Effect modification by statin use status on the association between fine particulate matter (PM2.5) and cardiovascular mortality.

BACKGROUND: Numerous studies have linked fine particulate matter (PM2.5) to increased cardiovascular mortality. Less is known how the PM2.5-cardiovascular mortality association varies by use of cardiovascular medications. This study sought to quantify effect modification by statin use status on the associations between long-term exposure to PM2.5 and mortality from any cardiovascular cause, coronary heart disease (CHD), and stroke. METHODS: In this nested case-control study, we followed 1.2 million community-dwelling adults aged ≥66 years who lived in Ontario, Canada from 2000 through 2018. Cases were patients who died from the three causes. Each case was individually matched to up to 30 randomly selected controls using incidence density sampling. Conditional logistic regression models were used to estimate odds ratios (ORs) for the associations between PM2.5 and mortality. We evaluated the presence of effect modification considering both multiplicative (ratio of ORs) and additive scales (the relative excess risk due to interaction, RERI). RESULTS: Exposure to PM2.5 increased the risks for cardiovascular, CHD, and stroke mortality. For all three causes of death, compared with statin users, stronger PM2.5-mortality associations were observed among non-users [e.g. for cardiovascular mortality corresponding to each interquartile range increase in PM2.5, OR = 1.042 (95% CI, 1.032-1.053) vs OR = 1.009 (95% CI, 0.996-1.022) in users, ratio of ORs = 1.033 (95% CI, 1.019-1.047), RERI = 0.039 (95% CI, 0.025-0.050)]. Among users, partially adherent users exhibited a higher risk of PM2.5-associated mortality than fully adherent users. CONCLUSIONS: The associations of chronic exposure to PM2.5 with cardiovascular and CHD mortality were stronger among statin non-users compared to users.

Ambient air pollution and daily mortality in ten cities of India: a causal modelling study.

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.

The impact of air pollution on the facial skin of Caucasian women using real-life pollutant exposure measurements.

BACKGROUND: To date, studies examining the effect of air pollution on skin characteristics have relied on regional pollution estimates obtained from fixed monitoring sites. Hence, there remains a need to characterize the impact of air pollution in vivo in real-time conditions. We conducted an initial investigation under real-life conditions, with the purpose of characterizing the in vivo impact of various pollutants on the facial skin condition of women living in Paris over a 6-month period. MATERIALS AND METHODS: A smartphone application linked to the Breezometer platform was used to collect participants' individual exposures to pollutants through the recovery of global positioning system (GPS) data over a 6-month period. Daily exposure to fine particulate matter (PM 2.5 µm and PM 10 µm), pollen, and air quality was measured. Facial skin color, roughness, pore, hydration, elasticity, and wrinkle measurements were taken at the end of the 6-month period. Participants' cumulated pollutant exposure over 6 months was calculated. Data were stratified into two groups (lower vs. higher pollutant exposure) for each pollutant. RESULTS: 156 women (20-60 years-old) were recruited, with 124 women completing the study. Higher PM 2.5 µm exposure was associated with altered skin color and increased roughness under the eye. Higher PM 10 µm exposure with increased wrinkles and roughness under the eye, increased pore appearance, and decreased skin hydration. Exposure to poorer air quality was linked with increased forehead wrinkles and decreased skin elasticity, while higher pollen exposure increased skin roughness and crow's feet. CONCLUSION: This study suggests a potential correlation between air pollution and facial skin in real-life conditions. Prolonged exposure to PM, gases, and pollen may be linked to clinical signs of skin ageing. This study highlights the importance of longer monitoring over time in real conditions to characterize the effect of pollution on the skin.

Air pollution disproportionately impairs beneficial invertebrates: a meta-analysis.

Air pollution has the potential to disrupt ecologically- and economically-beneficial services provided by invertebrates, including pollination and natural pest regulation. To effectively predict and mitigate this disruption requires an understanding of how the impacts of air pollution vary between invertebrate groups. Here we conduct a global meta-analysis of 120 publications comparing the performance of different invertebrate functional groups in unpolluted and polluted atmospheres. We focus on the pollutants ozone, nitrogen oxides, sulfur dioxide and particulate matter. We show that beneficial invertebrate performance is reduced by air pollution, whereas the performance of plant pest invertebrates is not significantly affected. Ozone pollution has the most detrimental impacts, and these occur at concentrations below national and international air quality standards. Changes in invertebrate performance are not dependent on air pollutant concentrations, indicating that even low levels of pollution are damaging. Predicted increases in tropospheric ozone could result in unintended consequences to global invertebrate populations and their valuable ecological services.

Exposure to Air Pollution, Genetic Susceptibility, and Psoriasis Risk in the UK.

Importance: Psoriasis is a common autoinflammatory disease influenced by complex interactions between environmental and genetic factors. The influence of long-term air pollution exposure on psoriasis remains underexplored. Objective: To examine the association between long-term exposure to air pollution and psoriasis and the interaction between air pollution and genetic susceptibility for incident psoriasis. Design, Setting, and Participants: This prospective cohort study used data from the UK Biobank. The analysis sample included individuals who were psoriasis free at baseline and had available data on air pollution exposure. Genetic analyses were restricted to White participants. Data were analyzed between November 1 and December 10, 2023. Exposures: Exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter with a diameter less than 2.5 µm (PM2.5), and particulate matter with a diameter less than 10 µm (PM10) and genetic susceptibility for psoriasis. Main Outcomes and Measures: To ascertain the association of long-term exposure to NO2, NOx, PM2.5, and PM10 with the risk of psoriasis, a Cox proportional hazards model with time-varying air pollution exposure was used. Cox models were also used to explore the potential interplay between air pollutant exposure and genetic susceptibility for the risk of psoriasis incidence. Results: A total of 474 055 individuals were included, with a mean (SD) age of 56.54 (8.09) years and 257 686 (54.36%) female participants. There were 9186 participants (1.94%) identified as Asian or Asian British, 7542 (1.59%) as Black or Black British, and 446 637 (94.22%) as White European. During a median (IQR) follow-up of 11.91 (11.21-12.59) years, 4031 incident psoriasis events were recorded. There was a positive association between the risk of psoriasis and air pollutant exposure. For every IQR increase in PM2.5, PM10, NO2, and NOx, the hazard ratios (HRs) were 1.41 (95% CI, 1.35-1.46), 1.47 (95% CI, 1.41-1.52), 1.28 (95% CI, 1.23-1.33), and 1.19 (95% CI, 1.14-1.24), respectively. When comparing individuals in the lowest exposure quartile (Q1) with those in the highest exposure quartile (Q4), the multivariate-adjusted HRs were 2.01 (95% CI, 1.83-2.20) for PM2.5, 2.21 (95% CI, 2.02-2.43) for PM10, 1.64 (95% CI, 1.49-1.80) for NO2, and 1.34 (95% CI, 1.22-1.47) for NOx. Moreover, significant interactions between air pollution and genetic predisposition for incident psoriasis were observed. In the subset of 446 637 White individuals, the findings indicated a substantial risk of psoriasis development in participants exposed to the highest quartile of air pollution levels concomitant with high genetic risk compared with those in the lowest quartile of air pollution levels with low genetic risk (PM2.5: HR, 4.11; 95% CI, 3.46-4.90; PM10: HR, 4.29; 95% CI, 3.61-5.08; NO2: HR, 2.95; 95% CI, 2.49-3.50; NOx: HR, 2.44; 95% CI, 2.08-2.87). Conclusions and Relevance: In this prospective cohort study of the association between air pollution and psoriasis, long-term exposure to air pollution was associated with increased psoriasis risk. There was an interaction between air pollution and genetic susceptibility on psoriasis risk.

Prenatal exposure to PM2.5 and childhood body mass index growth trajectories from birth to 6 years old.

This study aimed to determine the relationships between prenatal PM2.5 exposure and childhood growth trajectories during the first 6 years of life. A total of 47,625 pairs of mothers and children were recruited from a prospective birth cohort conducted between 2011 and 2013 in Wuhan, China, and followed for 6 years. We used the group-based trajectory models to classify the population into three trajectory groups: slow growth (n = 13,671, 28.7%), normal growth (n = 29,736, 62.4%), and rapid growth (n = 4218, 8.9%). Multinomial logistic regression models were used to determine the associations of prenatal PM2.5 exposure and childhood growth trajectories. Compared to normal growth trajectory, increased PM2.5 exposure in trimester 1, trimester 2 and the entire pregnancy showed significant associations with an increased risk of the slow growth trajectory but reduced the risk for the rapid growth trajectory, significant association of prenatal PM2.5 exposure with rapid growth trajectory was only observed in the trimester 3. Stratified analyses displayed relatively stronger associations among those mothers with maternal age over 35 years, pre-pregnancy BMI ≥ 25 kg/m2, and previous delivery experience. Prenatal exposure to PM2.5, particularly during the midpoint period of pregnancy, was more likely to have a slow growth trajectory and a lower risk of rapid growth trajectory. Maternal age, pre-pregnancy BMI, and previous delivery experience might modify these associations.

Effects of particulate matter (PM2.5) concentration and components on mortality in chronic kidney disease patients: a nationwide spatial-temporal analysis.

Chronic kidney disease (CKD) is a major global public health issue and the leading cause of death in Thailand. This study investigated the spatial-temporal association between PM2.5 and its components (organic carbon, black carbon, dust, sulfate, and sea salt) and CKD mortality in Thailand from 2012 to 2021. The Modern-Era Retrospective analysis for Research and Application version 2 (MERRA-2), a NASA atmospheric satellite model, was assessed for the temporal data of PM2.5 concentration and aerosol components. Spatial resources of 77 provinces were integrated using the Geographical Information System (GIS). Multivariate Poisson regression and Bayesian inference analyses were conducted to explore the effects of PM2.5 on CKD mortality across the provinces. Our analysis included 718,686 CKD-related deaths, resulting in a mortality rate of 1107 cases per 100,000 population where was the highest rate in Northeast region. The average age of the deceased was 72.43 ± 13.10 years, with males comprising 50.46% of the cases. Adjusting for age, sex, underlying diseases, co-morbidities, CKD complications, replacement therapy, population density, and income, each 1 µg/m3 increase in PM2.5, black carbon, dust, sulfate, and organic carbon was significantly associated with increased CKD mortality across 77 provinces. Incidence rate ratios were 1.04 (95% CI 1.03-1.04) for PM2.5, 1.11 (95% CI 1.10-1.13) for black carbon, 1.24 (95% CI 1.22-1.25) for dust, 1.16 (95% CI 1.16-1.17) for sulfate, and 1.05 (95% CI 1.04-1.05) for organic carbon. These findings emphasize the significant impact of PM2.5 on CKD mortality and underscore the need for strategies to reduce PM emissions and manage CKD co-morbidities effectively.

Moderating effect of a sodium-rich diet on the association between long-term exposure to fine particulate matter and blood lipids in children and adolescents.

BACKGROUND: Several studies reported that exposure to higher levels of fine particulate matter (PM2.5) was associated with deteriorated lipid profiles in children and adolescents. However, whether a sodium-rich diet could modify the associations remains unknown. We aimed to examine the associations of long-term exposure to PM2.5 with blood lipids in children and adolescents, and further examine the effect modification by dietary and urinary sodium levels based on a multi-community population in China. METHODS: The 3711 study participants were from a cross-sectional study, which interviewed children and adolescents aged 6 to 17 years across Sichuan Province, China between 2015 and 2017. Blood lipid outcomes including blood total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) were assessed. Information on daily dietary sodium consumption was estimated with a semi-quantitative food frequency questionnaire (FFQ), and urinary sodium was used as an internal exposure biomarker. A linear regression model was applied to estimate the associations of prior 2-years' average exposure to ambient PM2.5 with blood lipids. The effect modification by dietary and urinary sodium was examined by stratified analyses. RESULTS: The participants from rural areas had higher levels of daily sodium consumptions. The results of multivariable regression analysis indicated that per 10 µg/m3 incremental change in PM2.5 was associated with a 1.56% (95% confidence interval 0.90%-2.23%) and a 2.26% (1.15%-3.38%) higher blood TC and LDL-C levels, respectively. Among the study participants with higher levels of dietary sodium or urinary sodium, exposure to higher levels of PM2.5 was significantly associated with deteriorated lipid profiles. For example, each 10 µg/m3 incremental change in exposure to PM2.5 was correlated with a 2.83 (-4.65 to -0.97) lower percentage decrease in blood HDL-C levels among the participants who were from the highest quartile of urinary sodium levels. While, these associations changed to be nonsignificant in the participants who were from the lowest quartile of dietary sodium levels. CONCLUSION: Exposure to higher levels of PM2.5 was associated with deteriorated blood lipid levels in children and adolescents. It is noteworthy that these associations might be ameliorated through the adoption of a low-sodium dietary regimen.

From Inhalation to Neurodegeneration: Air Pollution as a Modifiable Risk Factor for Alzheimer's Disease.

Air pollution, a growing concern for public health, has been linked to various respiratory and cardiovascular diseases. Emerging evidence also suggests a link between exposure to air pollutants and neurodegenerative diseases, particularly Alzheimer's disease (AD). This review explores the composition and sources of air pollutants, including particulate matter, gases, persistent organic pollutants, and heavy metals. The pathophysiology of AD is briefly discussed, highlighting the role of beta-amyloid plaques, neurofibrillary tangles, and genetic factors. This article also examines how air pollutants reach the brain and exert their detrimental effects, delving into the neurotoxicity of air pollutants. The molecular mechanisms linking air pollution to neurodegeneration are explored in detail, focusing on oxidative stress, neuroinflammation, and protein aggregation. Preclinical studies, including in vitro experiments and animal models, provide evidence for the direct effects of pollutants on neuronal cells, glial cells, and the blood-brain barrier. Epidemiological studies have reported associations between exposure to air pollution and an increased risk of AD and cognitive decline. The growing body of evidence supporting air pollution as a modifiable risk factor for AD underscores the importance of considering environmental factors in the etiology and progression of neurodegenerative diseases, in the face of worsening global air quality.

Age and sex differences in the effects of short- and long-term exposure to air pollution on endothelial dysfunction.

BACKGROUND: The effects of air pollution on endothelial function remain unclear across populations. We aimed to use brachial artery flow-mediated dilatation (FMD) to identify demographic differences in the effects of air pollution exposure on endothelial dysfunction. METHODS: We measured FMD in 850 participants from October 2016 to January 2020. Location-specific concentrations of fine particulate matter < 2.5 µm aerodynamic diameter (PM2.5), inhalable particulate matter < 10 µm aerodynamic diameter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3) measured by fixed ambient air monitoring stations were collected for short- and long-term exposure assessment. Multiple linear regression models and restricted cubic splines were used to assess the associations before and after stratification by age and sex. RESULTS: This study eventually included 828 participants [551 (66.5%) younger than 65 years and 553 (66.8%) men]. Each 10 µg/m3 increase in 7-day exposure to PM2.5 and PM10 was significantly linearly associated with a 0.07% (ß = -0.07, 95% CI: -0.13 to -0.004) and 0.05% (ß = -0.05, 95% CI: -0.10 to -0.004) decrease in FMD in the fully adjusted model. After full adjustment, long-term exposure to all air pollutants was significantly associated with impaired FMD. Each 10 µg/m3 increase in long-term exposure to PM2.5 and PM10 was significantly associated with a -0.18% (95% CI: -0.34 to -0.03) and - 0.23% (95% CI: -0.40 to -0.06) change in FMD, respectively. After stratification, the associations of lower FMD with long-term exposure to PM2.5, PM10, SO2, NO2, and CO significantly persisted in men and participants younger than 65 years instead of women or older participants. For short-term exposure, we observed differences consistent with long-term exposure and a stronger effect of 7-day exposure to SO2 in men due to a significant interaction effect. CONCLUSION: Short- and long-term exposure to different air pollutants are strongly associated with decreased endothelial function, and susceptibility to air pollution varies significantly with age and sex.

Prenatal Exposure to Ambient Air Pollution and Cerebral Palsy.

Importance: Air pollution is associated with structural brain changes, disruption of neurogenesis, and neurodevelopmental disorders. The association between prenatal exposure to ambient air pollution and risk of cerebral palsy (CP), which is the most common motor disability in childhood, has not been thoroughly investigated. Objective: To evaluate the associations between prenatal residential exposure to ambient air pollution and risk of CP among children born at term gestation in a population cohort in Ontario, Canada. Design, Setting, and Participants: Population-based cohort study in Ontario, Canada using linked, province-wide health administrative databases. Participants were singleton full term births (≥37 gestational weeks) born in Ontario hospitals between April 1, 2002, and March 31, 2017. Data were analyzed from January to December 2022. Exposures: Weekly average concentrations of ambient fine particulate matter with a diameter 2.5 µm (PM2.5) or smaller, nitrogen dioxide (NO2), and ozone (O3) during pregnancy assigned by maternal residence reported at delivery from satellite-based estimates and ground-level monitoring data. Main outcome and measures: CP cases were ascertained by a single inpatient hospitalization diagnosis or at least 2 outpatient diagnoses for children from birth to age 18 years. Results: The present study included 1 587 935 mother-child pairs who reached term gestation, among whom 3170 (0.2%) children were diagnosed with CP. The study population had a mean (SD) maternal age of 30.1 (5.6) years and 811 745 infants (51.1%) were male. A per IQR increase (2.7 µg/m3) in prenatal ambient PM2.5 concentration was associated with a cumulative hazard ratio (CHR) of 1.12 (95% CI, 1.03-1.21) for CP. The CHR in male infants (1.14; 95% CI, 1.02-1.26) was higher compared with the CHR in female infants (1.08; 95% CI, 0.96-1.22). No specific window of susceptibility was found for prenatal PM2.5 exposure and CP in the study population. No associations or windows of susceptibility were found for prenatal NO2 or O3 exposure and CP risk. Conclusions and relevance: In this large cohort study of singleton full term births in Canada, prenatal ambient PM2.5 exposure was associated with an increased risk of CP in offspring. Further studies are needed to explore this association and its potential biological pathways, which could advance the identification of environmental risk factors of CP in early life.

Exposure to source-specific air pollution in residential areas and its association with dementia incidence: a cohort study in Northern Sweden.

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population's average exposure to annual mean total PM10 and PM2.5 lag 1-5 years was 9.50 µg/m3 and 5.61 µg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0-82%]) and PM2.5-Exhaust (33% [95% CI - 2 to 79%]) in the second exposure tertile for lag 1-5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure-response relationships were evident.

An investigation of inequalities in exposure to PM2.5 air pollution across small areas in Ireland.

The link between exposure to air pollution and adverse effects on human health is well documented. Yet, in a European context, research on the spatial distribution of air pollution and the characteristics of areas is relatively scarce, and there is a need for research using different spatial scales, a wider variety of socioeconomic indicators (such as ethnicity) and new methodologies to assess these relationships. This study uses comprehensive data on a wide range of demographic and socioeconomic indicators, matched to data on PM2.5 concentrations for small areas in Ireland, to assess the relationship between social vulnerability and PM2.5 air pollution. Examining a wide range of socioeconomic indicators revealed some differentials in PM2.5 concentration levels by measure and by rural and urban classification. However, statistical modelling using concentration curves and concentration indices did not present substantial evidence of inequalities in PM2.5 concentrations across small areas. In common with other western European countries, an overall decline in the levels of PM2.5 between 2011 and 2016 was observed in Ireland, though the data indicates that almost all small areas in Ireland were found to have exceeded the World Health Organization (WHO)'s PM2.5 annual guideline (of 5 µg/m3), calling for greater policy efforts to reduce air pollution in Ireland. The recent Clean Air Strategy contains a commitment to achieve the WHO guideline limits for PM2.5 by 2040, with interim targets at various points over the next two decades. Achieving these targets will require policy measures to decarbonise home heating, promote active travel and the transition to electric vehicles, and further regulations on burning fossil fuels and enforcing environmental regulations more tightly. From a research and information-gathering perspective, installing more monitoring stations at key points could improve the quality and spatial dimension of the data collected and facilitate the assessment of the implementation of the measures in the Clean Air Strategy.

Causal relationship and shared genes between air pollutants and amyotrophic lateral sclerosis: A large-scale genetic analysis.

OBJECTIVE: Air pollutants have been reported to have a potential relationship with amyotrophic lateral sclerosis (ALS). The causality and underlying mechanism remained unknown despite several existing observational studies. We aimed to investigate the potential causality between air pollutants (PM2.5, NOX, and NO2) and the risk of ALS and elucidate the underlying mechanisms associated with this relationship. METHODS: The data utilized in our study were obtained from publicly available genome-wide association study data sets, in which single nucleotide polymorphisms (SNPs) were employed as the instrumental variantswith three principles. Two-sample Mendelian randomization and transcriptome-wide association (TWAS) analyses were conducted to evaluate the effects of air pollutants on ALS and identify genes associated with both pollutants and ALS, followed by regulatory network prediction. RESULTS: We observed that exposure to a high level of PM2.5 (OR: 2.40 [95% CI: 1.26-4.57], p = 7.46E-3) and NOx (OR: 2.35 [95% CI: 1.32-4.17], p = 3.65E-3) genetically increased the incidence of ALS in MR analysis, while the effects of NO2 showed a similar trend but without sufficient significance. In the TWAS analysis, TMEM175 and USP35 turned out to be the genes shared between PM2.5 and ALS in the same direction. CONCLUSION: Higher exposure to PM2.5 and NOX might causally increase the risk of ALS. Avoiding exposure to air pollutants and air cleaning might be necessary for ALS prevention.

Assessing long-term effects of gaseous air pollution exposure on mortality in the United States using a variant of difference-in-differences analysis.

Long-term mortality effects of particulate air pollution have been investigated in a causal analytic frame, while causal evidence for associations with gaseous air pollutants remains extensively lacking, especially for carbon monoxide (CO) and sulfur dioxide (SO2). In this study, we estimated the causal relationship of long-term exposure to nitrogen dioxide (NO2), CO, SO2, and ozone (O3) with mortality. Utilizing the data from National Morbidity, Mortality, and Air Pollution Study, we applied a variant of difference-in-differences (DID) method with conditional Poisson regression and generalized weighted quantile sum regression (gWQS) to investigate the independent and joint effects. Independent exposures to NO2, CO, and SO2 were causally associated with increased risks of total, nonaccidental, and cardiovascular mortality, while no evident associations with O3 were identified in the entire population. In gWQS analyses, an interquartile range-equivalent increase in mixture exposure was associated with a relative risk of 1.067 (95% confidence interval: 1.010-1.126) for total mortality, 1.067 (1.009-1.128) for nonaccidental mortality, and 1.125 (1.060-1.193) for cardiovascular mortality, where NO2 was identified as the most significant contributor to the overall effect. This nationwide DID analysis provided causal evidence for independent and combined effects of NO2, CO, SO2, and O3 on increased mortality risks among the US general population.

[Research progress on the association between prenatal exposure to air pollutants and hypospadias in the offspring].

Recent epidemiological studies have increasingly found that pregnant women who are exposed to air pollutants (for example airborne particulate matter, nitrogen oxides, ozone, and sulfur dioxide) increase the risk of various birth defects in their offspring, such as congenital heart disease, neural tube defects, cleft lip and palate, and hypospadias. Hypospadias not only impairs the sexual function of infants but also causes major social and psychological problems during their growth period, therefore, the prevention and treatment of hypospadias infant carry substantial public health importance. However, the association between prenatal exposure to air pollution and hypospadias remains controversial. The study reviews the epidemiological research progress and potential biological mechanisms of prenatal maternal exposure to air pollutants such as particulate matter, nitrogen oxides, ozone, sulfur dioxide, and the risk of hypospadias in offspring. The study also summarizes the limitations of previous research and looks forward to future research directions, to provide scientific evidence for creating a healthy living environment for pregnant women, and reducing the risk of hypospadias in offspring.

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.

Exposure to ambient fine particulate matter components during pregnancy and early childhood and its association with asthma, allergies, and sensitization in school-age children.

BACKGROUND: Exposure to fine particulate matter (PM2.5) has been associated with allergic diseases, including asthma. However, information about the effects of specific PM2.5 components is limited. This study aimed to investigate the relationship of exposure to chemical components of PM2.5 during pregnancy and early childhood with the development of asthma, allergies, and sensitization in school-age children. METHODS: This study included 2,408 children in the second grade of elementary school. Questionnaire surveys of respiratory/allergic symptoms and measurements of serum total IgE and specific IgE levels to house dust mite (HDM) and animal proteins were conducted. Exposures to ambient PM2.5 mass, sulfate (SO42-), nitrate (NO3-), ammonium (NH4+), elemental carbon (EC), and organic carbon (OC) of PM2.5 in participants' residences from conception to age six were estimated using predictive models. Multiple logistic regression analysis was used to analyze the association of respiratory/allergic symptoms and allergen sensitization with estimated exposure concentrations, after adjustment for survey year, sex, season of birth, feeding method during infancy, presence of siblings, history of lower respiratory tract infection, use of childcare facilities, passive smoking, presence of pets, mother's age, history of allergic diseases, smoking during pregnancy, and annual household income. RESULTS: No significant association was found between PM2.5 and its component concentrations and asthma. However, wheezing significantly increased with mean NO3- concentrations during pregnancy (odds ratio of 1.64 [95% confidence interval: 1.10, 2.47] for an interquartile range increase). Significant associations were also found between EC in the second trimester of pregnancy and PM2.5, NO3-, EC, and OC concentrations in early childhood. Higher PM2.5, SO4-, and NH4+ concentrations during the second trimester increased the risk of rhinitis. Sensitizations to HDM and animal proteins were significantly associated with exposure to components such as SO42- and NH4+ during pregnancy but not with postnatal exposure. CONCLUSIONS: Exposures to NO3-, EC, and OC during pregnancy and early childhood were associated with wheezing. SO42- and NH4+ exposures during pregnancy were associated with sensitization to HDM and animal proteins. Asthma was not associated with exposure to PM2.5 and its main components at any period.