Ambient air pollution and low birth weight in Brazil: a nationwide study of more than 10 million births between 2001 and 2018.

Low birth weight (LBW) is a global health concern. While it is commonly associated with maternal health and behavior, exposure to ambient air pollution, can also play a role in contributing to LBW. In Brazil, where diverse environmental conditions and regional disparities exist, assessing the impact of ambient air pollution on LBW becomes particularly pertinent. To our knowledge, there is a gap in the existing literature, as no previous study has specifically investigated the relationship between ambient air pollution and LBW nationwide in Brazil. This study aims to fill this gap by examining the association between ambient air pollution and LBW in each trimester of pregnancy across the Brazilian states. In this work, birth data from January 1, 2001, to December 31, 2018 has been used. We utilized logistic regression models to estimate the odds ratio (OR) for low birth weight (LBW) associated with ambient air pollution (PM2.5, NO2, and O3) during each trimester of pregnancy (1st to 3rd trimester) across all 27 Brazilian states in our nationwide case-control study. We adjusted our model for several variables, including ambient temperature, relative humidity, and socioeconomic status (SES) variables at the individual level. We also conducted effect modification analyses by infant sex, mother's age, and the number of prenatal visits. Our study comprises over 10,213,144 birth records nationwide. Of these, 479,204 (4.92%) infants were included as cases of LBW. Our results indicate positive associations between PM2.5 and LBW, mainly in the Southern region. For example, in the state of Santa Catarina (South region), ORs were 1.003 (95% CI: 1.002, 1.004), 1.003 (95% CI: 1.002, 1.004), and 1.005 (95% CI: 1.003, 1.007) for the 1st, 2nd, and 3rd trimesters of exposure, respectively. NO2 had a robust association with LBW in the Northern and Northeastern states, including the state of Amapá (North region, where the Amazon Forest is located) with ORs of 1.377 (95% CI: 1.010, 1.878), 1.390 (95% CI: 1.020, 1.894), and 1.747 (95% CI: 1.297, 2.352) for the 1st, 2nd, and 3rd trimesters of exposure, respectively. Similarly, O3 had a robust association in the North and Midwest states, as observed in the state of Amapá with ORs of 1.033 (95% CI: 1.012, 1.054), and 1.033 (95% CI: 1.013, 1.053) for the 2nd, and 3rd trimesters, respectively. In the stratified analysis, boys were more vulnerable than girls, and the lower number of prenatal visits was associated with higher OR. Our findings are essential to the development of guidelines to prevent maternal exposure and protection of newborns in Brazil. This study provides valuable insights for region-specific strategies to improve maternal and neonatal health.

Associations of Lifestyle, Ambient Air Pollution With Progression of Asthma in Adults: A Comprehensive Analysis of UK Biobank Cohort.

Objectives: We aim to investigate the associations between lifestyle, ambient air pollution with crucial outcomes in the progression of adult asthma, including asthma new-onset and asthma hospitalisation. Methods: 176,800 participants were included to assess the prospective association between baseline risk exposures and the subsequent asthma onset, 17,387 participants were used to evaluate asthma hospitalisation. Cox regression models were employed to examine the associations. Results: In terms of lifestyle factors, the HRs (95% CIs) of the least healthy lifestyle categories for asthma incidence and hospitalization were 1.099 (1.017-1.187) and 1.064 (1.008-1.123), respectively. For pollutants, PM2.5, especially the traffic-related PM2.5 component, was consistently recognized as a significant risk factor for asthma onset (HR = 1.064, 95% CI: 1.034-1.094) and hospitalisation (HR = 1.031, 95% CI: 1.010-1.052) under various model adjustments. Low socioeconomic status also played a major role in the progression of adult asthma. Conclusion: Our study provides crucial insights into factors influencing the progression of adult asthma. Monitoring and reducing exposure to air pollution, particularly PM2.5, promoting healthier lifestyle, and addressing socioeconomic inequity are important in preventing and managing asthma.

Prenatal exposure to ambient air pollution and subsequent risk of lower respiratory tract infections in childhood and adolescence: A systematic review.

BACKGROUND: Pregnancy represents a critical window of vulnerability to the harmful effects of air pollution on health. However, long-term consequences such as risk of having lower respiratory tract infections (LRTIs) are less explored. This systematic review aims to synthesize previous research on prenatal exposure to ambient (outdoor) air pollution and LRTIs in childhood and adolescence. METHODS: We systematically searched Embase, MEDLINE, Web of Science Core Collection, CINAHL, and Global Health up to May 17, 2024. We included peer-reviewed publications of studies which investigated the association between prenatal exposure to ambient air pollution and LRTIs up to the age of 19. We excluded conference abstracts, study protocols, review articles, and grey literature. Screening and data extraction was conducted by two reviewers independently. We used the Office of Health Assessment and Translation tool to assess risk of bias and conducted a narrative synthesis. RESULTS: The search yielded 6056 records, of which 16 publications describing 12 research studies were eligible for the synthesis. All studies were conducted in high- or upper-middle-income countries in Europe or Asia. Half (6) of the studies focused on LRTIs occurring within the first three years of life, and the others also included LRTIs in older children (up to age 14). Air pollutants investigated included nitrogen dioxide, sulphur dioxide, particulate matter (PM2.5: diameter ≤2.5 µm and PM10: diameter ≤10 µm), carbon monoxide, ozone, and benzene. Findings on a potential association between prenatal ambient air pollution exposure and LRTIs were inconclusive, without a clear and consistent direction. There was some suggestion of a positive association with prenatal PM2.5 exposure. The small number of studies identified, their poor geographical representation, and their methodological limitations including concerns for risk of bias preclude more definitive conclusions. CONCLUSION: The available published evidence is insufficient to establish whether prenatal exposure to ambient air pollution increases risk of LRTIs in children and adolescents. With many populations exposed to high levels of air pollution, there is an urgent need for research in more diverse settings, more transparent reporting of methods, and exploring how, when, and for whom prenatal exposure to ambient air pollution leads to the greatest health risks. PROSPERO REGISTRATION NUMBER: CRD42023407689.

Prenatal exposure to ambient air pollution and persistent postpartum depression.

BACKGROUND: Ambient air pollution during pregnancy has been linked with postpartum depression up to 12 months, but few studies have investigated its impact on persistent depression beyond 12 months postpartum. This study aimed to evaluate prenatal ambient air pollution exposure and the risk of persistent depression over 3 years after childbirth and to identify windows of susceptibility. METHODS: This study included 361 predominantly low-income Hispanic/Latina participants with full-term pregnancies in the Maternal and Developmental Risks from Environmental and Social Stressors (MADRES) cohort. We estimated daily residential PM2.5, PM10, NO2, and O3 concentrations throughout 37 gestational weeks using inverse-distance squared spatial interpolation from monitoring data and calculated weekly averaged levels. Depression was assessed by the 20-item Center for Epidemiologic Studies-Depression (CES-D) scale at 12, 24, and 36 months postpartum, with persistent postpartum depression defined as a CES-D score ≥16 at any of these timepoints. We performed robust Poisson log-linear distributed lag models (DLM) via generalized estimating equations (GEE) to estimate the adjusted risk ratio (RR). RESULTS: Depression was observed in 17.8 %, 17.5 %, and 13.4 % of participants at 12, 24, and 36 months, respectively. We found one IQR increase (3.9 ppb) in prenatal exposure to NO2 during the identified sensitive window of gestational weeks 13-29 was associated with a cumulative risk ratio of 3.86 (95 % CI: 3.24, 4.59) for persistent depression 1-3 years postpartum. We also found one IQR increase (7.4 µg/m3) in prenatal exposure to PM10 during gestation weeks 12-28 was associated a cumulative risk ratio of 3.88 (95 % CI: 3.04, 4.96) for persistent depression. No clear sensitive windows were identified for PM2.5 or O3. CONCLUSIONS: Mid-pregnancy PM10 and NO2 exposures were associated with nearly 4-fold increased risks of persistent depression after pregnancy, which has critical implications for prevention of perinatal mental health outcomes.

Ambient air pollution, low-grade inflammation, and lung function: Evidences from the UK Biobank.

The associations of ambient air pollution exposure and low-grade inflammation with lung function remain uncertain. In this study, 276,289 subjects were enrolled in the UK Biobank. Individual exposure to ambient air pollution (including nitrogen dioxide [NO2], nitrogen oxides [NOx]), and particulate matter [PM2.5, PM10, PMcoarse]) were estimated by using the land-use regression model. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were tested, and low-grade inflammation score (INFLA score) was calculated for each subject. In this cross-sectional study, the median concentrations of air pollution were 9.89 µg/m3 for PM2.5, 15.98 µg/m3 for PM10, 6.09 µg/m3 for PMcoarse, 25.60 µg/m3 for NO2, and 41.46 µg/m3 for NOx, respectively. We observed that PM2.5, PM10, PMcoarse, NO2, NOx was negatively associated with lung function. Besides, significant positive associations between PM exposure and low-grade inflammation were noted. Per interquartile range (IQR) increase in PM2.5, PM10, and PMcoarse was related to higher INFLA score, and the ß (95 % CI) was 0.06 (0.03, 0.08), 0.03 (0.02, 0.05), and 0.03 (0.01, 0.04), respectively. Additionally, we found significant negative associations between INFLA scores and lung function. One-unit increase in INFLA score was linked with 12.41- and 11.31-ml decreases in FVC and FEV1, respectively. Compared with individuals with low air pollution exposure and low INFLA scores, participants with high air pollution and high INFLA scores had the lowest FVC and FEV1. Additionally, we observed that INFLA scores could modify the relationships of PM2.5, NO2, and NOx with FVC and FEV1 (Pinteraction <0.05). The negative impact of air pollutants on lung function was more pronounced in subjects with high INFLA scores in comparison to those with low INFLA scores. In conclusion, we demonstrated negative associations between ambient air pollution and lung function, and the observed associations were strengthened and modified by low-grade inflammation.

The Impact of Ambient Air Pollution on Allergic Rhinitis Symptoms: A Prospective Follow-Up Study.

Air pollution has become a serious public health problem and there is evidence that air pollution affects the incidence of allergic rhinitis. To further investigate the effect of ambient air pollutants on the severity of allergic rhinitis symptoms, a prospective follow-up study in patients with allergic rhinitis was conducted. A total of 167 allergic rhinitis patients with a mean age of 35.4 years, who were visiting the hospital, were enrolled. The daily symptom severity of allergic rhinitis and the concentrations of six air pollutants, including PM2.5, PM10, SO2, CO, O3 and NO2, were collected through follow-up investigations. The impact of ambient air pollutants on symptom severity was assessed via multi-pollutant models. Among several typical ambient air pollutants, we observed correlations of allergic rhinitis symptoms with PM2.5, PM10, CO, SO2 and NO2, whereas O3 showed no such correlation. Specifically, PM2.5 and PM10 were significantly associated with sneezing and nasal blockage. NO2 was significantly correlated with symptoms of rhinorrhea, itchy nose and itchy eyes. CO was significantly linked to sneezing and nasal blockage symptoms. These air pollutants not only had a direct impact on allergic rhinitis symptoms but also exhibited a lagging effect. This study indicates that short-term exposure to air pollutants is associated with exacerbation of nasal symptoms in patients with allergic rhinitis, leading to a decline in their quality of life.

Time-varying ambient air pollution exposure is associated with gut microbiome variation in the first 2 years of life.

The infant gut microbiome matures greatly in the first year of life. Ambient air pollution (AAP) exposure is associated with the infant gut microbiome. However, whether time-varying AAP influences infant gut microbiome variation is rarely investigated. This study aimed to investigate the effects of PM2.5, PM10, and O3 on infant gut microbiome variation longitudinally. Demographic information, stool samples, and AAP exposure concentrations were collected at 6, 12, 24 months from infants. Gut microbiome was processed and analyzed using 16S rRNA V3-V4 gene regions. AAP exposure concentrations were calculated using the China High Air Pollutants (CHAP) database. Multiple pollutant models were used to assess the mixed effects of PM2.5, PM10, and O3 on infant gut microbiome variation. Infants' gut microbiomes at 6, 12, 24 months old had significant differences in alpha diversity, beta diversity, and community composition. PM2.5 and O3 respectively explained 6.3% and 5.3% of the differences in community composition for 24-month-old infants. Single pollutant exposure and multiple pollutant exposure in different periods were both associated with alpha diversity indices and specific gut microbial phyla and genera. AAP was more associated with infant gut microbial alpha diversity indices, phyla variations, and genera variations at 12-24 months than 6-12 months. Multiple pollutant exposure in 0-2 lag months showed negative correlations with 12-24 months variation in Escherichia-Shigella (ß = -0.854, 95%CI: 1.398 to -0.310) and Enterococcus (ß = -0.979, 95%CI: 1.429 to -0.530). This study highlighted that time-varying PM2.5, PM10, and O3 synergistically influenced the variation of alpha diversity and abundance of gut microbial taxa in infants. Further research is needed to explore the effects and mechanisms of other environmental exposures on infant gut microbiome variation.

Ambient air pollutants exposure during gestation and incidence risk of hypertensive disorders of pregnancy or preeclampsia in China.

The relationships between the exposure to ambient air pollutants during gestation and the incidence of hypertensive disorders in pregnancy (HDPs) or preeclampsia are contradictory. This prospective cohort study enrolled the participants between January 2020 and December 2021 from the Maternal and Child Health Hospital of Hubei Province, Tongji Medical College, Huazhong University of Science and Technology. The exposure to ambient air pollutants and daily temperatures were obtained from the ChinaHighAirPollutants dataset and the Big Earth Data Platform for Three Poles, respectively. Logistic regression models were used as single- and two-pollutant models. Restricted cubic splines were applied to each ambient air pollutant exposure to further evaluate the exposure-response relationships. Quantile G-computation approaches were employed to evaluate the cumulative impact of mixed ambient air pollutants on the incidence risk HDPs and preeclampsia. Among 19,325 participants (median age: 30.2 years), 1669 (8.64%) were diagnosed with HDPs and 180 (0.94%) with preeclampsia. While mostly null risk estimates were observed, exposure to PM1, PM2.5, PM10, and NO2 correlated with a decreased incidence risk for HDPs and preeclampsia during most gestational periods. Additionally, our multi-pollutant model presented that an increase by one quartile in the cumulative effect of ambient air pollutants was associated with a significantly decreased incidence risk for HDPs in the trimester before gestation and in the third trimester during gestation, as well as for preeclampsia in the third trimester during gestation. These findings warrant further investigation into the mechanisms underlying these associations.

Short-term exposure to sulfur dioxide and the occurrence of chronic obstructive pulmonary disease: An updated systematic review and meta-analysis based on risk of bias and certainty of evidence.

Several studies have documented a relationship between short-term exposure to atmospheric sulfur dioxide (SO2) and chronic obstructive pulmonary disease (COPD). However, findings vary across different regions. This meta-analysis employed a random-effects model to calculate the combined risk estimate for each 10-µg/m3 increase in ambient SO2 concentration. Subgroup analysis aimed to identify sources of heterogeneity. To assess potential bias, studies were evaluated using a domain-based assessment tool developed by the World Health Organization. Sensitivity analyses, based on bias risk, explored how model assumptions influenced associations. An evidence certainty framework was used to evaluate overall evidence quality. The study protocol was registered with PROSPERO (CRD42023446823). We thoroughly reviewed 191 full-text articles, ultimately including 15 in the meta-analysis. The pooled relative risk for COPD was 1.26 (95 % CI 0.94-1.70) per 10-µg/m3 increase in ambient SO2. Eleven studies were deemed high risk due to inadequate handling of missing data. Overall evidence certainty was rated as medium. Given SO2's significant public health implications, continuous monitoring is crucial. Future research should include countries in Africa and Oceania to enhance global understanding of atmospheric SO2-related health issues.

Causal relationships between genetically predicted particulate air pollutants and neurodegenerative diseases: A two-sample Mendelian randomization study.

Accumulating observational studies have linked particulate air pollutants to neurodegenerative diseases (NDDs). However, the causal links and the direction of their associations remain unclear. Therefore, we adopted a two-sample Mendelian randomization (TSMR) design using the GWAS-based genetic instruments of particulate air pollutants (PM2.5 and PM10) from the UK Biobank to explore their causal influence on four common neurodegenerative diseases. Estimates of causative relationships were generated by the Inverse variance weighted (IVW) method with multiple sensitive analyses. The heterogeneity and pleiotropy tests were additionally performed to verify whether our findings were robust. Genetically predicted PM2.5 and PM10 could elevate the occurrence of AD (odds ratio [OR] = 2.22, 95 % confidence interval [CI] 1.53-3.22, PIVW = 2.85×10-5, PFalsediscovery rate[FDR]= 2.85×10-4 and OR = 2.41, 95 % CI: 1.26-4.60, PIVW = 0.008, PFDR=0.039, respectively). The results were robust in sensitive analysis. However, no evidence of causality was found for other NDDs. Our present study suggests that PM2.5 and PM10 have a detrimental effect on AD, which indicates that improving air quality to prevent AD may have pivotal public health implications.

Association of ambient air pollution and pesticide mixtures on respiratory inflammatory markers in agricultural communities.

Air pollution exposure is associated with adverse respiratory health outcomes. Evidence from occupational and community-based studies also suggests agricultural pesticides have negative health impacts on respiratory health. Although populations are exposed to multiple inhalation hazards simultaneously, multidomain mixtures (e.g. environmental and chemical pollutants of different classes) are rarely studied. We investigated the association of ambient air pollution-pesticide exposure mixtures with urinary leukotriene E4 (LTE4), a respiratory inflammation biomarker, for 75 participants in four Central California communities over two seasons. Exposures included three criteria air pollutants estimated via the Community Multiscale Air Quality model (fine particulate matter, ozone, and nitrogen dioxide) and urinary metabolites of organophosphate (OP) pesticides (total dialkyl phosphates (DAPs), total diethyl phosphates (DE), and total dimethyl phosphates (DM)). We implemented multiple linear regression models to examine associations in single pollutant models adjusted for age, sex, asthma status, occupational status, household member occupational status, temperature, and relative humidity, and evaluated whether associations changed seasonally. We then implemented Bayesian kernel machine regression (BKMR) to analyse these criteria air pollutants, DE, and DM as a mixture. Our multiple linear regression models indicated an interquartile range (IQR) increase in total DAPs was associated with an increase in urinary LTE4 in winter (ß: 0.04, 95% CI: [0.01, 0.07]). Similarly, an IQR increase in total DM was associated with an increase in urinary LTE4 in winter (ß:0.03, 95% CI: [0.004, 0.06]). Confidence intervals for all criteria air pollutant effect estimates included the null value. BKMR analysis revealed potential non-linear interactions between exposures in our air pollution-pesticide mixture, but all confidence intervals contained the null value. Our analysis demonstrated a positive association between OP pesticide metabolites and urinary LTE4 in a low asthma prevalence population and adds to the limited research on the joint effects of ambient air pollution and pesticides mixtures on respiratory health.

Cardiovascular disease mortality and air pollution in countries with different socioeconomic status.

Background: Cardiovascular diseases (CVDs) account for 17.9 million deaths annually. Behavioral risk factors increase the risk of dying from CVD. Air pollution is not included in this risk calculation since the appreciation of air pollution as a modifiable risk factor is still limited. The purpose of this study was to analyze CVD mortality attributed to air pollution in all World Health Organization WHO member states and demonstrate the association of CVD mortality with air pollution depending on countries' income level. Methods: The CVD death rate was calculated by dividing the number of deaths by the total population. The proportion of the population with primary reliance on clean fuels and technologies for cooking was calculated as an indicator of household air pollution. The annual mean concentration of fine particulate matter ≤2.5 µg/m3 and ≤10.0 µg/m3 to which the population is exposed was used as an indicator of ambient air pollution. Results: There is a gradual increase in CVD mortality attributed to air pollution from high-income countries (HICs) to low-income countries (LICs). Household air pollution is the major cause of CVD mortality in LICs. Ischemic heart disease mortality attributed to ambient air pollution in all countries is higher than stroke mortality attributed to ambient air pollution. In LIC, mortality from stroke is attributed to household air pollution of 39.27 ± 14.47, which is more than twice the stroke mortality attributed to ambient air pollution at 18.60 ± 5.64, t = 7.17, p < 0.01. Conclusion: Air pollution control should be an essential component of the CVD preventive strategy, along with lifestyle modifications and effective disease management.

Beyond lung cancer: air pollution and bladder, breast and prostate cancer incidence.

BACKGROUND: The carcinogenicity of air pollution and its impact on the risk of lung cancer is well known; however, there are still knowledge gaps and mixed results for other sites of cancer. METHODS: The current study aimed to evaluate the associations between ambient air pollution [fine particulate matter (PM2.5) and nitrogen oxides (NOx)] and cancer incidence. Exposure assessment was based on historical addresses of >900 000 participants. Cancer incidence included primary cancer cases diagnosed from 2007 to 2015 (n = 30 979). Cox regression was used to evaluate the associations between ambient air pollution and cancer incidence [hazard ratio (HR), 95% CI]. RESULTS: In the single-pollutant models, an increase of one interquartile range (IQR) (2.11 µg/m3) of PM2.5 was associated with an increased risk of all cancer sites (HR = 1.51, 95% CI: 1.47-1.54), lung cancer (HR = 1.73, 95% CI: 1.60-1.87), bladder cancer (HR = 1.50, 95% CI: 1.37-1.65), breast cancer (HR = 1.50, 95% CI: 1.42-1.58) and prostate cancer (HR = 1.41, 95% CI: 1.31-1.52). In the single-pollutant and the co-pollutant models, the estimates for PM2.5 were stronger compared with NOx for all the investigated cancer sites. CONCLUSIONS: Our findings confirm the carcinogenicity of ambient air pollution on lung cancer and provide additional evidence for bladder, breast and prostate cancers. Further studies are needed to confirm our observation regarding prostate cancer. However, the need for more research should not be a barrier to implementing policies to limit the population's exposure to air pollution.

Public Health Impacts of Ambient Particulate Matter Pollution in Libya from 1990 to 2019: An Analysis of the 2019 Global Burden of Disease (GBD) Study.

Air pollution is recognized as a critical global health risk, yet there has been no comprehensive assessment of its impact on public health in Libya until now. This study evaluates the burden of disease associated with ambient particulate matter (PM2.5) in Libya, drawing on data from the Global Burden of Disease Study 2019. By integrating satellite-based estimates, chemical transport models, and ground-level measurements, PM2.5 exposure and its effects on mortality and disability-adjusted life years (DALYs) across the different sexes and all age groups from 1990 to 2019 are estimated. Our findings reveal that the annual population-weighted mean PM2.5 concentration in Libya was 38.6 µg/m3 in 2019, marking a 3% increase since 1990. In the same year, PM2.5 was responsible for approximately 3368 deaths, accounting for 11% of all annual deaths in the country. Moreover, a total of 107,207 DALYs were attributable to PM2.5, with ischemic heart disease being the leading cause, representing 46% of these DALYs. The analysis also highlights a significant burden of years of life lost (YLLs) at 89,113 and years lived with disability (YLDs) at 18,094, due to PM2.5. Given the substantial health risks associated with air pollution, particularly from ambient particulate matter, Libyan authorities must implement effective policies aimed at reducing air pollution to enhance healthcare outcomes and preventive services.

Does Exposure to Ambient Air Pollution Affect Gestational Age and Newborn Weight?-A Systematic Review.

Current evidence suggests that airborne pollutants have a detrimental effect on fetal growth through the emergence of small for gestational age (SGA) or term low birth weight (TLBW). The study's objective was to critically evaluate the available literature on the association between environmental pollution and the incidence of SGA or TLBW occurrence. A comprehensive literature search was conducted across Pubmed/MEDLINE, Web of Science, Cochrane Library, EMBASE, and Google Scholar using predefined inclusion and exclusion criteria. The methodology adhered to the PRISMA guidelines. The systematic review protocol was registered in PROSPERO with ID number: CRD42022329624. As a result, 69 selected papers described the influence of environmental pollutants on SGA and TLBW occurrence with an Odds Ratios (ORs) of 1.138 for particulate matter ≤ 10 µm (PM10), 1.338 for particulate matter ≤ 2.5 µm (PM2.5), 1.173 for ozone (O3), 1.287 for sulfur dioxide (SO2), and 1.226 for carbon monoxide (CO). All eight studies analyzed validated that exposure to volatile organic compounds (VOCs) is a risk factor for SGA or TLBW. Pregnant women in the high-risk group of SGA occurrence, i.e., those living in urban areas or close to sources of pollution, are at an increased risk of complications. Understanding the exact exposure time of pregnant women could help improve prenatal care and timely intervention for fetuses with SGA. Nevertheless, the pervasive air pollution underscored in our findings suggests a pressing need for adaptive measures in everyday life to mitigate worldwide environmental pollution.

Airborne Nanoparticle Concentrations Are Associated with Increased Mortality Risk in Canada's Two Largest Cities.

RATIONALE: Outdoor fine particulate air pollution (PM2.5) contributes to millions of deaths around the world each year, but much less is known about the long-term health impacts of other particulate air pollutants including ultrafine particles (a.k.a. nanoparticles) which are in the nanometer size range (<100 nm), widespread in urban environments, and not currently regulated. OBJECTIVES: Estimate the associations between long-term exposure to outdoor ultrafine particles and mortality. METHODS: Outdoor air pollution levels were linked to the residential addresses of a large, population-based cohort from 2001 - 2016. Associations between long-term exposure to outdoor ultrafine particles and nonaccidental and cause-specific mortality were estimated using Cox proportional hazards models. MEASUREMENTS: An increase in long-term exposure to outdoor ultrafine particles was associated with an increased risk of nonaccidental mortality (Hazard Ratio = 1. 073, 95% Confidence Interval = 1. 061, 1. 085) and cause-specific mortality, the strongest of which was respiratory mortality (Hazard Ratio = 1.174, 95% Confidence Interval = 1.130, 1.220). MAIN RESULTS: Long-term exposure to outdoor ultrafine particles was associated with increased risk of mortality. We estimated the mortality burden for outdoor ultrafine particles in Montreal and Toronto, Canada to be approximately 1100 additional nonaccidental deaths every year. Furthermore, we observed possible confounding by particle size which suggests that previous studies may have underestimated or missed important health risks associated with ultrafine particles. CONCLUSIONS: As outdoor ultrafine particles are not currently regulated, there is great potential for future regulatory interventions to improve population health by targeting these common outdoor air pollutants.

Variability in personal exposure to ultrafine and fine particles by microenvironment among adolescents in Cincinnati.

Personal exposure to air pollution is influenced by an individual's time-activity patterns, but data regarding personal exposure to air pollution among children populations is lacking. The objective of this study was to characterize personal exposure to both PM2.5 and ultrafine particles (UFPs) using two portable real-time monitors, combined with GPS logging, and describe the relationship between these exposures across time and microenvironments among adolescents with asthma. Participants completed personal exposure monitoring for seven consecutive days and PM2.5 and UFP concentrations experienced in five microenvironments were determined using GPS location and mobility data. Average UFP and PM2.5 exposure varied across microenvironments with the highest average UFP exposure concentrations observed in transit (10,910 ± 27,297 p/cc), though correlations between UFP and PM2.5 concentrations in transit were low (0.24) and did not reach statistical significance (p > 0.05). We calculated exposure time ratios for each participant. Across participants, UFP exposures within the transit environment demonstrated the highest ratio (average exposure-time ratio = 1.91) though only 3 % of overall sampling time among all participants was monitored in transit (74/2840 h). We did not observe similar trends among PM2.5 exposures. The correlations between UFP and PM2.5 exposures varied throughout the day, with an overall correlation ranging from moderate to high among participants. Identifying microenvironments and activities where high exposure to PM occurs may offer potential targets for interventions to reduce overall exposures among sensitive groups.

Epidemiological trends and age-period-cohort effects on cardiovascular diseases burden attributable to ambient air pollution across BRICS.

Long-term exposure to ambient air pollution raises the risk of deaths and morbidity worldwide. From 1990 to 2019, we observed the epidemiological trends and age-period-cohort effects on the cardiovascular diseases (CVD) burden attributable to ambient air pollution across Brazil, Russia, India, China, and South Africa (BRICS). The number of CVD deaths related to ambient particulate matter (PM) pollution increased nearly fivefold in China [5.0% (95% CI 4.7, 5.2)] and India [5.7% (95% CI 5.1, 6.3)] during the study period. The age-standardized CVD deaths and disability-adjusted life years (DALYs) due to ambient PM pollution significantly increased in India and China but decreased in Brazil and Russia. Due to air pollution, the relative risk (RR) of premature CVD mortality (< 70 years) was higher in Russia [RR 12.6 (95% CI 8.7, 17.30)] and India [RR 9.2 (95% CI 7.6, 11.20)]. A higher period risk (2015-2019) for CVD deaths was found in India [RR 1.4 (95% CI 1.4, 1.4)] followed by South Africa [RR 1.3 (95% CI 1.3, 1.3)]. Across the BRICS countries, the RR of CVD mortality markedly decreased from the old birth cohort to young birth cohorts. In conclusion, China and India showed an increasing trend of CVD mortality and morbidity due to ambient PM pollution and higher risk of premature CVD deaths were observed in Russia and India.

Fine particulate matter air pollution and health implications for Nairobi, Kenya.

Background: Continuous ambient air quality monitoring in Kenya has been limited, resulting in a sparse data base on the health impacts of air pollution for the country. We have operated a centrally located monitor in Nairobi for measuring fine particulate matter (PM2.5), the pollutant that has demonstrated impact on health. Here, we describe the temporal levels and trends in PM2.5 data for Nairobi and evaluate associated health implications. Methods: We used a centrally located reference sensor, the beta attenuation monitor (BAM-1022), to measure hourly PM2.5 concentrations over a 3-year period (21 August 2019 to 20 August 2022). We used, at minimum, 75% of the daily hourly concentration to represent the 24-hour concentrations for a given calendar day. To estimate the deaths attributable to air pollution, we used the World Health Organization (WHO) AirQ+ tool with input as PM2.5 concentration data, local mortality statistics, and population sizes. Results: The daily (24-hour) mean (±SEM) PM2.5 concentration was 19. 2 ± 0.6 (µg/m3). Pollutant levels were lowest at 03:00 and, peaked at 20:00. Sundays had the lowest daily concentrations, which increased on Mondays and remained high through Saturdays. By season, the pollutant concentrations were lowest in April and highest in August. The mean annual concentration was 18.4 ± 7.1 (µg/m3), which was estimated to lead to between 400 and 1,400 premature deaths of the city's population in 2021 hence contributing 5%-8% of the 17,432 adult deaths excluding accidents when referenced to WHO recommended 2021 air quality guideline for annual thresholds of 5 µg/m3. Conclusion: Fine particulate matter air pollution in Nairobi showed daily, day-of-week, and seasonal fluctuations consistent with the anthropogenic source mix, particularly from motor vehicles. The long-term population exposure to PM2.5 was 3.7 times higher than the WHO annual guideline of 5 µg/m3 and estimated to lead to a substantial burden of attributable deaths. An updated regulation targeting measures to reduce vehicular emissions is recommended.