPH , Tian Tang BSc , Qiang Xu PhD , Chen-Long Lv PhD , Bao-Gui Jiang PhD , Prof Nick Golding PhD , Max L Mehlman PhD , Prof Simon I Hay DSc , Prof Li-Qun Fang PhD , Prof Wei Liu MD

Background

Nipah virus is a zoonotic paramyxovirus responsible for disease outbreaks with high fatality rates in south and southeast Asia. However, knowledge of the potential geographical extent and risk patterns of the virus is poor. We aimed to establish an integrated spatiotemporal and phylogenetic database of Nipah virus infections in humans and animals across south and southeast Asia.

Methods

In this geospatial modelling analysis, we developed an integrated database containing information on the distribution of Nipah virus infections in humans and animals from 1998 to 2021. We conducted phylodynamic analysis to examine the evolution and migration pathways of the virus and meta-analyses to estimate the adjusted case-fatality rate. We used two boosted regression tree models to identify the potential ecological drivers of Nipah virus occurrences in spillover events and endemic areas, and mapped potential risk areas for Nipah virus endemicity.

Findings

749 people and eight bat species across nine countries were documented as being infected with Nipah virus. On the basis of 66 complete genomes of the virus, we identified two clades—the Bangladesh clade and the Malaysia clade—with the time of the most recent common ancestor estimated to be 1863. Adjusted case-fatality rates varied widely between countries and were higher for the Bangladesh clade than for the Malaysia clade. Multivariable meta-regression analysis revealed significant relationships between case-fatality rate estimates and viral clade (p=0·0021), source country (p=0·016), proportion of male patients (p=0·036), and travel time to health-care facilities (p=0·036). Temperature-related bioclimate variables and the probability of occurrence of Pteropus medius were important contributors to both the spillover and the endemic infection models.

Interpretation

The suitable niches for Nipah virus are more extensive than previously reported. Future surveillance efforts should focus on high-risk areas informed by updated projections. Specifically, intensifying zoonotic surveillance efforts, enhancing laboratory testing capacity, and implementing public health education in projected high-risk areas where no human cases have been reported to date will be crucial. Additionally, strengthening wildlife surveillance and investigating potential modes of transmission in regions with documented human cases is needed.

Funding

The Key Research and Development Program of China.

背景:尼帕病毒是一种人畜共患的副黏液病毒,在南亚和东南亚爆发的疾病致死率很高。然而,人们对该病毒的潜在地理范围和风险模式知之甚少。我们的目标是建立南亚和东南亚地区人畜感染尼帕病毒的时空和系统发育综合数据库:在这项地理空间建模分析中,我们开发了一个综合数据库,其中包含 1998 年至 2021 年期间尼帕病毒在人类和动物中的感染分布信息。我们进行了系统动力学分析以研究病毒的进化和迁移途径,并进行了荟萃分析以估算调整后的病死率。我们使用了两个提升回归树模型来确定尼帕病毒在溢出事件和流行地区发生的潜在生态驱动因素,并绘制了尼帕病毒流行的潜在风险区域图:9个国家的749人和8种蝙蝠被记录为尼帕病毒感染者。根据病毒的 66 个完整基因组,我们确定了两个支系--孟加拉国支系和马来西亚支系--最近共同祖先的时间估计为 1863 年。不同国家的调整后病死率差异很大,孟加拉国支系的病死率高于马来西亚支系。多变量元回归分析显示,病死率估计值与病毒支系(p=0-0021)、来源国(p=0-016)、男性患者比例(p=0-036)和前往医疗机构的旅行时间(p=0-036)之间存在显著关系。与气温相关的生物气候变量和中翅蝶形花的发生概率对溢出效应模型和地方性感染模型都有重要影响:尼帕病毒的适宜生存环境比以前报告的更为广泛。未来的监测工作应根据最新预测,重点关注高风险地区。具体而言,在迄今尚未报告人类病例的预计高风险地区,加强人畜共患病监测工作、提高实验室检测能力和开展公共卫生教育至关重要。此外,还需要在有人类病例记录的地区加强野生动物监测并调查潜在的传播方式:资金来源:中国重点研发计划。
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引用次数: 0
Global health costs of ambient PM2·5 from combustion sources: a modelling study supporting air pollution control strategies 来自燃烧源的环境 PM2-5 的全球健康成本:支持空气污染控制策略的模型研究。
IF 24.1 1区 医学 Q1 ENVIRONMENTAL SCIENCES Pub Date : 2024-07-01 DOI: 10.1016/S2542-5196(24)00098-6
Hao Yin PhD , Erin E McDuffie PhD , Prof Randall V Martin PhD , Prof Michael Brauer ScD

Background

Climate actions targeting combustion sources can generate large ancillary health benefits via associated air-quality improvements. Therefore, understanding the health costs associated with ambient fine particulate matter (PM2·5) from combustion sources can guide policy design for both air pollution and climate mitigation efforts.

Methods

In this modelling study, we estimated the health costs attributable to ambient PM2·5 from six major combustion sources across 204 countries using updated concentration–response models and an age-adjusted valuation method. We defined major combustion sources as the sum of total coal, liquid fuel and natural gas, solid biofuel, agricultural waste burning, other fires, and 50% of the anthropogenic fugitive, combustion, and industrial dust source.

Findings

Global long-term exposure to ambient PM2·5 from combustion sources imposed US$1·1 (95% uncertainty interval 0·8–1·5) trillion in health costs in 2019, accounting for 56% of the total health costs from all PM2·5 sources. Comparing source contributions to PM2·5 concentrations and health costs, we observed a higher share of health costs from combustion sources compared to their contribution to population-weighted PM2·5 concentration across 134 countries, accounting for more than 87% of the global population. This disparity was primarily attributed to the non-linear relationship between PM2·5 concentration and its associated health costs. Globally, phasing out fossil fuels can generate 23% higher relative health benefits compared to their share of PM2·5 reductions. Specifically, the share of health costs for total coal was 36% higher than the source's contributions to corresponding PM2·5 concentrations and the share of health costs for liquid fuel and natural gas was 12% higher. Other than fossil fuels, South Asia was expected to show 16% greater relative health benefits than the percentage reduction in PM2·5 from the abatement of solid biofuel emissions.

Interpretation

In most countries, targeting combustion sources might offer greater health benefits than non-combustion sources. This finding provides additional rationale for climate actions aimed at phasing out combustion sources, especially those related to fossil fuels and solid biofuel. Mitigation efforts designed according to source-specific health costs can more effectively avoid health costs than strategies that depend solely on the source contributions to overall PM2·5 concentration.

Funding

The Health Effects Institute, the National Natural Science Foundation of China, and NASA.

背景:针对燃烧源的气候行动可通过相关的空气质量改善产生巨大的附带健康效益。因此,了解与燃烧源产生的环境细颗粒物(PM2-5)相关的健康成本可以为空气污染和气候减缓工作的政策设计提供指导:在这项建模研究中,我们使用最新的浓度-反应模型和年龄调整估值法,估算了 204 个国家六种主要燃烧源产生的环境 PM2-5 的健康成本。我们将主要燃烧源定义为煤炭、液体燃料和天然气、固体生物燃料、农业废弃物燃烧、其他火灾的总和,以及人为逃逸源、燃烧源和工业粉尘源的 50%:全球长期暴露于燃烧源产生的环境 PM2-5 将在 2019 年造成 1-1 万亿美元(95% 不确定区间为 0-8-1-5)的健康成本,占所有 PM2-5 源健康成本总额的 56%。比较各种来源对 PM2-5 浓度和健康成本的贡献,我们发现在 134 个国家(占全球人口的 87% 以上)中,燃烧源的健康成本份额高于其对人口加权 PM2-5 浓度的贡献。这种差异主要归因于 PM2-5 浓度与相关健康成本之间的非线性关系。在全球范围内,与减少 PM2-5 的份额相比,逐步淘汰化石燃料产生的相对健康效益要高出 23%。具体来说,总煤的健康成本份额比该来源对相应 PM2-5 浓度的贡献高出 36%,液体燃料和天然气的健康成本份额高出 12%。除化石燃料外,预计南亚的相对健康效益比减少固体生物燃料排放所减少的 PM2-5 百分比高出 16%:在大多数国家,针对燃烧源可能比非燃烧源带来更大的健康效益。这一发现为旨在逐步淘汰燃烧源的气候行动提供了更多理由,尤其是那些与化石燃料和固体生物燃料相关的行动。根据特定污染源的健康成本而设计的减排措施,比那些仅依赖于污染源对 PM2-5 整体浓度贡献的策略,能更有效地避免健康成本:资金来源:健康效应研究所、国家自然科学基金委员会和美国国家航空航天局。
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引用次数: 0
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Lancet Planetary Health
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