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Sand and dust storms increasingly threaten global environmental and public health. To date, 150 countries are directly affected, with more than 100 classified as non-dust source regions. With climate change, these storms are expected to become more frequent and severe. Despite international awareness and initiatives, such as those led by the UN, crucial knowledge gaps continue to hinder effective, evidence-based public responses to sand and dust storms. In this Viewpoint, we review existing gaps in health research and highlight four key research priorities: the comprehensive health effects of sand and dust storms, including short-term and long-term exposures, diseases, regions, and health outcomes; the key particle sizes and toxic components of particles during sand and dust storms; the design of multicentre studies accounting for region-specific exposure patterns; and research on health outcomes attributable to particulate matter mixtures dominated by windblown dust versus other sources. We urgently call for international, collaborative, and multidisciplinary health studies considering sand and dust storm exposure characteristics and for the adoption of scientifically robust epidemiological methods in these studies., Competing Interests: Declaration of interests PP is employed by the Health Effects Institute, a non-profit corporation that receives balanced funding from the United States Environmental Protection Agency, the worldwide motor vehicle industry, and philanthropic organisations, and serves as Chair of the Governing Board for OpenAQ, a non-profit organisation providing universal access to air quality data. This is a voluntary position with no financial renumeration. All other authors declare no competing interests., (Copyright © 2025 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: In 2019, the Global Burden of Diseases, Injuries, and Risk Factors Study attributed 0·98 million deaths to ambient air pollution in India based on potentially inappropriate exposure-response functions from countries with low air pollution levels. Instead, using data from India, we investigated long-term exposure to PM 2·5 and all-cause mortality with a causal inference method., Methods: We collected national counts of annual mortality from 2009 to 2019 from the Civil Registration System at the district level to calculate annual district-level mortality rate as our main outcome and obtained annual PM 2·5 concentrations from a high-resolution spatiotemporal model. We applied an extended version of the difference-in-differences design by use of generalised additive models with quasi-Poisson distribution, including indicator variables and separate time trends for spatial administrative divisions. PM 2·5 concentrations obtained at 1 km × 1 km spatial resolution across the country were used to calculate annual district-level mean PM 2·5 concentrations. Similarly, we collected confounders at the district level, such as mean and SD of quarterly temperatures, gross domestic product per capita, population aged 60 years or older, clean cooking fuel usage, literacy in women, and median age. The spatial unit of analysis was administrative division., Findings: The annual median population-weighted PM 2·5 was 38·9 μg/m 3 (5-95th percentile 19·7-71·8 μg/m 3 ). The full population lived in areas with PM 2·5 concentrations exceeding the 5 μg/m 3 annual mean recommended in the WHO guidelines, and 1·1 billion of 1·4 billion (81·9% of the total population) lived in areas above the Indian National Ambient Air Quality Standards for annual mean PM 2·5 not exceeding 40 μg/m 3 . A 10 μg/m 3 increase in annual PM 2·5 concentration was associated with an 8·6% (95% CI 6·4-10·8) higher annual mortality. Based on the Indian National Ambient Air Quality Standards, a total of 3·8 million (95% CI 2·9-4·9) deaths between 2009 and 2019 were attributable to PM 2·5 , amounting to 5·0% (3·8-6·4) of total mortality. Based on the WHO guidelines, a total of 16·6 million (13·0-21·8) deaths were attributable to PM 2·5 , amounting to 24·9% (19·5-32·5) of total mortality., Interpretation: Our difference-in-differences approach allowed us to assess the full extent of registered deaths in the most populated country in the world, which has high levels of air pollution. We provide new evidence of increased mortality risk from long-term PM 2·5 , which emphasises the need for tighter regulatory standards to potentially substantially reduce mortality across India., Funding: Swedish Research Council for Sustainable Development., Competing Interests: Declaration of interests PP reports working as a consultant for World Bank for climate change and health outcomes. GAW reports receiving consulting income from the Health Effects Institute and Google. PL has received air travel and hotel accommodation paid by Fondazione Menarini to attend and hold a presentation at the Respirami meeting in Milan, Italy. He is the Scientific Secretary of the Swedish Society of Cardiology and co-chair of the European Chapter of International Society of Environmental Epidemiology (both unpaid). He was a paid member of the ethical committee board for the Swedish Ethical Authority 2022–23. All other authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Ambient air pollution, including particulate matter (such as PM 10 and PM 2·5 ) and nitrogen dioxide (NO 2 ), 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 NO 2 , PM 10 , and PM 2·5 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 PM 10 , PM 2·5 , or NO 2 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/m 3 increase in PM 2·5 . Two-pollutant models generally showed similar results to single-pollutant models for PM fractions and indicated temporal differences for NO 2 ., 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., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

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 PM 2·5 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 PM 2·5 concentrations using a novel hybrid nationwide spatiotemporal model and estimated city-specific effects of PM 2·5 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 PM 2·5 guideline of 15 μg/m 3 . 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 3 )., Findings: We observed that a 10 μg/m 3 increase in 2-day moving average of PM 2·5 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/m 3 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 2·5 concentrations higher than the WHO guidelines., Interpretation: Short-term PM 2·5 exposure was associated with a high risk of death in India, even at concentrations well below the current Indian PM 2·5 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., Competing Interests: Declaration of interests PP reports working as a consultant for World Bank for climate change and health outcomes. GAW reports receiving consulting income from the Health Efects Institute and Google. PL has received air travel and hotel accommodation paid by Fondazione Menarini to attend and hold a presentation at the Respirami meeting in Milan. He is the Scientific Secretary of the Swedish Society of Cardiology and co-chair of the European Chapter of International Society of Environmental Epidemiology (both unpaid). He was a paid member of the ethical committee board for the Swedish Ethical Authority 2022–23. All other authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Heat and cold are established environmental risk factors for human health. However, mapping the related health burden is a difficult task due to the complexity of the associations and the differences in vulnerability and demographic distributions. In this study, we did a comprehensive mortality impact assessment due to heat and cold in European urban areas, considering geographical differences and age-specific risks., Methods: We included urban areas across Europe between Jan 1, 2000, and Dec 12, 2019, using the Urban Audit dataset of Eurostat and adults aged 20 years and older living in these areas. Data were extracted from Eurostat, the Multi-country Multi-city Collaborative Research Network, Moderate Resolution Imaging Spectroradiometer, and Copernicus. We applied a three-stage method to estimate risks of temperature continuously across the age and space dimensions, identifying patterns of vulnerability on the basis of city-specific characteristics and demographic structures. These risks were used to derive minimum mortality temperatures and related percentiles and raw and standardised excess mortality rates for heat and cold aggregated at various geographical levels., Findings: Across the 854 urban areas in Europe, we estimated an annual excess of 203 620 (empirical 95% CI 180 882-224 613) deaths attributed to cold and 20 173 (17 261-22 934) attributed to heat. These corresponded to age-standardised rates of 129 (empirical 95% CI 114-142) and 13 (11-14) deaths per 100 000 person-years. Results differed across Europe and age groups, with the highest effects in eastern European cities for both cold and heat., Interpretation: Maps of mortality risks and excess deaths indicate geographical differences, such as a north-south gradient and increased vulnerability in eastern Europe, as well as local variations due to urban characteristics. The modelling framework and results are crucial for the design of national and local health and climate policies and for projecting the effects of cold and heat under future climatic and socioeconomic scenarios., Funding: Medical Research Council of UK, the Natural Environment Research Council UK, the EU's Horizon 2020, and the EU's Joint Research Center., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Long-term exposure to ambient air pollution has been associated with premature mortality, but associations at concentrations lower than current annual limit values are uncertain. We analysed associations between low-level air pollution and mortality within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE)., Methods: In this multicentre longitudinal study, we analysed seven population-based cohorts of adults (age ≥30 years) within ELAPSE, from Belgium, Denmark, England, the Netherlands, Norway, Rome (Italy), and Switzerland (enrolled in 2000-11; follow-up until 2011-17). Mortality registries were used to extract the underlying cause of death for deceased individuals. Annual average concentrations of fine particulate matter (PM 2·5 ), nitrogen dioxide (NO 2 ), black carbon, and tropospheric warm-season ozone (O 3 ) from Europe-wide land use regression models at 100 m spatial resolution were assigned to baseline residential addresses. We applied cohort-specific Cox proportional hazard models with adjustment for area-level and individual-level covariates to evaluate associations with non-accidental mortality, as the main outcome, and with cardiovascular, non-malignant respiratory, and lung cancer mortality. Subset analyses of participants living at low pollutant concentrations (as per predefined values) and natural splines were used to investigate the concentration-response function. Cohort-specific effect estimates were pooled in a random-effects meta-analysis., Findings: We analysed 28 153 138 participants contributing 257 859 621 person-years of observation, during which 3 593 741 deaths from non-accidental causes occurred. We found significant positive associations between non-accidental mortality and PM 2·5 , NO 2 , and black carbon, with a hazard ratio (HR) of 1·053 (95% CI 1·021-1·085) per 5 μg/m 3 increment in PM 2·5 , 1·044 (1·019-1·069) per 10 μg/m 3 NO 2 , and 1·039 (1·018-1·059) per 0·5 × 10 -5 /m black carbon. Associations with PM 2·5 , NO 2 , and black carbon were slightly weaker for cardiovascular mortality, similar for non-malignant respiratory mortality, and stronger for lung cancer mortality. Warm-season O 3 was negatively associated with both non-accidental and cause-specific mortality. Associations were stronger at low concentrations: HRs for non-accidental mortality at concentrations lower than the WHO 2005 air quality guideline values for PM 2·5 (10 μg/m 3 ) and NO 2 (40 μg/m 3 ) were 1·078 (1·046-1·111) per 5 μg/m 3 PM 2·5 and 1·049 (1·024-1·075) per 10 μg/m 3 NO 2 . Similarly, the association between black carbon and non-accidental mortality was highest at low concentrations, with a HR of 1·061 (1·032-1·092) for exposure lower than 1·5× 10 -5 /m, and 1·081 (0·966-1·210) for exposure lower than 1·0× 10 -5 /m., Interpretation: Long-term exposure to concentrations of PM 2·5 and NO 2 lower than current annual limit values was associated with non-accidental, cardiovascular, non-malignant respiratory, and lung cancer mortality in seven large European cohorts. Continuing research on the effects of low concentrations of air pollutants is expected to further inform the process of setting air quality standards in Europe and other global regions., Funding: Health Effects Institute., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Many regions of the world are now facing more frequent and unprecedentedly large wildfires. However, the association between wildfire-related PM 2·5 and mortality has not been well characterised. We aimed to comprehensively assess the association between short-term exposure to wildfire-related PM 2·5 and mortality across various regions of the world., Methods: For this time series study, data on daily counts of deaths for all causes, cardiovascular causes, and respiratory causes were collected from 749 cities in 43 countries and regions during 2000-16. Daily concentrations of wildfire-related PM 2·5 were estimated using the three-dimensional chemical transport model GEOS-Chem at a 0·25° × 0·25° resolution. The association between wildfire-related PM 2·5 exposure and mortality was examined using a quasi-Poisson time series model in each city considering both the current-day and lag effects, and the effect estimates were then pooled using a random-effects meta-analysis. Based on these pooled effect estimates, the population attributable fraction and relative risk (RR) of annual mortality due to acute wildfire-related PM 2·5 exposure was calculated., Findings: 65·6 million all-cause deaths, 15·1 million cardiovascular deaths, and 6·8 million respiratory deaths were included in our analyses. The pooled RRs of mortality associated with each 10 μg/m 3 increase in the 3-day moving average (lag 0-2 days) of wildfire-related PM 2·5 exposure were 1·019 (95% CI 1·016-1·022) for all-cause mortality, 1·017 (1·012-1·021) for cardiovascular mortality, and 1·019 (1·013-1·025) for respiratory mortality. Overall, 0·62% (95% CI 0·48-0·75) of all-cause deaths, 0·55% (0·43-0·67) of cardiovascular deaths, and 0·64% (0·50-0·78) of respiratory deaths were annually attributable to the acute impacts of wildfire-related PM 2·5 exposure during the study period., Interpretation: Short-term exposure to wildfire-related PM 2·5 was associated with increased risk of mortality. Urgent action is needed to reduce health risks from the increasing wildfires., Funding: Australian Research Council, Australian National Health & Medical Research Council., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM 2·5 ), nitrogen dioxide (NO 2 ), black carbon, and warm-season ozone (O 3 ) with the incidence of stroke and acute coronary heart disease., Methods: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values., Findings: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM 2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 μg/m 3 increase), NO 2 (1·08 [1·04-1·12] per 10 μg/m 3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10 -5 /m increase), whereas coronary heart disease incidence was only associated with NO 2 (1·04 [1·01-1·07]). Warm-season O 3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM 2·5 and NO 2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 μg/m 3 for PM 2·5 and 40 μg/m 3 for NO 2 ., Interpretation: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values., Funding: Health Effects Institute., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Epidemiological evidence on short-term association between ambient carbon monoxide (CO) and mortality is inconclusive and limited to single cities, regions, or countries. Generalisation of results from previous studies is hindered by potential publication bias and different modelling approaches. We therefore assessed the association between short-term exposure to ambient CO and daily mortality in a multicity, multicountry setting., Methods: We collected daily data on air pollution, meteorology, and total mortality from 337 cities in 18 countries or regions, covering various periods from 1979 to 2016. All included cities had at least 2 years of both CO and mortality data. We estimated city-specific associations using confounder-adjusted generalised additive models with a quasi-Poisson distribution, and then pooled the estimates, accounting for their statistical uncertainty, using a random-effects multilevel meta-analytical model. We also assessed the overall shape of the exposure-response curve and evaluated the possibility of a threshold below which health is not affected., Findings: Overall, a 1 mg/m 3 increase in the average CO concentration of the previous day was associated with a 0·91% (95% CI 0·32-1·50) increase in daily total mortality. The pooled exposure-response curve showed a continuously elevated mortality risk with increasing CO concentrations, suggesting no threshold. The exposure-response curve was steeper at daily CO levels lower than 1 mg/m 3 , indicating greater risk of mortality per increment in CO exposure, and persisted at daily concentrations as low as 0·6 mg/m 3 or less. The association remained similar after adjustment for ozone but was attenuated after adjustment for particulate matter or sulphur dioxide, or even reduced to null after adjustment for nitrogen dioxide., Interpretation: This international study is by far the largest epidemiological investigation on short-term CO-related mortality. We found significant associations between ambient CO and daily mortality, even at levels well below current air quality guidelines. Further studies are warranted to disentangle its independent effect from other traffic-related pollutants., Funding: EU Horizon 2020, UK Medical Research Council, and Natural Environment Research Council., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Background: Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer (BC). Little is known about whether exposure to air pollution influences BC in the general population., Objective: To evaluate the association between long-term exposure to ambient air pollution and BC incidence., Design, Setting, and Participants: We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303431; mean follow-up 14.1 yr). We estimated exposure to nitrogen oxides (NO 2 and NO x ), particulate matter (PM) with diameter <10μm (PM 10 ), <2.5μm (PM 2.5 ), between 2.5 and 10μm (PM 2.5-10 ), PM 2.5 absorbance (soot), elemental constituents of PM, organic carbon, and traffic density at baseline home addresses using standardized land-use regression models from the European Study of Cohorts for Air Pollution Effects project., Outcome Measurements and Statistical Analysis: We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for BC incidence., Results and Limitations: During follow-up, 943 incident BC cases were diagnosed. In the meta-analysis, none of the exposures were associated with BC risk. The summary HRs associated with a 10-μg/m 3 increase in NO 2 and 5-μg/m 3 increase in PM 2.5 were 0.98 (95% confidence interval [CI] 0.89-1.08) and 0.86 (95% CI 0.63-1.18), respectively. Limitations include the lack of information about lifetime exposure., Conclusions: There was no evidence of an association between exposure to outdoor air pollution levels at place of residence and risk of BC., Patient Summary: We assessed the link between outdoor air pollution at place of residence and bladder cancer using the largest study population to date and extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at place of residence and bladder cancer risk., (Copyright © 2016 European Association of Urology. Published by Elsevier B.V. All rights reserved.)