Long-term Air Pollution Exposure Research Articles

Associations between long-term air pollution exposure and the incidence of cardiovascular diseases among American older adults

Background & aimNumerous studies have linked air pollution with cardiovascular diseases. Fewer studies examined the associations at low concentration levels or assessed potential modifiers. Some investigations only examined hospitalizations, which can miss incident cases. This study aims to address these gaps through a nationwide cohort study of Medicare enrollees. MethodsOur study cohort comprise all Medicare enrollees (≥65 years old) continuously enrolled in the fee-for-service program and both Medicare part A and B across the contiguous U.S. from 2000 to 2016. We examined the associations of population-weighted ZIP code-level annual average PM2.5, NO2, and warm-season O3 (May-October), with the first diagnoses of atrial fibrillation (AF), congestive heart failure (CHF), and stroke. We fit multi-pollutant Cox proportional hazards models adjusted for individual demographic characteristics and area-level covariates. We further examined these associations at low pollutant concentration levels and the potential effect modifications by race/ethnicity and comorbidities (diabetes, hypertension, hyperlipidemia). ResultsElevated PM2.5 and NO2 levels were associated with increased incidence of AF, CHF, and stroke. For each 1 μg/m3 increase in annual PM2.5, hazard ratios (HRs) were 1.0059 (95%CI: 1.0054-1.0064), 1.0260 (95%CI: 1.0256-1.0264), and 1.0279 (95%CI: 1.0274-1.0284), respectively. For each1 ppb increase in annual NO2, HRs are 1.0057 (95%CI: 1.0056-1.0059), 1.0112 (95%CI: 1.0110-1.0113), and 1.0095 (95%CI: 1.0093-1.0096), respectively. For warm-season O3, each 1 ppb increase was associated with increased incidence of CHF (HR=1.0035, 95%CI: 1.0033–1.0037) and stroke (HR=1.0026, 95%CI: 1.0023–1.0028). Larger magnitudes of HRs were observed when restricted to pollutants levels lower than NAAQS standards. Generally higher risks were observed for Black people and diabetics. ConclusionsLong-term exposure to PM2.5, NO2, and warm-season O3 were associated with increased incidence of cardiovascular diseases, even at low pollutant concentration levels. Black people and people with diabetes were found to be vulnerable populations.

Long-term exposure to particulate matter was associated with increased dementia risk using both traditional approaches and novel machine learning methods

Air pollution exposure has been linked to various diseases, including dementia. However, a novel method for investigating the associations between air pollution exposure and disease is lacking. The objective of this study was to investigate whether long-term exposure to ambient particulate air pollution increases dementia risk using both the traditional Cox model approach and a novel machine learning (ML) with random forest (RF) method. We used health data from a national population-based cohort in Taiwan from 2000 to 2017. We collected the following ambient air pollution data from the Taiwan Environmental Protection Administration (EPA): fine particulate matter (PM2.5) and gaseous pollutants, including sulfur dioxide (SO2), carbon monoxide (CO), ozone (O3), nitrogen oxide (NOx), nitric oxide (NO), and nitrogen dioxide (NO2). Spatiotemporal-estimated air quality data calculated based on a geostatistical approach, namely, the Bayesian maximum entropy method, were collected. Each subject's residential county and township were reviewed monthly and linked to air quality data based on the corresponding township and month of the year for each subject. The Cox model approach and the ML with RF method were used. Increasing the concentration of PM2.5 by one interquartile range (IQR) increased the risk of dementia by approximately 5% (HR = 1.05 with 95% CI = 1.04–1.05). The comparison of the performance of the extended Cox model approach with the RF method showed that the prediction accuracy was approximately 0.7 by the RF method, but the AUC was lower than that of the Cox model approach. This national cohort study over an 18-year period provides supporting evidence that long-term particulate air pollution exposure is associated with increased dementia risk in Taiwan. The ML with RF method appears to be an acceptable approach for exploring associations between air pollutant exposure and disease.

Breast Cancer Incidence in Relation to Long-Term Low-Level Exposure to Air Pollution in the ELAPSE Pooled Cohort.

Established risk factors for breast cancer include genetic disposition, reproductive factors, hormone therapy, and lifestyle-related factors such as alcohol consumption, physical inactivity, smoking, and obesity. More recently a role of environmental exposures, including air pollution, has also been suggested. The aim of this study, was to investigate the relationship between long-term air pollution exposure and breast cancer incidence. We conducted a pooled analysis among six European cohorts (n = 199,719) on the association between long-term residential levels of ambient nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone in the warm season (O3) and breast cancer incidence in women. The selected cohorts represented the lower range of air pollutant concentrations in Europe. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 3,592,885 person-years of follow-up, we observed a total of 9,659 incident breast cancer cases. The results of the fully adjusted linear analyses showed a HR (95% confidence interval) of 1.03 (1.00-1.06) per 10 μg/m³ NO2, 1.06 (1.01-1.11) per 5 μg/m³ PM2.5, 1.03 (0.99-1.06) per 0.5 10-5 m-1 BC, and 0.98 (0.94-1.01) per 10 μg/m³ O3. The effect estimates were most pronounced in the group of middle-aged women (50-54 years) and among never smokers. The results were in support of an association between especially PM2.5 and breast cancer. The findings of this study suggest a role of exposure to NO2, PM2.5, and BC in development of breast cancer.

Association of long-term air pollution exposure with the risk of prediabetes and diabetes: Systematic perspective from inflammatory mechanisms, glucose homeostasis pathway to preventive strategies

BackgroundLimited evidence suggests the association of air pollutants with a series of diabetic cascades including inflammatory pathways, glucose homeostasis disorder, and prediabetes and diabetes. Subclinical strategies for preventing such pollutants-induced effects remain unknown. MethodsWe conducted a cross-sectional study in two typically air-polluted Chinese cities in 2018–2020. One-year average PM1, PM2.5, PM10, SO2, NO2, and O3 were calculated according to participants' residence. GAM multinomial logistic regression was performed to investigate the association of air pollutants with diabetes status. GAM and quantile g-computation were respectively performed to investigate individual and joint effects of air pollutants on glucose homeostasis markers (glucose, insulin, HbA1c, HOMA-IR, HOMA-B and HOMA-S). Complement C3 and hsCRP were analyzed as potential mediators. The ABCS criteria and hemoglobin glycation index (HGI) were examined for their potential in preventive strategy. ResultsLong-term air pollutants exposure was associated with the risk of prediabetes [Prevalence ratio for O3 (PR_O3) = 1.96 (95% CI: 1.24, 3.03)] and diabetes [PR_PM1 = 1.18 (95% CI: 1.05, 1.32); PR_PM2.5 = 1.08 (95% CI: 1.00, 1.16); PR_O3 = 1.35 (95% CI: 1.03, 1.74)]. PM1, PM10, SO2 or O3 exposure was associated with glucose-homeostasis disorder. For example, O3 exposure was associated with increased levels of glucose [7.67% (95% CI: 1.75, 13.92)], insulin [19.98% (95% CI: 4.53, 37.72)], HOMA-IR [34.88% (95% CI: 13.81, 59.84)], and decreased levels of HOMA-S [-25.88% (95% CI: −37.46, −12.16)]. Complement C3 and hsCRP played mediating roles in these relationships with proportion mediated ranging from 6.95% to 60.64%. Participants with HGI ≤ −0.53 were protected from the adverse effects of air pollutants. ConclusionOur study provides comprehensive insights into air pollutant–associated diabetic cascade and suggests subclinical preventive strategies.

Long-term air pollution exposure and COVID-19 case-severity: An analysis of individual-level data from Switzerland

Several studies are pointing out that exposure to elevated air pollutants could contribute to increased COVID-19 mortality. However, literature on the associations between air pollution exposure and COVID-19 severe morbidity is rather sparse. In addition, the majority of the studies used an ecological study design and were applied in regions with rather high air pollution levels. Here, we study the differential effects of long-term exposure to air pollution on severe morbidity and mortality risks from COVID-19 in various population subgroups in Switzerland, a country known for clean air. We perform individual-level analyses using data covering the first two major waves of COVID-19 between February 2020 and May 2021. High-resolution maps of particulate matter (PM2.5) and nitrogen dioxide (NO2) concentrations were produced for the 6 years preceding the pandemic using Bayesian geostatistical models. Air pollution exposure for each patient was measured by the long-term average concentration across the municipality of residence. The models were adjusted for the effects of individual characteristics, socio-economic, health-system, and climatic factors. The variables with an important association to COVID-19 case-severity were identified using Bayesian spatial variable selection. The results have shown that the individual-level characteristics are important factors related to COVID-19 morbidity and mortality in all the models. Long-term exposure to air pollution appears to influence the severity of the disease only when analyzing data during the first wave; this effect is attenuated upon adjustment for health-system related factors during the entire study period. Our findings suggest that the burden of air pollution increased the risks of COVID-19 in Switzerland during the first wave of the pandemic, but not during the second wave, when the national health system was better prepared.

Estimating ambient air pollution mortality and disease burden and its economic cost in Barcelona

BackgroundThe new WHO air quality guidelines indicate that the air pollution disease burden is greater than previously reported. We aimed to estimate the air pollution disease burden and its economic cost in Barcelona to inform local action. MethodsWe used a quantitative health impact assessment to estimate the non-accidental mortality and incidence of childhood asthma and lung cancer attributable to long-term air pollution exposure in the city of Barcelona (Spain) in 2018–2019. We used the population weighted mean of PM2.5 and NO2 assigned at the geocoded address during the study period and the 2021 WHO air quality guidelines as counterfactual scenario to estimate new annual cases attributable to each pollutant separately and combined. We estimated the social cost of attributable deaths and the health care cost of childhood asthma and lung cancer attributable cases. We also estimated attributable mortality by city district and the mortality avoidable by achieving the WHO air quality interim targets. ResultsMean exposure was 17 μg/m3 for PM2.5 and 39 μg/m3 for NO2. Total combined air pollution attributable mortality was 13% (95%CI = 9%–17%), corresponding to 1,886 deaths (95%CI = 1,296–2,571) and a social cost of €1,292 million (95%CI = 888–1,762) annually. Fifty-one percent (95%CI = 21%–71%) and 17% (95%CI = 7%–29%) of new cases of childhood asthma and lung cancer were attributable to air pollution with a health care cost of €4.3 and €2.7 million, respectively. Achieving the first unmet WHO air quality interim targets for PM2.5 and for NO2 would avoid 410 deaths and €281 million annually. ConclusionAir pollution in Barcelona represents a huge disease and economic burden, which is greater than previous estimates. Much stronger measures to reduce PM2.5 and NO2 levels are urgently needed. Until the WHO air quality guidelines are met in the city, achieving each WHO air quality interim targets would avoid hundreds of deaths each year.

Long-term ambient air pollution exposure and DNA methylation of peripheral brain-derived neurotrophic factor promoter.

This study aimed to investigate the association between air pollutants and methylation of peripheral brain-derived neurotrophic factor (BDNF) promoters. A total of 101 individuals were recruited in this panel study. BDNF promoter methylation was detected by bisulfite-PCR amplification and pyrosequencing. Participants' exposure to air pollutants was estimated using a satellite-based random forests approach. A generalized estimated equation model with natural cubic splines was employed to examine the associations between air pollutants and BDNF promoter methylation levels. The associations between air pollution and BDNF promoter methylation showed nonlinear curves with threshold effects. The threshold concentration for the association of nitrogen dioxide (NO2) with average methylation level was 59.7μg/m3, and that for the association of particulate matter ≤1µm in diameter (PM1) with CpG2 methylation level was 70.9μg/m3. The percent change of average methylation level at the 95th percentile of NO2 against the threshold concentration was 43.25% (95%CI: 13.10%, 73.40%), and that of CpG2 methylation at the 95th percentile of PM1 was 128.29% (95%CI: 43.27%, 213.31%). Overall, long-term exposures of PM1, PM2.5, PM10, and NO2 were associated with significant changes in BDNF promoter methylation levels with threshold effects.

Residential greenness attenuated association of long-term air pollution exposure with elevated blood pressure: Findings from polluted areas in Northern China.

BackgroundEvidence on the hypertensive effects of long-term air pollutants exposure are mixed, and the joint hypertensive effects of air pollutants are also unclear. Sparse evidence exists regarding the modifying role of residential greenness in such effects.MethodsA cross-sectional study was conducted in typically air-polluted areas in northern China. Particulate matter with diameter < 1 μm (PM1), particulate matter with diameter < 2.5 μm (PM2.5), particulate matter with diameter < 10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), and ozone (O3) were predicted by space–time extremely randomized trees model. We used the Normalized Difference Vegetation Index (NDVI) to reflect residential green space. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were examined. We also calculated the pulse pressure (PP) and mean arterial pressure (MAP). Generalized additive model and quantile g-computation were, respectively, conducted to investigate individual and joint effects of air pollutants on blood pressure. Furthermore, beneficial effect of NDVI and its modification effect were explored.ResultsLong-term air pollutants exposure was associated with elevated DBP and MAP. Specifically, we found a 10-μg/m3 increase in PM2.5, PM10, and SO2 were associated with 2.36% (95% CI: 0.97, 3.76), 1.51% (95% CI: 0.70, 2.34), and 3.54% (95% CI: 1.55, 5.56) increase in DBP; a 10-μg/m3 increase in PM2.5, PM10, and SO2 were associated with 1.84% (95% CI: 0.74, 2.96), 1.17% (95% CI: 0.52, 1.83), and 2.43% (95% CI: 0.71, 4.18) increase in MAP. Air pollutants mixture (one quantile increase) was positively associated with increased values of DBP (8.22%, 95% CI: 5.49, 11.02) and MAP (4.15%, 95% CI: 2.05, 6.30), respectively. These identified harmful effect of air pollutants mainly occurred among these lived with low NDVI values. And participants aged ≥50 years were more susceptible to the harmful effect of PM2.5 and PM10 compared to younger adults.ConclusionsOur study indicated the harmful effect of long-term exposure to air pollutants and these effects may be modified by living within higher green space place. These evidence suggest increasing residential greenness and air pollution control may have simultaneous effect on decreasing the risk of hypertension.

Long term exposure to air pollution and kidney parenchyma cancer – Effects of low-level air pollution: a Study in Europe (ELAPSE)

Background: Particulate matter (PM) is classified as a group 1 human carcinogen. Previous experimental studies suggest that particles in diesel exhaust induce oxidative stress, inflammation and DNA damage in kidney cells, but the evidence from population studies linking air pollution to kidney cancer is limited.Methods: We pooled six European cohorts (N = 302,493) to assess the association of residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) with cancer of the kidney parenchyma. The main exposure model was developed for year 2010. We defined kidney parenchyma cancer according to the International Classification of Diseases 9th and 10th Revision codes 189.0 and C64. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level.Results: The participants were followed from baseline (1985–2005) to 2011–2015. A total of 847 cases occurred during 5,497,514 person-years of follow-up (average 18.2 years). Median (5–95%) exposure levels of NO2, PM2.5, BC and O3 were 24.1 μg/m3 (12.8–39.2), 15.3 μg/m3 (8.6–19.2), 1.6 10−5 m−1 (0.7–2.1), and 87.0 μg/m3 (70.3–97.4), respectively. The results of the fully adjusted linear analyses showed a hazard ratio (HR) of 1.03 (95% confidence interval [CI]: 0.92, 1.15) per 10 μg/m³ NO2, 1.04 (95% CI: 0.88, 1.21) per 5 μg/m³ PM2.5, 0.99 (95% CI: 0.89, 1.11) per 0.5 10−5 m−1 BCE, and 0.88 (95% CI: 0.76, 1.02) per 10 μg/m³ O3. We did not find associations between any of the elemental components of PM2.5 and cancer of the kidney parenchyma.Conclusion: We did not observe an association between long-term ambient air pollution exposure and incidence of kidney parenchyma cancer.

Investigation on associations between long-term air pollution exposure and osteoporotic fracture using nationwide cohort study data in South Korea

BACKGROUND AND AIM Bone health is a major concern for aging populations globally. Human and animal studies have suggested biological mechanisms for osteoporosis and bone density associated with air pollution, but less is known about the impacts of air pollution on osteoporotic fracture. We examined the associations between long-term air pollution exposure and risk of osteoporotic fracture in adults in seven large Korean cities. METHODS We used Cox proportional hazard models to estimate hazard rations (HRs) of time-varying moving window of past exposures of particulate matter (PM₁₀), sulfur dioxide (SO₂), carbon monoxide (CO), nitrogen dioxide (NO₂), and ozone (O₃) for osteoporotic fracture in Korean adults (age &amp;#x2265;50 years) in the National Health Insurance Service-National Sample Cohort data, followed 2002 to 2015. HRs were calculated for an interquartile range (IQR) increase of 3-year moving average concentration of each pollutant. Data of 56,467 participants over 535,481 person-years of follow-up were used. The model adjusted for individual-level confounders (comorbidity, prescription for osteoporosis, age, sex, body mass index, health behaviors, income). RESULTS Linear and positive exposure-response associations were found for SO₂, while PM₁₀ and NO₂ showed nonlinear associations. SO₂ was associated with osteoporosis-related fracture with marginal significance (HR for an IQR [2 ppb] increase = 1.04, 95% CI: 1.00–1.09). The SO₂ HR estimates were robust in analyses applying various moving windows of exposure (from one to three years of past exposure) and two-pollutant models. The O₃ HR estimate was positive but not significant (HR for 0.007 ppm increase = 1.01, 95% CI: 0.97–1.06). PM₁₀, CO, and NO₂ did not show associations. Vulnerable groups by sex, age, exercise, and income varied across air pollutants and there was no evidence of effect modifications. CONCLUSIONS Long-term exposure to SO₂ was associated with increased osteoporotic fracture risks in Korean adults. KEYWORDS Air pollution, bone fracture, cohort studies, osteoporosis.

Long-Term Air Pollution Exposure and Loss of Independence in the U.S.

Long-Term Air Pollution Exposure and Loss of Independence in the U.S.

Long-term air pollution exposure and diabetes risk in American older adults: a national cohort study

Long-term air pollution exposure and diabetes risk in American older adults: a national cohort study

Residential greenness, air pollution, and incident ischemic heart disease: A prospective cohort study in China

Background and aim: Green living environments are associated with beneficial health outcomes, whereas higher air pollution exposure might increase the risk of chronic diseases. Moreover, few studies have explored the interaction between residential greenness and air pollution on the risk of ischemic heart disease (IHD). Therefore we aimed to estimate the associations of residential greenness and air pollution with IHD and their interaction. Methods: We performed a prospective cohort study that included 29,141 adult participants recruited from Yinzhou District, Ningbo, China. Normalized Difference Vegetation Index (NDVI) around each participant’s residence was calculated to measure residential greenness exposure. Land-use regression models were conducted to estimate long-term individual exposure to air pollutants, including nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters &amp;#x2264; 2.5 &amp;#x3bc;m (PM2.5) and &amp;#x2264;10 &amp;#x3bc;m (PM10). Cox proportional hazard models were used to calculate the hazard ratios (HRs) and 95% confidence intervals (95% CIs) for the association of residential greenness and air pollutants with the risk of incident IHD. Results: During 101,172.5 person-years of follow-up, 1,392 incident IHD cases were reported in the study population. Residential greenness, expressed as an interquartile range (IQR) increase in NDVI within 300m, was inversely associated with incident IHD. However, long-term air pollution exposures were associated with higher IHD incidence. Mediation analyses suggested that the beneficial effect of residential greenness on incident IHD could be partly mediated by reducing the exposure to PM2.5. Conclusion: Higher greenness was associated with decreased risk of IHD, while air pollutants were positively associated with incident IHD. Meanwhile, residential greenness may decrease the risk of IHD by reducing PM2.5 exposure. Keywords: Residential greenness; Air pollution; Ischemic heart disease; Cohort study; Effect mediation

Associations between long-term air pollution exposure and physical function in older adults

Associations between long-term air pollution exposure and physical function in older adults

Long-term Air Pollution Exposure on COVID-19 Risk and Severity

Since the emergence of the COVID-19 pandemic, long-term exposure to air pollution has emerged as a possible risk factor for increased COVID-19 disease risk, severity, and mortality. The objective of this study was to examine the association between COVID-19 and long-term exposure to air pollution. This retrospective cohort study included patients who had a COVID-19 test at the University of Chicago Medicine Center from March 18, 2020, to March 30, 2021. Air pollution exposure was assessed using models developed for Chicago by the MESA Air Study and data from the Environmental Protection Agency’s EJSCREEN. Air pollution exposure estimates were linked to the University of Chicago Medicine patients using residential addresses. Air pollution measurements included PM2.5 (MESA Air and EPA), NO2, diesel PM, the respiratory hazard index, traffic proximity, and ozone. The outcome was COVID-19 risk and severity (ICU admission). Mixed effect analyses were performed to test whether poor air quality status was associated with COVID-19 risk and severity, controlling for demographic, smoking, and comorbidity indicators collected from the medical records. A total of 74,004 patients (mean [SD] age 44.0 [22.51] years; 42,979 [58.09%] women; and 32,870 [49.09%] African Americans) were linked to air quality exposure based on residence and other covariates using electronic medical record data in addition to COVID-19 test results. Overall, 8,463 participants (11.4%) tested positive for COVID-19. In the mixed effect analysis, long-term PM2.5 exposure was associated with increased risk of testing positive for COVID-19 (odds ratio [OR], 1.30; 95% CI, 1.23-1.38; P &amp;#x3c;0.01) and increased severity from COVID-19 (OR= 2.28; 95% CI, 2.00-2.60; P = &amp;#x3c;0.01). The results of this retrospective cohort study provide some evidence of the effect of long-term air pollution exposure on COVID-19 risk and severity.

Long-term exposure to air pollution, cause-specific mortality and incidence of stroke and acute coronary heart disease in the Rome Longitudinal Study: the BIGEPI project

Background and Aim Long-term air pollution exposure increases cause-specific mortality and incidence of cardiovascular diseases. Within the BIGEPI project, we aimed to investigate the association between long-term exposure to air pollutants, cause-specific mortality, incidence of coronary heart diseases and stroke in 6 large Italian administrative cohorts. We report preliminary results for Rome. Methods We enrolled 1,739,277 adults from the Rome Longitudinal Study at 2011 census, and followed them up until 2018. We analysed natural, cardiovascular and respiratory mortality, stroke and acute coronary heart disease (CHD) incidence. We assigned annual mean concentrations of particular matter &amp;#x3c;10 &amp;#x3bc;m (PM₁₀), PM &amp;#x3c;2.5 &amp;#x3bc;m (PM₂.₅), nitrogen dioxide (NO₂) and warm-season ozone (warm-O₃) at baseline residential addresses from satellite-based spatiotemporal models. We applied Cox proportional hazards models adjusted for individual and area-level covariates, in single- and two-exposure models. We investigated effect modification by age, sex, educational level, employment status and socioeconomic deprivation index. Results We observed 167,300 deaths from natural causes (62,368 cardiovascular, 12,286 respiratory), 42,241 CHD incident cases and 24,835 cases of incident stroke. PM₂.₅ was positively associated with natural, cardiovascular, respiratory mortality and stroke incidence: interquartile range (IQR) increases of 1.69 &amp;#x3bc;g/m³ were associated with hazard ratios (HR) of 1.007 (95% confidence interval: 1.000-1.014), 1.018 (1.006-1.030), 1.028 (1.001-1.056) and 1.025 (1.007-1.044), respectively. We found positive associations between NO₂ and cardiovascular mortality (HR=1.021; 1.007-1.034 per IQR=11.53 &amp;#x3bc;g/m³) and between warm-O₃ and CHD incidence (HR=1.024; 1.011-1.037 per 3.57 &amp;#x3bc;g/m³). Associations tended to attenuate in two-exposure models. The effects were stronger for females and in the age group 30-64 years, with no major differences by individual or area-level socioeconomic indicators. Conclusions We estimated consistent associations between long-term air pollution exposure and cause-specific mortality and CVD incidence. Similar analyses will be conducted in other 5 administrative cohorts. Keywords: air pollution, cause-specific mortality, stroke, acute coronary heart disease.

Effects of short- and long-term air pollution exposure on the course of idiopathic pulmonary fibrosis

Effects of short- and long-term air pollution exposure on the course of idiopathic pulmonary fibrosis

Long-term air pollution exposure and the incidence of cardiovascular diseases among American elderly population

Long-term air pollution exposure and the incidence of cardiovascular diseases among American elderly population

Road traffic noise and incidence of primary hypertension: a prospective analysis in UK Biobank

BACKGROUND AND AIM The quality of evidence regarding the associations between road traffic noise and hypertension is low due to the limitations of cross-sectional study design, with the role of air pollution remains to be further clarified. To evaluate associations of long-term road traffic noise and air pollution exposure with incident primary hypertension, we conducted a prospective population-based analysis in UK Biobank. METHODS Road traffic noise was estimated at baseline residential address using the Common Noise Assessment Method model. Incident primary hypertension (ICD 10: I10) was ascertained through linkage with medical records for ~250 000 participants. Cox proportional hazard models were used to estimate hazard ratios (HRs) for association between road traffic noise and incident primary hypertension, adjusting for covariates determined via directed acyclic graph. RESULTS During a median of 8.1 years follow up, 21 185 incident primary hypertension cases were ascertained. The HR for a 10 dB[A] increase in mean weighted average 24-h road traffic noise level (Lden) exposure was 1.08 [95% confidence interval (CI) 1.02, 1.14]. A dose-response relationship was found, with HRs of 1.14 (95% CI: 1.04, 1.26) for Lden &amp;#x3e; 65dB[A] vs. &amp;#x2264; 55dB[A] (P trend &amp;#x3c;0.05), and HRs of 1.15 (95% CI: 1.04, 1.26) for night-time road traffic noise (Lnight)&amp;#x3e;55 dB[A] vs. &amp;#x2264; 45dB[A] (P trend &amp;#x3c;0.05). The associations were all robust to adjustment for fine particulate matter (PM2.5) and nitrogen dioxide (NO2). Furthermore, the highest incident hypertension risk was seen in the group who were exposed to the highest level of both road traffic noise and air pollution. CONCLUSIONS Long-term exposure to road traffic noise was associated with increased incidence of primary hypertension, and the effect estimates were greater in those with higher air pollution exposure. KEYWORDS road traffic noise; air pollution; primary hypertension; prospective analysis

Association between long-term ambient air pollution exposure and handgrip strength change in the French CONSTANCES cohort

Association between long-term ambient air pollution exposure and handgrip strength change in the French CONSTANCES cohort